---
APC_amount: 4215,38 EUR
DOAJ_listed: '1'
OA_place: publisher
OA_type: gold
PlanS_conform: '1'
_id: '19963'
abstract:
- lang: eng
text: The acquisition of cellular identity requires large-scale alterations in cellular
state. The noncanonical proteasome activator PSME3 is known to regulate diverse
cellular processes, but its importance for differentiation remains unclear. Here,
we demonstrate that PSME3 binds dynamically to highly active promoters over the
course of differentiation. However, loss of PSME3 does not globally affect mRNA
transcription. We find instead that PSME3 influences the levels of several adhesion-related
proteins and acts upstream of the HSP90 co-chaperone NUDC to regulate cell motility
and myoblast differentiation in a proteasome-independent manner. Our findings
reveal several new facets of PSME3 functionality and highlight its importance
for the differentiation of myogenic cells.
acknowledged_ssus:
- _id: LifeSc
- _id: Bio
acknowledgement: 'All proteomics analysis was done by the ISTA LSF Mass Spectrometry
Service: Ewelina Dutkiewicz-Kopczynska processed the samples (digest and cleanup);
Bella Bruszel optimized the acquisition methods, acquired the data, and performed
all searches; and Armel Nicolas provided pre- and post-project consulting and post-processed
the search results using a development version of their data analysis package, proteoCraft
(publication pending). The authors would like to thank Saki for their clarity of
thought and insight, as well as Dr. Lorenzo Puri and the members of his laboratory
for invaluable discussions relating to the project. This research was further supported
by the Lab Support Facility and the Imaging and Optics Facility of ISTA.'
article_number: e202503208
article_processing_charge: Yes
article_type: original
author:
- first_name: Kenneth D
full_name: Kuhn, Kenneth D
id: 7deed7e0-0133-11f0-8590-c4600b08d0f4
last_name: Kuhn
- first_name: Ukrae H.
full_name: Cho, Ukrae H.
last_name: Cho
- first_name: Martin W
full_name: Hetzer, Martin W
id: 86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed
last_name: Hetzer
orcid: 0000-0002-2111-992X
citation:
ama: Kuhn KD, Cho UH, Hetzer M. PSME3 regulates migration and differentiation of
myoblasts. Life Science Alliance. 2025;8(9). doi:10.26508/lsa.202503208
apa: Kuhn, K. D., Cho, U. H., & Hetzer, M. (2025). PSME3 regulates migration
and differentiation of myoblasts. Life Science Alliance. Embo Press. https://doi.org/10.26508/lsa.202503208
chicago: Kuhn, Kenneth D, Ukrae H. Cho, and Martin Hetzer. “PSME3 Regulates Migration
and Differentiation of Myoblasts.” Life Science Alliance. Embo Press, 2025.
https://doi.org/10.26508/lsa.202503208.
ieee: K. D. Kuhn, U. H. Cho, and M. Hetzer, “PSME3 regulates migration and differentiation
of myoblasts,” Life Science Alliance, vol. 8, no. 9. Embo Press, 2025.
ista: Kuhn KD, Cho UH, Hetzer M. 2025. PSME3 regulates migration and differentiation
of myoblasts. Life Science Alliance. 8(9), e202503208.
mla: Kuhn, Kenneth D., et al. “PSME3 Regulates Migration and Differentiation of
Myoblasts.” Life Science Alliance, vol. 8, no. 9, e202503208, Embo Press,
2025, doi:10.26508/lsa.202503208.
short: K.D. Kuhn, U.H. Cho, M. Hetzer, Life Science Alliance 8 (2025).
corr_author: '1'
date_created: 2025-07-06T22:01:22Z
date_published: 2025-09-01T00:00:00Z
date_updated: 2026-05-20T08:38:04Z
day: '01'
ddc:
- '570'
department:
- _id: MaHe
doi: 10.26508/lsa.202503208
external_id:
isi:
- '001511452100001'
pmid:
- '40537284'
file:
- access_level: open_access
checksum: 591d47aa39fc969986c7d3b966890f5f
content_type: application/pdf
creator: dernst
date_created: 2025-12-30T09:17:09Z
date_updated: 2025-12-30T09:17:09Z
file_id: '20904'
file_name: 2025_LifeScienceAlliance_Kuhn.pdf
file_size: 5471288
relation: main_file
success: 1
file_date_updated: 2025-12-30T09:17:09Z
fulldoi: https://doi.org/10.26508/lsa.202503208
has_accepted_license: '1'
intvolume: ' 8'
isi: 1
issue: '9'
language:
- iso: eng
month: '09'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: B67AFEDC-15C9-11EA-A837-991A96BB2854
name: IST Austria Open Access Fund
publication: Life Science Alliance
publication_identifier:
eissn:
- 2575-1077
publication_status: published
publisher: Embo Press
quality_controlled: '1'
scopus_import: '1'
status: public
title: PSME3 regulates migration and differentiation of myoblasts
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: 8
year: '2025'
...
---
OA_place: publisher
OA_type: hybrid
PlanS_conform: '1'
_id: '20154'
abstract:
- lang: eng
text: In long-lived mammals, including humans, brain cell homeostasis is critical
for maintaining brain function throughout life. Most neurons are generated during
development and must maintain their cellular identity and plasticity to preserve
brain function. Although extensive studies indicate the importance of recycling
and regenerating cellular molecules to maintain cellular homeostasis, recent evidence
has shown that some proteins and RNAs do not turn over for months and even years.
We propose that these long-lived cellular molecules may be the basis for maintaining
brain function in the long term, but also a potential convergent target of brain
aging. We highlight key discoveries and challenges, and propose potential directions
to unravel the mystery of brain cell longevity.
acknowledgement: The work was supported by the Deutsche Forschungsgemeinschaft (DFG,
German Research Foundation) (470322152 – T1347/3-1; 497658532 – T1347/4-1; 507965872
– T1347/5-1; and 460333672 – CRC1540 Exploring Brain Mechanics) to T.T., the Schram
Foundation (T.T.), the European Research Council (ERC-2018-STG, 804468 EAGER; ERC-2023-COG,
101125034 NEUTIME) to T.T., the Hans-Georg Geis und Xue Hong Dong-Geis Foundation
and Forschungsstiftung Medizin am Universitätsklinikum Erlangen to T.T., and the
Interdisciplinary Centre for Clinical Research Erlangen (Interdisziplinäres Zentrum
für Klinische Forschung, Universitätsklinikum Erlangen; P162 to T.T.). We thank
Dr Laura J. Harrison for editing assistance.
article_processing_charge: Yes (in subscription journal)
article_type: original
author:
- first_name: Martin W
full_name: Hetzer, Martin W
id: 86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed
last_name: Hetzer
orcid: 0000-0002-2111-992X
- first_name: Tomohisa
full_name: Toda, Tomohisa
last_name: Toda
citation:
ama: Hetzer M, Toda T. Long-lived cellular molecules in the brain. Trends in
Neurosciences. 2025;48(9):645-654. doi:10.1016/j.tins.2025.07.004
apa: Hetzer, M., & Toda, T. (2025). Long-lived cellular molecules in the brain.
Trends in Neurosciences. Elsevier. https://doi.org/10.1016/j.tins.2025.07.004
chicago: Hetzer, Martin, and Tomohisa Toda. “Long-Lived Cellular Molecules in the
Brain.” Trends in Neurosciences. Elsevier, 2025. https://doi.org/10.1016/j.tins.2025.07.004.
ieee: M. Hetzer and T. Toda, “Long-lived cellular molecules in the brain,” Trends
in Neurosciences, vol. 48, no. 9. Elsevier, pp. 645–654, 2025.
ista: Hetzer M, Toda T. 2025. Long-lived cellular molecules in the brain. Trends
in Neurosciences. 48(9), 645–654.
mla: Hetzer, Martin, and Tomohisa Toda. “Long-Lived Cellular Molecules in the Brain.”
Trends in Neurosciences, vol. 48, no. 9, Elsevier, 2025, pp. 645–54, doi:10.1016/j.tins.2025.07.004.
short: M. Hetzer, T. Toda, Trends in Neurosciences 48 (2025) 645–654.
corr_author: '1'
date_created: 2025-08-10T22:01:29Z
date_published: 2025-09-01T00:00:00Z
date_updated: 2025-12-29T13:47:58Z
day: '01'
ddc:
- '570'
department:
- _id: MaHe
doi: 10.1016/j.tins.2025.07.004
external_id:
isi:
- '001568965400001'
pmid:
- '40744775'
file:
- access_level: open_access
checksum: 90942491b499f70b0bf48b8aec2e7387
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creator: dernst
date_created: 2025-12-29T13:47:27Z
date_updated: 2025-12-29T13:47:27Z
file_id: '20873'
file_name: 2025_TrendsNeurosciences_Hetzer.pdf
file_size: 327847
relation: main_file
success: 1
file_date_updated: 2025-12-29T13:47:27Z
fulldoi: https://doi.org/10.1016/j.tins.2025.07.004
has_accepted_license: '1'
intvolume: ' 48'
isi: 1
issue: '9'
language:
- iso: eng
month: '09'
oa: 1
oa_version: Published Version
page: 645-654
pmid: 1
publication: Trends in Neurosciences
publication_identifier:
eissn:
- 1878-108X
issn:
- 0166-2236
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: Long-lived cellular molecules in the brain
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: 48
year: '2025'
...
---
DOAJ_listed: '1'
OA_place: publisher
OA_type: gold
_id: '18480'
abstract:
- lang: eng
text: Caloric restriction (CR) can extend the organism life- and health-span by
improving glucose homeostasis. How CR affects the structure-function of pancreatic
beta cells remains unknown. We used single nucleus transcriptomics to show that
CR increases the expression of genes for beta cell identity, protein processing,
and organelle homeostasis. Gene regulatory network analysis reveal that CR activates
transcription factors important for beta cell identity and homeostasis, while
imaging metabolomics demonstrates that beta cells upon CR are more energetically
competent. In fact, high-resolution microscopy show that CR reduces beta cell
mitophagy to increase mitochondria mass and the potential for ATP generation.
However, CR beta cells have impaired adaptive proliferation in response to high
fat diet feeding. Finally, we show that long-term CR delays the onset of beta
cell aging hallmarks and promotes cell longevity by reducing beta cell turnover.
Therefore, CR could be a feasible approach to preserve compromised beta cell structure-function
during aging and diabetes.
acknowledgement: We are thankful to Michelle Reyzer from the Vanderbilt Mass Spectrometry
Research Center for assistance with MALDI-MS imaging and analysis, to the outstanding
team at the Vanderbilt Mouse Metabolic Phenotyping Center for all the assistance
with in vivo glucose homeostasis tests (DK135073, 1S10RR028101-01). We also thank
the University of Michigan Animal Phenotyping Core for conducting the bomb calorimetry
experiments (1U2CDK110768, DK020575, and DK089503). This research was supported
by recruitment funds from the Vanderbilt’s Department of Molecular Physiology and
Biophysics and NIH grants 1R03DK127484, 5U24DK097771, and 1R01DK138141 to RAeD,
by a grant from the Canadian Institutes of Health Research (CIHR; 487188) to PEM,
by and NIH DK132669 to D.D. PEM holds the Canada Research Chair in Islet Biology.
article_number: '9063'
article_processing_charge: Yes
article_type: original
author:
- first_name: Cristiane
full_name: Dos Santos, Cristiane
last_name: Dos Santos
- first_name: Amanda
full_name: Cambraia, Amanda
last_name: Cambraia
- first_name: Shristi
full_name: Shrestha, Shristi
last_name: Shrestha
- first_name: Melanie
full_name: Cutler, Melanie
last_name: Cutler
- first_name: Matthew
full_name: Cottam, Matthew
last_name: Cottam
- first_name: Guy
full_name: Perkins, Guy
last_name: Perkins
- first_name: Varda
full_name: Lev-Ram, Varda
last_name: Lev-Ram
- first_name: Birbickram
full_name: Roy, Birbickram
last_name: Roy
- first_name: Christopher
full_name: Acree, Christopher
last_name: Acree
- first_name: Keun Young
full_name: Kim, Keun Young
last_name: Kim
- first_name: Thomas
full_name: Deerinck, Thomas
last_name: Deerinck
- first_name: Danielle
full_name: Dean, Danielle
last_name: Dean
- first_name: Jean Philippe
full_name: Cartailler, Jean Philippe
last_name: Cartailler
- first_name: Patrick E.
full_name: Macdonald, Patrick E.
last_name: Macdonald
- first_name: Martin W
full_name: Hetzer, Martin W
id: 86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed
last_name: Hetzer
orcid: 0000-0002-2111-992X
- first_name: Mark
full_name: Ellisman, Mark
last_name: Ellisman
- first_name: Rafael
full_name: Arrojo E Drigo, Rafael
last_name: Arrojo E Drigo
citation:
ama: Dos Santos C, Cambraia A, Shrestha S, et al. Calorie restriction increases
insulin sensitivity to promote beta cell homeostasis and longevity in mice. Nature
Communications. 2024;15. doi:10.1038/s41467-024-53127-2
apa: Dos Santos, C., Cambraia, A., Shrestha, S., Cutler, M., Cottam, M., Perkins,
G., … Arrojo E Drigo, R. (2024). Calorie restriction increases insulin sensitivity
to promote beta cell homeostasis and longevity in mice. Nature Communications.
