Challenging the “chromatin hypothesis” of cardiac laminopathies with LMNA mutant iPS cells

Lamins A and C are intermediate filaments that provide structural support to the nuclear envelope and regulate gene expression. In this issue, Bertero et al. (2019. J. Cell Biol. https://doi.org/10.1083/jcb.201902117) report that although lamin A/C haploinsufficient cardiomyocytes show disease-assoc...

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Detalles Bibliográficos
Autores principales: Mozzetta, Chiara, Tedesco, Francesco Saverio
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Rockefeller University Press 2019
Materias:
Commentaries
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6719444/
https://www.ncbi.nlm.nih.gov/pubmed/31427369
http://dx.doi.org/10.1083/jcb.201907166
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author Mozzetta, Chiara
Tedesco, Francesco Saverio
author_facet Mozzetta, Chiara
Tedesco, Francesco Saverio
author_sort Mozzetta, Chiara
collection PubMed
description Lamins A and C are intermediate filaments that provide structural support to the nuclear envelope and regulate gene expression. In this issue, Bertero et al. (2019. J. Cell Biol. https://doi.org/10.1083/jcb.201902117) report that although lamin A/C haploinsufficient cardiomyocytes show disease-associated phenotypes, those changes cannot be explained by alterations in chromatin compartmentalization.
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spelling pubmed-67194442020-03-02 Challenging the “chromatin hypothesis” of cardiac laminopathies with LMNA mutant iPS cells Mozzetta, Chiara Tedesco, Francesco Saverio J Cell Biol Commentaries Lamins A and C are intermediate filaments that provide structural support to the nuclear envelope and regulate gene expression. In this issue, Bertero et al. (2019. J. Cell Biol. https://doi.org/10.1083/jcb.201902117) report that although lamin A/C haploinsufficient cardiomyocytes show disease-associated phenotypes, those changes cannot be explained by alterations in chromatin compartmentalization. Rockefeller University Press 2019-09-02 2019-08-19 /pmc/articles/PMC6719444/ /pubmed/31427369 http://dx.doi.org/10.1083/jcb.201907166 Text en © 2019 Mozzetta and Tedesco http://www.rupress.org/terms/https://creativecommons.org/licenses/by-nc-sa/4.0/This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms/). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 International license, as described at https://creativecommons.org/licenses/by-nc-sa/4.0/).
spellingShingle Commentaries
Mozzetta, Chiara
Tedesco, Francesco Saverio
Challenging the “chromatin hypothesis” of cardiac laminopathies with LMNA mutant iPS cells
title Challenging the “chromatin hypothesis” of cardiac laminopathies with LMNA mutant iPS cells
title_full Challenging the “chromatin hypothesis” of cardiac laminopathies with LMNA mutant iPS cells
title_fullStr Challenging the “chromatin hypothesis” of cardiac laminopathies with LMNA mutant iPS cells
title_full_unstemmed Challenging the “chromatin hypothesis” of cardiac laminopathies with LMNA mutant iPS cells
title_short Challenging the “chromatin hypothesis” of cardiac laminopathies with LMNA mutant iPS cells
title_sort challenging the “chromatin hypothesis” of cardiac laminopathies with lmna mutant ips cells
topic Commentaries
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6719444/
https://www.ncbi.nlm.nih.gov/pubmed/31427369
http://dx.doi.org/10.1083/jcb.201907166
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