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10.1158/1541-7786.MCR-14-0411 http://scihub22266oqcxt.onion/10.1158/1541-7786.MCR-14-0411 C4369191!4369191!25392346     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 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       Mol+Cancer+Res 2015 ; 13 (3): 575-83 Nephropedia Template TP {{tp|p=25392346|t=2015. The TWEAK Receptor Fn14 is a Src-inducible Protein and a Positive Regulator of Src-driven Cell Invasion |pdf=|usr=}}{{25392346}} gab.com Text The TWEAK Receptor Fn14 is a Src-inducible Protein and a Positive Regulator of Src-driven Cell Invasion JO: Mol Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=25392346 #FOAvip The TNF receptor superfamily member Fn14 (TNFRSF12A) is the sole signaling receptor for the pro-inflammatory cytokine TWEAK (TNFSF12). TWEAK:Fn14 engagement stimulates multiple signal transduction pathways, including the NF-?B pathway, and this triggers important cellular processes (e.g., growth, differentiation, migration, invasion). The TWEAK/Fn14 axis is thought to be a major physiological mediator of tissue repair after acute injury. Various studies have revealed that Fn14 is highly expressed in many solid tumor types and that Fn14 signaling may play a role in tumor growth and metastasis. Previously it was shown that Fn14 levels are frequently elevated in non-small cell lung cancer (NSCLC) tumors and cell lines that exhibit constitutive EGFR phosphorylation (activation). Furthermore, elevated Fn14 levels increased NSCLC cell invasion in vitro and lung metastatic tumor colonization in vivo. The present study reveals that EGFR-mutant NSCLC cells that express high levels of Fn14 exhibit constitutive activation of the cytoplasmic tyrosine kinase Src and that treatment with the Src family kinase (SFK) inhibitor dasatinib decreases Fn14 gene expression at both the mRNA and protein levels. Importantly, siRNA-mediated depletion of the SFK member Src in NSCLC cells also decreases Fn14 expression. Finally, expression of the constitutively active v-Src oncoprotein in NIH 3T3 cells induces Fn14 gene expression and NIH 3T3/v-Src cells require Fn14 expression for full invasive capacity. Twit Text FOAVip The TWEAK Receptor Fn14 is a Src-inducible Protein and a Positive Regulator of Src-driven Cell Invasion ????Mol Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=25392346 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25392346 #FOAvip English Wikipedia <ref>{{Cite pmid|25392346}}</ref> The TWEAK Receptor Fn14 is a Src-inducible Protein and a Positive Regulator of Src-driven Cell Invasion #MMPMID25392346 Cheng E; Whitsett TG; Tran NL; Winkles JA Mol Cancer Res 2015[Mar]; 13 (3): 575-83 PMID25392346show ga The TNF receptor superfamily member Fn14 (TNFRSF12A) is the sole signaling receptor for the pro-inflammatory cytokine TWEAK (TNFSF12). TWEAK:Fn14 engagement stimulates multiple signal transduction pathways, including the NF-?B pathway, and this triggers important cellular processes (e.g., growth, differentiation, migration, invasion). The TWEAK/Fn14 axis is thought to be a major physiological mediator of tissue repair after acute injury. Various studies have revealed that Fn14 is highly expressed in many solid tumor types and that Fn14 signaling may play a role in tumor growth and metastasis. Previously it was shown that Fn14 levels are frequently elevated in non-small cell lung cancer (NSCLC) tumors and cell lines that exhibit constitutive EGFR phosphorylation (activation). Furthermore, elevated Fn14 levels increased NSCLC cell invasion in vitro and lung metastatic tumor colonization in vivo. The present study reveals that EGFR-mutant NSCLC cells that express high levels of Fn14 exhibit constitutive activation of the cytoplasmic tyrosine kinase Src and that treatment with the Src family kinase (SFK) inhibitor dasatinib decreases Fn14 gene expression at both the mRNA and protein levels. Importantly, siRNA-mediated depletion of the SFK member Src in NSCLC cells also decreases Fn14 expression. Finally, expression of the constitutively active v-Src oncoprotein in NIH 3T3 cells induces Fn14 gene expression and NIH 3T3/v-Src cells require Fn14 expression for full invasive capacity. äThe TWEAK Receptor Fn14 is a Src-inducible Protein and a Positive Regu(epmc).pdf DeepDyve Pubget Overpricing