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AKT1 — HIF1A

Pathways - manually collected, often from reviews:

• NCI Pathway Database HIF-1-alpha transcription factor network: AKT1 (AKT1) → HIF1A/ARNT complex (HIF1A-ARNT) (modification, activates)
  Roth et al., J Biol Chem 2004
  Evidence: mutant phenotype, other species

Text-mined interactions from Literome

Laughner et al., Mol Cell Biol 2001 (Breast Neoplasms) : Increased phosphatidylinositol 3-kinase (PI3K) and AKT or decreased PTEN activity in prostate cancer cells also increases HIF-1alpha expression by an undefined mechanism
Bárdos et al., Mol Cell Biol 2004 : We found that growth factor stimulation, overexpression of Akt/PKB , or loss of PTEN resulted in enhanced expression of both HIF-1alpha and HDM2
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
Schnitzer et al., FEBS Lett 2005 : We investigated how PI3K/Akt and glycogen synthase kinase 3beta ( GSK3beta ) affect HIF-1alpha in human RKO cells under prolonged periods of severe hypoxia/anoxia
Shi et al., J Pathol 2005 (Breast Neoplasms) : The data show that HIF-1alpha expression is induced by bFGF in a dose- and time dependent fashion, while increased HIF-1alpha protein expression and transactivity of HIF-1 are due to the phosphorylation of Akt by bFGF, as indicated by application of the phosphatidylinositol 3-kinase (PI-3K) inhibitor LY294002
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
Sasabe et al., Cancer Sci 2005 (Carcinoma, Squamous Cell...) : Overexpression of HIF-1alpha also increased the levels of phosphorylation of Akt and extracellular signal regulated kinases ( ERK )
Zhang et al., Exp Cell Res 2006 (Keloid) : Our results also indicated that the enhancement of hypoxia mediated activation of ERK1/2 and Akt requires direct cell-cell interaction between mast cells and keloid fibroblasts, and activation of both ERK1/2 and Akt is involved in the hypoxia dependent HIF-1alpha protein accumulation and VEGF expression in the co-culture system
Bedogni et al., Cancer Cell 2005 (Cell Transformation, Neoplastic) : Taken together, these findings demonstrate that Akt hyperactivation and HIF1alpha induction by normally occurring hypoxia in the skin significantly contribute to melanoma development
Gort et al., Oncogene 2006 (Breast Neoplasms...) : Overexpression of dominant-active Akt1 restored HIF-1alpha expression, whereas inhibition of PI 3-kinase activity reduced hypoxic HIF-1alpha protein levels to a similar extent as serum deprivation
Kobayashi et al., Pathobiology 2006 (Adenocarcinoma...) : We investigated the role of phosphatidyl inositol-3 OH kinase (PI3K)-Akt signaling in the regulation of HIF-1alpha and VEGF expression in human gastric adenocarcinoma
Pore et al., Mol Cancer Res 2006 (Glioblastoma) : Therefore, our results indicate that Akt can augment HIF-1alpha expression by increasing its translation under both normoxic and hypoxic conditions ; however, the pathway we are investigating seems to be rapamycin insensitive and mTOR independent
Ardyanto et al., Int J Oncol 2006 (Stomach Neoplasms) : Phosphorylation of Akt was inhibited by CoCl ( 2 ) treatment and LY294002 treatment inhibited HIF-1alpha expression in a dose dependent manner
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
Tanaka et al., Cancer Res 2006 (Anoxia...) : On the other hand, Akt, the pathway of which can up-regulate HIF-1alpha expression, was activated in the mouse lesions, whereas HIF-1alpha was markedly down-regulated in the mouse hepatocellular carcinoma ( HCC ) cell lines after treatment with a phosphatidylinositol 3-kinase (PI3K) inhibitor, LY294002, indicating that HIF-1alpha expression is dependent on PI3K/Akt signaling
Jin et al., Cell Signal 2007 : Also, suppression of Akt activation blocked the expression of Redd1 and the activation of HIF-1alpha and Sp1 by CoCl ( 2 ) and HCD
Dimova et al., Ann N Y Acad Sci 2006 (Carcinoma, Hepatocellular...) : Furthermore, the insulin effect was associated with activation of HIF-1alpha via mitogen activated protein kinases ( MAPKs ) but not PDK1 and PKB in HepG2 cells
Barry et al., Eur J Cell Biol 2007 : Reduction of HIF1alpha levels using antimycin-A or siRNA targeting HIF1alpha did not affect PKB/Akt activation in hypoxia ... Reduction of HIF1alpha levels using antimycin-A or siRNA targeting HIF1alpha did not affect PKB/Akt activation in hypoxia ... Pharmacologic stabilization of HIF1alpha independent of hypoxia did not increase insulin stimulated PKB/Akt activation ... Pharmacologic stabilization of HIF1alpha independent of hypoxia did not increase insulin stimulated PKB/Akt activation
Tang et al., J Biol Chem 2007 (Disease Models, Animal...) : Moreover, the use of pharmacological inhibitors or genetic inhibition revealed that both ILK/Akt and mTOR signaling pathway were potentially required for US-induced HIF-1alpha activation and subsequent iNOS up-regulation