Springer Nature. https://doi.org/10.1038/s41467-024-53127-2
chicago: Dos Santos, Cristiane, Amanda Cambraia, Shristi Shrestha, Melanie Cutler,
Matthew Cottam, Guy Perkins, Varda Lev-Ram, et al. “Calorie Restriction Increases
Insulin Sensitivity to Promote Beta Cell Homeostasis and Longevity in Mice.” Nature
Communications. Springer Nature, 2024. https://doi.org/10.1038/s41467-024-53127-2.
ieee: C. Dos Santos et al., “Calorie restriction increases insulin sensitivity
to promote beta cell homeostasis and longevity in mice,” Nature Communications,
vol. 15. Springer Nature, 2024.
ista: Dos Santos C, Cambraia A, Shrestha S, Cutler M, Cottam M, Perkins G, Lev-Ram
V, Roy B, Acree C, Kim KY, Deerinck T, Dean D, Cartailler JP, Macdonald PE, Hetzer
M, Ellisman M, Arrojo E Drigo R. 2024. Calorie restriction increases insulin sensitivity
to promote beta cell homeostasis and longevity in mice. Nature Communications.
15, 9063.
mla: Dos Santos, Cristiane, et al. “Calorie Restriction Increases Insulin Sensitivity
to Promote Beta Cell Homeostasis and Longevity in Mice.” Nature Communications,
vol. 15, 9063, Springer Nature, 2024, doi:10.1038/s41467-024-53127-2.
short: C. Dos Santos, A. Cambraia, S. Shrestha, M. Cutler, M. Cottam, G. Perkins,
V. Lev-Ram, B. Roy, C. Acree, K.Y. Kim, T. Deerinck, D. Dean, J.P. Cartailler,
P.E. Macdonald, M. Hetzer, M. Ellisman, R. Arrojo E Drigo, Nature Communications
15 (2024).
das_tickbox: '1'
dataavailabilitystatement: Tabular and processed sequencing data is deposited in Zenodo
(https://doi.org/10.5281/zenodo.6491943). The single nucleus multiome sequencing
data has been deposited in the GEO repository (GSE276572, https://www.ncbi.xyz/geo/query/acc.cgi?acc=GSE276572).
Source data are provided with this paper.
date_created: 2024-10-27T23:01:44Z
date_published: 2024-10-21T00:00:00Z
date_updated: 2026-10-16T09:00:16Z
day: '21'
ddc:
- '570'
department:
- _id: MaHe
doi: 10.1038/s41467-024-53127-2
external_id:
isi:
- '001426270600023'
pmid:
- '39433757'
file:
- access_level: open_access
checksum: b936b1c047f41cd427f00e3dc79327d3
content_type: application/pdf
creator: dernst
date_created: 2024-11-04T10:37:56Z
date_updated: 2024-11-04T10:37:56Z
file_id: '18502'
file_name: 2024_NatureComm_dosSantos.pdf
file_size: 7358742
relation: main_file
success: 1
file_date_updated: 2024-11-04T10:37:56Z
fulldoi: https://doi.org/10.1038/s41467-024-53127-2
has_accepted_license: '1'
intvolume: ' 15'
isi: 1
language:
- iso: eng
month: '10'
oa: 1
oa_version: Published Version
pmid: 1
publication: Nature Communications
publication_identifier:
eissn:
- 2041-1723
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
related_material:
record:
- id: '22865'
relation: research_data
status: public
researchdata_availability: yes
scopus_import: '1'
status: public
supplementarymaterial: yes
title: Calorie restriction increases insulin sensitivity to promote beta cell homeostasis
and longevity in mice
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: 15
year: '2024'
...
---
OA_place: repository
OA_type: green
_id: '15316'
abstract:
- lang: eng
text: Genomic DNA that resides in the nuclei of mammalian neurons can be as old
as the organism itself. The life span of nuclear RNAs, which are critical for
proper chromatin architecture and transcription regulation, has not been determined
in adult tissues. In this work, we identified and characterized nuclear RNAs that
do not turn over for at least 2 years in a subset of postnatally born cells in
the mouse brain. These long-lived RNAs were stably retained in nuclei in a neural
cell type–specific manner and were required for the maintenance of heterochromatin.
Thus, the life span of neural cells may depend on both the molecular longevity
of DNA for the storage of genetic information and also the extreme stability of
RNA for the functional organization of chromatin.
acknowledgement: 'European Research Council: ERC-2018-STG, 804468 EAGER; European
Research Council: ERC-2023-COG, 101125034 NEUTIME; Deutsche Forschungsgemeinschaft:
TO1347/4-1; Boehringer Ingelheim Stiftung; Deutsches Zentrum für Neurodegenerative
Erkrankungen'
article_processing_charge: No
article_type: original
author:
- first_name: Sara
full_name: Zocher, Sara
last_name: Zocher
- first_name: Asako
full_name: Mccloskey, Asako
last_name: Mccloskey
- first_name: Anne
full_name: Karasinsky, Anne
last_name: Karasinsky
- first_name: Roberta
full_name: Schulte, Roberta
last_name: Schulte
- first_name: Ulrike
full_name: Friedrich, Ulrike
last_name: Friedrich
- first_name: Mathias
full_name: Lesche, Mathias
last_name: Lesche
- first_name: Nicole
full_name: Rund, Nicole
last_name: Rund
- first_name: Fred H.
full_name: Gage, Fred H.
last_name: Gage
- first_name: Martin W
full_name: Hetzer, Martin W
id: 86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed
last_name: Hetzer
orcid: 0000-0002-2111-992X
- first_name: Tomohisa
full_name: Toda, Tomohisa
last_name: Toda
citation:
ama: Zocher S, Mccloskey A, Karasinsky A, et al. Lifelong persistence of nuclear
RNAs in the mouse brain. Science. 2024;384(6691):53-59. doi:10.1126/science.adf3481
apa: Zocher, S., Mccloskey, A., Karasinsky, A., Schulte, R., Friedrich, U., Lesche,
M., … Toda, T. (2024). Lifelong persistence of nuclear RNAs in the mouse brain.
Science. AAAS. https://doi.org/10.1126/science.adf3481
chicago: Zocher, Sara, Asako Mccloskey, Anne Karasinsky, Roberta Schulte, Ulrike
Friedrich, Mathias Lesche, Nicole Rund, Fred H. Gage, Martin Hetzer, and Tomohisa
Toda. “Lifelong Persistence of Nuclear RNAs in the Mouse Brain.” Science.
AAAS, 2024. https://doi.org/10.1126/science.adf3481.
ieee: S. Zocher et al., “Lifelong persistence of nuclear RNAs in the mouse
brain,” Science, vol. 384, no. 6691. AAAS, pp. 53–59, 2024.
ista: Zocher S, Mccloskey A, Karasinsky A, Schulte R, Friedrich U, Lesche M, Rund
N, Gage FH, Hetzer M, Toda T. 2024. Lifelong persistence of nuclear RNAs in the
mouse brain. Science. 384(6691), 53–59.
mla: Zocher, Sara, et al. “Lifelong Persistence of Nuclear RNAs in the Mouse Brain.”
Science, vol. 384, no. 6691, AAAS, 2024, pp. 53–59, doi:10.1126/science.adf3481.
short: S. Zocher, A. Mccloskey, A. Karasinsky, R. Schulte, U. Friedrich, M. Lesche,
N. Rund, F.H. Gage, M. Hetzer, T. Toda, Science 384 (2024) 53–59.
corr_author: '1'
das_tickbox: '1'
dataavailabilitystatement: All data are available in the main text, figures, or supplementary
materials. EU-RNA-seq data were submitted to the Gene Expression Omnibus (GEO) under
accession no. GSE248101.
date_created: 2024-04-14T22:01:01Z
date_published: 2024-04-04T00:00:00Z
date_updated: 2026-10-16T08:59:32Z
day: '04'
department:
- _id: MaHe
doi: 10.1126/science.adf3481
external_id:
isi:
- '001253335100031'
pmid:
- '38574132'
fulldoi: https://doi.org/10.1126/science.adf3481
intvolume: ' 384'
isi: 1
issue: '6691'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7615865
month: '04'
oa: 1
oa_version: Submitted Version
page: 53-59
pmid: 1
publication: Science
publication_identifier:
eissn:
- 1095-9203
issn:
- 0036-8075
publication_status: published
publisher: AAAS
quality_controlled: '1'
related_material:
link:
- description: News on ISTA website
relation: press_release
url: https://ista.ac.at/en/news/nerve-cells-old-at-heart/
researchdata_availability: yes
scopus_import: '1'
status: public
supplementarymaterial: yes
title: Lifelong persistence of nuclear RNAs in the mouse brain
type: journal_article
user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 384
year: '2024'
...
---
_id: '12880'
abstract:
- lang: eng
text: Peripheral heterochromatin positioning depends on nuclear envelope associated
proteins and repressive histone modifications. Here we show that overexpression
(OE) of Lamin B1 (LmnB1) leads to the redistribution of peripheral heterochromatin
into heterochromatic foci within the nucleoplasm. These changes represent a perturbation
of heterochromatin binding at the nuclear periphery (NP) through a mechanism independent
from altering other heterochromatin anchors or histone post-translational modifications.
We further show that LmnB1 OE alters gene expression. These changes do not correlate
with different levels of H3K9me3, but a significant number of the misregulated
genes were likely mislocalized away from the NP upon LmnB1 OE. We also observed
an enrichment of developmental processes amongst the upregulated genes. ~74% of
these genes were normally repressed in our cell type, suggesting that LmnB1 OE
promotes gene de-repression. This demonstrates a broader consequence of LmnB1
OE on cell fate, and highlights the importance of maintaining proper levels of
LmnB1.
acknowledgement: 'We thank members of the Hetzer lab for critical review of the manuscript;
Novogene for mRNA library preparation and sequencing; the Next-Generation Sequencing
Core Facility at the Salk Institute, with funding from NIH-NCI CCSG: P30 014195,
the Chapman Foundation, and the Helmsley Charitable Trust, for sequencing Cut&Run
libraries; and the Waitt Advanced Biophotonics Core Facility at the Salk Institute,
with funding from NIH-NCI CCSG: P30 014195, the Waitt Foundation, and the Chan-Zuckerberg
Initiative Imaging Scientist Award, for electron microscopy sample preparation and
imaging.'
article_number: '2202548'
article_processing_charge: No
article_type: original
author:
- first_name: Jeanae M.
full_name: Kaneshiro, Jeanae M.
last_name: Kaneshiro
- first_name: Juliana S.
full_name: Capitanio, Juliana S.
last_name: Capitanio
- first_name: Martin W
full_name: Hetzer, Martin W
id: 86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed
last_name: Hetzer
orcid: 0000-0002-2111-992X
citation:
ama: Kaneshiro JM, Capitanio JS, Hetzer M. Lamin B1 overexpression alters chromatin
organization and gene expression. Nucleus. 2023;14(1). doi:10.1080/19491034.2023.2202548
apa: Kaneshiro, J. M., Capitanio, J. S., & Hetzer, M. (2023). Lamin B1 overexpression
alters chromatin organization and gene expression. Nucleus. Taylor &
Francis. https://doi.org/10.1080/19491034.2023.2202548
chicago: Kaneshiro, Jeanae M., Juliana S. Capitanio, and Martin Hetzer. “Lamin B1
Overexpression Alters Chromatin Organization and Gene Expression.” Nucleus.
