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UCSC Genome Browser Gene Interaction Graph
Gene interactions and pathways from curated databases and text-mining

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HIF1A — MTOR

Pathways - manually collected, often from reviews:

Text-mined interactions from Literome

Tan et al., Cancer Cell 2004 (Neovascularization, Pathologic) : We show that integrin linked kinase (ILK) stimulates the expression of VEGF by stimulating HIF-1alpha protein expression in a PKB/Akt- and mTOR/FRAP dependent manner
Yuan et al., J Cell Physiol 2008 (Calcium Signaling) : Thus, both increased mTOR dependent HIF-1alpha synthesis and decreased hydroxylase dependent HIF-1alpha degradation contribute to IH-evoked HIF-1alpha accumulation
Zhong et al., Cancer Res 2000 (Anoxia...) : Here we demonstrate that in human prostate cancer cells, basal-, growth factor-, and mitogen induced expression of hypoxia-inducible factor 1 (HIF-1) alpha , the regulated subunit of the transcription factor HIF-1, is blocked by LY294002 and rapamycin, inhibitors of PI3K and FRAP , respectively
Gao et al., Toxicol Appl Pharmacol 2004 (Ovarian Neoplasms) : Our results also indicated that the mTOR/FRAP inhibitor, rapamycin, inhibited 4-OHE2 induced HIF-1alpha and VEGF-A expression
Lee et al., Clin Cancer Res 2006 (Neoplasm Invasiveness...) : In OVCAR-3 and PC-3 cells, the phosphoinositide 3-kinase/Akt/mammalian target of rapamycin/p70S6K and p42/p44 mitogen activated protein kinase pathways were required for LPA induced HIF-1alpha and VEGF expressions, whereas only the phosphoinositide 3-kinase/mammalian target of rapamycin/p70S6K pathway was important in SK-Hep1 cells
Michaylira et al., Cancer Biol Ther 2006 (Cell Transformation, Neoplastic...) : HIF-1alpha activity was found to be required in Akt induced melanocyte transformation and tumor growth and it was suppressed greatly by mTOR inhibition with rapamycin
Pistollato et al., PloS one 2009 (Brain Neoplasms...) : HIF-1alpha is controlled at the transcriptional and translational level by mTOR and, alike BMP, also mTOR pathway modulates glial differentiation in central nervous system ( CNS ) stem cells ... Here, we investigate the role of mTOR signaling in the regulation of HIF-1alpha stability in primary GBM derived cells maintained under hypoxia ( 2 % oxygen )
Hwang et al., Carcinogenesis 2004 (Prostatic Neoplasms) : Phosphatidylinositol-3 kinase/Akt/mammalian target of rapamycin signaling was also involved in vanadate induced HIF-1alpha expression, but it was independent of AMPK signaling pathway
Zheng et al., Cell Biol Int 2009 (Polycystic Kidney, Autosomal Recessive) : Therefore, we investigated the relationship between the decreased FPC and the protein levels of mTOR and the inhibitory effects of rapamycin on the expression of mTOR, Hypoxia-inducible factor-1 alpha ( HIF-1alpha ) and vascular endothelial growth factor ( VEGF ) in the human 293T cell line
Gelse et al., Osteoarthritis Cartilage 2008 (Cartilage Diseases) : The functional role of phosphatidylinositol 3-kinase (PI3K)/mammalian target of rapamycin (mTOR) and mitogen activated protein kinase ( MEK ) /extracellular signal regulated kinase ( ERK ) signaling on BMP-2/IGF-1 induced HIF-1alpha expression was assessed in vitro by employing specific inhibitors
Petrella et al., Cancer Biol Ther 2009 (Carcinoma, Renal Cell...) : Activation of PI3K/Akt/mTOR leads to increased HIF-1alpha expression in certain cancer cells, supporting the rationale of using mTOR inhibitors as anti-cancer agents
Ji et al., Mol Pharmacol 2010 : Stimulation of endogenous EP1 receptors in human HepG2 hepatocellular carcinoma cells recapitulated the normoxic up-regulation of HIF-1 alpha observed in HEK cells, was sensitive to pertussis toxin, and involved the activation of mTOR signaling and phosphorylation of rpS6
Hasaneen et al., Am J Physiol Lung Cell Mol Physiol 2007 : Our results show : 1 ) a significant increase in human lung microvascular endothelial cell ( HMVEC-L ) proliferation, migration, and tube formation following incubation in conditioned media ( CM ) from HASM cells exposed to mechanical strain ; 2 ) mechanical strain of HASM cells induced VEGF expression and release ; 3 ) VEGF neutralizing antibodies inhibited the proliferation, migration, and tube formations of HMVEC-L induced by the strained airway smooth muscle CM ; 4 ) mechanical strain of HASM induced a significant increase in hypoxia-inducible factor-1alpha ( HIF-1alpha ) mRNA and protein, a transcription factor required for VEGF gene transcription ; and 5 ) mechanical strain of HASM induced HIF-1alpha/VEGF through dual phosphatidylinositol 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) and ERK pathways
Phillips et al., J Biol Chem 2005 (Anoxia...) : A molecular analysis of these events indicated that augmented CXCR4 expression was regulated by the phosphatidylinositol 3-kinase/PTEN/AKT/mammalian target of rapamycin signal transduction pathway, activation of hypoxia inducible factor (HIF) 1alpha , and ultimately HIF-1 dependent transcription of the CXCR4 gene
Land et al., J Biol Chem 2007 (Neoplasms...) : Hypoxia-inducible factor 1alpha is regulated by the mammalian target of rapamycin (mTOR) via an mTOR signaling motif ... Our work shows that activation of mTOR by Ras homologue enriched in brain (Rheb) overexpression potently enhances the activity of HIF1alpha and vascular endothelial growth factor ( VEGF ) -A secretion during hypoxia, which is reversed with rapamycin
Toschi et al., J Biol Chem 2008 : Expression of HIF1 alpha is dependent on the mammalian target of rapamycin (mTOR) and is sensitive to rapamycin ... These data indicate that although HIF1 alpha is dependent on both mTORC1 and mTORC2 , HIF2 alpha is dependent only on mTORC2 ... These data indicate that although HIF1 alpha is dependent on both mTORC1 and mTORC2, HIF2 alpha is dependent only on mTORC2
Majumder et al., Nat Med 2004 (Prostatic Neoplasms) : These data suggest that the expansion of AKT-driven prostate epithelial cells requires mTOR dependent survival signaling and activation of HIF-1 alpha , and that clinical resistance to mTOR inhibitors may emerge through BCL2 expression and/or upregulation of HIF-1 alpha activity