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UCSC Genome Browser Gene Interaction Graph
Gene interactions and pathways from curated databases and text-mining

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Text-mined interactions from Literome

Fortress et al., Learn Mem 2013 (MAP Kinase Signaling System) : Here, we asked whether the enhancement of object recognition memory consolidation produced by dorsal hippocampal infusion of 17ß-estradiol ( E ( 2 ) ) is dependent on mTOR signaling in the dorsal hippocampus, and whether E ( 2 ) -induced mTOR signaling is dependent on dorsal hippocampal phosphatidylinositol 3-kinase (PI3K) and extracellular signal regulated kinase ( ERK ) activation
Patterson et al., Bioelectromagnetics 2006 : Inhibition of PI3-kinase activity with the chemical inhibitor LY294002 blocked PEMF dependent activation of mTOR in both the pre-osteoblast and fibroblast cell lines
Muise-Helmericks et al., J Biol Chem 1998 : PI 3-kinase inhibitors such as wortmannin and LY294002, and rapamycin, an inhibitor of FRAP/TOR , cause a decline in the level of D-cyclins, whereas inhibitors of mitogen activated protein kinase kinase and farnesyltransferase do not
Razmara et al., Cell communication and signaling : CCS 2013 : Inhibition of phosphatidylinositol 3-kinase (PI3K) inhibited PDGF-BB activation of both mTORC1 and mTORC2 ... Inhibition of phosphatidylinositol 3-kinase (PI3K) inhibited PDGF-BB activation of both mTORC1 and mTORC2
Sheriff et al., Mol Cell Endocrinol 2012 (Burns...) : PI3 kinase inhibition by LY294002 and mTOR inhibition by rapamycin blocked the reversal of the anti-anabolic effects of TNF+IFN treated myotubes by DAG
Sekulić et al., Cancer Res 2000 : The involvement of phosphoinositide 3'-kinase (PI3K) in the regulation of mTOR activity was further suggested by findings that mTOR was phosphorylated in vitro and in vivo by the PI3K regulated protein kinase, AKT/PKB
Pawelczyk et al., Exp Cell Res 2003 (Diabetes Mellitus, Experimental...) : Exposure of rat lymphocytes to wortmannin, an inhibitor of phosphatidylinositol 3-kinase (PI3K) , or rapamycin, an inhibitor of mTOR , did not affect the ability of insulin to stimulate expression of AK
Solà-Villà et al., Kidney Int 2006 : SB 203580, a p38 mitogen activated protein kinase inhibitor, weakly inhibited the induction of VEGF by IL-1beta in a concentration dependent manner, whereas LY 294002, a phosphoinoside 3-kinase (PI3-K) inhibitor, and rapamycin, a mammalian target of rapamycin (mTOR) inhibitor , strongly inhibited both IL-1beta- and tumor necrosis factor-alpha induced VEGF formation in a concentration dependent manner
Peffley et al., Arch Biochem Biophys 2007 (Neoplasms) : Suppressive effects were similar to or greater than that observed with a PI3 kinase inhibitor or rapamycin, an mTOR inhibitor
Doi et al., Biochem Biophys Res Commun 2003 : The isoleucine effect on glucose uptake was mediated by phosphatidylinositol 3-kinase (PI3K) , but was independent of mammalian target of rapamycin (mTOR)
Banerjee et al., Mol Cancer Ther 2011 (Disease Models, Animal...) : Third, the incomplete suppression of Nf1-deficient glial cell proliferation in vivo following 5 mg/kg/day rapamycin treatment reflects mTOR mediated AKT activation, such that combined 5 mg/kg/day rapamycin and PI3-kinase (PI3K) inhibition or dual PI3K/mTOR inhibition recapitulates the growth suppressive effects of 20 mg/kg/day rapamycin
