---
_id: '11067'
abstract:
- lang: eng
text: Neural progenitor cells (NeuPCs) possess a unique nuclear architecture that
changes during differentiation. Nucleoporins are linked with cell-type-specific
gene regulation, coupling physical changes in nuclear structure to transcriptional
output; but, whether and how they coordinate with key fate-determining transcription
factors is unclear. Here we show that the nucleoporin Nup153 interacts with Sox2
in adult NeuPCs, where it is indispensable for their maintenance and controls
neuronal differentiation. Genome-wide analyses show that Nup153 and Sox2 bind
and co-regulate hundreds of genes. Binding of Nup153 to gene promoters or transcriptional
end sites correlates with increased or decreased gene expression, respectively,
and inhibiting Nup153 expression alters open chromatin configurations at its target
genes, disrupts genomic localization of Sox2, and promotes differentiation in
vitro and a gliogenic fate switch in vivo. Together, these findings reveal that
nuclear structural proteins may exert bimodal transcriptional effects to control
cell fate.
article_processing_charge: No
article_type: original
author:
- first_name: Tomohisa
full_name: Toda, Tomohisa
last_name: Toda
- first_name: Jonathan Y.
full_name: Hsu, Jonathan Y.
last_name: Hsu
- first_name: Sara B.
full_name: Linker, Sara B.
last_name: Linker
- first_name: Lauren
full_name: Hu, Lauren
last_name: Hu
- first_name: Simon T.
full_name: Schafer, Simon T.
last_name: Schafer
- first_name: Jerome
full_name: Mertens, Jerome
last_name: Mertens
- first_name: Filipe V.
full_name: Jacinto, Filipe V.
last_name: Jacinto
- 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: Fred H.
full_name: Gage, Fred H.
last_name: Gage
citation:
ama: Toda T, Hsu JY, Linker SB, et al. Nup153 interacts with Sox2 to enable bimodal
gene regulation and maintenance of neural progenitor cells. Cell Stem Cell.
2017;21(5):618-634.e7. doi:10.1016/j.stem.2017.08.012
apa: Toda, T., Hsu, J. Y., Linker, S. B., Hu, L., Schafer, S. T., Mertens, J., …
Gage, F. H. (2017). Nup153 interacts with Sox2 to enable bimodal gene regulation
and maintenance of neural progenitor cells. Cell Stem Cell. Elsevier. https://doi.org/10.1016/j.stem.2017.08.012
chicago: Toda, Tomohisa, Jonathan Y. Hsu, Sara B. Linker, Lauren Hu, Simon T. Schafer,
Jerome Mertens, Filipe V. Jacinto, Martin Hetzer, and Fred H. Gage. “Nup153 Interacts
with Sox2 to Enable Bimodal Gene Regulation and Maintenance of Neural Progenitor
Cells.” Cell Stem Cell. Elsevier, 2017. https://doi.org/10.1016/j.stem.2017.08.012.
ieee: T. Toda et al., “Nup153 interacts with Sox2 to enable bimodal gene
regulation and maintenance of neural progenitor cells,” Cell Stem Cell,
vol. 21, no. 5. Elsevier, p. 618–634.e7, 2017.
ista: Toda T, Hsu JY, Linker SB, Hu L, Schafer ST, Mertens J, Jacinto FV, Hetzer
M, Gage FH. 2017. Nup153 interacts with Sox2 to enable bimodal gene regulation
and maintenance of neural progenitor cells. Cell Stem Cell. 21(5), 618–634.e7.
mla: Toda, Tomohisa, et al. “Nup153 Interacts with Sox2 to Enable Bimodal Gene Regulation
and Maintenance of Neural Progenitor Cells.” Cell Stem Cell, vol. 21, no.
5, Elsevier, 2017, p. 618–634.e7, doi:10.1016/j.stem.2017.08.012.
short: T. Toda, J.Y. Hsu, S.B. Linker, L. Hu, S.T. Schafer, J. Mertens, F.V. Jacinto,
M. Hetzer, F.H. Gage, Cell Stem Cell 21 (2017) 618–634.e7.
date_created: 2022-04-07T07:46:12Z
date_published: 2017-11-02T00:00:00Z
date_updated: 2022-07-18T08:33:07Z
day: '02'
doi: 10.1016/j.stem.2017.08.012
extern: '1'
external_id:
pmid:
- '28919367'
intvolume: ' 21'
issue: '5'
keyword:
- Cell Biology
- Genetics
- Molecular Medicine
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1016/j.stem.2017.08.012
month: '11'
oa: 1
oa_version: Published Version
page: 618-634.e7
pmid: 1
publication: Cell Stem Cell
publication_identifier:
issn:
- 1934-5909
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: Nup153 interacts with Sox2 to enable bimodal gene regulation and maintenance
of neural progenitor cells
type: journal_article
user_id: 72615eeb-f1f3-11ec-aa25-d4573ddc34fd
volume: 21
year: '2017'
...
---
_id: '5560'
abstract:
- lang: eng
text: "This repository contains the data collected for the manuscript \"Biased partitioning
of the multi-drug efflux pump AcrAB-TolC underlies long-lived phenotypic heterogeneity\".\r\nThe
data is compressed into a single archive. Within the archive, different folders
correspond to figures of the main text and the SI of the related publication.\r\nData
is saved as plain text, with each folder containing a separate readme file describing
the format. Typically, the data is from fluorescence microscopy measurements of
single cells growing in a microfluidic \"mother machine\" device, and consists
of relevant values (primarily arbitrary unit or normalized fluorescence measurements,
and division times / growth rates) after raw microscopy images have been processed,
segmented, and their features extracted, as described in the methods section of
the related publication."
article_processing_charge: No
author:
- first_name: Tobias
full_name: Bergmiller, Tobias
id: 2C471CFA-F248-11E8-B48F-1D18A9856A87
last_name: Bergmiller
orcid: 0000-0001-5396-4346
- first_name: Anna M
full_name: Andersson, Anna M
id: 2B8A40DA-F248-11E8-B48F-1D18A9856A87
last_name: Andersson
orcid: 0000-0003-2912-6769
- first_name: Kathrin
full_name: Tomasek, Kathrin
id: 3AEC8556-F248-11E8-B48F-1D18A9856A87
last_name: Tomasek
orcid: 0000-0003-3768-877X
- first_name: Enrique
full_name: Balleza, Enrique
last_name: Balleza
- first_name: Daniel
full_name: Kiviet, Daniel
last_name: Kiviet
- first_name: Robert
full_name: Hauschild, Robert
id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87
last_name: Hauschild
orcid: 0000-0001-9843-3522
- first_name: Gasper
full_name: Tkacik, Gasper
id: 3D494DCA-F248-11E8-B48F-1D18A9856A87
last_name: Tkacik
orcid: 0000-0002-6699-1455
- first_name: Calin C
full_name: Guet, Calin C
id: 47F8433E-F248-11E8-B48F-1D18A9856A87
last_name: Guet
orcid: 0000-0001-6220-2052
citation:
ama: Bergmiller T, Andersson AM, Tomasek K, et al. Biased partitioning of the multi-drug
efflux pump AcrAB-TolC underlies long-lived phenotypic heterogeneity. 2017. doi:10.15479/AT:ISTA:53
apa: Bergmiller, T., Andersson, A. M., Tomasek, K., Balleza, E., Kiviet, D., Hauschild,
R., … Guet, C. C. (2017). Biased partitioning of the multi-drug efflux pump AcrAB-TolC
underlies long-lived phenotypic heterogeneity. Institute of Science and Technology
Austria. https://doi.org/10.15479/AT:ISTA:53
chicago: Bergmiller, Tobias, Anna M Andersson, Kathrin Tomasek, Enrique Balleza,
Daniel Kiviet, Robert Hauschild, Gašper Tkačik, and Calin C Guet. “Biased Partitioning
of the Multi-Drug Efflux Pump AcrAB-TolC Underlies Long-Lived Phenotypic Heterogeneity.”
