| Literature DB >> 19682467 |
Abstract
Nucleotide excision repair operating throughout the mammalian genome plays a crucial role in the suppression of mutagenesis and carcinogenesis, which can arise from DNA lesions induced by a wide variety of genotoxic agents, such as ultraviolet light and chemical compounds. A key process of this DNA repair pathway, damage recognition, is accomplished through multiple steps including concerted actions of the damaged DNA binding factors XPC and UV-DDB, both of which are implicated in a human cancer-prone genetic disorder, xeroderma pigmentosum. Accumulating evidence indicates that the expression and functions of these damage recognition factors are subject to exquisite regulation at diverse levels, including transcriptional activation, post-translational modification, complex formation, and protein degradation through ubiquitination. Copyright (c) 2009 Elsevier B.V. All rights reserved.Entities:
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Year: 2009 PMID: 19682467 DOI: 10.1016/j.mrfmmm.2009.08.004
Source DB: PubMed Journal: Mutat Res ISSN: 0027-5107 Impact factor: 2.433