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抗Human XRCC1 抗体:
抗Mouse (Murine) XRCC1 抗体:
抗Rat (Rattus) XRCC1 抗体:
This study found that an XRCC1 fragment, comprising residues 166-436, binds tightly to PNKP and DNA and efficiently activates PNKP's kinase activity.
Polymorphic variant XRCC1 HNSCC patients treated with CCRT have significantly increased acute radiation morbidities
carrying the allele T of XRCC1 rs1799782 polymorphism and the allele G of APEX rs1130409 polymorphism increased the risk of developing Paget's disease of bone.
a significant association between XRCC1 Arg399Gln and hepatocellular carcinoma risk was found in healthy controls in the general population but not in hospital controls.
XRCC1 gene is highly associated with susceptibility to cervical cancer risk in a female population in southwestern China.
Via interference with XRCC1/PARP1-mediated base excision repair.
we showed that CHK2-dependent phosphorylation of PARP1 not only regulates its cellular localization but also promotes its catalytic activity and its interaction with XRCC1. These findings indicate that CHK2 exerts a multifaceted impact on PARP1 in response to oxidative stress to facilitate DNA repair and to maintain cell survival.
Study shows that polymorphisms in the genes coding for the DNA damage repair enzymes - OGG1 Ser326Cys (rs1052133) and XRCC1 Arg399Gln (rs25487) - may be associated with poor sperm parameters and male infertility.
Data suggest that phosphorylation of T358 and T367 and p38 signaling are important for proper regulation of XRCC1 recruitment to DNA damage.
our study therefore identified a pathway in which DNA damage-induced poly(ADP-ribosyl)ation (PARylation) promotes SUMOylation of XRCC1, which leads to more efficient recruitment of POLB to complete base excision repair
Increased lung cancer risk was revealed in workers-carriers of homozygous minor genotype of genes OGG1] Ser326Cys (OR - 4.67, p = 0.007), APE1 Asp148Glu (OR = 1.82, p = 0.063) and XRCC1 Gln399Arg (OR = 2.86, p = 0.026).
Low XRCC1 rs25487 AA is associated with breast Cancer.
restriction fragment length polymorphism (RFLP) method was used for evaluating of XPD (-751), XRCC4 (-1394 and a variable number of tandem repeats in intron 3), and XRCC1 (-399) genes.We did not observe any noteworthy discrepancy in patients in the SH, CH, CAH, and NE groups in terms of XRCC1 (-399)
A statistically significant association between methylenetetrahydrofolate reductase (MTHFR) 677T/T, thymidylate synthase (TS) 5'-untranslated region (UTR) 3RG, TS 3'-UTR -6 bp/-6 bp, XRCC1 399G/G genotypes and short survival was found in patients receiving best supportive care (BSC)by multivariate analysis
The methylation status of XRCC1 (methylated at T0) and hOGG1 (unmethylated at T0) remained unchanged in the three sampling times. In conclusion, this study showed modulations of hOGG1 and XRCC1 expression especially 1 day after elective surgery in patients undergoing PROP and ISO anaesthesia
The TP53 codon 72 Arg allele and XRCC1 codon 399 Gln allele are likely to have a protective effect against lung adenocarcinoma, especially in individuals older than 50 years of age. XRCC1 and TP53 genotyping might be a useful low-cost tool for evaluating individual lung cancer risk.
Polymorphic variants of XRCC1 Arg399Gln and XPD Lys751Gln are not associated with the risk of gastric cancer in the Kashmiri population.
The effects of chronic smoking on oral mucosa led to the methylation of genes MRE11A PMS2, XRCC1 and MLH3, but resulted in a reduction of gene expression of MRE11A and PMS2, which showed >/=50% methylation. These results provide evidence that smoking cause methylation and reduced expression of repair genes.
T-77C and Arg399Gln polymorphisms of the XRCC1 gene, as well as the 186C>T and Val158Met polymorphisms of the COMT gene, increased the risk of lung cancer in non-smoking women.
