Jachimowicz, Ron D. and Reinhardt, H. Christian (2019). UBQLN4 promotes non-homologous end joining by repressing DNA end-resection. MOL. CELL ONCOL., 6 (2). PHILADELPHIA: TAYLOR & FRANCIS INC. ISSN 2372-3548

Full text not available from this repository.

Abstract

Ataxia-telangiectasia-mutated (ATM) promotes homologous recombination (HR)-mediated DNA double strand break repair. It was recently shown that the proteasomal shuttle factor UBQLN4 facilitates MRE11 degradation to repress HR. Surprisingly, the UBQLN4-MRE11 interaction is ATM-dependent, suggesting that the proximal DNA damage kinase ATM does not only initiate HR, but also limits excessive end resection.

Item Type: Journal Article
Creators:
CreatorsEmailORCIDORCID Put Code
Jachimowicz, Ron D.UNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Reinhardt, H. ChristianUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
URN: urn:nbn:de:hbz:38-138858
DOI: 10.1080/23723556.2019.1575692
Journal or Publication Title: MOL. CELL ONCOL.
Volume: 6
Number: 2
Date: 2019
Publisher: TAYLOR & FRANCIS INC
Place of Publication: PHILADELPHIA
ISSN: 2372-3548
Language: English
Faculty: Unspecified
Divisions: Unspecified
Subjects: no entry
Uncontrolled Keywords:
KeywordsLanguage
ATMMultiple languages
OncologyMultiple languages
Refereed: Yes
URI: http://kups.ub.uni-koeln.de/id/eprint/13885

Downloads

Downloads per month over past year

Altmetric

Export

Actions (login required)

View Item View Item