PuSH - Publication Server of Helmholtz Zentrum München: Depletion of histone demethylase Jarid1A resulting in histone hyperacetylation and radiation sensitivity does not affect DNA double-strand break repair.

Navigation

Home

Deutsch

Research

Advanced Search

Browse by ...

... Journal

... Publication Type

... Research Data

... Publication Year

Publication overview

Support & Contact

Contact persons

Help

Data protection

Penterling, C.* ; Drexler, G.A.* ; Böhland, C.* ; Stamp, R.* ; Wilke, C. ; Braselmann, H. ; Caldwell, R.B. ; Reindl, J.* ; Girst, S.* ; Greubel, C.* ; Siebenwirth, C.* ; Mansour, W.Y.* ; Borgmann, K.* ; Dollinger, G.* ; Unger, K. ; Friedl, A.A.

Depletion of histone demethylase Jarid1A resulting in histone hyperacetylation and radiation sensitivity does not affect DNA double-strand break repair.

PLoS ONE 11:e0156599 (2016)

Publ. Version/Full Text

Research data

DOI

PMC

	Open Access Gold

Abstract
Metrics
Extra information

Histone demethylases have recently gained interest as potential targets in cancer treatment and several histone demethylases have been implicated in the DNA damage response. We investigated the effects of siRNA-mediated depletion of histone demethylase Jarid1A (KDM5A, RBP2), which demethylates transcription activating tri- and dimethylated lysine 4 at histone H3 (H3K4me3/me2), on growth characteristics and cellular response to radiation in several cancer cell lines. In unirradiated cells Jarid1A depletion lead to histone hyperacetylation while not affecting cell growth. In irradiated cells, depletion of Jarid1A significantly increased cellular radiosensitivity. Unexpectedly, the hyperacetylation phenotype did not lead to disturbed accumulation of DNA damage response and repair factors 53BP1, BRCA1, or Rad51 at damage sites, nor did it influence resolution of radiation-induced foci or rejoining of reporter constructs. We conclude that the radiation sensitivity observed following depletion of Jarid1A is not caused by a deficiency in repair of DNA double-strand breaks.

Altmetric

Additional Metrics?

[➜Log in]

Edit extra informations Login

Publication type Article: Journal article

Document type Scientific Article

Corresponding Author

Keywords Damage Response Protein; Deacetylase Inhibitors; Chromatin Compaction; Valproic Acid; Cancer-cells; Oncometabolite 2-hydroxyglutarate; Transcriptional Repression; Lysine Demethylases; H3k4 Demethylase; Gastric-cancer

ISSN (print) / ISBN 1932-6203

Journal PLoS ONE

Quellenangaben Volume: 11, Issue: 6, Article Number: e0156599

Publisher Public Library of Science (PLoS)

Publishing Place Lawrence, Kan.

Non-patent literature Publications

Reviewing status Peer reviewed

Institute(s) CCG Personalized Radiotherapy in Head and Neck Cancer (KKG-KRT)
Translational Metabolic Oncology (TMO)