Chromatin Remodeling in Response to BRCA2-Crisis

Joshua J. Gruber; Justin Chen; Benjamin Geller; Natalie Jäger; Andrew M. Lipchik; Guangwen Wang; Allison W. Kurian; James M. Ford; Michael P. Snyder

doi:10.1016/j.celrep.2019.07.057

Chromatin Remodeling in Response to BRCA2-Crisis

Joshua J. Gruber, Justin Chen, Benjamin Geller, Natalie Jäger, Andrew M. Lipchik, Guangwen Wang, Allison W. Kurian, James M. Ford, Michael P. Snyder

Research output: Contribution to journal › Article › peer-review

6 Scopus citations

Abstract

Gruber et al. identify EGF-independent proliferation in mammary cells following transient BRCA2 depletion (“BRCA2-crisis”). In the absence of recurrent genomic mutations, chromatin remodeling mediated by NF-κB signaling drives gene expression changes. This in vitro model shares molecular commonalities observed in BRCA2^+/− carriers.

Original language	English (US)
Pages (from-to)	2182-2193.e6
Journal	Cell Reports
Volume	28
Issue number	8
DOIs	https://doi.org/10.1016/j.celrep.2019.07.057
State	Published - Aug 20 2019
Externally published	Yes

Keywords

BRCA2
H4K12Ac
NF-κB
breast cancer
carcinogenesis
epigenetics
haploinsufficiency
histone acetylation

ASJC Scopus subject areas

General Biochemistry, Genetics and Molecular Biology

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10.1016/j.celrep.2019.07.057

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title = "Chromatin Remodeling in Response to BRCA2-Crisis",

abstract = "Gruber et al. identify EGF-independent proliferation in mammary cells following transient BRCA2 depletion (“BRCA2-crisis”). In the absence of recurrent genomic mutations, chromatin remodeling mediated by NF-κB signaling drives gene expression changes. This in vitro model shares molecular commonalities observed in BRCA2+/− carriers.",

keywords = "BRCA2, H4K12Ac, NF-κB, breast cancer, carcinogenesis, epigenetics, haploinsufficiency, histone acetylation",

author = "Gruber, {Joshua J.} and Justin Chen and Benjamin Geller and Natalie J{\"a}ger and Lipchik, {Andrew M.} and Guangwen Wang and Kurian, {Allison W.} and Ford, {James M.} and Snyder, {Michael P.}",

note = "Publisher Copyright: {\textcopyright} 2019 The Author(s)",

year = "2019",

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doi = "10.1016/j.celrep.2019.07.057",

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T1 - Chromatin Remodeling in Response to BRCA2-Crisis

AU - Gruber, Joshua J.

AU - Chen, Justin

AU - Geller, Benjamin

AU - Jäger, Natalie

AU - Lipchik, Andrew M.

AU - Wang, Guangwen

AU - Kurian, Allison W.

AU - Ford, James M.

AU - Snyder, Michael P.

PY - 2019/8/20

Y1 - 2019/8/20

N2 - Gruber et al. identify EGF-independent proliferation in mammary cells following transient BRCA2 depletion (“BRCA2-crisis”). In the absence of recurrent genomic mutations, chromatin remodeling mediated by NF-κB signaling drives gene expression changes. This in vitro model shares molecular commonalities observed in BRCA2+/− carriers.

AB - Gruber et al. identify EGF-independent proliferation in mammary cells following transient BRCA2 depletion (“BRCA2-crisis”). In the absence of recurrent genomic mutations, chromatin remodeling mediated by NF-κB signaling drives gene expression changes. This in vitro model shares molecular commonalities observed in BRCA2+/− carriers.

KW - BRCA2

KW - H4K12Ac

KW - NF-κB

KW - breast cancer

KW - carcinogenesis

KW - epigenetics

KW - haploinsufficiency

KW - histone acetylation

UR - http://www.scopus.com/inward/record.url?scp=85070202032&partnerID=8YFLogxK

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DO - 10.1016/j.celrep.2019.07.057

M3 - Article

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AN - SCOPUS:85070202032

SN - 2211-1247

VL - 28

SP - 2182-2193.e6

JO - Cell Reports

JF - Cell Reports

IS - 8

ER -

Chromatin Remodeling in Response to BRCA2-Crisis

Abstract

Keywords

ASJC Scopus subject areas

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