---
_id: '834'
abstract:
- lang: eng
  text: 'Thermal and many-body localized phases are separated by a dynamical phase
    transition of a new kind. We analyze the distribution of off-diagonal matrix elements
    of local operators across this transition in two different models of disordered
    spin chains. We show that the behavior of matrix elements can be used to characterize
    the breakdown of thermalization and to extract the many-body Thouless energy.
    We find that upon increasing the disorder strength the system enters a critical
    region around the many-body localization transition. The properties of the system
    in this region are: (i) the Thouless energy becomes smaller than the level spacing,
    (ii) the matrix elements show critical dependence on the energy difference, and
    (iii) the matrix elements, viewed as amplitudes of a fictitious wave function,
    exhibit strong multifractality. This critical region decreases with the system
    size, which we interpret as evidence for a diverging correlation length at the
    many-body localization transition. Our findings show that the correlation length
    becomes larger than the accessible system sizes in a broad range of disorder strength
    values and shed light on the critical behavior near the many-body localization
    transition.'
acknowledgement: We   acknowledge   useful   discussions with V. Kravtsov, T. Grover,
  and R. Vasseur.  M.S. was supported by Gordon and Betty Moore Foundation’s EPiQS
  Initiative through Grant GBMF4307.  M.S. and D.A.  acknowledge  hospitality  of  KITP,  where  parts  of
  this work were completed (supported in part by the National Science Foundation under
  Grant No. NSF PHY11-25915)
article_number: '104201'
article_processing_charge: No
arxiv: 1
author:
- first_name: Maksym
  full_name: Serbyn, Maksym
  id: 47809E7E-F248-11E8-B48F-1D18A9856A87
  last_name: Serbyn
  orcid: 0000-0002-2399-5827
- first_name: Papic
  full_name: Zlatko, Papic
  last_name: Zlatko
- first_name: Dmitry
  full_name: Abanin, Dmitry
  last_name: Abanin
citation:
  ama: Serbyn M, Zlatko P, Abanin D. Thouless energy and multifractality across the
    many-body localization transition. <i>Physical Review B</i>. 2017;96(10). doi:<a
    href="https://doi.org/10.1103/PhysRevB.96.104201">10.1103/PhysRevB.96.104201</a>
  apa: Serbyn, M., Zlatko, P., &#38; Abanin, D. (2017). Thouless energy and multifractality
    across the many-body localization transition. <i>Physical Review B</i>. American
    Physical Society. <a href="https://doi.org/10.1103/PhysRevB.96.104201">https://doi.org/10.1103/PhysRevB.96.104201</a>
  chicago: Serbyn, Maksym, Papic Zlatko, and Dmitry Abanin. “Thouless Energy and Multifractality
    across the Many-Body Localization Transition.” <i>Physical Review B</i>. American
    Physical Society, 2017. <a href="https://doi.org/10.1103/PhysRevB.96.104201">https://doi.org/10.1103/PhysRevB.96.104201</a>.
  ieee: M. Serbyn, P. Zlatko, and D. Abanin, “Thouless energy and multifractality
    across the many-body localization transition,” <i>Physical Review B</i>, vol.
    96, no. 10. American Physical Society, 2017.
  ista: Serbyn M, Zlatko P, Abanin D. 2017. Thouless energy and multifractality across
    the many-body localization transition. Physical Review B. 96(10), 104201.
  mla: Serbyn, Maksym, et al. “Thouless Energy and Multifractality across the Many-Body
    Localization Transition.” <i>Physical Review B</i>, vol. 96, no. 10, 104201, American
    Physical Society, 2017, doi:<a href="https://doi.org/10.1103/PhysRevB.96.104201">10.1103/PhysRevB.96.104201</a>.
  short: M. Serbyn, P. Zlatko, D. Abanin, Physical Review B 96 (2017).
