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 EBV transcription factor EB1, is a key determinant of the switch from the latent infection to the lytic cycle. EB1 belongs to the Jun, Fos, ATF, CREB, C/EBP and GCN4 family of proteins, carrying a sequence-specific DNA-binding domain called "basic-Zipper" (bZIP). The N-terminal region of EB1 is required for transcriptional activation, whereas the C-terminal region contains the DNA-binding domain. The mechanism by which site-specific transcription factors increase specific initiation at polymerase II dependent promoters is thought to occur via recruitment and stabilization of components that form the initiation complex, i.e., TFIID, TFIIA, TFIIB, TFIIE, TFIIG, TFIIH, TFIIJ and pol II. TFIID is not a single protein but consists of the TATA-binding protein TBP plus several distinct and tightly associated proteins called TAFs. More specifically, in vitro studies have revealed that the TAFs are not required for basal transcription, but are essential for mediating regulated transcription by different upstream activators. TFIID binding at the promoter sites is one of the limiting steps in the assembly of the initiation complex. Direct interactions with TBP or with one or several TAFs, mediated by the activation domain of site specific activators, could influence the binding rate of TFIID, and thus provide one of the mechanisms by which transcription is regulated. We show here that EB1 interacts directly with TBP in vitro, and that it is the bZIP domain, likely the region contacting the DNA rather than the activation domain, which is required for physical contact between EB1 and TBP.
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PMID:The bZIP motif of the Epstein-Barr virus (EBV) transcription factor EB1 mediates a direct interaction with TBP. 808 22

We report the characterization of lambda and P1 phage clones containing the entire human mitochondrial 3-hydroxy-3-methylglutaryl CoA synthase (mHS) gene. The human mHS locus (HMGCS2) on chromosome 1p12-13 spans 25 kb and contains 10 exons. Exon 1 contains most of the mitochondrial leader, consistent with a recent hypothesis of the evolution of the ketogenic pathway. By primer extension and cDNA amplification (RACE-PCR) we localized the transcription start point (tsp) to 60 bp upstream of the initiation codon. Nine blocks of conserved sequence were identified by comparing the 5' flanking regions of the mHS genes of human and rat. The 5' flanking region contains potential binding sites for TATA-binding protein, Sp1, nuclear factor 1 (NF1), CAAT-box binding protein (C/EBP), hepatocyte nuclear factors 1 and 5 (HNF1, HNF5) and activator proteins 1 and 2 (AP1, AP2).
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PMID:Cloning and characterization of the human mitochondrial 3-hydroxy-3-methylglutaryl CoA synthase gene. 930 55

Direct interaction between bacteria and epithelial cells may initiate or amplify the airway response through induction of epithelial defense gene expression by nuclear factor-kappaB (NF-kappaB). However, multiple signaling pathways modify NF-kappaB effects to modulate gene expression. In this study, the effects of CCAAT/enhancer binding protein (C/EBP) family members on induction of the leukocyte adhesion glycoprotein intercellular adhesion molecule-1 (ICAM-1) was examined in primary cultures of human tracheobronchial epithelial cells incubated with nontypeable Haemophilus influenzae. Increased ICAM-1 gene transcription in response to H. influenzae required gene sequences located at -200 to -135 in the 5'-flanking region that contain a C/EBP-binding sequence immediately upstream of the NF-kappaB enhancer site. Constitutive C/EBPbeta was found to have an important role in epithelial cell ICAM-1 regulation, while the adjacent NF-kappaB sequence binds the RelA/p65 and NF-kappaB1/p50 members of the NF-kappaB family to induce ICAM-1 expression in response to H. influenzae. The expression of C/EBP proteins is not regulated by p38 mitogen-activated protein kinase activation, but p38 affects gene transcription by increasing the binding of TATA-binding protein to TATA-box-containing gene sequences. Epithelial cell ICAM-1 expression in response to H. influenzae was decreased by expressing dominant-negative protein or RNA interference against C/EBPbeta, confirming its role in ICAM-1 regulation. Although airway epithelial cells express multiple constitutive and inducible C/EBP family members that bind C/EBP sequences, the results indicate that C/EBPbeta plays a central role in modulation of NF-kappaB-dependent defense gene expression in human airway epithelial cells after exposure to H. influenzae.
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PMID:Regulation of bacteria-induced intercellular adhesion molecule-1 by CCAAT/enhancer binding proteins. 1870 96