Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P20226 (TATA-binding protein)
 1,297 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

RB, the protein product of the retinoblastoma tumor-suppressor gene, regulates the activity of specific transcription factors. This regulation appears to be mediated either directly through interactions with specific transcription factors or through an alternative mechanism. Here we report that stimulation of Sp1-mediated transcription by RB is partially abrogated at the nonpermissive temperature in ts13 cells. These cells contain a temperature-sensitive mutation in the TATA-binding protein-associated factor TAFII250, first identified as the cell cycle regulatory protein CCG1. The stimulation of Sp1-mediated transcription by RB in ts13 cells at the nonpermissive temperature could be restored by the introduction of wild-type human TAFII250. Furthermore, we demonstrate that RB binds directly to hTAFII250 in vitro and in vivo. These results suggest that RB can confer transcriptional regulation and possibly cell cycle control and tumor suppression through an interaction with TFIID, in particular with TAFII250.
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PMID:The retinoblastoma-susceptibility gene product binds directly to the human TATA-binding protein-associated factor TAFII250. 772 24

The retinoblastoma tumor suppressor gene product (Rb) binds directly to the largest TFIID subunit, TATA-binding protein associated factor TAF(II)250, first identified as the cell cycle regulatory protein CCG1. Here we map the domains in Rb and TAF(II)250 important for their interaction in vitro and in vivo. Both the amino terminus and the large pocket of Rb are able to associate independently with TAF(II)250. The binding domain(s) within the large pocket are distinct from the viral oncoprotein and E2F binding region since certain pocket mutations, which abolish E1A binding, do not abolish TAF(II)250 binding. Consistent with the large pocket of Rb binding to TAF(II)250, the large pocket domains of both p107 and p130 are able to bind to TAF(II)250 in vivo. We also demonstrate that at least two regions of TAF(II)250 are able to bind to the large pocket of Rb independently whereas the amino terminus of Rb binds to a distinct domain in TAF(II)250. We further demonstrate that Rb can bind to TFIID in vitro, presumably in part through an interaction with TAF(II)250. Our results suggest a complex interaction between Rb and TAF(II)250 and imply that TAF(II)250, TFIID, and potentially other basal transcription factors are targets for regulation by Rb and Rb-related proteins.
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PMID:Rb interacts with TAF(II)250/TFIID through multiple domains. 924 74

The TATA-binding protein-associated factor TAF(II)250, the largest subunit of TFIID, was first identified as the cell cycle regulatory protein CCG1. The ts13 Syrian hamster ovary fibroblast cell line, which contains a temperature-sensitive point mutation in TAF(II)250/CCG1, is arrested in G1 following a shift to the nonpermissive temperature. Here we demonstrate that the level of the D-type cyclins, in particular D1, was reduced, whereas the level of the cyclin-dependent kinase inhibitor p21 was stimulated in ts13 cells at the nonpermissive temperature. The levels of expression of cyclins A and E were not affected by temperature shift. We further show that at least part of the regulation of D1 and p21 levels in ts13 cells is mediated at the level of transcription initiation. These results suggest that the effect of the temperature-sensitive mutation TAF(II)250 on cell growth can be mediated through the differential regulation of transcription of specific cell growth regulatory genes, such as cyclin D1 and p21.
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PMID:Differential regulation of transcription of p21 and cyclin D1 conferred by TAF(II)250. 934 88