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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

Function and Regulation of CREB Family Transcription Factors in the Nervous System

TL;DR: This review focuses on the current level of understanding of where, when, and how CREB family members function in the nervous system.
Journal ArticleDOI

Transcriptional Paradigms in Mammalian Mitochondrial Biogenesis and Function

TL;DR: These transcriptional paradigms provide a basic framework for understanding the integration of mitochondrial biogenesis and function with signaling events that dictate cell- and tissue-specific energetic properties.
Journal ArticleDOI

Synaptic versus extrasynaptic NMDA receptor signalling: implications for neurodegenerative disorders

TL;DR: Perturbations in the balance between synaptic and extrasynaptic NMDAR activity contribute to neuronal dysfunction in acute ischaemia and Huntington's disease, and could be a common theme in the aetiology of neurodegenerative diseases.
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Astrocyte-Neuron Lactate Transport Is Required for Long-Term Memory Formation

TL;DR: It is concluded that astrocyte-neuron lactate transport is required for long-term memory formation, suggesting that lactate import into neurons is necessary for long -term memory.
Journal ArticleDOI

The many faces of CREB

TL;DR: Emerging evidence suggests that strategies that exploit regional differences in upstream factors or that target specific CREB-regulated genes, rather than CREB itself, could make a promising contribution to the treatment of neuropsychiatric conditions.
References
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Journal ArticleDOI

Activation of cAMP and mitogen responsive genes relies on a common nuclear factor

TL;DR: It is reported here that micro-injection of an anti-CBP antiserum into fibroblasts can inhibit transcription from a cAMP responsive promoter, and proposed that CBP is recruited to the promoter through interaction with certain phosphorylated factors, and may thus play a critical role in the transmission of inductive signals from cell surface receptor to the transcriptional apparatus.
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Differential activation of CREB by Ca2+/calmodulin-dependent protein kinases type II and type IV involves phosphorylation of a site that negatively regulates activity.

TL;DR: Evidence is provided for a new mechanism for regulation of CREB activity involving phosphorylation of a negative regulatory site in the transcriptional activation domain and new insights are provided into possible interactions between the cAMP and Ca2+ signaling pathways in the regulation of transcription.
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Nerve growth factor activates a Ras-dependent protein kinase that stimulates c-fos transcription via phosphorylation of CREB

TL;DR: Findings suggest that CREB has a more widespread function than previously believed and functions in the nucleus as a general mediator of growth factor responses.
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Solution structure of the KIX domain of CBP bound to the transactivation domain of CREB: a model for activator:coactivator interactions.

TL;DR: The solution structure of the complex formed by the phosphorylated kinase-inducible domain (pKID) of CREB with KIX reveals that pKID undergoes a coil-->helix folding transition upon binding to KIX, forming two alpha helices.
Journal ArticleDOI

Cyclic AMP-responsive DNA-binding protein: structure based on a cloned placental cDNA.

TL;DR: The putative DNA-binding domain of CREB is structurally similar to the corresponding domains in the phorbol ester-responsive c-jun protein and the yeast transcription factor GCN4.
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