ArticleMolecular biology of the cell2013
Lamin A tail modification by SUMO1 is disrupted by familial partial lipodystrophy-causing mutations.
Article in Molecular biology of the cell, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 40 citations in OpenAlex.
- MMP-3 cleavage of Lamin A induces pro-migratory nuclear deformity, nucleophagy, and their autophagic secretion with extracellular vesicles in metastatic cancer.Cell communication and signaling : CCS · 2026Article
- Role of Nuclear Lamins in the Regulation of the Genome: Focus on CardioLaminopathy.Sub-cellular biochemistry · 2025Review
- Case Report: ConcurrentFrontiers in genetics · 2024Article
- The E262K mutation in Lamin A links nuclear proteostasis imbalance to laminopathy-associated premature aging.Aging cell · 2022Article
- Phenotypic Differences Among Familial Partial Lipodystrophy Due toJournal of the Endocrine Society · 2022Article
- SUMOylation of Matrix Protein M1 and Filamentous Morphology Collectively Contribute to the Replication and Virulence of Highly Pathogenic H5N1 Avian Influenza Viruses in Mammals.Journal of virology · 2022Article
- Regulation of Lipid Metabolism by Lamin in Mutation-Related Diseases.Frontiers in pharmacology · 2022Review
- Lamin post-translational modifications: emerging toggles of nuclear organization and function.Trends in biochemical sciences · 2021Review
- Whole transcriptome RNA-seq reveals key regulatory factors involved in type 2 diabetes pathology in peripheral fat of Asian Indians.Scientific reports · 2021Article
- Posttranslational modifications of the cytoskeleton.Cytoskeleton (Hoboken, N.J.) · 2021Review
- Functional mechanisms and abnormalities of the nuclear lamina.Nature cell biology · 2021Review
- Not So Slim Anymore-Evidence for the Role of SUMO in the Regulation of Lipid Metabolism.Biomolecules · 2020Review
- Genotype-phenotype analysis of LMNA-related diseases predicts phenotype-selective alterations in lamin phosphorylation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Review
- Biosynthesis ofThe Journal of biological chemistry · 2019Article
- Nuclear accumulation of UBC9 contributes to SUMOylation of lamin A/C and nucleophagy in response to DNA damage.Journal of experimental & clinical cancer research : CR · 2019Article
- The SUMO-specific isopeptidase SENP2 is targeted to intracellular membranes via a predicted N-terminal amphipathic α-helix.Molecular biology of the cell · 2018Article
- Lipodystrophic syndromes due to LMNA mutations: recent developments on biomolecular aspects, pathophysiological hypotheses and therapeutic perspectives.Nucleus (Austin, Tex.) · 2018Review
- The Roles of SUMO in Metabolic Regulation.Advances in experimental medicine and biology · 2017Review
- Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Lamin filaments are major components of the nucleoskeleton that bind LINC complexes and many nuclear membrane proteins. The tail domain of lamin A directly binds 21 known partners, including actin, emerin, and SREBP1, but how these interactions are regulated is unknown. We report small ubiquitin-like modifier 1 (SUMO1) as a major new posttranslational modification of the lamin A tail. Two SUMO1 modification sites were identified based on in vitro SUMOylation assays and studies of Cos-7 cells. One site (K420) matches the SUMO1 target consensus; the other (K486) does not. On the basis of the position of K486 on the lamin A Ig-fold, we hypothesize the SUMO1 E2 enzyme recognizes a folded structure-dependent motif that includes residues genetically linked to familial partial lipodystrophy (FPLD). Supporting this model, SUMO1-modification of the lamin A tail is reduced by two FPLD-causing mutations, G465D and K486N, and by single mutations in acidic residues E460 and D461. These results suggest a novel mode of functional control over lamin A in cells.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.