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)

The archetypal TATA-box deficient G+C-rich promoter of the murine adenosine deaminase gene (Ada) requires a 48-bp minimal self-sufficient promoter element (MSPE) for function. This MSPE was used to isolate a novel full-length cDNA clone that encodes a 66-kDa murine G+C-rich promoter binding protein (mGPBP). The mGPBP mRNAs are ubiquitously expressed as either 3.0- or 3.5-kb forms differing in 3' polyadenylation site usage. Purified recombinant mGPBP, in the absence of any other mammalian cofactors, binds specifically to both the murine Ada gene promoter's MSPE and the nonhomologous human Topo IIalpha gene's G+C-rich promoter. In situ binding assays, immunoprecipitation, and Western blot analyses demonstrated that mGPBP is a nuclear factor that can form complexes with TATA-binding protein, TFIIB, TFIIF, RNA polymerase II, and P300/CBP both in vitro and in intact cells. In cotransfection assays, increased mGPBP expression transactivated the murine Ada gene's promoter. Sequestering of GPBP present in HeLa cell nuclear extract by immunoabsorption completely and reversibly suppressed extract-dependent in vitro transcription from the murine Ada gene's G+C-rich promoter. However, transcription from the human Topo IIalpha gene's TATA box-containing G+C-rich promoter was only partially suppressed and the adenovirus major late gene's classical TATA box-dependent promoter is totally unaffected under identical assay conditions. These results implicate GPBP as a requisite G+C-rich promoter-specific transcription factor and provide a mechanistic basis for distinguishing transcription initiated at a TATA box-deficient G+C-rich promoter from that initiated at a TATA box-dependent promoter.
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PMID:The murine G+C-rich promoter binding protein mGPBP is required for promoter-specific transcription. 1461 17

The histone deacetylase (HDAC) inhibitor trichostatin A (TSA) and hexamethylene bisacetamide (HMBA), which lacks HDAC inhibitory activity, both possess the capacity to induce leukemia cell differentiation and to enhance the expression of a wide range of transiently transfected reporter genes in 3T3 Swiss cells. In addition, known inducers of leukemia cell differentiation, including hypoxanthine, diazepam, 6-thioguanine and phorbol 12-myristate 13-acetate, also exhibited the ability to enhance reporter gene expression, while randomly chosen compounds that did not induce leukemia cell differentiation did not enhance reporter gene expression. The activity of TSA in the transfection system was modified by co-expression of histone acetyltransferase p300 and HDAC1; whereas, that of HMBA was enhanced by co-expression of the TATA-binding protein TBP. The stimulatory effects of diverse chemical inducers on transiently transfected genes suggest the existence of multiple exploitable targets for the selection of novel inducers of differentiation that function as modulators of gene activity.
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PMID:Relationship between the induction of leukemia cell differentiation and the enhancement of reporter gene expression in 3T3 Swiss cells. 1762 56