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10.4161/23723548.2014.970489 http://scihub22266oqcxt.onion/10.4161/23723548.2014.970489 C4904989!4904989!27308421     free     free     free Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\27308421.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Mol+Cell+Oncol 2015 ; 2 (2): ä Nephropedia Template TP {{tp|p=27308421|t=2015. Molecular mechanisms of mTOR regulation by stress |pdf=|usr=}}{{27308421}} gab.com Text Molecular mechanisms of mTOR regulation by stress JO: Mol Cell Oncol http://www.kidney.de/pget.php?&tw=1&pmid=27308421 #FOAvip Tumors are prime examples of cell growth in unfavorable environments that elicit cellular stress. The high metabolic demand and insufficient vascularization of tumors cause a deficiency of oxygen and nutrients. Oncogenic mutations map to signaling events via mammalian target of rapamycin (mTOR), metabolic pathways, and mitochondrial function. These alterations have been linked with cellular stresses, in particular endoplasmic reticulum (ER) stress, hypoxia, and oxidative stress. Yet tumors survive these challenges and acquire highly energy-demanding traits, such as overgrowth and invasiveness. In this review we focus on stresses that occur in cancer cells and discuss them in the context of mTOR signaling. Of note, many tumor traits require mTOR complex 1 (mTORC1) activity, but mTORC1 hyperactivation eventually sensitizes cells to apoptosis. Thus, mTORC1 activity needs to be balanced in cancer cells. We provide an overview of the mechanisms contributing to mTOR regulation by stress and suggest a model wherein stress granules function as guardians of mTORC1 signaling, allowing cancer cells to escape stress-induced cell death. Twit Text FOAVip Molecular mechanisms of mTOR regulation by stress ????Mol Cell Oncol http://www.kidney.de/pget.php?&tw=1&pmid=27308421 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27308421 #FOAvip English Wikipedia <ref>{{Cite pmid|27308421}}</ref> Molecular mechanisms of mTOR regulation by stress #MMPMID27308421 Heberle AM; Prentzell MT; van Eunen K; Bakker BM; Grellscheid SN; Thedieck K Mol Cell Oncol 2015[Apr]; 2 (2): ä PMID27308421show ga Tumors are prime examples of cell growth in unfavorable environments that elicit cellular stress. The high metabolic demand and insufficient vascularization of tumors cause a deficiency of oxygen and nutrients. Oncogenic mutations map to signaling events via mammalian target of rapamycin (mTOR), metabolic pathways, and mitochondrial function. These alterations have been linked with cellular stresses, in particular endoplasmic reticulum (ER) stress, hypoxia, and oxidative stress. Yet tumors survive these challenges and acquire highly energy-demanding traits, such as overgrowth and invasiveness. In this review we focus on stresses that occur in cancer cells and discuss them in the context of mTOR signaling. Of note, many tumor traits require mTOR complex 1 (mTORC1) activity, but mTORC1 hyperactivation eventually sensitizes cells to apoptosis. Thus, mTORC1 activity needs to be balanced in cancer cells. We provide an overview of the mechanisms contributing to mTOR regulation by stress and suggest a model wherein stress granules function as guardians of mTORC1 signaling, allowing cancer cells to escape stress-induced cell death. äMolecular mechanisms of mTOR regulation by stress (epmc).pdf DeepDyve Pubget Overpricing