Institute of Science and Technology Austria, 2017. https://doi.org/10.15479/AT:ISTA:53.
ieee: T. Bergmiller et al., “Biased partitioning of the multi-drug efflux
pump AcrAB-TolC underlies long-lived phenotypic heterogeneity.” Institute of Science
and Technology Austria, 2017.
ista: Bergmiller T, Andersson AM, Tomasek K, Balleza E, Kiviet D, Hauschild R, Tkačik
G, Guet CC. 2017. Biased partitioning of the multi-drug efflux pump AcrAB-TolC
underlies long-lived phenotypic heterogeneity, Institute of Science and Technology
Austria, 10.15479/AT:ISTA:53.
mla: Bergmiller, Tobias, et al. Biased Partitioning of the Multi-Drug Efflux
Pump AcrAB-TolC Underlies Long-Lived Phenotypic Heterogeneity. Institute of
Science and Technology Austria, 2017, doi:10.15479/AT:ISTA:53.
short: T. Bergmiller, A.M. Andersson, K. Tomasek, E. Balleza, D. Kiviet, R. Hauschild,
G. Tkačik, C.C. Guet, (2017).
datarep_id: '53'
date_created: 2018-12-12T12:31:32Z
date_published: 2017-03-10T00:00:00Z
date_updated: 2024-02-21T13:49:00Z
day: '10'
ddc:
- '571'
department:
- _id: CaGu
- _id: GaTk
- _id: Bio
doi: 10.15479/AT:ISTA:53
file:
- access_level: open_access
checksum: d77859af757ac8025c50c7b12b52eaf3
content_type: application/zip
creator: system
date_created: 2018-12-12T13:02:38Z
date_updated: 2020-07-14T12:47:03Z
file_id: '5603'
file_name: IST-2017-53-v1+1_Data_MDE.zip
file_size: 6773204
relation: main_file
file_date_updated: 2020-07-14T12:47:03Z
has_accepted_license: '1'
keyword:
- single cell microscopy
- mother machine microfluidic device
- AcrAB-TolC pump
- multi-drug efflux
- Escherichia coli
month: '03'
oa: 1
oa_version: Published Version
publisher: Institute of Science and Technology Austria
related_material:
record:
- id: '665'
relation: research_paper
status: public
status: public
title: Biased partitioning of the multi-drug efflux pump AcrAB-TolC underlies long-lived
phenotypic heterogeneity
tmp:
image: /images/cc_0.png
legal_code_url: https://creativecommons.org/publicdomain/zero/1.0/legalcode
name: Creative Commons Public Domain Dedication (CC0 1.0)
short: CC0 (1.0)
type: research_data
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
year: '2017'
...
---
_id: '5570'
abstract:
- lang: eng
text: Matlab script to calculate the forward migration indexes (/) from
TrackMate spot-statistics files.
article_processing_charge: No
author:
- first_name: Robert
full_name: Hauschild, Robert
id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87
last_name: Hauschild
orcid: 0000-0001-9843-3522
citation:
ama: Hauschild R. Forward migration indexes. 2017. doi:10.15479/AT:ISTA:75
apa: Hauschild, R. (2017). Forward migration indexes. Institute of Science and Technology
Austria. https://doi.org/10.15479/AT:ISTA:75
chicago: Hauschild, Robert. “Forward Migration Indexes.” Institute of Science and
Technology Austria, 2017. https://doi.org/10.15479/AT:ISTA:75.
ieee: R. Hauschild, “Forward migration indexes.” Institute of Science and Technology
Austria, 2017.
ista: Hauschild R. 2017. Forward migration indexes, Institute of Science and Technology
Austria, 10.15479/AT:ISTA:75.
mla: Hauschild, Robert. Forward Migration Indexes. Institute of Science and
Technology Austria, 2017, doi:10.15479/AT:ISTA:75.
short: R. Hauschild, (2017).
datarep_id: '75'
date_created: 2018-12-12T12:31:35Z
date_published: 2017-10-04T00:00:00Z
date_updated: 2024-02-21T13:47:14Z
day: '04'
ddc:
- '570'
department:
- _id: Bio
doi: 10.15479/AT:ISTA:75
file:
- access_level: open_access
checksum: cb7a2fa622460eca6231d659ce590e32
content_type: application/octet-stream
creator: system
date_created: 2018-12-12T13:02:29Z
date_updated: 2020-07-14T12:47:04Z
file_id: '5596'
file_name: IST-2017-75-v1+1_FMI.m
file_size: 799
relation: main_file
file_date_updated: 2020-07-14T12:47:04Z
has_accepted_license: '1'
keyword:
- Cell migration
- tracking
- forward migration index
- FMI
month: '10'
oa: 1
oa_version: Published Version
publisher: Institute of Science and Technology Austria
status: public
title: Forward migration indexes
tmp:
image: /images/cc_0.png
legal_code_url: https://creativecommons.org/publicdomain/zero/1.0/legalcode
name: Creative Commons Public Domain Dedication (CC0 1.0)
short: CC0 (1.0)
type: research_data
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
year: '2017'
...
---
_id: '11069'
abstract:
- lang: eng
text: Repeated rounds of nuclear envelope (NE) rupture and repair have been observed
in laminopathy and cancer cells and result in intermittent loss of nucleus compartmentalization.
Currently, the causes of NE rupture are unclear. Here, we show that NE rupture
in cancer cells relies on the assembly of contractile actin bundles that interact
with the nucleus via the linker of nucleoskeleton and cytoskeleton (LINC) complex.
We found that the loss of actin bundles or the LINC complex did not rescue nuclear
lamina defects, a previously identified determinant of nuclear membrane stability,
but did decrease the number and size of chromatin hernias. Finally, NE rupture
inhibition could be rescued in cells treated with actin-depolymerizing drugs by
mechanically constraining nucleus height. These data suggest a model of NE rupture
where weak membrane areas, caused by defects in lamina organization, rupture because
of an increase in intranuclear pressure from actin-based nucleus confinement.
article_processing_charge: No
article_type: original
author:
- first_name: Emily M.
full_name: Hatch, Emily M.
last_name: Hatch
- 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: Hatch EM, Hetzer M. Nuclear envelope rupture is induced by actin-based nucleus
confinement. Journal of Cell Biology. 2016;215(1):27-36. doi:10.1083/jcb.201603053
apa: Hatch, E. M., & Hetzer, M. (2016). Nuclear envelope rupture is induced
by actin-based nucleus confinement. Journal of Cell Biology. Rockefeller
University Press. https://doi.org/10.1083/jcb.201603053
chicago: Hatch, Emily M., and Martin Hetzer. “Nuclear Envelope Rupture Is Induced
by Actin-Based Nucleus Confinement.” Journal of Cell Biology. Rockefeller
University Press, 2016. https://doi.org/10.1083/jcb.201603053.
ieee: E. M. Hatch and M. Hetzer, “Nuclear envelope rupture is induced by actin-based
nucleus confinement,” Journal of Cell Biology, vol. 215, no. 1. Rockefeller
University Press, pp. 27–36, 2016.
ista: Hatch EM, Hetzer M. 2016. Nuclear envelope rupture is induced by actin-based
nucleus confinement. Journal of Cell Biology. 215(1), 27–36.
mla: Hatch, Emily M., and Martin Hetzer. “Nuclear Envelope Rupture Is Induced by
Actin-Based Nucleus Confinement.” Journal of Cell Biology, vol. 215, no.
1, Rockefeller University Press, 2016, pp. 27–36, doi:10.1083/jcb.201603053.
short: E.M. Hatch, M. Hetzer, Journal of Cell Biology 215 (2016) 27–36.
date_created: 2022-04-07T07:47:42Z
date_published: 2016-10-03T00:00:00Z
date_updated: 2022-07-18T08:33:47Z
day: '03'
doi: 10.1083/jcb.201603053
extern: '1'
external_id:
pmid:
- '27697922'
intvolume: ' 215'
issue: '1'
keyword:
- Cell Biology
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1083/jcb.201603053
month: '10'
oa: 1
oa_version: Published Version
page: 27-36
pmid: 1
publication: Journal of Cell Biology
publication_identifier:
issn:
- 0021-9525
- 1540-8140
publication_status: published
publisher: Rockefeller University Press
quality_controlled: '1'
scopus_import: '1'
status: public
title: Nuclear envelope rupture is induced by actin-based nucleus confinement
type: journal_article
user_id: 72615eeb-f1f3-11ec-aa25-d4573ddc34fd
volume: 215
year: '2016'
...
---
_id: '5555'
abstract:
- lang: eng
text: This FIJI script calculates the population average of the migration speed
as a function of time of all cells from wide field microscopy movies.
article_processing_charge: No
author:
- first_name: Robert
full_name: Hauschild, Robert
id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87
last_name: Hauschild
orcid: 0000-0001-9843-3522
citation:
ama: Hauschild R. Fiji script to determine average speed and direction of migration
of cells. 2016. doi:10.15479/AT:ISTA:44
apa: Hauschild, R. (2016). Fiji script to determine average speed and direction
of migration of cells. Institute of Science and Technology Austria. https://doi.org/10.15479/AT:ISTA:44
chicago: Hauschild, Robert. “Fiji Script to Determine Average Speed and Direction
of Migration of Cells.” Institute of Science and Technology Austria, 2016. https://doi.org/10.15479/AT:ISTA:44.
ieee: R. Hauschild, “Fiji script to determine average speed and direction of migration
of cells.” Institute of Science and Technology Austria, 2016.
ista: Hauschild R. 2016. Fiji script to determine average speed and direction of
migration of cells, Institute of Science and Technology Austria, 10.15479/AT:ISTA:44.
mla: Hauschild, Robert. Fiji Script to Determine Average Speed and Direction
of Migration of Cells. Institute of Science and Technology Austria, 2016,
doi:10.15479/AT:ISTA:44.
short: R. Hauschild, (2016).
datarep_id: '44'
date_created: 2018-12-12T12:31:31Z
date_published: 2016-07-08T00:00:00Z
date_updated: 2024-02-21T13:50:06Z
day: '08'
ddc:
- '570'
department:
- _id: Bio
doi: 10.15479/AT:ISTA:44
file:
- access_level: open_access
checksum: 9f96cddbcd4ed689f48712ffe234d5e5
content_type: application/zip
creator: system
date_created: 2018-12-12T13:03:03Z
date_updated: 2020-07-14T12:47:02Z
file_id: '5621'
file_name: IST-2016-44-v1+1_migrationAnalyzer.zip
file_size: 20692
relation: main_file
file_date_updated: 2020-07-14T12:47:02Z
has_accepted_license: '1'
keyword:
- cell migration
- wide field microscopy
- FIJI
month: '07'
oa: 1
oa_version: Published Version
publisher: Institute of Science and Technology Austria
status: public
title: Fiji script to determine average speed and direction of migration of cells
tmp:
image: /images/cc_0.png
legal_code_url: https://creativecommons.org/publicdomain/zero/1.0/legalcode
name: Creative Commons Public Domain Dedication (CC0 1.0)
short: CC0 (1.0)
type: research_data
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
year: '2016'
...