Taylor & Francis, 2023. https://doi.org/10.1080/19491034.2023.2202548.
ieee: J. M. Kaneshiro, J. S. Capitanio, and M. Hetzer, “Lamin B1 overexpression
alters chromatin organization and gene expression,” Nucleus, vol. 14, no.
1. Taylor & Francis, 2023.
ista: Kaneshiro JM, Capitanio JS, Hetzer M. 2023. Lamin B1 overexpression alters
chromatin organization and gene expression. Nucleus. 14(1), 2202548.
mla: Kaneshiro, Jeanae M., et al. “Lamin B1 Overexpression Alters Chromatin Organization
and Gene Expression.” Nucleus, vol. 14, no. 1, 2202548, Taylor & Francis,
2023, doi:10.1080/19491034.2023.2202548.
short: J.M. Kaneshiro, J.S. Capitanio, M. Hetzer, Nucleus 14 (2023).
corr_author: '1'
date_created: 2023-04-30T22:01:06Z
date_published: 2023-04-18T00:00:00Z
date_updated: 2024-10-09T21:05:01Z
day: '18'
ddc:
- '570'
department:
- _id: MaHe
doi: 10.1080/19491034.2023.2202548
external_id:
isi:
- '000971629400001'
pmid:
- '37071033'
file:
- access_level: open_access
checksum: 8e707eda84f64dbad7f03545ae0a83ef
content_type: application/pdf
creator: dernst
date_created: 2023-05-02T07:24:55Z
date_updated: 2023-05-02T07:24:55Z
file_id: '12884'
file_name: 2023_Nucleus_Kaneshiro.pdf
file_size: 3811113
relation: main_file
success: 1
file_date_updated: 2023-05-02T07:24:55Z
fulldoi: https://doi.org/10.1080/19491034.2023.2202548
has_accepted_license: '1'
intvolume: ' 14'
isi: 1
issue: '1'
language:
- iso: eng
month: '04'
oa: 1
oa_version: Published Version
pmid: 1
publication: Nucleus
publication_identifier:
eissn:
- 1949-1042
issn:
- 1949-1034
publication_status: published
publisher: Taylor & Francis
quality_controlled: '1'
scopus_import: '1'
status: public
title: Lamin B1 overexpression alters chromatin organization and gene expression
tmp:
image: /images/cc_by_nc.png
legal_code_url: https://creativecommons.org/licenses/by-nc/4.0/legalcode
name: Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0)
short: CC BY-NC (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 14
year: '2023'
...
---
_id: '14315'
abstract:
- lang: eng
text: During apoptosis, caspases degrade 8 out of ~30 nucleoporins to irreversibly
demolish the nuclear pore complex. However, for poorly understood reasons, caspases
are also activated during cell differentiation. Here, we show that sublethal activation
of caspases during myogenesis results in the transient proteolysis of four peripheral
Nups and one transmembrane Nup. ‘Trimmed’ NPCs become nuclear export-defective,
and we identified in an unbiased manner several classes of cytoplasmic, plasma
membrane, and mitochondrial proteins that rapidly accumulate in the nucleus. NPC
trimming by non-apoptotic caspases was also observed in neurogenesis and endoplasmic
reticulum stress. Our results suggest that caspases can reversibly modulate nuclear
transport activity, which allows them to function as agents of cell differentiation
and adaptation at sublethal levels.
acknowledgement: 'We thank the members of the Hetzer laboratory, Tony Hunter (Salk),
Lorenzo Puri (Sanford Burnham Prebys), and Jongmin Kim (Massachusetts General Hospital)
for the critical reading of the manuscript; Kenneth Diffenderfer and Aimee Pankonin
(Stem Cell Core at the Salk Institute) for help with neurogenesis; Carol Marchetto
and Fred Gage (Salk) for providing H9 embryonic stem cells; Lorenzo Puri, Alexandra
Sacco, and Luca Caputo (Sanford Burnham Prebys) for helpful discussions and sharing
mouse primary myoblasts. This work was supported by a Glenn Foundation for Medical
Research Postdoctoral Fellowship in Aging Research (UHC), the NOMIS foundation (MWH),
and the National Institutes of Health (R01 NS096786 to MWH and K01 AR080828 to UHC).
This work was also supported by the Mass Spectrometry Core of the Salk Institute
with funding from NIH-NCI CCSG: P30 014195 and the Helmsley Center for Genomic Medicine.
We thank Jolene Diedrich and Antonio Pinto for technical support.'
article_number: RP89066
article_processing_charge: Yes
article_type: original
author:
- first_name: Ukrae H.
full_name: Cho, Ukrae H.
last_name: Cho
- first_name: Martin W
full_name: Hetzer, Martin W
id: 86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed
last_name: Hetzer
orcid: 0000-0002-2111-992X
citation:
ama: Cho UH, Hetzer M. Caspase-mediated nuclear pore complex trimming in cell differentiation
and endoplasmic reticulum stress. eLife. 2023;12. doi:10.7554/eLife.89066
apa: Cho, U. H., & Hetzer, M. (2023). Caspase-mediated nuclear pore complex
trimming in cell differentiation and endoplasmic reticulum stress. ELife.
eLife Sciences Publications. https://doi.org/10.7554/eLife.89066
chicago: Cho, Ukrae H., and Martin Hetzer. “Caspase-Mediated Nuclear Pore Complex
Trimming in Cell Differentiation and Endoplasmic Reticulum Stress.” ELife.
eLife Sciences Publications, 2023. https://doi.org/10.7554/eLife.89066.
ieee: U. H. Cho and M. Hetzer, “Caspase-mediated nuclear pore complex trimming in
cell differentiation and endoplasmic reticulum stress,” eLife, vol. 12.
eLife Sciences Publications, 2023.
ista: Cho UH, Hetzer M. 2023. Caspase-mediated nuclear pore complex trimming in
cell differentiation and endoplasmic reticulum stress. eLife. 12, RP89066.
mla: Cho, Ukrae H., and Martin Hetzer. “Caspase-Mediated Nuclear Pore Complex Trimming
in Cell Differentiation and Endoplasmic Reticulum Stress.” ELife, vol.
12, RP89066, eLife Sciences Publications, 2023, doi:10.7554/eLife.89066.
short: U.H. Cho, M. Hetzer, ELife 12 (2023).
corr_author: '1'
date_created: 2023-09-10T22:01:11Z
date_published: 2023-09-04T00:00:00Z
date_updated: 2024-10-09T21:06:57Z
day: '04'
ddc:
- '570'
department:
- _id: MaHe
doi: 10.7554/eLife.89066
external_id:
pmid:
- '37665327'
file:
- access_level: open_access
checksum: db24bf3d595507387b48d3799c33e289
content_type: application/pdf
creator: dernst
date_created: 2023-09-15T06:59:10Z
date_updated: 2023-09-15T06:59:10Z
file_id: '14336'
file_name: 2023_eLife_Cho.pdf
file_size: 3703097
relation: main_file
success: 1
file_date_updated: 2023-09-15T06:59:10Z
fulldoi: https://doi.org/10.7554/eLife.89066
has_accepted_license: '1'
intvolume: ' 12'
language:
- iso: eng
month: '09'
oa: 1
oa_version: Published Version
pmid: 1
publication: eLife
publication_identifier:
eissn:
- 2050-084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
scopus_import: '1'
status: public
title: Caspase-mediated nuclear pore complex trimming in cell differentiation and
endoplasmic reticulum stress
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: '2023'
...
---
_id: '14868'
abstract:
- lang: eng
text: The role of nuclear pore complexes (NPCs) in genome organization remains poorly
characterized due to technical limitations in probing genome-wide protein-DNA
interactions specific to the nuclear periphery. Here, we developed a new sensitive
method, NPC-DamID, which combines in vitro reconstitution of nuclear import and
DamID technology. The fixation-free method identifies chromatin interactions at
the NPCs in intact nuclei from cells and tissues. We found that NPCs are preferentially
associated with common and hierarchically arranged super-enhancers (SEs) across
multiple cell types. We also uncovered phase-separated condensates at NPCs that
compartmentalize and concentrate transcriptional coactivators and structural proteins
at SE-regulated genes. Our results support NPCs as anchoring sites for SE regulatory
hubs and cell-type-specific transcriptional control.
acknowledgement: "This work was supported by M.H.’s NIH R01 grants (NS096786, GM126829)
and Salk Cancer Center Support Grant P30 CA014195. M.H. also received financial
support from the W.M. Keck Foundation and the NOMIS Foundation. Further, M.H. received
support from the AHA-Allen Initiative in Brain Health and Cognitive Impairment award
made jointly through the American Heart Association and The Paul G. Allen Frontiers
Group (19PABH134610000).\r\n\r\nS.T. and J.C. were supported by Salk’s Women & Science
Awards. S.T. also received financial support from the Hewitt Foundation fellowship,
and J.C. is a Paul F. Glenn Biology of Aging fellow. J.H. was supported by the National
Natural Science Foundation of China (31871317 and 32070635).\r\n\r\nWe thank Roberta
Schulte for assistance with in vitro transport assays, for comments that greatly
improved the manuscript, and for helping refine the figures presented in this work.
We thank Shefali Krishna for creating the diagram for the NPC-DamID method, for
her input on super-resolution microscopy analysis, and her insightful comments on
this manuscript. We thank all members of the Hetzer lab for helpful discussions
of these research ideas and their thoughtful comments on this manuscript. We are
also grateful to Salk’s core facilities for their assistance. Specifically, we thank
the Next Generation Sequencing Core (NGS) for sequencing our DamID and RNA NGS libraries,
the Advanced Biophotonics Core for assistance with super-resolution microscopy,
and the Razavi Newman Integrative Genomics and Bioinformatics Core (IGC) for their
input on analysis methods for DamID experiments."
article_processing_charge: Yes
article_type: original
author:
- first_name: Swati
full_name: Tyagi, Swati
last_name: Tyagi
- first_name: Juliana S.
full_name: Capitanio, Juliana S.
last_name: Capitanio
- first_name: Jiawei
full_name: Xu, Jiawei
last_name: Xu
- first_name: Fei
full_name: Chen, Fei
last_name: Chen
- first_name: Rahul
full_name: Sharma, Rahul
last_name: Sharma
- first_name: Jialiang
full_name: Huang, Jialiang
last_name: Huang
- first_name: Martin W
full_name: HETZER, Martin W
id: 86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed
last_name: HETZER
orcid: 0000-0002-2111-992X
citation:
ama: Tyagi S, Capitanio JS, Xu J, et al. High-precision mapping of nuclear pore-chromatin
interactions reveals new principles of genome organization at the nuclear envelope.
eLife. 2023. doi:10.7554/elife.87462
apa: Tyagi, S., Capitanio, J. S., Xu, J., Chen, F., Sharma, R., Huang, J., &
Hetzer, M. (2023). High-precision mapping of nuclear pore-chromatin interactions
reveals new principles of genome organization at the nuclear envelope. ELife.
eLife Sciences Publications. https://doi.org/10.7554/elife.87462
chicago: Tyagi, Swati, Juliana S. Capitanio, Jiawei Xu, Fei Chen, Rahul Sharma,
Jialiang Huang, and Martin Hetzer. “High-Precision Mapping of Nuclear Pore-Chromatin
Interactions Reveals New Principles of Genome Organization at the Nuclear Envelope.”
ELife. eLife Sciences Publications, 2023. https://doi.org/10.7554/elife.87462.
ieee: S. Tyagi et al., “High-precision mapping of nuclear pore-chromatin
interactions reveals new principles of genome organization at the nuclear envelope,”
eLife. eLife Sciences Publications, 2023.
ista: Tyagi S, Capitanio JS, Xu J, Chen F, Sharma R, Huang J, Hetzer M. 2023. High-precision
mapping of nuclear pore-chromatin interactions reveals new principles of genome
organization at the nuclear envelope. eLife.
mla: Tyagi, Swati, et al. “High-Precision Mapping of Nuclear Pore-Chromatin Interactions
Reveals New Principles of Genome Organization at the Nuclear Envelope.” ELife,
eLife Sciences Publications, 2023, doi:10.7554/elife.87462.
short: S. Tyagi, J.S. Capitanio, J. Xu, F. Chen, R. Sharma, J. Huang, M. Hetzer,
ELife (2023).
corr_author: '1'
date_created: 2024-01-22T12:21:56Z
date_published: 2023-06-23T00:00:00Z
date_updated: 2024-07-31T11:56:25Z
day: '23'
department:
- _id: MaHe
doi: 10.7554/elife.87462
fulldoi: https://doi.org/10.7554/elife.87462
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.7554/eLife.87462.1
month: '06'
oa: 1
oa_version: Submitted Version
publication: eLife
publication_status: epub_ahead
publisher: eLife Sciences Publications
status: public
title: High-precision mapping of nuclear pore-chromatin interactions reveals new principles
of genome organization at the nuclear envelope
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
year: '2023'
...
