Gene interactions and pathways from curated databases and text-mining

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Text-mined interactions from Literome

Campbell et al., Circ Res 2004 (MAP Kinase Signaling System) : ERK1/2 phosphorylation was reduced not only by MAPK pathway inhibitors but also by PI3K and mTOR inhibitors ; when PI3K was inhibited, ERK phosphorylation could be induced by microinjected activated Akt, indicating important cross-talk between the PI3K and ERK1/2 pathways
Rolfe et al., Biochem J 2005 : However, it remained unclear whether ERK activation was required and which downstream components were involved in activating mTOR and protein synthesis ... Activation and phosphorylation of S6K1 ( ribosomal protein S6 kinase 1 ) and phosphorylation of eIF4E ( eukaryotic initiation factor 4E ) -binding protein ( both are mTOR targets ) were also inhibited by MKP3, suggesting that ERK is also required for the activation of mTOR signalling
Lenz et al., J Biol Chem 2005 : 2-Amino-5-phosphonovaleric acid, an inhibitor of N'-methyl-D-aspartate receptors, abolishes glutamatergic activation of ERK1/2 but not the activation of mTOR-S6K ; the latter is completely abolished by inhibitors of voltage dependent calcium channels
Yamamoto et al., Mol Carcinog 2006 (Carcinoma, Hepatocellular...) : While MEK-ERK1/2 inhibition by PD98059 and mTOR inhibition by rapamycin affected the cyclin D1 nuclear shift and cell proliferation to a lesser extent, both these inhibitors reduced cyclin D1 levels
Ishida et al., J Biol Chem 2007 (Carcinoma, Hepatocellular) : Similar data indicated that mTOR is regulated by both phosphatidylinositol 3-kinase/Akt and ERK
Tsokas et al., J Neurosci 2007 (MAP Kinase Signaling System) : In addition, ERK mediated the stimulation of mTOR by HFS ... The possibility that ERK regulates mTOR by acting at a component further upstream in the phosphatidylinositide 3-kinase (PI3K)-mTOR pathway was tested by probing the phosphorylation of p90-S6 kinase, phosphoinositide dependent kinase 1 ( PDK1 ), and Akt
Fonseca et al., Biochem J 2008 : The binding of PRAS40 to 14-3-3 proteins is not required for activation of mTORC1 signalling by phorbol esters/ERK
Lee et al., Life Sci 2009 : The inhibition of mTOR blocked CAPE induced ERK phosphorylation
Mi et al., J Genet Genomics 2009 (Disease Models, Animal...) : Investigation of this hypothesis in a TSC cell model revealed that mTOR suppression with an mTOR inhibitor, rapamycin ( sirolimus ), led to up-regulation of ERK/MAPK signaling in mouse Tsc2 knockout cells and that this augmented signaling was attenuated by concurrent administration of a MEK1/2 inhibitor, PD98059
Albert et al., Cancer Genomics Proteomics 2009 (Glioblastoma...) : Small interfering RNA suppression of mTOR resulted in higher pERK1/2 levels and pre-treatment with RAPA potentiated PDGF induced activation of ERK1/2
Chen et al., Mol Carcinog 2010 (Neoplasms) : In this report, we focused on studying the role of mTORC1 and mTORC2 in rapamycin mediated Akt and ERK phosphorylation, and the antitumor effect of rapamycin in cancer cells in combination with Akt and ERK inhibitors ... In this report, we focused on studying the role of mTORC1 and mTORC2 in rapamycin mediated Akt and ERK phosphorylation, and the antitumor effect of rapamycin in cancer cells in combination with Akt and ERK inhibitors ... Collectively, we conclude that mTORC2 plays a much more important role than mTORC1 in rapamycin mediated phosphorylation of Akt and ERK , and cotargeting AKT and ERK signaling may be a new strategy for enhancing the efficacy of rapamycin based therapeutic approaches in cancer cells
