Excess Podocyte Semaphorin-3A Leads to Glomerular Disease Involving PlexinA 1 –Nephrin Interaction
Open Access
- 1 October 2013
- journal article
- Published by Elsevier in The American Journal of Pathology
- Vol. 183 (4) , 1156-1168
Abstract
No abstract availableKeywords
This publication has 62 references indexed in Scilit:
- Integrin α1/Akita double-knockout mice on a Balb/c background develop advanced features of human diabetic nephropathyKidney International, 2012
- Diverse roles for semaphorin−plexin signaling in the immune systemTrends in Immunology, 2012
- Vascular Endothelial Growth Factor Receptor 2 Direct Interaction with Nephrin Links VEGF-A Signals to Actin in Kidney PodocytesJournal of Biological Chemistry, 2011
- Semaphorins in kidney development and disease: modulators of ureteric bud branching, vascular morphogenesis, and podocyte-endothelial crosstalkPediatric Nephrology, 2011
- Extracellular inhibitors, repellents, and semaphorin/plexin/MICAL‐mediated actin filament disassemblyCytoskeleton, 2011
- Podocyte vascular endothelial growth factor (Vegf 164 ) overexpression causes severe nodular glomerulosclerosis in a mouse model of type 1 diabetesDiabetologia, 2011
- Semaphorins guide the entry of dendritic cells into the lymphatics by activating myosin IINature Immunology, 2010
- VEGF Inhibition and Renal Thrombotic MicroangiopathyNew England Journal of Medicine, 2008
- Glomerular endothelial cells and podocytes jointly synthesize laminin-1 and -11 chainsKidney International, 2001
- Positionally Cloned Gene for a Novel Glomerular Protein—Nephrin—Is Mutated in Congenital Nephrotic SyndromeMolecular Cell, 1998