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RPTOR — TP53

Text-mined interactions from Literome

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
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
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
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