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10.18632/oncotarget.18995 http://scihub22266oqcxt.onion/10.18632/oncotarget.18995 C5593539!5593539!28915568     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       Oncotarget 2017 ; 8 (34): 55984-97 Nephropedia Template TP {{tp|p=28915568|t=2017. Hyperosmotic stress stimulates autophagy via polycystin-2 |pdf=|usr=}}{{28915568}} gab.com Text Hyperosmotic stress stimulates autophagy via polycystin-2 JO: Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=28915568 #FOAvip Various intracellular mechanisms are activated in response to stress, leading to adaptation or death. Autophagy, an intracellular process that promotes lysosomal degradation of proteins, is an adaptive response to several types of stress. Osmotic stress occurs under both physiological and pathological conditions, provoking mechanical stress and activating various osmoadaptive mechanisms. Polycystin-2 (PC2), a membrane protein of the polycystin family, is a mechanical sensor capable of activating the cell signaling pathways required for cell adaptation and survival. Here we show that hyperosmotic stress provoked by treatment with hyperosmolar concentrations of sorbitol or mannitol induces autophagy in HeLa and HCT116 cell lines. In addition, we show that mTOR and AMPK, two stress sensor proteins involved modulating autophagy, are downregulated and upregulated, respectively, when cells are subjected to hyperosmotic stress. Finally, our findings show that PC2 is required to promote hyperosmotic stress-induced autophagy. Downregulation of PC2 prevents inhibition of hyperosmotic stress-induced mTOR pathway activation. In conclusion, our data provide new insight into the role of PC2 as a mechanosensor that modulates autophagy under hyperosmotic stress conditions. Twit Text FOAVip Hyperosmotic stress stimulates autophagy via polycystin-2 ????Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=28915568 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28915568 #FOAvip English Wikipedia <ref>{{Cite pmid|28915568}}</ref> Hyperosmotic stress stimulates autophagy via polycystin-2 #MMPMID28915568 Peņa-Oyarzun D; Troncoso R; Kretschmar C; Hernando C; Budini M; Morselli E; Lavandero S; Criollo A Oncotarget 2017[Aug]; 8 (34): 55984-97 PMID28915568show ga Various intracellular mechanisms are activated in response to stress, leading to adaptation or death. Autophagy, an intracellular process that promotes lysosomal degradation of proteins, is an adaptive response to several types of stress. Osmotic stress occurs under both physiological and pathological conditions, provoking mechanical stress and activating various osmoadaptive mechanisms. Polycystin-2 (PC2), a membrane protein of the polycystin family, is a mechanical sensor capable of activating the cell signaling pathways required for cell adaptation and survival. Here we show that hyperosmotic stress provoked by treatment with hyperosmolar concentrations of sorbitol or mannitol induces autophagy in HeLa and HCT116 cell lines. In addition, we show that mTOR and AMPK, two stress sensor proteins involved modulating autophagy, are downregulated and upregulated, respectively, when cells are subjected to hyperosmotic stress. Finally, our findings show that PC2 is required to promote hyperosmotic stress-induced autophagy. Downregulation of PC2 prevents inhibition of hyperosmotic stress-induced mTOR pathway activation. In conclusion, our data provide new insight into the role of PC2 as a mechanosensor that modulates autophagy under hyperosmotic stress conditions. äHyperosmotic stress stimulates autophagy via polycystin-2 (epmc).pdf DeepDyve Pubget Overpricing