Gene interactions and pathways from curated databases and text-mining

◀ Back to MTOR


Pathways - manually collected, often from reviews:

Text-mined interactions from Literome

Simpson et al., Mol Cell Biol 2001 (Breast Neoplasms) : In addition, PTEN , LY294002, and rapamycin, an inhibitor of mammalian target of rapamycin , caused a reduction in the molecular weight of IRS-2 and an increase in the association of IRS-2 with PI3K
Tee et al., Semin Cell Dev Biol 2005 (Disease...) : Recent studies reveal that the tuberous sclerosis complex (TSC)-1/2, PTEN , and LKB1 tumor suppressor proteins tightly control mTOR
Chang et al., Invest New Drugs 2005 (Anemia...) : Loss of PTEN , which is common in glioblastoma multiforme ( GBM ), results in activation of the mammalian target of rapapmycin (mTOR) , thereby increasing mRNA translation of a number of key proteins required for cell-cycle progression
Levitt et al., Biochem Biophys Res Commun 2005 (Glioma) : However, the rapamycin analog CCI-779 did not affect IGFBP-2 expression, suggesting that the PTEN induced decrease in IGFBP-2 expression is not attributable to decreased mTOR signalling
Cheung et al., Trends Mol Med 2006 (Leukemia) : Thus, the regulation of HSCs and leukemic cells seems to be governed by cell-context dependent , PTEN mediated regulation of mTOR
Steelman et al., Oncogene 2008 (Breast Neoplasms) : Interference with the lipid phosphatase activity of PTEN was sufficient to activate Akt/mTOR/p70S6K signaling
Sherbakova et al., Mol Biol (Mosk) 2008 (Prostatic Neoplasms) : Transfection of PTEN into PTEN-deficient PC3 as well as rapamycin treatment caused the inhibition of PI3K/Akt/mTOR signaling and resulted in cell sensitization to the action of doxorubicin and vinblastine
Chan et al., Cell Biol Int 2009 : Collectively, these findings suggest that PP2A and PTEN may be involved in fine tuning the regulation of Akt/tuberin/mTOR/p70S6K in PC12 cells by M ( 4 ) mAChR and TrkA, respectively
Li et al., Mol Cancer Ther 2009 (Glioblastoma...) : We also assessed the experimental therapeutic effects of combining anti-HGF/c-Met approaches with PTEN restoration or mTOR inhibition ... These preclinical studies show for the first time that PTEN loss amplifies c-Met induced glioblastoma malignancy and suggest that combining anti-HGF/c-Met approaches with PTEN restoration or mTOR inhibition is worth testing in a clinical setting
Bleau et al., Cell stem cell 2009 (Glioma) : In this cell population, Akt, but not its downstream target mTOR , regulates ABCG2 activity, and loss of PTEN increases the SP
Han et al., Clin Cancer Res 2009 (Chordoma) : Strikingly, expression of PTEN , a negative regulator of mTORC1 signaling, was not detected or significantly reduced in chordoma derived cell lines and primary tumors
Wang et al., Zhongguo Fei Ai Za Zhi 2010 (Carcinoma, Non-Small-Cell Lung...) : PTEN could negatively regulate mTOR signal pathway and inhibit its activity
Liu et al., Nat Neurosci 2010 (Spinal Cord Injuries) : Forced upregulation of mTOR activity in corticospinal neurons by conditional deletion of Pten , a negative regulator of mTOR , enhanced compensatory sprouting of uninjured CST axons and enabled successful regeneration of a cohort of injured CST axons past a spinal cord lesion
Morrow et al., J Clin Oncol 2011 (Breast Neoplasms...) : Phosphatase and tensin homolog (PTEN) is a dual phosphatase that counteracts the PI3K function ; PTEN loss leads to activation of the Akt cascade and the downstream mammalian target of rapamycin (mTOR)
Li et al., Mol Cell Biochem 2012 (Endometrial Neoplasms) : Loss of PTEN promoted cell proliferation and led to significant increases in the levels of EGFR, phospho-EGFR, AKT, phospho-AKT, and phospho-mTOR proteins
Leibinger et al., Neurobiol Dis 2012 (Optic Nerve Injuries) : Similar effects are achieved by the genetic deletion of phosphatase and tensin homolog (PTEN) and subsequent mammalian target of rapamycin (mTOR) activation
Jung et al., Oncogene 2013 (Carcinoma, Non-Small-Cell Lung...) : Pharmacological inhibition of phosphatidyl inositol 3-kinase or transfection with wild-type PTEN suppressed phosphorylation of Akt, mTOR and STAT3 ( Y705 ), sphere formation, and CXCR4 expression in A549/GR cells, whereas mutant PTEN enhanced these events
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
Wang et al., Cancer Res 2012 (Disease Models, Animal...) : Here we describe a new genetically engineered mouse model of prostate cancer in which PI3K-Akt-mTOR signaling is activated by inducible disruption of PTEN , and extracellular signal regulated kinase 1/2 ( ERK1/2 ) MAPK signaling is activated by inducible expression of a BRAF ( V600E ) oncogene
Weston et al., J Neurosci 2012 (Synaptic Transmission) : We therefore performed an electrophysiological and morphological comparison of glutamatergic and GABAergic neurons in which mTOR signaling was either increased by loss of the repressor Pten or decreased by treatment with rapamycin
Tanwar et al., PLoS Genet 2012 (Adenoma...) : Loss of PTEN , an upstream regulator of mTORC1 signaling, along with Lkb1 deletion significantly increased tumor burden in uteri and induced tumorigenesis in the cervix and vagina
Magee et al., Cell stem cell 2012 (Leukemia) : Pten is therefore required in adult, but not neonatal, HSCs to negatively regulate mTORC2 signaling
Tumaneng et al., Nat Cell Biol 2012 : We have identified the tumour suppressor PTEN , an upstream negative regulator of mTOR , as a critical mediator of YAP in mTOR regulation
Mao et al., Neuroscience 2013 (Brain Ischemia...) : Moreover, PTEN expression persistently remained high in the ischemic brain over 14 days after MCAO, and BPV treatment increased post-ischemic activation of Akt and mTOR in the ischemic brain
Adhikari et al., PloS one 2013 (Primary Ovarian Insufficiency) : Lack of PTEN leads to increased phosphatidylinositol 3-kinase (PI3K)-Akt and mammalian target of rapamycin complex 1 ( mTORC1 ) signaling in the oocytes