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10.3390/cancers9040037 http://scihub22266oqcxt.onion/10.3390/cancers9040037 C5406712!5406712!28430130     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cancers+(Basel) 2017 ; 9 (4): ä Nephropedia Template TP {{tp|p=28430130|t=2017. Timp1 Promotes Cell Survival by Activating the PDK1 Signaling Pathway in Melanoma |pdf=|usr=}}{{28430130}} gab.com Text Timp1 Promotes Cell Survival by Activating the PDK1 Signaling Pathway in Melanoma JO: Cancers (Basel) http://www.kidney.de/pget.php?&tw=1&pmid=28430130 #FOAvip High TIMP1 expression is associated with poor prognosis in melanoma, where it can bind to CD63 and ?1 integrin, inducing PI3-kinase pathway and cell survival. Phosphatidylinositol (3,4,5)-trisphosphate (PIP3), generated under phosphatidylinositol-3-kinase (PI3K) activation, enables the recruitment and activation of protein kinase B (PKB/AKT) and phosphoinositide-dependent kinase 1 (PDK1) at the membrane, resulting in the phosphorylation of a host of other proteins. Using a melanoma progression model, we evaluated the impact of Timp1 and AKT silencing, as well as PI3K, PDK1, and protein kinase C (PKC) inhibitors on aggressiveness characteristics. Timp1 downregulation resulted in decreased anoikis resistance, clonogenicity, dacarbazine resistance, and in vivo tumor growth and lung colonization. In metastatic cells, pAKTThr308 is highly expressed, contributing to anoikis resistance. We showed that PDK1Ser241 and PKC?IISer660 are activated by Timp1 in different stages of melanoma progression, contributing to colony formation and anoikis resistance. Moreover, simultaneous inhibition of Timp1 and AKT in metastatic cells resulted in more effective anoikis inhibition. Our findings demonstrate that Timp1 promotes cell survival with the participation of PDK1 and PKC in melanoma. In addition, Timp1 and AKT act synergistically to confer anoikis resistance in advanced tumor stages. This study brings new insights about the mechanisms by which Timp1 promotes cell survival in melanoma, and points to novel perspectives for therapeutic approaches. Twit Text FOAVip Timp1 Promotes Cell Survival by Activating the PDK1 Signaling Pathway in Melanoma ????Cancers (Basel) http://www.kidney.de/pget.php?&tw=1&pmid=28430130 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28430130 #FOAvip English Wikipedia <ref>{{Cite pmid|28430130}}</ref> Timp1 Promotes Cell Survival by Activating the PDK1 Signaling Pathway in Melanoma #MMPMID28430130 Toricelli M; Melo FHM; Hunger A; Zanatta D; Strauss BE; Jasiulionis MG Cancers (Basel) 2017[Apr]; 9 (4): ä PMID28430130show ga High TIMP1 expression is associated with poor prognosis in melanoma, where it can bind to CD63 and ?1 integrin, inducing PI3-kinase pathway and cell survival. Phosphatidylinositol (3,4,5)-trisphosphate (PIP3), generated under phosphatidylinositol-3-kinase (PI3K) activation, enables the recruitment and activation of protein kinase B (PKB/AKT) and phosphoinositide-dependent kinase 1 (PDK1) at the membrane, resulting in the phosphorylation of a host of other proteins. Using a melanoma progression model, we evaluated the impact of Timp1 and AKT silencing, as well as PI3K, PDK1, and protein kinase C (PKC) inhibitors on aggressiveness characteristics. Timp1 downregulation resulted in decreased anoikis resistance, clonogenicity, dacarbazine resistance, and in vivo tumor growth and lung colonization. In metastatic cells, pAKTThr308 is highly expressed, contributing to anoikis resistance. We showed that PDK1Ser241 and PKC?IISer660 are activated by Timp1 in different stages of melanoma progression, contributing to colony formation and anoikis resistance. Moreover, simultaneous inhibition of Timp1 and AKT in metastatic cells resulted in more effective anoikis inhibition. Our findings demonstrate that Timp1 promotes cell survival with the participation of PDK1 and PKC in melanoma. In addition, Timp1 and AKT act synergistically to confer anoikis resistance in advanced tumor stages. This study brings new insights about the mechanisms by which Timp1 promotes cell survival in melanoma, and points to novel perspectives for therapeutic approaches. äTimp1 Promotes Cell Survival by Activating the PDK1 Signaling Pathway (epmc).pdf DeepDyve Pubget Overpricing