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Silvia Crasto
National Research Council
6Publications
1H-index
8Citations
Publications 6
Newest
#1Vittoria Di Mauro (University of Milan)
#2Silvia CrastoH-Index: 1
Last.Daniele CatalucciH-Index: 29
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MiR-133a is a muscle-enriched miRNA, which plays a key role for proper skeletal and cardiac muscle function via regulation of transduction cascades, including the Wnt signalling. MiR-133a modulates its targets via canonical mRNA repression, a process that has been largely demonstrated to occur within the cytoplasm. However, recent evidence has shown that miRNAs play additional roles in other sub-cellular compartments, such as nuclei. Here, we show that miR-133a translocates to the nucleus of car...
#1Nicolò Salvarani (National Research Council)H-Index: 9
#2Silvia Crasto (National Research Council)H-Index: 1
Last.Elisa Di Pasquale (National Research Council)H-Index: 12
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Mutations in LMNA, which encodes the nuclear proteins Lamin A/C, can cause cardiomyopathy and conduction disorders. Here, we employ induced pluripotent stem cells (iPSCs) generated from human cells carrying heterozygous K219T mutation on LMNA to develop a disease model. Cardiomyocytes differentiated from these iPSCs, and which thus carry K219T-LMNA, have altered action potential, reduced peak sodium current and diminished conduction velocity. Moreover, they have significantly downregulated Nav1....
#1Maria Chatzifrangkeskou (UPMC: Pierre-and-Marie-Curie University)H-Index: 2
#2David Yadin (FU: Free University of Berlin)H-Index: 3
Last.Antoine Muchir (UPMC: Pierre-and-Marie-Curie University)H-Index: 2
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#1Silvia CrastoH-Index: 1
#2Nicolò SalvaraniH-Index: 9
Last.Elisa Di PasqualeH-Index: 12
view all 10 authors...
Mutations of the LMNA gene, encoding the nuclear lamina proteins Lamin A/C, are a common cause of dilated cardiomyopathy, typically manifesting in association with cardiac conduction defects. LaminA/C regulate various nuclear activities, including maintenance of the nuclear structure, gene transcription and chromatin organization. Most studies on the consequences of Lamin A/C defects were conducted on fibroblasts, while studies on human cardiomyocytes (CMs) are scarce. We therefore generated a c...
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