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10.1038/s41419-018-0548-3 http://scihub22266oqcxt.onion/10.1038/s41419-018-0548-3 C5938705!5938705!29725063     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cell+Death+Dis 2018 ; 9 (5): ä Nephropedia Template TP {{tp|p=29725063|t=2018. Actin like-6A promotes glioma progression through stabilization of transcriptional regulators YAP/TAZ |pdf=|usr=}}{{29725063}} gab.com Text Actin like-6A promotes glioma progression through stabilization of transcriptional regulators YAP/TAZ JO: Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=29725063 #FOAvip Increased Actin-like 6A (ACTL6A) expression has been implicated in the development of diverse cancers and recently associated with the Hippo signaling pathway, which is known to regulate biological properties, including proliferation, tissue regeneration, stem cell biology, as well as tumorigenesis. Here we first show that ACTL6A is upregulated in human gliomas and its expression is associated with glioma patient survival. ACTL6A promotes malignant behaviors of glioma cells in vitro and in orthotopic xenograft model. In co-immunoprecipitation assays, we discover that ACTL6A physically associated with YAP/TAZ and furthermore disrupts the interaction between YAP and ?-TrCP E3 ubiquitin ligase, which promotes YAP protein degradation. Moreover, effects of ACTL6A on glioma cells proliferation, migration, and invasion could be mediated by YAP/TAZ. These data indicate that ACTL6A may contribute to cancer progression by stabilizing YAP/TAZ and therefore provide a novel therapeutic target for the treatment of human gliomas. Twit Text FOAVip Actin like-6A promotes glioma progression through stabilization of transcriptional regulators YAP/TAZ ????Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=29725063 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29725063 #FOAvip English Wikipedia <ref>{{Cite pmid|29725063}}</ref> Actin like-6A promotes glioma progression through stabilization of transcriptional regulators YAP/TAZ #MMPMID29725063 Ji J; Xu R; Zhang X; Han M; Xu Y; Wei Y; Ding K; Wang S; Bin Huang; Chen A; Di Zhang; Jiang Z; Xu S; Zhang Q; Li W; Ni S; Wang J; Li X Cell Death Dis 2018[May]; 9 (5): ä PMID29725063show ga Increased Actin-like 6A (ACTL6A) expression has been implicated in the development of diverse cancers and recently associated with the Hippo signaling pathway, which is known to regulate biological properties, including proliferation, tissue regeneration, stem cell biology, as well as tumorigenesis. Here we first show that ACTL6A is upregulated in human gliomas and its expression is associated with glioma patient survival. ACTL6A promotes malignant behaviors of glioma cells in vitro and in orthotopic xenograft model. In co-immunoprecipitation assays, we discover that ACTL6A physically associated with YAP/TAZ and furthermore disrupts the interaction between YAP and ?-TrCP E3 ubiquitin ligase, which promotes YAP protein degradation. Moreover, effects of ACTL6A on glioma cells proliferation, migration, and invasion could be mediated by YAP/TAZ. These data indicate that ACTL6A may contribute to cancer progression by stabilizing YAP/TAZ and therefore provide a novel therapeutic target for the treatment of human gliomas. äActin like-6A promotes glioma progression through stabilization of tra(epmc).pdf DeepDyve Pubget Overpricing