date_created: 2018-12-11T11:48:45Z
date_published: 2017-09-06T00:00:00Z
date_updated: 2026-08-12T14:24:27Z
day: '06'
department:
- _id: MaSe
doi: 10.1103/PhysRevB.96.104201
external_id:
  arxiv:
  - '1610.02389'
  isi:
  - '000409429300004'
fulldoi: https://doi.org/10.1103/PhysRevB.96.104201
intvolume: '        96'
isi: 1
issue: '10'
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://arxiv.org/abs/1610.02389
month: '09'
oa: 1
oa_version: Submitted Version
publication: Physical Review B
publication_identifier:
  issn:
  - 2469-9950
publication_status: published
publisher: American Physical Society
publist_id: '6814'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Thouless energy and multifractality across the many-body localization transition
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 96
year: '2017'
...
---
_id: '947'
abstract:
- lang: eng
  text: Viewing the ways a living cell can organize its metabolism as the phase space
    of a physical system, regulation can be seen as the ability to reduce the entropy
    of that space by selecting specific cellular configurations that are, in some
    sense, optimal. Here we quantify the amount of regulation required to control
    a cell's growth rate by a maximum-entropy approach to the space of underlying
    metabolic phenotypes, where a configuration corresponds to a metabolic flux pattern
    as described by genome-scale models. We link the mean growth rate achieved by
    a population of cells to the minimal amount of metabolic regulation needed to
    achieve it through a phase diagram that highlights how growth suppression can
    be as costly (in regulatory terms) as growth enhancement. Moreover, we provide
    an interpretation of the inverse temperature β controlling maximum-entropy distributions
    based on the underlying growth dynamics. Specifically, we show that the asymptotic
    value of β for a cell population can be expected to depend on (i) the carrying
    capacity of the environment, (ii) the initial size of the colony, and (iii) the
    probability distribution from which the inoculum was sampled. Results obtained
    for E. coli and human cells are found to be remarkably consistent with empirical
    evidence.
article_number: '010401'
article_processing_charge: No
arxiv: 1
author:
- first_name: Daniele
  full_name: De Martino, Daniele
  id: 3FF5848A-F248-11E8-B48F-1D18A9856A87
  last_name: De Martino
  orcid: 0000-0002-5214-4706
- first_name: Fabrizio
  full_name: Capuani, Fabrizio
  last_name: Capuani
- first_name: Andrea
  full_name: De Martino, Andrea
  last_name: De Martino
citation:
  ama: De Martino D, Capuani F, De Martino A. Quantifying the entropic cost of cellular
    growth control. <i>Physical Review E</i>. 2017;96(1). doi:<a href="https://doi.org/10.1103/PhysRevE.96.010401">10.1103/PhysRevE.96.010401</a>
  apa: De Martino, D., Capuani, F., &#38; De Martino, A. (2017). Quantifying the entropic
    cost of cellular growth control. <i>Physical Review E</i>. American Physical Society.
    <a href="https://doi.org/10.1103/PhysRevE.96.010401">https://doi.org/10.1103/PhysRevE.96.010401</a>
  chicago: De Martino, Daniele, Fabrizio Capuani, and Andrea De Martino. “Quantifying
    the Entropic Cost of Cellular Growth Control.” <i>Physical Review E</i>. American
    Physical Society, 2017. <a href="https://doi.org/10.1103/PhysRevE.96.010401">https://doi.org/10.1103/PhysRevE.96.010401</a>.
  ieee: D. De Martino, F. Capuani, and A. De Martino, “Quantifying the entropic cost
    of cellular growth control,” <i>Physical Review E</i>, vol. 96, no. 1. American
    Physical Society, 2017.
  ista: De Martino D, Capuani F, De Martino A. 2017. Quantifying the entropic cost
    of cellular growth control. Physical Review E. 96(1), 010401.
  mla: De Martino, Daniele, et al. “Quantifying the Entropic Cost of Cellular Growth
    Control.” <i>Physical Review E</i>, vol. 96, no. 1, 010401, American Physical
    Society, 2017, doi:<a href="https://doi.org/10.1103/PhysRevE.96.010401">10.1103/PhysRevE.96.010401</a>.