Guillaumot et al., PloS one 2010 : Very recently, three studies have reported on the same protein under two other names : the human p27RF-Rho that regulates RhoA activation and actin dynamics, and its rodent orthologue p18 that controls both LE/LY dynamics through the MERK-ERK pathway and the lysosomal activation of mammalian target of rapamycin complex 1 by amino acids
Li et al., Cancer Immunol Immunother 2011 : Rapamycin inhibited these phosphorylation events without impacting Akt or Erk activation, even though specific inhibition of Akt or Erk in turn reduced the activation of mTOR
Winter et al., Am J Physiol Cell Physiol 2011 : Previous studies have shown that, in part, Akt and ERK promote mTORC1 signaling through phosphorylation of a GTPase activator protein (GAP), referred to as tuberous sclerosis complex 2 (TSC2), that acts as an upstream inhibitor of mTORC1
Fonseca et al., J Biol Chem 2011 : Our data also reveal striking diversity in the requirements for MEK/ERK in the control of mTORC1 between different cell types, pointing to additional signaling connections between phorbol esters and mTORC1, which do not involve MEK/ERK
Gundermann et al., J Appl Physiol 2012 (Hyperemia) : BFR exercise increased the phosphorylation of mTOR, S6 kinase 1, ribosomal protein S6, ERK1/2 , and Mnk1 interacting kinase 1 ( P < 0.05 ) with no changes in mTORC1 signaling in the SNP trial ( P > 0.05 )
O'Brien et al., Arch Immunol Ther Exp (Warsz) 2012 (MAP Kinase Signaling System) : Furthermore, we highlight the importance of tight control of mTOR signaling by tuberous sclerosis complex 1 for T-cell homeostasis, and the regulation of mTOR signaling by diacylglycerol kinases and the RasGRP1-Ras-Erk1/2 pathway in the context of TCR signaling
Nölting et al., J Mol Endocrinol 2012 : Lovastatin alone significantly reduced MPC and MTT cell viability at therapeutically relevant doses and inhibited both ERK and AKT signalling, but increased mTORC1/p70S6K signalling
You et al., PloS one 2012 (MAP Kinase Signaling System...) : Hence, we reasoned that a mechanically induced increase in PA might promote mTOR signaling via an ERK dependent mechanism
Parrales et al., Cell Signal 2013 : ERK1/2 dependent activation of mTOR/mTORC1/p70S6K regulates thrombin induced RPE cell proliferation
Sajjad et al., Endocr Pathol 2013 (Growth Hormone-Secreting Pituitary Adenoma...) : mTOR kinase phosphorylation was independent of Erk and Akt in primary cultures
Stoklosa et al., Exp Hematol 2013 (Blast Crisis...) : In this study, we demonstrate that mTOR activation in CML CD34 ( + ) progenitor cells is ERK dependent in chronic phase of the disease and ERK independent in blast crisis
Fortress et al., Learn Mem 2013 (MAP Kinase Signaling System) : Collectively, these data demonstrate for the first time that activation of the dorsal hippocampal mTOR signaling pathway is necessary for E ( 2 ) to enhance object recognition memory consolidation and that E ( 2 ) -induced mTOR activation is dependent on upstream activation of ERK and PI3K signaling
Le Borgne et al., PloS one 2013 (Listeriosis...) : We showed that activation of ERK following TCR engagement is required for sustained mTOR complex 1 (mTORC1) activation ... Absence of kinase suppressor of Ras 1 (KSR1), a scaffold protein of the ERK signaling pathway, or inhibition of ERK resulted in decreased mTORC1 activity following T cell activation
Soares et al., PloS one 2013 (Carcinoma, Pancreatic Ductal...) : Conversely, active-site inhibitors of mTOR cause a marked increase in ERK activation whereas rapamycin did not have any stimulatory effect on ERK activation
Potter et al., PLoS Biol 2013 (Tuberous Sclerosis) : Inhibition of mGluR5 or Erk signaling restores appropriate mTOR-dependence to LTD, and significantly reduces epileptiform bursting in TSC2 ( +/- ) hippocampal slices