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10.1159/000191075 http://scihub22266oqcxt.onion/10.1159/000191075 19142027!2881215!19142027     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=19142027&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\19142027.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Nephron+Physiol 2009 ; 111 (2): p9-15 Nephropedia Template TP {{tp|p=19142027|t=2009. Signaling in regulation of podocyte phenotypes |pdf=|usr=}}{{19142027}} gab.com Text Signaling in regulation of podocyte phenotypes JO: Nephron Physiol http://www.kidney.de/pget.php?&tw=1&pmid=19142027 #FOAvip The kidney podocyte is a terminally differentiated and highly specialized cell. The function of the glomerular filtration barrier depends on the integrity of the podocyte. Podocyte injury and loss have been observed in human and experimental models of glomerular diseases. Three major podocyte phenotypes have been described in glomerular diseases: effacement, apoptosis, and proliferation. Here, we highlight the signaling cascades that are responsible for the manifestation of these pathologic phenotypes. The integrity of the podocyte foot process is determined by the interaction of nephrin with proteins in the slit diaphragm complex, the regulation of actin dynamics by the Rho family of GTPases, and the transduction of extracellular signals through focal adhesion complexes. Activation of the p38 mitogen-activated protein kinase and transforming growth factor-beta1 causes podocyte apoptosis. Phosphoinositide 3-kinase and its downstream target AKT protect podocytes from apoptosis. In human immunodeficiency virus-associated nephropathy, Src-dependent activation of Stat3, mitogen-activated protein kinase 1,2, and hypoxia-inducible factor 2alpha is an important driver of podocyte proliferation. At the level of intracellular signaling, it appears that different extracellular signals can converge onto a few pathways to induce changes in the phenotype of podocytes. Twit Text FOAVip Signaling in regulation of podocyte phenotypes ????Nephron Physiol http://www.kidney.de/pget.php?&tw=1&pmid=19142027 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=19142027 #FOAvip English Wikipedia <ref>{{Cite pmid|19142027}}</ref> Signaling in regulation of podocyte phenotypes #MMPMID19142027 Chuang PY; He JC Nephron Physiol 2009[]; 111 (2): p9-15 PMID19142027show ga The kidney podocyte is a terminally differentiated and highly specialized cell. The function of the glomerular filtration barrier depends on the integrity of the podocyte. Podocyte injury and loss have been observed in human and experimental models of glomerular diseases. Three major podocyte phenotypes have been described in glomerular diseases: effacement, apoptosis, and proliferation. Here, we highlight the signaling cascades that are responsible for the manifestation of these pathologic phenotypes. The integrity of the podocyte foot process is determined by the interaction of nephrin with proteins in the slit diaphragm complex, the regulation of actin dynamics by the Rho family of GTPases, and the transduction of extracellular signals through focal adhesion complexes. Activation of the p38 mitogen-activated protein kinase and transforming growth factor-beta1 causes podocyte apoptosis. Phosphoinositide 3-kinase and its downstream target AKT protect podocytes from apoptosis. In human immunodeficiency virus-associated nephropathy, Src-dependent activation of Stat3, mitogen-activated protein kinase 1,2, and hypoxia-inducible factor 2alpha is an important driver of podocyte proliferation. At the level of intracellular signaling, it appears that different extracellular signals can converge onto a few pathways to induce changes in the phenotype of podocytes. |*Signal Transduction[MESH] |Animals[MESH] |Apoptosis[MESH] |Cell Dedifferentiation[MESH] |Cell Proliferation[MESH] |Cytoskeleton/metabolism[MESH] |Glomerular Basement Membrane/*metabolism/pathology[MESH] |Humans[MESH] |Intracellular Signaling Peptides and Proteins/*metabolism[MESH] |Kidney Diseases/enzymology/*metabolism/pathology[MESH] |Phenotype[MESH]Signaling in regulation of podocyte phenotypes (epmc).pdf DeepDyve Pubget Overpricing