  short: D. De Martino, F. Capuani, A. De Martino, Physical Review E 96 (2017).
das_tickbox: '1'
date_created: 2018-12-11T11:49:21Z
date_published: 2017-07-10T00:00:00Z
date_updated: 2026-08-12T14:29:46Z
day: '10'
department:
- _id: GaTk
doi: 10.1103/PhysRevE.96.010401
ec_funded: 1
external_id:
  arxiv:
  - '1703.00219'
  isi:
  - '000405194200002'
fulldoi: https://doi.org/10.1103/PhysRevE.96.010401
intvolume: '        96'
isi: 1
issue: '1'
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://arxiv.org/abs/1703.00219
month: '07'
oa: 1
oa_version: Submitted Version
project:
- _id: 25681D80-B435-11E9-9278-68D0E5697425
  call_identifier: FP7
  grant_number: '291734'
  name: International IST Postdoc Fellowship Programme
publication: Physical Review E
publication_identifier:
  issn:
  - 2470-0045
publication_status: published
publisher: American Physical Society
publist_id: '6470'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Quantifying the entropic cost of cellular growth control
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 96
year: '2017'
...
---
_id: '700'
abstract:
- lang: eng
  text: Microtubules provide the mechanical force required for chromosome separation
    during mitosis. However, little is known about the dynamic (high-frequency) mechanical
    properties of microtubules. Here, we theoretically propose to control the vibrations
    of a doubly clamped microtubule by tip electrodes and to detect its motion via
    the optomechanical coupling between the vibrational modes of the microtubule and
    an optical cavity. In the presence of a red-detuned strong pump laser, this coupling
    leads to optomechanical-induced transparency of an optical probe field, which
    can be detected with state-of-the art technology. The center frequency and line
    width of the transparency peak give the resonance frequency and damping rate of
    the microtubule, respectively, while the height of the peak reveals information
    about the microtubule-cavity field coupling. Our method opens the new possibilities
    to gain information about the physical properties of microtubules, which will
    enhance our capability to design physical cancer treatment protocols as alternatives
    to chemotherapeutic drugs.
article_number: '012404'
article_processing_charge: No
arxiv: 1
author:
- first_name: Shabir
  full_name: Barzanjeh, Shabir
  id: 2D25E1F6-F248-11E8-B48F-1D18A9856A87
  last_name: Barzanjeh
  orcid: 0000-0003-0415-1423
- first_name: Vahid
  full_name: Salari, Vahid
  last_name: Salari
- first_name: Jack
  full_name: Tuszynski, Jack
  last_name: Tuszynski
- first_name: Michal
  full_name: Cifra, Michal
  last_name: Cifra
- first_name: Christoph
  full_name: Simon, Christoph
  last_name: Simon
citation:
  ama: Barzanjeh S, Salari V, Tuszynski J, Cifra M, Simon C. Optomechanical proposal
    for monitoring microtubule mechanical vibrations. <i>Physical Review E</i>. 2017;96(1).
    doi:<a href="https://doi.org/10.1103/PhysRevE.96.012404">10.1103/PhysRevE.96.012404</a>
  apa: Barzanjeh, S., Salari, V., Tuszynski, J., Cifra, M., &#38; Simon, C. (2017).
    Optomechanical proposal for monitoring microtubule mechanical vibrations. <i>Physical
    Review E</i>. American Physical Society. <a href="https://doi.org/10.1103/PhysRevE.96.012404">https://doi.org/10.1103/PhysRevE.96.012404</a>
  chicago: Barzanjeh, Shabir, Vahid Salari, Jack Tuszynski, Michal Cifra, and Christoph
    Simon. “Optomechanical Proposal for Monitoring Microtubule Mechanical Vibrations.”
