about
Lysosomal integral membrane protein 2 is a novel component of the cardiac intercalated disc and vital for load-induced cardiac myocyte hypertrophySatellite cell loss and impaired muscle regeneration in selenoprotein N deficiencyFHL1 protein isoforms in Emery-Dreifuss muscular dystrophySevere dystonia, cerebellar atrophy, and cardiomyopathy likely caused by a missense mutation in TOR1AIP1.Apoptosis-inducing factor regulates skeletal muscle progenitor cell number and muscle phenotypeLamin A/C mutants disturb sumo1 localization and sumoylation in vitro and in vivo.Type B mandibuloacral dysplasia with congenital myopathy due to homozygous ZMPSTE24 missense mutation.New role for serum response factor in postnatal skeletal muscle growth and regeneration via the interleukin 4 and insulin-like growth factor 1 pathwaysMyocyte apoptosis in heart failure.Mutations of the FHL1 gene cause Emery-Dreifuss muscular dystrophy.199th ENMC international workshop: FHL1 related myopathies, June 7-9, 2013, Naarden, The Netherlands.Clinical and genetic heterogeneity in laminopathies.Striated muscle laminopathies.Muscle electrotransfer as a tool for studying muscle fiber-specific and nerve-dependent activity of promoters.Heterozygous LmnadelK32 mice develop dilated cardiomyopathy through a combined pathomechanism of haploinsufficiency and peptide toxicity.Mouse muscle identity: the position-dependent and fast fiber-specific expression of a transgene in limb muscles is methylation-independent and cell-autonomous.Cellular microenvironments reveal defective mechanosensing responses and elevated YAP signaling in LMNA-mutated muscle precursors.CAPON expression in skeletal muscle is regulated by position, repair, NOS activity, and dystrophy.Gene Therapy for LMNA-related Congenital Muscular Dystrophy (L-CMD) by Trans-Splicing.Nuclear accumulation of androgen receptor in gender difference of dilated cardiomyopathy due to lamin A/C mutations.FHL1B Interacts with Lamin A/C and Emerin at the Nuclear Lamina and is Misregulated in Emery-Dreifuss Muscular Dystrophy.Mutation in lamin A/C sensitizes the myocardium to exercise-induced mechanical stress but has no effect on skeletal muscles in mouse.Gene Therapy via Trans-Splicing for LMNA-Related Congenital Muscular Dystrophy.SMAD6 overexpression leads to accelerated myogenic differentiation of LMNA mutated cells.The Pathogenesis and Therapies of Striated Muscle LaminopathiesDelK32-lamin A/C has abnormal location and induces incomplete tissue maturation and severe metabolic defects leading to premature deathLaminopathies : un seul gène, de nombreuses pathologiesEUK-8, a Superoxide Dismutase and Catalase Mimetic, Reduces Cardiac Oxidative Stress and Ameliorates Pressure Overload-Induced Heart Failure in the Harlequin Mouse Mutant
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description
hulumtuese
@sq
researcher
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wetenschapper
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հետազոտող
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name
Anne Bertrand
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Anne Bertrand
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Anne Bertrand
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Anne Bertrand
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type
label
Anne Bertrand
@ast
Anne Bertrand
@en
Anne Bertrand
@es
Anne Bertrand
@nl
prefLabel
Anne Bertrand
@ast
Anne Bertrand
@en
Anne Bertrand
@es
Anne Bertrand
@nl
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P21
P31
P496
0000-0001-7153-848X