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
Belaiba et al., Mol Biol Cell 2007 (Anoxia) : Furthermore, inhibition of the phosphatidylinositol 3-kinase (PI3K)/AKT but not extracellular signal regulated kinase 1/2 pathway blocked the hypoxia dependent induction of HIF-1alpha mRNA and HIF-1alpha promoter activity, suggesting involvement of a PI3K/AKT regulated transcription factor
Park et al., J Cell Biochem 2008 : But our study revealed, through p53 mutant-type as well as p53 null cell lines, that neither the PI3K/Akt nor the p53 signaling pathway is required for quercetin induced HIF-1alpha accumulation
Lee et al., Carcinogenesis 2008 (Neovascularization, Pathologic...) : Western blot analysis and reverse transcription-polymerase chain reaction in cell experiments revealed that the over-expression of constitutively active AKT ( CA-AKT ) promotes the expressions of HIF-1alpha protein and VEGF messenger ribonucleic acid in Seoul national university ( SNU ) -216 and SNU-668 gastric cancer cells under normoxic conditions, whereas kinase-dead mutant of AKT down-regulated these expressions under the same conditions
Krieg et al., Photochem Photobiol Sci 2007 : Analysis of caspase-3 and -9 expression, the activation of HIF-1alpha , Bcl2, Cox2 and the phosphorylation of AKT reveals signal activation due to a PDT-stimulus in correlation with the positive controls
Li et al., Zhongguo Xiu Fu Chong Jian Wai Ke Za Zhi 2008 (Hypoxia-Ischemia, Brain) : To investigate the expression of hypoxia inducible factor 1alpha ( HIF-1alpha ) protein and the activation of phosphoinositide 3-kinase/Akt (PI3K/Akt) signaling pathway in neurons under hypoxia ischemia condition, and to elucidate the role of PI3K/Akt on HIF-1alpha regulation in the developing neurons after hypoxia ischemia brain damage ( HIBD )
Thomas et al., Prostate 2009 (Prostatic Neoplasms) : We detected a time dependent increase in Akt activation during serum deprivation, and inhibition of Akt activation attenuated the serum deprivation mediated increase in HIF-1alpha and cell survival ... Furthermore, HIF-1alpha suppression attenuated the serum deprivation mediated increase in Akt and IGF-IR activation
Song et al., Cancer Sci 2008 (Disease Progression...) : Taken together, these results indicate that OPN can increase the survival of ovarian cancer cells under stress conditions in vitro and promote the late progression of ovarian cancer in vivo, and the survival promoting functions of OPN are mediated through Akt activation and the induction of HIF-1alpha expression
Yang et al., Invest Ophthalmol Vis Sci 2009 (Anoxia...) : Role of PI3K/Akt and MEK/ERK in mediating hypoxia induced expression of HIF-1alpha and VEGF in laser induced rat choroidal neovascularization ... A well established rat model of CNV and cultured human retinal pigment epithelium ( hRPE ) was used to investigate the role of PI3K/Akt and MEK/ERK pathways in regulating HIF-1alpha and VEGF expression in CNV in rat and hRPE under hypoxia by immunohistochemistry, Western blot analysis, real-time PCR, and ELISA
Lau et al., Clin Cancer Res 2009 (Liver Neoplasms...) : Akt/HIF-1alpha/PDGF-BB signaling regulated Akt to confer cisplatin resistance to HCC cell lines in vitro
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
Lee et al., Carcinogenesis 2009 (Anoxia) : Methyl-beta cyclodextrin ( MbetaCD ), which induces cholesterol depletion, upregulated HIF-1alpha even under normoxic conditions and this upregulation required epidermal growth factor receptor (EGFR) and extracellular signal regulated kinase 1 and 2 activation, but not Akt activation
Koshikawa et al., J Biol Chem 2009 (Carcinoma, Lewis Lung) : Stimulation of HIF-1alpha transcription by the ND6 mutation was mediated by overproduction of reactive oxygen species ( ROS ) and subsequent activation of phosphatidylinositol 3-kinase (PI3K)-Akt and protein kinase C ( PKC ) signaling pathways
Choy et al., J Cell Physiol 2010 (Cardiomegaly...) : PKB/Akt activation inhibits p53 mediated HIF1A degradation that is independent of MDM2 ... PKB/Akt activation inhibits p53 mediated HIF1A degradation that is independent of MDM2
Zeng et al., Eur J Cancer 2010 (Lung Neoplasms...) : The data indicate that in a relatively hypoxic environment HIF-1alpha may play a role in mediating the anti-cancer effect of rapamycin and cyclophosphamide may prevent the feedback activation of Akt by rapamycin
Tseng et al., J Cell Physiol 2010 : Moreover, the use of pharmacological inhibitors or genetic inhibition revealed that both ILK/Akt and mTOR signaling pathway were potentially required for hypoxia induced HIF-1alpha activation and subsequent BMP-2 up-regulation