---
_id: '11075'
abstract:
- lang: eng
text: Previously, we identified the nucleoporin gp210/Nup210 as a critical regulator
of muscle and neuronal differentiation, but how this nucleoporin exerts its function
and whether it modulates nuclear pore complex (NPC) activity remain unknown. Here,
we show that gp210/Nup210 mediates muscle cell differentiation in vitro via its
conserved N-terminal domain that extends into the perinuclear space. Removal of
the C-terminal domain, which partially mislocalizes gp210/Nup210 away from NPCs,
efficiently rescues the differentiation defect caused by the knockdown of endogenous
gp210/Nup210. Unexpectedly, a gp210/Nup210 mutant lacking the NPC-targeting transmembrane
and C-terminal domains is sufficient for C2C12 myoblast differentiation. We demonstrate
that the endoplasmic reticulum (ER) stress-specific caspase cascade is exacerbated
during Nup210 depletion and that blocking ER stress-mediated apoptosis rescues
differentiation of Nup210-deficient cells. Our results suggest that the role of
gp210/Nup210 in cell differentiation is mediated by its large luminal domain,
which can act independently of NPC association and appears to play a pivotal role
in the maintenance of nuclear envelope/ER homeostasis.
article_processing_charge: No
article_type: original
author:
- first_name: J. Sebastian
full_name: Gomez-Cavazos, J. Sebastian
last_name: Gomez-Cavazos
- 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: Gomez-Cavazos JS, Hetzer M. The nucleoporin gp210/Nup210 controls muscle differentiation
by regulating nuclear envelope/ER homeostasis. Journal of Cell Biology.
2015;208(6):671-681. doi:10.1083/jcb.201410047
apa: Gomez-Cavazos, J. S., & Hetzer, M. (2015). The nucleoporin gp210/Nup210
controls muscle differentiation by regulating nuclear envelope/ER homeostasis.
Journal of Cell Biology. Rockefeller University Press. https://doi.org/10.1083/jcb.201410047
chicago: Gomez-Cavazos, J. Sebastian, and Martin Hetzer. “The Nucleoporin Gp210/Nup210
Controls Muscle Differentiation by Regulating Nuclear Envelope/ER Homeostasis.”
Journal of Cell Biology. Rockefeller University Press, 2015. https://doi.org/10.1083/jcb.201410047.
ieee: J. S. Gomez-Cavazos and M. Hetzer, “The nucleoporin gp210/Nup210 controls
muscle differentiation by regulating nuclear envelope/ER homeostasis,” Journal
of Cell Biology, vol. 208, no. 6. Rockefeller University Press, pp. 671–681,
2015.
ista: Gomez-Cavazos JS, Hetzer M. 2015. The nucleoporin gp210/Nup210 controls muscle
differentiation by regulating nuclear envelope/ER homeostasis. Journal of Cell
Biology. 208(6), 671–681.
mla: Gomez-Cavazos, J. Sebastian, and Martin Hetzer. “The Nucleoporin Gp210/Nup210
Controls Muscle Differentiation by Regulating Nuclear Envelope/ER Homeostasis.”
Journal of Cell Biology, vol. 208, no. 6, Rockefeller University Press,
2015, pp. 671–81, doi:10.1083/jcb.201410047.
short: J.S. Gomez-Cavazos, M. Hetzer, Journal of Cell Biology 208 (2015) 671–681.
date_created: 2022-04-07T07:49:10Z
date_published: 2015-03-16T00:00:00Z
date_updated: 2022-07-18T08:43:00Z
day: '16'
doi: 10.1083/jcb.201410047
extern: '1'
external_id:
pmid:
- '25778917'
intvolume: ' 208'
issue: '6'
keyword:
- Cell Biology
language:
- iso: eng
month: '03'
oa_version: Published Version
page: 671-681
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: The nucleoporin gp210/Nup210 controls muscle differentiation by regulating
nuclear envelope/ER homeostasis
type: journal_article
user_id: 72615eeb-f1f3-11ec-aa25-d4573ddc34fd
volume: 208
year: '2015'
...
---
_id: '11078'
abstract:
- lang: eng
text: Aging is associated with the decline of protein, cell, and organ function.
Here, we use an integrated approach to characterize gene expression, bulk translation,
and cell biology in the brains and livers of young and old rats. We identify 468
differences in protein abundance between young and old animals. The majority are
a consequence of altered translation output, that is, the combined effect of changes
in transcript abundance and translation efficiency. In addition, we identify 130
proteins whose overall abundance remains unchanged but whose sub-cellular localization,
phosphorylation state, or splice-form varies. While some protein-level differences
appear to be a generic property of the rats’ chronological age, the majority are
specific to one organ. These may be a consequence of the organ’s physiology or
the chronological age of the cells within the tissue. Taken together, our study
provides an initial view of the proteome at the molecular, sub-cellular, and organ
level in young and old rats.
article_processing_charge: No
article_type: original
author:
- first_name: Alessandro
full_name: Ori, Alessandro
last_name: Ori
- first_name: Brandon H.
full_name: Toyama, Brandon H.
last_name: Toyama
- first_name: Michael S.
full_name: Harris, Michael S.
last_name: Harris
- first_name: Thomas
full_name: Bock, Thomas
last_name: Bock
- first_name: Murat
full_name: Iskar, Murat
last_name: Iskar
- first_name: Peer
full_name: Bork, Peer
last_name: Bork
- first_name: Nicholas T.
full_name: Ingolia, Nicholas T.
last_name: Ingolia
- 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: Martin
full_name: Beck, Martin
last_name: Beck
citation:
ama: Ori A, Toyama BH, Harris MS, et al. Integrated transcriptome and proteome analyses
reveal organ-specific proteome deterioration in old rats. Cell Systems.
2015;1(3):P224-237. doi:10.1016/j.cels.2015.08.012
apa: Ori, A., Toyama, B. H., Harris, M. S., Bock, T., Iskar, M., Bork, P., … Beck,
M. (2015). Integrated transcriptome and proteome analyses reveal organ-specific
proteome deterioration in old rats. Cell Systems. Elsevier. https://doi.org/10.1016/j.cels.2015.08.012
chicago: Ori, Alessandro, Brandon H. Toyama, Michael S. Harris, Thomas Bock, Murat
Iskar, Peer Bork, Nicholas T. Ingolia, Martin Hetzer, and Martin Beck. “Integrated
Transcriptome and Proteome Analyses Reveal Organ-Specific Proteome Deterioration
in Old Rats.” Cell Systems. Elsevier, 2015. https://doi.org/10.1016/j.cels.2015.08.012.
ieee: A. Ori et al., “Integrated transcriptome and proteome analyses reveal
organ-specific proteome deterioration in old rats,” Cell Systems, vol.
1, no. 3. Elsevier, pp. P224-237, 2015.
ista: Ori A, Toyama BH, Harris MS, Bock T, Iskar M, Bork P, Ingolia NT, Hetzer M,
Beck M. 2015. Integrated transcriptome and proteome analyses reveal organ-specific
proteome deterioration in old rats. Cell Systems. 1(3), P224-237.
mla: Ori, Alessandro, et al. “Integrated Transcriptome and Proteome Analyses Reveal
Organ-Specific Proteome Deterioration in Old Rats.” Cell Systems, vol.
1, no. 3, Elsevier, 2015, pp. P224-237, doi:10.1016/j.cels.2015.08.012.
short: A. Ori, B.H. Toyama, M.S. Harris, T. Bock, M. Iskar, P. Bork, N.T. Ingolia,
M. Hetzer, M. Beck, Cell Systems 1 (2015) P224-237.
date_created: 2022-04-07T07:49:39Z
date_published: 2015-09-23T00:00:00Z
date_updated: 2022-07-18T08:44:07Z
day: '23'
doi: 10.1016/j.cels.2015.08.012
extern: '1'
external_id:
pmid:
- '27135913'
intvolume: ' 1'
issue: '3'
keyword:
- Cell Biology
- Histology
- Pathology and Forensic Medicine
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1016/j.cels.2015.08.012
month: '09'
oa: 1
oa_version: Published Version
page: P224-237
pmid: 1
publication: Cell Systems
publication_identifier:
issn:
- 2405-4712
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: Integrated transcriptome and proteome analyses reveal organ-specific proteome
deterioration in old rats
type: journal_article
user_id: 72615eeb-f1f3-11ec-aa25-d4573ddc34fd
volume: 1
year: '2015'
...
---
_id: '11079'
abstract:
- lang: eng
text: Aging is a major risk factor for many human diseases, and in vitro generation
of human neurons is an attractive approach for modeling aging-related brain disorders.
However, modeling aging in differentiated human neurons has proved challenging.
