Inhibition of apoptosis improves outcome in a model of congenital muscular dystrophy. - sprookjes - yvandenbroek - TriplyDB

Inhibition of apoptosis improves outcome in a model of congenital muscular dystrophy.

Inhibition of apoptosis improves outcome in a model of congenital muscular dystrophy.

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Skeletal muscle laminin and MDC1A: pathogenesis and treatment strategies.Apoptosis inhibitors and mini-agrin have additive benefits in congenital muscular dystrophy mice The zebrafish candyfloss mutant implicates extracellular matrix adhesion failure in laminin alpha2-deficient congenital muscular dystrophy.Diseased muscles that lack dystrophin or laminin-alpha2 have altered compositions and proliferation of mononuclear cell populations Distinct roles for laminin globular domains in laminin alpha1 chain mediated rescue of murine laminin alpha2 chain deficiency Apoptosis repressor with a CARD domain (ARC) restrains Bax-mediated pathogenesis in dystrophic skeletal muscle Magnetic Resonance Imaging Is Sensitive to Pathological Amelioration in a Model for Laminin-Deficient Congenital Muscular Dystrophy (MDC1A)BAG3 deficiency results in fulminant myopathy and early lethality Enhancing muscle membrane repair by gene delivery of MG53 ameliorates muscular dystrophy and heart failure in δ-Sarcoglycan-deficient hamsters.Potent pro-inflammatory and pro-fibrotic molecules, osteopontin and galectin-3, are not major disease modulators of laminin α2 chain-deficient muscular dystrophy.Improving Reproducibility of Phenotypic Assessments in the DyW Mouse Model of Laminin-α2 Related Congenital Muscular Dystrophy.Bcl-2 inhibits the innate immune response during early pathogenesis of murine congenital muscular dystrophy P38α MAPK underlies muscular dystrophy and myofiber death through a Bax-dependent mechanism.Doxycycline attenuates and delays toxicity of the oculopharyngeal muscular dystrophy mutation in transgenic mice.Soleus muscle in glycosylation-deficient muscular dystrophy is protected from contraction-induced injury Over-expression of BCL2 rescues muscle weakness in a mouse model of oculopharyngeal muscular dystrophy.Omigapil treatment decreases fibrosis and improves respiratory rate in dy(2J) mouse model of congenital muscular dystrophy Muscle-specific expression of insulin-like growth factor 1 improves outcome in Lama2Dy-w mice, a model for congenital muscular dystrophy type 1A Peripheral nerve pathology, including aberrant Schwann cell differentiation, is ameliorated by doxycycline in a laminin-α2-deficient mouse model of congenital muscular dystrophy.Deficiency of the Bax gene attenuates denervation-induced apoptosis Quantitative proteomic analysis reveals metabolic alterations, calcium dysregulation, and increased expression of extracellular matrix proteins in laminin α2 chain-deficient muscle.Life or death by NFκB, Losartan promotes survival in dy2J/dy2J mouse of MDC1A.Proinflammatory signals and the loss of lymphatic vessel hyaluronan receptor-1 (LYVE-1) in the early pathogenesis of laminin alpha2-deficient skeletal muscle.Laminin-111 protein therapy reduces muscle pathology and improves viability of a mouse model of merosin-deficient congenital muscular dystrophy Mesoangioblast delivery of miniagrin ameliorates murine model of merosin-deficient congenital muscular dystrophy type 1A.Linker molecules between laminins and dystroglycan ameliorate laminin-alpha2-deficient muscular dystrophy at all disease stages Laminin-211 in skeletal muscle function.The cell biology of disease: cellular and molecular mechanisms underlying muscular dystrophy.The role of cell death in sexually dimorphic muscle development: male-specific muscles are retained in female bax/bak knockout mice.Pathology is alleviated by doxycycline in a laminin-alpha2-null model of congenital muscular dystrophy Wasting mechanisms in muscular dystrophy.Ku70 regulates Bax-mediated pathogenesis in laminin-alpha2-deficient human muscle cells and mouse models of congenital muscular dystrophy.Immortalized myogenic cells from congenital muscular dystrophy type1A patients recapitulate aberrant caspase activation in pathogenesis: a new tool for MDC1A research The collagen VI-related myopathies: muscle meets its matrix.Basement membranes and human disease.Congenital muscular dystrophies: toward molecular therapeutic interventions.Exacerbation of pathology by oxidative stress in respiratory and locomotor muscles with Duchenne muscular dystrophy.Cell-matrix interactions in muscle disease.The dystrophin-glycoprotein complex in the prevention of muscle damage.Absence of microRNA-21 does not reduce muscular dystrophy in mouse models of LAMA2-CMD

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Inhibition of apoptosis improves outcome in a model of congenital muscular dystrophy.

http://www.wikidata.org/entity/Q37625936

description

article científic

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article scientifique

@fr

articolo scientifico

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artigo científico

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bilimsel makale

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scientific article published on December 2004

@en

vedecký článok

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vetenskaplig artikel

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videnskabelig artikel

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vědecký článek

@cs

name

Inhibition of apoptosis improves outcome in a model of congenital muscular dystrophy.

@en

Inhibition of apoptosis improves outcome in a model of congenital muscular dystrophy.

@nl

type

label

Inhibition of apoptosis improves outcome in a model of congenital muscular dystrophy.

@en

Inhibition of apoptosis improves outcome in a model of congenital muscular dystrophy.

@nl

prefLabel

Inhibition of apoptosis improves outcome in a model of congenital muscular dystrophy.

@en

Inhibition of apoptosis improves outcome in a model of congenital muscular dystrophy.

@nl

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Journal of Clinical Investigation

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Inhibition of apoptosis improves outcome in a model of congenital muscular dystrophy.

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Christine A Kostek

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

Janice A Dominov

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

Mahasweta Girgenrath

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

P2860

Immortalization of mouse myogenic cells can occur without loss of p16INK4a, p19ARF, or p53 and is accelerated by inactivation of Bax

Activation of the lama2 gene in muscle regeneration: abortive regeneration in laminin alpha2-deficiency

Merosin and congenital muscular dystrophy

Bax-deficient mice with lymphoid hyperplasia and male germ cell death

Pro- and anti-apoptotic members of the Bcl-2 family in skeletal muscle: a distinct role for Bcl-2 in later stages of myogenesis

Characterization of ARC, apoptosis repressor interacting with CARD, in normal and dystrophin-deficient skeletal muscle

An agrin minigene rescues dystrophic symptoms in a mouse model for congenital muscular dystrophy.

Pharmacological strategies for muscular dystrophy.

Immunohistochemical analysis of Mcl-1 protein in human tissues. Differential regulation of Mcl-1 and Bcl-2 protein production suggests a unique role for Mcl-1 in control of programmed cell death in vivo.

Immunohistochemical determination of in vivo distribution of Bax, a dominant inhibitor of Bcl-2.

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1635-1639

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scholarly article

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10.1172/JCI22928

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11

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114

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2004-12-01T00:00:00Z

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15578095

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apoptotic process

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529286

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