---
_id: '11051'
abstract:
- lang: eng
text: Nuclear pore complexes (NPCs) bridge the nucleus and the cytoplasm and are
indispensable for crucial cellular activities, such as bidirectional molecular
trafficking and gene transcription regulation. The discovery of long-lived proteins
(LLPs) in NPCs from postmitotic cells raises the exciting possibility that the
maintenance of NPC integrity might play an inherent role in lifelong cell function.
Age-dependent deterioration of NPCs and loss of nuclear integrity have been linked
to age-related decline in postmitotic cell function and degenerative diseases.
In this review, we discuss our current understanding of NPC maintenance in proliferating
and postmitotic cells, and how malfunction of nucleoporins (Nups) might contribute
to the pathogenesis of various neurodegenerative and cardiovascular diseases.
article_processing_charge: No
article_type: review
author:
- first_name: Jinqiang
full_name: Liu, Jinqiang
last_name: Liu
- first_name: Martin W
full_name: HETZER, Martin W
id: 86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed
last_name: HETZER
orcid: 0000-0002-2111-992X
citation:
ama: Liu J, Hetzer M. Nuclear pore complex maintenance and implications for age-related
diseases. Trends in Cell Biology. 2022;32(3):P216-227. doi:10.1016/j.tcb.2021.10.001
apa: Liu, J., & Hetzer, M. (2022). Nuclear pore complex maintenance and implications
for age-related diseases. Trends in Cell Biology. Elsevier. https://doi.org/10.1016/j.tcb.2021.10.001
chicago: Liu, Jinqiang, and Martin Hetzer. “Nuclear Pore Complex Maintenance and
Implications for Age-Related Diseases.” Trends in Cell Biology. Elsevier,
2022. https://doi.org/10.1016/j.tcb.2021.10.001.
ieee: J. Liu and M. Hetzer, “Nuclear pore complex maintenance and implications for
age-related diseases,” Trends in Cell Biology, vol. 32, no. 3. Elsevier,
pp. P216-227, 2022.
ista: Liu J, Hetzer M. 2022. Nuclear pore complex maintenance and implications for
age-related diseases. Trends in Cell Biology. 32(3), P216-227.
mla: Liu, Jinqiang, and Martin Hetzer. “Nuclear Pore Complex Maintenance and Implications
for Age-Related Diseases.” Trends in Cell Biology, vol. 32, no. 3, Elsevier,
2022, pp. P216-227, doi:10.1016/j.tcb.2021.10.001.
short: J. Liu, M. Hetzer, Trends in Cell Biology 32 (2022) P216-227.
date_created: 2022-04-07T07:43:01Z
date_published: 2022-03-01T00:00:00Z
date_updated: 2024-10-14T11:14:57Z
day: '01'
doi: 10.1016/j.tcb.2021.10.001
extern: '1'
external_id:
pmid:
- '34782239'
fulldoi: https://doi.org/10.1016/j.tcb.2021.10.001
intvolume: ' 32'
issue: '3'
keyword:
- Cell Biology
language:
- iso: eng
month: '03'
oa_version: None
page: P216-227
pmid: 1
publication: Trends in Cell Biology
publication_identifier:
issn:
- 0962-8924
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: Nuclear pore complex maintenance and implications for age-related diseases
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 32
year: '2022'
...
---
_id: '11052'
abstract:
- lang: eng
text: In order to combat molecular damage, most cellular proteins undergo rapid
turnover. We have previously identified large nuclear protein assemblies that
can persist for years in post-mitotic tissues and are subject to age-related decline.
Here, we report that mitochondria can be long lived in the mouse brain and reveal
that specific mitochondrial proteins have half-lives longer than the average proteome.
These mitochondrial long-lived proteins (mitoLLPs) are core components of the
electron transport chain (ETC) and display increased longevity in respiratory
supercomplexes. We find that COX7C, a mitoLLP that forms a stable contact site
between complexes I and IV, is required for complex IV and supercomplex assembly.
Remarkably, even upon depletion of COX7C transcripts, ETC function is maintained
for days, effectively uncoupling mitochondrial function from ongoing transcription
of its mitoLLPs. Our results suggest that modulating protein longevity within
the ETC is critical for mitochondrial proteome maintenance and the robustness
of mitochondrial function.
article_processing_charge: No
article_type: original
author:
- first_name: Shefali
full_name: Krishna, Shefali
last_name: Krishna
- first_name: Rafael
full_name: Arrojo e Drigo, Rafael
last_name: Arrojo e Drigo
- first_name: Juliana S.
full_name: Capitanio, Juliana S.
last_name: Capitanio
- first_name: Ranjan
full_name: Ramachandra, Ranjan
last_name: Ramachandra
- first_name: Mark
full_name: Ellisman, Mark
last_name: Ellisman
- first_name: Martin W
full_name: HETZER, Martin W
id: 86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed
last_name: HETZER
orcid: 0000-0002-2111-992X
citation:
ama: Krishna S, Arrojo e Drigo R, Capitanio JS, Ramachandra R, Ellisman M, Hetzer
M. Identification of long-lived proteins in the mitochondria reveals increased
stability of the electron transport chain. Developmental Cell. 2021;56(21):P2952-2965.e9.
doi:10.1016/j.devcel.2021.10.008
apa: Krishna, S., Arrojo e Drigo, R., Capitanio, J. S., Ramachandra, R., Ellisman,
M., & Hetzer, M. (2021). Identification of long-lived proteins in the mitochondria
reveals increased stability of the electron transport chain. Developmental
Cell. Elsevier. https://doi.org/10.1016/j.devcel.2021.10.008
chicago: Krishna, Shefali, Rafael Arrojo e Drigo, Juliana S. Capitanio, Ranjan Ramachandra,
Mark Ellisman, and Martin Hetzer. “Identification of Long-Lived Proteins in the
Mitochondria Reveals Increased Stability of the Electron Transport Chain.” Developmental
Cell. Elsevier, 2021. https://doi.org/10.1016/j.devcel.2021.10.008.
ieee: S. Krishna, R. Arrojo e Drigo, J. S. Capitanio, R. Ramachandra, M. Ellisman,
and M. Hetzer, “Identification of long-lived proteins in the mitochondria reveals
increased stability of the electron transport chain,” Developmental Cell,
vol. 56, no. 21. Elsevier, p. P2952–2965.e9, 2021.
ista: Krishna S, Arrojo e Drigo R, Capitanio JS, Ramachandra R, Ellisman M, Hetzer
M. 2021. Identification of long-lived proteins in the mitochondria reveals increased
stability of the electron transport chain. Developmental Cell. 56(21), P2952–2965.e9.
mla: Krishna, Shefali, et al. “Identification of Long-Lived Proteins in the Mitochondria
Reveals Increased Stability of the Electron Transport Chain.” Developmental
Cell, vol. 56, no. 21, Elsevier, 2021, p. P2952–2965.e9, doi:10.1016/j.devcel.2021.10.008.
short: S. Krishna, R. Arrojo e Drigo, J.S. Capitanio, R. Ramachandra, M. Ellisman,
M. Hetzer, Developmental Cell 56 (2021) P2952–2965.e9.
date_created: 2022-04-07T07:43:14Z
date_published: 2021-11-08T00:00:00Z
date_updated: 2025-12-15T10:01:56Z
day: '08'
department:
- _id: MaHe
doi: 10.1016/j.devcel.2021.10.008
extern: '1'
external_id:
pmid:
- '34715012'
fulldoi: https://doi.org/10.1016/j.devcel.2021.10.008
intvolume: ' 56'
issue: '21'
keyword:
- Developmental Biology
- Cell Biology
- General Biochemistry
- Genetics and Molecular Biology
- Molecular Biology
language:
- iso: eng
month: '11'
oa_version: None
page: P2952-2965.e9
pmid: 1
publication: Developmental Cell
publication_identifier:
issn:
- 1534-5807
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: Identification of long-lived proteins in the mitochondria reveals increased
stability of the electron transport chain
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 56
year: '2021'
...
---
_id: '11053'
abstract:
- lang: eng
text: Understanding basic mechanisms of aging holds great promise for developing
interventions that prevent or delay many age-related declines and diseases simultaneously
to increase human healthspan. However, a major confounding factor in aging research
is the heterogeneity of the aging process itself. At the organismal level, it
is clear that chronological age does not always predict biological age or susceptibility
to frailty or pathology. While genetics and environment are major factors driving
variable rates of aging, additional complexity arises because different organs,
tissues, and cell types are intrinsically heterogeneous and exhibit different
aging trajectories normally or in response to the stresses of the aging process
(e.g., damage accumulation). Tackling the heterogeneity of aging requires new
and specialized tools (e.g., single-cell analyses, mass spectrometry-based approaches,
and advanced imaging) to identify novel signatures of aging across scales. Cutting-edge
computational approaches are then needed to integrate these disparate datasets
and elucidate network interactions between known aging hallmarks. There is also
a need for improved, human cell-based models of aging to ensure that basic research
findings are relevant to human aging and healthspan interventions. The San Diego
Nathan Shock Center (SD-NSC) provides access to cutting-edge scientific resources
to facilitate the study of the heterogeneity of aging in general and to promote
the use of novel human cell models of aging. The center also has a robust Research
Development Core that funds pilot projects on the heterogeneity of aging and organizes
innovative training activities, including workshops and a personalized mentoring
program, to help investigators new to the aging field succeed. Finally, the SD-NSC
participates in outreach activities to educate the general community about the
importance of aging research and promote the need for basic biology of aging research
in particular.
article_processing_charge: No
article_type: original
author:
- first_name: Gerald S.
full_name: Shadel, Gerald S.
last_name: Shadel
- first_name: Peter D.
full_name: Adams, Peter D.
last_name: Adams
- first_name: W. Travis
full_name: Berggren, W. Travis
last_name: Berggren
- first_name: Jolene K.
full_name: Diedrich, Jolene K.
last_name: Diedrich
- first_name: Kenneth E.
full_name: Diffenderfer, Kenneth E.
last_name: Diffenderfer
- first_name: Fred H.
full_name: Gage, Fred H.
last_name: Gage
- first_name: Nasun
full_name: Hah, Nasun
last_name: Hah
- first_name: Malene
full_name: Hansen, Malene
last_name: Hansen
- first_name: Martin W
full_name: HETZER, Martin W
id: 86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed
last_name: HETZER
orcid: 0000-0002-2111-992X
- first_name: Anthony J. A.
full_name: Molina, Anthony J. A.
last_name: Molina
- first_name: Uri
full_name: Manor, Uri
last_name: Manor
- first_name: Kurt
full_name: Marek, Kurt
last_name: Marek
- first_name: David D.
full_name: O’Keefe, David D.
last_name: O’Keefe
- first_name: Antonio F. M.
full_name: Pinto, Antonio F. M.
last_name: Pinto
- first_name: Alessandra
full_name: Sacco, Alessandra
last_name: Sacco
- first_name: Tatyana O.
full_name: Sharpee, Tatyana O.
last_name: Sharpee
- first_name: Maxim N.
full_name: Shokriev, Maxim N.
last_name: Shokriev
- first_name: Stefania
full_name: Zambetti, Stefania
last_name: Zambetti
citation:
ama: 'Shadel GS, Adams PD, Berggren WT, et al. The San Diego Nathan Shock Center:
Tackling the heterogeneity of aging. GeroScience. 2021;43(5):2139-2148.
doi:10.1007/s11357-021-00426-x'
apa: 'Shadel, G. S., Adams, P. D., Berggren, W. T., Diedrich, J. K., Diffenderfer,
K. E., Gage, F. H., … Zambetti, S. (2021). The San Diego Nathan Shock Center:
Tackling the heterogeneity of aging. GeroScience. Springer Nature. https://doi.org/10.1007/s11357-021-00426-x'
chicago: 'Shadel, Gerald S., Peter D. Adams, W. Travis Berggren, Jolene K. Diedrich,
Kenneth E. Diffenderfer, Fred H. Gage, Nasun Hah, et al. “The San Diego Nathan
Shock Center: Tackling the Heterogeneity of Aging.” GeroScience. Springer
Nature, 2021. https://doi.org/10.1007/s11357-021-00426-x.'
ieee: 'G. S. Shadel et al., “The San Diego Nathan Shock Center: Tackling
the heterogeneity of aging,” GeroScience, vol. 43, no. 5. Springer Nature,
pp. 2139–2148, 2021.'
ista: 'Shadel GS, Adams PD, Berggren WT, Diedrich JK, Diffenderfer KE, Gage FH,
Hah N, Hansen M, Hetzer M, Molina AJA, Manor U, Marek K, O’Keefe DD, Pinto AFM,
Sacco A, Sharpee TO, Shokriev MN, Zambetti S. 2021. The San Diego Nathan Shock
Center: Tackling the heterogeneity of aging. GeroScience. 43(5), 2139–2148.'
mla: 'Shadel, Gerald S., et al. “The San Diego Nathan Shock Center: Tackling the
Heterogeneity of Aging.” GeroScience, vol. 43, no. 5, Springer Nature,
2021, pp. 2139–48, doi:10.1007/s11357-021-00426-x.'
short: G.S. Shadel, P.D. Adams, W.T. Berggren, J.K. Diedrich, K.E. Diffenderfer,
F.H. Gage, N. Hah, M. Hansen, M. Hetzer, A.J.A. Molina, U. Manor, K. Marek, D.D.
