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10.1038/srep27454 http://scihub22266oqcxt.onion/10.1038/srep27454 C4897636!4897636 !27273450     free     free     free Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\27273450 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Sci+Rep 2016 ; 6 (ä): 27454 Nephropedia Template TP {{tp|p=27273450 |t=2016. CRAF R391W is a melanoma driver oncogene |pdf=|usr=}}{{27273450 }} gab.com Text CRAF R391W is a melanoma driver oncogene JO: Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=27273450 #FOAvip Approximately 75% of melanomas have known driver oncogenic mutations in BRAF, NRAS, GNA11 or GNAQ, while the mutations providing constitutive oncogenic signaling in the remaining melanomas are not known. We established a melanoma cell line from a tumor with none of the common driver mutations. This cell line demonstrated a signaling profile similar to BRAF-mutants, but lacked sensitivity to the BRAF inhibitor vemurafenib. RNA-seq mutation data implicated CRAF R391W as the alternative driver mutation of this melanoma. CRAF R391W was homozygous and over expressed. These melanoma cells were highly sensitive to CRAF, but not BRAF knockdown. In reconstitution experiments, CRAF R391W, but not CRAF WT, transformed NIH3T3 cells in soft-agar colony formation assays, increased kinase activity in vitro, induced MAP kinase signaling and conferred vemurafenib resistance. MAP kinase inducing activity was dependent on CRAF dimerization. Thus, CRAF is a bona fide alternative oncogene for BRAF/NRAS/GNAQ/GNA11 wild type melanomas. Twit Text FOAVip CRAF R391W is a melanoma driver oncogene ????Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=27273450 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27273450 #FOAvip English Wikipedia <ref>{{Cite pmid|27273450 }}</ref> CRAF R391W is a melanoma driver oncogene #MMPMID27273450 Atefi M ; Titz B ; Tsoi J ; Avramis E ; Le A ; Ng C ; Lomova A ; Lassen A ; Friedman M ; Chmielowski B ; Ribas A ; Graeber TG Sci Rep 2016[Jun]; 6 (ä): 27454 PMID27273450 show ga Approximately 75% of melanomas have known driver oncogenic mutations in BRAF, NRAS, GNA11 or GNAQ, while the mutations providing constitutive oncogenic signaling in the remaining melanomas are not known. We established a melanoma cell line from a tumor with none of the common driver mutations. This cell line demonstrated a signaling profile similar to BRAF-mutants, but lacked sensitivity to the BRAF inhibitor vemurafenib. RNA-seq mutation data implicated CRAF R391W as the alternative driver mutation of this melanoma. CRAF R391W was homozygous and over expressed. These melanoma cells were highly sensitive to CRAF, but not BRAF knockdown. In reconstitution experiments, CRAF R391W, but not CRAF WT, transformed NIH3T3 cells in soft-agar colony formation assays, increased kinase activity in vitro, induced MAP kinase signaling and conferred vemurafenib resistance. MAP kinase inducing activity was dependent on CRAF dimerization. Thus, CRAF is a bona fide alternative oncogene for BRAF/NRAS/GNAQ/GNA11 wild type melanomas. |*Oncogenes [MESH] |Aged [MESH] |Animals [MESH] |Humans [MESH] |MAP Kinase Signaling System [MESH] |Melanoma/*genetics [MESH] |Mice [MESH] |NIH 3T3 Cells [MESH]CRAF R391W is a melanoma driver oncogene (epmc).pdf DeepDyve Pubget Overpricing