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10.1158/0008-5472.CAN-15-0989 http://scihub22266oqcxt.onion/10.1158/0008-5472.CAN-15-0989 C4558210!4558210 !26282175     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26282175 &cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\26282175 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Cancer+Res 2015 ; 75 (17 ): 3436-41 Nephropedia Template TP {{tp|p=26282175 |t=2015. Ligand-Independent EGFR Signaling |pdf=|usr=}}{{26282175 }} gab.com Text Ligand-Independent EGFR Signaling JO: Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=26282175 #FOAvip Constitutive activation of the EGFR is common in cancer due to EGFR wild-type (EGFRwt) overexpression or the presence of mutant EGFR. Signaling by constitutively active NSCLC EGFR mutants or the EGFRvIII mutant in glioblastoma has been studied intensively and the downstream signals are known. Normally, the EGFRwt is activated when it is exposed to ligand, resulting in activation of canonical signals such as ERK and Akt. The EGFRwt also becomes tyrosine phosphorylated and constitutively activated without ligand when it is overexpressed, but downstream signals are unclear. Recent studies have identified a noncanonical form of signaling triggered by EGFRwt exclusively in the absence of ligand that does not involve ERK or Akt activation but, instead, results in activation of the transcription factor IRF3. The addition of ligand turns off IRF3-dependent transcription and activates ERK and Akt. Thus, the EGFR triggers distinct and mutually exclusive signaling networks, depending on the presence of ligand. Furthermore, noncanonical EGFRwt signaling may influence response to treatment in cancer. Also, there are reports of both synergistic and antagonistic interactions between ligand-dependent EGFRwt and EGFRvIII signaling. Here, we discuss ligand-independent EGFR signal transduction by oncogenic EGFR mutants and EGFRwt, and review the interplay between EGFRwt and EGFRvIII. Twit Text FOAVip Ligand-Independent EGFR Signaling ????Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=26282175 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26282175 #FOAvip English Wikipedia <ref>{{Cite pmid|26282175 }}</ref> Ligand-Independent EGFR Signaling #MMPMID26282175 Guo G ; Gong K ; Wohlfeld B ; Hatanpaa KJ ; Zhao D ; Habib AA Cancer Res 2015[Sep]; 75 (17 ): 3436-41 PMID26282175 show ga Constitutive activation of the EGFR is common in cancer due to EGFR wild-type (EGFRwt) overexpression or the presence of mutant EGFR. Signaling by constitutively active NSCLC EGFR mutants or the EGFRvIII mutant in glioblastoma has been studied intensively and the downstream signals are known. Normally, the EGFRwt is activated when it is exposed to ligand, resulting in activation of canonical signals such as ERK and Akt. The EGFRwt also becomes tyrosine phosphorylated and constitutively activated without ligand when it is overexpressed, but downstream signals are unclear. Recent studies have identified a noncanonical form of signaling triggered by EGFRwt exclusively in the absence of ligand that does not involve ERK or Akt activation but, instead, results in activation of the transcription factor IRF3. The addition of ligand turns off IRF3-dependent transcription and activates ERK and Akt. Thus, the EGFR triggers distinct and mutually exclusive signaling networks, depending on the presence of ligand. Furthermore, noncanonical EGFRwt signaling may influence response to treatment in cancer. Also, there are reports of both synergistic and antagonistic interactions between ligand-dependent EGFRwt and EGFRvIII signaling. Here, we discuss ligand-independent EGFR signal transduction by oncogenic EGFR mutants and EGFRwt, and review the interplay between EGFRwt and EGFRvIII. |Carcinoma, Non-Small-Cell Lung/*genetics/pathology [MESH] |ErbB Receptors/biosynthesis/*genetics [MESH] |Gene Expression Regulation, Neoplastic [MESH] |Humans [MESH] |Interferon Regulatory Factor-3/genetics [MESH] |Ligands [MESH] |MAP Kinase Signaling System/genetics [MESH] |Mutation [MESH] |Proto-Oncogene Proteins c-akt [MESH]Ligand-Independent EGFR Signaling (epmc).pdf DeepDyve Pubget Overpricing