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

The androgen receptor (AR) is a member of the steroid receptor subfamily of nuclear receptors and is important for normal male sexual differentiation and fertility. The major transactivation function of the AR, termed activation function 1 (AF1), is modular in structure and has been mapped to the N terminus of the protein. To understand better the mechanisms whereby the AR activates transcription, we have established a novel cell-free transcription assay. This is based on the use of a dual reporter gene template, containing promoter proximal and distal G-less cassettes, which result in different size transcripts that can be easily detected and quantified. The promoter proximal transcript gives an indication of transcription initiation and promoter escape, whereas the relative levels of the distal transcript indicate elongation efficiency. The AR-AF1-Lex protein enhanced production of both transcripts whereas, in the absence of DNA binding, the AF1 domain squelched both initiation and elongation. Mutations in the transactivation domain that impaired transactivation and/or binding of the general transcription factor IIF (TFIIF) were found to reduce the ability of AR-AF1 to squelch transcription. Addition of recombinant TFIIF reversed squelching of the promoter-proximal but not the -distal G-less transcript, whereas addition of TATA-binding protein failed to reverse squelching of either transcript. Taken together, these results demonstrate that the AR N-terminal transactivation function, AF1, has the potential to regulate transcription at both the level of initiation and elongation, and that interactions with TFIIF are important during preinitiation complex assembly/open complex formation and/or promoter escape.
Mol Endocrinol 2006 Sep
PMID:The role of the general transcription factor IIF in androgen receptor-dependent transcription. 1664 39

In kinetoplastids a 39-nucleotide spliced leader RNA is trans-spliced to the 5' end of nuclear mRNAs before they can be translated, thus the spliced leader is central to gene expression in kinetoplastid biology. The spliced leader RNA genes in Leishmania tarentolae contain promoters with important sites at approximately -60 and -30. A complex forms specifically on the -60 element as shown by electrophoretic mobility shift. The -60 shift complex has an estimated mass of 159 kDa. An L. tarentolae homologue of TATA-binding protein, LtTBP, co-fractionates with the -60 shift complex. Inclusion of anti-LtTBP antiserum in the shift assay disrupts the shift, indicating that LtTBP is a component of the complex that interacts with the TATA-less -60 element of the spliced leader RNA gene promoter. Both LtTBP and LtSNAP50 are found near the spliced leader RNA gene promoter and the promoters important for tRNAAla and/or U2 snRNA gene transcription, as demonstrated by chromatin immunoprecipitation. The LtTBP appears to interact with a subset of promoters in kinetoplastids with an affinity for short transcription units.
Int J Parasitol 2006 Sep
PMID:A non-universal transcription factor? The Leishmania tarentolae TATA box-binding protein LtTBP associates with a subset of promoters. 1675 68

In addition to TATA-binding protein (TBP), a key factor for transcription initiation, the metazoan-specific TBP-like factor TLF/TRF2 and the vertebrate-specific factor TBP2/TRF3 are known to be required for transcription of specific subsets of genes. We have combined an antisense-knockdown approach with transcriptome profiling to determine the significance and biological role of TBP-independent transcription in early gastrula-stage Xenopus laevis embryos. Here, we report that, although each of the TBP family members is essential for embryonic development, relatively few genes depend on TBP in the embryo. Most of the transcripts that depend on TBP in the embryo are also expressed maternally and in adult stages, and show no functional specialization. In contrast, TLF is linked to preferential expression in embryos and shows functional specialization in catabolism. A requirement for TBP2 is linked to vertebrate-specific embryonic genes and ventral-specific expression. Therefore TBP paralogs are essential for the gene-regulatory repertoire that is directly linked to early embryogenesis.
EMBO J 2007 Sep 05
PMID:TBP paralogs accommodate metazoan- and vertebrate-specific developmental gene regulation. 1770 92

