Gene interactions and pathways from curated databases and text-mining

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MLST8 — MLST8

Pathways - manually collected, often from reviews:

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
Rahimi et al., Cancer Res 2009 : mTORC2 promotes TGF-beta induced morphologic transformation and is required for TGF-beta induced Akt S473 phosphorylation but not mTORC1 activation
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 ... 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 ... 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 ... 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
Zhang et al., PloS one 2009 : Loss of function of the TSC1-TSC2 complex results in constitutive mTORC1 signaling and, through mTORC1 dependent feedback mechanisms and loss of mTORC2 activity, leads to a concomitant block of Akt signaling to its other downstream targets
Boletta , PathoGenetics 2009 : The mTORC1 complex regulates cell growth ( size ), proliferation, translation and autophagy, and mTORC2 regulates the actin cytoskeleton and apoptosis
Harston et al., Am J Physiol Heart Circ Physiol 2011 (Hypertrophy) : Another molecular keystone involved in the hypertrophic growth process is the mammalian target of rapamycin (mTOR), which forms two distinct functional complexes : mTORC1 that activates p70S6 kinase-1 to enhance protein synthesis and mTORC2 that activates Akt to promote cell survival
Völkers et al., Proc Natl Acad Sci U S A 2013 (Cardiomegaly) : Inhibition of mTORC1 by PRAS40 preferentially promotes protective mTORC2 signaling in chronic diseased myocardium
Guertin et al., Dev Cell 2006 : Thus, mTORC1 function is essential in early development, mLST8 is required only for mTORC2 signaling, and mTORC2 is a necessary component of the Akt-FOXO and PKCalpha pathways
Rao et al., Immunity 2012 : The Foxo1 inactivation was dependent on mTORC1 kinase, given that blockade of mTORC1 abrogated mTORC2 mediated Akt ( Ser473 ) kinase phosphorylation, resulting in Foxo1 dependent switch from T-bet to Eomesodermin transcription factor activation and increase in memory precursors
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
Chong et al., Prog Neurobiol 2012 (Neurodegenerative Diseases) : mTOR signaling is dependent upon the mTORC1 and mTORC2 complexes that are composed of mTOR and several regulatory proteins including the tuberous sclerosis complex ( TSC1, hamartin/TSC2, tuberin )
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