We generated neurons from human donors across a broad range of ages, either by
iPSC-based reprogramming and differentiation or by direct conversion into induced
neurons (iNs). While iPSCs and derived neurons did not retain aging-associated
gene signatures, iNs displayed age-specific transcriptional profiles and revealed
age-associated decreases in the nuclear transport receptor RanBP17. We detected
an age-dependent loss of nucleocytoplasmic compartmentalization (NCC) in donor
fibroblasts and corresponding iNs and found that reduced RanBP17 impaired NCC
in young cells, while iPSC rejuvenation restored NCC in aged cells. These results
show that iNs retain important aging-related signatures, thus allowing modeling
of the aging process in vitro, and they identify impaired NCC as an important
factor in human aging.
article_processing_charge: No
article_type: original
author:
- first_name: Jerome
full_name: Mertens, Jerome
last_name: Mertens
- first_name: Apuã C.M.
full_name: Paquola, Apuã C.M.
last_name: Paquola
- first_name: Manching
full_name: Ku, Manching
last_name: Ku
- first_name: Emily
full_name: Hatch, Emily
last_name: Hatch
- first_name: Lena
full_name: Böhnke, Lena
last_name: Böhnke
- first_name: Shauheen
full_name: Ladjevardi, Shauheen
last_name: Ladjevardi
- first_name: Sean
full_name: McGrath, Sean
last_name: McGrath
- first_name: Benjamin
full_name: Campbell, Benjamin
last_name: Campbell
- first_name: Hyungjun
full_name: Lee, Hyungjun
last_name: Lee
- first_name: Joseph R.
full_name: Herdy, Joseph R.
last_name: Herdy
- first_name: J. Tiago
full_name: Gonçalves, J. Tiago
last_name: Gonçalves
- first_name: Tomohisa
full_name: Toda, Tomohisa
last_name: Toda
- first_name: Yongsung
full_name: Kim, Yongsung
last_name: Kim
- first_name: Jürgen
full_name: Winkler, Jürgen
last_name: Winkler
- first_name: Jun
full_name: Yao, Jun
last_name: Yao
- 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: Fred H.
full_name: Gage, Fred H.
last_name: Gage
citation:
ama: Mertens J, Paquola ACM, Ku M, et al. Directly reprogrammed human neurons retain
aging-associated transcriptomic signatures and reveal age-related nucleocytoplasmic
defects. Cell Stem Cell. 2015;17(6):705-718. doi:10.1016/j.stem.2015.09.001
apa: Mertens, J., Paquola, A. C. M., Ku, M., Hatch, E., Böhnke, L., Ladjevardi,
S., … Gage, F. H. (2015). Directly reprogrammed human neurons retain aging-associated
transcriptomic signatures and reveal age-related nucleocytoplasmic defects. Cell
Stem Cell. Elsevier. https://doi.org/10.1016/j.stem.2015.09.001
chicago: Mertens, Jerome, Apuã C.M. Paquola, Manching Ku, Emily Hatch, Lena Böhnke,
Shauheen Ladjevardi, Sean McGrath, et al. “Directly Reprogrammed Human Neurons
Retain Aging-Associated Transcriptomic Signatures and Reveal Age-Related Nucleocytoplasmic
Defects.” Cell Stem Cell. Elsevier, 2015. https://doi.org/10.1016/j.stem.2015.09.001.
ieee: J. Mertens et al., “Directly reprogrammed human neurons retain aging-associated
transcriptomic signatures and reveal age-related nucleocytoplasmic defects,” Cell
Stem Cell, vol. 17, no. 6. Elsevier, pp. 705–718, 2015.
ista: Mertens J, Paquola ACM, Ku M, Hatch E, Böhnke L, Ladjevardi S, McGrath S,
Campbell B, Lee H, Herdy JR, Gonçalves JT, Toda T, Kim Y, Winkler J, Yao J, Hetzer
M, Gage FH. 2015. Directly reprogrammed human neurons retain aging-associated
transcriptomic signatures and reveal age-related nucleocytoplasmic defects. Cell
Stem Cell. 17(6), 705–718.
mla: Mertens, Jerome, et al. “Directly Reprogrammed Human Neurons Retain Aging-Associated
Transcriptomic Signatures and Reveal Age-Related Nucleocytoplasmic Defects.” Cell
Stem Cell, vol. 17, no. 6, Elsevier, 2015, pp. 705–18, doi:10.1016/j.stem.2015.09.001.
short: J. Mertens, A.C.M. Paquola, M. Ku, E. Hatch, L. Böhnke, S. Ladjevardi, S.
McGrath, B. Campbell, H. Lee, J.R. Herdy, J.T. Gonçalves, T. Toda, Y. Kim, J.
Winkler, J. Yao, M. Hetzer, F.H. Gage, Cell Stem Cell 17 (2015) 705–718.
date_created: 2022-04-07T07:49:51Z
date_published: 2015-12-03T00:00:00Z
date_updated: 2022-07-18T08:44:21Z
day: '03'
doi: 10.1016/j.stem.2015.09.001
extern: '1'
external_id:
pmid:
- '26456686'
intvolume: ' 17'
issue: '6'
keyword:
- Cell Biology
- Genetics
- Molecular Medicine
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1016/j.stem.2015.09.001
month: '12'
oa: 1
oa_version: Published Version
page: 705-718
pmid: 1
publication: Cell Stem Cell
publication_identifier:
issn:
- 1934-5909
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: Directly reprogrammed human neurons retain aging-associated transcriptomic
signatures and reveal age-related nucleocytoplasmic defects
type: journal_article
user_id: 72615eeb-f1f3-11ec-aa25-d4573ddc34fd
volume: 17
year: '2015'
...
---
_id: '12196'
abstract:
- lang: eng
text: SNC1 (SUPPRESSOR OF NPR1, CONSTITUTIVE 1) is one of a suite of intracellular
Arabidopsis NOD-like receptor (NLR) proteins which, upon activation, result in
the induction of defense responses. However, the molecular mechanisms underlying
NLR activation and the subsequent provocation of immune responses are only partially
characterized. To identify negative regulators of NLR-mediated immunity, a forward
genetic screen was undertaken to search for enhancers of the dwarf, autoimmune
gain-of-function snc1 mutant. To avoid lethality resulting from severe dwarfism,
the screen was conducted using mos4 (modifier of snc1, 4) snc1 plants, which display
wild-type-like morphology and resistance. M2 progeny were screened for mutant,
snc1-enhancing (muse) mutants displaying a reversion to snc1-like phenotypes.
The muse9 mos4 snc1 triple mutant was found to exhibit dwarf morphology, elevated
expression of the pPR2-GUS defense marker reporter gene and enhanced resistance
to the oomycete pathogen Hyaloperonospora arabidopsidis Noco2. Via map-based cloning
and Illumina sequencing, it was determined that the muse9 mutation is in the gene
encoding the SWI/SNF chromatin remodeler SYD (SPLAYED), and was thus renamed syd-10.
The syd-10 single mutant has no observable alteration from wild-type-like resistance,
although the syd-4 T-DNA insertion allele displays enhanced resistance to the
bacterial pathogen Pseudomonas syringae pv. maculicola ES4326. Transcription of
SNC1 is increased in both syd-4 and syd-10. These data suggest that SYD plays
a subtle, specific role in the regulation of SNC1 expression and SNC1-mediated
immunity. SYD may work with other proteins at the chromatin level to repress SNC1
transcription; such regulation is important for fine-tuning the expression of
NLR-encoding genes to prevent unpropitious autoimmunity.
acknowledgement: "This work was supported by the National Sciences and Engineering
Research Council of Canada [Canada Graduate\r\nScholarship–Doctoral to K.J.; Discovery
Grant to X.L.]; the department of Botany at the University of f British Columbia\r\n[the
Dewar Cooper Memorial Fund to X.L.].The authors would like to thank Dr. Yuelin Zhang
and Ms. Yan Li for their assistance with next-generation sequencing, and Mr. Charles
Copeland for critical reading of the manuscript."
article_processing_charge: No
article_type: original
author:
- first_name: Kaeli C.M.
full_name: Johnson, Kaeli C.M.
last_name: Johnson
- first_name: Shitou
full_name: Xia, Shitou
last_name: Xia
- first_name: Xiaoqi
full_name: Feng, Xiaoqi
id: e0164712-22ee-11ed-b12a-d80fcdf35958
last_name: Feng
orcid: 0000-0002-4008-1234
- first_name: Xin
full_name: Li, Xin
last_name: Li
citation:
ama: Johnson KCM, Xia S, Feng X, Li X. The chromatin remodeler SPLAYED negatively
regulates SNC1-mediated immunity. Plant and Cell Physiology. 2015;56(8):1616-1623.
doi:10.1093/pcp/pcv087
apa: Johnson, K. C. M., Xia, S., Feng, X., & Li, X. (2015). The chromatin remodeler
SPLAYED negatively regulates SNC1-mediated immunity. Plant and Cell Physiology.
