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10.1038/ncomms13171 http://scihub22266oqcxt.onion/10.1038/ncomms13171 C5080445!5080445!27786175     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Nat+Commun 2016 ; 7 (ä): ä Nephropedia Template TP {{tp|p=27786175|t=2016. Mitochondrial function controls intestinal epithelial stemness and proliferation |pdf=|usr=}}{{27786175}} gab.com Text Mitochondrial function controls intestinal epithelial stemness and proliferation JO: Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=27786175 #FOAvip Control of intestinal epithelial stemness is crucial for tissue homeostasis. Disturbances in epithelial function are implicated in inflammatory and neoplastic diseases of the gastrointestinal tract. Here we report that mitochondrial function plays a critical role in maintaining intestinal stemness and homeostasis. Using intestinal epithelial cell (IEC)-specific mouse models, we show that loss of HSP60, a mitochondrial chaperone, activates the mitochondrial unfolded protein response (MT-UPR) and results in mitochondrial dysfunction. HSP60-deficient crypts display loss of stemness and cell proliferation, accompanied by epithelial release of WNT10A and RSPO1. Sporadic failure of Cre-mediated Hsp60 deletion gives rise to hyperproliferative crypt foci originating from OLFM4+ stem cells. These effects are independent of the MT-UPR-associated transcription factor CHOP. In conclusion, compensatory hyperproliferation of HSP60+ escaper stem cells suggests paracrine release of WNT-related factors from HSP60-deficient, functionally impaired IEC to be pivotal in the control of the proliferative capacity of the stem cell niche. Twit Text FOAVip Mitochondrial function controls intestinal epithelial stemness and proliferation ????Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=27786175 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27786175 #FOAvip English Wikipedia <ref>{{Cite pmid|27786175}}</ref> Mitochondrial function controls intestinal epithelial stemness and proliferation #MMPMID27786175 Berger E; Rath E; Yuan D; Waldschmitt N; Khaloian S; Allgäuer M; Staszewski O; Lobner EM; Schöttl T; Giesbertz P; Coleman OI; Prinz M; Weber A; Gerhard M; Klingenspor M; Janssen KP; Heikenwalder M; Haller D Nat Commun 2016[]; 7 (ä): ä PMID27786175show ga Control of intestinal epithelial stemness is crucial for tissue homeostasis. Disturbances in epithelial function are implicated in inflammatory and neoplastic diseases of the gastrointestinal tract. Here we report that mitochondrial function plays a critical role in maintaining intestinal stemness and homeostasis. Using intestinal epithelial cell (IEC)-specific mouse models, we show that loss of HSP60, a mitochondrial chaperone, activates the mitochondrial unfolded protein response (MT-UPR) and results in mitochondrial dysfunction. HSP60-deficient crypts display loss of stemness and cell proliferation, accompanied by epithelial release of WNT10A and RSPO1. Sporadic failure of Cre-mediated Hsp60 deletion gives rise to hyperproliferative crypt foci originating from OLFM4+ stem cells. These effects are independent of the MT-UPR-associated transcription factor CHOP. In conclusion, compensatory hyperproliferation of HSP60+ escaper stem cells suggests paracrine release of WNT-related factors from HSP60-deficient, functionally impaired IEC to be pivotal in the control of the proliferative capacity of the stem cell niche. äMitochondrial function controls intestinal epithelial stemness and pro(epmc).pdf DeepDyve Pubget Overpricing