ReviewCell2013
When lamins go bad: nuclear structure and disease.
Review in Cell, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 242 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
242 citing papers in PubMed, 389 citations in OpenAlex.
- August in focus in HCB: biomarker expression in specific tumor cell types.Histochemistry and cell biology · 2026Article
- The Underexplored Mechanobiology of Lamin A Biogenesis and Homeostasis.Biology of the cell · 2026Review
- Emerin loss of function inhibits MyoD-driven differentiation of human iPSCs into skeletal myotubes.bioRxiv : the preprint server for biology · 2026Article
- Review
- Epigenetics, Modifiers, and Molecular Noise: Rethinking Pathophysiology in Dilated and Hypertrophic Cardiomyopathies.International journal of molecular sciences · 2026Review
- Stem cell-associated osteogenic deficiency causes craniofacial deformities with progeroid accumulation of prelamin A.JCI insight · 2026Article
- Article
- Dynamic expression of lamin B1 during adult neurogenesis in the vertebrate brain.Developmental dynamics : an official publication of the American Association of Anatomists · 2026Article
- Lamin A/C-regulated cysteine catabolic flux modulates stem cell fate through epigenome reprogramming.Nature metabolism · 2026Article
- Interpreting the functional impact of genetic variants: The need for context qualifiers.American journal of human genetics · 2026Review
- Nucleoskeletal Proteins in Early Embryogenesis.Advances in experimental medicine and biology · 2026Review
- Epigenetic Regulation in Dilated Cardiomyopathy.Heart failure clinics · 2026Review
- Decreased RYR2 Cluster Size and Abnormal SR CaAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The dual guardians of cellular stability: exploring nesprin and lamin in senescence.Cell death & disease · 2025Review
- An evolutionarily conserved role for separase in the regulation of nuclear lamins.Cell death discovery · 2025Article
- Mechanically knocking out titin reveals protein tension loss as a trigger of muscle disease.Nature biomedical engineering · 2025Article
- Inhibitory Effect of S0859 on the Antioxidant Master Switch Nuclear Factor Erythroid 2-Related Factor 2 in Lung Cancer Cells.Antioxidants (Basel, Switzerland) · 2025Article
- Lamin B1 and LAP2β resist cytoskeletal force to maintain lamin A/C meshwork organization and preserve nuclear integrity.Molecular biology of the cell · 2025Article
- Transmembrane Protein 43: Molecular and Pathogenetic Implications in Arrhythmogenic Cardiomyopathy and Various Other Diseases.International journal of molecular sciences · 2025Review
- Lamin A/C regulates cerebellar granule cell maturation.Cell biology and toxicology · 2025Article
182 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 2 countries.
Funding
Abstract
Mutations in nuclear lamins or other proteins of the nuclear envelope are the root cause of a group of phenotypically diverse genetic disorders known as laminopathies, which have symptoms that range from muscular dystrophy to neuropathy to premature aging syndromes. Although precise disease mechanisms remain unclear, there has been substantial progress in our understanding of not only laminopathies, but also the biological roles of nuclear structure. Nuclear envelope dysfunction is associated with altered nuclear activity, impaired structural dynamics, and aberrant cell signaling. Building on these findings, small molecules are being discovered that may become effective therapeutic agents.
Indexed as
Identifiers
What OpenQuestion holds
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.