Key result
Expression of a non-phosphorylatable S910A-FAK mutant reduced sarcomere reorganization and cell spreading in cardiomyocytes, and FAK-S910 phosphorylation was reduced in end-stage DCM.
FAK-S910 phosphorylation is critical for cardiomyocyte sarcomere reorganization, and its reduction may contribute to the pathogenesis of dilated cardiomyopathy.
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May implicate FAK-S910 in DCM pathogenesis; animal data leaves open human validation and therapeutic targeting.
Chu et al. (2011) studied Dilated cardiomyopathy. S910A-FAK mutant adenovirus vs. Wild-type (WT) FAK adenovirus was evaluated on Sarcomere reorganization and cell spreading. Expression of a non-phosphorylatable S910A-FAK mutant reduced sarcomere reorganization and cell spreading in cardiomyocytes, and FAK-S910 phosphorylation was reduced in end-stage DCM.
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