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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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Perinatal brain injury and regulation of transcription.

TL;DR: Investigation of the transcriptional mechanisms of neuro-survival is likely to reveal other novel transcription factors whose activation by small molecules or drugs will complement current medication in activating the salutary gene program.
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Distinct mechanisms of regulation by Ca2+/calmodulin of type 1 and 8 adenylyl cyclases support their different physiological roles.

TL;DR: Different patterns of regulation and Ca2+ dependence of AC1 and AC8 seems to emanate from their mode of regulation by CaM, which may contribute significantly to the divergent physiological roles in which these ACs have been implicated.
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Capsaicin ameliorates stress-induced Alzheimer's disease-like pathological and cognitive impairments in rats.

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High-Throughput Proteomics Reveals the Unicellular Roots of Animal Phosphosignaling and Cell Differentiation.

TL;DR: It is shown that life-cycle transitions are linked to extensive proteome and phosphoproteome remodeling and that they affect key genes involved in animal multicellularity, such as transcription factors and tyrosine kinases.
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Gene expression induced by drugs of abuse

TL;DR: It is now important to identify which of these changes are causally related to the compulsive behavior associated with drug addiction, and which are non-specific changes related to general features of arousal or other physiological responses (e.g. stress, altered body temperature or energy metabolism).
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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