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Werner syndrome protein participates in a complex with RAD51, RAD54, RAD54B and ATR in response to ICL-induced replication arrest

22 Nov 2006

Abstract excerpt

Werner syndrome (WS) is a rare genetic disorder characterized by genomic instability caused by defects in the WRN gene encoding a member of the human RecQ helicase family. RecQ helicases are involved in several DNA metabolic pathways including homologous recombination (HR) processes during repair of stalled replication forks. Following introduction of interstrand DNA crosslinks (ICL), WRN relocated from nucleoli...

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PMID: 17118963
DOI: 10.1242/jcs.03291

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Related research

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Werner syndrome protein participates in a complex with RAD51, RAD54, RAD54B and ATR in response to ICL-induced replication arrestPMID 17118963Read ↗

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The RecQ helicase WRN is required for normal replication fork progression after DNA damage or replication fork arrestSemantic proximity Read ↗

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Replication fork stalling in WRN-deficient cells is overcome by prompt activation of a MUS81-dependent pathwaySemantic proximity Read ↗

WRN as a Novel Target of Synthetic Lethality: Current Advances and Future PerspectivesSemantic proximity Read ↗

Functional role of the Werner syndrome RecQ helicase in human fibroblasts.Semantic proximity Read ↗

Werner Syndrome, aging and cancer.Semantic proximity Read ↗

Werner syndrome RECQ helicase participates in and directs maintenance of the protein complexes of constitutive heterochromatin in proliferating human cellsSemantic proximity Read ↗

WRN is recruited to damaged telomeres via its RQC domain and tankyrase1-mediated poly-ADP-ribosylation of TRF1Semantic proximity Read ↗

Telomere dysfunction as a cause of genomic instability in Werner syndromeSemantic proximity Read ↗

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