---
_id: '999'
abstract:
- lang: eng
  text: 'In multi-task learning, a learner is given a collection of prediction tasks
    and needs to solve all of them. In contrast to previous work, which required that
    annotated training data must be available for all tasks, we consider a new setting,
    in which for some tasks, potentially most of them, only unlabeled training data
    is provided. Consequently, to solve all tasks, information must be transferred
    between tasks with labels and tasks without labels. Focusing on an instance-based
    transfer method we analyze two variants of this setting: when the set of labeled
    tasks is fixed, and when it can be actively selected by the learner. We state
    and prove a generalization bound that covers both scenarios and derive from it
    an algorithm for making the choice of labeled tasks (in the active case) and for
    transferring information between the tasks in a principled way. We also illustrate
    the effectiveness of the algorithm on synthetic and real data. '
alternative_title:
- PMLR
article_processing_charge: No
arxiv: 1
author:
- first_name: Anastasia
  full_name: Pentina, Anastasia
  id: 42E87FC6-F248-11E8-B48F-1D18A9856A87
  last_name: Pentina
- first_name: Christoph
  full_name: Lampert, Christoph
  id: 40C20FD2-F248-11E8-B48F-1D18A9856A87
  last_name: Lampert
  orcid: 0000-0001-8622-7887
citation:
  ama: 'Pentina A, Lampert C. Multi-task learning with labeled and unlabeled tasks.
    In: Vol 70. ML Research Press; 2017:2807-2816.'
  apa: 'Pentina, A., &#38; Lampert, C. (2017). Multi-task learning with labeled and
    unlabeled tasks (Vol. 70, pp. 2807–2816). Presented at the ICML: International
    Conference on Machine Learning, Sydney, Australia: ML Research Press.'
  chicago: Pentina, Anastasia, and Christoph Lampert. “Multi-Task Learning with Labeled
    and Unlabeled Tasks,” 70:2807–16. ML Research Press, 2017.
  ieee: 'A. Pentina and C. Lampert, “Multi-task learning with labeled and unlabeled
    tasks,” presented at the ICML: International Conference on Machine Learning, Sydney,
    Australia, 2017, vol. 70, pp. 2807–2816.'
  ista: 'Pentina A, Lampert C. 2017. Multi-task learning with labeled and unlabeled
    tasks. ICML: International Conference on Machine Learning, PMLR, vol. 70, 2807–2816.'
  mla: Pentina, Anastasia, and Christoph Lampert. <i>Multi-Task Learning with Labeled
    and Unlabeled Tasks</i>. Vol. 70, ML Research Press, 2017, pp. 2807–16.
  short: A. Pentina, C. Lampert, in:, ML Research Press, 2017, pp. 2807–2816.
conference:
  end_date: 2017-08-11
  location: Sydney, Australia
  name: 'ICML: International Conference on Machine Learning'
  start_date: 2017-08-06
corr_author: '1'
date_created: 2018-12-11T11:49:37Z
date_published: 2017-06-08T00:00:00Z
date_updated: 2025-06-04T08:19:03Z
day: '08'
department:
- _id: ChLa
ec_funded: 1
external_id:
  arxiv:
  - '1602.06518'
  isi:
  - '000683309502093'
intvolume: '        70'
isi: 1
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://arxiv.org/abs/1602.06518
month: '06'
oa: 1
oa_version: Submitted Version
page: 2807 - 2816
project:
- _id: 2532554C-B435-11E9-9278-68D0E5697425
  call_identifier: FP7
  grant_number: '308036'
  name: Lifelong Learning of Visual Scene Understanding
publication_identifier:
  isbn:
  - '9781510855144'
publication_status: published
publisher: ML Research Press
publist_id: '6399'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Multi-task learning with labeled and unlabeled tasks
type: conference
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 70
year: '2017'
...
---
OA_place: repository
OA_type: green
_id: '22071'
abstract:
- lang: eng
  text: "We consider the cubic–quintic nonlinear Schrödinger equation: (mathematical
    formular)\r\nIn the first part of the paper, we analyze the one-parameter family
    of ground state solitons associated to this equation with particular attention
    to the shape of the associated mass/energy curve. Additionally, we are able to
    characterize the kernel of the linearized operator about such solitons and to
    demonstrate that they occur as optimizers for a one-parameter family of inequalities
    of Gagliardo–Nirenberg type. Building on this work, in the latter part of the
    paper we prove that scattering holds for solutions belonging to the region R of
    the mass/energy plane where the virial is positive. We show that this region is
    partially bounded by solitons also by rescalings of solitons (which are not soliton
    solutions in their own right). The discovery of rescaled solitons in this context
    is new and highlights an unexpected limitation of any virial-based methodology."
article_processing_charge: No
article_type: original
arxiv: 1
author:
- first_name: Rowan
  full_name: Killip, Rowan
  last_name: Killip
- first_name: Tadahiro
  full_name: Oh, Tadahiro
  last_name: Oh
- first_name: Oana
  full_name: Pocovnicu, Oana
  last_name: Pocovnicu
- first_name: Monica
  full_name: Visan, Monica
  id: 056daca0-b8d1-11f0-964f-f91054abf8ca
  last_name: Visan
citation:
  ama: Killip R, Oh T, Pocovnicu O, Vişan M. Solitons and scattering for the cubic-quintic
    nonlinear Schrödinger equation on R^3. <i>Archive for Rational Mechanics and Analysis</i>.
    2017;225:469-548. doi:<a href="https://doi.org/10.1007/s00205-017-1109-0">10.1007/s00205-017-1109-0</a>
  apa: Killip, R., Oh, T., Pocovnicu, O., &#38; Vişan, M. (2017). Solitons and scattering
    for the cubic-quintic nonlinear Schrödinger equation on R^3. <i>Archive for Rational
    Mechanics and Analysis</i>. Springer Nature. <a href="https://doi.org/10.1007/s00205-017-1109-0">https://doi.org/10.1007/s00205-017-1109-0</a>
  chicago: Killip, Rowan, Tadahiro Oh, Oana Pocovnicu, and Monica Vişan. “Solitons
    and Scattering for the Cubic-Quintic Nonlinear Schrödinger Equation on R^3.” <i>Archive
    for Rational Mechanics and Analysis</i>. Springer Nature, 2017. <a href="https://doi.org/10.1007/s00205-017-1109-0">https://doi.org/10.1007/s00205-017-1109-0</a>.
  ieee: R. Killip, T. Oh, O. Pocovnicu, and M. Vişan, “Solitons and scattering for
    the cubic-quintic nonlinear Schrödinger equation on R^3,” <i>Archive for Rational
    Mechanics and Analysis</i>, vol. 225. Springer Nature, pp. 469–548, 2017.
  ista: Killip R, Oh T, Pocovnicu O, Vişan M. 2017. Solitons and scattering for the
    cubic-quintic nonlinear Schrödinger equation on R^3. Archive for Rational Mechanics
    and Analysis. 225, 469–548.
  mla: Killip, Rowan, et al. “Solitons and Scattering for the Cubic-Quintic Nonlinear
    Schrödinger Equation on R^3.” <i>Archive for Rational Mechanics and Analysis</i>,
    vol. 225, Springer Nature, 2017, pp. 469–548, doi:<a href="https://doi.org/10.1007/s00205-017-1109-0">10.1007/s00205-017-1109-0</a>.
  short: R. Killip, T. Oh, O. Pocovnicu, M. Vişan, Archive for Rational Mechanics
    and Analysis 225 (2017) 469–548.
date_created: 2026-06-19T08:21:38Z
date_published: 2017-07-01T00:00:00Z
date_updated: 2026-06-30T10:52:12Z
day: '01'
doi: 10.1007/s00205-017-1109-0
extern: '1'
external_id:
  arxiv:
  - '1409.6734'
intvolume: '       225'
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://doi.org/10.48550/arXiv.1409.6734
month: '07'
oa: 1
oa_version: Preprint
page: 469-548
publication: Archive for Rational Mechanics and Analysis
publication_identifier:
  eissn:
  - 1432-0673
  issn:
  - 0003-9527
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
scopus_import: '1'
status: public
title: Solitons and scattering for the cubic-quintic nonlinear Schrödinger equation
  on R^3
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 225
year: '2017'
...
---
_id: '704'
abstract:
- lang: eng
  text: 'How the organization of genes on a chromosome shapes adaptation is essential
    for understanding evolutionary paths. Here, we investigate how adaptation to rapidly
    increasing levels of antibiotic depends on the chromosomal neighborhood of a drug-resistance
    gene inserted at different positions of the Escherichia coli chromosome. Using
    a dual-fluorescence reporter that allows us to distinguish gene amplifications
    from other up-mutations, we track in real-time adaptive changes in expression
    of the drug-resistance gene. We find that the relative contribution of several
    mutation types differs systematically between loci due to properties of neighboring
    genes: essentiality, expression, orientation, termination, and presence of duplicates.
    These properties determine rate and fitness effects of gene amplification, deletions,
    and mutations compromising transcriptional termination. Thus, the adaptive potential
    of a gene under selection is a system-property with a complex genetic basis that
    is specific for each chromosomal locus, and it can be inferred from detailed functional
    and genomic data.'
article_number: e25100
article_processing_charge: No
author:
- first_name: Magdalena
  full_name: Steinrück, Magdalena
  id: 2C023F40-F248-11E8-B48F-1D18A9856A87
  last_name: Steinrück
  orcid: 0000-0003-1229-9719
- first_name: Calin C
  full_name: Guet, Calin C
  id: 47F8433E-F248-11E8-B48F-1D18A9856A87
  last_name: Guet
  orcid: 0000-0001-6220-2052
citation:
  ama: Steinrück M, Guet CC. Complex chromosomal neighborhood effects determine the
    adaptive potential of a gene under selection. <i>eLife</i>. 2017;6. doi:<a href="https://doi.org/10.7554/eLife.25100">10.7554/eLife.25100</a>
  apa: Steinrück, M., &#38; Guet, C. C. (2017). Complex chromosomal neighborhood effects
    determine the adaptive potential of a gene under selection. <i>ELife</i>. eLife
    Sciences Publications. <a href="https://doi.org/10.7554/eLife.25100">https://doi.org/10.7554/eLife.25100</a>
  chicago: Steinrück, Magdalena, and Calin C Guet. “Complex Chromosomal Neighborhood
    Effects Determine the Adaptive Potential of a Gene under Selection.” <i>ELife</i>.
    eLife Sciences Publications, 2017. <a href="https://doi.org/10.7554/eLife.25100">https://doi.org/10.7554/eLife.25100</a>.
  ieee: M. Steinrück and C. C. Guet, “Complex chromosomal neighborhood effects determine
    the adaptive potential of a gene under selection,” <i>eLife</i>, vol. 6. eLife
    Sciences Publications, 2017.
  ista: Steinrück M, Guet CC. 2017. Complex chromosomal neighborhood effects determine
    the adaptive potential of a gene under selection. eLife. 6, e25100.
  mla: Steinrück, Magdalena, and Calin C. Guet. “Complex Chromosomal Neighborhood
    Effects Determine the Adaptive Potential of a Gene under Selection.” <i>ELife</i>,
    vol. 6, e25100, eLife Sciences Publications, 2017, doi:<a href="https://doi.org/10.7554/eLife.25100">10.7554/eLife.25100</a>.
  short: M. Steinrück, C.C. Guet, ELife 6 (2017).
corr_author: '1'
date_created: 2018-12-11T11:48:01Z
date_published: 2017-07-25T00:00:00Z
date_updated: 2026-06-30T22:30:12Z
day: '25'
ddc:
- '576'
department:
- _id: CaGu
doi: 10.7554/eLife.25100
external_id:
  isi:
  - '000406183700001'
file:
- access_level: open_access
  checksum: 6b908b5db9f61f6820ebd7f8fa815571
  content_type: application/pdf
  creator: system
  date_created: 2018-12-12T10:12:54Z
  date_updated: 2020-07-14T12:47:48Z
  file_id: '4975'
  file_name: IST-2017-890-v1+1_elife-25100-v1.pdf
  file_size: 2092088
  relation: main_file
- access_level: open_access
  checksum: ca21530389b720243552678125fdba35
  content_type: application/pdf
  creator: system
  date_created: 2018-12-12T10:12:55Z
  date_updated: 2020-07-14T12:47:48Z
  file_id: '4976'
  file_name: IST-2017-890-v1+2_elife-25100-figures-v1.pdf
  file_size: 3428681
  relation: main_file
file_date_updated: 2020-07-14T12:47:48Z
has_accepted_license: '1'
intvolume: '         6'
isi: 1
language:
- iso: eng
month: '07'
oa: 1
oa_version: Published Version
publication: eLife
publication_identifier:
  issn:
  - 2050-084X
publication_status: published
publisher: eLife Sciences Publications
publist_id: '6990'
pubrep_id: '890'
quality_controlled: '1'
related_material:
  record:
  - id: '5564'
    relation: popular_science
    status: public
  - id: '26'
    relation: dissertation_contains
    status: public
scopus_import: '1'
status: public
title: Complex chromosomal neighborhood effects determine the adaptive potential of
  a gene under selection
tmp:
  image: /images/cc_by.png
  legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
  name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
  short: CC BY (4.0)
type: journal_article
user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 6
year: '2017'
...
