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MAPK3 — RPTOR
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
Text-mined interactions from Literome
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
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
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
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 )
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