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Human Polyclonal ERCC3 Primary Antibody for ChIP, IP - ABIN253199
Gray, Vallur, Eddy, Maizels: G quadruplexes are genomewide targets of transcriptional helicases XPB and XPD. in Nature chemical biology 2014
Cow (Bovine) Polyclonal ERCC3 Primary Antibody for WB - ABIN2780326
Vijai, Topka, Villano, Ravichandran, Maxwell, Maria, Thomas, Gaddam, Lincoln, Kazzaz, Wenz, Carmi, Schrader, Hart, Lipkin, Neuhausen, Walsh, Zhang, Lejbkowicz, Rennert, Stadler, Robson, Weitzel et al.: A Recurrent ERCC3 Truncating Mutation Confers Moderate Risk for Breast Cancer. ... in Cancer discovery 2016
Spironolactone-induced degradation of the TFIIH core complex XPB subunit suppresses NF-kappaB and AP-1 signalling, preventing inflammation in pulmonary hypertension.
Reduced protein expression levels of DNA excision repair protein ERCC-3 (ERCC3) and XPA nucleotide excision repair protein (XPA) were associated with an increased risk of squamous cell carcinoma of head and neck (SCCHN).
We found that the T allele of ERCC2-rs1799793 and the A allele of ERCC3-rs4150441, interaction between rs1799793 and rs4150441, and haplotype containing the rs1799793T and rs11615-T alleles were all associated with increased osteosarcoma risk
This study demonstrates that CpG-specific DNA methylation in the ERCC3 promoter region may be involved in benzene-induced epigenetic modification and it may contribute to benzene-induced hematotoxicity.
An essential role of MYC-ERCC3 interactions in PDAC.
similar to tumors arising in the background of homologous repair defects, mutations in nucleotide excision repair genes such as ERCC3 could constitute potential therapeutic targets in a subset of hereditary breast cancers.
results reveal a previously unknown role for transcription factor IIH in ATR kinase activation in non-replicating, non-cycling cells
Study shows that: mRNA synthesis is sensitive to the inhibition of the ATPase activity of XPB; mRNA synthesis accommodates the depletion of XPB; XPB-depleted TFIIH participates in mRNA synthesis, and finally, XPB ATPase overcomes transcription initiation block imposed by its helicase motifs.
significant interactions between ERCC2 (Lys751Gln) and ERCC3 (7122 A>G) genotypes polymorphism and cadmium exposure in association with nasal polyposis disease
Data did not find any association between ERCC2 or ERCC3 gene polymorphisms and the development of osteosarcoma.
Transcriptional differences found between various TFIIH subunit variants participate in the phenotypic variability observed among xeroderma pigmentosum, XP associated with Cockayne syndrome, and trichothiodystrophy individuals.
XPB and XPD enrichment at G4 motifs characterizes specific signaling pathways and regulatory pathways associated with specific cancers
findings suggest that benzene exposure may be associated with hypermethylation in ERCC3, and that genetic variants in EPHX1 may play an important role in epigenetic changes and hematotoxicity among benzene-exposed workers
The crystal structure of the C-terminal half of the XPB subunit of TFIIH (residues 494-782) is reported, containing XPB helicase domain (HD)2 and a C-terminal extension which shares structural similarity with RIG-I.
results identify the ARCH domain of XPD as a platform for the recruitment of CAK and as a molecular switch that might control TFIIH composition and play a role in conversion of TFIIH from a factor active in transcription to a factor involved in DNA repair
XPB and XPD helicases differentially regulate TFIIH compositional change during nucleotide excision repair.
Phenotype-specific adverse effects of XPD mutations on human prenatal development implicate impairment of TFIIH-mediated functions in placenta.
reduction in ERCC3 by siRNA interference in human melanocytes in vitro reduced their tyrosinase production ability
high expression of ERCC1, XPB and ILF3 was observed in human epithelial ovarian cancer
These results indicated that persistent HBV infection might trigger NER impairment in part through upregulation of miR-192, which suppressed the levels of ERCC3 and ERCC4.
ERCC3 is an ATP-dependent DNA helicase that functions in nucleotide excision repair and complements xeroderma pigmentosum group B mutations. It also is the 89 kDa subunit of basal transcription factor 2 (TFIIH) and thus functions in class II transcription.
excision repair cross-complementing rodent repair deficiency, complementation group 3 (xeroderma pigmentosum group B complementing)
, BTF2 p89
, DNA excision repair protein ERCC-3
, DNA repair protein complementing XP-B cells
, TFIIH 89 kDa subunit
, TFIIH basal transcription factor complex 89 kDa subunit
, TFIIH basal transcription factor complex helicase XPB subunit
, TFIIH p89
, basic transcription factor 2 89 kDa subunit
, xeroderma pigmentosum group B-complementing protein
, xeroderma pigmentosum, complementation group B
, excision repair 3