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10.1074/jbc.M114.593392 http://scihub22266oqcxt.onion/10.1074/jbc.M114.593392 C4263869!4263869 !25344606     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 251.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 251.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 251.2 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\25344606 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       J+Biol+Chem 2014 ; 289 (50 ): 34627-41 Nephropedia Template TP {{tp|p=25344606 |t=2014. ?-Galactoside ?2,6-sialyltranferase 1 promotes transforming growth factor-?-mediated epithelial-mesenchymal transition |pdf=|usr=}}{{25344606 }} gab.com Text -Galactoside 2,6-sialyltranferase 1 promotes transforming growth factor- -mediated epithelial-mesenchymal transition JO: J Biol Chem http://www.kidney.de/pget.php?&tw=1&pmid=25344606 #FOAvip ?-Galactoside ?2,6-sialyltranferase 1 (ST6GAL1) catalyzes the addition of terminal ?2,6-sialylation to N-glycans. Increased expression of ST6GAL1 has been reported in diverse carcinomas and highly correlates with tumor progression. Here, we report that St6gal1 transcription and ?2,6-sialylated N-glycans are up-regulated during TGF-?-induced epithelial-mesenchymal transition (EMT) in GE11 cells, requiring the Sp1 element within the St6gal1 promoter. Knockdown of St6gal1 strongly suppressed TGF-?-induced EMT with a concomitant increase in E-cadherin expression, a major determinant of epithelial cell adherens junctions. Conversely, overexpression of ST6GAL1 increased the turnover of cell surface E-cadherin and promoted TGF-?-induced EMT. Overexpressing ?-galactoside ?2,3-sialyltranferase 4 had little influence on EMT, indicating specificity for ?2,6-sialylation. The basal mesenchymal phenotype of MDA-MB-231 human breast cancer cells was partially reversed by ST6GAL1 silencing. Moreover, ST6GAL1 knockdown inhibited the phosphorylation of Akt, but not Smad2, suggesting that ST6GAL1 contributes to EMT through a non-Smad signaling pathway. Taken together, our data indicate that ST6GAL1 promotes TGF-?-dependent EMT as well as maintenance of the mesenchymal state by growth signaling, providing a plausible mechanism whereby up-regulated ST6GAL1 may promote malignant progression. Twit Text FOAVip -Galactoside 2,6-sialyltranferase 1 promotes transforming growth factor- -mediated epithelial-mesenchymal transition ????J Biol Chem http://www.kidney.de/pget.php?&tw=1&pmid=25344606 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25344606 #FOAvip English Wikipedia <ref>{{Cite pmid|25344606 }}</ref> ?-Galactoside ?2,6-sialyltranferase 1 promotes transforming growth factor-?-mediated epithelial-mesenchymal transition #MMPMID25344606 Lu J ; Isaji T ; Im S ; Fukuda T ; Hashii N ; Takakura D ; Kawasaki N ; Gu J J Biol Chem 2014[Dec]; 289 (50 ): 34627-41 PMID25344606 show ga ?-Galactoside ?2,6-sialyltranferase 1 (ST6GAL1) catalyzes the addition of terminal ?2,6-sialylation to N-glycans. Increased expression of ST6GAL1 has been reported in diverse carcinomas and highly correlates with tumor progression. Here, we report that St6gal1 transcription and ?2,6-sialylated N-glycans are up-regulated during TGF-?-induced epithelial-mesenchymal transition (EMT) in GE11 cells, requiring the Sp1 element within the St6gal1 promoter. Knockdown of St6gal1 strongly suppressed TGF-?-induced EMT with a concomitant increase in E-cadherin expression, a major determinant of epithelial cell adherens junctions. Conversely, overexpression of ST6GAL1 increased the turnover of cell surface E-cadherin and promoted TGF-?-induced EMT. Overexpressing ?-galactoside ?2,3-sialyltranferase 4 had little influence on EMT, indicating specificity for ?2,6-sialylation. The basal mesenchymal phenotype of MDA-MB-231 human breast cancer cells was partially reversed by ST6GAL1 silencing. Moreover, ST6GAL1 knockdown inhibited the phosphorylation of Akt, but not Smad2, suggesting that ST6GAL1 contributes to EMT through a non-Smad signaling pathway. Taken together, our data indicate that ST6GAL1 promotes TGF-?-dependent EMT as well as maintenance of the mesenchymal state by growth signaling, providing a plausible mechanism whereby up-regulated ST6GAL1 may promote malignant progression. |Antigens, CD/genetics/*metabolism [MESH] |Binding Sites [MESH] |Breast Neoplasms/pathology [MESH] |Cadherins/metabolism [MESH] |Cell Line, Tumor [MESH] |Cell Movement/drug effects [MESH] |Disease Progression [MESH] |Epithelial-Mesenchymal Transition/*drug effects [MESH] |Gene Knockdown Techniques [MESH] |Gene Silencing [MESH] |Humans [MESH] |Phenotype [MESH] |Promoter Regions, Genetic/genetics [MESH] |Sialyltransferases/deficiency/genetics/*metabolism [MESH] |Sp1 Transcription Factor/metabolism [MESH] |Transcriptional Activation/drug effects [MESH] |Transforming Growth Factor beta/*pharmacology [MESH]?-Galactoside ?2,6-sialyltranferase 1 promotes transforming growth f(epmc).pdf DeepDyve Pubget Overpricing