Oxford University Press. https://doi.org/10.1093/pcp/pcv087
chicago: Johnson, Kaeli C.M., Shitou Xia, Xiaoqi Feng, and Xin Li. “The Chromatin
Remodeler SPLAYED Negatively Regulates SNC1-Mediated Immunity.” Plant and Cell
Physiology. Oxford University Press, 2015. https://doi.org/10.1093/pcp/pcv087.
ieee: K. C. M. Johnson, S. Xia, X. Feng, and X. Li, “The chromatin remodeler SPLAYED
negatively regulates SNC1-mediated immunity,” Plant and Cell Physiology,
vol. 56, no. 8. Oxford University Press, pp. 1616–1623, 2015.
ista: Johnson KCM, Xia S, Feng X, Li X. 2015. The chromatin remodeler SPLAYED negatively
regulates SNC1-mediated immunity. Plant and Cell Physiology. 56(8), 1616–1623.
mla: Johnson, Kaeli C. M., et al. “The Chromatin Remodeler SPLAYED Negatively Regulates
SNC1-Mediated Immunity.” Plant and Cell Physiology, vol. 56, no. 8, Oxford
University Press, 2015, pp. 1616–23, doi:10.1093/pcp/pcv087.
short: K.C.M. Johnson, S. Xia, X. Feng, X. Li, Plant and Cell Physiology 56 (2015)
1616–1623.
date_created: 2023-01-16T09:20:22Z
date_published: 2015-08-01T00:00:00Z
date_updated: 2023-05-08T11:03:23Z
department:
- _id: XiFe
doi: 10.1093/pcp/pcv087
extern: '1'
external_id:
pmid:
- '26063389'
intvolume: ' 56'
issue: '8'
keyword:
- Cell Biology
- Plant Science
- Physiology
- General Medicine
language:
- iso: eng
month: '08'
oa_version: None
page: 1616-1623
pmid: 1
publication: Plant and Cell Physiology
publication_identifier:
issn:
- 0032-0781
- 1471-9053
publication_status: published
publisher: Oxford University Press
quality_controlled: '1'
scopus_import: '1'
status: public
title: The chromatin remodeler SPLAYED negatively regulates SNC1-mediated immunity
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 56
year: '2015'
...
---
_id: '11081'
abstract:
- lang: eng
text: In eukaryotic cells the nuclear genome is enclosed by the nuclear envelope
(NE). In metazoans, the NE breaks down in mitosis and it has been assumed that
the physical barrier separating nucleoplasm and cytoplasm remains intact during
the rest of the cell cycle and cell differentiation. However, recent studies suggest
that nonmitotic NE remodeling plays a critical role in development, virus infection,
laminopathies, and cancer. Although the mechanisms underlying these NE restructuring
events are currently being defined, one common theme is activation of protein
kinase C family members in the interphase nucleus to disrupt the nuclear lamina,
demonstrating the importance of the lamina in maintaining nuclear integrity.
article_processing_charge: No
article_type: review
author:
- first_name: Emily
full_name: Hatch, Emily
last_name: Hatch
- 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: Hatch E, Hetzer M. Breaching the nuclear envelope in development and disease.
Journal of Cell Biology. 2014;205(2):133-141. doi:10.1083/jcb.201402003
apa: Hatch, E., & Hetzer, M. (2014). Breaching the nuclear envelope in development
and disease. Journal of Cell Biology. Rockefeller University Press. https://doi.org/10.1083/jcb.201402003
chicago: Hatch, Emily, and Martin Hetzer. “Breaching the Nuclear Envelope in Development
and Disease.” Journal of Cell Biology. Rockefeller University Press, 2014.
https://doi.org/10.1083/jcb.201402003.
ieee: E. Hatch and M. Hetzer, “Breaching the nuclear envelope in development and
disease,” Journal of Cell Biology, vol. 205, no. 2. Rockefeller University
Press, pp. 133–141, 2014.
ista: Hatch E, Hetzer M. 2014. Breaching the nuclear envelope in development and
disease. Journal of Cell Biology. 205(2), 133–141.
mla: Hatch, Emily, and Martin Hetzer. “Breaching the Nuclear Envelope in Development
and Disease.” Journal of Cell Biology, vol. 205, no. 2, Rockefeller University
Press, 2014, pp. 133–41, doi:10.1083/jcb.201402003.
short: E. Hatch, M. Hetzer, Journal of Cell Biology 205 (2014) 133–141.
date_created: 2022-04-07T07:50:13Z
date_published: 2014-04-21T00:00:00Z
date_updated: 2022-07-18T08:45:09Z
day: '21'
doi: 10.1083/jcb.201402003
extern: '1'
external_id:
pmid:
- '24751535'
intvolume: ' 205'
issue: '2'
keyword:
- Cell Biology
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1083/jcb.201402003
month: '04'
oa: 1
oa_version: Published Version
page: 133-141
pmid: 1
publication: Journal of Cell Biology
publication_identifier:
issn:
- 1540-8140
- 0021-9525
publication_status: published
publisher: Rockefeller University Press
quality_controlled: '1'
scopus_import: '1'
status: public
title: Breaching the nuclear envelope in development and disease
type: journal_article
user_id: 72615eeb-f1f3-11ec-aa25-d4573ddc34fd
volume: 205
year: '2014'
...
---
_id: '11082'
abstract:
- lang: eng
text: The nuclear pore complex (NPC) plays a critical role in gene expression by
mediating import of transcription regulators into the nucleus and export of RNA
transcripts to the cytoplasm. Emerging evidence suggests that in addition to mediating
transport, a subset of nucleoporins (Nups) engage in transcriptional activation
and elongation at genomic loci that are not associated with NPCs. The underlying
mechanism and regulation of Nup mobility on and off nuclear pores remain unclear.
Here we show that Nup50 is a mobile Nup with a pronounced presence both at the
NPC and in the nucleoplasm that can move between these different localizations.
Strikingly, the dynamic behavior of Nup50 in both locations is dependent on active
transcription by RNA polymerase II and requires the N-terminal half of the protein,
which contains importin α– and Nup153-binding domains. However, Nup50 dynamics
are independent of importin α, Nup153, and Nup98, even though the latter two proteins
also exhibit transcription-dependent mobility. Of interest, depletion of Nup50
from C2C12 myoblasts does not affect cell proliferation but inhibits differentiation
into myotubes. Taken together, our results suggest a transport-independent role
for Nup50 in chromatin biology that occurs away from the NPC.
article_processing_charge: No
article_type: original
author:
- first_name: Abigail L.
full_name: Buchwalter, Abigail L.
last_name: Buchwalter
- first_name: Yun
full_name: Liang, Yun
last_name: Liang
- 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 AL, Liang Y, Hetzer M. Nup50 is required for cell differentiation
and exhibits transcription-dependent dynamics. Molecular Biology of the Cell.
2014;25(16):2472-2484. doi:10.1091/mbc.e14-04-0865
apa: Buchwalter, A. L., Liang, Y., & Hetzer, M. (2014). Nup50 is required for
cell differentiation and exhibits transcription-dependent dynamics. Molecular
Biology of the Cell. American Society for Cell Biology. https://doi.org/10.1091/mbc.e14-04-0865
chicago: Buchwalter, Abigail L., Yun Liang, and Martin Hetzer. “Nup50 Is Required
for Cell Differentiation and Exhibits Transcription-Dependent Dynamics.” Molecular
Biology of the Cell. American Society for Cell Biology, 2014. https://doi.org/10.1091/mbc.e14-04-0865.
ieee: A. L. Buchwalter, Y. Liang, and M. Hetzer, “Nup50 is required for cell differentiation
and exhibits transcription-dependent dynamics,” Molecular Biology of the Cell,
vol. 25, no. 16. American Society for Cell Biology, pp. 2472–2484, 2014.
ista: Buchwalter AL, Liang Y, Hetzer M. 2014. Nup50 is required for cell differentiation
and exhibits transcription-dependent dynamics. Molecular Biology of the Cell.
25(16), 2472–2484.
mla: Buchwalter, Abigail L., et al. “Nup50 Is Required for Cell Differentiation
and Exhibits Transcription-Dependent Dynamics.” Molecular Biology of the Cell,
vol. 25, no. 16, American Society for Cell Biology, 2014, pp. 2472–84, doi:10.1091/mbc.e14-04-0865.
short: A.L. Buchwalter, Y. Liang, M. Hetzer, Molecular Biology of the Cell 25 (2014)
2472–2484.
date_created: 2022-04-07T07:50:24Z
date_published: 2014-08-15T00:00:00Z
date_updated: 2022-07-18T08:45:20Z
day: '15'
doi: 10.1091/mbc.e14-04-0865
extern: '1'
intvolume: ' 25'
issue: '16'
keyword:
- Cell Biology
- Molecular Biology
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1091/mbc.e14-04-0865
month: '08'
oa: 1
oa_version: Published Version
page: 2472-2484
publication: Molecular Biology of the Cell
publication_identifier:
issn:
- 1059-1524
- 1939-4586
publication_status: published
publisher: American Society for Cell Biology
quality_controlled: '1'
scopus_import: '1'
status: public
title: Nup50 is required for cell differentiation and exhibits transcription-dependent
dynamics
type: journal_article
user_id: 72615eeb-f1f3-11ec-aa25-d4573ddc34fd
volume: 25
year: '2014'
...
---
_id: '11083'
abstract:
- lang: eng
text: Nuclear pore complex (NPC) proteins are known for their critical roles in
regulating nucleocytoplasmic traffic of macromolecules across the nuclear envelope.
