Gene interactions and pathways from curated databases and text-mining

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AKT1 — RPTOR

Pathways - manually collected, often from reviews:

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

Text-mined interactions from Literome

Wang et al., Oncology 2007 (Disease Models, Animal...) : Either siRNA Raptor or siRNA Rictor suppressed TNF-alpha expression, but the latter suppressed the effects of GM3 on TNF-alpha expression and Akt phosphorylation at Ser ( 473 ), indicating the GM3 signal to be transduced via Rictor/mTOR and Akt ( Ser ( 473 ) ), leading to TNF-alpha stimulation
Wang et al., Cancer Res 2008 (Lung Neoplasms) : Collectively, we conclude that inhibition of the mTOR/raptor complex initiates Akt activation independent of mTOR/rictor
Wu et al., Urol Oncol 2012 (Carcinoma, Transitional Cell...) : The present findings also suggest rictor dependent AKT activation as a consequence of mTORC1 inhibition
Julien et al., Mol Cell Biol 2010 : Interestingly, mTORC1 negatively regulates Akt activation, but whether mTORC1 signaling directly targets mTORC2 remains unknown
Castillo-Pichardo et al., Nutr Cancer 2012 (Breast Neoplasms) : RQC was found to reduce Akt activity, induce the activation of AMPK, and inhibit mTOR signaling in breast cancer cells
Hwang et al., BMB Rep 2011 (Ischemia) : The loss of TSC2, which is upstream of mTOR, activates S6K1, promotes cell growth and survival, activates mTOR kinase activities, inhibits mTORC1 and mTORC2 via mTOR inhibitors, and suppresses S6K1 and Akt
Han et al., Oncogene 2007 : Small interfering RNA mediated knockdown of mTOR or Rictor, components of the rapamycin-insensitive mTORC2 complex, but not the mTORC1 component Raptor , also inhibited Akt Ser-473 phosphorylation induced by A-443654
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
Magri et al., Cell stem cell 2011 (Epilepsy...) : Notably, mTORC1 dependent Akt inhibition and STAT3 activation were involved in the reduced self-renewal and earlier neuronal and astroglial differentiation of mutant NSCs
Willems et al., Leukemia 2012 (Leukemia, Myeloid, Acute) : In addition, the mTORC1 dependent PI3K/Akt feedback activation was fully abrogated in AZD8055 treated AML cells
Vadlakonda et al., Frontiers in oncology 2013 : We present in this article, a hypothesis that activation of Akt-T308 phosphorylation in the presence of high ATP : AMP ratio promotes the stability of its phosphorylations and activates mTORC1 and the energy consuming biosynthetic processes
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
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
Finlay et al., J Exp Med 2012 : The present study now demonstrates that mTORC1 activity in CD8 ( + ) T cells is not dependent on PI3K or Akt but is critical to sustain glucose uptake and glycolysis in CD8 ( + ) T cells
Jung et al., J Nutr Biochem 2013 : The results suggested that fisetin treatment inhibits mTORC1 activity in an Akt dependent manner
White et al., Mol Cell Endocrinol 2013 : Acute Akt activation in C ( 2 ) C ( 12 ) myotubes is sensitive to a high concentration of testosterone, and low concentrations of testosterone can activate mTOR signaling independent of Akt
Espona-Fiedler et al., Biochem Pharmacol 2012 (Melanoma) : The inhibition of mTORC1 and mTORC2 complexes by PG or OBX resulted in a loss of AKT phosphorylation at S473, preventing its full activation, with no significant effect on T308
Pollizzi et al., Molecular cancer 2009 (Disease Models, Animal...) : Recent studies indicate that inhibition of mTORC1 with RAD001 ( everolimus ) leads to rebound activation of AKT , which could protect tumors from drug induced cell death
Tanaka et al., Clin Cancer Res 2011 (Neoplasms) : Effects on Akt phosphorylation induced by mTORC1 inhibition were tested with CH5132799 and compared with mTORC1 and PI3K/mTOR inhibitors
Park et al., Haematologica 2010 (Leukemia, Myeloid, Acute) : However, as mTORC1 activation is independent of PI3K/AKT in acute myeloid leukemia, dual PI3K and mTOR inhibitors may induce apoptosis in blast cells
