TATA-Box Binding Protein (TATA-Binding Protein)

A general transcription factor that plays a major role in the activation of eukaryotic genes transcribed by RNA POLYMERASES. It binds specifically to the TATA BOX promoter element, which lies close to the position of transcription initiation in RNA transcribed by RNA POLYMERASE II. Although considered a principal component of TRANSCRIPTION FACTOR TFIID it also takes part in general transcription factor complexes involved in RNA POLYMERASE I and RNA POLYMERASE III transcription.

Also Known As:

Networked: 153 relevant articles (0 outcomes, 12 trials/studies)

Bio-Agent Context: Research Results

Experts

1.	Lee-Chen, Guey-Jen: 9 articles (04/2015 - 02/2009)
2.	Chen, Chiung-Mei: 7 articles (12/2014 - 02/2009)
3.	Su, Ming-Tsan: 6 articles (12/2014 - 02/2009)
4.	Lee, Li-Ching: 6 articles (12/2014 - 02/2009)
5.	Hsieh-Li, Hsiu-Mei: 4 articles (12/2014 - 02/2009)
6.	Li, Shihua: 4 articles (01/2014 - 12/2007)
7.	Li, Xiao-Jiang: 4 articles (01/2014 - 12/2007)
8.	Zühlke, Christine: 4 articles (01/2007 - 02/2003)
9.	Lee, Guan-Chiun: 3 articles (04/2015 - 02/2009)
10.	Quadt, Ilja: 3 articles (06/2014 - 11/2002)

Related Diseases

1.	Spinocerebellar Ataxias (Spinocerebellar Ataxia) 06/01/2014 - "Spinocerebellar ataxia type 17 (SCA17) is caused by CAG repeat expansion in the TATA-box binding protein gene. " 07/01/2011 - "Spinocerebellar ataxia type 17 (SCA17) is an autosomal dominant inherited disorder characterized by degeneration of spinocerebellar tracts and selected brainstem neurons owing to the expansion of a CAG repeat of the human TATA-binding protein (hTBP) gene. " 07/01/2011 - "To investigate the pathogenesis of spinocerebellar ataxia 17, we generated a conditional knock-in mouse model that expresses one copy of the mutant TATA box-binding protein gene, which encodes a 105-glutamine repeat, selectively in neuronal cells at the endogenous level. " 02/01/2010 - "A spinocerebellar ataxia family with expanded alleles in the TATA-binding protein gene and ataxin-3 gene." 09/11/2007 - "Spinocerebellar ataxia type 17 (SCA17) is associated with an expansion of CAG/CAA trinucleotide repeats in the gene encoding the TATA-binding protein. "
2.	Infection 06/01/2014 - "Expression and nuclear localization of the TATA-box-binding protein during baculovirus infection." 10/10/2013 - "Upon infection, this phosphorylation is lost, and the activity of MEF2 changes--MEF2 now associates with the TATA binding protein to bind a distinct TATA box sequence and promote antimicrobial peptide expression. " 07/01/1994 - "Characterization of the Spodoptera frugiperda TATA-binding protein: nucleotide sequence and response to baculovirus infection." 01/01/2016 - "Investigation of reference gene expression during human herpesvirus 6B infection indicates peptidylprolyl isomerase A as a stable reference gene and TATA box binding protein as a gene up-regulated by this virus." 11/01/2002 - "Baculovirus infection raises the level of TATA-binding protein that colocalizes with viral DNA replication sites."
3.	Shock 08/01/1999 - "These effects on the promoter are specific, since the mutation does not affect TATA box occupancy or, in the case of HSP82, recruitment of TATA-binding protein to the TATA element or that of heat shock factor to heat shock elements. " 09/15/1993 - "The interaction between the Hsp70 heat shock gene promoter and a Drosophila protein complex which contains the TATA-binding protein depends on sequence-specific interactions located in the region downstream of the transcription start site. " 02/10/2004 - "Phylogenetic analysis of the heat-shock gene hsp82 and the TATA-box-binding protein gene tbp in multiple bdelloid species suggested that for each gene, each copy belonged to one of two lineages that began to diverge before the bdelloid radiation. " 05/01/1995 - "In vivo KMnO4 footprinting reveals that the interaction of the TATA-binding protein (TBP) with this promoter is also modulated: heat shock slightly increases TBP binding to the promoter and this binding is reduced upon recovery from heat shock. " 11/01/2007 - "To test the generality of the yield enhancement, we have investigated the benefits of using approximately 150 fs UV pulses to crosslink TATA-binding protein, glucocorticoid receptor and heat shock factor to oligonucleotides in vitro. "
4.	Huntington Disease (Huntington's Disease) 12/30/2002 - "In this study the distribution and cellular localisation of TATA-binding protein was compared to the distribution and cellular localisation of the huntingtin protein in the middle frontal gyrus of Huntington's disease and neurologically normal subjects. " 12/30/2002 - "Seven different morphological forms of TATA-binding protein-positive structures were detected in Huntington's disease but not in control brain. " 12/30/2002 - "Insoluble TATA-binding protein accumulation in Huntington's disease cortex." 12/30/2002 - "We were therefore interested in testing the hypothesis that TATA-binding protein may play a role in Huntington's disease as it contains an elongated polymorphic polyglutamine stretch that ranges in size from 26 to 42 amino acids in normal individuals. " 01/01/2007 - "Huntington's disease, spinal and bulbar muscular atrophy, and spinocerebellar ataxia 17 (SCA17) are caused by expansions in the polyglutamine (polyQ) repeats in Huntingtin protein (Htt), androgen receptor protein (AR), and TATA-binding protein (TBP), respectively. "
5.	Progressive Myoclonic Epilepsies (Progressive Myoclonic Epilepsy) 08/01/2001 - "In this immunohistochemical study, we showed recruitment of ataxin-2, ataxin-3 and TATA box binding protein (TBP) into NIIs of the pontine neurons of spinocerebellar ataxia type (SCA) 1, SCA2, SCA3 and dentatorubral-pallidoluysian atrophy brains. " 12/01/2000 - "It has been demonstrated that the inclusions in dentatorubral-pallidoluysian atrophy (DRPLA) and Machado-Joseph disease (MJD) were immunopositive for several transcription factors such as TATA-binding protein (TBP), TBP-associated factor (TAF(II)130), Sp1, cAMP-responsive element-binding protein (CREB) and CREB-binding protein, suggesting that neuronal degeneration in polyglutamine diseases may result from nuclear depletion of transcription factors containing the glutamine-rich domain. "

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