Cyclic Amp Response Element Binding Protein
Mostrando 1-12 de 141 artigos, teses e dissertações.
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1. Vias intracelulares da ação do Sildenafil no diabetes insipidus induzido pelo lítio / Sildenafil action in lithium-induced NDI: intracellular pathway
Patients taking lithium to treat bipolar disorder often present polyuria and urinary concentrating defect. In addition, lithium-treated animals present lower cyclic adenosine monophosphate production in response to vasopressin. Sildenafil (Sil), a phosphodiesterase 5 (PDE5) inhibitor, elevates intracellular cyclic guanosine monophosphate (cGMP) levels, leadi
IBICT - Instituto Brasileiro de Informação em Ciência e Tecnologia. Publicado em: 13/06/2012
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2. The amino terminus of Tax is required for interaction with the cyclic AMP response element binding protein.
Tax of human T-cell leukemia virus type 1 was analyzed for interaction with the cyclic AMP response element binding protein (CREB) in vitro with and without Tax response element DNA. Mutations in the carboxy terminus of Tax (L296G and L320G) did not affect binding to CREB and led to supershifts. In contrast, mutants with changes in the amino-terminal cystein
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3. The cAMP response element binding protein, CREB, is a potent inhibitor of diverse transcriptional activators.
Cyclic AMP response element binding protein (CREB) activates transcription of cAMP response element (CRE)-containing promoters following an elevation of intracellular cAMP. Here we show that CREB and the highly related protein ATF-1 are also potent transcription inhibitors. Strikingly, CREB inhibits transcription of multiple activators, whose DNA-binding dom
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4. Cyclic AMP response element binding protein CREB and modulator protein CREM are products of distinct genes.
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5. Transcription from a murine T-cell receptor V beta promoter depends on a conserved decamer motif similar to the cyclic AMP response element.
We identified a regulatory region of the murine V beta promoter by both in vivo and in vitro analyses. The results of transient transfection assays indicated that the dominant transcription-activating element within the V beta 8.3 promoter is the palindromic motif identified previously as the conserved V beta decamer. Elimination of this element, by linear d
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6. A small molecule inhibitor of β-catenin/cyclic AMP response element-binding protein transcription
Inherited and somatic mutations in the adenomatous polyposis coli occur in most colon cancers, leading to activation of β-catenin-responsive genes. To identify small molecule antagonists of this pathway, we challenged transformed colorectal cells with a secondary structure-templated chemical library, looking for compounds that inhibit a β-catenin-responsiv
National Academy of Sciences.
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7. Induction of a cyclic AMP-responsive gene in living cells requires the nuclear factor CREB.
We constructed cell lines containing various enhancer elements cloned upstream from a marker gene. By microinjection of specific antibodies directed against transcriptional activator proteins into these cell lines, we have developed a functional assay for factors which regulate the activity of target promoters. Here we show that microinjection of a highly sp
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8. Doxorubicin-induced Id2A gene transcription is targeted at an activating transcription factor/cyclic AMP response element motif through novel mechanisms involving protein kinases distinct from protein kinase C and protein kinase A.
We have recently shown that doxorubicin (Dox), an antineoplastic drug and an inhibitor of terminal differentiation of myogenic and adipogenic cells, induces expression of Id, a gene encoding a helix-loop-helix transcriptional inhibitor. In this study we have investigated the molecular mechanisms underlying Dox-induced Id2A expression. We have also attempted
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9. A cDNA for a human cyclic AMP response element-binding protein which is distinct from CREB and expressed preferentially in brain.
The cyclic AMP response element (CRE) is found in many cellular genes regulated by cyclic AMP, and similar elements are present in the early genes of adenovirus that are activated by E1A. The transcription factor CREB has previously been shown to bind this site, and cDNAs for CREB have recently been characterized. We report here the isolation of a cDNA encod
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10. Cyclic AMP response element-binding protein and the catalytic subunit of protein kinase A are present in F9 embryonal carcinoma cells but are unable to activate the somatostatin promoter.
The cyclic AMP (cAMP) response elements (CREs) of the somatostatin and vasoactive intestinal peptide (VIP) promoters contain binding sites for CRE-binding protein (CREB) that are essential for cAMP-regulated transcription. Using F9 embryonal carcinoma cells, we show that the somatostatin and VIP promoters exhibit a differentiation-dependent cAMP response, de
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11. Nuclear localization of v-Abl leads to complex formation with cyclic AMP response element (CRE)-binding protein and transactivation through CRE motifs.
Deregulated expression of v-abl and BCR/abl genes has been associated with myeloproliferative syndromes and myelodysplasia, both of which can progress to acute leukemia. These studies identify the localization of the oncogenic form of the abl gene product encoded by the Abelson murine leukemia virus in the nuclei of myeloid cells and the association of the v
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12. Multiple regulatory elements in the interleukin-6 gene mediate induction by prostaglandins, cyclic AMP, and lipopolysaccharide.
Induction of interleukin-6 (IL-6) gene expression is mediated by numerous agents involving all major signal transduction pathways. We have compared the effects of prostaglandins and their second messenger cyclic AMP (cAMP) with the effect of lipopolysaccharide (LPS) on IL-6 gene expression. We demonstrate that secretion of IL-6 is induced by cAMP in murine m