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p44 of TFIIH has a role in binding to the nonstructural protein of Rift Valley fever virus to form nuclear filamentous structures
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.
Advanced oxidation protein products down-regulate the expression of calcium transport channels through p44/42 MAPK signaling mechanisms in the small intestinal epithelium.
Together, these results suggest that p44/WDR77 expression causes the non-sensitivity of proliferating cells to TGFbeta signaling, thereby contributing to cellular proliferation during lung tumorigenesis.
No correlation was found for p44 and occludin gene copy number and spinal muscular atrophy
miR-27a was identified as a key regulator of p44 mRNA. Moreover, miR-27a was shown to destabilize the p44 subunit of the TFIIH complex during the G2-M phase, thereby modulating the transcriptional shutdown observed during this transition.
p52 Mediates XPB function within the transcription/repair factor
solution structure of p44-(321-395) shows topology differs from other reported RING domains by a circular permutation of the extended secondary structure elements; mutagenesis suggests tight binding to p34 is mediated by hydrophobic interactions
Impaired transcription in IPF is associated with decreased concentrations of transcription factor II-H in alveolar macrophages and may alter the intraalveolar milieu in IPF.
This gene is part of a 500 kb inverted duplication on chromosome 5q13. This duplicated region contains at least four genes and repetitive elements which make it prone to rearrangements and deletions. The repetitiveness and complexity of the sequence have also caused difficulty in determining the organization of this genomic region. This gene is within the telomeric copy of the duplication. Deletion of this gene sometimes accompanies deletion of the neighboring SMN1 gene in spinal muscular atrophy (SMA) patients but it is unclear if deletion of this gene contributes to the SMA phenotype. This gene encodes the 44 kDa subunit of RNA polymerase II transcription initiation factor IIH which is involved in basal transcription and nucleotide excision repair. Transcript variants for this gene have been described, but their full length nature has not been determined. A second copy of this gene within the centromeric copy of the duplication has been described in the literature. It is reported to be different by either two or four base pairs\; however, no sequence data is currently available for the centromeric copy of the gene.
TFIIH basal transcription factor complex p44 subunit
, basal transcription factor 2, p44 subunit
, basic transcription factor 2 44 kDa subunit
, general transcription factor II H, polypeptide 2 (44 kDa subunit)
, general transcription factor IIH subunit 2
, general transcription factor IIH, polypeptide 2 (44 kDa subunit)
, BTF2 p44
, general transcription factor IIH polypeptide 2
, general transcription factor IIH, polypeptide 2, 44kD subunit