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10.18632/oncotarget.13338 http://scihub22266oqcxt.onion/10.18632/oncotarget.13338 C5356633!5356633!27863380     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 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Oncotarget 2016 ; 7 (51): 83893-906 Nephropedia Template TP {{tp|p=27863380|t=2016. Arctigenin functions as a selective agonist of estrogen receptor ? to restrict mTORC1 activation and consequent Th17 differentiation |pdf=|usr=}}{{27863380}} gab.com Text Arctigenin functions as a selective agonist of estrogen receptor to restrict mTORC1 activation and consequent Th17 differentiation JO: Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=27863380 #FOAvip Arctigenin was previously proven to inhibit Th17 cell differentiation and thereby attenuate colitis in mice by down-regulating the activation of mechanistic target of rapamycin complex 1 (mTORC1). The present study was performed to address its underlying mechanism in view of estrogen receptor (ER). The specific antagonist PHTPP or siRNA of ER? largely diminished the inhibitory effect of arctigenin on the mTORC1 activation in T cell lines and primary CD4+ T cells under Th17-polarization condition, suggesting that arctigenin functioned in an ER?-dependent manner. Moreover, arctigenin was recognized to be an agonist of ER?, which could bind to ER? with a moderate affinity, promote dissociation of ER?/HSP90 complex and nuclear translocation and phosphorylation of ER?, and increase the transcription activity. Following activation of ER?, arctigenin inhibited the activity of mTORC1 by disruption of ER?-raptor-mTOR complex assembly. Deficiency of ER? markedly abolished arctigenin-mediated inhibition of Th17 cell differentiation. In colitis mice, the activation of ER?, inhibition of mTORC1 activation and Th17 response by arctigenin were abolished by PHTPP treatment. In conclusion, ER? might be the target protein of arctigenin responsible for inhibition of mTORC1 activation and resultant prevention of Th17 cell differentiation and colitis development. Twit Text FOAVip Arctigenin functions as a selective agonist of estrogen receptor to restrict mTORC1 activation and consequent Th17 differentiation ????Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=27863380 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27863380 #FOAvip English Wikipedia <ref>{{Cite pmid|27863380}}</ref> Arctigenin functions as a selective agonist of estrogen receptor ? to restrict mTORC1 activation and consequent Th17 differentiation #MMPMID27863380 Wu X; Tong B; Yang Y; Luo J; Yuan X; Wei Z; Yue M; Xia Y; Dai Y Oncotarget 2016[Dec]; 7 (51): 83893-906 PMID27863380show ga Arctigenin was previously proven to inhibit Th17 cell differentiation and thereby attenuate colitis in mice by down-regulating the activation of mechanistic target of rapamycin complex 1 (mTORC1). The present study was performed to address its underlying mechanism in view of estrogen receptor (ER). The specific antagonist PHTPP or siRNA of ER? largely diminished the inhibitory effect of arctigenin on the mTORC1 activation in T cell lines and primary CD4+ T cells under Th17-polarization condition, suggesting that arctigenin functioned in an ER?-dependent manner. Moreover, arctigenin was recognized to be an agonist of ER?, which could bind to ER? with a moderate affinity, promote dissociation of ER?/HSP90 complex and nuclear translocation and phosphorylation of ER?, and increase the transcription activity. Following activation of ER?, arctigenin inhibited the activity of mTORC1 by disruption of ER?-raptor-mTOR complex assembly. Deficiency of ER? markedly abolished arctigenin-mediated inhibition of Th17 cell differentiation. In colitis mice, the activation of ER?, inhibition of mTORC1 activation and Th17 response by arctigenin were abolished by PHTPP treatment. In conclusion, ER? might be the target protein of arctigenin responsible for inhibition of mTORC1 activation and resultant prevention of Th17 cell differentiation and colitis development. äArctigenin functions as a selective agonist of estrogen receptor ? to (epmc).pdf DeepDyve Pubget Overpricing