RAD23B
Lua error in Module:Infobox_gene at line 33: attempt to index field 'wikibase' (a nil value). UV excision repair protein RAD23 homolog B is a protein that in humans is encoded by the RAD23B gene.[1][2]
Contents
Function
The protein encoded by this gene is one of two human homologs of Saccharomyces cerevisiae Rad23, a protein involved in nucleotide excision repair (NER). This protein was found to be a component of the protein complex that specifically complements the NER defect of xeroderma pigmentosum group C (XP-c) cell extracts in vitro. This protein was also shown to interact with, and elevate the nucleotide excision activity of 3-methyladenine-DNA glycosylase (MPG), which suggested a role in DNA damage recognition in base excision repair. This protein contains an N-terminal ubiquitin-like domain, which was reported to interact with 26S proteasome, and thus this protein may be involved in the ubiquitin mediated proteolytic pathway in cells.[3]
Role in DNA repair
The complex of XPC-RAD23B is the initial damage recognition factor in global genomic nucleotide excision repair (GG-NER). XPC-RAD23B recognizes a wide variety of lesions that thermodynamically destabilize DNA duplexes, including UV-induced photoproducts (cyclopyrimidine dimers and 6-4 photoproducts ), adducts formed by environmental mutagens such as benzo[a]pyrene or various aromatic amines, certain oxidative endogenous lesions such as cyclopurines and adducts formed by cancer chemotherapeutic drugs such as cisplatin. The presence of XPC-RAD23B is required for assembly of the other core NER factors and progression through the NER pathway both in vitro and in vivo.[4] Although most studies have been performed with XPC-RAD23B, it is part of a trimeric complex with centrin-2, a calcium-binding protein of the calmodulin family.[4]
Epigenetic repression of RAD23
The protein expression level of RAD23B can be epigenetically repressed, either by promoter methylation of the RAD23B gene[5][6] or by either of two microRNAs (miR-744-3p[7] or miR-373[8]).
Deficiency of RAD23B in cancer
A deficiency in expression of a DNA repair gene increases the risk for cancer (see Deficient DNA repair in carcinogenesis). The expression of RAD23B is reduced in tumor tissue of women with breast cancer.[9] A low percentage of RAD23B positive nuclei in high grade breast cancer was also observed.[10]
RAD23B was substantially reduced by promoter methylation in a cell line derived from multiple myeloma.[5] and reduced by promoter methylation in a small proportion of non-small cell lung cancer (NSCLC) tumours.[6]
RAD23B appears to be one of 26 DNA repair genes that are epigenetically repressed in various cancers (see Cancer epigenetics).
Interactions
RAD23B has been shown to interact with PSMD4[11] and Ataxin 3.[12]
References
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