作者: C. Masutani , K. Sugasawa , J. Yanagisawa , T. Sonoyama , M. Ui
DOI: 10.1002/J.1460-2075.1994.TB06452.X
关键词: Biology 、 Nucleotide excision repair 、 Molecular biology 、 Nucleotide-excision repair complex 、 Nucleic acid sequence 、 Global genome nucleotide-excision repair 、 Complementation 、 Xeroderma pigmentosum 、 DNA repair 、 Homology directed repair
摘要: Abstract Complementation group C of xeroderma pigmentosum (XP) represents one the most common forms this cancer-prone DNA repair syndrome. The primary defect is located in subpathway nucleotide excision system, dealing with removal lesions from non-transcribing sequences ('genome-overall' repair). Here we report purification to homogeneity and subsequent cDNA cloning a complex by vitro complementation XP-C cell-free system containing UV-damaged SV40 minichromosomes. has high affinity for ssDNA consists two tightly associated proteins 125 58 kDa. kDa subunit an N-terminally extended version previously reported XPCC gene product which thought represent human homologue Saccharomyces cerevisiae RAD4. species turned out be yeast RAD23. Unexpectedly, second counterpart RAD23 was identified. All derivatives share ubiquitin-like N-terminus. nature implies that exerts unique function genome-overall pathway important prevention skin cancer.