    <i>Physical Review E</i>. American Physical Society, 2017. <a href="https://doi.org/10.1103/PhysRevE.96.012404">https://doi.org/10.1103/PhysRevE.96.012404</a>.
  ieee: S. Barzanjeh, V. Salari, J. Tuszynski, M. Cifra, and C. Simon, “Optomechanical
    proposal for monitoring microtubule mechanical vibrations,” <i>Physical Review
    E</i>, vol. 96, no. 1. American Physical Society, 2017.
  ista: Barzanjeh S, Salari V, Tuszynski J, Cifra M, Simon C. 2017. Optomechanical
    proposal for monitoring microtubule mechanical vibrations. Physical Review E.
    96(1), 012404.
  mla: Barzanjeh, Shabir, et al. “Optomechanical Proposal for Monitoring Microtubule
    Mechanical Vibrations.” <i>Physical Review E</i>, vol. 96, no. 1, 012404, American
    Physical Society, 2017, doi:<a href="https://doi.org/10.1103/PhysRevE.96.012404">10.1103/PhysRevE.96.012404</a>.
  short: S. Barzanjeh, V. Salari, J. Tuszynski, M. Cifra, C. Simon, Physical Review
    E 96 (2017).
das_tickbox: '1'
date_created: 2018-12-11T11:48:00Z
date_published: 2017-07-12T00:00:00Z
date_updated: 2026-08-12T14:29:59Z
day: '12'
department:
- _id: JoFi
doi: 10.1103/PhysRevE.96.012404
ec_funded: 1
external_id:
  arxiv:
  - '1612.07061'
  isi:
  - '000405367200012'
fulldoi: https://doi.org/10.1103/PhysRevE.96.012404
intvolume: '        96'
isi: 1
issue: '1'
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://arxiv.org/abs/1612.07061
month: '07'
oa: 1
oa_version: Submitted Version
project:
- _id: 258047B6-B435-11E9-9278-68D0E5697425
  call_identifier: H2020
  grant_number: '707438'
  name: 'Microwave-to-Optical Quantum Link: Quantum Teleportation and Quantum Illumination
    with cavity Optomechanics'
publication: Physical Review E
publication_identifier:
  issn:
  - 2470-0045
publication_status: published
publisher: American Physical Society
publist_id: '6997'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Optomechanical proposal for monitoring microtubule mechanical vibrations
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 96
year: '2017'
...
---
_id: '959'
abstract:
- lang: eng
  text: In this work it is shown that scale-free tails in metabolic flux distributions
    inferred in stationary models are an artifact due to reactions involved in thermodynamically
    unfeasible cycles, unbounded by physical constraints and in principle able to
    perform work without expenditure of free energy. After implementing thermodynamic
    constraints by removing such loops, metabolic flux distributions scale meaningfully
    with the physical limiting factors, acquiring in turn a richer multimodal structure
    potentially leading to symmetry breaking while optimizing for objective functions.
article_processing_charge: No
arxiv: 1
author:
- first_name: Daniele
  full_name: De Martino, Daniele
  id: 3FF5848A-F248-11E8-B48F-1D18A9856A87
  last_name: De Martino
  orcid: 0000-0002-5214-4706
citation:
  ama: De Martino D. Scales and multimodal flux distributions in stationary metabolic
    network models via thermodynamics. <i>Physical Review E</i>. 2017;95(6):062419.
    doi:<a href="https://doi.org/10.1103/PhysRevE.95.062419">10.1103/PhysRevE.95.062419</a>
  apa: De Martino, D. (2017). Scales and multimodal flux distributions in stationary
    metabolic network models via thermodynamics. <i>Physical Review E</i>. American
    Physical Society. <a href="https://doi.org/10.1103/PhysRevE.95.062419">https://doi.org/10.1103/PhysRevE.95.062419</a>
  chicago: De Martino, Daniele. “Scales and Multimodal Flux Distributions in Stationary
    Metabolic Network Models via Thermodynamics.” <i>Physical Review E</i>. American
    Physical Society, 2017. <a href="https://doi.org/10.1103/PhysRevE.95.062419">https://doi.org/10.1103/PhysRevE.95.062419</a>.
  ieee: D. De Martino, “Scales and multimodal flux distributions in stationary metabolic
    network models via thermodynamics,” <i>Physical Review E</i>, vol. 95, no. 6.