---
_id: '679'
abstract:
- lang: eng
  text: Protective responses against pathogens require a rapid mobilization of resting
    neutrophils and the timely removal of activated ones. Neutrophils are exceptionally
    short-lived leukocytes, yet it remains unclear whether the lifespan of pathogen-engaged
    neutrophils is regulated differently from that in the circulating steady-state
    pool. Here, we have found that under homeostatic conditions, the mRNA-destabilizing
    protein tristetraprolin (TTP) regulates apoptosis and the numbers of activated
    infiltrating murine neutrophils but not neutrophil cellularity. Activated TTP-deficient
    neutrophils exhibited decreased apoptosis and enhanced accumulation at the infection
    site. In the context of myeloid-specific deletion of Ttp, the potentiation of
    neutrophil deployment protected mice against lethal soft tissue infection with
    Streptococcus pyogenes and prevented bacterial dissemination. Neutrophil transcriptome
    analysis revealed that decreased apoptosis of TTP-deficient neutrophils was specifically
    associated with elevated expression of myeloid cell leukemia 1 (Mcl1) but not
    other antiapoptotic B cell leukemia/ lymphoma 2 (Bcl2) family members. Higher
    Mcl1 expression resulted from stabilization of Mcl1 mRNA in the absence of TTP.
    The low apoptosis rate of infiltrating TTP-deficient neutrophils was comparable
    to that of transgenic Mcl1-overexpressing neutrophils. Our study demonstrates
    that posttranscriptional gene regulation by TTP schedules the termination of the
    antimicrobial engagement of neutrophils. The balancing role of TTP comes at the
    cost of an increased risk of bacterial infections.
acknowledgement: This work was supported by grants from the Austrian Science Fund
  (FWF) (P27538-B21, I1621-B22, and SFB 43, to PK); by funding from the European Union
  Seventh Framework Programme Marie Curie Initial Training Networks (FP7-PEOPLE-2012-ITN)
  for the project INBIONET (INfection BIOlogy Training NETwork under grant agreement
  PITN-GA-2012-316682; and by a joint research cluster initiative of the University
  of Vienna and the Medical University of Vienna.
article_processing_charge: No
author:
- first_name: Florian
  full_name: Ebner, Florian
  last_name: Ebner
- first_name: Vitaly
  full_name: Sedlyarov, Vitaly
  last_name: Sedlyarov
- first_name: Saren
  full_name: Tasciyan, Saren
  id: 4323B49C-F248-11E8-B48F-1D18A9856A87
  last_name: Tasciyan
  orcid: 0000-0003-1671-393X
- first_name: Masa
  full_name: Ivin, Masa
  last_name: Ivin
- first_name: Franz
  full_name: Kratochvill, Franz
  last_name: Kratochvill
- first_name: Nina
  full_name: Gratz, Nina
  last_name: Gratz
- first_name: Lukas
  full_name: Kenner, Lukas
  last_name: Kenner
- first_name: Andreas
  full_name: Villunger, Andreas
  last_name: Villunger
- first_name: Michael K
  full_name: Sixt, Michael K
  id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
  last_name: Sixt
  orcid: 0000-0002-6620-9179
- first_name: Pavel
  full_name: Kovarik, Pavel
  last_name: Kovarik
citation:
  ama: Ebner F, Sedlyarov V, Tasciyan S, et al. The RNA-binding protein tristetraprolin
    schedules apoptosis of pathogen-engaged neutrophils during bacterial infection.
    <i>The Journal of Clinical Investigation</i>. 2017;127(6):2051-2065. doi:<a href="https://doi.org/10.1172/JCI80631">10.1172/JCI80631</a>
  apa: Ebner, F., Sedlyarov, V., Tasciyan, S., Ivin, M., Kratochvill, F., Gratz, N.,
    … Kovarik, P. (2017). The RNA-binding protein tristetraprolin schedules apoptosis
    of pathogen-engaged neutrophils during bacterial infection. <i>The Journal of
    Clinical Investigation</i>. American Society for Clinical Investigation. <a href="https://doi.org/10.1172/JCI80631">https://doi.org/10.1172/JCI80631</a>
  chicago: Ebner, Florian, Vitaly Sedlyarov, Saren Tasciyan, Masa Ivin, Franz Kratochvill,
    Nina Gratz, Lukas Kenner, Andreas Villunger, Michael K Sixt, and Pavel Kovarik.
    “The RNA-Binding Protein Tristetraprolin Schedules Apoptosis of Pathogen-Engaged
    Neutrophils during Bacterial Infection.” <i>The Journal of Clinical Investigation</i>.
    American Society for Clinical Investigation, 2017. <a href="https://doi.org/10.1172/JCI80631">https://doi.org/10.1172/JCI80631</a>.
  ieee: F. Ebner <i>et al.</i>, “The RNA-binding protein tristetraprolin schedules
    apoptosis of pathogen-engaged neutrophils during bacterial infection,” <i>The
    Journal of Clinical Investigation</i>, vol. 127, no. 6. American Society for Clinical
    Investigation, pp. 2051–2065, 2017.
  ista: Ebner F, Sedlyarov V, Tasciyan S, Ivin M, Kratochvill F, Gratz N, Kenner L,
    Villunger A, Sixt MK, Kovarik P. 2017. The RNA-binding protein tristetraprolin
    schedules apoptosis of pathogen-engaged neutrophils during bacterial infection.
    The Journal of Clinical Investigation. 127(6), 2051–2065.
  mla: Ebner, Florian, et al. “The RNA-Binding Protein Tristetraprolin Schedules Apoptosis
    of Pathogen-Engaged Neutrophils during Bacterial Infection.” <i>The Journal of
    Clinical Investigation</i>, vol. 127, no. 6, American Society for Clinical Investigation,
    2017, pp. 2051–65, doi:<a href="https://doi.org/10.1172/JCI80631">10.1172/JCI80631</a>.
  short: F. Ebner, V. Sedlyarov, S. Tasciyan, M. Ivin, F. Kratochvill, N. Gratz, L.
    Kenner, A. Villunger, M.K. Sixt, P. Kovarik, The Journal of Clinical Investigation
    127 (2017) 2051–2065.
date_created: 2018-12-11T11:47:53Z
date_published: 2017-06-01T00:00:00Z
date_updated: 2026-06-30T22:30:14Z
day: '01'
department:
- _id: MiSi
doi: 10.1172/JCI80631
external_id:
  isi:
  - '000402620800008'
  pmid:
  - '28504646'
intvolume: '       127'
isi: 1
issue: '6'
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5451238/
month: '06'
oa: 1
oa_version: Submitted Version
page: 2051 - 2065
pmid: 1
project:
- _id: 25985A36-B435-11E9-9278-68D0E5697425
  call_identifier: FWF
  grant_number: T00817-B21
  name: The biochemical basis of PAR polarization
- _id: 25E9AF9E-B435-11E9-9278-68D0E5697425
  call_identifier: FWF
  grant_number: P27201-B22
  name: Revealing the mechanisms underlying drug interactions
publication: The Journal of Clinical Investigation
publication_identifier:
  issn:
  - 0021-9738
publication_status: published
publisher: American Society for Clinical Investigation
publist_id: '7038'
quality_controlled: '1'
related_material:
  record:
  - id: '12401'
    relation: dissertation_contains
    status: public
scopus_import: '1'
status: public
title: The RNA-binding protein tristetraprolin schedules apoptosis of pathogen-engaged
  neutrophils during bacterial infection
type: journal_article
user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 127
year: '2017'
...
---
_id: '682'
abstract:
- lang: eng
  text: Left-right asymmetry is a fundamental feature of higher-order brain structure;
    however, the molecular basis of brain asymmetry remains unclear. We recently identified
    structural and functional asymmetries in mouse hippocampal circuitry that result
    from the asymmetrical distribution of two distinct populations of pyramidal cell
    synapses that differ in the density of the NMDA receptor subunit GluRε2 (also
    known as NR2B, GRIN2B or GluN2B). By examining the synaptic distribution of ε2
    subunits, we previously found that β2-microglobulin-deficient mice, which lack
    cell surface expression of the vast majority of major histocompatibility complex
    class I (MHCI) proteins, do not exhibit circuit asymmetry. In the present study,
    we conducted electrophysiological and anatomical analyses on the hippocampal circuitry
    of mice with a knockout of the paired immunoglobulin-like receptor B (PirB), an
    MHCI receptor. As in β2-microglobulin-deficient mice, the PirB-deficient hippocampus
    lacked circuit asymmetries. This finding that MHCI loss-of-function mice and PirB
    knockout mice have identical phenotypes suggests that MHCI signals that produce
    hippocampal asymmetries are transduced through PirB. Our results provide evidence
    for a critical role of the MHCI/PirB signaling system in the generation of asymmetries
    in hippocampal circuitry.
article_number: e0179377
article_processing_charge: No
article_type: original
author:
- first_name: Hikari
  full_name: Ukai, Hikari
  last_name: Ukai
- first_name: Aiko
  full_name: Kawahara, Aiko
  last_name: Kawahara
- first_name: Keiko
  full_name: Hirayama, Keiko
  last_name: Hirayama
- first_name: Matthew J
  full_name: Case, Matthew J
  id: 44B7CA5A-F248-11E8-B48F-1D18A9856A87
  last_name: Case
- first_name: Shotaro
  full_name: Aino, Shotaro
  last_name: Aino
- first_name: Masahiro
  full_name: Miyabe, Masahiro
  last_name: Miyabe
- first_name: Ken
  full_name: Wakita, Ken
  last_name: Wakita
- first_name: Ryohei
  full_name: Oogi, Ryohei
  last_name: Oogi
- first_name: Michiyo
  full_name: Kasayuki, Michiyo
  last_name: Kasayuki
- first_name: Shihomi
  full_name: Kawashima, Shihomi
  last_name: Kawashima
- first_name: Shunichi
  full_name: Sugimoto, Shunichi
  last_name: Sugimoto
- first_name: Kanako
  full_name: Chikamatsu, Kanako
  last_name: Chikamatsu
- first_name: Noritaka
  full_name: Nitta, Noritaka
  last_name: Nitta
- first_name: Tsuneyuki
  full_name: Koga, Tsuneyuki
  last_name: Koga
- first_name: Ryuichi
  full_name: Shigemoto, Ryuichi
  id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
  last_name: Shigemoto
  orcid: 0000-0001-8761-9444
- first_name: Toshiyuki
  full_name: Takai, Toshiyuki
  last_name: Takai
- first_name: Isao
  full_name: Ito, Isao
  last_name: Ito
citation:
  ama: Ukai H, Kawahara A, Hirayama K, et al. PirB regulates asymmetries in hippocampal
    circuitry. <i>PLoS One</i>. 2017;12(6). doi:<a href="https://doi.org/10.1371/journal.pone.0179377">10.1371/journal.pone.0179377</a>
  apa: Ukai, H., Kawahara, A., Hirayama, K., Case, M. J., Aino, S., Miyabe, M., …
    Ito, I. (2017). PirB regulates asymmetries in hippocampal circuitry. <i>PLoS One</i>.
    Public Library of Science. <a href="https://doi.org/10.1371/journal.pone.0179377">https://doi.org/10.1371/journal.pone.0179377</a>
  chicago: Ukai, Hikari, Aiko Kawahara, Keiko Hirayama, Matthew J Case, Shotaro Aino,
    Masahiro Miyabe, Ken Wakita, et al. “PirB Regulates Asymmetries in Hippocampal
    Circuitry.” <i>PLoS One</i>. Public Library of Science, 2017. <a href="https://doi.org/10.1371/journal.pone.0179377">https://doi.org/10.1371/journal.pone.0179377</a>.
  ieee: H. Ukai <i>et al.</i>, “PirB regulates asymmetries in hippocampal circuitry,”
    <i>PLoS One</i>, vol. 12, no. 6. Public Library of Science, 2017.
  ista: Ukai H, Kawahara A, Hirayama K, Case MJ, Aino S, Miyabe M, Wakita K, Oogi
    R, Kasayuki M, Kawashima S, Sugimoto S, Chikamatsu K, Nitta N, Koga T, Shigemoto
    R, Takai T, Ito I. 2017. PirB regulates asymmetries in hippocampal circuitry.
    PLoS One. 12(6), e0179377.
  mla: Ukai, Hikari, et al. “PirB Regulates Asymmetries in Hippocampal Circuitry.”
    <i>PLoS One</i>, vol. 12, no. 6, e0179377, Public Library of Science, 2017, doi:<a
    href="https://doi.org/10.1371/journal.pone.0179377">10.1371/journal.pone.0179377</a>.
  short: H. Ukai, A. Kawahara, K. Hirayama, M.J. Case, S. Aino, M. Miyabe, K. Wakita,
    R. Oogi, M. Kasayuki, S. Kawashima, S. Sugimoto, K. Chikamatsu, N. Nitta, T. Koga,
    R. Shigemoto, T. Takai, I. Ito, PLoS One 12 (2017).
date_created: 2018-12-11T11:47:54Z
date_published: 2017-06-01T00:00:00Z
date_updated: 2026-06-30T22:30:36Z
day: '01'
ddc:
- '571'
department:
- _id: RySh
doi: 10.1371/journal.pone.0179377
external_id:
  isi:
  - '000402923200125'
file:
- access_level: open_access
  checksum: 24dd19c46fb1c761b0bcbbcd1025a3a8
  content_type: application/pdf
  creator: system
  date_created: 2018-12-12T10:12:16Z
  date_updated: 2020-07-14T12:47:40Z
  file_id: '4934'
  file_name: IST-2017-897-v1+1_journal.pone.0179377.pdf
  file_size: 5798454
  relation: main_file
file_date_updated: 2020-07-14T12:47:40Z
has_accepted_license: '1'
intvolume: '        12'
isi: 1
issue: '6'
language:
- iso: eng
month: '06'
oa: 1
oa_version: Published Version
publication: PLoS One
publication_identifier:
  issn:
  - 1932-6203
publication_status: published
publisher: Public Library of Science
publist_id: '7034'
pubrep_id: '897'
quality_controlled: '1'
related_material:
  record:
  - id: '51'
    relation: dissertation_contains
    status: public
scopus_import: '1'
status: public
title: PirB regulates asymmetries in hippocampal circuitry
tmp:
  image: /images/cc_by.png
  legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
  name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
  short: CC BY (4.0)
type: journal_article
user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 12
year: '2017'
...
