Gene interactions and pathways from curated databases and text-mining

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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

Avruch et al., Am J Physiol Endocrinol Metab 2009 : In contrast, amino acids, especially leucine, regulate mTORC1 by controlling the ability of Rheb-GTP to activate mTORC1
Wang et al., Oncogene 2008 (Prostatic Neoplasms) : Inhibition of both mTORC1 and mTORC2 by rapamycin induced apoptosis, whereas rapamycin-stimulation of AR transcriptional activity resulted from the inhibition of mTORC1 , but not mTORC2
Delgoffe et al., Mol Immunol 2009 : Enhanced interaction between Hsp90 and raptor regulates mTOR signaling upon T cell activation
Shao et al., J Hepatol 2012 (Carcinoma, Hepatocellular...) : The inhibition of both mTORC1/2 not only efficiently blocked mTORC1 signaling, but also abrogated AKT-feedback activation caused by selective mTORC1 inhibition
Wu et al., J Biol Chem 2011 : The phosphorylation of Raptor on these sites enhances mTORC1 activity, and contributes largely to arsenite induced mTORC1 activation ... The phosphorylation of Raptor on these sites enhances mTORC1 activity, and contributes largely to arsenite induced mTORC1 activation
Kato et al., PloS one 2013 : Knockdown of Raptor , a positive regulator of mTORC1 , also had the similar effect
Wang et al., J Biol Chem 2009 : Raptor ( regulatory associated protein of mammalian target of rapamycin (mTOR) ), a constitutively binding protein of mTORC1, is essential for mTORC1 activity and critical for the regulation of mTORC1 activity in response to insulin signaling and nutrient and energy sufficiency
Foster et al., J Biol Chem 2010 (MAP Kinase Signaling System) : These data suggest that mTORC1 activation leads to raptor multisite phosphorylation and that raptor Ser ( 863 ) phosphorylation functions as a master biochemical switch that modulates hierarchical raptor phosphorylation ( e.g. on Ser ( 859 ) and Ser ( 855 ) )
Jung et al., Autophagy 2011 : In addition, ULK1 was found to bind raptor , induce its phosphorylation, and inhibit the kinase activity of mTORC1
Ramírez-Valle et al., Mol Cell Biol 2010 : Mitotic raptor promotes mTORC1 activity, G ( 2 ) /M cell cycle progression, and internal ribosome entry site mediated mRNA translation
Gwinn et al., Mol Cell 2008 : The phosphorylation of raptor by AMPK is required for the inhibition of mTORC1 and cell-cycle arrest induced by energy stress
Chong et al., Oxidative medicine and cellular longevity 2010 (Neurodegenerative Diseases) : The function of mTOR signaling is mediated primarily through two mTOR complexes : mTORC1 and mTORC2
Wagner et al., Am J Physiol Cell Physiol 2010 : Notably, mTORC1 activity was elevated in VSMC isolated from an intimal hyperplastic patient lesion compared with normal media, and lovastatin treatment inhibited mTORC1 activity in these cultures
Dunlop et al., Autophagy 2011 : ULK1 inhibits mTORC1 signaling, promotes multisite Raptor phosphorylation and hinders substrate binding
Wolff et al., Mol Cell Biol 2011 (Anoxia) : AMPK activation ( using 5-aminoimidazole-4-carboxamide riboside [ AICAR ] ) induces raptor phosphorylation and inhibits mTORC1 in both mouse embryo fibroblasts ( MEFs ) and hepatocytes, but whereas mTORC1 inhibition is Tsc1/Tsc2 dependent in MEFs, it is independent in hepatocytes