Abstract
The bulky adduct lesions of DNA known to cause deleterious phenotypes in mammals, are mostly acted upon and removed from the genomic DNA by nucleotide excision repair (NER) pathway. NER pathways with its TFIIH multi-protein complex containing an important helicase–xeroderma pigmentosum protein (XPD) serves as the pivotal factor for identification and opening up of the damaged DNA lesion site so as to carry out the repair process. In this chapter, we’ll be exploring the new visions in scientific research on the functioning of the NER pathway, the role of TFIIH as the central complex of NER, the pivotal helicase XPD as the lynchpin of NER, and the effects of various single nucleotide polymorphisms (SNPs) of XPD on its functioning and their consequent role in development and progression of colorectal cancer.
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