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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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Epigenetic treatments of adult rats promote recovery from visual acuity deficits induced by long-term monocular deprivation.

TL;DR: It is found that chronic intraperitoneal administration of valproic acid or sodium butyrate to long‐term monocularly deprived adult rats coupled with reverse lid‐suturing caused a complete recovery of visual acuity.
Journal ArticleDOI

CREB is a critical regulator of normal hematopoiesis and leukemogenesis.

TL;DR: It is shown that cAMP-responsive element binding protein (CREB) is most highly expressed in lineage negative hematopoietic stem cells (HSCs), suggesting that CREB is critical for normal myelopoiesis and leukemia cell proliferation.
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Proatherogenic abnormalities of lipid metabolism in SirT1 transgenic mice are mediated through Creb deacetylation.

TL;DR: It is proposed that SirT1-dependent Creb deacetylation regulates the balance between glucose and lipid metabolism, integrating fasting signals.
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Neurological Enhancement Effects of Melatonin against Brain Injury-Induced Oxidative Stress, Neuroinflammation, and Neurodegeneration via AMPK/CREB Signaling

TL;DR: It is demonstrated that traumatic brain injury (TBI) evokes oxidative stress, disrupts brain energy homeostasis, and boosts neuroinflammation, which further contributes to neuronal degeneration and cognitive dysfunction in the mouse brain, and that melatonin treatment overcomes energy depletion and protects against brain damage via the regulation of p-AMPK/p-CREB signaling pathways.
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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