ArticleScientific reports2018
Nexilin/NEXN controls actin polymerization in smooth muscle and is regulated by myocardin family coactivators and YAP.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 35 citations in OpenAlex.
- Impaired stem cell migration and divisions in Duchenne muscular dystrophy revealed by live imaging.Nature communications · 2026Article
- Nexilin promotes calcium-dependent endo-lysosomal fission required for retrograde transport.Cell communication and signaling : CCS · 2026Article
- Integrating transcriptome and proteome profiles to compare carcass and meat quality traits between Songliao and Songlei black pigs.Frontiers in nutrition · 2026Article
- YAP/TAZ deletion in vascular smooth muscle cells mirrors atherosclerosis-associated transcriptional programs.Journal of molecular and cellular cardiology plus · 2025Article
- NEXN protects against vascular calcification by promoting SERCA2 SUMOylation and stabilization.Nature communications · 2025Article
- NEXN deficiency leads to dilated cardiomyopathy in human pluripotent stem cell-derived cardiomyocytes.Stem cell research & therapy · 2025Article
- NEXN regulates vascular smooth muscle cell phenotypic switching and neointimal hyperplasia.JCI insight · 2025Article
- Hippo in smooth muscle - a therapeutic target in vascular diseases driven by aging and hypertension.Frontiers in physiology · 2025Review
- Nexilin in cardiomyopathy: unveiling its diverse roles with special focus on endocardial fibroelastosis.Heart failure reviews · 2024Review
- Myeloid-derived growth factor suppresses VSMC dedifferentiation and attenuates postinjury neointimal formation in rats by activating S1PR2 and its downstream signaling.Acta pharmacologica Sinica · 2024Article
- Article
- Myocardin regulates exon usage in smooth muscle cells through induction of splicing regulatory factors.Cellular and molecular life sciences : CMLS · 2022Article
- Loss of Nexilin function leads to a recessive lethal fetal cardiomyopathy characterized by cardiomegaly and endocardial fibroelastosis.American journal of medical genetics. Part A · 2022Article
- Understanding the molecular basis of cardiomyopathy.American journal of physiology. Heart and circulatory physiology · 2022Review
- Two genetic variants inFrontiers in cardiovascular medicine · 2022Article
- Deciphering the Nature ofCancers · 2021Article
- NG2/CSPG4, CD146/MCAM and VAP1/AOC3 are regulated by myocardin-related transcription factors in smooth muscle cells.Scientific reports · 2021Article
- The transcriptome-wide association search for genes and genetic variants which associate with BMI and gestational weight gain in women with type 1 diabetes.Molecular medicine (Cambridge, Mass.) · 2021Article
- Identification of tumor mutation burden-related hub genes and the underlying mechanism in melanoma.Journal of Cancer · 2021Article
- Gastrointestinal dysfunction in autism displayed by altered motility and achalasia inProceedings of the National Academy of Sciences of the United States of America · 2019Article
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nexilin, encoded by the NEXN gene, is expressed in striated muscle and localizes to Z-discs, influencing mechanical stability. We examined Nexilin/NEXN in smooth muscle cells (SMCs), and addressed if Nexilin localizes to dense bodies and dense bands and whether it is regulated by actin-controlled coactivators from the MRTF (MYOCD, MKL1, MKL2) and YAP/TAZ (YAP1 and WWTR1) families. NEXN expression in SMCs was comparable to that in striated muscles. Immunofluorescence and immunoelectron microscopy suggested that Nexilin localizes to dense bodies and dense bands. Correlations at the mRNA level suggested that NEXN expression might be controlled by actin polymerization. Depolymerization of actin using Latrunculin B repressed the NEXN mRNA and protein in bladder and coronary artery SMCs. Overexpression and knockdown supported involvement of both YAP/TAZ and MRTFs in the transcriptional control of NEXN. YAP/TAZ and MRTFs appeared equally important in bladder SMCs, whereas MRTFs dominated in vascular SMCs. Expression of NEXN was moreover reduced in situations of SMC phenotypic modulation in vivo. The proximal promoter of NEXN conferred control by MRTF-A/MKL1 and MYOCD. NEXN silencing reduced actin polymerization and cell migration, as well as SMC marker expression. NEXN targeting by actin-controlled coactivators thus amplifies SMC differentiation through the actin cytoskeleton, probably via dense bodies and dense bands.
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