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XPC is an RNA polymerase II cofactor recruiting ATAC coactivator complex to promoters by interacting with E2F1.
CC genotype for XPC A>C polymorphism is associated with the risk of squamous cell carcinoma head and neck.
Results show that XPC deficiency leads to alterations in mitochondrial redox balance with a respiratory complex CI/CII shift as a possible adaptation to lower CI activity, but at the cost of sensitizing XP-C cells to mitochondrial oxidative stress.
Chronic low-dose of UVB (CLUV) treatment activates p53, which corroborate with the increased level of DDB2 and XPC proteins. DDB2 and XPC recruited at chromatin bound, suggesting a more efficient cyclobutane pyrimidine dimer (CPD) recognition by NER and more efficient repair of CDP.
Demethylation using decitabine increased XPC and apoptosis after sequential carboplatin. These results confirm that sequential decitabine and carboplatin requires further investigation as a combination treatment for melanoma.
These findings support that loss of XPC, possibly due to chronic Cigarette smoke exposure, promotes emphysema development and further supports a link between DNA damage, impaired DNA repair, and development of emphysema.
Poly(ADP-ribose) polymerase-1 (PARP1) interacts with xeroderma pigmentosum, complementation group C protein (XPC) in the nucleoplasmic and chromatin fractions in UV irradiated HEK293 cells.
hospital workers as a category are at risk for genotoxic damage caused by chronic exposure to xenobiotics. The higher levels of cytogenetic damage observed among GSTT1 null, XPD 751 and XPC 939 CC homozygote subjects confirm the importance of the genetic polymorphisms analysis associated to genotoxicological studies.
XPC Ala499Val substitution increases urinary bladder cancer risk, but Lys939Gln appears to be neutral. (Meta-analysis)
low XPC and global genome repair have roles in reduced repair of UVB-induced DNA damage in melanoma
Several mutations in the two parts of the central "crest" of the arrestin molecule, middle-loop and C-loop, enhanced or reduced arrestin-3 interactions with several GPCRs in receptor subtype and functional state-specific manner.
these studies found that carriers of the T allele of ERCC1 rs11615, XPC rs2228000 and rs50872, particularly in postmenopausal females, have an increased risk of breast cancer
analysis confirms that XP-C patients without increased sun sensitivity develop non-melanoma skin cancers earlier than sun-sensitive XP-C patients. Reduced cellular mRNA levels are characteristic for XP complementation group C and qRT-PCR represents a rapid diagnostic tool.
Data suggest that a common TFIIH subunit p62 recruitment mechanism is shared by UV-stimulated scaffold protein A (UVSSA) in transcription-coupled repair (TCR) and xeroderma pigmentosum, complementation group C protein (XPC) in global genome repair (GGR).
CHD1 facilitates substrate handover from XPC to the downstream TFIIH (transcription factor IIH).
results provide insights into an unexpected biological role of XPC in response to DNA replication stress
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) of certain types of DNA adducts, leading to repression of NER.
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 and XPC in combination showed an increased risk towards ESCC.
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