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10.1097/01.asn.0000067648.75923.68 http://scihub22266oqcxt.onion/10.1097/01.asn.0000067648.75923.68 12761234!ä!12761234 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Am+Soc+Nephrol 2003 ; 14 Suppl 1 (ä): S22-6 Nephropedia Template TP {{tp|p=12761234|t=2003. Podocyte differentiation and hereditary proteinuria/nephrotic syndromes |pdf=|usr=}}{{12761234}} gab.com Text Podocyte differentiation and hereditary proteinuria/nephrotic syndromes JO: J Am Soc Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=12761234 #FOAvip The study of familial nephrotic syndromes (NS) and the analysis of murine models of glomerular diseases resulted in major progresses in the knowledge of podocyte physiology and pathology. Numerous proteins participating in the composition of the slit diaphragm region have been identified. The importance of several of them (nephrin, podocin, CD2AP, and Neph1) in the maintenance of the glomerular filtration barrier has been demonstrated by the occurrence of massive proteinuria when they are defective. The role of the cytoskeleton has been revealed by the development of proteinuria/NS in patients with ACTN4 mutation and the occurrence of early and severe NS in alpha-actinin-4-deficient mice. Given the genetic heterogeneity of familial NS and the many other genes to be identified, further insights in the molecular basis of the role of the podocyte in the maintenance of the glomerular filtration barrier may be expected in the near future. Twit Text FOAVip Podocyte differentiation and hereditary proteinuria/nephrotic syndromes ????J Am Soc Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=12761234 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=12761234 #FOAvip English Wikipedia <ref>{{Cite pmid|12761234}}</ref> Podocyte differentiation and hereditary proteinuria/nephrotic syndromes #MMPMID12761234 Gubler MC J Am Soc Nephrol 2003[Jun]; 14 Suppl 1 (ä): S22-6 PMID12761234show ga The study of familial nephrotic syndromes (NS) and the analysis of murine models of glomerular diseases resulted in major progresses in the knowledge of podocyte physiology and pathology. Numerous proteins participating in the composition of the slit diaphragm region have been identified. The importance of several of them (nephrin, podocin, CD2AP, and Neph1) in the maintenance of the glomerular filtration barrier has been demonstrated by the occurrence of massive proteinuria when they are defective. The role of the cytoskeleton has been revealed by the development of proteinuria/NS in patients with ACTN4 mutation and the occurrence of early and severe NS in alpha-actinin-4-deficient mice. Given the genetic heterogeneity of familial NS and the many other genes to be identified, further insights in the molecular basis of the role of the podocyte in the maintenance of the glomerular filtration barrier may be expected in the near future. |Animals[MESH] |Cell Differentiation[MESH] |Humans[MESH] |Kidney Glomerulus/*pathology[MESH] |Nephrotic Syndrome/congenital/*genetics/*pathology[MESH]Podocyte differentiation and hereditary proteinuria/nephrotic syndrome(epmc).pdf DeepDyve Pubget Overpricing