---
_id: '676'
abstract:
- lang: eng
  text: The segregation of different cell types into distinct tissues is a fundamental
    process in metazoan development. Differences in cell adhesion and cortex tension
    are commonly thought to drive cell sorting by regulating tissue surface tension
    (TST). However, the role that differential TST plays in cell segregation within
    the developing embryo is as yet unclear. Here, we have analyzed the role of differential
    TST for germ layer progenitor cell segregation during zebrafish gastrulation.
    Contrary to previous observations that differential TST drives germ layer progenitor
    cell segregation in vitro, we show that germ layers display indistinguishable
    TST within the gastrulating embryo, arguing against differential TST driving germ
    layer progenitor cell segregation in vivo. We further show that the osmolarity
    of the interstitial fluid (IF) is an important factor that influences germ layer
    TST in vivo, and that lower osmolarity of the IF compared with standard cell culture
    medium can explain why germ layers display differential TST in culture but not
    in vivo. Finally, we show that directed migration of mesendoderm progenitors is
    required for germ layer progenitor cell segregation and germ layer formation.
article_processing_charge: No
article_type: original
author:
- first_name: Gabriel
  full_name: Krens, Gabriel
  id: 2B819732-F248-11E8-B48F-1D18A9856A87
  last_name: Krens
  orcid: 0000-0003-4761-5996
- first_name: Jim
  full_name: Veldhuis, Jim
  last_name: Veldhuis
- first_name: Vanessa
  full_name: Barone, Vanessa
  id: 419EECCC-F248-11E8-B48F-1D18A9856A87
  last_name: Barone
  orcid: 0000-0003-2676-3367
- first_name: Daniel
  full_name: Capek, Daniel
  id: 31C42484-F248-11E8-B48F-1D18A9856A87
  last_name: Capek
  orcid: 0000-0001-5199-9940
- first_name: Jean-Léon
  full_name: Maître, Jean-Léon
  id: 48F1E0D8-F248-11E8-B48F-1D18A9856A87
  last_name: Maître
  orcid: 0000-0002-3688-1474
- first_name: Wayne
  full_name: Brodland, Wayne
  last_name: Brodland
- first_name: Carl-Philipp J
  full_name: Heisenberg, Carl-Philipp J
  id: 39427864-F248-11E8-B48F-1D18A9856A87
  last_name: Heisenberg
  orcid: 0000-0002-0912-4566
citation:
  ama: Krens G, Veldhuis J, Barone V, et al. Interstitial fluid osmolarity modulates
    the action of differential tissue surface tension in progenitor cell segregation
    during gastrulation. <i>Development</i>. 2017;144(10):1798-1806. doi:<a href="https://doi.org/10.1242/dev.144964">10.1242/dev.144964</a>
  apa: Krens, G., Veldhuis, J., Barone, V., Capek, D., Maître, J.-L., Brodland, W.,
    &#38; Heisenberg, C.-P. J. (2017). Interstitial fluid osmolarity modulates the
    action of differential tissue surface tension in progenitor cell segregation during
    gastrulation. <i>Development</i>. Company of Biologists. <a href="https://doi.org/10.1242/dev.144964">https://doi.org/10.1242/dev.144964</a>
  chicago: Krens, Gabriel, Jim Veldhuis, Vanessa Barone, Daniel Capek, Jean-Léon Maître,
    Wayne Brodland, and Carl-Philipp J Heisenberg. “Interstitial Fluid Osmolarity
    Modulates the Action of Differential Tissue Surface Tension in Progenitor Cell
    Segregation during Gastrulation.” <i>Development</i>. Company of Biologists, 2017.
    <a href="https://doi.org/10.1242/dev.144964">https://doi.org/10.1242/dev.144964</a>.
  ieee: G. Krens <i>et al.</i>, “Interstitial fluid osmolarity modulates the action
    of differential tissue surface tension in progenitor cell segregation during gastrulation,”
    <i>Development</i>, vol. 144, no. 10. Company of Biologists, pp. 1798–1806, 2017.
  ista: Krens G, Veldhuis J, Barone V, Capek D, Maître J-L, Brodland W, Heisenberg
    C-PJ. 2017. Interstitial fluid osmolarity modulates the action of differential
    tissue surface tension in progenitor cell segregation during gastrulation. Development.
    144(10), 1798–1806.
  mla: Krens, Gabriel, et al. “Interstitial Fluid Osmolarity Modulates the Action
    of Differential Tissue Surface Tension in Progenitor Cell Segregation during Gastrulation.”
    <i>Development</i>, vol. 144, no. 10, Company of Biologists, 2017, pp. 1798–806,
    doi:<a href="https://doi.org/10.1242/dev.144964">10.1242/dev.144964</a>.
  short: G. Krens, J. Veldhuis, V. Barone, D. Capek, J.-L. Maître, W. Brodland, C.-P.J.
    Heisenberg, Development 144 (2017) 1798–1806.
corr_author: '1'
date_created: 2018-12-11T11:47:52Z
date_published: 2017-05-15T00:00:00Z
date_updated: 2026-06-30T22:30:39Z
day: '15'
ddc:
- '570'
department:
- _id: Bio
- _id: CaHe
doi: 10.1242/dev.144964
external_id:
  isi:
  - '000402275900007'
  pmid:
  - '28512197'
file:
- access_level: open_access
  checksum: bc25125fb664706cdf180e061429f91d
  content_type: application/pdf
  creator: dernst
  date_created: 2019-09-24T06:56:22Z
  date_updated: 2020-07-14T12:47:39Z
  file_id: '6905'
  file_name: 2017_Development_Krens.pdf
  file_size: 8194516
  relation: main_file
file_date_updated: 2020-07-14T12:47:39Z
has_accepted_license: '1'
intvolume: '       144'
isi: 1
issue: '10'
language:
- iso: eng
month: '05'
oa: 1
oa_version: Published Version
page: 1798 - 1806
pmid: 1
publication: Development
publication_identifier:
  issn:
  - 0950-1991
publication_status: published
publisher: Company of Biologists
publist_id: '7047'
quality_controlled: '1'
related_material:
  record:
  - id: '961'
    relation: dissertation_contains
    status: public
  - id: '50'
    relation: dissertation_contains
    status: public
scopus_import: '1'
status: public
title: Interstitial fluid osmolarity modulates the action of differential tissue surface
  tension in progenitor cell segregation during gastrulation
tmp:
  image: /images/cc_by.png
  legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
  name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
  short: CC BY (4.0)
type: journal_article
user_id: ba8df636-2132-11f1-aed0-ed93e2281fdd
volume: 144
year: '2017'
...
---
_id: '1024'
abstract:
- lang: eng
  text: The history of auxin and cytokinin biology including the initial discoveries
    by father–son duo Charles Darwin and Francis Darwin (1880), and Gottlieb Haberlandt
    (1919) is a beautiful demonstration of unceasing continuity of research. Novel
    findings are integrated into existing hypotheses and models and deepen our understanding
    of biological principles. At the same time new questions are triggered and hand
    to hand with this new methodologies are developed to address these new challenges.
alternative_title:
- Methods in Molecular Biology
article_processing_charge: No
author:
- first_name: Andrej
  full_name: Hurny, Andrej
  id: 4DC4AF46-F248-11E8-B48F-1D18A9856A87
  last_name: Hurny
  orcid: 0000-0003-3638-1426
- first_name: Eva
  full_name: Benková, Eva
  id: 38F4F166-F248-11E8-B48F-1D18A9856A87
  last_name: Benková
  orcid: 0000-0002-8510-9739
citation:
  ama: Hurny A, Benková E. Methodological advances in auxin and cytokinin biology.
    <i>Auxins and Cytokinins in Plant Biology</i>. 2017;1569:1-29. doi:<a href="https://doi.org/10.1007/978-1-4939-6831-2_1">10.1007/978-1-4939-6831-2_1</a>
  apa: Hurny, A., &#38; Benková, E. (2017). Methodological advances in auxin and cytokinin
    biology. <i>Auxins and Cytokinins in Plant Biology</i>. Springer. <a href="https://doi.org/10.1007/978-1-4939-6831-2_1">https://doi.org/10.1007/978-1-4939-6831-2_1</a>
  chicago: Hurny, Andrej, and Eva Benková. “Methodological Advances in Auxin and Cytokinin
    Biology.” <i>Auxins and Cytokinins in Plant Biology</i>. Springer, 2017. <a href="https://doi.org/10.1007/978-1-4939-6831-2_1">https://doi.org/10.1007/978-1-4939-6831-2_1</a>.
  ieee: A. Hurny and E. Benková, “Methodological advances in auxin and cytokinin biology,”
    <i>Auxins and Cytokinins in Plant Biology</i>, vol. 1569. Springer, pp. 1–29,
    2017.
  ista: Hurny A, Benková E. 2017. Methodological advances in auxin and cytokinin biology.
    Auxins and Cytokinins in Plant Biology. 1569, 1–29.
  mla: Hurny, Andrej, and Eva Benková. “Methodological Advances in Auxin and Cytokinin
    Biology.” <i>Auxins and Cytokinins in Plant Biology</i>, vol. 1569, Springer,
    2017, pp. 1–29, doi:<a href="https://doi.org/10.1007/978-1-4939-6831-2_1">10.1007/978-1-4939-6831-2_1</a>.
  short: A. Hurny, E. Benková, Auxins and Cytokinins in Plant Biology 1569 (2017)
    1–29.
corr_author: '1'
date_created: 2018-12-11T11:49:45Z
date_published: 2017-03-17T00:00:00Z
date_updated: 2026-06-30T22:30:38Z
day: '17'
ddc:
- '575'
department:
- _id: EvBe
doi: 10.1007/978-1-4939-6831-2_1
file:
- access_level: open_access
  content_type: application/pdf
  creator: system
  date_created: 2018-12-12T10:14:18Z
  date_updated: 2019-10-15T07:47:05Z
  file_id: '5068'
  file_name: IST-2018-1019-v1+1_Hurny_MethodsMolBiol_2017.pdf
  file_size: 840646
  relation: main_file
file_date_updated: 2019-10-15T07:47:05Z
has_accepted_license: '1'
intvolume: '      1569'
language:
- iso: eng
month: '03'
oa: 1
oa_version: Submitted Version
page: 1 - 29
project:
- _id: 2542D156-B435-11E9-9278-68D0E5697425
  call_identifier: FWF
  grant_number: I 1774-B16
  name: Hormone cross-talk drives nutrient dependent plant development
publication: Auxins and Cytokinins in Plant Biology
publication_identifier:
  issn:
  - 1064-3745
publication_status: published
publisher: Springer
publist_id: '6369'
pubrep_id: '1019'
quality_controlled: '1'
related_material:
  record:
  - id: '539'
    relation: dissertation_contains
    status: public
scopus_import: '1'
status: public
title: Methodological advances in auxin and cytokinin biology
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 1569
year: '2017'
...
---
_id: '696'
abstract:
- lang: eng
  text: Mutator strains are expected to evolve when the availability and effect of
    beneficial mutations are high enough to counteract the disadvantage from deleterious
    mutations that will inevitably accumulate. As the population becomes more adapted
    to its environment, both availability and effect of beneficial mutations necessarily
    decrease and mutation rates are predicted to decrease. It has been shown that
    certain molecular mechanisms can lead to increased mutation rates when the organism
    finds itself in a stressful environment. While this may be a correlated response
    to other functions, it could also be an adaptive mechanism, raising mutation rates
    only when it is most advantageous. Here, we use a mathematical model to investigate
    the plausibility of the adaptive hypothesis. We show that such a mechanism can
    be mantained if the population is subjected to diverse stresses. By simulating
    various antibiotic treatment schemes, we find that combination treatments can
    reduce the effectiveness of second-order selection on stress-induced mutagenesis.
    We discuss the implications of our results to strategies of antibiotic therapy.
article_number: e1005609
article_processing_charge: No
article_type: original
author:
- first_name: Marta
  full_name: Lukacisinova, Marta
  id: 4342E402-F248-11E8-B48F-1D18A9856A87
  last_name: Lukacisinova
  orcid: 0000-0002-2519-8004
- first_name: Sebastian
  full_name: Novak, Sebastian
  id: 461468AE-F248-11E8-B48F-1D18A9856A87
  last_name: Novak
  orcid: 0000-0002-2519-824X
- first_name: Tiago
  full_name: Paixao, Tiago
  id: 2C5658E6-F248-11E8-B48F-1D18A9856A87
  last_name: Paixao
  orcid: 0000-0003-2361-3953
citation:
  ama: 'Lukacisinova M, Novak S, Paixao T. Stress induced mutagenesis: Stress diversity
    facilitates the persistence of mutator genes. <i>PLoS Computational Biology</i>.
    2017;13(7). doi:<a href="https://doi.org/10.1371/journal.pcbi.1005609">10.1371/journal.pcbi.1005609</a>'
  apa: 'Lukacisinova, M., Novak, S., &#38; Paixao, T. (2017). Stress induced mutagenesis:
    Stress diversity facilitates the persistence of mutator genes. <i>PLoS Computational
    Biology</i>. Public Library of Science. <a href="https://doi.org/10.1371/journal.pcbi.1005609">https://doi.org/10.1371/journal.pcbi.1005609</a>'
  chicago: 'Lukacisinova, Marta, Sebastian Novak, and Tiago Paixao. “Stress Induced
    Mutagenesis: Stress Diversity Facilitates the Persistence of Mutator Genes.” <i>PLoS
    Computational Biology</i>. Public Library of Science, 2017. <a href="https://doi.org/10.1371/journal.pcbi.1005609">https://doi.org/10.1371/journal.pcbi.1005609</a>.'
  ieee: 'M. Lukacisinova, S. Novak, and T. Paixao, “Stress induced mutagenesis: Stress
    diversity facilitates the persistence of mutator genes,” <i>PLoS Computational
    Biology</i>, vol. 13, no. 7. Public Library of Science, 2017.'
  ista: 'Lukacisinova M, Novak S, Paixao T. 2017. Stress induced mutagenesis: Stress
    diversity facilitates the persistence of mutator genes. PLoS Computational Biology.
