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10.1016/j.cell.2015.10.034 http://scihub22266oqcxt.onion/10.1016/j.cell.2015.10.034 C4640214!4640214 !26544941     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\26544941 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Cell 2015 ; 163 (4 ): 960-74 Nephropedia Template TP {{tp|p=26544941 |t=2015. Estrogen Receptor ? Modulates Apoptosis Complexes and the Inflammasome to Drive the Pathogenesis of Endometriosis |pdf=|usr=}}{{26544941 }} gab.com Text Estrogen Receptor Modulates Apoptosis Complexes and the Inflammasome to Drive the Pathogenesis of Endometriosis JO: Cell http://www.kidney.de/pget.php?&tw=1&pmid=26544941 #FOAvip Alterations in estrogen-mediated cellular signaling play an essential role in the pathogenesis of endometriosis. In addition to higher estrogen receptor (ER) ? levels, enhanced ER? activity was detected in endometriotic tissues, and the inhibition of enhanced ER? activity by an ER?-selective antagonist suppressed mouse ectopic lesion growth. Notably, gain of ER? function stimulated the progression of endometriosis. As a mechanism to evade endogenous immune surveillance for cell survival, ER? interacts with cellular apoptotic machinery in the cytoplasm to inhibit TNF-?-induced apoptosis. ER? also interacts with components of the cytoplasmic inflammasome to increase interleukin-1? and thus enhance its cellular adhesion and proliferation properties. Furthermore, this gain of ER? function enhances epithelial-mesenchymal transition signaling, thereby increasing the invasion activity of endometriotic tissues for establishment of ectopic lesions. Collectively, we reveal how endometrial tissue generated by retrograde menstruation can escape immune surveillance and develop into sustained ectopic lesions via gain of ER? function. Twit Text FOAVip Estrogen Receptor Modulates Apoptosis Complexes and the Inflammasome to Drive the Pathogenesis of Endometriosis ????Cell http://www.kidney.de/pget.php?&tw=1&pmid=26544941 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26544941 #FOAvip English Wikipedia <ref>{{Cite pmid|26544941 }}</ref> Estrogen Receptor ? Modulates Apoptosis Complexes and the Inflammasome to Drive the Pathogenesis of Endometriosis #MMPMID26544941 Han SJ ; Jung SY ; Wu SP ; Hawkins SM ; Park MJ ; Kyo S ; Qin J ; Lydon JP ; Tsai SY ; Tsai MJ ; DeMayo FJ ; O'Malley BW Cell 2015[Nov]; 163 (4 ): 960-74 PMID26544941 show ga Alterations in estrogen-mediated cellular signaling play an essential role in the pathogenesis of endometriosis. In addition to higher estrogen receptor (ER) ? levels, enhanced ER? activity was detected in endometriotic tissues, and the inhibition of enhanced ER? activity by an ER?-selective antagonist suppressed mouse ectopic lesion growth. Notably, gain of ER? function stimulated the progression of endometriosis. As a mechanism to evade endogenous immune surveillance for cell survival, ER? interacts with cellular apoptotic machinery in the cytoplasm to inhibit TNF-?-induced apoptosis. ER? also interacts with components of the cytoplasmic inflammasome to increase interleukin-1? and thus enhance its cellular adhesion and proliferation properties. Furthermore, this gain of ER? function enhances epithelial-mesenchymal transition signaling, thereby increasing the invasion activity of endometriotic tissues for establishment of ectopic lesions. Collectively, we reveal how endometrial tissue generated by retrograde menstruation can escape immune surveillance and develop into sustained ectopic lesions via gain of ER? function. |Animals [MESH] |Apoptosis [MESH] |Cell Adhesion [MESH] |Cell Proliferation [MESH] |Endometriosis/metabolism/*pathology [MESH] |Estrogen Receptor alpha/metabolism [MESH] |Estrogen Receptor beta/*metabolism [MESH] |Female [MESH] |Humans [MESH] |Immunologic Surveillance [MESH] |Inflammasomes/*metabolism [MESH] |Interleukin-1beta/metabolism [MESH] |Menstruation/*metabolism [MESH] |Mice [MESH]Estrogen Receptor ? Modulates Apoptosis Complexes and the Inflammasome(epmc).pdf DeepDyve Pubget Overpricing