XRCC1 Arg194Trp, Arg280His, and Arg399Gln did not affect overall survival after platinum-based chemotherapy in ovarian cancer patients. However, disease status could affect the relationship between Arg399Gln and overall survival in these patients
Unrepaired single strand DNA breaks (SSBs) activate DNA damage response and increase the expression of inflammatory cytokines through NF-kappaB signalling. Pressure overload-induced heart failure is more severe in the mice lacking XRCC1, an essential protein for SSB repair.
Interaction with phosphorylated XRCC1 is a requirement for significant APTX recruitment to cellular DNA damage and enzymatic activity in cell extracts.
this review focuses on the role of the oxidized form of XRCC1 in protection against extreme oxidative stress
Repair independent of the well documented XRCC1-PNKP interaction was studied. XRCC1 can mediate repair of strand breaks without PNKP binding.
data establish the importance of XRCC1 protein complexes for normal neurological function and identify PARP1 as a therapeutic target in DNA strand break repair-defective disease
We have characterized the nuclear localization signal (NLS) of XRCC1 structurally using X-ray crystallography and functionally using fluorescence imaging.
Its allelic loss results in increased brain damage and reduced recovery from ischemic stroke.
Data indicate that maternal folate depletion during pregnancy and high-fat feeding from weaning altered gene expression of Ogg1, Neil1, Mutyh and Xrcc1 in the brain of adult offspring.
In cells with DNA base damage, PAR serves to recruit XRCC1 that in turn binds and recruits pol beta, the primary DNA polymerase of the base excision repair pathway.
Lig4 and XRCC1 double-deficient cells switch as efficiently as Lig4-deficient cells, clearly indicating that XRCC1 is dispensable for A-EJ in CH12F3 cells during class switch recombination
findings firmly demonstrate that XRCC1 is not a requisite factor for A-EJ of chromosomal DSBs and raise the possibility that DNA ligase 1 (Lig1) may contribute more to A-EJ than previously considered
Data support a role for XRCC1 in microhomology-mediated joining, and imply that AID-induced single-strand breaks in Igh variable and switch regions become substrates simultaneously for BER and mutagenesis pathways.
Results indicates that XRCC1 haploinsufficiency has little effect on chronological longevity and many key biological markers of aging, but may adversely affect normal animal development or increase disease susceptibility to a relevant genotoxic exposure.
data reveal that the critical biological role of Lig3 is to maintain mtDNA integrity and not Xrcc1-dependent DNA repair
results establish a role for Lig3 in mitochondria, but distinguish it from its interacting protein Xrcc1
poly(ADP-ribose) polymerase-1 and XRCC1/DNA ligase III utilize an alternative route for DNA double-strand breaks rejoining
These results identify a novel role for FoxM1 in the transcriptional response during DNA damage/checkpoint signaling and show a novel mechanism by which Chk2 protein regulates expression of DNA repair enzymes.
the XRCC1 Arg399Gln and RAD51 5'UTR G135C polymorphisms have roles in breast cancer aggressiveness
E2F1 regulates the base excision repair gene XRCC1 and promotes DNA repair
The protein encoded by this gene is involved in the efficient repair of DNA single-strand breaks formed by exposure to ionizing radiation and alkylating agents. This protein interacts with DNA ligase III, polymerase beta and poly (ADP-ribose) polymerase to participate in the base excision repair pathway. It may play a role in DNA processing during meiogenesis and recombination in germ cells. A rare microsatellite polymorphism in this gene is associated with cancer in patients of varying radiosensitivity.
X-ray repair complementing defective repair in Chinese hamster cells 1
, X-ray repair cross complementing protein 1
, DNA repair protein XRCC1-like
, DNA repair protein XRCC1
, X-ray repair cross-complementing protein 1
, X-ray-repair, complementing defective, repair in Chinese hamster
, x-ray repair cross-complementing group 1 protein