O’Keefe, A.F.M. Pinto, A. Sacco, T.O. Sharpee, M.N. Shokriev, S. Zambetti, GeroScience
43 (2021) 2139–2148.
date_created: 2022-04-07T07:43:25Z
date_published: 2021-10-01T00:00:00Z
date_updated: 2022-07-18T08:27:24Z
day: '01'
doi: 10.1007/s11357-021-00426-x
extern: '1'
external_id:
pmid:
- '34370163'
fulldoi: https://doi.org/10.1007/s11357-021-00426-x
intvolume: ' 43'
issue: '5'
keyword:
- Geriatrics and Gerontology
- Aging
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8599742/
month: '10'
oa: 1
oa_version: Published Version
page: 2139-2148
pmid: 1
publication: GeroScience
publication_identifier:
issn:
- 2509-2715
- 2509-2723
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
scopus_import: '1'
status: public
title: 'The San Diego Nathan Shock Center: Tackling the heterogeneity of aging'
type: journal_article
user_id: 72615eeb-f1f3-11ec-aa25-d4573ddc34fd
volume: 43
year: '2021'
...
---
_id: '11054'
abstract:
- lang: eng
text: In recent years, the nuclear pore complex (NPC) has emerged as a key player
in genome regulation and cellular homeostasis. New discoveries have revealed that
the NPC has multiple cellular functions besides mediating the molecular exchange
between the nucleus and the cytoplasm. In this review, we discuss non-transport
aspects of the NPC focusing on the NPC-genome interaction, the extreme longevity
of the NPC proteins, and NPC dysfunction in age-related diseases. The examples
summarized herein demonstrate that the NPC, which first evolved to enable the
biochemical communication between the nucleus and the cytoplasm, now doubles as
the gatekeeper of cellular identity and aging.
article_processing_charge: No
article_type: review
author:
- first_name: Ukrae H.
full_name: Cho, Ukrae H.
last_name: Cho
- first_name: Martin W
full_name: HETZER, Martin W
id: 86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed
last_name: HETZER
orcid: 0000-0002-2111-992X
citation:
ama: 'Cho UH, Hetzer M. Nuclear periphery takes center stage: The role of nuclear
pore complexes in cell identity and aging. Neuron. 2020;106(6):899-911.
doi:10.1016/j.neuron.2020.05.031'
apa: 'Cho, U. H., & Hetzer, M. (2020). Nuclear periphery takes center stage:
The role of nuclear pore complexes in cell identity and aging. Neuron.
Elsevier. https://doi.org/10.1016/j.neuron.2020.05.031'
chicago: 'Cho, Ukrae H., and Martin Hetzer. “Nuclear Periphery Takes Center Stage:
The Role of Nuclear Pore Complexes in Cell Identity and Aging.” Neuron.
Elsevier, 2020. https://doi.org/10.1016/j.neuron.2020.05.031.'
ieee: 'U. H. Cho and M. Hetzer, “Nuclear periphery takes center stage: The role
of nuclear pore complexes in cell identity and aging,” Neuron, vol. 106,
no. 6. Elsevier, pp. 899–911, 2020.'
ista: 'Cho UH, Hetzer M. 2020. Nuclear periphery takes center stage: The role of
nuclear pore complexes in cell identity and aging. Neuron. 106(6), 899–911.'
mla: 'Cho, Ukrae H., and Martin Hetzer. “Nuclear Periphery Takes Center Stage: The
Role of Nuclear Pore Complexes in Cell Identity and Aging.” Neuron, vol.
106, no. 6, Elsevier, 2020, pp. 899–911, doi:10.1016/j.neuron.2020.05.031.'
short: U.H. Cho, M. Hetzer, Neuron 106 (2020) 899–911.
date_created: 2022-04-07T07:43:36Z
date_published: 2020-06-17T00:00:00Z
date_updated: 2024-10-14T11:15:26Z
day: '17'
doi: 10.1016/j.neuron.2020.05.031
extern: '1'
external_id:
pmid:
- '32553207'
fulldoi: https://doi.org/10.1016/j.neuron.2020.05.031
intvolume: ' 106'
issue: '6'
keyword:
- General Neuroscience
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1016/j.neuron.2020.05.031
month: '06'
oa: 1
oa_version: Published Version
page: 899-911
pmid: 1
publication: Neuron
publication_identifier:
issn:
- 0896-6273
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: 'Nuclear periphery takes center stage: The role of nuclear pore complexes in
cell identity and aging'
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 106
year: '2020'
...
---
_id: '11055'
abstract:
- lang: eng
text: Vascular dysfunctions are a common feature of multiple age-related diseases.
However, modeling healthy and pathological aging of the human vasculature represents
an unresolved experimental challenge. Here, we generated induced vascular endothelial
cells (iVECs) and smooth muscle cells (iSMCs) by direct reprogramming of healthy
human fibroblasts from donors of different ages and Hutchinson-Gilford Progeria
Syndrome (HGPS) patients. iVECs induced from old donors revealed upregulation
of GSTM1 and PALD1, genes linked to oxidative stress, inflammation and endothelial
junction stability, as vascular aging markers. A functional assay performed on
PALD1 KD VECs demonstrated a recovery in vascular permeability. We found that
iSMCs from HGPS donors overexpressed bone morphogenetic protein (BMP)−4, which
plays a key role in both vascular calcification and endothelial barrier damage
observed in HGPS. Strikingly, BMP4 concentrations are higher in serum from HGPS
vs. age-matched mice. Furthermore, targeting BMP4 with blocking antibody recovered
the functionality of the vascular barrier in vitro, hence representing a potential
future therapeutic strategy to limit cardiovascular dysfunction in HGPS. These
results show that iVECs and iSMCs retain disease-related signatures, allowing
modeling of vascular aging and HGPS in vitro.
article_number: e54383
article_processing_charge: No
article_type: original
author:
- first_name: Simone
full_name: Bersini, Simone
last_name: Bersini
- first_name: Roberta
full_name: Schulte, Roberta
last_name: Schulte
- first_name: Ling
full_name: Huang, Ling
last_name: Huang
- first_name: Hannah
full_name: Tsai, Hannah
last_name: Tsai
- first_name: Martin W
full_name: HETZER, Martin W
id: 86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed
last_name: HETZER
orcid: 0000-0002-2111-992X
citation:
ama: Bersini S, Schulte R, Huang L, Tsai H, Hetzer M. Direct reprogramming of human
smooth muscle and vascular endothelial cells reveals defects associated with aging
and Hutchinson-Gilford progeria syndrome. eLife. 2020;9. doi:10.7554/elife.54383
apa: Bersini, S., Schulte, R., Huang, L., Tsai, H., & Hetzer, M. (2020). Direct
reprogramming of human smooth muscle and vascular endothelial cells reveals defects
associated with aging and Hutchinson-Gilford progeria syndrome. ELife.
eLife Sciences Publications. https://doi.org/10.7554/elife.54383
chicago: Bersini, Simone, Roberta Schulte, Ling Huang, Hannah Tsai, and Martin Hetzer.
“Direct Reprogramming of Human Smooth Muscle and Vascular Endothelial Cells Reveals
Defects Associated with Aging and Hutchinson-Gilford Progeria Syndrome.” ELife.
eLife Sciences Publications, 2020. https://doi.org/10.7554/elife.54383.
ieee: S. Bersini, R. Schulte, L. Huang, H. Tsai, and M. Hetzer, “Direct reprogramming
of human smooth muscle and vascular endothelial cells reveals defects associated
with aging and Hutchinson-Gilford progeria syndrome,” eLife, vol. 9. eLife
Sciences Publications, 2020.
ista: Bersini S, Schulte R, Huang L, Tsai H, Hetzer M. 2020. Direct reprogramming
of human smooth muscle and vascular endothelial cells reveals defects associated
with aging and Hutchinson-Gilford progeria syndrome. eLife. 9, e54383.
mla: Bersini, Simone, et al. “Direct Reprogramming of Human Smooth Muscle and Vascular
Endothelial Cells Reveals Defects Associated with Aging and Hutchinson-Gilford
Progeria Syndrome.” ELife, vol. 9, e54383, eLife Sciences Publications,
2020, doi:10.7554/elife.54383.
short: S. Bersini, R. Schulte, L. Huang, H. Tsai, M. Hetzer, ELife 9 (2020).
date_created: 2022-04-07T07:43:48Z
date_published: 2020-09-08T00:00:00Z
date_updated: 2024-10-14T11:17:02Z
day: '08'
ddc:
- '570'
doi: 10.7554/elife.54383
extern: '1'
external_id:
pmid:
- '32896271'
file:
- access_level: open_access
checksum: f8b3821349a194050be02570d8fe7d4b
content_type: application/pdf
creator: dernst
date_created: 2022-04-08T06:53:10Z
date_updated: 2022-04-08T06:53:10Z
file_id: '11132'
file_name: 2020_eLife_Bersini.pdf
file_size: 4399825
relation: main_file
success: 1
file_date_updated: 2022-04-08T06:53:10Z
fulldoi: https://doi.org/10.7554/elife.54383
has_accepted_license: '1'
intvolume: ' 9'
keyword:
- General Immunology and Microbiology
- General Biochemistry
- Genetics and Molecular Biology
- General Medicine
- General Neuroscience
language:
- iso: eng
month: '09'
oa: 1
oa_version: Published Version
pmid: 1
publication: eLife
publication_identifier:
issn:
- 2050-084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
scopus_import: '1'
status: public
title: Direct reprogramming of human smooth muscle and vascular endothelial cells
reveals defects associated with aging and Hutchinson-Gilford progeria syndrome
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: 9
year: '2020'
...
---
_id: '11056'
abstract:
- lang: eng
text: Aging of the circulatory system correlates with the pathogenesis of a large
spectrum of diseases. However, it is largely unknown which factors drive the age-dependent
or pathological decline of the vasculature and how vascular defects relate to
tissue aging. The goal of the study is to design a multianalytical approach to
identify how the cellular microenvironment (i.e., fibroblasts) and serum from
healthy donors of different ages or Alzheimer disease (AD) patients can modulate
the functionality of organ-specific vascular endothelial cells (VECs). Long-living
human microvascular networks embedding VECs and fibroblasts from skin biopsies
are generated. RNA-seq, secretome analyses, and microfluidic assays demonstrate
that fibroblasts from young donors restore the functionality of aged endothelial
cells, an effect also achieved by serum from young donors. New biomarkers of vascular
aging are validated in human biopsies and it is shown that young serum induces
angiopoietin-like-4, which can restore compromised vascular barriers. This strategy
is then employed to characterize transcriptional/functional changes induced on
the blood–brain barrier by AD serum, demonstrating the importance of PTP4A3 in
the regulation of permeability. Features of vascular degeneration during aging
and AD are recapitulated, and a tool to identify novel biomarkers that can be
exploited to develop future therapeutics modulating vascular function is established.
article_number: '2000044'
article_processing_charge: No
article_type: original
author:
- first_name: Simone
full_name: Bersini, Simone
last_name: Bersini
- first_name: Rafael
full_name: Arrojo e Drigo, Rafael
last_name: Arrojo e Drigo
- first_name: Ling
full_name: Huang, Ling
last_name: Huang
- first_name: Maxim N.
full_name: Shokhirev, Maxim N.
last_name: Shokhirev
- first_name: Martin W
full_name: HETZER, Martin W
id: 86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed
last_name: HETZER
orcid: 0000-0002-2111-992X
citation:
ama: Bersini S, Arrojo e Drigo R, Huang L, Shokhirev MN, Hetzer M. Transcriptional
and functional changes of the human microvasculature during physiological aging
and Alzheimer disease. Advanced Biosystems. 2020;4(5). doi:10.1002/adbi.202000044
apa: Bersini, S., Arrojo e Drigo, R., Huang, L., Shokhirev, M. N., & Hetzer,
M. (2020). Transcriptional and functional changes of the human microvasculature
during physiological aging and Alzheimer disease. Advanced Biosystems.
