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10.1681/ASN.2013090984 http://scihub22266oqcxt.onion/10.1681/ASN.2013090984 C4341469!4341469!25313256     free     free     free Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Am+Soc+Nephrol 2015 ; 26 (3): 553-64 Nephropedia Template TP {{tp|p=25313256|t=2015. ?-Catenin Links von Hippel-Lindau to Aurora Kinase A and Loss of Primary Cilia in Renal Cell Carcinoma |pdf=|usr=}}{{25313256}} gab.com Text -Catenin Links von Hippel-Lindau to Aurora Kinase A and Loss of Primary Cilia in Renal Cell Carcinoma JO: J Am Soc Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=25313256 #FOAvip von Hippel-Lindau (VHL) gene mutations are associated with clear cell renal cell carcinoma (ccRCC). A hallmark of ccRCC is loss of the primary cilium. Loss of this key organelle in ccRCC is caused by loss of VHL and associated with increased Aurora kinase A (AURKA) and histone deacetylase 6 (HDAC6) activities, which drive disassembly of the primary cilium. However, the underlying mechanism by which VHL loss increases AURKA levels has not been clearly elucidated, although it has been suggested that hypoxia-inducible factor-1? (HIF-1?) mediates increased AURKA expression in VHL-null cells. By contrast, we found that elevated AURKA expression is not increased by HIF-1?, suggesting an alternate mechanism for AURKA dysregulation in VHL-null cells. We report here that AURKA expression is driven by ?-catenin transcription in VHL-null cells. In a panel of RCC cell lines, we observed nuclear accumulation of ?-catenin and increased AURKA signaling to HDAC6. Moreover, HIF-1? inhibited AURKA expression by inhibiting ?-catenin transcription. VHL knockdown activated ?-catenin and elevated AURKA expression, decreased primary cilia formation, and caused significant shortening of cilia length in cells that did form cilia. The ?-catenin responsive transcription inhibitor iCRT14 reduced AURKA levels and rescued ciliary defects, inducing a significant increase in primary cilia formation in VHL-deficient cells. These data define a role for ?-catenin in regulating AURKA and formation of primary cilia in the setting of VHL deficiency, opening new avenues for treatment with ?-catenin inhibitors to rescue ciliogenesis in ccRCC. Twit Text FOAVip -Catenin Links von Hippel-Lindau to Aurora Kinase A and Loss of Primary Cilia in Renal Cell Carcinoma ????J Am Soc Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=25313256 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25313256 #FOAvip English Wikipedia <ref>{{Cite pmid|25313256}}</ref> ?-Catenin Links von Hippel-Lindau to Aurora Kinase A and Loss of Primary Cilia in Renal Cell Carcinoma #MMPMID25313256 Dere R; Perkins AL; Bawa-Khalfe T; Jonasch D; Walker CL J Am Soc Nephrol 2015[Mar]; 26 (3): 553-64 PMID25313256show ga von Hippel-Lindau (VHL) gene mutations are associated with clear cell renal cell carcinoma (ccRCC). A hallmark of ccRCC is loss of the primary cilium. Loss of this key organelle in ccRCC is caused by loss of VHL and associated with increased Aurora kinase A (AURKA) and histone deacetylase 6 (HDAC6) activities, which drive disassembly of the primary cilium. However, the underlying mechanism by which VHL loss increases AURKA levels has not been clearly elucidated, although it has been suggested that hypoxia-inducible factor-1? (HIF-1?) mediates increased AURKA expression in VHL-null cells. By contrast, we found that elevated AURKA expression is not increased by HIF-1?, suggesting an alternate mechanism for AURKA dysregulation in VHL-null cells. We report here that AURKA expression is driven by ?-catenin transcription in VHL-null cells. In a panel of RCC cell lines, we observed nuclear accumulation of ?-catenin and increased AURKA signaling to HDAC6. Moreover, HIF-1? inhibited AURKA expression by inhibiting ?-catenin transcription. VHL knockdown activated ?-catenin and elevated AURKA expression, decreased primary cilia formation, and caused significant shortening of cilia length in cells that did form cilia. The ?-catenin responsive transcription inhibitor iCRT14 reduced AURKA levels and rescued ciliary defects, inducing a significant increase in primary cilia formation in VHL-deficient cells. These data define a role for ?-catenin in regulating AURKA and formation of primary cilia in the setting of VHL deficiency, opening new avenues for treatment with ?-catenin inhibitors to rescue ciliogenesis in ccRCC. ä?-Catenin Links von Hippel-Lindau to Aurora Kinase A and Loss of Prima(epmc).pdf DeepDyve Pubget Overpricing