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10.1681/ASN.2013101067 http://scihub22266oqcxt.onion/10.1681/ASN.2013101067 C4341470!4341470!25071087     free     free     free 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 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 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 2015 ; 26 (3): 677-91 Nephropedia Template TP {{tp|p=25071087|t=2015. Mutual Antagonism of Wilms? Tumor 1 and ?-Catenin Dictates Podocyte Health and Disease |pdf=|usr=}}{{25071087}} gab.com Text Mutual Antagonism of Wilms Tumor 1 and -Catenin Dictates Podocyte Health and Disease JO: J Am Soc Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=25071087 #FOAvip Activation of ?-catenin, the intracellular mediator of canonical Wnt signaling, has a critical role in mediating podocyte injury and proteinuria. However, the underlying mechanisms remain poorly understood. Here, we show that ?-catenin triggers ubiquitin-mediated protein degradation of Wilms? tumor 1 (WT1) and functionally antagonizes its action. In mice injected with adriamycin, WT1 protein was progressively lost in glomerular podocytes at 1, 3, and 5 weeks after injection. Notably, loss of WT1 apparently did not result from podocyte depletion but was closely associated with upregulation of ?-catenin. This change in WT1/?-catenin ratio was accompanied by loss of podocyte-specific nephrin, podocalyxin, and synaptopodin and acquisition of mesenchymal markers Snail1, ?-smooth muscle actin, and fibroblast-specific protein 1. In vitro, overexpression of ?-catenin induced WT1 protein degradation through the ubiquitin proteasomal pathway, which was blocked by MG-132. WT1 and ?-catenin also competed for binding to common transcriptional coactivator CREB-binding protein and mutually repressed the expression of their respective target genes. In glomerular miniorgan culture, activation of ?-catenin by Wnt3a repressed WT1 and its target gene expression. In vivo, blockade of Wnt/?-catenin signaling by endogenous antagonist Klotho induced WT1 and restored podocyte integrity in adriamycin nephropathy. These results show that ?-catenin specifically targets WT1 for ubiquitin-mediated degradation, leading to podocyte dedifferentiation and mesenchymal transition. Our data also suggest that WT1 and ?-catenin have opposing roles in podocyte biology, and that the ratio of their expression levels dictates the state of podocyte health and disease in vivo. Twit Text FOAVip Mutual Antagonism of Wilms Tumor 1 and -Catenin Dictates Podocyte Health and Disease ????J Am Soc Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=25071087 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25071087 #FOAvip English Wikipedia <ref>{{Cite pmid|25071087}}</ref> Mutual Antagonism of Wilms? Tumor 1 and ?-Catenin Dictates Podocyte Health and Disease #MMPMID25071087 Zhou L; Li Y; He W; Zhou D; Tan RJ; Nie J; Hou FF; Liu Y J Am Soc Nephrol 2015[Mar]; 26 (3): 677-91 PMID25071087show ga Activation of ?-catenin, the intracellular mediator of canonical Wnt signaling, has a critical role in mediating podocyte injury and proteinuria. However, the underlying mechanisms remain poorly understood. Here, we show that ?-catenin triggers ubiquitin-mediated protein degradation of Wilms? tumor 1 (WT1) and functionally antagonizes its action. In mice injected with adriamycin, WT1 protein was progressively lost in glomerular podocytes at 1, 3, and 5 weeks after injection. Notably, loss of WT1 apparently did not result from podocyte depletion but was closely associated with upregulation of ?-catenin. This change in WT1/?-catenin ratio was accompanied by loss of podocyte-specific nephrin, podocalyxin, and synaptopodin and acquisition of mesenchymal markers Snail1, ?-smooth muscle actin, and fibroblast-specific protein 1. In vitro, overexpression of ?-catenin induced WT1 protein degradation through the ubiquitin proteasomal pathway, which was blocked by MG-132. WT1 and ?-catenin also competed for binding to common transcriptional coactivator CREB-binding protein and mutually repressed the expression of their respective target genes. In glomerular miniorgan culture, activation of ?-catenin by Wnt3a repressed WT1 and its target gene expression. In vivo, blockade of Wnt/?-catenin signaling by endogenous antagonist Klotho induced WT1 and restored podocyte integrity in adriamycin nephropathy. These results show that ?-catenin specifically targets WT1 for ubiquitin-mediated degradation, leading to podocyte dedifferentiation and mesenchymal transition. Our data also suggest that WT1 and ?-catenin have opposing roles in podocyte biology, and that the ratio of their expression levels dictates the state of podocyte health and disease in vivo. äMutual Antagonism of Wilms? Tumor 1 and ?-Catenin Dictates Podocyte He(epmc).pdf DeepDyve Pubget Overpricing