Wiley. https://doi.org/10.1002/adbi.202000044
chicago: Bersini, Simone, Rafael Arrojo e Drigo, Ling Huang, Maxim N. Shokhirev,
and Martin Hetzer. “Transcriptional and Functional Changes of the Human Microvasculature
during Physiological Aging and Alzheimer Disease.” Advanced Biosystems.
Wiley, 2020. https://doi.org/10.1002/adbi.202000044.
ieee: S. Bersini, R. Arrojo e Drigo, L. Huang, M. N. Shokhirev, and M. Hetzer, “Transcriptional
and functional changes of the human microvasculature during physiological aging
and Alzheimer disease,” Advanced Biosystems, vol. 4, no. 5. Wiley, 2020.
ista: Bersini S, Arrojo e Drigo R, Huang L, Shokhirev MN, Hetzer M. 2020. Transcriptional
and functional changes of the human microvasculature during physiological aging
and Alzheimer disease. Advanced Biosystems. 4(5), 2000044.
mla: Bersini, Simone, et al. “Transcriptional and Functional Changes of the Human
Microvasculature during Physiological Aging and Alzheimer Disease.” Advanced
Biosystems, vol. 4, no. 5, 2000044, Wiley, 2020, doi:10.1002/adbi.202000044.
short: S. Bersini, R. Arrojo e Drigo, L. Huang, M.N. Shokhirev, M. Hetzer, Advanced
Biosystems 4 (2020).
date_created: 2022-04-07T07:43:57Z
date_published: 2020-05-01T00:00:00Z
date_updated: 2024-10-14T11:18:07Z
day: '01'
ddc:
- '570'
doi: 10.1002/adbi.202000044
extern: '1'
external_id:
pmid:
- '32402127'
file:
- access_level: open_access
checksum: 5584d9a1609812dc75c02ce1e35d2ec0
content_type: application/pdf
creator: dernst
date_created: 2022-04-08T07:06:05Z
date_updated: 2022-04-08T07:06:05Z
file_id: '11134'
file_name: 2020_AdvancedBiosystems_Bersini.pdf
file_size: 2490829
relation: main_file
success: 1
file_date_updated: 2022-04-08T07:06:05Z
fulldoi: https://doi.org/10.1002/adbi.202000044
has_accepted_license: '1'
intvolume: ' 4'
issue: '5'
keyword:
- General Biochemistry
- Genetics and Molecular Biology
- Biomedical Engineering
- Biomaterials
language:
- iso: eng
month: '05'
oa: 1
oa_version: Published Version
pmid: 1
publication: Advanced Biosystems
publication_identifier:
issn:
- 2366-7478
- 2366-7478
publication_status: published
publisher: Wiley
quality_controlled: '1'
scopus_import: '1'
status: public
title: Transcriptional and functional changes of the human microvasculature during
physiological aging and Alzheimer disease
tmp:
image: /images/cc_by_nc_nd.png
legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
(CC BY-NC-ND 4.0)
short: CC BY-NC-ND (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 4
year: '2020'
...
---
_id: '11057'
abstract:
- lang: eng
text: During mitosis, transcription of genomic DNA is dramatically reduced, before
it is reactivated during nuclear reformation in anaphase/telophase. Many aspects
of the underlying principles that mediate transcriptional memory and reactivation
in the daughter cells remain unclear. Here, we used ChIP-seq on synchronized cells
at different stages after mitosis to generate genome-wide maps of histone modifications.
Combined with EU-RNA-seq and Hi-C analyses, we found that during prometaphase,
promoters, enhancers, and insulators retain H3K4me3 and H3K4me1, while losing
H3K27ac. Enhancers globally retaining mitotic H3K4me1 or locally retaining mitotic
H3K27ac are associated with cell type-specific genes and their transcription factors
for rapid transcriptional activation. As cells exit mitosis, promoters regain
H3K27ac, which correlates with transcriptional reactivation. Insulators also gain
H3K27ac and CCCTC-binding factor (CTCF) in anaphase/telophase. This increase of
H3K27ac in anaphase/telophase is required for posttranscriptional activation and
may play a role in the establishment of topologically associating domains (TADs).
Together, our results suggest that the genome is reorganized in a sequential order,
in which histone methylations occur first in prometaphase, histone acetylation,
and CTCF in anaphase/telophase, transcription in cytokinesis, and long-range chromatin
interactions in early G1. We thus provide insights into the histone modification
landscape that allows faithful reestablishment of the transcriptional program
and TADs during cell division.
article_processing_charge: No
article_type: original
author:
- first_name: Hyeseon
full_name: Kang, Hyeseon
last_name: Kang
- first_name: Maxim N.
full_name: Shokhirev, Maxim N.
last_name: Shokhirev
- first_name: Zhichao
full_name: Xu, Zhichao
last_name: Xu
- first_name: Sahaana
full_name: Chandran, Sahaana
last_name: Chandran
- first_name: Jesse R.
full_name: Dixon, Jesse R.
last_name: Dixon
- first_name: Martin W
full_name: HETZER, Martin W
id: 86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed
last_name: HETZER
orcid: 0000-0002-2111-992X
citation:
ama: Kang H, Shokhirev MN, Xu Z, Chandran S, Dixon JR, Hetzer M. Dynamic regulation
of histone modifications and long-range chromosomal interactions during postmitotic
transcriptional reactivation. Genes & Development. 2020;34(13-14):913-930.
doi:10.1101/gad.335794.119
apa: Kang, H., Shokhirev, M. N., Xu, Z., Chandran, S., Dixon, J. R., & Hetzer,
M. (2020). Dynamic regulation of histone modifications and long-range chromosomal
interactions during postmitotic transcriptional reactivation. Genes & Development.
Cold Spring Harbor Laboratory Press. https://doi.org/10.1101/gad.335794.119
chicago: Kang, Hyeseon, Maxim N. Shokhirev, Zhichao Xu, Sahaana Chandran, Jesse
R. Dixon, and Martin Hetzer. “Dynamic Regulation of Histone Modifications and
Long-Range Chromosomal Interactions during Postmitotic Transcriptional Reactivation.”
Genes & Development. Cold Spring Harbor Laboratory Press, 2020. https://doi.org/10.1101/gad.335794.119.
ieee: H. Kang, M. N. Shokhirev, Z. Xu, S. Chandran, J. R. Dixon, and M. Hetzer,
“Dynamic regulation of histone modifications and long-range chromosomal interactions
during postmitotic transcriptional reactivation,” Genes & Development,
vol. 34, no. 13–14. Cold Spring Harbor Laboratory Press, pp. 913–930, 2020.
ista: Kang H, Shokhirev MN, Xu Z, Chandran S, Dixon JR, Hetzer M. 2020. Dynamic
regulation of histone modifications and long-range chromosomal interactions during
postmitotic transcriptional reactivation. Genes & Development. 34(13–14),
913–930.
mla: Kang, Hyeseon, et al. “Dynamic Regulation of Histone Modifications and Long-Range
Chromosomal Interactions during Postmitotic Transcriptional Reactivation.” Genes
& Development, vol. 34, no. 13–14, Cold Spring Harbor Laboratory Press,
2020, pp. 913–30, doi:10.1101/gad.335794.119.
short: H. Kang, M.N. Shokhirev, Z. Xu, S. Chandran, J.R. Dixon, M. Hetzer, Genes
& Development 34 (2020) 913–930.
date_created: 2022-04-07T07:44:09Z
date_published: 2020-04-28T00:00:00Z
date_updated: 2024-10-14T11:18:25Z
day: '28'
ddc:
- '570'
doi: 10.1101/gad.335794.119
extern: '1'
external_id:
pmid:
- '32499403'
file:
- access_level: open_access
checksum: 84e92d40e67936c739628315c238daf9
content_type: application/pdf
creator: dernst
date_created: 2022-04-08T07:12:33Z
date_updated: 2022-04-08T07:12:33Z
file_id: '11136'
file_name: 2020_GenesDevelopment_Kang.pdf
file_size: 4406772
relation: main_file
success: 1
file_date_updated: 2022-04-08T07:12:33Z
fulldoi: https://doi.org/10.1101/gad.335794.119
has_accepted_license: '1'
intvolume: ' 34'
issue: 13-14
keyword:
- Developmental Biology
- Genetics
language:
- iso: eng
month: '04'
oa: 1
oa_version: Published Version
page: 913-930
pmid: 1
publication: Genes & Development
publication_identifier:
issn:
- 0890-9369
- 1549-5477
publication_status: published
publisher: Cold Spring Harbor Laboratory Press
quality_controlled: '1'
scopus_import: '1'
status: public
title: Dynamic regulation of histone modifications and long-range chromosomal interactions
during postmitotic transcriptional reactivation
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: 34
year: '2020'
...
---
_id: '11058'
abstract:
- lang: eng
text: Nucleoporin 93 (Nup93) expression inversely correlates with the survival of
triple-negative breast cancer patients. However, our knowledge of Nup93 function
in breast cancer besides its role as structural component of the nuclear pore
complex is not understood. Combination of functional assays and genetic analyses
suggested that chromatin interaction of Nup93 partially modulates the expression
of genes associated with actin cytoskeleton remodeling and epithelial to mesenchymal
transition, resulting in impaired invasion of triple-negative, claudin-low breast
cancer cells. Nup93 depletion induced stress fiber formation associated with reduced
cell migration/proliferation and impaired expression of mesenchymal-like genes.
Silencing LIMCH1, a gene responsible for actin cytoskeleton remodeling and up-regulated
upon Nup93 depletion, partially restored the invasive phenotype of cancer cells.
Loss of Nup93 led to significant defects in tumor establishment/propagation in
vivo, whereas patient samples revealed that high Nup93 and low LIMCH1 expression
correlate with late tumor stage. Our approach identified Nup93 as contributor
of triple-negative, claudin-low breast cancer cell invasion and paves the way
to study the role of nuclear envelope proteins during breast cancer tumorigenesis.
article_number: e201900623
article_processing_charge: No
article_type: original
author:
- first_name: Simone
full_name: Bersini, Simone
last_name: Bersini
- first_name: Nikki K
full_name: Lytle, Nikki K
last_name: Lytle
- first_name: Roberta
full_name: Schulte, Roberta
last_name: Schulte
- first_name: Ling
full_name: Huang, Ling
last_name: Huang
- first_name: Geoffrey M
full_name: Wahl, Geoffrey M
last_name: Wahl
- first_name: Martin W
full_name: HETZER, Martin W
id: 86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed
last_name: HETZER
orcid: 0000-0002-2111-992X
citation:
ama: Bersini S, Lytle NK, Schulte R, Huang L, Wahl GM, Hetzer M. Nup93 regulates
breast tumor growth by modulating cell proliferation and actin cytoskeleton remodeling.
Life Science Alliance. 2020;3(1). doi:10.26508/lsa.201900623
apa: Bersini, S., Lytle, N. K., Schulte, R., Huang, L., Wahl, G. M., & Hetzer,
M. (2020). Nup93 regulates breast tumor growth by modulating cell proliferation
and actin cytoskeleton remodeling. Life Science Alliance. Life Science
Alliance. https://doi.org/10.26508/lsa.201900623
chicago: Bersini, Simone, Nikki K Lytle, Roberta Schulte, Ling Huang, Geoffrey M
Wahl, and Martin Hetzer. “Nup93 Regulates Breast Tumor Growth by Modulating Cell
Proliferation and Actin Cytoskeleton Remodeling.” Life Science Alliance.