    American Physical Society, p. 062419, 2017.
  ista: De Martino D. 2017. Scales and multimodal flux distributions in stationary
    metabolic network models via thermodynamics. Physical Review E. 95(6), 062419.
  mla: De Martino, Daniele. “Scales and Multimodal Flux Distributions in Stationary
    Metabolic Network Models via Thermodynamics.” <i>Physical Review E</i>, vol. 95,
    no. 6, American Physical Society, 2017, p. 062419, doi:<a href="https://doi.org/10.1103/PhysRevE.95.062419">10.1103/PhysRevE.95.062419</a>.
  short: D. De Martino, Physical Review E 95 (2017) 062419.
das_tickbox: '1'
date_created: 2018-12-11T11:49:25Z
date_published: 2017-06-28T00:00:00Z
date_updated: 2026-08-12T14:29:35Z
day: '28'
department:
- _id: GaTk
doi: 10.1103/PhysRevE.95.062419
ec_funded: 1
external_id:
  arxiv:
  - '1703.00853'
  isi:
  - '000404546400004'
fulldoi: https://doi.org/10.1103/PhysRevE.95.062419
intvolume: '        95'
isi: 1
issue: '6'
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://arxiv.org/abs/1703.00853
month: '06'
oa: 1
oa_version: Submitted Version
page: '062419'
project:
- _id: 25681D80-B435-11E9-9278-68D0E5697425
  call_identifier: FP7
  grant_number: '291734'
  name: International IST Postdoc Fellowship Programme
publication: Physical Review E
publication_identifier:
  issn:
  - 2470-0045
publication_status: published
publisher: American Physical Society
publist_id: '6446'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Scales and multimodal flux distributions in stationary metabolic network models
  via thermodynamics
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 95
year: '2017'
...
---
_id: '1077'
abstract:
- lang: eng
  text: Viral capsids are structurally constrained by interactions among the amino
    acids (AAs) of their constituent proteins. Therefore, epistasis is expected to
    evolve among physically interacting sites and to influence the rates of substitution.
    To study the evolution of epistasis, we focused on the major structural protein
    of the fX174 phage family by first reconstructing the ancestral protein sequences
    of 18 species using a Bayesian statistical framework. The inferred ancestral reconstruction
    differed at eight AAs, for a total of 256 possible ancestral haplotypes. For each
    ancestral haplotype and the extant species, we estimated, in silico, the distribution
    of free energies and epistasis of the capsid structure. We found that free energy
    has not significantly increased but epistasis has. We decomposed epistasis up
    to fifth order and found that higher-order epistasis sometimes compensates pairwise
    interactions making the free energy seem additive. The dN/dS ratio is low, suggesting
    strong purifying selection, and that structure is under stabilizing selection.
    We synthesized phages carrying ancestral haplotypes of the coat protein gene and
    measured their fitness experimentally. Our findings indicate that stabilizing
    mutations can have higher fitness, and that fitness optima do not necessarily
    coincide with energy minima.