Early steps of embryo development are directed by maternal gene products and trace levels of zygotic gene activity in vertebrates. A major activation of zygotic transcription occurs together with degradation of maternal mRNAs during the midblastula transition in several vertebrate systems. How these processes are regulated in preparation for the onset of differentiation in the vertebrate embryo is mostly unknown. Here, we studied the function of TATA-binding protein (TBP) by knock down and DNA microarray analysis of gene expression in early embryo development. We show that a subset of polymerase II-transcribed genes with ontogenic stage-dependent regulation requires TBP for their zygotic activation. TBP is also required for limiting the activation of genes during development. We reveal that TBP plays an important role in the degradation of a specific subset of maternal mRNAs during late blastulation/early gastrulation, which involves targets of the miR-430 pathway. Hence, TBP acts as a specific regulator of the key processes underlying the transition from maternal to zygotic regulation of embryogenesis. These results implicate core promoter recognition as an additional level of differential gene regulation during development.
EMBO J 2007 Sep 05
PMID:The TATA-binding protein regulates maternal mRNA degradation and differential zygotic transcription in zebrafish. 1770 93

Transcriptional mechanisms that govern cellular differentiation typically include sequence-specific DNA-binding proteins and chromatin-modifying activities. These regulatory factors are assumed necessary and sufficient to drive both divergent programs of proliferation and terminal differentiation. By contrast, potential contributions of the basal transcriptional apparatus to orchestrate cell-specific gene expression have been poorly explored. In order to probe alternative mechanisms that control differentiation, we have assessed the fate of the core promoter recognition complex, TFIID, during skeletal myogenesis. Here we report that differentiation of myoblast to myotubes involves the disruption of the canonical holo-TFIID and replacement by a novel TRF3/TAF3 (TBP-related factor 3/TATA-binding protein-associated factor 3) complex. This required switching of core promoter complexes provides organisms a simple yet effective means to selectively turn on one transcriptional program while silencing many others. Although this drastic but parsimonious transcriptional switch had previously escaped our attention, it may represent a more general mechanism for regulating cell type-specific terminal differentiation.
Genes Dev 2007 Sep 01
PMID:Switching of the core transcription machinery during myogenesis. 1778 21

Huntington's disease (HD), which is caused by a triplet-repeat expansion in the IT15 gene (also known as huntingtin or HD), accounts for about 90% of cases of chorea of genetic etiology. In recent years, several other distinct genetic disorders have been identified that can present with a clinical picture indistinguishable from that of HD. These disorders are termed Huntington's disease-like (HDL) syndromes. So far, four such conditions have been recognized, namely disorders attributable to mutations in the prion protein gene (HDL1), the junctophilin 3 gene (HDL2), and the gene encoding the TATA box-binding protein (HDL4/SCA17), and a recessively inherited HD phenocopy in a single family (HDL3), the genetic basis of which is currently poorly understood. These disorders, however, account for only a small proportion of cases with the HD phenotype but a negative genetic test for HD, and the list of HDL genes and conditions is set to grow. In this article, we review the most important HD phenocopy disorders identified to date and discuss the clinical clues that guide further investigation. We will concentrate on the four so-called HDL syndromes mentioned above, as well as other genetic disorders such as dentatorubral-pallidoluysian atrophy, neuroferritinopathy, pantothenate-kinase-associated neurodegeneration and chorea-acanthocytosis.
Nat Clin Pract Neurol 2007 Sep
PMID:The Huntington's disease-like syndromes: what to consider in patients with a negative Huntington's disease gene test. 1780 46

Toxoplasma gondii GRA10 expressed as a GFP-GRA10 fusion protein in HeLa cells moved to the nucleoli within the nucleus rapidly and entirely. GRA10 was concentrated specifically in the dense fibrillar component of the nucleolus morphologically by the overlap of GFP-GRA10 transfection image with IFA images by monoclonal antibodies against GRA10 (Tg378), B23 (nucleophosmin) and C23 (nucleolin). The nucleolar translocalization of GRA10 was caused by a putative nucleolar localizing sequence (NoLS) of GRA10. Interaction of GRA10 with TATA-binding protein associated factor 1B (TAF1B) in the yeast two-hybrid technique was confirmed by GST pull-down assay and immunoprecipitation assay. GRA10 and TAF1B were also co-localized in the nucleolus after co-transfection. The nucleolar condensation of GRA10 was affected by actinomycin D. Expressed GFP-GRA10 was evenly distributed over the nucleoplasm and the nucleolar locations remained as hollows in the nucleoplasm under a low dose of actinomycin D. Nucleolar localizing and interacting of GRA10 with TAF1B suggested the participation of GRA10 in rRNA synthesis of host cells to favor the parasitism of T. gondii.
Korean J Parasitol 2007 Sep
PMID:Nucleolar translocalization of GRA10 of Toxoplasma gondii transfectionally expressed in HeLa cells. 1787 61