    13(7), e1005609.'
  mla: 'Lukacisinova, Marta, et al. “Stress Induced Mutagenesis: Stress Diversity
    Facilitates the Persistence of Mutator Genes.” <i>PLoS Computational Biology</i>,
    vol. 13, no. 7, e1005609, Public Library of Science, 2017, doi:<a href="https://doi.org/10.1371/journal.pcbi.1005609">10.1371/journal.pcbi.1005609</a>.'
  short: M. Lukacisinova, S. Novak, T. Paixao, PLoS Computational Biology 13 (2017).
corr_author: '1'
date_created: 2018-12-11T11:47:58Z
date_published: 2017-07-18T00:00:00Z
date_updated: 2026-06-30T22:30:40Z
day: '18'
ddc:
- '576'
department:
- _id: ToBo
- _id: NiBa
- _id: CaGu
doi: 10.1371/journal.pcbi.1005609
ec_funded: 1
external_id:
  isi:
  - '000406619800014'
file:
- access_level: open_access
  checksum: 9143c290fa6458ed2563bff4b295554a
  content_type: application/pdf
  creator: system
  date_created: 2018-12-12T10:15:01Z
  date_updated: 2020-07-14T12:47:46Z
  file_id: '5117'
  file_name: IST-2017-894-v1+1_journal.pcbi.1005609.pdf
  file_size: 3775716
  relation: main_file
file_date_updated: 2020-07-14T12:47:46Z
has_accepted_license: '1'
intvolume: '        13'
isi: 1
issue: '7'
language:
- iso: eng
month: '07'
oa: 1
oa_version: Published Version
project:
- _id: 25B1EC9E-B435-11E9-9278-68D0E5697425
  call_identifier: FP7
  grant_number: '618091'
  name: Speed of Adaptation in Population Genetics and Evolutionary Computation
publication: PLoS Computational Biology
publication_identifier:
  issn:
  - 1553-734X
publication_status: published
publisher: Public Library of Science
publist_id: '7004'
pubrep_id: '894'
quality_controlled: '1'
related_material:
  record:
  - id: '9849'
    relation: research_data
    status: public
  - id: '9850'
    relation: research_data
    status: public
  - id: '9851'
    relation: research_data
    status: public
  - id: '9852'
    relation: research_data
    status: public
  - id: '6263'
    relation: dissertation_contains
    status: public
scopus_import: '1'
status: public
title: 'Stress induced mutagenesis: Stress diversity facilitates the persistence of
  mutator genes'
tmp:
  image: /images/cc_by.png
  legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
  name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
  short: CC BY (4.0)
type: journal_article
user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 13
year: '2017'
...
---
_id: '1027'
abstract:
- lang: eng
  text: The rising prevalence of antibiotic resistant bacteria is an increasingly
    serious public health challenge. To address this problem, recent work ranging
    from clinical studies to theoretical modeling has provided valuable insights into
    the mechanisms of resistance, its emergence and spread, and ways to counteract
    it. A deeper understanding of the underlying dynamics of resistance evolution
    will require a combination of experimental and theoretical expertise from different
    disciplines and new technology for studying evolution in the laboratory. Here,
    we review recent advances in the quantitative understanding of the mechanisms
    and evolution of antibiotic resistance. We focus on key theoretical concepts and
    new technology that enables well-controlled experiments. We further highlight
    key challenges that can be met in the near future to ultimately develop effective
    strategies for combating resistance.
article_processing_charge: Yes (in subscription journal)
article_type: original
author:
- first_name: Marta
  full_name: Lukacisinova, Marta
  id: 4342E402-F248-11E8-B48F-1D18A9856A87
  last_name: Lukacisinova
  orcid: 0000-0002-2519-8004
- first_name: Mark Tobias
  full_name: Bollenbach, Mark Tobias
  id: 3E6DB97A-F248-11E8-B48F-1D18A9856A87
  last_name: Bollenbach
  orcid: 0000-0003-4398-476X
citation:
  ama: Lukacisinova M, Bollenbach MT. Toward a quantitative understanding of antibiotic
    resistance evolution. <i>Current Opinion in Biotechnology</i>. 2017;46:90-97.
    doi:<a href="https://doi.org/10.1016/j.copbio.2017.02.013">10.1016/j.copbio.2017.02.013</a>
  apa: Lukacisinova, M., &#38; Bollenbach, M. T. (2017). Toward a quantitative understanding
    of antibiotic resistance evolution. <i>Current Opinion in Biotechnology</i>. Elsevier.
    <a href="https://doi.org/10.1016/j.copbio.2017.02.013">https://doi.org/10.1016/j.copbio.2017.02.013</a>
  chicago: Lukacisinova, Marta, and Mark Tobias Bollenbach. “Toward a Quantitative
    Understanding of Antibiotic Resistance Evolution.” <i>Current Opinion in Biotechnology</i>.
    Elsevier, 2017. <a href="https://doi.org/10.1016/j.copbio.2017.02.013">https://doi.org/10.1016/j.copbio.2017.02.013</a>.
  ieee: M. Lukacisinova and M. T. Bollenbach, “Toward a quantitative understanding
    of antibiotic resistance evolution,” <i>Current Opinion in Biotechnology</i>,
    vol. 46. Elsevier, pp. 90–97, 2017.
  ista: Lukacisinova M, Bollenbach MT. 2017. Toward a quantitative understanding of
    antibiotic resistance evolution. Current Opinion in Biotechnology. 46, 90–97.
  mla: Lukacisinova, Marta, and Mark Tobias Bollenbach. “Toward a Quantitative Understanding
    of Antibiotic Resistance Evolution.” <i>Current Opinion in Biotechnology</i>,
    vol. 46, Elsevier, 2017, pp. 90–97, doi:<a href="https://doi.org/10.1016/j.copbio.2017.02.013">10.1016/j.copbio.2017.02.013</a>.
  short: M. Lukacisinova, M.T. Bollenbach, Current Opinion in Biotechnology 46 (2017)
    90–97.
corr_author: '1'
date_created: 2018-12-11T11:49:45Z
date_published: 2017-08-01T00:00:00Z
date_updated: 2026-06-30T22:30:40Z
day: '01'
ddc:
- '570'
department:
- _id: ToBo
doi: 10.1016/j.copbio.2017.02.013
ec_funded: 1
external_id:
  isi:
  - '000408077400015'
file:
- access_level: open_access
  content_type: application/pdf
  creator: dernst
  date_created: 2019-01-18T09:57:57Z
  date_updated: 2019-01-18T09:57:57Z
  file_id: '5846'
  file_name: 2017_CurrentOpinion_Lukaciinova.pdf
  file_size: 858338
  relation: main_file
  success: 1
file_date_updated: 2019-01-18T09:57:57Z
has_accepted_license: '1'
intvolume: '        46'
isi: 1
language:
- iso: eng
month: '08'
oa: 1
oa_version: Published Version
page: 90 - 97
project:
- _id: 25E9AF9E-B435-11E9-9278-68D0E5697425
  call_identifier: FWF
  grant_number: P27201-B22
  name: Revealing the mechanisms underlying drug interactions
- _id: 25E83C2C-B435-11E9-9278-68D0E5697425
  call_identifier: FP7
  grant_number: '303507'
  name: Optimality principles in responses to antibiotics
- _id: 25EB3A80-B435-11E9-9278-68D0E5697425
  grant_number: RGP0042/2013
  name: Revealing the fundamental limits of cell growth
publication: Current Opinion in Biotechnology
publication_status: published
publisher: Elsevier
publist_id: '6364'
pubrep_id: '801'
quality_controlled: '1'
related_material:
  record:
  - id: '6263'
    relation: dissertation_contains
    status: public
scopus_import: '1'
status: public
title: Toward a quantitative understanding of antibiotic resistance evolution
tmp:
  image: /images/cc_by_nc_nd.png
  legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode
  name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
    (CC BY-NC-ND 4.0)
  short: CC BY-NC-ND (4.0)
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 46
year: '2017'
...
---
_id: '1029'
abstract:
- lang: eng
  text: RNA Polymerase II pauses and backtracks during transcription, with many consequences
    for gene expression and cellular physiology. Here, we show that the energy required
    to melt double-stranded nucleic acids in the transcription bubble predicts pausing
    in Saccharomyces cerevisiae far more accurately than nucleosome roadblocks do.
    In addition, the same energy difference also determines when the RNA polymerase
    backtracks instead of continuing to move forward. This data-driven model corroborates—in
    a genome wide and quantitative manner—previous evidence that sequence-dependent
    thermodynamic features of nucleic acids influence both transcriptional pausing
    and backtracking.
article_number: e0174066
article_processing_charge: Yes
author:
- first_name: Martin
  full_name: Lukacisin, Martin
  id: 298FFE8C-F248-11E8-B48F-1D18A9856A87
  last_name: Lukacisin
  orcid: 0000-0001-6549-4177
- first_name: Matthieu
  full_name: Landon, Matthieu
  last_name: Landon
- first_name: Rishi
  full_name: Jajoo, Rishi
  last_name: Jajoo
citation:
  ama: Lukacisin M, Landon M, Jajoo R. Sequence-specific thermodynamic properties
    of nucleic acids influence both transcriptional pausing and backtracking in yeast.
    <i>PLoS One</i>. 2017;12(3). doi:<a href="https://doi.org/10.1371/journal.pone.0174066">10.1371/journal.pone.0174066</a>
  apa: Lukacisin, M., Landon, M., &#38; Jajoo, R. (2017). Sequence-specific thermodynamic
    properties of nucleic acids influence both transcriptional pausing and backtracking
    in yeast. <i>PLoS One</i>. Public Library of Science. <a href="https://doi.org/10.1371/journal.pone.0174066">https://doi.org/10.1371/journal.pone.0174066</a>
  chicago: Lukacisin, Martin, Matthieu Landon, and Rishi Jajoo. “Sequence-Specific
    Thermodynamic Properties of Nucleic Acids Influence Both Transcriptional Pausing
    and Backtracking in Yeast.” <i>PLoS One</i>. Public Library of Science, 2017.
    <a href="https://doi.org/10.1371/journal.pone.0174066">https://doi.org/10.1371/journal.pone.0174066</a>.
  ieee: M. Lukacisin, M. Landon, and R. Jajoo, “Sequence-specific thermodynamic properties
    of nucleic acids influence both transcriptional pausing and backtracking in yeast,”
    <i>PLoS One</i>, vol. 12, no. 3. Public Library of Science, 2017.
  ista: Lukacisin M, Landon M, Jajoo R. 2017. Sequence-specific thermodynamic properties
    of nucleic acids influence both transcriptional pausing and backtracking in yeast.
    PLoS One. 12(3), e0174066.
  mla: Lukacisin, Martin, et al. “Sequence-Specific Thermodynamic Properties of Nucleic
    Acids Influence Both Transcriptional Pausing and Backtracking in Yeast.” <i>PLoS
    One</i>, vol. 12, no. 3, e0174066, Public Library of Science, 2017, doi:<a href="https://doi.org/10.1371/journal.pone.0174066">10.1371/journal.pone.0174066</a>.
  short: M. Lukacisin, M. Landon, R. Jajoo, PLoS One 12 (2017).
date_created: 2018-12-11T11:49:46Z
date_published: 2017-03-16T00:00:00Z
date_updated: 2026-06-30T22:30:39Z
day: '16'
ddc:
- '570'
department:
- _id: ToBo
doi: 10.1371/journal.pone.0174066
external_id:
  isi:
  - '000396318300121'
file:
- access_level: open_access
  content_type: application/pdf
  creator: system
  date_created: 2018-12-12T10:09:47Z
  date_updated: 2018-12-12T10:09:47Z
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  file_name: IST-2017-800-v1+1_journal.pone.0174066.pdf
  file_size: 3429381
  relation: main_file
file_date_updated: 2018-12-12T10:09:47Z
has_accepted_license: '1'
intvolume: '        12'
isi: 1
issue: '3'
language:
- iso: eng
month: '03'
oa: 1
oa_version: Published Version
publication: PLoS One
publication_identifier:
  issn:
  - 1932-6203
publication_status: published
publisher: Public Library of Science
publist_id: '6361'
pubrep_id: '800'
quality_controlled: '1'
related_material:
  record:
  - id: '5556'
    relation: popular_science
    status: public
  - id: '6392'
    relation: dissertation_contains
    status: public
scopus_import: '1'
status: public
title: Sequence-specific thermodynamic properties of nucleic acids influence both
  transcriptional pausing and backtracking in yeast
tmp:
  image: /images/cc_by.png
  legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
  name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
  short: CC BY (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 12
year: '2017'
...