article_number: '20160139'
article_processing_charge: Yes (in subscription journal)
author:
- first_name: Rodrigo A
  full_name: Fernandes Redondo, Rodrigo A
  id: 409D5C96-F248-11E8-B48F-1D18A9856A87
  last_name: Fernandes Redondo
  orcid: 0000-0002-5837-2793
- first_name: Harold
  full_name: Vladar, Harold
  id: 2A181218-F248-11E8-B48F-1D18A9856A87
  last_name: Vladar
  orcid: 0000-0002-5985-7653
- first_name: Tomasz
  full_name: Włodarski, Tomasz
  last_name: Włodarski
- first_name: Jonathan P
  full_name: Bollback, Jonathan P
  id: 2C6FA9CC-F248-11E8-B48F-1D18A9856A87
  last_name: Bollback
  orcid: 0000-0002-4624-4612
citation:
  ama: Fernandes Redondo RA, de Vladar H, Włodarski T, Bollback JP. Evolutionary interplay
    between structure, energy and epistasis in the coat protein of the ϕX174 phage
    family. <i>Journal of the Royal Society Interface</i>. 2017;14(126). doi:<a href="https://doi.org/10.1098/rsif.2016.0139">10.1098/rsif.2016.0139</a>
  apa: Fernandes Redondo, R. A., de Vladar, H., Włodarski, T., &#38; Bollback, J.
    P. (2017). Evolutionary interplay between structure, energy and epistasis in the
    coat protein of the ϕX174 phage family. <i>Journal of the Royal Society Interface</i>.
    Royal Society. <a href="https://doi.org/10.1098/rsif.2016.0139">https://doi.org/10.1098/rsif.2016.0139</a>
  chicago: Fernandes Redondo, Rodrigo A, Harold de Vladar, Tomasz Włodarski, and Jonathan
    P Bollback. “Evolutionary Interplay between Structure, Energy and Epistasis in
    the Coat Protein of the ΦX174 Phage Family.” <i>Journal of the Royal Society Interface</i>.
    Royal Society, 2017. <a href="https://doi.org/10.1098/rsif.2016.0139">https://doi.org/10.1098/rsif.2016.0139</a>.
  ieee: R. A. Fernandes Redondo, H. de Vladar, T. Włodarski, and J. P. Bollback, “Evolutionary
    interplay between structure, energy and epistasis in the coat protein of the ϕX174
    phage family,” <i>Journal of the Royal Society Interface</i>, vol. 14, no. 126.
    Royal Society, 2017.
  ista: Fernandes Redondo RA, de Vladar H, Włodarski T, Bollback JP. 2017. Evolutionary
    interplay between structure, energy and epistasis in the coat protein of the ϕX174
    phage family. Journal of the Royal Society Interface. 14(126), 20160139.
  mla: Fernandes Redondo, Rodrigo A., et al. “Evolutionary Interplay between Structure,
    Energy and Epistasis in the Coat Protein of the ΦX174 Phage Family.” <i>Journal
    of the Royal Society Interface</i>, vol. 14, no. 126, 20160139, Royal Society,
    2017, doi:<a href="https://doi.org/10.1098/rsif.2016.0139">10.1098/rsif.2016.0139</a>.
  short: R.A. Fernandes Redondo, H. de Vladar, T. Włodarski, J.P. Bollback, Journal
    of the Royal Society Interface 14 (2017).
date_created: 2018-12-11T11:50:01Z
date_published: 2017-01-04T00:00:00Z
date_updated: 2026-08-27T12:09:33Z
day: '04'
ddc:
- '570'
department:
- _id: NiBa
- _id: JoBo
doi: 10.1098/rsif.2016.0139
ec_funded: 1
external_id:
  isi:
  - '000393380400001'
file:
- access_level: open_access
  content_type: application/pdf
  creator: dernst
  date_created: 2019-01-18T09:14:02Z
  date_updated: 2019-01-18T09:14:02Z
  file_id: '5843'
  file_name: 2017_JRSI_Redondo.pdf
  file_size: 1092015
  relation: main_file
  success: 1
file_date_updated: 2019-01-18T09:14:02Z
fulldoi: https://doi.org/10.1098/rsif.2016.0139
has_accepted_license: '1'
intvolume: '        14'
isi: 1
issue: '126'
language:
- iso: eng
license: https://creativecommons.org/licenses/by/4.0/
month: '01'
oa: 1
oa_version: Published Version
project:
- _id: 25B07788-B435-11E9-9278-68D0E5697425
  call_identifier: FP7
  grant_number: '250152'
  name: Limits to selection in biology and in evolutionary computation
- _id: 2578D616-B435-11E9-9278-68D0E5697425
  call_identifier: H2020
  grant_number: '648440'
  name: Selective Barriers to Horizontal Gene Transfer
publication: Journal of the Royal Society Interface
publication_identifier:
  issn:
  - 1742-5689
publication_status: published
publisher: Royal Society
publist_id: '6303'
quality_controlled: '1'
related_material:
  record:
  - id: '9864'
    relation: research_data
    status: public
scopus_import: '1'
status: public
title: Evolutionary interplay between structure, energy and epistasis in the coat
  protein of the ϕX174 phage family
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: 14
year: '2017'
...