However, recent findings suggest that some nucleoporins (Nups), including Nup98,
have additional functions in developmental gene regulation. Nup98, which exhibits
transcription-dependent mobility at the NPC but can also bind chromatin away from
the nuclear envelope, is frequently involved in chromosomal translocations in
a subset of patients suffering from acute myeloid leukemia (AML). A common paradigm
suggests that Nup98 translocations cause aberrant transcription when they are
recuited to aberrant genomic loci. Importantly, this model fails to account for
the potential loss of wild type (WT) Nup98 function in the presence of Nup98 translocation
mutants. Here we examine how the cell might regulate Nup98 nucleoplasmic protein
levels to control transcription in healthy cells. In addition, we discuss the
possibility that dominant negative Nup98 fusion proteins disrupt the transcriptional
activity of WT Nup98 in the nucleoplasm to drive AML.
article_processing_charge: No
article_type: letter_note
author:
- first_name: Tobias M.
full_name: Franks, Tobias M.
last_name: Franks
- 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: Franks TM, Hetzer M. The role of Nup98 in transcription regulation in healthy
and diseased cells. Trends in Cell Biology. 2013;23(3):112-117. doi:10.1016/j.tcb.2012.10.013
apa: Franks, T. M., & Hetzer, M. (2013). The role of Nup98 in transcription
regulation in healthy and diseased cells. Trends in Cell Biology. Elsevier.
https://doi.org/10.1016/j.tcb.2012.10.013
chicago: Franks, Tobias M., and Martin Hetzer. “The Role of Nup98 in Transcription
Regulation in Healthy and Diseased Cells.” Trends in Cell Biology. Elsevier,
2013. https://doi.org/10.1016/j.tcb.2012.10.013.
ieee: T. M. Franks and M. Hetzer, “The role of Nup98 in transcription regulation
in healthy and diseased cells,” Trends in Cell Biology, vol. 23, no. 3.
Elsevier, pp. 112–117, 2013.
ista: Franks TM, Hetzer M. 2013. The role of Nup98 in transcription regulation in
healthy and diseased cells. Trends in Cell Biology. 23(3), 112–117.
mla: Franks, Tobias M., and Martin Hetzer. “The Role of Nup98 in Transcription Regulation
in Healthy and Diseased Cells.” Trends in Cell Biology, vol. 23, no. 3,
Elsevier, 2013, pp. 112–17, doi:10.1016/j.tcb.2012.10.013.
short: T.M. Franks, M. Hetzer, Trends in Cell Biology 23 (2013) 112–117.
date_created: 2022-04-07T07:50:33Z
date_published: 2013-03-01T00:00:00Z
date_updated: 2022-07-18T08:45:34Z
day: '01'
doi: 10.1016/j.tcb.2012.10.013
extern: '1'
external_id:
pmid:
- '23246429'
intvolume: ' 23'
issue: '3'
keyword:
- Cell Biology
language:
- iso: eng
month: '03'
oa_version: None
page: 112-117
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: The role of Nup98 in transcription regulation in healthy and diseased cells
type: journal_article
user_id: 72615eeb-f1f3-11ec-aa25-d4573ddc34fd
volume: 23
year: '2013'
...
---
_id: '11084'
abstract:
- lang: eng
text: Protein turnover is an effective way of maintaining a functional proteome,
as old and potentially damaged polypeptides are destroyed and replaced by newly
synthesized copies. An increasing number of intracellular proteins, however, have
been identified that evade this turnover process and instead are maintained over
a cell's lifetime. This diverse group of long-lived proteins might be particularly
prone to accumulation of damage and thus have a crucial role in the functional
deterioration of key regulatory processes during ageing.
article_processing_charge: No
article_type: original
author:
- first_name: Brandon H.
full_name: Toyama, Brandon H.
last_name: Toyama
- 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, Hetzer M. Protein homeostasis: Live long, won’t prosper. Nature
Reviews Molecular Cell Biology. 2013;14:55-61. doi:10.1038/nrm3496'
apa: 'Toyama, B. H., & Hetzer, M. (2013). Protein homeostasis: Live long, won’t
prosper. Nature Reviews Molecular Cell Biology. Springer Nature. https://doi.org/10.1038/nrm3496'
chicago: 'Toyama, Brandon H., and Martin Hetzer. “Protein Homeostasis: Live Long,
Won’t Prosper.” Nature Reviews Molecular Cell Biology. Springer Nature,
2013. https://doi.org/10.1038/nrm3496.'
ieee: 'B. H. Toyama and M. Hetzer, “Protein homeostasis: Live long, won’t prosper,”
Nature Reviews Molecular Cell Biology, vol. 14. Springer Nature, pp. 55–61,
2013.'
ista: 'Toyama BH, Hetzer M. 2013. Protein homeostasis: Live long, won’t prosper.
Nature Reviews Molecular Cell Biology. 14, 55–61.'
mla: 'Toyama, Brandon H., and Martin Hetzer. “Protein Homeostasis: Live Long, Won’t
Prosper.” Nature Reviews Molecular Cell Biology, vol. 14, Springer Nature,
2013, pp. 55–61, doi:10.1038/nrm3496.'
short: B.H. Toyama, M. Hetzer, Nature Reviews Molecular Cell Biology 14 (2013) 55–61.
date_created: 2022-04-07T07:50:43Z
date_published: 2013-01-01T00:00:00Z
date_updated: 2022-07-18T08:37:53Z
day: '01'
doi: 10.1038/nrm3496
extern: '1'
external_id:
pmid:
- '23258296'
intvolume: ' 14'
keyword:
- Cell Biology
- Molecular Biology
language:
- iso: eng
month: '01'
oa_version: None
page: 55-61
pmid: 1
publication: Nature Reviews Molecular Cell Biology
publication_identifier:
issn:
- 1471-0072
- 1471-0080
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
scopus_import: '1'
status: public
title: 'Protein homeostasis: Live long, won''t prosper'
type: journal_article
user_id: 72615eeb-f1f3-11ec-aa25-d4573ddc34fd
volume: 14
year: '2013'
...
---
_id: '11089'
abstract:
- lang: eng
text: The Nuclear Envelope (NE) contains over 100 different proteins that associate
with nuclear components such as chromatin, the lamina and the transcription machinery.
Mutations in genes encoding NE proteins have been shown to result in tissue-specific
defects and disease, suggesting cell-type specific differences in NE composition
and function. Consistent with these observations, recent studies have revealed
unexpected functions for numerous NE associated proteins during cell differentiation
and development. Here we review the latest insights into the roles played by the
NE in cell differentiation, development, disease and aging, focusing primarily
on inner nuclear membrane (INM) proteins and nuclear pore components.
article_processing_charge: No
article_type: original
author:
- first_name: J Sebastian
full_name: Gomez-Cavazos, J Sebastian
last_name: Gomez-Cavazos
- 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: 'Gomez-Cavazos JS, Hetzer M. Outfits for different occasions: tissue-specific
roles of Nuclear Envelope proteins. Current Opinion in Cell Biology. 2012;24(6):775-783.
doi:10.1016/j.ceb.2012.08.008'
apa: 'Gomez-Cavazos, J. S., & Hetzer, M. (2012). Outfits for different occasions:
tissue-specific roles of Nuclear Envelope proteins. Current Opinion in Cell
Biology. Elsevier. https://doi.org/10.1016/j.ceb.2012.08.008'
chicago: 'Gomez-Cavazos, J Sebastian, and Martin Hetzer. “Outfits for Different
Occasions: Tissue-Specific Roles of Nuclear Envelope Proteins.” Current Opinion
in Cell Biology. Elsevier, 2012. https://doi.org/10.1016/j.ceb.2012.08.008.'
ieee: 'J. S. Gomez-Cavazos and M. Hetzer, “Outfits for different occasions: tissue-specific
roles of Nuclear Envelope proteins,” Current Opinion in Cell Biology, vol.
24, no. 6. Elsevier, pp. 775–783, 2012.'
ista: 'Gomez-Cavazos JS, Hetzer M. 2012. Outfits for different occasions: tissue-specific
roles of Nuclear Envelope proteins. Current Opinion in Cell Biology. 24(6), 775–783.'
mla: 'Gomez-Cavazos, J. Sebastian, and Martin Hetzer. “Outfits for Different Occasions:
Tissue-Specific Roles of Nuclear Envelope Proteins.” Current Opinion in Cell
Biology, vol. 24, no. 6, Elsevier, 2012, pp. 775–83, doi:10.1016/j.ceb.2012.08.008.'
short: J.S. Gomez-Cavazos, M. Hetzer, Current Opinion in Cell Biology 24 (2012)
775–783.
date_created: 2022-04-07T07:51:37Z
date_published: 2012-12-01T00:00:00Z
date_updated: 2022-07-18T08:38:47Z
day: '01'
doi: 10.1016/j.ceb.2012.08.008
extern: '1'
external_id:
pmid:
- '22995343'
intvolume: ' 24'
issue: '6'
keyword:
- Cell Biology
language:
- iso: eng
month: '12'
oa_version: None
page: 775-783
pmid: 1
publication: Current Opinion in Cell Biology
publication_identifier:
issn:
- 0955-0674
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: 'Outfits for different occasions: tissue-specific roles of Nuclear Envelope
proteins'
type: journal_article
user_id: 72615eeb-f1f3-11ec-aa25-d4573ddc34fd
volume: 24
year: '2012'
...