---
_id: '1028'
abstract:
- lang: eng
  text: Optogenetics and photopharmacology provide spatiotemporally precise control
    over protein interactions and protein function in cells and animals. Optogenetic
    methods that are sensitive to green light and can be used to break protein complexes
    are not broadly available but would enable multichromatic experiments with previously
    inaccessible biological targets. Herein, we repurposed cobalamin (vitamin B12)
    binding domains of bacterial CarH transcription factors for green-light-induced
    receptor dissociation. In cultured cells, we observed oligomerization-induced
    cell signaling for the fibroblast growth factor receptor 1 fused to cobalamin-binding
    domains in the dark that was rapidly eliminated upon illumination. In zebrafish
    embryos expressing fusion receptors, green light endowed control over aberrant
    fibroblast growth factor signaling during development. Green-light-induced domain
    dissociation and light-inactivated receptors will critically expand the optogenetic
    toolbox for control of biological processes.
acknowledgement: "This work was supported by a grant from the European Union\U0010FC1Ds
  Seventh Framework Programme (CIG-303564). E.R. was supported by the graduate program
  MolecularDrugTargets (Austrian Science Fund (FWF), W1232) and a FemTech fellowship
  (Austrian Research Promotion Agency, 3580812)"
article_processing_charge: No
author:
- first_name: Stephanie
  full_name: Kainrath, Stephanie
  id: 32CFBA64-F248-11E8-B48F-1D18A9856A87
  last_name: Kainrath
  orcid: 0000-0002-6709-2195
- first_name: Manuela
  full_name: Stadler, Manuela
  last_name: Stadler
- first_name: Eva
  full_name: Gschaider-Reichhart, Eva
  id: 3FEE232A-F248-11E8-B48F-1D18A9856A87
  last_name: Gschaider-Reichhart
  orcid: 0000-0002-7218-7738
- first_name: Martin
  full_name: Distel, Martin
  last_name: Distel
- first_name: Harald L
  full_name: Janovjak, Harald L
  id: 33BA6C30-F248-11E8-B48F-1D18A9856A87
  last_name: Janovjak
  orcid: 0000-0002-8023-9315
citation:
  ama: Kainrath S, Stadler M, Gschaider-Reichhart E, Distel M, Janovjak HL. Green-light-induced
    inactivation of receptor signaling using cobalamin-binding domains. <i>Angewandte
    Chemie - International Edition</i>. 2017;56(16):4608-4611. doi:<a href="https://doi.org/10.1002/anie.201611998">10.1002/anie.201611998</a>
  apa: Kainrath, S., Stadler, M., Gschaider-Reichhart, E., Distel, M., &#38; Janovjak,
    H. L. (2017). Green-light-induced inactivation of receptor signaling using cobalamin-binding
    domains. <i>Angewandte Chemie - International Edition</i>. Wiley-Blackwell. <a
    href="https://doi.org/10.1002/anie.201611998">https://doi.org/10.1002/anie.201611998</a>
  chicago: Kainrath, Stephanie, Manuela Stadler, Eva Gschaider-Reichhart, Martin Distel,
    and Harald L Janovjak. “Green-Light-Induced Inactivation of Receptor Signaling
    Using Cobalamin-Binding Domains.” <i>Angewandte Chemie - International Edition</i>.
    Wiley-Blackwell, 2017. <a href="https://doi.org/10.1002/anie.201611998">https://doi.org/10.1002/anie.201611998</a>.
  ieee: S. Kainrath, M. Stadler, E. Gschaider-Reichhart, M. Distel, and H. L. Janovjak,
    “Green-light-induced inactivation of receptor signaling using cobalamin-binding
    domains,” <i>Angewandte Chemie - International Edition</i>, vol. 56, no. 16. Wiley-Blackwell,
    pp. 4608–4611, 2017.
  ista: Kainrath S, Stadler M, Gschaider-Reichhart E, Distel M, Janovjak HL. 2017.
    Green-light-induced inactivation of receptor signaling using cobalamin-binding
    domains. Angewandte Chemie - International Edition. 56(16), 4608–4611.
  mla: Kainrath, Stephanie, et al. “Green-Light-Induced Inactivation of Receptor Signaling
    Using Cobalamin-Binding Domains.” <i>Angewandte Chemie - International Edition</i>,
    vol. 56, no. 16, Wiley-Blackwell, 2017, pp. 4608–11, doi:<a href="https://doi.org/10.1002/anie.201611998">10.1002/anie.201611998</a>.
  short: S. Kainrath, M. Stadler, E. Gschaider-Reichhart, M. Distel, H.L. Janovjak,
    Angewandte Chemie - International Edition 56 (2017) 4608–4611.
corr_author: '1'
date_created: 2018-12-11T11:49:46Z
date_published: 2017-03-20T00:00:00Z
date_updated: 2026-06-30T22:31:00Z
day: '20'
ddc:
- '540'
department:
- _id: CaGu
- _id: HaJa
doi: 10.1002/anie.201611998
ec_funded: 1
external_id:
  isi:
  - '000398154000038'
file:
- access_level: open_access
  content_type: application/pdf
  creator: dernst
  date_created: 2019-01-18T09:39:55Z
  date_updated: 2019-01-18T09:39:55Z
  file_id: '5845'
  file_name: 2017_communications_Kainrath.pdf
  file_size: 2614942
  relation: main_file
  success: 1
file_date_updated: 2019-01-18T09:39:55Z
has_accepted_license: '1'
intvolume: '        56'
isi: 1
issue: '16'
language:
- iso: eng
month: '03'
oa: 1
oa_version: Published Version
page: 4608-4611
project:
- _id: 25548C20-B435-11E9-9278-68D0E5697425
  call_identifier: FP7
  grant_number: '303564'
  name: Microbial Ion Channels for Synthetic Neurobiology
- _id: 26AA4EF2-B435-11E9-9278-68D0E5697425
  call_identifier: FWF
  grant_number: W1232-B24
  name: Molecular Drug Targets
publication: Angewandte Chemie - International Edition
publication_identifier:
  issn:
  - 1433-7851
publication_status: published
publisher: Wiley-Blackwell
publist_id: '6362'
quality_controlled: '1'
related_material:
  record:
  - id: '418'
    relation: dissertation_contains
    status: public
  - id: '7680'
    relation: part_of_dissertation
    status: public
scopus_import: '1'
status: public
title: Green-light-induced inactivation of receptor signaling using cobalamin-binding
  domains
tmp:
  image: /images/cc_by.png
  legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
  name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
  short: CC BY (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 56
year: '2017'
...
---
_id: '661'
abstract:
- lang: eng
  text: During embryonic development, mechanical forces are essential for cellular
    rearrangements driving tissue morphogenesis. Here, we show that in the early zebrafish
    embryo, friction forces are generated at the interface between anterior axial
    mesoderm (prechordal plate, ppl) progenitors migrating towards the animal pole
    and neurectoderm progenitors moving in the opposite direction towards the vegetal
    pole of the embryo. These friction forces lead to global rearrangement of cells
    within the neurectoderm and determine the position of the neural anlage. Using
    a combination of experiments and simulations, we show that this process depends
    on hydrodynamic coupling between neurectoderm and ppl as a result of E-cadherin-mediated
    adhesion between those tissues. Our data thus establish the emergence of friction
    forces at the interface between moving tissues as a critical force-generating
    process shaping the embryo.
acknowledged_ssus:
- _id: SSU
article_processing_charge: No
author:
- first_name: Michael
  full_name: Smutny, Michael
  id: 3FE6E4E8-F248-11E8-B48F-1D18A9856A87
  last_name: Smutny
  orcid: 0000-0002-5920-9090
- first_name: Zsuzsa
  full_name: Ákos, Zsuzsa
  last_name: Ákos
- first_name: Silvia
  full_name: Grigolon, Silvia
  last_name: Grigolon
- first_name: Shayan
  full_name: Shamipour, Shayan
  id: 40B34FE2-F248-11E8-B48F-1D18A9856A87
  last_name: Shamipour
- first_name: Verena
  full_name: Ruprecht, Verena
  last_name: Ruprecht
- first_name: Daniel
  full_name: Capek, Daniel
  id: 31C42484-F248-11E8-B48F-1D18A9856A87
  last_name: Capek
  orcid: 0000-0001-5199-9940
- first_name: Martin
  full_name: Behrndt, Martin
  id: 3ECECA3A-F248-11E8-B48F-1D18A9856A87
  last_name: Behrndt
- first_name: Ekaterina
  full_name: Papusheva, Ekaterina
  id: 41DB591E-F248-11E8-B48F-1D18A9856A87
  last_name: Papusheva
- first_name: Masazumi
  full_name: Tada, Masazumi
  last_name: Tada
- first_name: Björn
  full_name: Hof, Björn
  id: 3A374330-F248-11E8-B48F-1D18A9856A87
  last_name: Hof
  orcid: 0000-0003-2057-2754
- first_name: Tamás
  full_name: Vicsek, Tamás
  last_name: Vicsek
- first_name: Guillaume
  full_name: Salbreux, Guillaume
  last_name: Salbreux
- first_name: Carl-Philipp J
  full_name: Heisenberg, Carl-Philipp J
  id: 39427864-F248-11E8-B48F-1D18A9856A87
  last_name: Heisenberg
  orcid: 0000-0002-0912-4566
citation:
  ama: Smutny M, Ákos Z, Grigolon S, et al. Friction forces position the neural anlage.
    <i>Nature Cell Biology</i>. 2017;19:306-317. doi:<a href="https://doi.org/10.1038/ncb3492">10.1038/ncb3492</a>
  apa: Smutny, M., Ákos, Z., Grigolon, S., Shamipour, S., Ruprecht, V., Capek, D.,
    … Heisenberg, C.-P. J. (2017). Friction forces position the neural anlage. <i>Nature
    Cell Biology</i>. Nature Publishing Group. <a href="https://doi.org/10.1038/ncb3492">https://doi.org/10.1038/ncb3492</a>
  chicago: Smutny, Michael, Zsuzsa Ákos, Silvia Grigolon, Shayan Shamipour, Verena
    Ruprecht, Daniel Capek, Martin Behrndt, et al. “Friction Forces Position the Neural
    Anlage.” <i>Nature Cell Biology</i>. Nature Publishing Group, 2017. <a href="https://doi.org/10.1038/ncb3492">https://doi.org/10.1038/ncb3492</a>.
  ieee: M. Smutny <i>et al.</i>, “Friction forces position the neural anlage,” <i>Nature
    Cell Biology</i>, vol. 19. Nature Publishing Group, pp. 306–317, 2017.
  ista: Smutny M, Ákos Z, Grigolon S, Shamipour S, Ruprecht V, Capek D, Behrndt M,
    Papusheva E, Tada M, Hof B, Vicsek T, Salbreux G, Heisenberg C-PJ. 2017. Friction
    forces position the neural anlage. Nature Cell Biology. 19, 306–317.
  mla: Smutny, Michael, et al. “Friction Forces Position the Neural Anlage.” <i>Nature
    Cell Biology</i>, vol. 19, Nature Publishing Group, 2017, pp. 306–17, doi:<a href="https://doi.org/10.1038/ncb3492">10.1038/ncb3492</a>.
  short: M. Smutny, Z. Ákos, S. Grigolon, S. Shamipour, V. Ruprecht, D. Capek, M.
    Behrndt, E. Papusheva, M. Tada, B. Hof, T. Vicsek, G. Salbreux, C.-P.J. Heisenberg,
    Nature Cell Biology 19 (2017) 306–317.
corr_author: '1'
date_created: 2018-12-11T11:47:46Z
date_published: 2017-03-27T00:00:00Z
date_updated: 2026-06-30T22:31:06Z
day: '27'
department:
- _id: CaHe
- _id: BjHo
- _id: Bio
doi: 10.1038/ncb3492
ec_funded: 1
external_id:
  isi:
  - '000397917000009'
  pmid:
  - '28346437'
intvolume: '        19'
isi: 1
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://europepmc.org/articles/pmc5635970
month: '03'
oa: 1
oa_version: Submitted Version
page: 306 - 317
pmid: 1
project:
- _id: 25152F3A-B435-11E9-9278-68D0E5697425
  call_identifier: FP7
  grant_number: '306589'
  name: Decoding the complexity of turbulence at its origin
- _id: 252ABD0A-B435-11E9-9278-68D0E5697425
  call_identifier: FWF
  grant_number: I930-B20
  name: Control of Epithelial Cell Layer Spreading in Zebrafish
publication: Nature Cell Biology
publication_identifier:
  issn:
  - 1465-7392
publication_status: published
publisher: Nature Publishing Group
publist_id: '7074'
quality_controlled: '1'
related_material:
  record:
  - id: '50'
    relation: dissertation_contains
    status: public
  - id: '8350'
    relation: dissertation_contains
    status: public
scopus_import: '1'
status: public
title: Friction forces position the neural anlage
type: journal_article
user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 19
year: '2017'
...
