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10.1158/0008-5472.CAN-13-3058 http://scihub22266oqcxt.onion/10.1158/0008-5472.CAN-13-3058 C4488067!4488067!24509905     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       Cancer+Res 2014 ; 74 (8): 2362-73 Nephropedia Template TP {{tp|p=24509905|t=2014. Cofilin Drives Cell-Invasive and Metastatic Responses to TGF-? in Prostate Cancer |pdf=|usr=}}{{24509905}} gab.com Text Cofilin Drives Cell-Invasive and Metastatic Responses to TGF- in Prostate Cancer JO: Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=24509905 #FOAvip Cofilin (CFL) is an F-actin?severing protein required for the cytoskeleton reorganization and filopodia formation, which drives cell migration. CFL binding and severing of F-actin is controlled by Ser3 phosphorylation, but the contributions of this step to cell migration during invasion and metastasis of cancer cells are unclear. In this study, we addressed the question in prostate cancer cells, including the response to TGF-?, a critical regulator of migration. In cells expressing wild-type CFL, TGF-? treatment increased LIMK-2 activity and cofilin phosphorylation, decreasing filopodia formation. Conversely, constitutively active CFL (SerAla) promoted filipodia formation and cell migration mediated by TGF-?. Notably, in cocultures of prostate cancer epithelial cells and cancer-associated fibroblasts, active CFL promoted invasive migration in response to TGF-? in the microenvironment. Further, constitutively active CFL elevated the metastatic ability of prostate cancer cells in vivo. We found that levels of active CFL correlated with metastasis in a mouse model of prostate tumor and that in human prostate cancer, CFL expression was increased significantly in metastatic tumors. Our findings show that the actin-severing protein CFL coordinates responses to TGF-? that are needed for invasive cancer migration and metastasis. Twit Text FOAVip Cofilin Drives Cell-Invasive and Metastatic Responses to TGF- in Prostate Cancer ????Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=24509905 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24509905 #FOAvip English Wikipedia <ref>{{Cite pmid|24509905}}</ref> Cofilin Drives Cell-Invasive and Metastatic Responses to TGF-? in Prostate Cancer #MMPMID24509905 Collazo J; Zhu B; Larkin S; Martin SK; Pu H; Horbinski C; Koochekpour S; Kyprianou N Cancer Res 2014[Apr]; 74 (8): 2362-73 PMID24509905show ga Cofilin (CFL) is an F-actin?severing protein required for the cytoskeleton reorganization and filopodia formation, which drives cell migration. CFL binding and severing of F-actin is controlled by Ser3 phosphorylation, but the contributions of this step to cell migration during invasion and metastasis of cancer cells are unclear. In this study, we addressed the question in prostate cancer cells, including the response to TGF-?, a critical regulator of migration. In cells expressing wild-type CFL, TGF-? treatment increased LIMK-2 activity and cofilin phosphorylation, decreasing filopodia formation. Conversely, constitutively active CFL (SerAla) promoted filipodia formation and cell migration mediated by TGF-?. Notably, in cocultures of prostate cancer epithelial cells and cancer-associated fibroblasts, active CFL promoted invasive migration in response to TGF-? in the microenvironment. Further, constitutively active CFL elevated the metastatic ability of prostate cancer cells in vivo. We found that levels of active CFL correlated with metastasis in a mouse model of prostate tumor and that in human prostate cancer, CFL expression was increased significantly in metastatic tumors. Our findings show that the actin-severing protein CFL coordinates responses to TGF-? that are needed for invasive cancer migration and metastasis. äCofilin Drives Cell-Invasive and Metastatic Responses to TGF-? in Pros(epmc).pdf DeepDyve Pubget Overpricing