Life Science Alliance, 2020. https://doi.org/10.26508/lsa.201900623.
ieee: S. Bersini, N. K. Lytle, R. Schulte, L. Huang, G. M. Wahl, and M. Hetzer,
“Nup93 regulates breast tumor growth by modulating cell proliferation and actin
cytoskeleton remodeling,” Life Science Alliance, vol. 3, no. 1. Life Science
Alliance, 2020.
ista: Bersini S, Lytle NK, Schulte R, Huang L, Wahl GM, Hetzer M. 2020. Nup93 regulates
breast tumor growth by modulating cell proliferation and actin cytoskeleton remodeling.
Life Science Alliance. 3(1), e201900623.
mla: Bersini, Simone, et al. “Nup93 Regulates Breast Tumor Growth by Modulating
Cell Proliferation and Actin Cytoskeleton Remodeling.” Life Science Alliance,
vol. 3, no. 1, e201900623, Life Science Alliance, 2020, doi:10.26508/lsa.201900623.
short: S. Bersini, N.K. Lytle, R. Schulte, L. Huang, G.M. Wahl, M. Hetzer, Life
Science Alliance 3 (2020).
date_created: 2022-04-07T07:44:18Z
date_published: 2020-01-01T00:00:00Z
date_updated: 2024-10-14T11:18:41Z
day: '01'
ddc:
- '570'
doi: 10.26508/lsa.201900623
extern: '1'
external_id:
pmid:
- '31959624'
file:
- access_level: open_access
checksum: 3bf33e7e93bef7823287807206b69b38
content_type: application/pdf
creator: dernst
date_created: 2022-04-08T07:33:01Z
date_updated: 2022-04-08T07:33:01Z
file_id: '11137'
file_name: 2020_LifeScienceAlliance_Bersini.pdf
file_size: 2653960
relation: main_file
success: 1
file_date_updated: 2022-04-08T07:33:01Z
fulldoi: https://doi.org/10.26508/lsa.201900623
has_accepted_license: '1'
intvolume: ' 3'
issue: '1'
keyword:
- Health
- Toxicology and Mutagenesis
- Plant Science
- Biochemistry
- Genetics and Molecular Biology (miscellaneous)
- Ecology
language:
- iso: eng
month: '01'
oa: 1
oa_version: Published Version
pmid: 1
publication: Life Science Alliance
publication_identifier:
issn:
- 2575-1077
publication_status: published
publisher: Life Science Alliance
quality_controlled: '1'
scopus_import: '1'
status: public
title: Nup93 regulates breast tumor growth by modulating cell proliferation and actin
cytoskeleton remodeling
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: 3
year: '2020'
...
---
_id: '11059'
abstract:
- lang: eng
text: The genome is packaged and organized nonrandomly within the 3D space of the
nucleus to promote efficient gene expression and to faithfully maintain silencing
of heterochromatin. The genome is enclosed within the nucleus by the nuclear envelope
membrane, which contains a set of proteins that actively participate in chromatin
organization and gene regulation. Technological advances are providing views of
genome organization at unprecedented resolution and are beginning to reveal the
ways that cells co-opt the structures of the nuclear periphery for nuclear organization
and gene regulation. These genome regulatory roles of proteins of the nuclear
periphery have important influences on development, disease and ageing.
article_processing_charge: No
article_type: review
author:
- first_name: Abigail
full_name: Buchwalter, Abigail
last_name: Buchwalter
- first_name: Jeanae M.
full_name: Kaneshiro, Jeanae M.
last_name: Kaneshiro
- first_name: Martin W
full_name: HETZER, Martin W
id: 86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed
last_name: HETZER
orcid: 0000-0002-2111-992X
citation:
ama: 'Buchwalter A, Kaneshiro JM, Hetzer M. Coaching from the sidelines: The nuclear
periphery in genome regulation. Nature Reviews Genetics. 2019;20(1):39-50.
doi:10.1038/s41576-018-0063-5'
apa: 'Buchwalter, A., Kaneshiro, J. M., & Hetzer, M. (2019). Coaching from the
sidelines: The nuclear periphery in genome regulation. Nature Reviews Genetics.
Springer Nature. https://doi.org/10.1038/s41576-018-0063-5'
chicago: 'Buchwalter, Abigail, Jeanae M. Kaneshiro, and Martin Hetzer. “Coaching
from the Sidelines: The Nuclear Periphery in Genome Regulation.” Nature Reviews
Genetics. Springer Nature, 2019. https://doi.org/10.1038/s41576-018-0063-5.'
ieee: 'A. Buchwalter, J. M. Kaneshiro, and M. Hetzer, “Coaching from the sidelines:
The nuclear periphery in genome regulation,” Nature Reviews Genetics, vol.
20, no. 1. Springer Nature, pp. 39–50, 2019.'
ista: 'Buchwalter A, Kaneshiro JM, Hetzer M. 2019. Coaching from the sidelines:
The nuclear periphery in genome regulation. Nature Reviews Genetics. 20(1), 39–50.'
mla: 'Buchwalter, Abigail, et al. “Coaching from the Sidelines: The Nuclear Periphery
in Genome Regulation.” Nature Reviews Genetics, vol. 20, no. 1, Springer
Nature, 2019, pp. 39–50, doi:10.1038/s41576-018-0063-5.'
short: A. Buchwalter, J.M. Kaneshiro, M. Hetzer, Nature Reviews Genetics 20 (2019)
39–50.
date_created: 2022-04-07T07:44:45Z
date_published: 2019-01-01T00:00:00Z
date_updated: 2024-10-14T11:18:54Z
day: '01'
doi: 10.1038/s41576-018-0063-5
extern: '1'
external_id:
pmid:
- '30356165'
fulldoi: https://doi.org/10.1038/s41576-018-0063-5
intvolume: ' 20'
issue: '1'
keyword:
- Genetics (clinical)
- Genetics
- Molecular Biology
language:
- iso: eng
month: '01'
oa_version: None
page: 39-50
pmid: 1
publication: Nature Reviews Genetics
publication_identifier:
eissn:
- 1471-0064
issn:
- 1471-0056
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
scopus_import: '1'
status: public
title: 'Coaching from the sidelines: The nuclear periphery in genome regulation'
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 20
year: '2019'
...
---
_id: '11060'
abstract:
- lang: eng
text: The inner nuclear membrane (INM) is a subdomain of the endoplasmic reticulum
(ER) that is gated by the nuclear pore complex. It is unknown whether proteins
of the INM and ER are degraded through shared or distinct pathways in mammalian
cells. We applied dynamic proteomics to profile protein half-lives and report
that INM and ER residents turn over at similar rates, indicating that the INM’s
unique topology is not a barrier to turnover. Using a microscopy approach, we
observed that the proteasome can degrade INM proteins in situ. However, we also
uncovered evidence for selective, vesicular transport-mediated turnover of a single
INM protein, emerin, that is potentiated by ER stress. Emerin is rapidly cleared
from the INM by a mechanism that requires emerin’s LEM domain to mediate vesicular
trafficking to lysosomes. This work demonstrates that the INM can be dynamically
remodeled in response to environmental inputs.
article_number: e49796
article_processing_charge: No
article_type: original
author:
- first_name: Abigail
full_name: Buchwalter, Abigail
last_name: Buchwalter
- first_name: Roberta
full_name: Schulte, Roberta
last_name: Schulte
- first_name: Hsiao
full_name: Tsai, Hsiao
last_name: Tsai
- first_name: Juliana
full_name: Capitanio, Juliana
last_name: Capitanio
- first_name: Martin W
full_name: HETZER, Martin W
id: 86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed
last_name: HETZER
orcid: 0000-0002-2111-992X
citation:
ama: Buchwalter A, Schulte R, Tsai H, Capitanio J, Hetzer M. Selective clearance
of the inner nuclear membrane protein emerin by vesicular transport during ER
stress. eLife. 2019;8. doi:10.7554/elife.49796
apa: Buchwalter, A., Schulte, R., Tsai, H., Capitanio, J., & Hetzer, M. (2019).
Selective clearance of the inner nuclear membrane protein emerin by vesicular
transport during ER stress. ELife. eLife Sciences Publications. https://doi.org/10.7554/elife.49796
chicago: Buchwalter, Abigail, Roberta Schulte, Hsiao Tsai, Juliana Capitanio, and
Martin Hetzer. “Selective Clearance of the Inner Nuclear Membrane Protein Emerin
by Vesicular Transport during ER Stress.” ELife. eLife Sciences Publications,
2019. https://doi.org/10.7554/elife.49796.
ieee: A. Buchwalter, R. Schulte, H. Tsai, J. Capitanio, and M. Hetzer, “Selective
clearance of the inner nuclear membrane protein emerin by vesicular transport
during ER stress,” eLife, vol. 8. eLife Sciences Publications, 2019.
ista: Buchwalter A, Schulte R, Tsai H, Capitanio J, Hetzer M. 2019. Selective clearance
of the inner nuclear membrane protein emerin by vesicular transport during ER
stress. eLife. 8, e49796.
mla: Buchwalter, Abigail, et al. “Selective Clearance of the Inner Nuclear Membrane
Protein Emerin by Vesicular Transport during ER Stress.” ELife, vol. 8,
e49796, eLife Sciences Publications, 2019, doi:10.7554/elife.49796.
short: A. Buchwalter, R. Schulte, H. Tsai, J. Capitanio, M. Hetzer, ELife 8 (2019).
date_created: 2022-04-07T07:45:02Z
date_published: 2019-10-10T00:00:00Z
date_updated: 2024-10-14T12:08:36Z
day: '10'
ddc:
- '570'
doi: 10.7554/elife.49796
extern: '1'
external_id:
pmid:
- '31599721'
file:
- access_level: open_access
checksum: 1e8672a1e9c3dc0a2d3d0dad89673616
content_type: application/pdf
creator: dernst
date_created: 2022-04-08T08:18:01Z
date_updated: 2022-04-08T08:18:01Z
file_id: '11138'
file_name: 2019_eLife_Buchwalter.pdf
file_size: 6984654
relation: main_file
success: 1
file_date_updated: 2022-04-08T08:18:01Z
fulldoi: https://doi.org/10.7554/elife.49796
has_accepted_license: '1'
intvolume: ' 8'
keyword:
- General Immunology and Microbiology
- General Biochemistry
- Genetics and Molecular Biology
- General Medicine
- General Neuroscience
language:
- iso: eng
month: '10'
oa: 1
oa_version: Published Version
pmid: 1
publication: eLife
publication_identifier:
issn:
- 2050-084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
related_material:
record:
- id: '13079'
relation: research_data
status: public
scopus_import: '1'
status: public
title: Selective clearance of the inner nuclear membrane protein emerin by vesicular
transport during ER stress
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: 8
year: '2019'
...
---
_id: '11061'
abstract:
- lang: eng
text: Many adult tissues contain postmitotic cells as old as the host organism.
The only organelle that does not turn over in these cells is the nucleus, and
its maintenance represents a formidable challenge, as it harbors regulatory proteins
that persist throughout adulthood. Here we developed strategies to visualize two
classes of such long-lived proteins, histones and nucleoporins, to understand
the function of protein longevity in nuclear maintenance. Genome-wide mapping
of histones revealed specific enrichment of long-lived variants at silent gene
loci. Interestingly, nuclear pores are maintained by piecemeal replacement of
subunits, resulting in mosaic complexes composed of polypeptides with vastly different
ages. In contrast, nondividing quiescent cells remove old nuclear pores in an
ESCRT-dependent manner. Our findings reveal distinct molecular strategies of nuclear
maintenance, linking lifelong protein persistence to gene regulation and nuclear
integrity.
article_processing_charge: No
article_type: original
author:
- first_name: Brandon H.
full_name: Toyama, Brandon H.
last_name: Toyama
- first_name: Rafael
full_name: Arrojo e Drigo, Rafael
last_name: Arrojo e Drigo
- first_name: Varda
full_name: Lev-Ram, Varda
last_name: Lev-Ram
- first_name: Ranjan
full_name: Ramachandra, Ranjan
last_name: Ramachandra
- first_name: Thomas J.
full_name: Deerinck, Thomas J.
last_name: Deerinck
- first_name: Claude
full_name: Lechene, Claude
last_name: Lechene
- first_name: Mark H.
full_name: Ellisman, Mark H.
last_name: Ellisman
- first_name: Martin W
full_name: HETZER, Martin W
id: 86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed
last_name: HETZER
orcid: 0000-0002-2111-992X
citation:
ama: Toyama BH, Arrojo e Drigo R, Lev-Ram V, et al. Visualization of long-lived
proteins reveals age mosaicism within nuclei of postmitotic cells. Journal
of Cell Biology. 2019;218(2):433-444. doi:10.1083/jcb.201809123
apa: Toyama, B. H., Arrojo e Drigo, R., Lev-Ram, V., Ramachandra, R., Deerinck,
T. J., Lechene, C., … Hetzer, M. (2019). Visualization of long-lived proteins
reveals age mosaicism within nuclei of postmitotic cells. Journal of Cell Biology.
