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anti-Rat (Rattus) GTF2H3 Antibodies:
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Using quantitative imaging of TFIIH in living mouse cells, we found that these molecules reduce the intracellular concentration of TFIIH and its transcriptional activity to levels similar to that observed in individuals with trichothiodystrophy owing to mutated TTD-A
extensive molecular analyses unveiled that wild-type TFIIH cooperated in an ATP-dependent manner with PGC1-alpha as well as with the deacetylase SIRT1, thereby contributing to the PGC1-a deacetylation by SIRT1
Mutations in TFIIH causing trichothiodystrophy are responsible for defects in ribosomal RNA production and processing.
Data show that that B2 RNA, when present with Pol II in promoter-bound complexes, specifically represses CTD phosphorylation by TFIIH.
Molecular analyses performed on the mice brain tissue demonstrate that TFIIH is required for the stabilization of thyroid hormone receptors (TR) to their DNA-responsive elements.
interface variants between the p34 and p44 subunits only mildly affected the association between the full length proteins and did not impinge on TFIIH activities due to the presence of an additional interface involving the C4 domain of p34.
This gene encodes a member of the TFB4 family. The encoded protein is a subunit of the core-TFIIH basal transcription factor and localizes to the nucleus. The encoded protein is involved in RNA transcription by RNA polymerase II and nucleotide excision repair and associates with the Cdk-activating kinase complex. Alternative splicing results in multiple transcript variants. A related pseudogene has been identified on chromosome 14.
general transcription factor IIH subunit 3
, TFIIH basal transcription factor complex p34 subunit
, basic transcription factor 2 34 kDa subunit
, general transcription factor IIH, polypeptide 3, 34kDa
, general transcription factor IIH polypeptide 3