---
_id: '735'
abstract:
- lang: eng
  text: Cell-cell contact formation constitutes an essential step in evolution, leading
    to the differentiation of specialized cell types. However, remarkably little is
    known about whether and how the interplay between contact formation and fate specification
    affects development. Here, we identify a positive feedback loop between cell-cell
    contact duration, morphogen signaling, and mesendoderm cell-fate specification
    during zebrafish gastrulation. We show that long-lasting cell-cell contacts enhance
    the competence of prechordal plate (ppl) progenitor cells to respond to Nodal
    signaling, required for ppl cell-fate specification. We further show that Nodal
    signaling promotes ppl cell-cell contact duration, generating a positive feedback
    loop between ppl cell-cell contact duration and cell-fate specification. Finally,
    by combining mathematical modeling and experimentation, we show that this feedback
    determines whether anterior axial mesendoderm cells become ppl or, instead, turn
    into endoderm. Thus, the interdependent activities of cell-cell signaling and
    contact formation control fate diversification within the developing embryo.
article_processing_charge: No
author:
- first_name: Vanessa
  full_name: Barone, Vanessa
  id: 419EECCC-F248-11E8-B48F-1D18A9856A87
  last_name: Barone
  orcid: 0000-0003-2676-3367
- first_name: Moritz
  full_name: Lang, Moritz
  id: 29E0800A-F248-11E8-B48F-1D18A9856A87
  last_name: Lang
- first_name: Gabriel
  full_name: Krens, Gabriel
  id: 2B819732-F248-11E8-B48F-1D18A9856A87
  last_name: Krens
  orcid: 0000-0003-4761-5996
- first_name: Saurabh
  full_name: Pradhan, Saurabh
  last_name: Pradhan
- first_name: Shayan
  full_name: Shamipour, Shayan
  id: 40B34FE2-F248-11E8-B48F-1D18A9856A87
  last_name: Shamipour
- first_name: Keisuke
  full_name: Sako, Keisuke
  id: 3BED66BE-F248-11E8-B48F-1D18A9856A87
  last_name: Sako
  orcid: 0000-0002-6453-8075
- first_name: Mateusz K
  full_name: Sikora, Mateusz K
  id: 2F74BCDE-F248-11E8-B48F-1D18A9856A87
  last_name: Sikora
- first_name: Calin C
  full_name: Guet, Calin C
  id: 47F8433E-F248-11E8-B48F-1D18A9856A87
  last_name: Guet
  orcid: 0000-0001-6220-2052
- first_name: Carl-Philipp J
  full_name: Heisenberg, Carl-Philipp J
  id: 39427864-F248-11E8-B48F-1D18A9856A87
  last_name: Heisenberg
  orcid: 0000-0002-0912-4566
citation:
  ama: Barone V, Lang M, Krens G, et al. An effective feedback loop between cell-cell
    contact duration and morphogen signaling determines cell fate. <i>Developmental
    Cell</i>. 2017;43(2):198-211. doi:<a href="https://doi.org/10.1016/j.devcel.2017.09.014">10.1016/j.devcel.2017.09.014</a>
  apa: Barone, V., Lang, M., Krens, G., Pradhan, S., Shamipour, S., Sako, K., … Heisenberg,
    C.-P. J. (2017). An effective feedback loop between cell-cell contact duration
    and morphogen signaling determines cell fate. <i>Developmental Cell</i>. Cell
    Press. <a href="https://doi.org/10.1016/j.devcel.2017.09.014">https://doi.org/10.1016/j.devcel.2017.09.014</a>
  chicago: Barone, Vanessa, Moritz Lang, Gabriel Krens, Saurabh Pradhan, Shayan Shamipour,
    Keisuke Sako, Mateusz K Sikora, Calin C Guet, and Carl-Philipp J Heisenberg. “An
    Effective Feedback Loop between Cell-Cell Contact Duration and Morphogen Signaling
    Determines Cell Fate.” <i>Developmental Cell</i>. Cell Press, 2017. <a href="https://doi.org/10.1016/j.devcel.2017.09.014">https://doi.org/10.1016/j.devcel.2017.09.014</a>.
  ieee: V. Barone <i>et al.</i>, “An effective feedback loop between cell-cell contact
    duration and morphogen signaling determines cell fate,” <i>Developmental Cell</i>,
    vol. 43, no. 2. Cell Press, pp. 198–211, 2017.
  ista: Barone V, Lang M, Krens G, Pradhan S, Shamipour S, Sako K, Sikora MK, Guet
    CC, Heisenberg C-PJ. 2017. An effective feedback loop between cell-cell contact
    duration and morphogen signaling determines cell fate. Developmental Cell. 43(2),
    198–211.
  mla: Barone, Vanessa, et al. “An Effective Feedback Loop between Cell-Cell Contact
    Duration and Morphogen Signaling Determines Cell Fate.” <i>Developmental Cell</i>,
    vol. 43, no. 2, Cell Press, 2017, pp. 198–211, doi:<a href="https://doi.org/10.1016/j.devcel.2017.09.014">10.1016/j.devcel.2017.09.014</a>.
  short: V. Barone, M. Lang, G. Krens, S. Pradhan, S. Shamipour, K. Sako, M.K. Sikora,
    C.C. Guet, C.-P.J. Heisenberg, Developmental Cell 43 (2017) 198–211.
corr_author: '1'
date_created: 2018-12-11T11:48:13Z
date_published: 2017-10-23T00:00:00Z
date_updated: 2026-06-30T22:31:06Z
day: '23'
department:
- _id: CaHe
- _id: CaGu
- _id: GaTk
doi: 10.1016/j.devcel.2017.09.014
ec_funded: 1
external_id:
  isi:
  - '000413443700011'
intvolume: '        43'
isi: 1
issue: '2'
language:
- iso: eng
month: '10'
oa_version: None
page: 198 - 211
project:
- _id: 25681D80-B435-11E9-9278-68D0E5697425
  call_identifier: FP7
  grant_number: '291734'
  name: International IST Postdoc Fellowship Programme
- _id: 252DD2A6-B435-11E9-9278-68D0E5697425
  call_identifier: FWF
  grant_number: I2058
  name: 'Cell segregation in gastrulation: the role of cell fate specification'
publication: Developmental Cell
publication_identifier:
  issn:
  - 1534-5807
publication_status: published
publisher: Cell Press
publist_id: '6934'
quality_controlled: '1'
related_material:
  record:
  - id: '961'
    relation: dissertation_contains
    status: public
  - id: '8350'
    relation: dissertation_contains
    status: public
scopus_import: '1'
status: public
title: An effective feedback loop between cell-cell contact duration and morphogen
  signaling determines cell fate
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 43
year: '2017'
...
---
_id: '949'
abstract:
- lang: eng
  text: The notion of treewidth of graphs has been exploited for faster algorithms
    for several problems arising in verification and program analysis. Moreover, various
    notions of balanced tree decompositions have been used for improved algorithms
    supporting dynamic updates and analysis of concurrent programs. In this work,
    we present a tool for constructing tree-decompositions of CFGs obtained from Java
    methods, which is implemented as an extension to the widely used Soot framework.
    The experimental results show that our implementation on real-world Java benchmarks
    is very efficient. Our tool also provides the first implementation for balancing
    tree-decompositions. In summary, we present the first tool support for exploiting
    treewidth in the static analysis problems on Java programs.
alternative_title:
- LNCS
article_processing_charge: No
author:
- first_name: Krishnendu
  full_name: Chatterjee, Krishnendu
  id: 2E5DCA20-F248-11E8-B48F-1D18A9856A87
  last_name: Chatterjee
  orcid: 0000-0002-4561-241X
- first_name: Amir
  full_name: Goharshady, Amir
  id: 391365CE-F248-11E8-B48F-1D18A9856A87
  last_name: Goharshady
  orcid: 0000-0003-1702-6584
- first_name: Andreas
  full_name: Pavlogiannis, Andreas
  id: 49704004-F248-11E8-B48F-1D18A9856A87
  last_name: Pavlogiannis
  orcid: 0000-0002-8943-0722
citation:
  ama: 'Chatterjee K, Goharshady AK, Pavlogiannis A. JTDec: A tool for tree decompositions
    in soot. In: D’Souza D, ed. Vol 10482. Springer; 2017:59-66. doi:<a href="https://doi.org/10.1007/978-3-319-68167-2_4">10.1007/978-3-319-68167-2_4</a>'
  apa: 'Chatterjee, K., Goharshady, A. K., &#38; Pavlogiannis, A. (2017). JTDec: A
    tool for tree decompositions in soot. In D. D’Souza (Ed.) (Vol. 10482, pp. 59–66).
    Presented at the ATVA: Automated Technology for Verification and Analysis, Pune,
    India: Springer. <a href="https://doi.org/10.1007/978-3-319-68167-2_4">https://doi.org/10.1007/978-3-319-68167-2_4</a>'
  chicago: 'Chatterjee, Krishnendu, Amir Kafshdar Goharshady, and Andreas Pavlogiannis.
    “JTDec: A Tool for Tree Decompositions in Soot.” edited by Deepak D’Souza, 10482:59–66.
    Springer, 2017. <a href="https://doi.org/10.1007/978-3-319-68167-2_4">https://doi.org/10.1007/978-3-319-68167-2_4</a>.'
  ieee: 'K. Chatterjee, A. K. Goharshady, and A. Pavlogiannis, “JTDec: A tool for
    tree decompositions in soot,” presented at the ATVA: Automated Technology for
    Verification and Analysis, Pune, India, 2017, vol. 10482, pp. 59–66.'
  ista: 'Chatterjee K, Goharshady AK, Pavlogiannis A. 2017. JTDec: A tool for tree
    decompositions in soot. ATVA: Automated Technology for Verification and Analysis,
    LNCS, vol. 10482, 59–66.'
  mla: 'Chatterjee, Krishnendu, et al. <i>JTDec: A Tool for Tree Decompositions in
    Soot</i>. Edited by Deepak D’Souza, vol. 10482, Springer, 2017, pp. 59–66, doi:<a
    href="https://doi.org/10.1007/978-3-319-68167-2_4">10.1007/978-3-319-68167-2_4</a>.'
  short: K. Chatterjee, A.K. Goharshady, A. Pavlogiannis, in:, D. D’Souza (Ed.), Springer,
    2017, pp. 59–66.
conference:
  end_date: 2017-10-06
  location: Pune, India
  name: 'ATVA: Automated Technology for Verification and Analysis'
  start_date: 2017-10-03
corr_author: '1'
date_created: 2018-12-11T11:49:22Z
date_published: 2017-01-01T00:00:00Z
date_updated: 2026-06-30T22:31:17Z
day: '01'
ddc:
- '005'
department:
- _id: KrCh
doi: 10.1007/978-3-319-68167-2_4
ec_funded: 1
editor:
- first_name: Deepak
  full_name: D'Souza, Deepak
  last_name: D'Souza
external_id:
  isi:
  - '000723567800004'
file:
- access_level: open_access
  checksum: a0d9f5f94dc594c4e71e78525c9942f1
  content_type: application/pdf
  creator: system
  date_created: 2018-12-12T10:10:45Z
  date_updated: 2020-07-14T12:48:16Z
  file_id: '4835'
  file_name: IST-2017-845-v1+1_2017_Chatterjee_JTDec.pdf
  file_size: 948514
  relation: main_file
file_date_updated: 2020-07-14T12:48:16Z
has_accepted_license: '1'
intvolume: '     10482'
isi: 1
language:
- iso: eng
month: '01'
oa: 1
oa_version: Submitted Version
page: 59 - 66
project:
- _id: 25863FF4-B435-11E9-9278-68D0E5697425
  call_identifier: FWF
  grant_number: S11407
  name: Game Theory
- _id: 2581B60A-B435-11E9-9278-68D0E5697425
  call_identifier: FP7
  grant_number: '279307'
  name: 'Quantitative Graph Games: Theory and Applications'
publication_identifier:
  issn:
  - 0302-9743
publication_status: published
publisher: Springer
publist_id: '6468'
pubrep_id: '845'
quality_controlled: '1'
related_material:
  record:
  - id: '8934'
    relation: dissertation_contains
    status: public
scopus_import: '1'
status: public
title: 'JTDec: A tool for tree decompositions in soot'
type: conference
user_id: ba8df636-2132-11f1-aed0-ed93e2281fdd
volume: 10482
year: '2017'
...
---
_id: '639'
abstract:
- lang: eng
  text: We study the problem of developing efficient approaches for proving worst-case
    bounds of non-deterministic recursive programs. Ranking functions are sound and
    complete for proving termination and worst-case bounds of non-recursive programs.
    First, we apply ranking functions to recursion, resulting in measure functions,
    and show that they provide a sound and complete approach to prove worst-case bounds
    of non-deterministic recursive programs. Our second contribution is the synthesis
    of measure functions in non-polynomial forms. We show that non-polynomial measure
    functions with logarithm and exponentiation can be synthesized through abstraction
    of logarithmic or exponentiation terms, Farkas’ Lemma, and Handelman’s Theorem
    using linear programming. While previous methods obtain worst-case polynomial
    bounds, our approach can synthesize bounds of the form O(n log n) as well as O(nr)
    where r is not an integer. We present experimental results to demonstrate that
    our approach can efficiently obtain worst-case bounds of classical recursive algorithms
    such as Merge-Sort, Closest-Pair, Karatsuba’s algorithm and Strassen’s algorithm.
alternative_title:
- LNCS
article_processing_charge: No
arxiv: 1
author:
- first_name: Krishnendu
  full_name: Chatterjee, Krishnendu
  id: 2E5DCA20-F248-11E8-B48F-1D18A9856A87
  last_name: Chatterjee
  orcid: 0000-0002-4561-241X
- first_name: Hongfei
  full_name: Fu, Hongfei
  last_name: Fu
- first_name: Amir
  full_name: Goharshady, Amir
  id: 391365CE-F248-11E8-B48F-1D18A9856A87
  last_name: Goharshady
  orcid: 0000-0003-1702-6584
citation:
  ama: 'Chatterjee K, Fu H, Goharshady AK. Non-polynomial worst case analysis of recursive
    programs. In: Majumdar R, Kunčak V, eds. Vol 10427. Springer; 2017:41-63. doi:<a
    href="https://doi.org/10.1007/978-3-319-63390-9_3">10.1007/978-3-319-63390-9_3</a>'
  apa: 'Chatterjee, K., Fu, H., &#38; Goharshady, A. K. (2017). Non-polynomial worst
    case analysis of recursive programs. In R. Majumdar &#38; V. Kunčak (Eds.) (Vol.