Rockefeller University Press. https://doi.org/10.1083/jcb.201809123
chicago: Toyama, Brandon H., Rafael Arrojo e Drigo, Varda Lev-Ram, Ranjan Ramachandra,
Thomas J. Deerinck, Claude Lechene, Mark H. Ellisman, and Martin Hetzer. “Visualization
of Long-Lived Proteins Reveals Age Mosaicism within Nuclei of Postmitotic Cells.”
Journal of Cell Biology. Rockefeller University Press, 2019. https://doi.org/10.1083/jcb.201809123.
ieee: B. H. Toyama et al., “Visualization of long-lived proteins reveals
age mosaicism within nuclei of postmitotic cells,” Journal of Cell Biology,
vol. 218, no. 2. Rockefeller University Press, pp. 433–444, 2019.
ista: Toyama BH, Arrojo e Drigo R, Lev-Ram V, Ramachandra R, Deerinck TJ, Lechene
C, Ellisman MH, Hetzer M. 2019. Visualization of long-lived proteins reveals age
mosaicism within nuclei of postmitotic cells. Journal of Cell Biology. 218(2),
433–444.
mla: Toyama, Brandon H., et al. “Visualization of Long-Lived Proteins Reveals Age
Mosaicism within Nuclei of Postmitotic Cells.” Journal of Cell Biology,
vol. 218, no. 2, Rockefeller University Press, 2019, pp. 433–44, doi:10.1083/jcb.201809123.
short: B.H. Toyama, R. Arrojo e Drigo, V. Lev-Ram, R. Ramachandra, T.J. Deerinck,
C. Lechene, M.H. Ellisman, M. Hetzer, Journal of Cell Biology 218 (2019) 433–444.
date_created: 2022-04-07T07:45:11Z
date_published: 2019-02-04T00:00:00Z
date_updated: 2024-10-14T11:19:21Z
day: '04'
ddc:
- '570'
doi: 10.1083/jcb.201809123
extern: '1'
external_id:
pmid:
- '30552100'
file:
- access_level: open_access
checksum: 7964ebbf833b0b35f9fba840eea9531d
content_type: application/pdf
creator: dernst
date_created: 2022-04-08T08:26:32Z
date_updated: 2022-04-08T08:26:32Z
file_id: '11139'
file_name: 2019_JCB_Toyama.pdf
file_size: 2503838
relation: main_file
success: 1
file_date_updated: 2022-04-08T08:26:32Z
fulldoi: https://doi.org/10.1083/jcb.201809123
has_accepted_license: '1'
intvolume: ' 218'
issue: '2'
keyword:
- Cell Biology
language:
- iso: eng
month: '02'
oa: 1
oa_version: Published Version
page: 433-444
pmid: 1
publication: Journal of Cell Biology
publication_identifier:
eissn:
- 1540-8140
issn:
- 0021-9525
publication_status: published
publisher: Rockefeller University Press
quality_controlled: '1'
scopus_import: '1'
status: public
title: Visualization of long-lived proteins reveals age mosaicism within nuclei of
postmitotic cells
tmp:
image: /images/cc_by_nc_sa.png
legal_code_url: https://creativecommons.org/licenses/by-nc-sa/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC
BY-NC-SA 4.0)
short: CC BY-NC-SA (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 218
year: '2019'
...
---
_id: '11062'
abstract:
- lang: eng
text: Most neurons are not replaced during an animal’s lifetime. This nondividing
state is characterized by extreme longevity and age-dependent decline of key regulatory
proteins. To study the lifespans of cells and proteins in adult tissues, we combined
isotope labeling of mice with a hybrid imaging method (MIMS-EM). Using 15N mapping,
we show that liver and pancreas are composed of cells with vastly different ages,
many as old as the animal. Strikingly, we also found that a subset of fibroblasts
and endothelial cells, both known for their replicative potential, are characterized
by the absence of cell division during adulthood. In addition, we show that the
primary cilia of beta cells and neurons contains different structural regions
with vastly different lifespans. Based on these results, we propose that age mosaicism
across multiple scales is a fundamental principle of adult tissue, cell, and protein
complex organization.
article_processing_charge: No
article_type: original
author:
- first_name: Rafael
full_name: Arrojo e Drigo, Rafael
last_name: Arrojo e Drigo
- first_name: Varda
full_name: Lev-Ram, Varda
last_name: Lev-Ram
- first_name: Swati
full_name: Tyagi, Swati
last_name: Tyagi
- first_name: Ranjan
full_name: Ramachandra, Ranjan
last_name: Ramachandra
- first_name: Thomas
full_name: Deerinck, Thomas
last_name: Deerinck
- first_name: Eric
full_name: Bushong, Eric
last_name: Bushong
- first_name: Sebastien
full_name: Phan, Sebastien
last_name: Phan
- first_name: Victoria
full_name: Orphan, Victoria
last_name: Orphan
- first_name: Claude
full_name: Lechene, Claude
last_name: Lechene
- first_name: Mark H.
full_name: Ellisman, Mark H.
last_name: Ellisman
- first_name: Martin W
full_name: HETZER, Martin W
id: 86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed
last_name: HETZER
orcid: 0000-0002-2111-992X
citation:
ama: Arrojo e Drigo R, Lev-Ram V, Tyagi S, et al. Age mosaicism across multiple
scales in adult tissues. Cell Metabolism. 2019;30(2):343-351.e3. doi:10.1016/j.cmet.2019.05.010
apa: Arrojo e Drigo, R., Lev-Ram, V., Tyagi, S., Ramachandra, R., Deerinck, T.,
Bushong, E., … Hetzer, M. (2019). Age mosaicism across multiple scales in adult
tissues. Cell Metabolism. Elsevier. https://doi.org/10.1016/j.cmet.2019.05.010
chicago: Arrojo e Drigo, Rafael, Varda Lev-Ram, Swati Tyagi, Ranjan Ramachandra,
Thomas Deerinck, Eric Bushong, Sebastien Phan, et al. “Age Mosaicism across Multiple
Scales in Adult Tissues.” Cell Metabolism. Elsevier, 2019. https://doi.org/10.1016/j.cmet.2019.05.010.
ieee: R. Arrojo e Drigo et al., “Age mosaicism across multiple scales in
adult tissues,” Cell Metabolism, vol. 30, no. 2. Elsevier, p. 343–351.e3,
2019.
ista: Arrojo e Drigo R, Lev-Ram V, Tyagi S, Ramachandra R, Deerinck T, Bushong E,
Phan S, Orphan V, Lechene C, Ellisman MH, Hetzer M. 2019. Age mosaicism across
multiple scales in adult tissues. Cell Metabolism. 30(2), 343–351.e3.
mla: Arrojo e Drigo, Rafael, et al. “Age Mosaicism across Multiple Scales in Adult
Tissues.” Cell Metabolism, vol. 30, no. 2, Elsevier, 2019, p. 343–351.e3,
doi:10.1016/j.cmet.2019.05.010.
short: R. Arrojo e Drigo, V. Lev-Ram, S. Tyagi, R. Ramachandra, T. Deerinck, E.
Bushong, S. Phan, V. Orphan, C. Lechene, M.H. Ellisman, M. Hetzer, Cell Metabolism
30 (2019) 343–351.e3.
date_created: 2022-04-07T07:45:21Z
date_published: 2019-08-06T00:00:00Z
date_updated: 2025-12-15T10:02:11Z
day: '06'
department:
- _id: MaHe
doi: 10.1016/j.cmet.2019.05.010
extern: '1'
external_id:
pmid:
- '31178361'
fulldoi: https://doi.org/10.1016/j.cmet.2019.05.010
intvolume: ' 30'
issue: '2'
keyword:
- Cell Biology
- Molecular Biology
- Physiology
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1016/j.cmet.2019.05.010
month: '08'
oa: 1
oa_version: Published Version
page: 343-351.e3
pmid: 1
publication: Cell Metabolism
publication_identifier:
issn:
- 1550-4131
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: Age mosaicism across multiple scales in adult tissues
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 30
year: '2019'
...
---
_id: '13079'
abstract:
- lang: eng
text: The inner nuclear membrane (INM) is a subdomain of the endoplasmic reticulum
(ER) that is gated by the nuclear pore complex. It is unknown whether proteins
of the INM and ER are degraded through shared or distinct pathways in mammalian
cells. We applied dynamic proteomics to profile protein half-lives and report
that INM and ER residents turn over at similar rates, indicating that the INM’s
unique topology is not a barrier to turnover. Using a microscopy approach, we
observed that the proteasome can degrade INM proteins in situ. However, we also
uncovered evidence for selective, vesicular transport-mediated turnover of a single
INM protein, emerin, that is potentiated by ER stress. Emerin is rapidly cleared
from the INM by a mechanism that requires emerin’s LEM domain to mediate vesicular
trafficking to lysosomes. This work demonstrates that the INM can be dynamically
remodeled in response to environmental inputs.
article_processing_charge: No
author:
- first_name: Abigail
full_name: Buchwalter, Abigail
last_name: Buchwalter
- first_name: Roberta
full_name: Schulte, Roberta
last_name: Schulte
- first_name: Hsiao
full_name: Tsai, Hsiao
last_name: Tsai
- first_name: Juliana
full_name: Capitanio, Juliana
last_name: Capitanio
- first_name: Martin W
full_name: HETZER, Martin W
id: 86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed
last_name: HETZER
orcid: 0000-0002-2111-992X
citation:
ama: 'Buchwalter A, Schulte R, Tsai H, Capitanio J, Hetzer M. Data from: Selective
clearance of the inner nuclear membrane protein emerin by vesicular transport
during ER stress. 2019. doi:10.5061/DRYAD.N0R525H'
apa: 'Buchwalter, A., Schulte, R., Tsai, H., Capitanio, J., & Hetzer, M. (2019).
Data from: Selective clearance of the inner nuclear membrane protein emerin by
vesicular transport during ER stress. Dryad. https://doi.org/10.5061/DRYAD.N0R525H'
chicago: 'Buchwalter, Abigail, Roberta Schulte, Hsiao Tsai, Juliana Capitanio, and
Martin Hetzer. “Data from: Selective Clearance of the Inner Nuclear Membrane Protein
Emerin by Vesicular Transport during ER Stress.” Dryad, 2019. https://doi.org/10.5061/DRYAD.N0R525H.'
ieee: 'A. Buchwalter, R. Schulte, H. Tsai, J. Capitanio, and M. Hetzer, “Data from:
Selective clearance of the inner nuclear membrane protein emerin by vesicular
transport during ER stress.” Dryad, 2019.'
ista: 'Buchwalter A, Schulte R, Tsai H, Capitanio J, Hetzer M. 2019. Data from:
Selective clearance of the inner nuclear membrane protein emerin by vesicular
transport during ER stress, Dryad, 10.5061/DRYAD.N0R525H.'
mla: 'Buchwalter, Abigail, et al. Data from: Selective Clearance of the Inner
Nuclear Membrane Protein Emerin by Vesicular Transport during ER Stress. Dryad,
2019, doi:10.5061/DRYAD.N0R525H.'
short: A. Buchwalter, R. Schulte, H. Tsai, J. Capitanio, M. Hetzer, (2019).
date_created: 2023-05-23T17:09:30Z
date_published: 2019-10-28T00:00:00Z
date_updated: 2024-10-14T12:08:37Z
day: '28'
ddc:
- '570'
doi: 10.5061/DRYAD.N0R525H
extern: '1'
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status: public
status: public
title: 'Data from: Selective clearance of the inner nuclear membrane protein emerin
by vesicular transport during ER stress'
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...