Phosphorylation of ACTN4 Leads to Podocyte Vulnerability and Proteinuric Glomerulosclerosis.
Di FengMukesh KumarJan MuntelSusan B GurleyGabriel BirraneIsaac E StillmanLai DingMinxian WangSaima AhmedJohannes SchlondorffSeth L AlperTom FerranteSusan L MarquezCarlos F NgRichard NovakDonald E IngberHanno SteenMartin R PollakPublished in: Journal of the American Society of Nephrology : JASN (2020)
These findings suggest that increased phosphorylation of ACTN4 at S159 leads to biochemical, cellular, and renal pathology that is similar to pathology resulting from human disease-causing mutations in ACTN4. ACTN4 may mediate podocyte injury as a consequence of both genetic mutations and signaling events that modulate phosphorylation.