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Journal ArticleDOI

Transcriptional regulation by the phosphorylation-dependent factor CREB

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TLDR
The transcription factor CREB functions in glucose homeostasis, growth-factor-dependent cell survival, and has been implicated in learning and memory, and how is specificity achieved in these signalling pathways?
Abstract
The transcription factor CREB -- for 'cyclic AMP response element-binding protein' -- functions in glucose homeostasis, growth-factor-dependent cell survival, and has been implicated in learning and memory. CREB is phosphorylated in response to various signals, but how is specificity achieved in these signalling pathways?

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Citations
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Journal ArticleDOI

Nuclear Redox Signaling

TL;DR: The redox state of the nucleus and several important nuclear redox regulators are introduced more precisely, and their necessity for regulation of transcription factors is emphasized.
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Effect of chronic citalopram on serotonin-related and stress-regulated genes in the dorsal raphe nucleus of the rat

TL;DR: It is demonstrated that in the dorsal raphe nucleus of chronically stressed rats, citalopram normalizes TPH expression and blocks stress effects on distinct genes related to neurotransmitter release and neuroplasticity.
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cAMP response element-binding protein (CREB) and nuclear factor κB mediate the tamoxifen-induced up-regulation of glutamate transporter 1 (GLT-1) in rat astrocytes.

TL;DR: These findings establish that TX regulates GLT-1 via the CREB and NF-κB pathways, which are important for the development of neuroprotectants against excitotoxicity.
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Expression of cyclic adenosine monophosphate response-element binding protein in acute leukemia

TL;DR: It is suggested that CREB expression could be a useful marker for leukemia in patients with acute disease and a role for CREB in leukemogenesis is suggested.
Journal ArticleDOI

Cyclic adenosine 3',5'-monophosphate-elevating agents inhibit transforming growth factor-beta-induced SMAD3/4-dependent transcription via a protein kinase A-dependent mechanism.

TL;DR: It is suggested that suppression of TGF-β/SMAD signaling and resulting gene transactivation by cAMP-inducing agents occurs via PKA-dependent, CREB-mediated, disruption of SMAD–CBP/p300 complexes.
References
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Journal ArticleDOI

Cyclic AMP stimulates somatostatin gene transcription by phosphorylation of CREB at serine 133

TL;DR: Results suggest that phosphorylation of CREB may stimulate transcription by a mechanism other than by simply providing negative charge, as CREB mutants containing acidic residues in place of the Ser-133 phosphoacceptor were also transcriptionally inactive.
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Phosphorylated CREB binds specifically to the nuclear protein CBP

TL;DR: It is proposed that CBP may participate in cAMP-regulated gene expression by interacting with the activated phosphorylated form of CREB, which is activated as a result of phosphorylation by protein kinase A7.
Journal ArticleDOI

Cell survival promoted by the Ras-MAPK signaling pathway by transcription-dependent and -independent mechanisms.

TL;DR: The findings suggest that the MAPK signaling pathway promotes cell survival by a dual mechanism comprising the posttranslational modification and inactivation of a component of the cell death machinery and the increased transcription of pro-survival genes.
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Deficient long-term memory in mice with a targeted mutation of the cAMP-responsive element-binding protein

TL;DR: Consistent with models claiming a role for long-term potentiation (LTP) in memory, LTP in hippocampal slices from CREB mutants decayed to baseline 90 min after tetanic stimulation, however, paired-pulse facilitation and posttetanic potentiation are normal.
Journal ArticleDOI

Nuclear protein CBP is a coactivator for the transcription factor CREB

TL;DR: Fluorescence anisotropy measurements are used to define the equi-librium binding parameters of the phosphoCREB:CBP interaction and report here that CBP can activate transcription through a region in its carboxy terminus.
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