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10.1371/journal.pone.0152695 http://scihub22266oqcxt.onion/10.1371/journal.pone.0152695 C4839611!4839611!27100093     free     free     free Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 269.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\27100093.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       PLoS+One 2016 ; 11 (4): ä Nephropedia Template TP {{tp|p=27100093|t=2016. Diverse Basis of ?-Catenin Activation in Human Hepatocellular Carcinoma: Implications in Biology and Prognosis |pdf=|usr=}}{{27100093}} gab.com Text Diverse Basis of -Catenin Activation in Human Hepatocellular Carcinoma: Implications in Biology and Prognosis JO: PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=27100093 #FOAvip Aim: ?-catenin signaling is a major oncogenic pathway in hepatocellular carcinoma (HCC). Since ?-catenin phosphorylation by glycogen synthase kinase 3? (GSK3?) and casein kinase 1? (CK1?) results in its degradation, mutations affecting these phosphorylation sites cause ?-catenin stabilization. However, the relevance of missense mutations in non-phosphorylation sites in exon 3 remains unclear. The current study explores significance of such mutations in addition to addressing the clinical and biological implications of ?-catenin activation in human HCC. Methods: Gene alteration in exon3 of CTNNB1, gene expression of ?-catenin targets such as glutamate synthetase (GS), axin2, lect2 and regucalcin (RGN), and protein expression of ?-catenin were examined in 125 human HCC tissues. Results: Sixteen patients (12.8%) showed conventional missense mutations affecting codons 33, 37, 41, and 45. Fifteen additional patients (12.0%) had other missense mutations in codon 32, 34, and 35. Induction of exon3 mutation caused described ?-catenin target gene upregulation in HCC cell line. Interestingly, conventional and non-phosphorylation site mutations were equally associated with upregulation of ?-catenin target genes. Nuclear localization of ?-catenin was associated with poor overall survival (p = 0.0461). Of these patients with nuclear ?-catenin localization, loss of described ?-catenin target gene upregulation showed significant poorer overall survival than others (p = 0.0001). Conclusion: This study suggests that both conventional and other missense mutations in exon 3 of CTNNB1 lead to ?-catenin activation in human HCC. Additionally, the mechanism of nuclear ?-catenin localization without upregulation of described ?-catenin target genes might be of clinical importance depending on distinct mechanism. Twit Text FOAVip Diverse Basis of -Catenin Activation in Human Hepatocellular Carcinoma: Implications in Biology and Prognosis ????PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=27100093 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27100093 #FOAvip English Wikipedia <ref>{{Cite pmid|27100093}}</ref> Diverse Basis of ?-Catenin Activation in Human Hepatocellular Carcinoma: Implications in Biology and Prognosis #MMPMID27100093 Okabe H; Kinoshita H; Imai K; Nakagawa S; Higashi T; Arima K; Uchiyama H; Ikegami T; Harimoto N; Itoh S; Ishiko T; Yoshizumi T; Beppu T; Monga SPS; Baba H; Maehara Y PLoS One 2016[]; 11 (4): ä PMID27100093show ga Aim: ?-catenin signaling is a major oncogenic pathway in hepatocellular carcinoma (HCC). Since ?-catenin phosphorylation by glycogen synthase kinase 3? (GSK3?) and casein kinase 1? (CK1?) results in its degradation, mutations affecting these phosphorylation sites cause ?-catenin stabilization. However, the relevance of missense mutations in non-phosphorylation sites in exon 3 remains unclear. The current study explores significance of such mutations in addition to addressing the clinical and biological implications of ?-catenin activation in human HCC. Methods: Gene alteration in exon3 of CTNNB1, gene expression of ?-catenin targets such as glutamate synthetase (GS), axin2, lect2 and regucalcin (RGN), and protein expression of ?-catenin were examined in 125 human HCC tissues. Results: Sixteen patients (12.8%) showed conventional missense mutations affecting codons 33, 37, 41, and 45. Fifteen additional patients (12.0%) had other missense mutations in codon 32, 34, and 35. Induction of exon3 mutation caused described ?-catenin target gene upregulation in HCC cell line. Interestingly, conventional and non-phosphorylation site mutations were equally associated with upregulation of ?-catenin target genes. Nuclear localization of ?-catenin was associated with poor overall survival (p = 0.0461). Of these patients with nuclear ?-catenin localization, loss of described ?-catenin target gene upregulation showed significant poorer overall survival than others (p = 0.0001). Conclusion: This study suggests that both conventional and other missense mutations in exon 3 of CTNNB1 lead to ?-catenin activation in human HCC. Additionally, the mechanism of nuclear ?-catenin localization without upregulation of described ?-catenin target genes might be of clinical importance depending on distinct mechanism. äDiverse Basis of ?-Catenin Activation in Human Hepatocellular Carcinom(epmc).pdf DeepDyve Pubget Overpricing