---
_id: '11091'
abstract:
- lang: eng
text: Neoplastic cells are often characterized by specific morphological abnormalities
of the nuclear envelope (NE), which have been used for cancer diagnosis for more
than a century. The NE is a double phospholipid bilayer that encapsulates the
nuclear genome, regulates all nuclear trafficking of RNAs and proteins and prevents
the passive diffusion of macromolecules between the nucleoplasm and the cytoplasm.
Whether there is a consequence to the proper functioning of the cell and loss
of structural integrity of the nucleus remains unclear. Using live cell imaging,
we characterize a phenomenon wherein nuclei of several proliferating human cancer
cell lines become temporarily ruptured during interphase. Strikingly, NE rupturing
was associated with the mislocalization of nucleoplasmic and cytoplasmic proteins
and, in the most extreme cases, the entrapment of cytoplasmic organelles in the
nuclear interior. In addition, we observed the formation of micronuclei-like structures
during interphase and the movement of chromatin out of the nuclear space. The
frequency of these NE rupturing events was higher in cells in which the nuclear
lamina, a network of intermediate filaments providing mechanical support to the
NE, was not properly formed. Our data uncover the existence of a NE instability
that has the potential to change the genomic landscape of cancer cells.
article_processing_charge: No
article_type: original
author:
- first_name: Jesse D.
full_name: Vargas, Jesse D.
last_name: Vargas
- first_name: Emily M.
full_name: Hatch, Emily M.
last_name: Hatch
- first_name: Daniel J.
full_name: Anderson, Daniel J.
last_name: Anderson
- 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: Vargas JD, Hatch EM, Anderson DJ, Hetzer M. Transient nuclear envelope rupturing
during interphase in human cancer cells. Nucleus. 2012;3(1):88-100. doi:10.4161/nucl.18954
apa: Vargas, J. D., Hatch, E. M., Anderson, D. J., & Hetzer, M. (2012). Transient
nuclear envelope rupturing during interphase in human cancer cells. Nucleus.
Taylor & Francis. https://doi.org/10.4161/nucl.18954
chicago: Vargas, Jesse D., Emily M. Hatch, Daniel J. Anderson, and Martin Hetzer.
“Transient Nuclear Envelope Rupturing during Interphase in Human Cancer Cells.”
Nucleus. Taylor & Francis, 2012. https://doi.org/10.4161/nucl.18954.
ieee: J. D. Vargas, E. M. Hatch, D. J. Anderson, and M. Hetzer, “Transient nuclear
envelope rupturing during interphase in human cancer cells,” Nucleus, vol.
3, no. 1. Taylor & Francis, pp. 88–100, 2012.
ista: Vargas JD, Hatch EM, Anderson DJ, Hetzer M. 2012. Transient nuclear envelope
rupturing during interphase in human cancer cells. Nucleus. 3(1), 88–100.
mla: Vargas, Jesse D., et al. “Transient Nuclear Envelope Rupturing during Interphase
in Human Cancer Cells.” Nucleus, vol. 3, no. 1, Taylor & Francis, 2012,
pp. 88–100, doi:10.4161/nucl.18954.
short: J.D. Vargas, E.M. Hatch, D.J. Anderson, M. Hetzer, Nucleus 3 (2012) 88–100.
date_created: 2022-04-07T07:51:53Z
date_published: 2012-01-01T00:00:00Z
date_updated: 2022-07-18T08:52:53Z
day: '01'
doi: 10.4161/nucl.18954
extern: '1'
external_id:
pmid:
- '22567193'
intvolume: ' 3'
issue: '1'
keyword:
- Cell Biology
language:
- iso: eng
month: '01'
oa_version: None
page: 88-100
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: Transient nuclear envelope rupturing during interphase in human cancer cells
type: journal_article
user_id: 72615eeb-f1f3-11ec-aa25-d4573ddc34fd
volume: 3
year: '2012'
...
---
_id: '11093'
abstract:
- lang: eng
text: Nuclear pore complexes (NPCs) are built from ∼30 different proteins called
nucleoporins or Nups. Previous studies have shown that several Nups exhibit cell-type-specific
expression and that mutations in NPC components result in tissue-specific diseases.
Here we show that a specific change in NPC composition is required for both myogenic
and neuronal differentiation. The transmembrane nucleoporin Nup210 is absent in
proliferating myoblasts and embryonic stem cells (ESCs) but becomes expressed
and incorporated into NPCs during cell differentiation. Preventing Nup210 production
by RNAi blocks myogenesis and the differentiation of ESCs into neuroprogenitors.
We found that the addition of Nup210 to NPCs does not affect nuclear transport
but is required for the induction of genes that are essential for cell differentiation.
Our results identify a single change in NPC composition as an essential step in
cell differentiation and establish a role for Nup210 in gene expression regulation
and cell fate determination.
article_processing_charge: No
article_type: original
author:
- first_name: Maximiliano A.
full_name: D'Angelo, Maximiliano A.
last_name: D'Angelo
- first_name: J. Sebastian
full_name: Gomez-Cavazos, J. Sebastian
last_name: Gomez-Cavazos
- first_name: Arianna
full_name: Mei, Arianna
last_name: Mei
- first_name: Daniel H.
full_name: Lackner, Daniel H.
last_name: Lackner
- 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: D’Angelo MA, Gomez-Cavazos JS, Mei A, Lackner DH, Hetzer M. A change in nuclear
pore complex composition regulates cell differentiation. Developmental Cell.
2012;22(2):446-458. doi:10.1016/j.devcel.2011.11.021
apa: D’Angelo, M. A., Gomez-Cavazos, J. S., Mei, A., Lackner, D. H., & Hetzer,
M. (2012). A change in nuclear pore complex composition regulates cell differentiation.
Developmental Cell. Elsevier. https://doi.org/10.1016/j.devcel.2011.11.021
chicago: D’Angelo, Maximiliano A., J. Sebastian Gomez-Cavazos, Arianna Mei, Daniel H.
Lackner, and Martin Hetzer. “A Change in Nuclear Pore Complex Composition Regulates
Cell Differentiation.” Developmental Cell. Elsevier, 2012. https://doi.org/10.1016/j.devcel.2011.11.021.
ieee: M. A. D’Angelo, J. S. Gomez-Cavazos, A. Mei, D. H. Lackner, and M. Hetzer,
“A change in nuclear pore complex composition regulates cell differentiation,”
Developmental Cell, vol. 22, no. 2. Elsevier, pp. 446–458, 2012.
ista: D’Angelo MA, Gomez-Cavazos JS, Mei A, Lackner DH, Hetzer M. 2012. A change
in nuclear pore complex composition regulates cell differentiation. Developmental
Cell. 22(2), 446–458.
mla: D’Angelo, Maximiliano A., et al. “A Change in Nuclear Pore Complex Composition
Regulates Cell Differentiation.” Developmental Cell, vol. 22, no. 2, Elsevier,
2012, pp. 446–58, doi:10.1016/j.devcel.2011.11.021.
short: M.A. D’Angelo, J.S. Gomez-Cavazos, A. Mei, D.H. Lackner, M. Hetzer, Developmental
Cell 22 (2012) 446–458.
date_created: 2022-04-07T07:52:10Z
date_published: 2012-01-19T00:00:00Z
date_updated: 2022-07-18T08:53:16Z
day: '19'
doi: 10.1016/j.devcel.2011.11.021
extern: '1'
external_id:
pmid:
- '22264802'
intvolume: ' 22'
issue: '2'
keyword:
- Developmental Biology
- Cell Biology
- General Biochemistry
- Genetics and Molecular Biology
- Molecular Biology
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1016/j.devcel.2011.11.021
month: '01'
oa: 1
oa_version: Published Version
page: 446-458
pmid: 1
publication: Developmental Cell
publication_identifier:
issn:
- 1534-5807
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: A change in nuclear pore complex composition regulates cell differentiation
type: journal_article
user_id: 72615eeb-f1f3-11ec-aa25-d4573ddc34fd
volume: 22
year: '2012'
...
---
_id: '11094'
abstract:
- lang: eng
text: Nuclear pore complexes (NPCs) assemble at the end of mitosis during nuclear
envelope (NE) reformation and into an intact NE as cells progress through interphase.
