PMID:23144634

Citation	Duquette, ML, Zhu, Q, Taylor, ER, Tsay, AJ, Shi, LZ, Berns, MW and McGowan, CH (2012) CtIP Is Required to Initiate Replication-Dependent Interstrand Crosslink Repair. PLoS Genet. 8:e1003050
Abstract	DNA interstrand crosslinks (ICLs) are toxic lesions that block the progression of replication and transcription. CtIP is a conserved DNA repair protein that facilitates DNA end resection in the double-strand break (DSB) repair pathway. Here we show that CtIP plays a critical role during initiation of ICL processing in replicating human cells that is distinct from its role in DSB repair. CtIP depletion sensitizes human cells to ICL inducing agents and significantly impairs the accumulation of DNA damage response proteins RPA, ATR, FANCD2, γH2AX, and phosphorylated ATM at sites of laser generated ICLs. In contrast, the appearance of γH2AX and phosphorylated ATM at sites of laser generated double strand breaks (DSBs) is CtIP-independent. We present a model in which CtIP functions early in ICL repair in a BRCA1- and FANCM-dependent manner prior to generation of DSB repair intermediates.
Links	PubMed Online version:10.1371/journal.pgen.1003050
Keywords
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Annotations

Gene product	Qualifier	GO Term	Evidence Code	with/from	Aspect	Extension	Notes	Status
HUMAN:COM1		GO:0006289: nucleotide-excision repair	ECO:0000315:		P		Figure 1. CtIP depletion sensitizes cells to ICL inducing agents.	complete CACAO 5872
HUMAN:COM1	involved_in	GO:0006289: nucleotide-excision repair	ECO:0000315: mutant phenotype evidence used in manual assertion		P		Seeded From UniProt	complete
HUMAN:CTIP	involved_in	GO:0006289: nucleotide-excision repair	ECO:0000315: mutant phenotype evidence used in manual assertion		P		Seeded From UniProt	complete

References

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