Alam et al., Endocrinology 2009 : These results indicate that FSH stimulated HIF-1 activation leading to up-regulation of targets such as vascular endothelial growth factor requires not only PI3-kinase/AKT mediated activation of mammalian target of rapamycin as well as phosphorylation of FOXO1 and possibly MDM2 but also a protein ( kinase ) activity that is inhibited by the classic ERK kinase inhibitor PD98059 but not ERK1/2 or 5
Ögmundsdóttir et al., PloS one 2012 : Mammalian Target of Rapamycin Complex 1 ( mTORC1 ) is activated by growth factor regulated phosphoinositide 3-kinase (PI3K)/Akt/Rheb signalling and extracellular amino acids ( AAs ) to promote growth and proliferation
Tzatsos , J Biol Chem 2009 : However, under diabetic mimicking conditions mTOR inhibits phosphatidylinositol (PI) 3-kinase/Akt signaling by phosphorylating insulin receptor substrate-1 (IRS-1) at Ser-636/639 ... Overall, these data provide new insights in the molecular mechanisms by which mTORC1 inhibits PI 3-kinase/Akt signaling at the level of IRS-1 and suggest that mTOR signaling toward Akt is scaffold dependent
Lipinski et al., Dev Cell 2010 (MAP Kinase Signaling System) : In a genome-wide human siRNA screen, we demonstrate that under normal nutrient conditions upregulation of autophagy requires the type III PI3 kinase, but not inhibition of mTORC1 , the essential negative regulator of starvation induced autophagy
Bhattacharya et al., Cancer Biol Ther 2012 (Stomach Neoplasms) : In AGS cells, PI3K inhibition alone enhanced 5-FU sensitivity as much as dual PI3K/mTOR inhibition
Kim et al., J Pharmacol Exp Ther 2006 : Treatment of cells with the phosphatidylinositol 3-kinase (PI3K) inhibitors wortmannin and LY294002 [ 2- ( 4-morpholinyl ) -8-phenyl-4H-1-benzopyran-4-one ] or rapamycin, an inhibitor of mammalian target of rapamycin and ribosomal p70 S6 kinase (p70S6K) phosphorylation, or with an adenovirus containing green fluorescent protein and a dominant negative and kinase-dead Akt, effectively inhibited the insulin mediated increase in alpha-class GST expression and GST activity toward NBD
Gual et al., Diabetologia 2003 : Moreover, inhibition of mTOR led to a persistent PI 3-kinase activation by insulin
Pham et al., J Cell Biochem 2000 : In several cell lines, mTOR or its downstream targets can be regulated by phosphatidylinositol (PI) 3-kinase ; protein kinases A, B, and C ; heterotrimeric G-proteins ; a PD98059-sensitive kinase or calcium ; as well as by amino acids
Reyes-Gordillo et al., Am J Pathol 2011 (Liver Cirrhosis) : The lack of AKT phosphorylation was not due to the inhibition of PDGF-ßr phosphorylation, the activation of phosphoinositide 3-kinase (PI3K) , pyruvate dehydrogenase kinase isozyme 1 ( PDK1 ), and mammalian target of rapamycin (mTOR)
Roux et al., Proc Natl Acad Sci U S A 2004 (MAP Kinase Signaling System...) : Phosphatidylinositol 3-kinase (PI3K) inactivates the tumor suppressor complex and enhances mTOR signaling by means of phosphorylation of tuberin by Akt
Kim et al., J Pharmacol Exp Ther 2004 : The phosphatidylinositol 3-kinase (PI3K) inhibitors, wortmannin and LY294002 [ 2- ( 4-morpholinyl ) -9-phenyl-4H-1-benzopyran-4-one ], dominant negative Akt, or rapamycin, an inhibitor of mTOR ( mammalian target of rapamycin ) and ribosomal p70 S6 kinase (p70S6K) phosphorylation, inhibited the insulin mediated increase in GCLC protein and GSH levels
Kumar et al., Mol Cell Biol 2008 : Since little is known about the role of either rictor or mTORC2 in PI-3 kinase mediated physiological processes in adult animals, we generated muscle-specific rictor knockout mice
Ballou et al., J Biol Chem 2007 : Several small molecules such as LY294002 inhibit mTOR kinase activity, but they also inhibit phosphatidylinositol 3-kinase (PI3K) at similar concentrations