ArticleMolecular biology of the cell2001
Focal adhesion kinase and p130Cas mediate both sarcomeric organization and activation of genes associated with cardiac myocyte hypertrophy.
Article in Molecular biology of the cell, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 93 citations in OpenAlex.
- Developmental and Evolutionary Heart Adaptations Through Structure-Function Relationships.Journal of cardiovascular development and disease · 2025Review
- Laminin-derived peptide drives the cardiomyogenic potential and cardiac cells functionality.Frontiers in bioengineering and biotechnology · 2025Article
- The role of p130Cas/BCAR1 adaptor protein in the pathogenesis of cardiovascular diseases: A literature review.American heart journal plus : cardiology research and practice · 2024Review
- Genome-Wide Analysis of Left Ventricular Maximum Wall Thickness in the UK Biobank Cohort Reveals a Shared Genetic Background With Hypertrophic Cardiomyopathy.Circulation. Genomic and precision medicine · 2023Article
- Cardiac Differentiation Promotes Focal Adhesions Assembly through Vinculin Recruitment.International journal of molecular sciences · 2023Article
- Cellular Biomechanic Impairment in Cardiomyocytes Carrying the Progeria Mutation: An Atomic Force Microscopy Investigation.Langmuir : the ACS journal of surfaces and colloids · 2022Article
- Cooperation between myofibril growth and costamere maturation in human cardiomyocytes.Frontiers in bioengineering and biotechnology · 2022Article
- Neuregulins: protective and reparative growth factors in multiple forms of cardiovascular disease.Clinical science (London, England : 1979) · 2020Review
- Coupling to substrate adhesions drives the maturation of muscle stress fibers into myofibrils within cardiomyocytes.Molecular biology of the cell · 2020Article
- Mechanical regulation of gene expression in cardiac myocytes and fibroblasts.Nature reviews. Cardiology · 2019Review
- Cardiac Resynchronisation Therapy and Cellular Bioenergetics: Effects Beyond Chamber Mechanics.European cardiology · 2019Review
- The Cardiomyopathy Lamin A/C D192G Mutation Disrupts Whole-Cell Biomechanics in Cardiomyocytes as Measured by Atomic Force Microscopy Loading-Unloading Curve Analysis.Scientific reports · 2015Article
- Mechanotransduction in cardiac hypertrophy and failure.Circulation research · 2015Review
- AFM single-cell force spectroscopy links altered nuclear and cytoskeletal mechanics to defective cell adhesion in cardiac myocytes with a nuclear lamin mutation.Nucleus (Austin, Tex.) · 2015Article
- Paxillin and focal adhesion kinase colocalise in human skeletal muscle and its associated microvasculature.Histochemistry and cell biology · 2014Article
- Focal adhesion signaling in heart failure.Pflugers Archiv : European journal of physiology · 2014Review
- Cardiac resynchronization sensitizes the sarcomere to calcium by reactivating GSK-3β.The Journal of clinical investigation · 2014Article
- ErbB/integrin signaling interactions in regulation of myocardial cell-cell and cell-matrix interactions.Biochimica et biophysica acta · 2013Review
- Mechanical stretching for tissue engineering: two-dimensional and three-dimensional constructs.Tissue engineering. Part B, Reviews · 2012Review
- Serine-910 phosphorylation of focal adhesion kinase is critical for sarcomere reorganization in cardiomyocyte hypertrophy.Cardiovascular research · 2011Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Hypertrophic terminally differentiated cardiac myocytes show increased sarcomeric organization and altered gene expression. Previously, we established a role for the nonreceptor tyrosine kinase Src in signaling cardiac myocyte hypertrophy. Here we report evidence that p130Cas (Cas) and focal adhesion kinase (FAK) regulate this process. In neonatal cardiac myocytes, tyrosine phosphorylation of Cas and FAK increased upon endothelin (ET) stimulation. FAK, Cas, and paxillin were localized in sarcomeric Z-lines, suggesting that the Z-line is an important signaling locus in these cells. Cas, alone or in cooperation with Src, modulated basal and ET-stimulated atrial natriuretic peptide (ANP) gene promoter activity, a marker of cardiac hypertrophy. Expression of the C-terminal focal adhesion-targeting domain of FAK interfered with localization of endogenous FAK to Z-lines. Expression of the Cas-binding proline-rich region 1 of FAK hindered association of Cas with FAK and impaired the structural stability of sarcomeres. Collectively, these results suggest that interaction of Cas with FAK, together with their localization to Z-lines, is critical to assembly of sarcomeric units in cardiac myocytes in culture. Moreover, expression of the focal adhesion-targeting and/or the Cas-binding proline-rich regions of FAK inhibited ANP promoter activity and suppressed ET-induced ANP and brain natriuretic peptide gene expression. In summary, assembly of signaling complexes that include the focal adhesion proteins Cas, FAK, and paxillin at Z-lines in the cardiac myocyte may regulate, either directly or indirectly, both cytoskeletal organization and gene expression associated with cardiac myocyte hypertrophy.
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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.