AT1 blockade abolishes left ventricular hypertrophy in heterozygous cMyBP-C null mice: role of FHL1.

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http://www.wikidata.org/entity/Q51060626

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2013 nî lūn-bûn

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2013年の論文

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2013年学术文章

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2013年学术文章

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2013年学术文章

@zh-cn

2013年学术文章

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2013年学术文章

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2013年学术文章

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2013年學術文章

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2013年學術文章

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AT1 blockade abolishes left ve ...... yBP-C null mice: role of FHL1.

@en

AT1 blockade abolishes left ve ...... yBP-C null mice: role of FHL1.

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type

Item

label

AT1 blockade abolishes left ve ...... yBP-C null mice: role of FHL1.

@en

AT1 blockade abolishes left ve ...... yBP-C null mice: role of FHL1.

@nl

prefLabel

AT1 blockade abolishes left ve ...... yBP-C null mice: role of FHL1.

@en

AT1 blockade abolishes left ve ...... yBP-C null mice: role of FHL1.

@nl

P1476

AT1 blockade abolishes left ve ...... MyBP-C null mice: role of FHL1

@en

P2093

Charlotte Blard

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Claude Delcayre

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

Feriel Azibani

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

Lucie Carrier

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

Lucien Sambin

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Saskia Schlossarek

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P2860

Novel splice donor site mutation in the cardiac myosin-binding protein-C gene in familial hypertrophic cardiomyopathy. Characterization Of cardiac transcript and protein

Extracellular signal-regulated kinase 2 interacts with and is negatively regulated by the LIM-only protein FHL2 in cardiomyocytes

Expression profiling of cardiac genes in human hypertrophic cardiomyopathy: insight into the pathogenesis of phenotypes

A newly created splice donor site in exon 25 of the MyBP-C gene is responsible for inherited hypertrophic cardiomyopathy with incomplete disease penetrance

Hypertrophic cardiomyopathy: distribution of disease genes, spectrum of mutations, and implications for a molecular diagnosis strategy

Subcellular targeting of metabolic enzymes to titin in heart muscle may be mediated by DRAL/FHL-2

Cardiac myosin-binding protein C mutations and hypertrophic cardiomyopathy: haploinsufficiency, deranged phosphorylation, and cardiomyocyte dysfunction

Impairment of the ubiquitin-proteasome system by truncated cardiac myosin binding protein C mutants

Cardiac myosin-binding protein C is required for complete relaxation in intact myocytes

Nonsense-mediated mRNA decay and ubiquitin-proteasome system regulate cardiac myosin-binding protein C mutant levels in cardiomyopathic mice

P304

249-256

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P31

scholarly article

P356

10.1111/FCP.12031

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P433

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

P478

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P50

Jin Bo Su

Philippe Le Corvoisier

Luc Hittinger

N Vignier

P577

2013-04-18T00:00:00Z

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P5875

236249475

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P698

23600722

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