LAP2alpha maintains a mobile and low assembly state of A-type lamins in the nuclear interior
Author:
Affiliation:
1. Max Perutz Labs, Center for Medical Biochemistry, Medical University of Vienna, Vienna Biocenter Campus (VBC), Vienna, Austria
2. Physics Department and Nanotechnology Institute, Bar Ilan University, Ramat Gan, Israel
Abstract
Funder
Austrian Science Fund
Austrian Academy of Sciences
Israel Science Foundation
European Cooperation in Science and Technology
European Molecular Biology Organization
S Grosskopf Grant
Publisher
eLife Sciences Publications, Ltd
Subject
General Immunology and Microbiology,General Biochemistry, Genetics and Molecular Biology,General Medicine,General Neuroscience
Link
https://cdn.elifesciences.org/articles/63476/elife-63476-v2.pdf
Reference69 articles.
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3. DelK32-lamin A/C has abnormal location and induces incomplete tissue maturation and severe metabolic defects leading to premature death;Bertrand;Human Molecular Genetics,2012
4. Dysfunctional polycomb transcriptional repression contributes to lamin A/C-dependent muscular dystrophy;Bianchi;Journal of Clinical Investigation,2020
5. The lipodystrophic hotspot lamin A p.r482w mutation deregulates the mesodermal inducer T/Brachyury and early vascular differentiation gene networks;Briand;Human Molecular Genetics,2018
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