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10.1074/jbc.M114.621011 http://scihub22266oqcxt.onion/10.1074/jbc.M114.621011 C4375497!4375497 !25657002     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25657002 &cmd=llinks): Failed to open stream: HTTP request failed! 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Loss of the polarity protein PAR3 activates STAT3 signaling via an atypical protein kinase C (aPKC)/NF-?B/interleukin-6 (IL-6) axis in mouse mammary cells |pdf=|usr=}}{{25657002 }} gab.com Text Loss of the polarity protein PAR3 activates STAT3 signaling via an atypical protein kinase C (aPKC)/NF- B/interleukin-6 (IL-6) axis in mouse mammary cells JO: J Biol Chem http://www.kidney.de/pget.php?&tw=1&pmid=25657002 #FOAvip PAR3 suppresses tumor growth and metastasis in vivo and cell invasion through matrix in vitro. We propose that PAR3 organizes and limits multiple signaling pathways and that inappropriate activation of these pathways occurs without PAR3. Silencing Pard3 in conjunction with oncogenic activation promotes invasion and metastasis via constitutive STAT3 activity in mouse models, but the mechanism for this is unknown. We now show that loss of PAR3 triggers increased production of interleukin-6, which induces STAT3 signaling in an autocrine manner. Activation of atypical protein kinase C ?/? (aPKC?/?) mediates this effect by stimulating NF-?B signaling and IL-6 expression. Our results suggest that PAR3 restrains aPKC?/? activity and thus prevents aPKC?/? from activating an oncogenic signaling network. Twit Text FOAVip Loss of the polarity protein PAR3 activates STAT3 signaling via an atypical protein kinase C (aPKC)/NF- B/interleukin-6 (IL-6) axis in mouse mammary cells ????J Biol Chem http://www.kidney.de/pget.php?&tw=1&pmid=25657002 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25657002 #FOAvip English Wikipedia <ref>{{Cite pmid|25657002 }}</ref> Loss of the polarity protein PAR3 activates STAT3 signaling via an atypical protein kinase C (aPKC)/NF-?B/interleukin-6 (IL-6) axis in mouse mammary cells #MMPMID25657002 Guyer RA ; Macara IG J Biol Chem 2015[Mar]; 290 (13 ): 8457-68 PMID25657002 show ga PAR3 suppresses tumor growth and metastasis in vivo and cell invasion through matrix in vitro. We propose that PAR3 organizes and limits multiple signaling pathways and that inappropriate activation of these pathways occurs without PAR3. Silencing Pard3 in conjunction with oncogenic activation promotes invasion and metastasis via constitutive STAT3 activity in mouse models, but the mechanism for this is unknown. We now show that loss of PAR3 triggers increased production of interleukin-6, which induces STAT3 signaling in an autocrine manner. Activation of atypical protein kinase C ?/? (aPKC?/?) mediates this effect by stimulating NF-?B signaling and IL-6 expression. Our results suggest that PAR3 restrains aPKC?/? activity and thus prevents aPKC?/? from activating an oncogenic signaling network. |Adaptor Proteins, Signal Transducing [MESH] |Animals [MESH] |Autocrine Communication [MESH] |Cell Adhesion Molecules/*genetics [MESH] |Cell Cycle Proteins [MESH] |Cells, Cultured [MESH] |Cytokine Receptor gp130/metabolism [MESH] |Enzyme Activation [MESH] |Epithelial Cells/metabolism [MESH] |Female [MESH] |Interleukin-6/*metabolism [MESH] |Mammary Glands, Animal/cytology [MESH] |Mice, Inbred C3H [MESH] |NF-kappa B/*metabolism [MESH] |Phosphorylation [MESH] |Protein Kinase C/*metabolism [MESH] |Protein Processing, Post-Translational [MESH] |STAT3 Transcription Factor/*metabolism [MESH]Loss of the polarity protein PAR3 activates STAT3 signaling via an aty(epmc).pdf DeepDyve Pubget Overpricing