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Disease-causing mutation in α-actinin-4 promotes podocyte detachment through maladaptation to periodic stretch

29 Jan 2018

Abstract excerpt

α-Actinin-4 (ACTN4) bundles and cross-links actin filaments to confer mechanical resilience to the reconstituted actin network. How this resilience is built and dynamically regulated in the podocyte, and the cause of its failure in ACTN4 mutation-associated focal segmental glomerulosclerosis (FSGS), remains poorly defined. Using primary podocytes isolated from wild-type (WT) and FSGS-causing point mutant Actn4...

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PMID: 29378953
DOI: 10.1073/pnas.1717870115

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