ArticleAging cell2018
Smurf2 regulates stability and the autophagic-lysosomal turnover of lamin A and its disease-associated form progerin.
Article in Aging cell, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 44 citations in OpenAlex.
- Progerin Hinders Autophagy Flux at Its Final Stages in Hutchinson-Gilford Progeria Syndrome Cells, Preventing Its Own Autophagic Degradation.Aging cell · 2026Article
- Paclitaxel compromises nuclear integrity in interphase through SUN2-mediated cytoskeletal coupling.Journal of cell science · 2026Article
- Lamin A/C as a Molecular Link Between Nuclear Organization, Chromatin Dynamics, and Tumor Progression.Cells · 2026Review
- Intermediate, but not average: The unusual lives of the nuclear lamin proteins.Current opinion in cell biology · 2023Review
- Article
- The role of NEDD4 related HECT-type E3 ubiquitin ligases in defective autophagy in cancer cells: molecular mechanisms and therapeutic perspectives.Molecular medicine (Cambridge, Mass.) · 2023Review
- The E3 ubiquitin ligase SMURF2 stabilizes RNA editase ADAR1p110 and promotes its adenosine-to-inosine (A-to-I) editing function.Cellular and molecular life sciences : CMLS · 2022Article
- Article
- Stabilization of SETD3 by deubiquitinase USP27 enhances cell proliferation and hepatocellular carcinoma progression.Cellular and molecular life sciences : CMLS · 2022Article
- A heterozygous p.S143P mutation inFrontiers in cell and developmental biology · 2022Article
- Post-Translational Modification of Lamins: Mechanisms and Functions.Frontiers in cell and developmental biology · 2022Review
- Atg39 selectively captures inner nuclear membrane into lumenal vesicles for delivery to the autophagosome.The Journal of cell biology · 2021Article
- Development and characterisation of SMURF2-targeting modifiers.Journal of enzyme inhibition and medicinal chemistry · 2021Article
- Sirolimus and Other Mechanistic Target of Rapamycin Inhibitors Directly Activate Latent Pathogenic Human Polyomavirus Replication.The Journal of infectious diseases · 2021Article
- Lamin post-translational modifications: emerging toggles of nuclear organization and function.Trends in biochemical sciences · 2021Review
- CRISPR/Cas9-engineered Drosophila knock-in models to study VCP diseases.Disease models & mechanisms · 2021Article
- A Non-stop identity complex (NIC) supervises enterocyte identity and protects from premature aging.eLife · 2021Article
- Functional mechanisms and abnormalities of the nuclear lamina.Nature cell biology · 2021Review
- Article
- The Nuclear Lamina: Protein Accumulation and Disease.Biomedicines · 2020Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A-lamins, encoded by the LMNA gene, are major structural components of the nuclear lamina coordinating essential cellular processes. Mutations in the LMNA gene and/or alterations in its expression levels have been linked to a distinct subset of human disorders, collectively known as laminopathies, and to cancer. Mechanisms regulating A-lamins are mostly obscure. Here, we identified E3 ubiquitin ligase Smurf2 as a physiological regulator of lamin A and its disease-associated mutant form progerin (LAΔ50), whose expression underlies the development of Hutchinson-Gilford progeria syndrome (HGPS), a devastating premature aging syndrome. We show that Smurf2 directly binds, ubiquitinates, and negatively regulates the expression of lamin A and progerin in Smurf2 dose- and E3 ligase-dependent manners. Overexpression of catalytically active Smurf2 promotes the autophagic-lysosomal breakdown of lamin A and progerin, whereas Smurf2 depletion increases lamin A levels. Remarkably, acute overexpression of Smurf2 in progeria fibroblasts was able to significantly reduce the nuclear deformability. Furthermore, we demonstrate that the reciprocal relationship between Smurf2 and A-lamins is preserved in different types of mouse and human normal and cancer tissues. These findings establish Smurf2 as an essential regulator of lamin A and progerin and lay a foundation for evaluating the efficiency of progerin clearance by Smurf2 in HGPS, and targeting of the Smurf2-lamin A axis in age-related diseases such as cancer.
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