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New functions of XPC in the protection of human skin cells from oxidative damage
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New functions of XPC in the protection of human skin cells from oxidative damage
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Journal Article
New functions of XPC in the protection of human skin cells from oxidative damage
2006
Overview
Xeroderma pigmentosum (XP) C is involved in the recognition of a variety of bulky DNA‐distorting lesions in nucleotide excision repair. Here, we show that XPC plays an unexpected and multifaceted role in cell protection from oxidative DNA damage. XP‐C primary keratinocytes and fibroblasts are hypersensitive to the killing effects of DNA‐oxidizing agents and this effect is reverted by expression of wild‐type XPC. Upon oxidant exposure, XP‐C primary keratinocytes and fibroblasts accumulate 8,5′‐cyclopurine 2′‐deoxynucleosides in their DNA, indicating that XPC is involved in their removal. In the absence of XPC, a decrease in the repair rate of 8‐hydroxyguanine (8‐OH‐Gua) is also observed. We demonstrate that XPC–HR23B complex acts as cofactor in base excision repair of 8‐OH‐Gua, by stimulating the activity of its specific DNA glycosylase OGG1.
In vitro
experiments suggest that the mechanism involved is a combination of increased loading and turnover of OGG1 by XPC‐HR23B complex. The accumulation of endogenous oxidative DNA damage might contribute to increased skin cancer risk and account for internal cancers reported for XP‐C patients.
Publisher
John Wiley & Sons, Ltd,Nature Publishing Group UK,Springer Nature B.V,EMBO Press
Subject
Biochemistry, Molecular Biology
/ Bromates
/ cancer
/ Cells
/ DNA
/ DNA Glycosylases - metabolism
/ DNA-Binding Proteins - deficiency
/ DNA-Binding Proteins - genetics
/ DNA-Binding Proteins - metabolism
/ EMBO13
/ Guanine
/ Guanine - analogs & derivatives
/ Humans
/ Keratinocytes - drug effects
/ Keratinocytes - radiation effects
/ Lesions
/ Oxidants
/ Skin
/ X-Rays
/ Xeroderma Pigmentosum - complications
