Gene interactions and pathways from curated databases and text-mining

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MTOR — STK11

Text-mined interactions from Literome

Shaw et al., Cancer Cell 2004 (Colonic Polyps...) : Here, we report that LKB1 is required for repression of mTOR under low ATP conditions in cultured cells in an AMPK- and TSC2 dependent manner, and that Lkb1 null MEFs and the hamartomatous gastrointestinal polyps from Lkb1 mutant mice show elevated signaling downstream of mTOR
Brugarolas et al., Genes Dev 2004 (Anoxia) : In contrast to energy depletion, mTOR inhibition by hypoxia does not require AMPK or LKB1
MariƱo et al., Hum Mol Genet 2008 (Aging, Premature...) : These Zmpste24 ( -/- ) mice metabolic alterations are also linked to substantial changes in circulating blood parameters, such as leptin, glucose, insulin or adiponectin which in turn lead to peripheral LKB1-AMPK activation and mTOR inhibition
Orlova et al., J Clin Invest 2010 : Consistent with the observations in human PMSE brain, knockdown of STRADalpha in vivo resulted in cortical malformation, enhanced mTORC1 activation , and abnormal nuclear localization of LKB1
Gurumurthy et al., Nature 2010 : The haematopoietic effects are largely independent of Lkb1 regulation of AMP activated protein kinase (AMPK) and mammalian target of rapamycin (mTOR) signalling
Xiao et al., Gynecol Oncol 2012 (Uterine Cervical Neoplasms) : Ectopic expression of LKB1 with stable transduction system or inducible expression construct in endogenous LKB1 deficient cells improved the activation of AMPK, promoted the inhibition of mTOR , and prompted the sensitivity of cells to metformin
Dong et al., Acta Pharmacol Sin 2013 (Carcinoma, Non-Small-Cell Lung...) : Negative regulation of mTOR activity by LKB1-AMPK signaling in non-small cell lung cancer cells ... To investigate the role of LKB1 in regulation of mTOR signaling in non-small cell lung cancer ( NSCLC ) cells ... In non-small cell lung cancer cells, LKB1/AMPK signaling negatively regulates mTOR activity and contributes to cell growth inhibition in response to energy stress