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MAPK3 — MTOR

Text-mined interactions from Literome

Iijima et al., J Biol Chem 2002 : Whereas p38 MAPK inhibitors exhibited only partial effect, MAPK-phosphatase-3 expression significantly blocked the TPA stimulated S6K1 and mTOR phosphorylation
Cinar et al., Cancer Res 2005 (Prostatic Neoplasms) : The signal to attenuate AR was mediated by the mammalian target of rapamycin , as shown by genetic and pharmacologic methods, and was independent of ErbB2/HER-2, extracellular signal regulated kinase 1/2 , and p38 mitogen activated protein kinase pathways
Williamson et al., Am J Physiol Endocrinol Metab 2006 (MAP Kinase Signaling System) : Overall, the data support the conclusion that AICAR induced AMPK activation suppresses protein synthesis through concurrent repression of mTOR signaling and activation of MAPK signaling, the combination of which modulates transient changes in the initiation and elongation phases of mRNA translation
Tang et al., Hum Mol Genet 2008 (Alexander Disease) : The activation of p38 MAPK by GFAP accumulation is in part responsible for the down-regulation of phosphorylated-mTOR and the subsequent activation of autophagy
Kim et al., Stem Cells 2008 : E ( 2 ) -injected TIS21 ( -/- ) male mice also increased LSK cells in BM. Taken together, expansion of hematopoietic progenitors in TIS21 ( -/- ) female mice might be through inhibition of Akt activation, and constitutive activation of mTOR via preferential binding of TIS21 to E ( 2 ) -induced p-Erk1/2 , compared with that of Akt
Recchia et al., Int J Biochem Cell Biol 2009 (Lung Neoplasms...) : A cross-talk between the androgen receptor and the epidermal growth factor receptor leads to p38MAPK dependent activation of mTOR and cyclinD1 expression in prostate and lung cancer cells
Carracedo et al., J Clin Invest 2008 (MAP Kinase Signaling System...) : Inhibition of mTORC1 leads to MAPK pathway activation through a PI3K dependent feedback loop in human cancer ... Taken together, our findings identify MAPK activation as a consequence of mTORC1 inhibition and underscore the potential of a combined therapeutic approach with mTORC1 and MAPK inhibitors, currently employed as single agents in the clinic, for the treatment of human cancers
James et al., Mol Cell Biol 2009 (Meningioma...) : Merlin does not regulate mTORC1 via the established mechanism of phosphoinositide 3-kinase-Akt or mitogen activated protein kinase/extracellular signal regulated kinase mediated TSC2 inactivation and may instead regulate TSC/mTOR signaling in a novel fashion ... Merlin does not regulate mTORC1 via the established mechanism of phosphoinositide 3-kinase-Akt or mitogen activated protein kinase/extracellular signal regulated kinase mediated TSC2 inactivation and may instead regulate TSC/mTOR signaling in a novel fashion
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
Dormond-Meuwly et al., Biochem Biophys Res Commun 2011 (Neoplasms...) : Downregulation of mTORC1 but not mTORC2 had similar effects showing that the inhibition of mTORC1 is responsible for the activation of MAPK ... Taken together these results show that blocking mTORC1 in endothelial cells activates MAPK and that a combined inhibition of MAPK and mTOR has additive anti-angiogenic effects
Chu et al., Cancer Chemother Pharmacol 2012 (Brain Neoplasms...) : Moreover, BO-1051 not only induced apoptotic cell death, but also enhanced autophagic flux via inhibition of Akt/mTOR and activation of Erk1/2
Gallagher et al., Oncogene 2012 (Cell Transformation, Neoplastic...) : We also investigated the effect of targeted PI3K/mTOR inhibition on PI3K/Akt/mTOR and Erk1/2 signaling, and the potential effects on glycemia
Liu et al., Mol Cancer Ther 2012 (Lung Neoplasms) : Inhibition of mTOR signaling by rapamycin has been shown to activate extracellular signal regulated kinase 1 or 2 ( ERK1/2 ) and Akt in various types of cancer cells, which contributes to rapamycin resistance
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 )
Gratia et al., Cardiovasc Res 2012 (Disease Models, Animal...) : Combined inhibition of AMPK and activation of Akt and MAPK lead to activation of growth stimulating mammalian target of rapamycin (mTOR) signalling
Gulhati et al., Carcinogenesis 2012 (Colorectal Neoplasms...) : In this study, we show that inhibition of mTORC1 with rapamycin leads to feedback activation of PI3K/Akt and Ras-MAPK signaling, resulting in cell survival and possible contribution to rapamycin resistance