ArticleMolecular biology of the cell2014
Systematic identification of pathological lamin A interactors.
Article in Molecular biology of the cell, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
51 citing papers in PubMed, 1 synthesis or guideline pooled it, 73 citations in OpenAlex.
- Pooled it
- Farnesylated prelamin A induces fibroblast polarity defects in premature aging disorders by inhibiting nesprin-2-SUN2 LINC complex function.Journal of cell science · 2026Article
- Decreased RYR2 Cluster Size and Abnormal SR CaAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Cardiac phenotypes in LMNA mutations.Current opinion in cardiology · 2025Review
- IgStrand: A universal residue numbering scheme for the immunoglobulin-fold (Ig-fold) to study Ig-proteomes and Ig-interactomes.PLoS computational biology · 2025Review
- MAM-STAT3-Driven Mitochondrial CaAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- SMAP3-ID for Identification of Endogenous Protein-Protein Interactions Reveals Regulation of Mitochondrial Activity by Lamins.JACS Au · 2025Article
- The syntaxin-binding protein STXBP5 regulates progerin expression.Scientific reports · 2024Article
- Nuclear lamin A/C phosphorylation by loss of androgen receptor leads to cancer-associated fibroblast activation.Nature communications · 2024Article
- Article
- Review
- Native lamin A/C proteomes and novel partners from heart and skeletal muscle in a mouse chronic inflammation model of human frailty.Frontiers in cell and developmental biology · 2023Article
- The E262K mutation in Lamin A links nuclear proteostasis imbalance to laminopathy-associated premature aging.Aging cell · 2022Article
- Combined alteration of lamin and nuclear morphology influences the localization of the tumor-associated factor AKTIP.Journal of experimental & clinical cancer research : CR · 2022Article
- Most myopathic lamin variants aggregate: a functional genomics approach for assessing variants of uncertain significance.NPJ genomic medicine · 2021Article
- Characterization of subcellular localization of eukaryotic clamp loader/unloader and its regulatory mechanism.Scientific reports · 2021Article
- In Silico and In Vivo Analysis of Amino Acid Substitutions That Cause Laminopathies.International journal of molecular sciences · 2021Article
- Increase in lamin B1 promotes telomere instability by disrupting the shelterin complex in human cells.Nucleic acids research · 2021Article
- Review
- An APEX2 proximity ligation method for mapping interactions with the nuclear lamina.The Journal of cell biology · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Laminopathies are a collection of phenotypically diverse diseases that include muscular dystrophies, cardiomyopathies, lipodystrophies, and premature aging syndromes. Laminopathies are caused by >300 distinct mutations in the LMNA gene, which encodes the nuclear intermediate filament proteins lamin A and C, two major architectural elements of the mammalian cell nucleus. The genotype-phenotype relationship and the basis for the pronounced tissue specificity of laminopathies are poorly understood. Here we seek to identify on a global scale lamin A-binding partners whose interaction is affected by disease-relevant LMNA mutations. In a screen of a human genome-wide ORFeome library, we identified and validated 337 lamin A-binding proteins. Testing them against 89 known lamin A disease mutations identified 50 disease-associated interactors. Association of progerin, the lamin A isoform responsible for the premature aging disorder Hutchinson-Gilford progeria syndrome, with its partners was largely mediated by farnesylation. Mapping of the interaction sites on lamin A identified the immunoglobulin G (IgG)-like domain as an interaction hotspot and demonstrated that lamin A variants, which destabilize the Ig-like domain, affect protein-protein interactions more globally than mutations of surface residues. Analysis of a set of LMNA mutations in a single residue, which result in three phenotypically distinct diseases, identified disease-specific interactors. The results represent a systematic map of disease-relevant lamin A interactors and suggest loss of tissue-specific lamin A interactions as a mechanism for the tissue-specific appearance of laminopathic phenotypes.
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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.