Lipodystrophic laminopathy: Lamin A mutation relaxes chromatin architecture to impair adipogenesis-Reference-Cited by-同舟云学术

Lipodystrophic laminopathy: Lamin A mutation relaxes chromatin architecture to impair adipogenesis

Published:2017-08-15 Issue:9 Volume:216 Page:2607-2610
ISSN:0021-9525
Container-title:Journal of Cell Biology
language:en
Short-container-title:

Author:

Elzeneini Eman¹,Wickström Sara A.¹²^ORCID

Affiliation:

1. Paul Gerson Unna Group, Skin Homeostasis and Ageing, Max Planck Institute for Biology of Ageing, Cologne, Germany

2. Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases, University of Cologne, Cologne, Germany

Abstract

The familial partial Dunnigan lipodystrophy, characterized by subcutaneous fat loss, is frequently caused by an R482W mutation in lamin A. In this issue, Oldenburg et al. (2017. J. Cell Biol. https://doi.org/10.1083/jcb.201701043) demonstrate that this mutation impairs the ability of lamin A to repress the anti-adipogenic miR-335, providing a potential molecular mechanism for the disease.

Funder

Deutsche Forschungsgemeinschaft

Max Planck

Publisher

Rockefeller University Press

Subject

Cell Biology

Link

http://rupress.org/jcb/article-pdf/216/9/2607/1377553/jcb_201707090.pdf

Reference10 articles.

1. Lamins: nuclear intermediate filament proteins with fundamental functions in nuclear mechanics and genome regulation;Gruenbaum;Annu. Rev. Biochem.,2015

2. Laminopathies: multisystem dystrophy syndromes;Jacob;Mol. Genet. Metab.,2006