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HIV-1 Tat specific factor 1

The protein encoded by this gene functions as a cofactor for the stimulation of transcriptional elongation by HIV-1 Tat, which binds to the HIV-1 promoter through Tat-TAR interaction. This protein may also serve as a dual-function factor to couple transcription and splicing and to facilitate their reciprocal activation. Alternatively spliced transcript variants have been found for this gene.[provided by RefSeq, Sep 2009] (from NCBI)
Top mentioned proteins: SF-1, POLYMERASE, CAN, TAK, Spt5
Papers on Tat-SF1
Impact of sustained RNAi-mediated suppression of cellular cofactor Tat-SF1 on HIV-1 replication in CD4+ T cells.
Weinberg et al., Johannesburg, South Africa. In Virol J, 2011
Cellular Tat-SF1 has long been ascribed a cofactor role in Tat-dependent transactivation of viral transcription elongation.
Identification of Tat-SF1 cellular targets by exon array analysis reveals dual roles in transcription and splicing.
Garcia-Blanco et al., Durham, United States. In Rna, 2011
these findings suggest that Tat-SF1 functions independently in transcription and splicing of cellular genes.
An investigation of a role for U2 snRNP spliceosomal components in regulating transcription.
Johnson et al., San Diego, United States. In Plos One, 2010
Previous studies have implicated the mammalian spliceosomal U2 snRNP as having a novel role in stimulating transcriptional elongation in vitro through interactions with the elongation factors P-TEFb and Tat-SF1; however, the mechanism remains unknown [1].
The transcriptional transactivator Tat selectively regulates viral splicing.
Caputi et al., Boca Raton, United States. In Nucleic Acids Res, 2010
We used a series of HIV-1 reporter minigenes to demonstrate that Tat's role in splicing is dependent on the cellular co-transcriptional splicing activators Tat-SF1 and CA150.
DSIF, the Paf1 complex, and Tat-SF1 have nonredundant, cooperative roles in RNA polymerase II elongation.
Handa et al., Yokohama, Japan. In Genes Dev, 2010
We show that the Paf1 complex (Paf1C) and Tat-SF1, two factors implicated previously in elongation control, collaborate with DSIF to facilitate efficient elongation.
Tat-SF1 is not required for Tat transactivation but does regulate the relative levels of unspliced and spliced HIV-1 RNAs.
Garcia-Blanco et al., Durham, United States. In Plos One, 2008
Tat-SF1 is not required for regulating HIV-1 transcription, but is required for maintaining the ratios of different classes of HIV-1 transcripts.
An influenza virus replicon system in yeast identified Tat-SF1 as a stimulatory host factor for viral RNA synthesis.
Nagata et al., Tsukuba, Japan. In Proc Natl Acad Sci U S A, 2007
We found that among them, Tat-SF1, a mammalian homologue of yeast CUS2, was a stimulatory host factor in influenza virus RNA synthesis.
Combined high-resolution array-based comparative genomic hybridization and expression profiling of ETV6/RUNX1-positive acute lymphoblastic leukemias reveal a high incidence of cryptic Xq duplications and identify several putative target genes within the commonly gained region.
Fioretos et al., Lund, Sweden. In Leukemia, 2007
By studying the expression profile and the proposed function of genes in the minimally gained region, several candidate target genes (SPANXB, HMGB3, FAM50A, HTATSF1 and RAP2C) were identified.
Intracellular HIV-1 Tat protein represses constitutive LMP2 transcription increasing proteasome activity by interfering with the binding of IRF-1 to STAT1.
Battistini et al., Roma, Italy. In Biochem J, 2006
Intracellular HIV-1 Tat protein represses constitutive LMP2 transcription increasing proteasome activity by interfering with the binding of IRF-1 to STAT1
Soluble HIV-1 gp120 enhances HIV-1 replication in non-dividing CD4+ T cells, mediated via cell signaling and Tat cofactor overexpression.
Veas et al., Montpellier, France. In Aids, 2005
Moreover, rgp120 enhances the gene, as well as protein expression of the cellular Tat cofactors Tat-Sf1 and SPT5 in primary CD4+/CXCR4+ T cells.
Coordination of transcription factor phosphorylation and histone methylation by the P-TEFb kinase during human immunodeficiency virus type 1 transcription.
Kumar et al., Washington, D.C., United States. In J Virol, 2004
phosphorylated by P-TEFb kinase during HIV-1 transcription in Tat/TAR dependent manner
FF domains of CA150 bind transcription and splicing factors through multiple weak interactions.
Pawson et al., Toronto, Canada. In Mol Cell Biol, 2004
Using mass spectrometry, we identify a number of nuclear binding partners for the CA150 FF domains and demonstrate a direct interaction between CA150 and Tat-SF1, a protein involved in the coupling of splicing and transcription.
p54(nrb) associates with the 5' splice site within large transcription/splicing complexes.
Konarska et al., New York City, United States. In Embo J, 2004
These RNAPIIO-snRNP complexes also contain other transcription/splicing factors, such as PSF and TLS, as well as transcription factors that interact with RNAPIIO during elongation, including P-TEFb, TAT-SF1 and TFIIF.
Proliferation inhibition of astrocytes, neurons, and non-glial cells by intracellularly expressed human immunodeficiency virus type 1 (HIV-1) Tat protein.
He et al., Indianapolis, United States. In Neurosci Lett, 2004
These results support the notion that Tat-induced neuropathogenesis is mediated by multiple mechanisms involving both intracellular and extracellular Tat protein.
Stimulatory effect of splicing factors on transcriptional elongation.
Zhou et al., Berkeley, United States. In Nature, 2002
The spliceosomal U small nuclear ribonucleoproteins (snRNPs) interact with human transcription elongation factor TAT-SF1 (refs 6,7,8,9) and strongly stimulate polymerase elongation when directed to an intron-free human immunodeficiency virus-1 (HIV-1) template.
Nef triggers a transcriptional program in T cells imitating single-signal T cell activation and inducing HIV virulence mediators.
McMichael et al., Oxford, United Kingdom. In Immunity, 2001
In contrast, Nef exclusively upregulates factors positively regulating HIV, including Tat-SF1, U1 SNRNP, and IRF-2.
Tat-SF1: cofactor for stimulation of transcriptional elongation by HIV-1 Tat.
Sharp et al., Cambridge, United States. In Science, 1996
Tat may stimulate transcriptional elongation by recruitment of a complex containing Tat-SF1 and a kinase to the human immunodeficiency virus-type 1 (HIV-1) promoter through a Tat-TAR interaction.
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