about
ERK1/2 directly acts on CTGF/CCN2 expression to mediate myocardial fibrosis in cardiomyopathy caused by mutations in the lamin A/C geneMolecular mechanisms of human lipodystrophies: from adipocyte lipid droplet to oxidative stress and lipotoxicity.Extracellular matrix remodeling and transforming growth factor-β signaling abnormalities induced by lamin A/C variants that cause lipodystrophy.Depletion of lamina-associated polypeptide 1 from cardiomyocytes causes cardiac dysfunction in mice.Decreased WNT/β-catenin signalling contributes to the pathogenesis of dilated cardiomyopathy caused by mutations in the lamin a/C gene.Lipodystrophic syndromes due to LMNA mutations: recent developments on biomolecular aspects, pathophysiological hypotheses and therapeutic perspectives.Microtubule cytoskeleton regulates Connexin 43 localization and cardiac conduction in cardiomyopathy caused by mutation in A-type lamins geneA homozygous mutation of prelamin-A preventing its farnesylation and maturation leads to a severe lipodystrophic phenotype: new insights into the pathogenicity of nonfarnesylated prelamin-A
P50
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P50
description
investigador
@es
researcher
@en
wetenschapper
@nl
name
Caroline Le Dour
@en
Caroline Le Dour
@nl
type
label
Caroline Le Dour
@en
Caroline Le Dour
@nl
prefLabel
Caroline Le Dour
@en
Caroline Le Dour
@nl
P108
P31
P496
0000-0001-8647-3252