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10.1038/cddis.2016.98 http://scihub22266oqcxt.onion/10.1038/cddis.2016.98 C4855677!4855677!27077812     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cell+Death+Dis 2016 ; 7 (4): e2196- Nephropedia Template TP {{tp|p=27077812|t=2016. TAK1 regulates Paneth cell integrity partly through blocking necroptosis |pdf=|usr=}}{{27077812}} gab.com Text TAK1 regulates Paneth cell integrity partly through blocking necroptosis JO: Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=27077812 #FOAvip Paneth cells reside at the base of crypts of the small intestine and secrete antimicrobial factors to control gut microbiota. Paneth cell loss is observed in the chronically inflamed intestine, which is often associated with increased reactive oxygen species (ROS). However, the relationship between Paneth cell loss and ROS is not yet clear. Intestinal epithelial-specific deletion of a protein kinase Tak1 depletes Paneth cells and highly upregulates ROS in the mouse model. We found that depletion of gut bacteria or myeloid differentiation factor 88 (Myd88), a mediator of bacteria-derived cell signaling, reduced ROS but did not block Paneth cell loss, suggesting that gut bacteria are the cause of ROS accumulation but bacteria-induced ROS are not the cause of Paneth cell loss. In contrast, deletion of the necroptotic cell death signaling intermediate, receptor-interacting protein kinase 3 (Ripk3), partially blocked Paneth cell loss. Thus, Tak1 deletion causes Paneth cell loss in part through necroptotic cell death. These results suggest that TAK1 participates in intestinal integrity through separately modulating bacteria-derived ROS and RIPK3-dependent Paneth cell loss. Twit Text FOAVip TAK1 regulates Paneth cell integrity partly through blocking necroptosis ????Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=27077812 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27077812 #FOAvip English Wikipedia <ref>{{Cite pmid|27077812}}</ref> TAK1 regulates Paneth cell integrity partly through blocking necroptosis #MMPMID27077812 Simmons AN; Kajino-Sakamoto R; Ninomiya-Tsuji J Cell Death Dis 2016[Apr]; 7 (4): e2196- PMID27077812show ga Paneth cells reside at the base of crypts of the small intestine and secrete antimicrobial factors to control gut microbiota. Paneth cell loss is observed in the chronically inflamed intestine, which is often associated with increased reactive oxygen species (ROS). However, the relationship between Paneth cell loss and ROS is not yet clear. Intestinal epithelial-specific deletion of a protein kinase Tak1 depletes Paneth cells and highly upregulates ROS in the mouse model. We found that depletion of gut bacteria or myeloid differentiation factor 88 (Myd88), a mediator of bacteria-derived cell signaling, reduced ROS but did not block Paneth cell loss, suggesting that gut bacteria are the cause of ROS accumulation but bacteria-induced ROS are not the cause of Paneth cell loss. In contrast, deletion of the necroptotic cell death signaling intermediate, receptor-interacting protein kinase 3 (Ripk3), partially blocked Paneth cell loss. Thus, Tak1 deletion causes Paneth cell loss in part through necroptotic cell death. These results suggest that TAK1 participates in intestinal integrity through separately modulating bacteria-derived ROS and RIPK3-dependent Paneth cell loss. äTAK1 regulates Paneth cell integrity partly through blocking necroptos(epmc).pdf DeepDyve Pubget Overpricing