Dysfunction of the CNS-heart axis in mouse models of Huntington's disease. - Wikidata - awgldk - TriplyDB

Dysfunction of the CNS-heart axis in mouse models of Huntington's disease.

Dysfunction of the CNS-heart axis in mouse models of Huntington's disease.

http://www.wikidata.org/entity/Q35220835

about

CRISPR/Cas9: a powerful genetic engineering tool for establishing large animal models of neurodegenerative diseases Developing stem cell therapies for juvenile and adult-onset Huntington's disease HDAC4-myogenin axis as an important marker of HD-related skeletal muscle atrophy CLIP-GENE: a web service of the condition specific context-laid integrative analysis for gene prioritization in mouse TF knockout experiments.High-resolution respirometry of fine-needle muscle biopsies in pre-manifest Huntington's disease expansion mutation carriers shows normal mitochondrial respiratory function.The pathogenic exon 1 HTT protein is produced by incomplete splicing in Huntington's disease patients Neurocardiovascular deficits in the Q175 mouse model of Huntington's disease.Early transcriptional alteration of histone deacetylases in a murine model of doxorubicin-induced cardiomyopathy.The Huntington's disease-related cardiomyopathy prevents a hypertrophic response in the R6/2 mouse model.Skeletal muscle pathology in Huntington's disease Cardiac Dysfunction in the BACHD Mouse Model of Huntington's Disease.SIRT1 Activity Is Linked to Its Brain Region-Specific Phosphorylation and Is Impaired in Huntington's Disease Mice.Longitudinal in vivo MRI in a Huntington's disease mouse model: Global atrophy in the absence of white matter microstructural damage.Correlations of Behavioral Deficits with Brain Pathology Assessed through Longitudinal MRI and Histopathology in the HdhQ150/Q150 Mouse Model of Huntington's Disease.Non-Hsp genes are essential for HSF1-mediated maintenance of whole body homeostasis.Impaired Nitric Oxide Mediated Vasodilation In The Peripheral Circulation In The R6/2 Mouse Model Of Huntington's Disease Frequency of nuclear mutant huntingtin inclusion formation in neurons and glia is cell-type-specific.Transcriptional Signature of an Altered Purine Metabolism in the Skeletal Muscle of a Huntington's Disease Mouse Model HDAC4 as a potential therapeutic target in neurodegenerative diseases: a summary of recent achievements Exogenous GDF11 induces cardiac and skeletal muscle dysfunction and wasting.Huntington's disease is a multi-system disorder.Motor phenotype is not associated with vascular dysfunction in symptomatic Huntington's disease transgenic R6/2 (160 CAG) mice HSF1-dependent and -independent regulation of the mammalian in vivo heat shock response and its impairment in Huntington's disease mouse models.A shared mechanism of muscle wasting in cancer and Huntington's disease.Allele-Specific Reduction of the Mutant Huntingtin Allele Using Transcription Activator-Like Effectors in Human Huntington's Disease Fibroblasts.Changes in cardiac nucleotide metabolism in Huntington's disease.Cardiac Fas-Dependent and Mitochondria-Dependent Apoptotic Pathways in a Transgenic Mouse Model of Huntington's Disease.Integrated genomics and proteomics define huntingtin CAG length-dependent networks in mice.Myostatin inhibition prevents skeletal muscle pathophysiology in Huntington's disease mice.Cardiac mTORC1 Dysregulation Impacts Stress Adaptation and Survival in Huntington's Disease.Neuro-Cardio Mechanisms in Huntington's Disease and Other Neurodegenerative Disorders.

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Dysfunction of the CNS-heart axis in mouse models of Huntington's disease.

http://www.wikidata.org/entity/Q35220835

description

2014 nî lūn-bûn

@nan

2014 թուականի Օգոստոսին հրատարակուած գիտական յօդուած

@hyw

2014 թվականի օգոստոսին հրատարակված գիտական հոդված

@hy

2014年の論文

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2014年論文

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2014年論文

@zh-hant

2014年論文

@zh-hk

2014年論文

@zh-mo

2014年論文

@zh-tw

2014年论文

@wuu

name

Dysfunction of the CNS-heart axis in mouse models of Huntington's disease.

@ast

Dysfunction of the CNS-heart axis in mouse models of Huntington's disease.

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type

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Dysfunction of the CNS-heart axis in mouse models of Huntington's disease.

@ast

Dysfunction of the CNS-heart axis in mouse models of Huntington's disease.

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prefLabel

Dysfunction of the CNS-heart axis in mouse models of Huntington's disease.

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Dysfunction of the CNS-heart axis in mouse models of Huntington's disease.

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JOURNAL.PGEN.1004550

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Dysfunction of the CNS-heart axis in mouse models of Huntington's disease.

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Andrea Protti

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Donna L Smith

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Georgina F Osborne

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Ivan Rattray

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Jim Rosinski

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Linda Inuabasi

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Marie K Bondulich

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Sophie A Franklin

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Thomas Muller

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P2860

Differential expression analysis for sequence count data

WGCNA: an R package for weighted correlation network analysis

SAHA decreases HDAC 2 and 4 levels in vivo and improves molecular phenotypes in the R6/2 mouse model of Huntington's disease

Huntington's disease induced cardiac amyloidosis is reversed by modulating protein folding and oxidative stress pathways in the Drosophila heart

Systematic and integrative analysis of large gene lists using DAVID bioinformatics resources

The hunt for huntingtin function: interaction partners tell many different stories

Formation of neuronal intranuclear inclusions underlies the neurological dysfunction in mice transgenic for the HD mutation

Arrhythmia and cardiac defects are a feature of spinal muscular atrophy model mice.

Conduction slowing and sudden arrhythmic death in mice with cardiac-restricted inactivation of connexin43

Neurological abnormalities in a knock-in mouse model of Huntington's disease

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8

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10

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Andreas Neueder

Michal Mielcarek

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2014-08-07T00:00:00Z

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264633935

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25101683

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Huntington disease

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4125112

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