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Article

A UVR-induced G2-phase checkpoint response to ssDNA gaps produced by replication fork bypass of unrepaired lesions is defective in melanoma.

The Journal of investigative dermatology - 1 Jun 2012

Wigan Matthew, Pinder Alex, Giles Nichole, Pavey Sandra, Burgess Andrew, Wong Shushyan, Sturm Rick A, Gabrielli Brian

Abstract excerpt

UVR is a major environmental risk factor for the development of melanoma. Here we describe a coupled DNA-damage tolerance (DDT) mechanism and G2-phase cell cycle checkpoint induced in response to suberythemal doses of UVR that is commonly defective in melanomas. This coupled response is triggered by a small number of UVR-induced DNA lesions incurred during G1 phase that are not repaired by nucleotide excision...

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Source

Identifiers

PMID: 22402442
DOI: 10.1038/jid.2012.41

Genes

RAD18
DDT
RAD51
ATR
BRCA1

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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