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Regulation of Nephrin Phosphorylation in Diabetes and Chronic Kidney Injury

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Protein Reviews

Part of the book series: Advances in Experimental Medicine and Biology ((PROTRE,volume 966))

Abstract

Diabetes is the leading cause of microalbuminuria and end-stage renal failure in industrial countries. Disruption of the filtration barrier, seen in almost all nephrotic diseases and diabetes, is the result of the loss or effacement of the podocyte foot process, notably damage of proteins within the slit diaphragm such as nephrin. For many years, nephrin has been viewed as a structural component of the slit diaphragm. It is now well recognized that nephrin contains several tyrosine residues in its cytoplasmic domain, which influences the development of glomerular injury. In this review, we propose an overview of nephrin signaling pathways in kidney injury.

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Abbreviations

DN:

diabetic nephropathy

FP:

foot process

NF-B:

nuclear factor-kappa B

LPS:

lipopolysaccharides

PAN:

puromycin aminonucleoside

PI3K:

phosphatidylinositol 3-kinase

PS:

protamin sulfate

SD:

slit diaphragm

SHP-1:

Src homology 2 domain phosphatase 1

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Denhez, B., Geraldes, P. (2017). Regulation of Nephrin Phosphorylation in Diabetes and Chronic Kidney Injury. In: Atassi, M. (eds) Protein Reviews. Advances in Experimental Medicine and Biology(), vol 966. Springer, Singapore. https://doi.org/10.1007/5584_2017_62

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