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This study demonstrates that CpG-specific DNA methylation (show HELLS Proteins) 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 (show MYC Proteins)-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 (show ERCC2 Proteins) (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 (show ERCC2 Proteins) or ERCC3 gene polymorphisms and the development of osteosarcoma.
Transcriptional differences found between various TFIIH subunit (show GTF2H4 Proteins) variants participate in the phenotypic variability observed among xeroderma pigmentosum, XP associated with Cockayne syndrome, and trichothiodystrophy individuals.
XPB (show GTF2H5 Proteins) and XPD (show ERCC2 Proteins) 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 (show EPHX1 Proteins) may play an important role in epigenetic changes and hematotoxicity among benzene-exposed workers
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