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 MTOR

MTOR — SETD2

Text-mined interactions from Literome

Cam et al., Mol Cell 2010 : mTORC1 signaling under hypoxic conditions is controlled by ATM dependent phosphorylation of HIF-1a
Srinivas et al., Cells Tissues Organs 2009 : Based on the 2 studies described above, and our previous observation that HIF-1 is required for the induction of autophagy, we put forward the hypothesis that autophagy is regulated by the activities of AMP kinase and mTOR in a HIF-1 dependent manner
Finlay , Biochem Soc Trans 2013 : mTORC1 regulates glucose metabolism in CTLs through regulating the expression of the transcription factor HIF1a ( hypoxia-inducible factor 1a )
Bohensky et al., Pediatr Nephrol 2010 : Chondrocyte autophagy is stimulated by HIF-1 dependent AMPK activation and mTOR suppression
Jham et al., PloS one 2011 (Inflammation...) : Conditioned media from vGPCR expressing cells lead to an mTOR dependent increase in HIF-1a and HIF-2a protein levels and VEGF upregulation
Nakamura et al., Mol Cell Neurosci 2011 : Pharmacologic inhibitors of the Trk tyrosine kinase, PI-3 kinase and mTOR paths prevent NGF stimulated increases in HIF-1a and VEGF
Kucejova et al., Mol Cancer Res 2011 (Carcinoma, Renal Cell) : REDD1 is upregulated by hypoxia-inducible factor (HIF)-1 , and forced REDD1 expression is sufficient to inhibit mTORC1
Sudhagar et al., Br J Cancer 2011 (Breast Neoplasms) : Rapid non-genomic signalling by 17ß-oestradiol through c-Src involves mTOR dependent expression of HIF-1a in breast cancer cells
Iqbal et al., Molecular cancer 2013 (Neoplasms) : We observed that insulin up-regulated PKM2 expression, through PI3K/mTOR mediated HIF1a induction, but significantly reduced PKM2 activity independent of this pathway
Frolova et al., Cancer Biol Ther 2012 (Precursor Cell Lymphoblastic Leukemia-Lymphoma) : mTOR blockade with everolimus reduced HIF-1a expression, diminished glucose uptake and glycolytic rate and partially restored the chemosensitivity of ALL cells under hypoxia/stroma co-cultures
Horak et al., Proc Natl Acad Sci U S A 2010 (Cell Transformation, Viral...) : Surprisingly, however, HIF-1 up-regulation in REDD1 ( -/- ) cells is largely independent of mTORC1 activity
Alam et al., Endocrinology 2009 : These results indicate that FSH stimulated HIF-1 activation leading to up-regulation of targets such as vascular endothelial growth factor requires not only PI3-kinase/AKT mediated activation of mammalian target of rapamycin as well as phosphorylation of FOXO1 and possibly MDM2 but also a protein ( kinase ) activity that is inhibited by the classic ERK kinase inhibitor PD98059 but not ERK1/2 or 5
Wu et al., J Neurosci 2012 (Brain Ischemia) : We found that mTOR activation leads to accumulation of the hypoxia-inducible factor-1a (HIF-1a) and induction and recruitment to the cell membrane of the HIF-1a regulated neuronal transporter of glucose GLUT3
Shin et al., PloS one 2013 (Neovascularization, Pathologic...) : Mechanistically, MEL specifically inhibited the EGF induced HIF-1a expression by suppressing the phosphorylation of ERK, mTOR and p70S6K
Choi et al., J Biol Chem 2010 : These translational signal events and HIF-1a protein level were suppressed by inhibitors of phosphatidylinositol 3-kinase (PI3K), MEK, and mTOR , suggesting that the PI3K/Akt/mTOR and MEK/ERK pathways are involved in a translational increase in HIF-1a