Gene interactions and pathways from curated databases and text-mining

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

Studies that report less than 10 interactions are marked with *

Text-mined interactions from Literome

Rai et al., American journal of physiology. Renal physiology 2013 (AIDS-Associated Nephropathy...) : To test our hypothesis, we evaluated the effect of an mTOR inhibitor, rapamycin, on kidney cell p53 expression, downstream signaling, and kidney cell injury in both in vivo and in vitro studies ... Since HP/HIV silenced for mTOR displayed a lack of expression of p53 as well as attenuated podocyte apoptosis, this suggests that mTOR is critical for kidney cell p53 activation and associated oxidative kidney cell injury in the HIV milieu
Zeng et al., Cell Res 2010 : We also found that p53 knockdown or inhibition of mTOR activity by rapamycin cotreatment impairs 6-TG- and 5-FU induced upregulation of BNIP3 protein levels and autophagy
Astle et al., Oncogene 2012 (Cell Transformation, Neoplastic) : We demonstrate that AKT induced senescence is p53 dependent and is characterised by mTORC1 dependent regulation of p53 translation and stabilisation of p53 protein following nucleolar localisation and inactivation of MDM2
Habib et al., Genes & cancer 2011 : These novel data provide evidence that loss of TSC-2, PTEN, and p53 as well as activation of PI 3-K and mTOR is associated with kidney cancer in the Eker rat, while sustained expression of TSC-2, PTEN, and p53 may prevent progression of kidney cancer in TSC patients
Zhu et al., Circulation 2009 (Acute Disease...) : These data suggest that doxorubicin treatment induces acute cardiac dysfunction and reduces cardiac mass via p53 dependent inhibition of mTOR signaling and that loss of myocardial mass, and not cardiomyocyte apoptosis, is the major contributor to acute doxorubicin cardiotoxicity
Castedo et al., EMBO J 2002 (HIV Infections) : Syncytia arising from the fusion of cells expressing the HIV-1 encoded Env gene with cells expressing the CD4/CXCR4 complex undergo apoptosis following the nuclear translocation of mammalian target of rapamycin (mTOR), mTOR mediated phosphorylation of p53 on Ser15 ( p53 ( S15 ) ), p53 dependent upregulation of Bax and activation of the mitochondrial death pathway
Zhang et al., J Biol Chem 2010 (Glioblastoma) : Activation of AMP activated protein kinase by temozolomide contributes to apoptosis in glioblastoma cells via p53 activation and mTORC1 inhibition ... Our study suggests that activation of AMPK by TMZ contributes to glioblastoma cell apoptosis, probably by promoting p53 activation and inhibiting mTORC1 signaling
Criollo et al., Cell cycle (Georgetown, Tex.) 2012 : Here, we show that in autophagy-competent mouse embryonic fibroblasts ( MEFs ), distinct autophagic triggers, including starvation, mTOR inhibition with rapamycin and p53 inhibition with cyclic pifithrin a lead to the activation of IKK, followed by the phosphorylation dependent degradation of I?Ba and nuclear translocation of NF?B
Lee et al., Oncogene 2012 (Carcinoma, Non-Small-Cell Lung...) : This demonstrates that the pro-oncogenic activity of TR3 in lung cancer cells was due to inhibition of p53 and activation of mTORC1
Hui et al., Mol Cell Biol 2004 : PLD1 stimulated increases in MDM2 expression and suppression of p53 activation were blocked by inhibition of mTOR and the mitogen activated protein kinase pathway
Mungamuri et al., Cancer Res 2006 (Breast Neoplasms...) : Survival signaling by Notch1 : mammalian target of rapamycin (mTOR) dependent inhibition of p53
Budanov et al., Cell 2008 : Although genotoxic stress has been suggested to inhibit mTOR via p53 mediated activation of mTOR inhibitors, the precise mechanism of this link was unknown
Feng et al., Proc Natl Acad Sci U S A 2005 : Moreover, the mechanisms by which p53 regulates mTOR involves AMP kinase activation and requires the tuberous sclerosis (TSC) 1/TSC2 complex, both of which respond to energy deprivation in cells