Desmin-related cardiomyopathy in transgenic mice: a cardiac amyloidosis. - Wikidata - awgldk - TriplyDB

Desmin-related cardiomyopathy in transgenic mice: a cardiac amyloidosis.

Desmin-related cardiomyopathy in transgenic mice: a cardiac amyloidosis.

http://www.wikidata.org/entity/Q35971521

about

Formation of soluble amyloid oligomers and amyloid fibrils by the multifunctional protein vitronectin Role for the Unfolded Protein Response in Heart Disease and Cardiac Arrhythmias New Insights in the Diagnosis and Treatment of Heart Failure Functional Amyloid Signaling via the Inflammasome, Necrosome, and Signalosome: New Therapeutic Targets in Heart Failure Role of heat shock proteins in stem cell behavior The ubiquitin-proteasome system and cardiovascular disease Neuropathy- and myopathy-associated mutations in human small heat shock proteins: Characteristics and evolutionary history of the mutation sites Huntington's disease induced cardiac amyloidosis is reversed by modulating protein folding and oxidative stress pathways in the Drosophila heart Priming the proteasome by protein kinase G: a novel cardioprotective mechanism of sildenafil Protein quality control and metabolism: bidirectional control in the heart Ubiquitin proteasome dysfunction in human hypertrophic and dilated cardiomyopathies Hold me tight: Role of the heat shock protein family of chaperones in cardiac disease Proteotoxicity: an underappreciated pathology in cardiac disease Cardiomyocyte-Specific Human Bcl2-Associated Anthanogene 3 P209L Expression Induces Mitochondrial Fragmentation, Bcl2-Associated Anthanogene 3 Haploinsufficiency, and Activates p38 Signaling Screening for toxic amyloid in yeast exemplifies the role of alternative pathway responsible for cytotoxicity Cardioprotective effect of nicorandil, a mitochondrial ATP-sensitive potassium channel opener, prolongs survival in HSPB5 R120G transgenic mice The specificity of the interaction between αB-crystallin and desmin filaments and its impact on filament aggregation and cell viability.Protective effect of geranylgeranylacetone via enhancement of HSPB8 induction in desmin-related cardiomyopathy.The ubiquitin-proteasome system in cardiac proteinopathy: a quality control perspective.Proteasomal and lysosomal protein degradation and heart disease.Evidence for proteotoxicity in beta cells in type 2 diabetes: toxic islet amyloid polypeptide oligomers form intracellularly in the secretory pathway.Genetic causes of human heart failure.Autophagy and the ubiquitin-proteasome system in cardiac dysfunction.Soluble and mature amyloid fibrils in drusen deposits Contesting the dogma of an age-related heat shock response impairment: implications for cardiac-specific age-related disorders.The ubiquitin proteasome system in human cardiomyopathies and heart failure.BAG3 directly interacts with mutated alphaB-crystallin to suppress its aggregation and toxicity.Manipulation of death pathways in desmin-related cardiomyopathy Proteomic profiling of endothelin-1-stimulated hypertrophic cardiomyocytes reveals the increase of four different desmin species and alpha-B-crystallin.Reversal of amyloid-induced heart disease in desmin-related cardiomyopathy.Human alpha B-crystallin mutation causes oxido-reductive stress and protein aggregation cardiomyopathy in mice Proteasome functional insufficiency activates the calcineurin-NFAT pathway in cardiomyocytes and promotes maladaptive remodelling of stressed mouse hearts.Drusen deposits associated with aging and age-related macular degeneration contain nonfibrillar amyloid oligomers.Mitochondrial dysfunction and apoptosis underlie the pathogenic process in alpha-B-crystallin desmin-related cardiomyopathy Enhancement of proteasome function by PA28α overexpression protects against oxidative stress.Tubulin hyperacetylation is adaptive in cardiac proteotoxicity by promoting autophagy.Regulation of neurite growth by inorganic pyrophosphatase 1 via JNK dephosphorylation.The interplay between autophagy and the ubiquitin-proteasome system in cardiac proteotoxicity The NADPH metabolic network regulates human αB-crystallin cardiomyopathy and reductive stress in Drosophila melanogaster Reactive γ-ketoaldehydes promote protein misfolding and preamyloid oligomer formation in rapidly-activated atrial cells.

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P2860

Desmin-related cardiomyopathy in transgenic mice: a cardiac amyloidosis.

http://www.wikidata.org/entity/Q35971521

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2004 nî lūn-bûn

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2004年論文

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2004年论文

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2004年论文

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2004年论文

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name

Desmin-related cardiomyopathy in transgenic mice: a cardiac amyloidosis.

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Desmin-related cardiomyopathy in transgenic mice: a cardiac amyloidosis.

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type

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Desmin-related cardiomyopathy in transgenic mice: a cardiac amyloidosis.

@ast

Desmin-related cardiomyopathy in transgenic mice: a cardiac amyloidosis.

@en

prefLabel

Desmin-related cardiomyopathy in transgenic mice: a cardiac amyloidosis.

@ast

Desmin-related cardiomyopathy in transgenic mice: a cardiac amyloidosis.

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Proceedings of the National Academy of Sciences of the United States of America

P1476

Desmin-related cardiomyopathy in transgenic mice: a cardiac amyloidosis.

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P2093

Alina Maloyan

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Atsushi Sanbe

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Charles G Glabe

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Hanna Osinska

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Jeffrey E Saffitz

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Jeffrey Robbins

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Rakez Kayed

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P2860

A missense mutation in the alphaB-crystallin chaperone gene causes a desmin-related myopathy

The cardiac mechanical stretch sensor machinery involves a Z disc complex that is defective in a subset of human dilated cardiomyopathy

Four small Drosophila heat shock proteins are related to each other and to mammalian alpha-crystallin

A simplified system for generating recombinant adenoviruses

The amyloid hypothesis of Alzheimer's disease: progress and problems on the road to therapeutics

Aggresomes: a cellular response to misfolded proteins

Targeted disruption of the mouse alpha A-crystallin gene induces cataract and cytoplasmic inclusion bodies containing the small heat shock protein alpha B-crystallin

Abundance and location of the small heat shock proteins HSP25 and alphaB-crystallin in rat and human heart

Ischemia-induced association of the stress protein alpha B-crystallin with I-band portion of cardiac titin

Common structure of soluble amyloid oligomers implies common mechanism of pathogenesis

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