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Allelic variants in the gene XPC are not associated with an increased risk for developing pre-senile cataract
XPC dissociation from the damage site could become a rate-limiting step in nucleotide excision repair (NER (zeige NR1H2 ELISA Kits)) of certain types of DNA adducts, leading to repression of NER (zeige NR1H2 ELISA Kits).
Histone deacetylation plays a significant role in the process of DNA damage recognition for nucleotide excision repair and the localization and functions of XPC can be regulated by acetylated states of histones.
The risk of esophageal squamous cell carcinoma associated with XPC rs-2228000 was determined. A homozygous minor allele showed strong association with ESCC risk, especially in smokers, those in adobe houses, and drinkers of salt tea. Variant genotypes of both XPA (zeige XPA ELISA Kits) and XPC in combination showed an increased risk towards ESCC.
the associations between three XPC gene polymorphisms (rs2228001 A>C, rs2228000 C>T, and rs2229090 G>C) and neuroblastoma risk with 256 neuroblastoma patients and 531 healthy controls in a Chinese Han population, were investigated.
XPC polymorphisms are associated with gastric cancer and atrophic gastritis risks.
A chirality change in XPC- and Sfi1-derived peptides affects their affinity for centrin (zeige CETN1 ELISA Kits).
XPC intron11 C/A polymorphism was associated with an increased risk of prostate cancer. Among non-smokers, the A/A genotype was significantly more prevalent in prostate cancer patients than in controls.
No association between XPC polymorphisms and grades/stages of tumors, but report significant association between XPC PAT and reduction of prostate cancer risk in this group of patients.
Structural insight into the mechanism of TFIIH (zeige GTF2H1 ELISA Kits) recognition by the acidic string of the nucleotide excision repair factor XPC has been uncovered.
results suggest that XPC may help repair DNA damage caused by KRAS-mediated production of ROS (zeige ROS1 ELISA Kits).
OCT4 (zeige POU5F1 ELISA Kits) and SOX2 (zeige SOX2 ELISA Kits) are the primary transcription factors recruiting SCC (zeige CYP11A1 ELISA Kits) to regulatory regions of pluripotency genes; the XPC subunit is essential for interaction with the two proteins
progerin and p16(INK4a) expression, beta-galactosidase (zeige GLB1 ELISA Kits) activity, and reactive oxygen species, which increase with age, were higher in young Xpc(-/-) mice than in young Xpc(+/+) ones
Study indicates that Xpc(-/-) mice have an increased mutational load upon induction of oxidative stress. The effect of non-functional XPC in vivo appears to have implications in mutagenesis, which can contribute to the carcinogenesis process.
The C-terminal region of Xpc is dispensable for the transcriptional activity of Oct3/4 (zeige POU5F1 ELISA Kits) in mouse embryonic stem cells.
BRAF (zeige BRAF ELISA Kits)(V600E) and ARF deletion synergize to inhibit nucleotide excision repair by epigenetically repressing XPC.
Dysmyelination not demyelination causes neurological symptoms in preweaned mice in a cs-b xp-c murine model of Cockayne syndrome
analysis of mHR23A/B double-mutant cells showed that HR23 proteins function in nucleotide excision repair by governing xeroderma pigmentosum group C protein stability via partial protection against proteasomal degradation
mutational hot spot is not at a dipyrimidine site and is apparently Xpc-specific, suggesting some form of non-dipyrimidine base damage is normally repaired in a manner distinct from conventional nucleotide excision repair, but that requires XPC protein
Deletion of Gadd45a (zeige GADD45A ELISA Kits) alone does not lead to increased lung tumors in mice, but coupled with an XPC deletion, it results in lung tumor progression
This gene encodes a component of the nucleotide excision repair (NER) pathway. There are multiple components involved in the NER pathway, including Xeroderma pigmentosum (XP) A-G and V, Cockayne syndrome (CS) A and B, and trichothiodystrophy (TTD) group A, etc. This component, XPC, plays an important role in the early steps of global genome NER, especially in damage recognition, open complex formation, and repair protein complex formation. Mutations in this gene or some other NER components result in Xeroderma pigmentosum, a rare autosomal recessive disorder characterized by increased sensitivity to sunlight with the development of carcinomas at an early age. Alternatively spliced transcript variants have been found for this gene.
xeroderma pigmentosum, complementation group C
, DNA repair protein complementing XP-C cells
, mutant xeroderma pigmentosum group C
, DNA repair protein complementing XP-C cells homolog
, xeroderma pigmentosum group C-complementing protein homolog