Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

A PALB2-interacting domain in RNF168 couples homologous recombination to DNA break-induced chromatin ubiquitylation

27 Feb 2017

Abstract excerpt

DNA double-strand breaks (DSB) elicit a ubiquitylation cascade that controls DNA repair pathway choice. This cascade involves the ubiquitylation of histone H2A by the RNF168 ligase and the subsequent recruitment of RIF1, which suppresses homologous recombination (HR) in G1 cells. The RIF1-dependent suppression is relieved in S/G2 cells, allowing PALB2-driven HR to occur. With the inhibitory impact of RIF1...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to DNA Repair Mechanisms
Share to PARP inhibition in cancer therapy
Share to Polyomavirus and related diseases

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 28240985
DOI: 10.7554/elife.20922

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 8 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

A PALB2-interacting domain in RNF168 couples homologous recombination to DNA break-induced chromatin ubiquitylationPMID 28240985Read ↗

RNF168 ubiquitylates 53BP1 and controls its response to DNA double-strand breaksSemantic proximity Read ↗

Human RNF169 is a negative regulator of the ubiquitin-dependent response to DNA double-strand breaksSemantic proximity Read ↗

Remodeling and spacing factor 1 (RSF1) deposits centromere proteins at DNA double-strand breaks to promote non-homologous end-joiningSemantic proximity Read ↗

Tumors overexpressing RNF168 show altered DNA repair and responses to genotoxic treatments, genomic instability and resistance to proteotoxic stress.Semantic proximity Read ↗

Fine-tuning of DNA damage-dependent ubiquitination by OTUB2 supports the DNA repair pathway choice.Semantic proximity Read ↗

RNF168 regulates R-loop resolution and genomic stability in BRCA1/2-deficient tumorsSemantic proximity Read ↗

RNF168 and USP10 regulate topoisomerase IIα function via opposing effects on its ubiquitylationSemantic proximity Read ↗

BRCA1-Dependent and Independent Recruitment of PALB2–BRCA2–RAD51 in the DNA Damage Response and CancerSemantic proximity Read ↗

RNF8 ubiquitylation of XRN2 facilitates R-loop resolution and restrains genomic instability in BRCA1 mutant cellsSemantic proximity Read ↗

NBS1 recruits RAD18 via a RAD6-like domain and regulates Pol η-dependent translesion DNA synthesis.Semantic proximity Read ↗

E3 ligases: a ubiquitous link between DNA repair, DNA replication and human diseaseSemantic proximity Read ↗

Genomic Instability, Defective Spermatogenesis, Immunodeficiency, and Cancer in a Mouse Model of the RIDDLE SyndromeSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.