CREB is a key regulator of striatal vulnerability in chemical and genetic models of Huntington's disease. - Wikidata - awgldk - TriplyDB

CREB is a key regulator of striatal vulnerability in chemical and genetic models of Huntington's disease.

CREB is a key regulator of striatal vulnerability in chemical and genetic models of Huntington's disease.

http://www.wikidata.org/entity/Q33908482

about

Phosphodiesterase Inhibition and Regulation of Dopaminergic Frontal and Striatal Functioning: Clinical Implications Genome-wide loss of 5-hmC is a novel epigenetic feature of Huntington's disease Neuroprotective effect of caffeic acid phenethyl ester in 3-nitropropionic acid-induced striatal neurotoxicity When cytokinin, a plant hormone, meets the adenosine A2A receptor: a novel neuroprotectant and lead for treating neurodegenerative disorders?Preclinical and clinical investigations of mood stabilizers for Huntington's disease: what have we learned?Mitogen- and stress-activated protein kinase 1-induced neuroprotection in Huntington's disease: role on chromatin remodeling at the PGC-1-alpha promoter.Transcription, epigenetics and ameliorative strategies in Huntington's Disease: a genome-wide perspective Reduction in subventricular zone-derived olfactory bulb neurogenesis in a rat model of Huntington's disease is accompanied by striatal invasion of neuroblasts.miR-196a Ameliorates Cytotoxicity and Cellular Phenotype in Transgenic Huntington's Disease Monkey Neural Cells Transducer of regulated CREB-binding proteins (TORCs) transcription and function is impaired in Huntington's disease.Acetyltransferases (HATs) as targets for neurological therapeutics CREB: a multifaceted regulator of neuronal plasticity and protection.Lysine acetyltransferases CBP and p300 as therapeutic targets in cognitive and neurodegenerative disorders.Adenyl cyclase activator forskolin protects against Huntington's disease-like neurodegenerative disorders.CREB influences timing and entrainment of the SCN circadian clock TAK-063, a Novel Phosphodiesterase 10A Inhibitor, Protects from Striatal Neurodegeneration and Ameliorates Behavioral Deficits in the R6/2 Mouse Model of Huntington's Disease.Ultrastructural and transcriptional profiling of neuropathological misregulation of CREB function.Transcriptional Dysregulation and Post-translational Modifications in Polyglutamine Diseases: From Pathogenesis to Potential Therapeutic Strategies.Large-scale transcriptomic analysis reveals that pridopidine reverses aberrant gene expression and activates neuroprotective pathways in the YAC128 HD mouse.

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P2860

CREB is a key regulator of striatal vulnerability in chemical and genetic models of Huntington's disease.

http://www.wikidata.org/entity/Q33908482

description

2009 nî lūn-bûn

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2009 թուականի Յուլիսին հրատարակուած գիտական յօդուած

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2009 թվականի հուլիսին հրատարակված գիտական հոդված

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2009年の論文

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2009年論文

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2009年論文

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2009年論文

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2009年論文

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2009年論文

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2009年论文

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name

CREB is a key regulator of str ...... odels of Huntington's disease.

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CREB is a key regulator of str ...... odels of Huntington's disease.

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CREB is a key regulator of str ...... odels of Huntington's disease.

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CREB is a key regulator of str ...... odels of Huntington's disease.

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CREB is a key regulator of str ...... odels of Huntington's disease.

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CREB is a key regulator of str ...... odels of Huntington's disease.

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P356

J.NBD.2009.07.014

P1433

Neurobiology of Disease

P1476

CREB is a key regulator of str ...... odels of Huntington's disease.

@en

P2093

Boyoung Lee

http://www.w3.org/2001/XMLSchema#string

Hee-Yeon Cho

http://www.w3.org/2001/XMLSchema#string

Iza B Reyes

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Karl Obrietan

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Takaomi C Saido

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Xin-An Pu

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Yun-Sik Choi

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P2860

Mitochondrial cyclic AMP response element-binding protein (CREB) mediates mitochondrial gene expression and neuronal survival

Suppression of reactive oxygen species and neurodegeneration by the PGC-1 transcriptional coactivators

Control of memory formation through regulated expression of a CaMKII transgene

A dominant-negative inhibitor of CREB reveals that it is a general mediator of stimulus-dependent transcription of c-fos

The CREB/CRE transcriptional pathway: protection against oxidative stress-mediated neuronal cell death

Disruption of CREB function in brain leads to neurodegeneration.

Apoptosis in neurodegenerative disorders.

Ca2+ influx regulates BDNF transcription by a CREB family transcription factor-dependent mechanism.

Predictive testing for Huntington disease: interpretation and significance of intermediate alleles.

cAMP response element-binding protein-mediated gene expression increases the intrinsic excitability of CA1 pyramidal neurons.

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259-268

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scholarly article

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10.1016/J.NBD.2009.07.014

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2

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36

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2009-07-24T00:00:00Z

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26695455

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19632326

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P921

corpus striatum

Huntington disease

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2884277

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