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Targeting VE-PTP phosphatase protects the kidney from diabetic injury.

J. Exp. Med.. 2019; 
CarotaIsabel A,Kenig-KozlovskyYael,OnayTuncer,ScottRizaldy,ThomsonBenjamin R,SoumaTomokazu,BartlettChristina S,LiYanyang,ProcissiDaniele,RamirezVeronica,YamaguchiShinji,TarjusAntoine,TannaChristine E,LiChengjin,EreminaVera,VestweberDietmar,OladipupoSunday S,BreyerMatthew D,QuagginSus
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Catalog Antibody The following antibodies were used for Western blot analysis: TIE2 antibody (Santa Cruz; C-20; SC-324), 4G-10 platinum anti-phosphotyrosine (EMD Millipore; 05–1050), α-tubulin antibody (Genscript; A01410), eNOS (Cell Signaling Technology; 49G3), phospho-eNOS (Cell Signaling Technology; C9C3), and FOXO1 (Cell Signaling Technology; C29H4). Get A Quote

摘要

Diabetic nephropathy is a leading cause of end-stage kidney failure. Reduced angiopoietin-TIE2 receptor tyrosine kinase signaling in the vasculature leads to increased vascular permeability, inflammation, and endothelial cell loss and is associated with the development of diabetic complications. Here, we identified a mechanism to explain how TIE2 signaling is attenuated in diabetic animals. Expression of vascular endothelial protein tyrosine phosphatase VE-PTP (also known as PTPRB), which dephosphorylates TIE2, is robustly up-regulated in the renal microvasculature of diabetic rodents, thereby reducing TIE2 activity. Increased VE-PTP expression was dependent on hypoxia-inducible factor transcription... More

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