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
Tzatsos , J Biol Chem 2009 : The molecular basis for the differential effect of mTOR signaling on Akt is poorly understood ... 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
Dan et al., Genes Dev 2008 (Prostatic Neoplasms) : Akt dependent regulation of NF-{kappa}B is controlled by mTOR and Raptor in association with IKK
Kato et al., Cell Death Differ 2012 (MAP Kinase Signaling System) : Activation of mTORC1 reduced Akt phosphorylation, which was an event upstream of IRE-JNK signaling and consequent apoptosis ... These results disclosed that, under ER stress conditions, mTORC1 causes apoptosis through suppression of Akt and consequent induction of the IRE1-JNK pathway
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 ... We found that low concentrations rapamycin increased Akt and ERK phosphorylation through a mTORC1 dependent mechanism because knockdowned raptor induced the activation of Akt and ERK, but higher doses of rapamycin inhibited Akt and ERK phosphorylation mainly via the mTORC2 signaling pathway because that the silencing of rictor led to the inhibition of Akt and ERK phosphorylation
Koketsu et al., Am J Physiol Endocrinol Metab 2008 (Glucose Intolerance...) : Hepatic overexpression of a dominant negative form of raptor enhances Akt phosphorylation and restores insulin sensitivity in K/KAy mice
Pang et al., World J Gastroenterol 2013 : Furthermore, TM treatment also activated mTORC1 , and in turn reduced Akt phosphorylation, which suggested the PI3K/Akt/mTOR signal pathway was involved in the TM-induced autophagic response in EC109 cells
Lee et al., Carcinogenesis 2010 (Colonic Neoplasms) : In contrast, the Akt dependent mTORC1 inhibition by selenium did not require AMPKalpha ( 1 )
Villa-Cuesta et al., PloS one 2011 (Carcinoma, Hepatocellular...) : The effects on mTOR signaling were independent of effects on AMP activated kinase or AKT
Gupta et al., Blood 2009 (Lymphoma, Large B-Cell, Diffuse) : Furthermore, knockdown of the mTORC2 component rictor, but not the mTORC1 component raptor , inhibited rapamycin induced Akt phosphorylation in lymphoma cells
Lee et al., PloS one 2010 (Endotoxemia) : Furthermore, in vitro cellular studies demonstrated that LPS ( lipopolysaccharide ) activation of mTORC1-S6K still occurs in the presence of PI3K-Akt inhibition alone, but can be suppressed by concurrent inhibition of PI3K-Akt and MEK-ERK pathways
Timmerman et al., J Clin Endocrinol Metab 2010 : During insulin infusion, blood flow and capillary recruitment increased in the control ( P < 0.05 ) group only ; Akt phosphorylation and glucose uptake increased in both groups ( P < 0.05 ), with no group differences ; and mTORC1 signaling increased more in control ( P < 0.05 ) than in L-NMMA
Wenner , J Cell Physiol 2012 (Neoplasms) : In addition, chemotherapeutic approaches based on Akt activated mTORC1 are described, and their relationship to the role of aerobic glycolysis in this protection
Wieman et al., Mol Biol Cell 2007 : Although Akt did not require mTOR/RAPTOR to maintain surface Glut1 levels, inhibition of mTOR/RAPTOR by rapamycin greatly diminished glucose uptake, suggesting Akt stimulated mTOR/RAPTOR may promote Glut1 transporter activity
Gupta et al., Blood 2012 (Lymphoma) : Dual mTORC1/mTORC2 inhibition diminishes Akt activation and induces Puma dependent apoptosis in lymphoid malignancies
Breuleux et al., Mol Cancer Ther 2009 (Neoplasms) : Strikingly, rictor down-regulation attenuated AKT S473 phosphorylation induced by mTORC1 inhibition
Urbanska et al., J Biol Chem 2012 : We also identified Akt as a downstream effector of mTORC2 needed for proper dendritic arbor morphology, the action of which required mTORC1 and p70S6K1
Brito et al., Atherosclerosis 2009 (Atherosclerosis) : The activation of mTOR signaling by oxLDL, requires the upstream activation of PI3K and Akt , as assessed by the inhibitory effect of the PI3K inhibitor Ly294002 on mTOR activation and DNA synthesis