PKCα Mediates β-Arrestin2-dependent Nephrin Endocytosis in Hyperglycemia
Open Access
- 1 April 2011
- journal article
- Published by Elsevier
- Vol. 286 (15) , 12959-12970
- https://doi.org/10.1074/jbc.m110.204024
Abstract
No abstract availableKeywords
This publication has 35 references indexed in Scilit:
- Acute hyperglycemia induces rapid, reversible increases in glomerular permeability in nondiabetic ratsAmerican Journal of Physiology-Renal Physiology, 2010
- Podocytic PKC-Alpha Is Regulated in Murine and Human Diabetes and Mediates Nephrin EndocytosisPLOS ONE, 2010
- Phosphorylation of Nephrin Triggers Its Internalization by Raft-Mediated EndocytosisJournal of the American Society of Nephrology, 2009
- Nephrin—signature molecule of the glomerular podocyte?The Journal of Pathology, 2009
- PKC-alpha Modulates TGF-β Signaling and Impairs Podocyte SurvivalCellular Physiology and Biochemistry, 2009
- Neph1 Cooperates with Nephrin To Transduce a Signal That Induces Actin PolymerizationMolecular and Cellular Biology, 2007
- β-Arrestin2 mediates nephrin endocytosis and impairs slit diaphragm integrityProceedings of the National Academy of Sciences, 2006
- Structure and Function of PICK1Neurosignals, 2006
- NEPH1 defines a novel family of podocin‐interacting proteinsThe FASEB Journal, 2002
- Heterologous Activation of Protein Kinase C Stimulates Phosphorylation of δ-Opioid Receptor at Serine 344, Resulting in β-Arrestin- and Clathrin-mediated Receptor InternalizationPublished by Elsevier ,2001