    10427, pp. 41–63). Presented at the CAV: Computer Aided Verification, Heidelberg,
    Germany: Springer. <a href="https://doi.org/10.1007/978-3-319-63390-9_3">https://doi.org/10.1007/978-3-319-63390-9_3</a>'
  chicago: Chatterjee, Krishnendu, Hongfei Fu, and Amir Kafshdar Goharshady. “Non-Polynomial
    Worst Case Analysis of Recursive Programs.” edited by Rupak Majumdar and Viktor
    Kunčak, 10427:41–63. Springer, 2017. <a href="https://doi.org/10.1007/978-3-319-63390-9_3">https://doi.org/10.1007/978-3-319-63390-9_3</a>.
  ieee: 'K. Chatterjee, H. Fu, and A. K. Goharshady, “Non-polynomial worst case analysis
    of recursive programs,” presented at the CAV: Computer Aided Verification, Heidelberg,
    Germany, 2017, vol. 10427, pp. 41–63.'
  ista: 'Chatterjee K, Fu H, Goharshady AK. 2017. Non-polynomial worst case analysis
    of recursive programs. CAV: Computer Aided Verification, LNCS, vol. 10427, 41–63.'
  mla: Chatterjee, Krishnendu, et al. <i>Non-Polynomial Worst Case Analysis of Recursive
    Programs</i>. Edited by Rupak Majumdar and Viktor Kunčak, vol. 10427, Springer,
    2017, pp. 41–63, doi:<a href="https://doi.org/10.1007/978-3-319-63390-9_3">10.1007/978-3-319-63390-9_3</a>.
  short: K. Chatterjee, H. Fu, A.K. Goharshady, in:, R. Majumdar, V. Kunčak (Eds.),
    Springer, 2017, pp. 41–63.
conference:
  end_date: 2017-07-28
  location: Heidelberg, Germany
  name: 'CAV: Computer Aided Verification'
  start_date: 2017-07-24
date_created: 2018-12-11T11:47:39Z
date_published: 2017-01-01T00:00:00Z
date_updated: 2026-06-30T22:31:17Z
day: '01'
department:
- _id: KrCh
doi: 10.1007/978-3-319-63390-9_3
ec_funded: 1
editor:
- first_name: Rupak
  full_name: Majumdar, Rupak
  last_name: Majumdar
- first_name: Viktor
  full_name: Kunčak, Viktor
  last_name: Kunčak
external_id:
  arxiv:
  - '1705.00317'
  isi:
  - '000431900900003'
intvolume: '     10427'
isi: 1
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://arxiv.org/abs/1705.00317
month: '01'
oa: 1
oa_version: Submitted Version
page: 41 - 63
project:
- _id: 25863FF4-B435-11E9-9278-68D0E5697425
  call_identifier: FWF
  grant_number: S11407
  name: Game Theory
- _id: 2581B60A-B435-11E9-9278-68D0E5697425
  call_identifier: FP7
  grant_number: '279307'
  name: 'Quantitative Graph Games: Theory and Applications'
publication_identifier:
  isbn:
  - 978-331963389-3
publication_status: published
publisher: Springer
publist_id: '7149'
quality_controlled: '1'
related_material:
  record:
  - id: '7014'
    relation: later_version
    status: public
  - id: '8934'
    relation: dissertation_contains
    status: public
scopus_import: '1'
status: public
title: Non-polynomial worst case analysis of recursive programs
type: conference
user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 10427
year: '2017'
...
---
_id: '664'
abstract:
- lang: eng
  text: Immune cells communicate using cytokine signals, but the quantitative rules
    of this communication aren't clear. In this issue of Immunity, Oyler-Yaniv et
    al. (2017) suggest that the distribution of a cytokine within a lymphatic organ
    is primarily governed by the local density of cells consuming it.
article_processing_charge: No
author:
- first_name: Frank P
  full_name: Assen, Frank P
  id: 3A8E7F24-F248-11E8-B48F-1D18A9856A87
  last_name: Assen
  orcid: 0000-0003-3470-6119
- first_name: Michael K
  full_name: Sixt, Michael K
  id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
  last_name: Sixt
  orcid: 0000-0002-6620-9179
citation:
  ama: Assen FP, Sixt MK. The dynamic cytokine niche. <i>Immunity</i>. 2017;46(4):519-520.
    doi:<a href="https://doi.org/10.1016/j.immuni.2017.04.006">10.1016/j.immuni.2017.04.006</a>
  apa: Assen, F. P., &#38; Sixt, M. K. (2017). The dynamic cytokine niche. <i>Immunity</i>.
    Cell Press. <a href="https://doi.org/10.1016/j.immuni.2017.04.006">https://doi.org/10.1016/j.immuni.2017.04.006</a>
  chicago: Assen, Frank P, and Michael K Sixt. “The Dynamic Cytokine Niche.” <i>Immunity</i>.
    Cell Press, 2017. <a href="https://doi.org/10.1016/j.immuni.2017.04.006">https://doi.org/10.1016/j.immuni.2017.04.006</a>.
  ieee: F. P. Assen and M. K. Sixt, “The dynamic cytokine niche,” <i>Immunity</i>,
    vol. 46, no. 4. Cell Press, pp. 519–520, 2017.
  ista: Assen FP, Sixt MK. 2017. The dynamic cytokine niche. Immunity. 46(4), 519–520.
  mla: Assen, Frank P., and Michael K. Sixt. “The Dynamic Cytokine Niche.” <i>Immunity</i>,
    vol. 46, no. 4, Cell Press, 2017, pp. 519–20, doi:<a href="https://doi.org/10.1016/j.immuni.2017.04.006">10.1016/j.immuni.2017.04.006</a>.
  short: F.P. Assen, M.K. Sixt, Immunity 46 (2017) 519–520.
corr_author: '1'
date_created: 2018-12-11T11:47:47Z
date_published: 2017-04-18T00:00:00Z
date_updated: 2026-06-30T22:31:22Z
day: '18'
department:
- _id: MiSi
doi: 10.1016/j.immuni.2017.04.006
external_id:
  isi:
  - '000399451100002'
intvolume: '        46'
isi: 1
issue: '4'
language:
- iso: eng
month: '04'
oa_version: None
page: 519 - 520
publication: Immunity
publication_identifier:
  issn:
  - 1074-7613
publication_status: published
publisher: Cell Press
publist_id: '7065'
quality_controlled: '1'
related_material:
  record:
  - id: '6947'
    relation: dissertation_contains
    status: public
scopus_import: '1'
status: public
title: The dynamic cytokine niche
type: journal_article
user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 46
year: '2017'
...
---
_id: '960'
abstract:
- lang: eng
  text: The human cerebral cortex is the seat of our cognitive abilities and composed
    of an extraordinary number of neurons, organized in six distinct layers. The establishment
    of specific morphological and physiological features in individual neurons needs
    to be regulated with high precision. Impairments in the sequential developmental
    programs instructing corticogenesis lead to alterations in the cortical cytoarchitecture
    which is thought to represent the major underlying cause for several neurological
    disorders including neurodevelopmental and psychiatric diseases. In this review
    we discuss the role of cell polarity at sequential stages during cortex development.
    We first provide an overview of morphological cell polarity features in cortical
    neural stem cells and newly-born postmitotic neurons. We then synthesize a conceptual
    molecular and biochemical framework how cell polarity is established at the cellular
    level through a break in symmetry in nascent cortical projection neurons. Lastly
    we provide a perspective how the molecular mechanisms applying to single cells
    could be probed and integrated in an in vivo and tissue-wide context.
article_number: '176'
article_processing_charge: Yes
author:
- first_name: Andi H
  full_name: Hansen, Andi H
  id: 38853E16-F248-11E8-B48F-1D18A9856A87
  last_name: Hansen
- first_name: Christian F
  full_name: Düllberg, Christian F
  id: 459064DC-F248-11E8-B48F-1D18A9856A87
  last_name: Düllberg
  orcid: 0000-0001-6335-9748
- first_name: Christine
  full_name: Mieck, Christine
  id: 34CAE85C-F248-11E8-B48F-1D18A9856A87
  last_name: Mieck
  orcid: 0000-0003-1919-7416
- first_name: Martin
  full_name: Loose, Martin
  id: 462D4284-F248-11E8-B48F-1D18A9856A87
  last_name: Loose
  orcid: 0000-0001-7309-9724
- first_name: Simon
  full_name: Hippenmeyer, Simon
  id: 37B36620-F248-11E8-B48F-1D18A9856A87
  last_name: Hippenmeyer
  orcid: 0000-0003-2279-1061
citation:
  ama: Hansen AH, Düllberg CF, Mieck C, Loose M, Hippenmeyer S. Cell polarity in cerebral
    cortex development - cellular architecture shaped by biochemical networks. <i>Frontiers
    in Cellular Neuroscience</i>. 2017;11. doi:<a href="https://doi.org/10.3389/fncel.2017.00176">10.3389/fncel.2017.00176</a>
  apa: Hansen, A. H., Düllberg, C. F., Mieck, C., Loose, M., &#38; Hippenmeyer, S.
    (2017). Cell polarity in cerebral cortex development - cellular architecture shaped
    by biochemical networks. <i>Frontiers in Cellular Neuroscience</i>. Frontiers
    Research Foundation. <a href="https://doi.org/10.3389/fncel.2017.00176">https://doi.org/10.3389/fncel.2017.00176</a>
  chicago: Hansen, Andi H, Christian F Düllberg, Christine Mieck, Martin Loose, and
    Simon Hippenmeyer. “Cell Polarity in Cerebral Cortex Development - Cellular Architecture
    Shaped by Biochemical Networks.” <i>Frontiers in Cellular Neuroscience</i>. Frontiers
    Research Foundation, 2017. <a href="https://doi.org/10.3389/fncel.2017.00176">https://doi.org/10.3389/fncel.2017.00176</a>.
  ieee: A. H. Hansen, C. F. Düllberg, C. Mieck, M. Loose, and S. Hippenmeyer, “Cell
    polarity in cerebral cortex development - cellular architecture shaped by biochemical
    networks,” <i>Frontiers in Cellular Neuroscience</i>, vol. 11. Frontiers Research
    Foundation, 2017.
  ista: Hansen AH, Düllberg CF, Mieck C, Loose M, Hippenmeyer S. 2017. Cell polarity
    in cerebral cortex development - cellular architecture shaped by biochemical networks.
    Frontiers in Cellular Neuroscience. 11, 176.
  mla: Hansen, Andi H., et al. “Cell Polarity in Cerebral Cortex Development - Cellular
    Architecture Shaped by Biochemical Networks.” <i>Frontiers in Cellular Neuroscience</i>,
    vol. 11, 176, Frontiers Research Foundation, 2017, doi:<a href="https://doi.org/10.3389/fncel.2017.00176">10.3389/fncel.2017.00176</a>.
  short: A.H. Hansen, C.F. Düllberg, C. Mieck, M. Loose, S. Hippenmeyer, Frontiers
    in Cellular Neuroscience 11 (2017).
date_created: 2018-12-11T11:49:25Z
date_published: 2017-06-28T00:00:00Z
date_updated: 2026-06-30T22:31:25Z
day: '28'
ddc:
- '570'
department:
- _id: SiHi
- _id: MaLo
doi: 10.3389/fncel.2017.00176
ec_funded: 1
external_id:
  isi:
  - '000404486700001'
file:
- access_level: open_access
  checksum: dc1f5a475b918d09a0f9f587400b1626
  content_type: application/pdf
  creator: system
  date_created: 2018-12-12T10:09:40Z
  date_updated: 2020-07-14T12:48:16Z
  file_id: '4764'
  file_name: IST-2017-830-v1+1_2017_Hansen_CellPolarity.pdf
  file_size: 2153858
  relation: main_file
file_date_updated: 2020-07-14T12:48:16Z
has_accepted_license: '1'
intvolume: '        11'
isi: 1
language:
- iso: eng
month: '06'
oa: 1
oa_version: Published Version
project:
- _id: 25D61E48-B435-11E9-9278-68D0E5697425
  call_identifier: FP7
  grant_number: '618444'
  name: Molecular Mechanisms of Cerebral Cortex Development
- _id: 25D7962E-B435-11E9-9278-68D0E5697425
  grant_number: RGP0053/2014
  name: Quantitative Structure-Function Analysis of Cerebral Cortex Assembly at Clonal
    Level
- _id: 25681D80-B435-11E9-9278-68D0E5697425
  call_identifier: FP7
  grant_number: '291734'
  name: International IST Postdoc Fellowship Programme
- _id: 25985A36-B435-11E9-9278-68D0E5697425
  call_identifier: FWF
  grant_number: T00817-B21
  name: The biochemical basis of PAR polarization
publication: Frontiers in Cellular Neuroscience
publication_identifier:
  issn:
  - 1662-5102
publication_status: published
publisher: Frontiers Research Foundation
publist_id: '6445'
pubrep_id: '830'
quality_controlled: '1'
related_material:
  record:
  - id: '9962'
    relation: dissertation_contains
    status: public
scopus_import: '1'
status: public
title: Cell polarity in cerebral cortex development - cellular architecture shaped
  by biochemical networks
tmp:
  image: /images/cc_by.png
  legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
  name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
  short: CC BY (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 11
year: '2017'
...
---
_id: '1082'
abstract:
- lang: eng
  text: In many applications, it is desirable to extract only the relevant aspects
    of data. A principled way to do this is the information bottleneck (IB) method,
    where one seeks a code that maximises information about a relevance variable,
    Y, while constraining the information encoded about the original data, X. Unfortunately
    however, the IB method is computationally demanding when data are high-dimensional
    and/or non-gaussian. Here we propose an approximate variational scheme for maximising
    a lower bound on the IB objective, analogous to variational EM. Using this method,
    we derive an IB algorithm to recover features that are both relevant and sparse.
