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10.1038/s41419-020-03114-4 http://scihub22266oqcxt.onion/10.1038/s41419-020-03114-4 33106485!7589503!33106485     free     free     free Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cell+Death+Dis 2020 ; 11 (10): 918 Nephropedia Template TP {{tp|p=33106485|t=2020. Activation of mTORC1 by LSECtin in macrophages directs intestinal repair in inflammatory bowel disease |pdf=|usr=}}{{33106485}} gab.com Text Activation of mTORC1 by LSECtin in macrophages directs intestinal repair in inflammatory bowel disease JO: Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=33106485 #FOAvip Damage to intestinal epithelial cells and the induction of cellular apoptosis are characteristics of inflammatory bowel disease. The C-type lectin receptor family member LSECtin promotes apoptotic cell clearance by macrophages and induces the production of anti-inflammatory/tissue growth factors, which direct intestinal repair in experimental colitis. However, the mechanisms by which the phagocytosis of apoptotic cells triggers the pro-repair function of macrophages remain largely undefined. Here, using immunoprecipitation in combination with mass spectrometry to identify LSECtin-interacting proteins, we found that LSECtin interacted with mTOR, exhibiting a role in activating mTORC1. Mechanistically, apoptotic cells enhance the interaction between LSECtin and mTOR, and increase the activation of mTORC1 induced by LSECtin in macrophages. Elevated mTORC1 signaling triggers macrophages to produce anti-inflammatory/tissue growth factors that contribute to the proliferation of epithelial cells and promote the reestablishment of tissue homeostasis. Collectively, our findings suggest that LSECtin-dependent apoptotic cell clearance by macrophages activates mTORC1, and thus contributes to intestinal regeneration and the remission of colitis. Twit Text FOAVip Activation of mTORC1 by LSECtin in macrophages directs intestinal repair in inflammatory bowel disease ????Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=33106485 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=33106485 #FOAvip English Wikipedia <ref>{{Cite pmid|33106485}}</ref> Activation of mTORC1 by LSECtin in macrophages directs intestinal repair in inflammatory bowel disease #MMPMID33106485 Li Q; Cheng H; Liu Y; Wang X; He F; Tang L Cell Death Dis 2020[Oct]; 11 (10): 918 PMID33106485show ga Damage to intestinal epithelial cells and the induction of cellular apoptosis are characteristics of inflammatory bowel disease. The C-type lectin receptor family member LSECtin promotes apoptotic cell clearance by macrophages and induces the production of anti-inflammatory/tissue growth factors, which direct intestinal repair in experimental colitis. However, the mechanisms by which the phagocytosis of apoptotic cells triggers the pro-repair function of macrophages remain largely undefined. Here, using immunoprecipitation in combination with mass spectrometry to identify LSECtin-interacting proteins, we found that LSECtin interacted with mTOR, exhibiting a role in activating mTORC1. Mechanistically, apoptotic cells enhance the interaction between LSECtin and mTOR, and increase the activation of mTORC1 induced by LSECtin in macrophages. Elevated mTORC1 signaling triggers macrophages to produce anti-inflammatory/tissue growth factors that contribute to the proliferation of epithelial cells and promote the reestablishment of tissue homeostasis. Collectively, our findings suggest that LSECtin-dependent apoptotic cell clearance by macrophages activates mTORC1, and thus contributes to intestinal regeneration and the remission of colitis. |Animals[MESH] |Humans[MESH] |Inflammatory Bowel Diseases/*genetics[MESH] |Lectins, C-Type/*metabolism[MESH] |Macrophages/*metabolism[MESH] |Mechanistic Target of Rapamycin Complex 1/*metabolism[MESH] |Mice[MESH]Activation of mTORC1 by LSECtin in macrophages directs intestinal repa(epmc).pdf DeepDyve Pubget Overpricing