We have a suspicion that you are an automated web bot software, not a real user. To keep our site fast for other users, we have slowed down this page. The slowdown will gradually disappear. If you think this is a mistake, please contact us at genome-www@soe.ucsc.edu. Also note that all data for hgGeneGraph can be obtained through our public MySQL server and all our software source code is available and can be installed locally onto your own computer. If you are unsure how to use these resources, do not hesitate to contact us.
UCSC Genome Browser Gene Interaction Graph
Gene interactions and pathways from curated databases and text-mining

◀ Back to ULK3

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