ArticleDevelopmental cell2019
ERK1/2 Phosphorylation of FHOD Connects Signaling and Nuclear Positioning Alternations in Cardiac Laminopathy.
Article in Developmental cell, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 44 citations in OpenAlex.
- Farnesylated prelamin A induces fibroblast polarity defects in premature aging disorders by inhibiting nesprin-2-SUN2 LINC complex function.Journal of cell science · 2026Article
- Nuclear Mechanotransduction at the Crossroads: How Membrane Receptors Remodel the Perinuclear Cytoskeleton to Drive Cancer and Disease.International journal of biological sciences · 2026Review
- Elevated SUN1 promotes migratory cell polarity defects through mechanically coupling microtubules to the nuclear lamina.Communications biology · 2025Article
- LMNA-related cardiomyopathy: From molecular pathology to cardiac gene therapy.Journal of advanced research · 2025Review
- Feeling the force from within - new tools and insights into nuclear mechanotransduction.Journal of cell science · 2025Review
- Apoptosis-induced translocation of nesprin-2 from the nuclear envelope to mitochondria is associated with mitochondrial dysfunction.Nucleus (Austin, Tex.) · 2024Article
- Non-Cell-Autonomous Cardiomyocyte Regulation Complicates Gene Supplementation Therapy forJACC. Basic to translational science · 2024Article
- FHOD-1 and profilin protect sarcomeres against contraction-induced deformation> inMolecular biology of the cell · 2024Article
- FHOD-1/profilin-mediated actin assembly protects sarcomeres against contraction-induced deformation inbioRxiv : the preprint server for biology · 2024Article
- From gene to mechanics: a comprehensive insight into the mechanobiology of LMNA mutations in cardiomyopathy.Cell communication and signaling : CCS · 2024Review
- LINC complex protein nesprin-2 has pro-apoptotic activity via Bcl-2 family proteins.Cell death discovery · 2024Article
- Purification of Human Cytoplasmic Actins FromBio-protocol · 2023Article
- Nesprin-1: novel regulator of striated muscle nuclear positioning and mechanotransduction.Biochemical Society transactions · 2023Review
- Purification of human β- and γ-actin from budding yeast.Journal of cell science · 2023Article
- FHODs: Nuclear tethered formins for nuclear mechanotransduction.Frontiers in cell and developmental biology · 2023Review
- Actin-microtubule cytoskeletal interplay mediated by MRTF-A/SRF signaling promotes dilated cardiomyopathy caused by LMNA mutations.Nature communications · 2022Article
- Nuclear envelope mechanobiology: linking the nuclear structure and function.Nucleus (Austin, Tex.) · 2021Review
- The non-muscle ADF/cofilin-1 controls sarcomeric actin filament integrity and force production in striated muscle laminopathies.Cell reports · 2021Article
- Structures of FHOD1-Nesprin1/2 complexes reveal alternate binding modes for the FH3 domain of formins.Structure (London, England : 1993) · 2021Article
- A LINC between the nucleus and the cytoskeleton takes form(in).Structure (London, England : 1993) · 2021Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Mutations in the lamin A/C gene (LMNA) cause cardiomyopathy and also disrupt nuclear positioning in fibroblasts. LMNA mutations causing cardiomyopathy elevate ERK1/2 activity in the heart, and inhibition of the ERK1/2 kinase activity ameliorates pathology, but the downstream effectors remain largely unknown. We now show that cardiomyocytes from mice with an Lmna mutation and elevated cardiac ERK1/2 activity have altered nuclear positioning. In fibroblasts, ERK1/2 activation negatively regulated nuclear movement by phosphorylating S498 of FHOD1. Expression of an unphosphorylatable FHOD1 variant rescued the nuclear movement defect in fibroblasts expressing a cardiomyopathy-causing lamin A mutant. In hearts of mice with LMNA mutation-induced cardiomyopathy, ERK1/2 mediated phosphorylation of FHOD3, an isoform highly expressed in cardiac tissue. Phosphorylation of FHOD1 and FHOD3 inhibited their actin bundling activity. These results show that phosphorylation of FHOD proteins by ERK1/2 is a critical switch for nuclear positioning and may play a role in the pathogenesis of cardiomyopathy caused by LMNA mutations.
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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.