The small GTPase regulatory protein Rac1 drives podocyte injury independent of cationic channel protein TRPC5-Reference-Cited by-同舟云学术

The small GTPase regulatory protein Rac1 drives podocyte injury independent of cationic channel protein TRPC5

Published:2023-06 Issue:6 Volume:103 Page:1056-1062
ISSN:0085-2538
Container-title:Kidney International
language:en
Short-container-title:Kidney International

Author:

Polat Onur K.,Isaeva Elena,Sudhini Yashwanth R.,Knott Brenna,Zhu Ke,Noben Manuel,Suresh Kumar Varsha,Endlich Nicole,Mangos Steve,Reddy Tejasree Vallapu,Samelko Beata,Wei Changli,Altintas Mehmet M.,Dryer Stuart E.,Sever Sanja,Staruschenko Alexander,Reiser Jochen

Funder

National Institutes of Health

U.S. Department of Veterans Affairs

Publisher

Elsevier BV

Subject

Nephrology

Reference33 articles.

1. A mutation in the TRPC6 cation channel causes familial focal segmental glomerulosclerosis;Winn;Science,2005

2. TRPC6 is a glomerular slit diaphragm-associated channel required for normal renal function;Reiser;Nat Genet,2005

3. Contribution of coiled-coil assembly to Ca2+/Calmodulin-dependent inactivation of TRPC6 channels and its impacts on FSGS-associated phenotypes;Polat;J Am Soc Nephrol,2019

4. Mechanisms underlying modulation of podocyte TRPC6 channels by suPAR: role of NADPH oxidases and Src family tyrosine kinases;Kim;Biochem Biophys Acta Mol Basis Dis,2018

5. Trpc6 inactivation confers protection in a model of severe nephrosis in rats;Kim;J Mol Med (Berl),2018

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