---
_id: '12905'
article_processing_charge: No
author:
- first_name: Alois
  full_name: Schlögl, Alois
  id: 45BF87EE-F248-11E8-B48F-1D18A9856A87
  last_name: Schlögl
  orcid: 0000-0002-5621-8100
- first_name: Janos
  full_name: Kiss, Janos
  id: 3D3A06F8-F248-11E8-B48F-1D18A9856A87
  last_name: Kiss
citation:
  ama: 'Schlögl A, Kiss J. Scientific Computing at IST Austria. In: <i>AHPC17 – Austrian
    HPC Meeting 2017</i>. FSP Scientific Computing; 2017:28.'
  apa: 'Schlögl, A., &#38; Kiss, J. (2017). Scientific Computing at IST Austria. In
    <i>AHPC17 – Austrian HPC Meeting 2017</i> (p. 28). Grundlsee, Austria: FSP Scientific
    Computing.'
  chicago: Schlögl, Alois, and Janos Kiss. “Scientific Computing at IST Austria.”
    In <i>AHPC17 – Austrian HPC Meeting 2017</i>, 28. FSP Scientific Computing, 2017.
  ieee: A. Schlögl and J. Kiss, “Scientific Computing at IST Austria,” in <i>AHPC17
    – Austrian HPC Meeting 2017</i>, Grundlsee, Austria, 2017, p. 28.
  ista: 'Schlögl A, Kiss J. 2017. Scientific Computing at IST Austria. AHPC17 – Austrian
    HPC Meeting 2017. AHPC: Austrian HPC Meeting, 28.'
  mla: Schlögl, Alois, and Janos Kiss. “Scientific Computing at IST Austria.” <i>AHPC17
    – Austrian HPC Meeting 2017</i>, FSP Scientific Computing, 2017, p. 28.
  short: A. Schlögl, J. Kiss, in:, AHPC17 – Austrian HPC Meeting 2017, FSP Scientific
    Computing, 2017, p. 28.
