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This study showed that XPG rs2296147 CT/TT variants conferred significant survival disadvantage in CRC (show CALR Proteins) patients in term of PFS.
These results indicated that none of the selected XPG polymorphism could significantly alter gastric cancer susceptibility alone.
XPG mRNA expression was not predictive of trabectedin efficacy as single agent in hormone-positive, HER-2 (show ERBB2 Proteins)-negative advanced breast cancer.
the XPG gene rs2094258 C>T polymorphism may contribute to neuroblastoma (show ARHGEF16 Proteins) susceptibility.
No strong evidence was found to support the use of XPG polymorphisms as tumor response and prognostic factors of patients with NSCLC receiving a platinum-based treatment regimen--(REVIEW)
Xpg thus helps to adequately induce DNA damage responses after IR, thereby keeping the expansion of damaged cells under control. This represents a new function of Xpg in the response to IR, in addition to its well-characterized role in nucleotide excision repair.
Meta-analysis indicated that the ERCC1 (show ERCC1 Proteins) rs3212986 polymorphism and 2 polymorphisms in ERCC2 (show ERCC2 Proteins) gene (rs13181 and rs1799793) contributed to the susceptibility of glioma. However, no association was observed between glioma risk and ERCC1 (show ERCC1 Proteins) rs11615, ERCC2 (show ERCC2 Proteins) rs238406, and ERCC5 rs17655 polymorphisms.
The rs751402 C/T SNP T allele and the T/T genotype were associated with an increased risk of GCA (show NPR1 Proteins) in younger individuals (>61 years) (odds ratio [OR] = 1.33 and 1.77, 95% confidence interval [CI] = 1.00-1.76 and 1.12-3.30, respectively). The rs873601 G/A SNP was not associated with susceptibility to GCA (show NPR1 Proteins).
The ERCC5 rs751402 gene polymorphism may influence the susceptibility to gastric cancer in the Chinese population.
we found that XPG rs2094258, rs751402, and rs17655 do not influence the development of breast cancer in a Chinese population
HIghlighted in this study is the crucial role of XPG's interactions with TFIIH (show GTF2H4 Proteins) for proper nucleotide excision repair
XPG gene expression can be influenced by an epigenetic mechanism. Restoration of NER (show NR1H2 Proteins) activity through XPG gene transfer or treatment with demethylating agents restored sensitivity to nemorubicin.
introduced a point mutation into the XPG gene which inactivates the nuclease (show DCLRE1C Proteins) catalytic site but leaves the remainder of the protein intact. The mutant mice are hypersensitive to UV irradiation.
Results suggest that the Cockayne syndrome phenotype results from C-terminal truncations in the XPG (xeroderma pigmentosum) gene in mice and humans.
This gene encodes a single-strand specific DNA endonuclease that makes the 3' incision in DNA excision repair following UV-induced damage. The protein may also function in other cellular processes, including RNA polymerase II transcription, and transcription-coupled DNA repair. Mutations in this gene cause xeroderma pigmentosum complementation group G (XP-G), which is also referred to as xeroderma pigmentosum VII (XP7), a skin disorder characterized by hypersensitivity to UV light and increased susceptibility for skin cancer development following UV exposure. Some patients also develop Cockayne syndrome, which is characterized by severe growth defects, mental retardation, and cachexia. Read-through transcription exists between this gene and the neighboring upstream BIVM (basic, immunoglobulin-like variable motif containing) gene.
DNA repair protein complementing XP-G cells
, excision repair cross-complementing rodent repair deficiency, complementation group 5 (xeroderma pigmentosum, complementation group G (Cockayne syndrome))
, DNA excision repair protein ERCC-5
, XPG-complementing protein
, xeroderma pigmentosum, complementation group G
, DNA repair protein complementing XP-G cells homolog
, DNA-repair protein complementing XP-G cells homolog
, XP-G related factor
, xeroderma pigmentosum group G-complementing protein homolog