Although recent studies have shown that NPC formation occurs by two different
molecular mechanisms at two distinct cell cycle stages, little is known about
the molecular players that mediate the fusion of the outer and inner nuclear membranes
to form pores. In this paper, we provide evidence that the transmembrane nucleoporin
(Nup), POM121, but not the Nup107–160 complex, is present at new pore assembly
sites at a time that coincides with inner nuclear membrane (INM) and outer nuclear
membrane (ONM) fusion. Overexpression of POM121 resulted in juxtaposition of the
INM and ONM. Additionally, Sun1, an INM protein that is known to interact with
the cytoskeleton, was specifically required for interphase assembly and localized
with POM121 at forming pores. We propose a model in which POM121 and Sun1 interact
transiently to promote early steps of interphase NPC assembly.
article_processing_charge: No
article_type: original
author:
- first_name: Jessica A.
full_name: Talamas, Jessica A.
last_name: Talamas
- 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: Talamas JA, Hetzer M. POM121 and Sun1 play a role in early steps of interphase
NPC assembly. Journal of Cell Biology. 2011;194(1):27-37. doi:10.1083/jcb.201012154
apa: Talamas, J. A., & Hetzer, M. (2011). POM121 and Sun1 play a role in early
steps of interphase NPC assembly. Journal of Cell Biology. Rockefeller
University Press. https://doi.org/10.1083/jcb.201012154
chicago: Talamas, Jessica A., and Martin Hetzer. “POM121 and Sun1 Play a Role in
Early Steps of Interphase NPC Assembly.” Journal of Cell Biology. Rockefeller
University Press, 2011. https://doi.org/10.1083/jcb.201012154.
ieee: J. A. Talamas and M. Hetzer, “POM121 and Sun1 play a role in early steps of
interphase NPC assembly,” Journal of Cell Biology, vol. 194, no. 1. Rockefeller
University Press, pp. 27–37, 2011.
ista: Talamas JA, Hetzer M. 2011. POM121 and Sun1 play a role in early steps of
interphase NPC assembly. Journal of Cell Biology. 194(1), 27–37.
mla: Talamas, Jessica A., and Martin Hetzer. “POM121 and Sun1 Play a Role in Early
Steps of Interphase NPC Assembly.” Journal of Cell Biology, vol. 194, no.
1, Rockefeller University Press, 2011, pp. 27–37, doi:10.1083/jcb.201012154.
short: J.A. Talamas, M. Hetzer, Journal of Cell Biology 194 (2011) 27–37.
date_created: 2022-04-07T07:52:18Z
date_published: 2011-07-04T00:00:00Z
date_updated: 2022-07-18T08:53:46Z
day: '04'
doi: 10.1083/jcb.201012154
extern: '1'
external_id:
pmid:
- '21727197'
intvolume: ' 194'
issue: '1'
keyword:
- Cell Biology
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1083/jcb.201012154
month: '07'
oa: 1
oa_version: Published Version
page: 27-37
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: POM121 and Sun1 play a role in early steps of interphase NPC assembly
type: journal_article
user_id: 72615eeb-f1f3-11ec-aa25-d4573ddc34fd
volume: 194
year: '2011'
...
---
_id: '11095'
article_processing_charge: No
article_type: letter_note
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: Giacomo
full_name: Cavalli, Giacomo
last_name: Cavalli
citation:
ama: Hetzer M, Cavalli G. Editorial overview. Current Opinion in Cell Biology.
2011;23(3):255-257. doi:10.1016/j.ceb.2011.04.013
apa: Hetzer, M., & Cavalli, G. (2011). Editorial overview. Current Opinion
in Cell Biology. Elsevier. https://doi.org/10.1016/j.ceb.2011.04.013
chicago: Hetzer, Martin, and Giacomo Cavalli. “Editorial Overview.” Current Opinion
in Cell Biology. Elsevier, 2011. https://doi.org/10.1016/j.ceb.2011.04.013.
ieee: M. Hetzer and G. Cavalli, “Editorial overview,” Current Opinion in Cell
Biology, vol. 23, no. 3. Elsevier, pp. 255–257, 2011.
ista: Hetzer M, Cavalli G. 2011. Editorial overview. Current Opinion in Cell Biology.
23(3), 255–257.
mla: Hetzer, Martin, and Giacomo Cavalli. “Editorial Overview.” Current Opinion
in Cell Biology, vol. 23, no. 3, Elsevier, 2011, pp. 255–57, doi:10.1016/j.ceb.2011.04.013.
short: M. Hetzer, G. Cavalli, Current Opinion in Cell Biology 23 (2011) 255–257.
date_created: 2022-04-07T07:52:27Z
date_published: 2011-06-01T00:00:00Z
date_updated: 2022-07-18T08:39:40Z
day: '01'
doi: 10.1016/j.ceb.2011.04.013
extern: '1'
external_id:
pmid:
- '21592757'
intvolume: ' 23'
issue: '3'
keyword:
- Cell Biology
language:
- iso: eng
month: '06'
oa_version: None
page: 255-257
pmid: 1
publication: Current Opinion in Cell Biology
publication_identifier:
issn:
- 0955-0674
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: Editorial overview
type: journal_article
user_id: 72615eeb-f1f3-11ec-aa25-d4573ddc34fd
volume: 23
year: '2011'
...
---
_id: '11096'
abstract:
- lang: eng
text: As the gatekeepers of the eukaryotic cell nucleus, nuclear pore complexes
(NPCs) mediate all molecular trafficking between the nucleoplasm and the cytoplasm.
In recent years, transport-independent functions of NPC components, nucleoporins,
have been identified including roles in chromatin organization and gene regulation.
Here, we summarize our current view of the NPC as a dynamic hub for the integration
of chromatin regulation and nuclear trafficking and discuss the functional interplay
between nucleoporins and the nuclear genome.
article_processing_charge: No
article_type: original
author:
- first_name: Yun
full_name: Liang, Yun
last_name: Liang
- 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: Liang Y, Hetzer M. Functional interactions between nucleoporins and chromatin.
Current Opinion in Cell Biology. 2011;23(1):65-70. doi:10.1016/j.ceb.2010.09.008
apa: Liang, Y., & Hetzer, M. (2011). Functional interactions between nucleoporins
and chromatin. Current Opinion in Cell Biology. Elsevier. https://doi.org/10.1016/j.ceb.2010.09.008
chicago: Liang, Yun, and Martin Hetzer. “Functional Interactions between Nucleoporins
and Chromatin.” Current Opinion in Cell Biology. Elsevier, 2011. https://doi.org/10.1016/j.ceb.2010.09.008.
ieee: Y. Liang and M. Hetzer, “Functional interactions between nucleoporins and
chromatin,” Current Opinion in Cell Biology, vol. 23, no. 1. Elsevier,
pp. 65–70, 2011.
ista: Liang Y, Hetzer M. 2011. Functional interactions between nucleoporins and
chromatin. Current Opinion in Cell Biology. 23(1), 65–70.
mla: Liang, Yun, and Martin Hetzer. “Functional Interactions between Nucleoporins
and Chromatin.” Current Opinion in Cell Biology, vol. 23, no. 1, Elsevier,
2011, pp. 65–70, doi:10.1016/j.ceb.2010.09.008.
short: Y. Liang, M. Hetzer, Current Opinion in Cell Biology 23 (2011) 65–70.
date_created: 2022-04-07T07:52:37Z
date_published: 2011-02-01T00:00:00Z
date_updated: 2022-07-18T08:53:48Z
day: '01'
doi: 10.1016/j.ceb.2010.09.008
extern: '1'
external_id:
pmid:
- '21030234'
intvolume: ' 23'
issue: '1'
keyword:
- Cell Biology
language:
- iso: eng
month: '02'
oa_version: None
page: 65-70
pmid: 1
publication: Current Opinion in Cell Biology
publication_identifier:
issn:
- 0955-0674
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: Functional interactions between nucleoporins and chromatin
type: journal_article
user_id: 72615eeb-f1f3-11ec-aa25-d4573ddc34fd
volume: 23
year: '2011'
...
---
_id: '11098'
article_processing_charge: No
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
citation:
ama: Hetzer M. The role of the nuclear pore complex in aging of post-mitotic cells.
Aging. 2010;2(2):74-75. doi:10.18632/aging.100125
apa: Hetzer, M. (2010). The role of the nuclear pore complex in aging of post-mitotic
cells. Aging. Impact Journals. https://doi.org/10.18632/aging.100125
chicago: Hetzer, Martin. “The Role of the Nuclear Pore Complex in Aging of Post-Mitotic
Cells.” Aging. Impact Journals, 2010. https://doi.org/10.18632/aging.100125.
ieee: M. Hetzer, “The role of the nuclear pore complex in aging of post-mitotic
cells,” Aging, vol. 2, no. 2. Impact Journals, pp. 74–75, 2010.
ista: Hetzer M. 2010. The role of the nuclear pore complex in aging of post-mitotic
cells. Aging. 2(2), 74–75.
mla: Hetzer, Martin. “The Role of the Nuclear Pore Complex in Aging of Post-Mitotic
Cells.” Aging, vol. 2, no. 2, Impact Journals, 2010, pp. 74–75, doi:10.18632/aging.100125.
short: M. Hetzer, Aging 2 (2010) 74–75.
date_created: 2022-04-07T07:52:58Z
date_published: 2010-02-01T00:00:00Z
date_updated: 2022-07-18T08:54:15Z
day: '01'
doi: 10.18632/aging.100125
extern: '1'
external_id:
pmid:
- '20354266'
intvolume: ' 2'
issue: '2'
keyword:
- Cell Biology
- Aging
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.18632/aging.100125
month: '02'
oa: 1
oa_version: Published Version
page: 74-75
pmid: 1
publication: Aging
publication_identifier:
issn:
- 1945-4589
publication_status: published
publisher: Impact Journals
quality_controlled: '1'
scopus_import: '1'
status: public
title: The role of the nuclear pore complex in aging of post-mitotic cells
type: journal_article
user_id: 72615eeb-f1f3-11ec-aa25-d4573ddc34fd
volume: 2
year: '2010'
...