ArticleExperimental cell research2011
Subcellular localization of SREBP1 depends on its interaction with the C-terminal region of wild-type and disease related A-type lamins.
Article in Experimental cell research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 48 citations in OpenAlex.
- Navigating Lipodystrophy: Insights from Laminopathies and Beyond.International journal of molecular sciences · 2024Review
- Overview of cellular homeostasis-associated nuclear envelope lamins and associated input signals.Frontiers in cell and developmental biology · 2023Review
- A Multisensory Network Drives Nuclear Mechanoadaptation.Biomolecules · 2022Review
- Transcription of the Envelope Protein by 1-L Protein-RNA Recognition Code Leads to Genes/Proteins That Are Relevant to the SARS-CoV-2 Life Cycle and Pathogenesis.Current issues in molecular biology · 2022Article
- Lamin regulates the dietary restriction response via the mTOR pathway in Caenorhabditis elegans.Journal of cell science · 2021Article
- Review
- Role of Elevated Intracellular S-Adenosylhomocysteine in the Pathogenesis of Alcohol-Related Liver Disease.Cells · 2020Article
- Lamina-associated domains: peripheral matters and internal affairs.Genome biology · 2020Review
- Interplay of lamin A and lamin B LADs on the radial positioning of chromatin.Nucleus (Austin, Tex.) · 2019Article
- Lipodystrophic syndromes due to LMNA mutations: recent developments on biomolecular aspects, pathophysiological hypotheses and therapeutic perspectives.Nucleus (Austin, Tex.) · 2018Review
- Itm2a silencing rescues lamin A mediated inhibition of 3T3-L1 adipocyte differentiation.Adipocyte · 2017Article
- A lipodystrophy-causing lamin A mutant alters conformation and epigenetic regulation of the anti-adipogenicThe Journal of cell biology · 2017Article
- Chrom3D: three-dimensional genome modeling from Hi-C and nuclear lamin-genome contacts.Genome biology · 2017Article
- A Novel Lamin A Mutant Responsible for Congenital Muscular Dystrophy Causes Distinct Abnormalities of the Cell Nucleus.PloS one · 2017Article
- Hutchinson-Gilford Progeria Syndrome: A premature aging disease caused by LMNA gene mutations.Ageing research reviews · 2017Review
- Lamin B1 mediated demyelination: Linking Lamins, Lipids and Leukodystrophies.Nucleus (Austin, Tex.) · 2016Review
- Comparative proteome analysis of abdominal adipose tissues between fat and lean broilers.Proteome science · 2016Article
- Muscular Dystrophy Mutations Impair the Nuclear Envelope Emerin Self-assembly Properties.ACS chemical biology · 2015Article
- Defects of Lipid Synthesis Are Linked to the Age-Dependent Demyelination Caused by Lamin B1 Overexpression.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Distinct features of lamin A-interacting chromatin domains mapped by ChIP-sequencing from sonicated or micrococcal nuclease-digested chromatin.Nucleus (Austin, Tex.) · 2015Article
Corrections and comments
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Authors and funding
15 authors at 6 institutions in 2 countries.
Funding
Abstract
Lamins A and C are nuclear intermediate filament proteins expressed in most differentiated somatic cells. Previous data suggested that prelamin A, the lamin A precursor, accumulates in some lipodystrophy syndromes caused by mutations in the lamin A/C gene, and binds and inactivates the sterol regulatory element binding protein 1 (SREBP1). Here we show that, in vitro, the tail regions of prelamin A, lamin A and lamin C bind a polypeptide of SREBP1. Such interactions also occur in HeLa cells, since expression of lamin tail regions impedes nucleolar accumulation of the SREBP1 polypeptide fused to a nucleolar localization signal sequence. In addition, the tail regions of A-type lamin variants that occur in Dunnigan-type familial partial lipodystrophy of (R482W) and Hutchison Gilford progeria syndrome (∆607-656) bind to the SREBP1 polypeptide in vitro, and the corresponding FLAG-tagged full-length lamin variants co-immunoprecipitate the SREBP1 polypeptide in cells. Overexpression of wild-type A-type lamins and variants favors SREBP1 polypeptide localization at the intranuclear periphery, suggesting its sequestration. Our data support the hypothesis that variation of A-type lamin protein level and spatial organization, in particular due to disease-linked mutations, influences the sequestration of SREBP1 at the nuclear envelope and thus contributes to the regulation of SREBP1 function.
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Registered trials
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