Gene interactions and pathways from curated databases and text-mining

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Text-mined interactions from Literome

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
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
Bohensky et al., Pediatr Nephrol 2010 : Chondrocyte autophagy is stimulated by HIF-1 dependent AMPK activation and mTOR suppression
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
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
Cam et al., Mol Cell 2010 : mTORC1 signaling under hypoxic conditions is controlled by ATM dependent phosphorylation of HIF-1a
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
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
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
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
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
Finlay et al., Biochem Soc Trans 2013 : mTORC1 regulates glucose metabolism in CTLs through regulating the expression of the transcription factor HIF1a ( hypoxia-inducible factor 1a )
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
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