    Finally, we demonstrate how kernelised versions of the algorithm can be used to
    address a broad range of problems with non-linear relation between X and Y.
alternative_title:
- Advances in Neural Information Processing Systems
article_processing_charge: No
arxiv: 1
author:
- first_name: Matthew J
  full_name: Chalk, Matthew J
  id: 2BAAC544-F248-11E8-B48F-1D18A9856A87
  last_name: Chalk
  orcid: 0000-0001-7782-4436
- first_name: Olivier
  full_name: Marre, Olivier
  last_name: Marre
- first_name: Gasper
  full_name: Tkacik, Gasper
  id: 3D494DCA-F248-11E8-B48F-1D18A9856A87
  last_name: Tkacik
  orcid: 0000-0002-6699-1455
citation:
  ama: 'Chalk MJ, Marre O, Tkačik G. Relevant sparse codes with variational information
    bottleneck. In: Vol 29. Neural Information Processing Systems Foundation; 2016:1965-1973.'
  apa: 'Chalk, M. J., Marre, O., &#38; Tkačik, G. (2016). Relevant sparse codes with
    variational information bottleneck (Vol. 29, pp. 1965–1973). Presented at the
    NIPS: Neural Information Processing Systems, Barcelona, Spain: Neural Information
    Processing Systems Foundation.'
  chicago: Chalk, Matthew J, Olivier Marre, and Gašper Tkačik. “Relevant Sparse Codes
    with Variational Information Bottleneck,” 29:1965–73. Neural Information Processing
    Systems Foundation, 2016.
  ieee: 'M. J. Chalk, O. Marre, and G. Tkačik, “Relevant sparse codes with variational
    information bottleneck,” presented at the NIPS: Neural Information Processing
    Systems, Barcelona, Spain, 2016, vol. 29, pp. 1965–1973.'
  ista: 'Chalk MJ, Marre O, Tkačik G. 2016. Relevant sparse codes with variational
    information bottleneck. NIPS: Neural Information Processing Systems, Advances
    in Neural Information Processing Systems, vol. 29, 1965–1973.'
  mla: Chalk, Matthew J., et al. <i>Relevant Sparse Codes with Variational Information
    Bottleneck</i>. Vol. 29, Neural Information Processing Systems Foundation, 2016,
    pp. 1965–73.
  short: M.J. Chalk, O. Marre, G. Tkačik, in:, Neural Information Processing Systems
    Foundation, 2016, pp. 1965–1973.
conference:
  end_date: 2016-12-10
  location: Barcelona, Spain
  name: 'NIPS: Neural Information Processing Systems'
  start_date: 2016-12-05
date_created: 2018-12-11T11:50:03Z
date_published: 2016-12-01T00:00:00Z
date_updated: 2025-06-03T11:33:51Z
day: '01'
department:
- _id: GaTk
external_id:
  arxiv:
  - '1605.07332'
intvolume: '        29'
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://arxiv.org/abs/1605.07332
month: '12'
oa: 1
oa_version: Preprint
page: 1965-1973
publication_status: published
publisher: Neural Information Processing Systems Foundation
publist_id: '6298'
quality_controlled: '1'
related_material:
  link:
  - relation: other
    url: https://papers.nips.cc/paper/6101-relevant-sparse-codes-with-variational-information-bottleneck
scopus_import: '1'
status: public
title: Relevant sparse codes with variational information bottleneck
type: conference
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 29
year: '2016'
...
---
_id: '1083'
abstract:
- lang: eng
  text: ' Cholecystokinin-expressing interneurons (CCK-INs) mediate behavior state-dependent
    inhibition in cortical circuits and themselves receive strong GABAergic input.
    However, it remains unclear to what extent GABABreceptors (GABABRs) contribute
    to their inhibitory control. Using immunoelectron microscopy, we found that CCK-INs
    in the rat hippocampus possessed high levels of dendritic GABABRs and KCTD12 auxiliary
    proteins, whereas postsynaptic effector Kir3 channels were present at lower levels.
    Consistently, whole-cell recordings revealed slow GABABR-mediated inhibitory postsynaptic
    currents (IPSCs) in most CCK-INs. In spite of the higher surface density of GABABRs
    in CCK-INs than in CA1 principal cells, the amplitudes of IPSCs were comparable,
    suggesting that the expression of Kir3 channels is the limiting factor for the
    GABABR currents in these INs. Morphological analysis showed that CCK-INs were
    diverse, comprising perisomatic-targeting basket cells (BCs), as well as dendrite-targeting
    (DT) interneurons, including a previously undescribed DT type. GABABR-mediated
    IPSCs in CCK-INs were large in BCs, but small in DT subtypes. In response to prolonged
    activation, GABABR-mediated currents displayed strong desensitization, which was
    absent in KCTD12-deficient mice. This study highlights that GABABRs differentially
    control CCK-IN subtypes, and the kinetics and desensitization of GABABR-mediated
    currents are modulated by KCTD12 proteins. '
acknowledgement: "This work was supported by the Deutsche Forschungsgemeinschaft (DFG
  SFB 780 A2, A.K.; SFB TR3 I.V. and EXC 257, I.V.; FOR 2143, A.K. and I.V.), Spemann
  Graduate School (D.A.), BIOSS-2 (A6, A.K.), the Swiss National Science Foundation
  (3100A0-117816, B.B.), The McNaught Bequest (S.A.B. and I.V.), and Tenovus Scotland
  (I.V.).\r\n\r\n\r\nWe thank Cheryl Hutton and Chinmaya Sadangi for their contributions
  to neuronal reconstruction as well as Natalie Wernet, Sigrun Nestel, Anikó Schneider,
  Ina Wolter, and Ulrich Noeller for their excellent technical support. VGAT-Venus
  transgenic rats were generated by Drs Y. Yanagawa, M. Hirabayashi, and Y. Kawaguchi
  in National Institute for Physiological Sciences, Okazaki, Japan, using pCS2-Venus
  provided by Dr A. Miyawaki. The monoclonal mouse CCK antibody was generously provided
  by Dr G.V. Ohning, CURE Center, UCLA, CA. "
article_processing_charge: No
author:
- first_name: Sam
  full_name: Booker, Sam
  last_name: Booker
- first_name: Daniel
  full_name: Althof, Daniel
  last_name: Althof
- first_name: Anna
  full_name: Gross, Anna
  last_name: Gross
- first_name: Desiree
  full_name: Loreth, Desiree
  last_name: Loreth
- first_name: Johanna
  full_name: Müller, Johanna
  last_name: Müller
- first_name: Andreas
  full_name: Unger, Andreas
  last_name: Unger
- first_name: Bernd
  full_name: Fakler, Bernd
  last_name: Fakler
- first_name: Andrea
  full_name: Varro, Andrea
  last_name: Varro
- first_name: Masahiko
  full_name: Watanabe, Masahiko
  last_name: Watanabe
- first_name: Martin
  full_name: Gassmann, Martin
  last_name: Gassmann
- first_name: Bernhard
  full_name: Bettler, Bernhard
  last_name: Bettler
- first_name: Ryuichi
  full_name: Shigemoto, Ryuichi
  id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
  last_name: Shigemoto
  orcid: 0000-0001-8761-9444
- first_name: Imre
  full_name: Vida, Imre
  last_name: Vida
- first_name: Ákos
  full_name: Kulik, Ákos
  last_name: Kulik
citation:
  ama: Booker S, Althof D, Gross A, et al. KCTD12 auxiliary proteins modulate kinetics
    of GABAB receptor-mediated inhibition in Cholecystokinin-containing interneurons.
    <i>Cerebral Cortex</i>. 2016;27(3):2318-2334. doi:<a href="https://doi.org/10.1093/cercor/bhw090">10.1093/cercor/bhw090</a>
  apa: Booker, S., Althof, D., Gross, A., Loreth, D., Müller, J., Unger, A., … Kulik,
    Á. (2016). KCTD12 auxiliary proteins modulate kinetics of GABAB receptor-mediated
    inhibition in Cholecystokinin-containing interneurons. <i>Cerebral Cortex</i>.
    Oxford University Press. <a href="https://doi.org/10.1093/cercor/bhw090">https://doi.org/10.1093/cercor/bhw090</a>
  chicago: Booker, Sam, Daniel Althof, Anna Gross, Desiree Loreth, Johanna Müller,
    Andreas Unger, Bernd Fakler, et al. “KCTD12 Auxiliary Proteins Modulate Kinetics
    of GABAB Receptor-Mediated Inhibition in Cholecystokinin-Containing Interneurons.”
    <i>Cerebral Cortex</i>. Oxford University Press, 2016. <a href="https://doi.org/10.1093/cercor/bhw090">https://doi.org/10.1093/cercor/bhw090</a>.
  ieee: S. Booker <i>et al.</i>, “KCTD12 auxiliary proteins modulate kinetics of GABAB
    receptor-mediated inhibition in Cholecystokinin-containing interneurons,” <i>Cerebral
    Cortex</i>, vol. 27, no. 3. Oxford University Press, pp. 2318–2334, 2016.
  ista: Booker S, Althof D, Gross A, Loreth D, Müller J, Unger A, Fakler B, Varro
    A, Watanabe M, Gassmann M, Bettler B, Shigemoto R, Vida I, Kulik Á. 2016. KCTD12
    auxiliary proteins modulate kinetics of GABAB receptor-mediated inhibition in
    Cholecystokinin-containing interneurons. Cerebral Cortex. 27(3), 2318–2334.
  mla: Booker, Sam, et al. “KCTD12 Auxiliary Proteins Modulate Kinetics of GABAB Receptor-Mediated
    Inhibition in Cholecystokinin-Containing Interneurons.” <i>Cerebral Cortex</i>,
    vol. 27, no. 3, Oxford University Press, 2016, pp. 2318–34, doi:<a href="https://doi.org/10.1093/cercor/bhw090">10.1093/cercor/bhw090</a>.
  short: S. Booker, D. Althof, A. Gross, D. Loreth, J. Müller, A. Unger, B. Fakler,
    A. Varro, M. Watanabe, M. Gassmann, B. Bettler, R. Shigemoto, I. Vida, Á. Kulik,
    Cerebral Cortex 27 (2016) 2318–2334.
date_created: 2018-12-11T11:50:03Z
date_published: 2016-04-12T00:00:00Z
date_updated: 2025-09-22T14:19:11Z
day: '12'
department:
- _id: RySh
doi: 10.1093/cercor/bhw090
external_id:
  isi:
  - '000397636600048'
intvolume: '        27'
isi: 1
issue: '3'
language:
- iso: eng
month: '04'
oa_version: None
page: 2318 - 2334
publication: Cerebral Cortex
publication_status: published
publisher: Oxford University Press
publist_id: '6297'
quality_controlled: '1'
scopus_import: '1'
status: public
title: KCTD12 auxiliary proteins modulate kinetics of GABAB receptor-mediated inhibition
  in Cholecystokinin-containing interneurons
type: journal_article
user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 27
year: '2016'
...
---
_id: '1088'
abstract:
- lang: eng
  text: Cell geometry is tightly coupled to gene expression patterns within the tissue
    microenvironment. This perspective synthesizes evidence that the 3D organization
    of chromosomes is a critical intermediate for geometric control of genomic programs.
    Using a combination of experiments and modeling we outline approaches to decipher
    the mechano-genomic code that governs cellular homeostasis and reprogramming.
author:
- first_name: Caroline
  full_name: Uhler, Caroline
  id: 49ADD78E-F248-11E8-B48F-1D18A9856A87
  last_name: Uhler
  orcid: 0000-0002-7008-0216
- first_name: G V
  full_name: Shivashankar, G V
  last_name: Shivashankar
citation:
  ama: Uhler C, Shivashankar GV. Geometric control and modeling of genome reprogramming.
    <i>BioArchitecture</i>. 2016;6(4):76-84. doi:<a href="https://doi.org/10.1080/19490992.2016.1201620">10.1080/19490992.2016.1201620</a>
  apa: Uhler, C., &#38; Shivashankar, G. V. (2016). Geometric control and modeling
    of genome reprogramming. <i>BioArchitecture</i>. Taylor &#38; Francis. <a href="https://doi.org/10.1080/19490992.2016.1201620">https://doi.org/10.1080/19490992.2016.1201620</a>
  chicago: Uhler, Caroline, and G V Shivashankar. “Geometric Control and Modeling
    of Genome Reprogramming.” <i>BioArchitecture</i>. Taylor &#38; Francis, 2016.
    <a href="https://doi.org/10.1080/19490992.2016.1201620">https://doi.org/10.1080/19490992.2016.1201620</a>.
  ieee: C. Uhler and G. V. Shivashankar, “Geometric control and modeling of genome
    reprogramming,” <i>BioArchitecture</i>, vol. 6, no. 4. Taylor &#38; Francis, pp.
    76–84, 2016.
  ista: Uhler C, Shivashankar GV. 2016. Geometric control and modeling of genome reprogramming.
    BioArchitecture. 6(4), 76–84.
  mla: Uhler, Caroline, and G. V. Shivashankar. “Geometric Control and Modeling of
    Genome Reprogramming.” <i>BioArchitecture</i>, vol. 6, no. 4, Taylor &#38; Francis,
    2016, pp. 76–84, doi:<a href="https://doi.org/10.1080/19490992.2016.1201620">10.1080/19490992.2016.1201620</a>.
  short: C. Uhler, G.V. Shivashankar, BioArchitecture 6 (2016) 76–84.
date_created: 2018-12-11T11:50:05Z
date_published: 2016-07-27T00:00:00Z
date_updated: 2021-01-12T06:48:11Z
day: '27'
doi: 10.1080/19490992.2016.1201620
extern: '1'
intvolume: '         6'
issue: '4'
language:
- iso: eng
month: '07'
oa_version: None
page: 76 - 84
publication: BioArchitecture
publication_status: published
publisher: Taylor & Francis
publist_id: '6289'
quality_controlled: '1'
status: public
title: Geometric control and modeling of genome reprogramming
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 6
year: '2016'
...