The stability of housekeeping genes (HKGs) is critical when performing real-time quantitative PCR. To date, the stability of common HKGs has not been systematically compared in human airway epithelial cells (AEC) in normal and atopic subjects. Expression levels of 12 HKGs were measured in AECs from a cohort of 30 healthy atopic nonasthmatic or atopic asthmatic children. Gene expression stability was determined using three different Visual Basic for Applications applets (geNorm, NormFinder and BestKeeper). All 12 HKGs were expressed in AECs. However, the hypoxanthine ribosyltransferase and TATA-binding protein genes were excluded from further analysis due to low expression levels. The cyclophilin A gene was ranked the most stable by all three methods. The expression levels of the beta-actin and glyceraldehyde-3-phosphate dehydrogenase genes were significantly different between the three groups of patients, with atopic asthmatics showing the highest expression levels for both genes. The results suggest that the cyclophilin A gene is the most suitable housekeeping gene analysed for expression studies utilising uncultured bronchial airway epithelial cells from healthy and asthmatic children, and highlight the importance of validating housekeeping genes for each experimental model.
Eur Respir J 2008 Sep
PMID:Selection of housekeeping genes for real-time PCR in atopic human bronchial epithelial cells. 1841 9

Mot1 is an essential, conserved TATA-binding protein (TBP)-associated factor in Saccharomyces cerevisiae and a member of the Snf2/Swi2 ATPase family. Mot1 uses ATP hydrolysis to displace TBP from DNA, an activity that can be readily reconciled with its global role in gene repression. Less well understood is how Mot1 directly activates gene expression. It has been suggested that Mot1-mediated activation can occur by displacement of inactive TBP-containing complexes from promoters, thereby permitting assembly of functional transcription complexes. Mot1 may also activate transcription by other mechanisms that have not yet been defined. A gap in our understanding has been the absence of biochemical information related to the activity of Mot1 on natural target genes. Using URA1 as a model Mot1-activated promoter, we show striking differences in the way that both TBP and Mot1 interact with DNA compared with other model DNA substrates analyzed previously. These differences are due at least in part to the propensity of TBP alone to bind to the URA1 promoter in the wrong orientation to direct appropriate assembly of the URA1 preinitiation complex. The results suggest that Mot1-mediated activation of URA1 transcription involves at least two steps, one of which is the removal of TBP bound to the promoter in the opposite orientation required for URA1 transcription.
J Biol Chem 2008 Sep 05
PMID:Function and structural organization of Mot1 bound to a natural target promoter. 1860 10

Although RNA polymerases (RNAPs) are able to use RNA as template, it is unknown how they recognize RNA promoters. In this study, we used an RNA fragment derived from the hepatitis delta virus (HDV) genome as a model to investigate the recognition of RNA promoters by RNAP II. Inhibition of the transcription reaction using an antibody specific to the largest subunit of RNAP II and the direct binding of purified RNAP II to the RNA promoter confirmed the involvement of RNAP II in the reaction. RNA affinity chromatography established that an active RNAP II preinitiation complex forms on the RNA promoter and indicated that this complex contains the core RNAP II subunit and the general transcription factors TFIIA, TFIIB, TFIID, TFIIE, TFIIF, TFIIH and TFIIS. Binding assays demonstrated the direct binding of the TATA-binding protein and suggested that this protein is required to nucleate the RNAP II complex on the RNA promoter. Our findings provide a better understanding of the events leading to RNA promoter recognition by RNAP II.
Nucleic Acids Res 2008 Sep
PMID:Formation of an RNA polymerase II preinitiation complex on an RNA promoter derived from the hepatitis delta virus RNA genome. 1868 25


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