conference:
  end_date: 2017-03-03
  location: Grundlsee, Austria
  name: 'AHPC: Austrian HPC Meeting'
  start_date: 2017-03-01
corr_author: '1'
date_created: 2023-05-05T12:58:53Z
date_published: 2017-03-03T00:00:00Z
date_updated: 2026-10-14T09:39:37Z
day: '03'
ddc:
- '000'
department:
- _id: ScienComp
file:
- access_level: open_access
  checksum: 7bcc499479d4f4c5ce6c0071c24ca6c6
  content_type: application/pdf
  creator: dernst
  date_created: 2023-05-16T07:20:50Z
  date_updated: 2023-05-16T07:20:50Z
  file_id: '12969'
  file_name: 2017_AHPC_Schloegl.pdf
  file_size: 1005486
  relation: main_file
  success: 1
file_date_updated: 2023-05-16T07:20:50Z
has_accepted_license: '1'
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://asc.ac.at/fileadmin/user_upload/vsc/conferences/ahpc17/BOOKLET_AHPC17.pdf
month: '03'
oa: 1
oa_version: Published Version
page: '28'
publication: AHPC17 – Austrian HPC Meeting 2017
publication_status: published
publisher: FSP Scientific Computing
status: public
title: Scientific Computing at IST Austria
type: conference_abstract
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
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: 2026-10-24T22:30:19Z
day: '01'
department:
- _id: MiSi
doi: 10.1172/JCI80631
external_id:
  isi:
  - '000402620800008'
  pmid:
  - '28504646'
fulldoi: https://doi.org/10.1172/JCI80631
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: '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: 2026-10-24T22:30:24Z
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
fulldoi: https://doi.org/10.7554/eLife.25100
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: '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: 2026-10-24T22:30:27Z
day: '23'
department:
- _id: CaHe
- _id: CaGu
- _id: GaTk
doi: 10.1016/j.devcel.2017.09.014
ec_funded: 1
external_id:
  isi:
  - '000413443700011'
fulldoi: https://doi.org/10.1016/j.devcel.2017.09.014
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: '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: 2026-10-24T22:31:04Z
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
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file_date_updated: 2018-12-12T10:09:47Z
fulldoi: https://doi.org/10.1371/journal.pone.0174066
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:
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  - id: '5556'
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    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: '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: 2026-10-24T22:31:11Z
day: '15'
ddc:
- '570'
department:
- _id: Bio
- _id: CaHe
doi: 10.1242/dev.144964
external_id:
  isi:
  - '000402275900007'
  pmid:
  - '28512197'
file:
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  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
fulldoi: https://doi.org/10.1242/dev.144964
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: '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: 2026-10-24T22:31:11Z
day: '27'
department:
- _id: CaHe
- _id: BjHo
- _id: Bio
doi: 10.1038/ncb3492
ec_funded: 1
external_id:
  isi:
  - '000397917000009'
  pmid:
  - '28346437'
fulldoi: https://doi.org/10.1038/ncb3492
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: '8350'
    relation: dissertation_contains
    status: public
  - id: '50'
    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: '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: 2026-10-24T22:31:24Z
day: '18'
department:
- _id: MiSi
doi: 10.1016/j.immuni.2017.04.006
external_id:
  isi:
  - '000399451100002'
fulldoi: https://doi.org/10.1016/j.immuni.2017.04.006
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: '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: 2026-10-24T22:31:35Z
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
fulldoi: https://doi.org/10.1007/978-3-319-68167-2_4
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: 2026-10-24T22:31:34Z
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'
fulldoi: https://doi.org/10.1007/978-3-319-63390-9_3
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:
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  - 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: '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: 2026-10-24T22:31:40Z
day: '28'
ddc:
- '570'
department:
- _id: SiHi
- _id: MaLo
doi: 10.3389/fncel.2017.00176
ec_funded: 1
external_id:
  isi:
  - '000404486700001'
file:
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  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
fulldoi: https://doi.org/10.3389/fncel.2017.00176
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: '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: 2026-10-24T22:31:45Z
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:
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  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
fulldoi: https://doi.org/10.1371/journal.pcbi.1005609
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: 2026-10-24T22:31:45Z
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
fulldoi: https://doi.org/10.1016/j.copbio.2017.02.013
has_accepted_license: '1'
intvolume: '        46'
isi: 1
language:
- iso: eng
license: https://creativecommons.org/licenses/by-nc-nd/4.0/
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:
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  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: '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: 2026-10-24T22:31:50Z
day: '01'
ddc:
- '571'
department:
- _id: RySh
doi: 10.1371/journal.pone.0179377
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title: PirB regulates asymmetries in hippocampal circuitry
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  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
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...
---
_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: 2026-10-24T22:31:51Z
day: '17'
ddc:
- '575'
department:
- _id: EvBe
doi: 10.1007/978-1-4939-6831-2_1
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file_date_updated: 2019-10-15T07:47:05Z
fulldoi: https://doi.org/10.1007/978-1-4939-6831-2_1
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:
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  - id: '539'
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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'
...
