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we investigated how specific XPF mutations found in patients affected with xeroderma pigmentosum(XP) , XP combined with Cockayne syndrome or Fanconi anemia impair the activity of the ERCC1-XPF complex in response to DNA damage induction by UV irradiation. We show that XPF with an XP mutation is inefficiently recruited into the NER machinery but retains repair activity.
XPF rs1799801 was associated with severe preeclampsia and early-onset preeclampsia in Chinese Han Women.
Study provides evidence that Replication forks can break quickly in S-phase upon DNA replication stress induction by an endonucleolytic mechanism independent of MUS81. Two nucleases ARTEMIS and XPF-ERCC1 are responsible for this Rapid-Replication Fork Breakage (RRFB) which takes place during S and G2 phases of the cell cycle.
For 11985 A>G polymorphism, lung cancer subjects treated with irinotecan cisplatin/carboplatin regimen having heterozygous genotype (AG) was associated with high mortality risk (p = 0.0001). 673 C>T polymorphism was associated with increased lung cancer risk.
common genetic variations in ERCC1/XPF genes predispose to neuroblastoma risk, which needs to be further validated by ongoing efforts.
Our results confirm that biallelic ERCC4 mutations cause a cerebellar ataxia-dominant phenotype with mild cutaneous symptoms, possibly accounting for a high proportion of the genetic causes of ARCA in Japan, where XP-F is prevalent.
ERCC1 was not detectable in the nucleus of the XPF knockout cells indicating the necessity of a functional XPF/ERCC1 heterodimer to allow ERCC1 to enter the nucleus.
Strikingly, the addition of the single-stranded DNA (ssDNA)-binding replication protein A (RPA) selectively restores XPF-ERCC1 endonuclease activity on this structure. The 5'-3' exonuclease SNM1A can load from the XPF-ERCC1-RPA-induced incisions and digest past the crosslink to quantitatively complete the unhooking reaction.
Based on structural models, NMR titrations, DNA-binding studies, site-directed mutagenesis, charge distribution, and sequence conservation, we propose that the HhH domain of ERCC1 binds to dsDNA upstream of the damage, and XPF binds to the non-damaged strand within a repair bubble
silenced XPF significantly increased the sensitivity and survival following treatment with cisplatin in xenograft mice bearing renal cell tumor.
C allele of the 30028T/C polymorphism significantly increased the risk of ischemic stroke.
Polymorphisms in XPF gene is associated with gastrointestinal stromal tumours.
inherited abnormalities in DNA repair pathway related to XPF 30028C and TP53 Arg72Pro polymorphisms act as prognostic factors for progression free survival and overall survival of cutaneous melanoma patients.
Based on these results, we conclude that the XPF gene polymorphism Ser835Ser may be associated with a decreased risk of colorectal cancer.
Polymorphisms of ERCC4 gene are associated with HPV-positive cervical cancer.
Helicobacter Pylori introduces double-stranded DNA breaks by the nucleotide excision repair endonucleases XPF and XPG, which, together with RelA, are recruited to chromatin in a highly coordinated, type IV secretion system-dependent manner.
SLX4 (FANCP) and XPF (FANCQ) proteins interact with each other and play a vital role in the Fanconi anemia (FA) DNA repair pathway.
Mus81-deficient cells fail to recover from exposure to low doses of replication inhibitors and cell viability is dependent on the XPF endonuclease.
Genotypes of ERCC1 (rs11615, rs3212986 and rs2298881) and XPF (rs2276465 and rs6498486) were performed by Polymerase Chain Reaction Restriction Fragment Length Polymorphism (PCR-RFLP) assay
XPF and XPC expression may be a potential predictive factor for bladder cancer, and smoking can not only influence the recurrence of bladder cancer as a single factor but also aggravate the results of the XPF defect and XPC defect.
ERCC1-XPF cooperates with CTCF and cohesin to facilitate the developmental silencing of imprinted genes and that persistent DNA damage triggers chromatin changes that affect gene expression programs associated with NER disorders.
these results establish USP45 as a new regulator of XPF-ERCC1 crucial for efficient DNA repair
SLX4 is a tumor suppressor, which activates XPF-ERCC1 nuclease specificity in DNA crosslink repair.
Data reveal an unanticipated involvement of the ERCC1/XPF NER endonuclease in the regulation of telomere integrity.
mitomycin C triggered sister chromatid exchanges in wild-type cells but chromatid fusions in Ercc1(-/-) and Xpf mutant cells, indicating that in their absence, repair of double-strand breaks(DSBs)is prevented.
In mice with overexpressed TRF2, telomere loss is mediated by Xpf.
These data support the conclusion that, as in yeast, ERCC1-XPF facilitates double-strand breaks repair via an end-joining mechanism that is Ku86 independent.
These data support a model in which the interstrand crosslink repair-specific function of XPF-ERCC1 is dependent on recruitment, positioning and substrate recognition.
The protein encoded by this gene forms a complex with ERCC1 and is involved in the 5' incision made during nucleotide excision repair. This complex is a structure specific DNA repair endonuclease that interacts with EME1. Defects in this gene are a cause of xeroderma pigmentosum complementation group F (XP-F), or xeroderma pigmentosum VI (XP6).
DNA excision repair protein ERCC-4
, DNA repair endonuclease XPF
, DNA repair protein complementing XP-F cells
, excision-repair, complementing defective, in Chinese hamster
, xeroderma pigmentosum group F-complementing protein
, xeroderma pigmentosum, complementation group F
, DNA repair endonuclease subunit
, Ercc4 protein-like
, excision repair cross-complementing rodent repair deficiency, complementation group 4
, DNA repair endonuclease XPF-like