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A novel regulation mechanism of DNA repair by damage-induced and RAD23-dependent stabilization of xeroderma pigmentosum group C protein.

Genes & development | Jul 1, 2003

Primary DNA damage sensing in mammalian global genome nucleotide excision repair (GG-NER) is performed by the xeroderma pigmentosum group C (XPC)/HR23B protein complex. HR23B and HR23A are human homologs of the yeast ubiquitin-domain repair factor RAD23, the function of which is unknown. Knockout mice revealed that mHR23A and mHR23B have a fully redundant role in NER, and a partially redundant function in embryonic development. Inactivation of both genes causes embryonic lethality, but appeared still compatible with cellular viability. Analysis of mHR23A/B double-mutant cells showed that HR23 proteins function in NER by governing XPC stability via partial protection against proteasomal degradation. Interestingly, NER-type DNA damage further stabilizes XPC and thereby enhances repair. These findings resolve the primary function of RAD23 in repair and reveal a novel DNA-damage-dependent regulation mechanism of DNA repair in eukaryotes, which may be part of a more global damage-response circuitry.

Pubmed ID: 12815074 RIS Download

Mesh terms: Acetoxyacetylaminofluorene | Animals | Cell Line | Cysteine Endopeptidases | DNA Damage | DNA Repair | DNA Repair Enzymes | DNA-Binding Proteins | Female | Gene Targeting | Hot Temperature | Humans | Male | Mice | Mice, Inbred C57BL | Mice, Knockout | Multienzyme Complexes | Proteasome Endopeptidase Complex | Recombinant Fusion Proteins | Transcription, Genetic | Transfection | Ubiquitin | Ultraviolet Rays

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Associated grants

  • Agency: NIA NIH HHS, Id: P01 AG017242

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