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10.1038/onc.2014.395 http://scihub22266oqcxt.onion/10.1038/onc.2014.395 C4459945!4459945!25486430     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Oncogene 2015 ; 34 (36): 4702-12 Nephropedia Template TP {{tp|p=25486430|t=2015. Casein Kinase 2 prevents mesenchymal transformation by maintaining Foxc2 in the cytoplasm |pdf=|usr=}}{{25486430}} gab.com Text Casein Kinase 2 prevents mesenchymal transformation by maintaining Foxc2 in the cytoplasm JO: Oncogene http://www.kidney.de/pget.php?&tw=1&pmid=25486430 #FOAvip Nuclear Foxc2 is a transcriptional regulator of mesenchymal transformation during developmental EMT and has been associated with EMT in malignant epithelia. Our laboratory has shown that in normal epithelial cells Foxc2 is maintained in the cytoplasm where it promotes an epithelial phenotype. The Foxc2 amino terminus has a consensus casein kinase 2 phosphorylation site at serine 124, and we now show that CK2 associates with Foxc2 and phosphorylates this site in vitro. Knock-down or inhibition of the CK2?/?? kinase subunit in epithelial cells causes de novo accumulation of Foxc2 in the nucleus. Mutation of serine 124 to leucine promotes constitutive nuclear localization of Foxc2 and expression of mesenchymal genes, whereas an S124D phosphomimetic leads to constitutive cytoplasmic localization and epithelial maintenance. In malignant breast cancer cells the CK2? regulatory subunit is downregulated and FOXC2 is found in the nucleus, correlating with an increase in ?-SMA expression. Restoration of CK2? expression in these cells results in cytoplasmic localization of Foxc2, decreased ?-SMA expression and reduced cell migration and invasion. In contrast, knockdown of CK2? in normal breast epithelial cells leads to FOXC2 nuclear localization, decreased E-cadherin expression, increased ?-SMA and vimentin expression, and enhanced cell migration and invasion. Based on these findings we propose that Foxc2 is functionally maintained in the cytoplasm of normal epithelial cells by CK2?/??-mediated phosphorylation at serine 124 that is dependent on proper targeting of the holoenzyme via the CK2? regulatory subunit. Twit Text FOAVip Casein Kinase 2 prevents mesenchymal transformation by maintaining Foxc2 in the cytoplasm ????Oncogene http://www.kidney.de/pget.php?&tw=1&pmid=25486430 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25486430 #FOAvip English Wikipedia <ref>{{Cite pmid|25486430}}</ref> Casein Kinase 2 prevents mesenchymal transformation by maintaining Foxc2 in the cytoplasm #MMPMID25486430 Golden D; Cantley LG Oncogene 2015[Sep]; 34 (36): 4702-12 PMID25486430show ga Nuclear Foxc2 is a transcriptional regulator of mesenchymal transformation during developmental EMT and has been associated with EMT in malignant epithelia. Our laboratory has shown that in normal epithelial cells Foxc2 is maintained in the cytoplasm where it promotes an epithelial phenotype. The Foxc2 amino terminus has a consensus casein kinase 2 phosphorylation site at serine 124, and we now show that CK2 associates with Foxc2 and phosphorylates this site in vitro. Knock-down or inhibition of the CK2?/?? kinase subunit in epithelial cells causes de novo accumulation of Foxc2 in the nucleus. Mutation of serine 124 to leucine promotes constitutive nuclear localization of Foxc2 and expression of mesenchymal genes, whereas an S124D phosphomimetic leads to constitutive cytoplasmic localization and epithelial maintenance. In malignant breast cancer cells the CK2? regulatory subunit is downregulated and FOXC2 is found in the nucleus, correlating with an increase in ?-SMA expression. Restoration of CK2? expression in these cells results in cytoplasmic localization of Foxc2, decreased ?-SMA expression and reduced cell migration and invasion. In contrast, knockdown of CK2? in normal breast epithelial cells leads to FOXC2 nuclear localization, decreased E-cadherin expression, increased ?-SMA and vimentin expression, and enhanced cell migration and invasion. Based on these findings we propose that Foxc2 is functionally maintained in the cytoplasm of normal epithelial cells by CK2?/??-mediated phosphorylation at serine 124 that is dependent on proper targeting of the holoenzyme via the CK2? regulatory subunit. äCasein Kinase 2 prevents mesenchymal transformation by maintaining Fox(epmc).pdf DeepDyve Pubget Overpricing