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The Molecular Mechanism of XPB Gene in Nucleotide Excision Repair and Gene Transcription
Xiao-Dong Hu, Ji -Xiang Zhang1*
The Key Laboratory of Molecular Medicine, the Second Affiliated Hospital of Jiangxi Medical College, Nanchang 330006, China
Abstract: Nucleotide excision repair (NER) mechanism is essential for the maintenance of organism genome integrity. Human xeroderma pigmentosum group B (XPB) gene， also named excision repair cross complementing 3 (ERCC3)， which codes the largest p89 subunit of the basal transcription factor TFIIH and involves in both NER pathway and RNA polymerase II (RNAP II) transcription. XPB， as the essential component of NER， presents a unique 3'→5' ATP-dependent single-stranded DNA (ssDNA) helicases which is absolutely required and indispensable for unwinding and opening the DNA around both a promote in RNAP II transcription and /or a lesion in NER functions. Mutations in human XPB gene are associated with three genetic disorders: xerodema pigmentosum (XP)， Cockayne抯 syndrome (CS) and trichothiodystrophys (TTD)， the phenotypes of which could be explained by specific deficiencies in both transcription and DNA repair. In addition， what抯 intriguing finding is the physical and functional interaction of XPB with p53.
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