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Human Polyclonal ERCC5 Primary Antibody for ICC, IF - ABIN261688
Wang, Han, Milum, Wani: Stem cell protein Piwil2 modulates chromatin modifications upon cisplatin treatment. in Mutation research 2011
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this meta-analysis shows that XPG gene polymorphisms are associated with lung cancer and gastric cancer
Relevant SNPs in DNA repair (ERCC1 (show ERCC1 Antibodies) and ERCC5) and apoptosis (MDM2 (show MDM2 Antibodies) and TP53 (show TP53 Antibodies)) genes might influence the severity of radiation-related side-effects in HNSCC patients. Prospective clinical SNP-based validation studies are needed on these bases
Nine case-control studies involving 3540 cases and 3953 controls were included in the meta-analysis, which revealed that the XPG rs751402 polymorphism is positively associated with GC risk and could be viewed as a risk factor of GC in three genetic models. The XPG gene rs751402 polymorphism is associated with an increased risk of GC in Chinese Han populations. This fi nding should be veri fi ed by larger studies.
In NBEC, T allele at SNP rs2296147 upregulates ERCC5.
XPG gene polymorphism rs751402 was associated with increased susceptibility to gastric cancer in Chinese populations (Meta-Analysis)
Overexpression of human XPG and FEN1 (show FEN1 Antibodies) increases genome instability in U2OS cells
This study showed that XPG rs2296147 CT/TT variants conferred significant survival disadvantage in CRC (show CALR Antibodies) 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 Antibodies)-negative advanced breast cancer.
the XPG gene rs2094258 C>T polymorphism may contribute to neuroblastoma (show ARHGEF16 Antibodies) susceptibility.
HIghlighted in this study is the crucial role of XPG's interactions with TFIIH (show GTF2H4 Antibodies) for proper nucleotide excision repair
XPG gene expression can be influenced by an epigenetic mechanism. Restoration of NER (show NR1H2 Antibodies) 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 Antibodies) 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