PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 33282728-9 2020 Together, these findings suggested that the PTEN-TXNIP-HIF-1alpha axis might be related to the E6/E7-mediated expression of GLUT1 and its glucose uptake. Glucose 138-145 hypoxia inducible factor 1 subunit alpha Homo sapiens 55-65 31944299-8 2020 Upon exposure to hypoxia, Jurkat T cells expressing Rai show (a) higher HIF-1alpha protein levels; (b) a decreased cell death and increased Akt/extracellular-signal-regulated kinase phosphorylation; (c) a decreased expression of proapoptotic markers, including caspase activities and poly(ADP-ribose) polymerase cleavage; (d) an increased glucose and lactate metabolism; (e) an increased activation of nuclear factor-kB pathway. Glucose 339-346 hypoxia inducible factor 1 subunit alpha Homo sapiens 72-82 32809974-5 2020 Improving glucose control in people with diabetes increases HIF-1alpha protein and has wide-ranging benefits, some of which are at least partially mediated by HIF-1alpha. Glucose 10-17 hypoxia inducible factor 1 subunit alpha Homo sapiens 60-70 33126773-0 2020 Pulsed Electromagnetic Fields Stimulate HIF-1alpha-Independent VEGF Release in 1321N1 Human Astrocytes Protecting Neuron-Like SH-SY5Y Cells from Oxygen-Glucose Deprivation. Glucose 152-159 hypoxia inducible factor 1 subunit alpha Homo sapiens 40-50 32809974-5 2020 Improving glucose control in people with diabetes increases HIF-1alpha protein and has wide-ranging benefits, some of which are at least partially mediated by HIF-1alpha. Glucose 10-17 hypoxia inducible factor 1 subunit alpha Homo sapiens 159-169 32412317-12 2020 Moreover, we found that most of the differentially expressed genes which were related to CDKN1B were the downstream molecules regulated by HIF-1alpha.Conclusion: The results indicated that berberine could dramatically overcome the low glucose and hypoxia induced radioresistance. Glucose 235-242 hypoxia inducible factor 1 subunit alpha Homo sapiens 139-149 32697943-0 2020 Elevated Glucose Levels Favor SARS-CoV-2 Infection and Monocyte Response through a HIF-1alpha/Glycolysis-Dependent Axis. Glucose 9-16 hypoxia inducible factor 1 subunit alpha Homo sapiens 83-93 32984331-6 2020 Mechanistically, we identify that the suppression of baicalein and baicalin on melanoma cells is due to inhibition of tumor cell glucose uptake and metabolism by affecting the mTOR-HIF-1alpha signaling pathway. Glucose 129-136 hypoxia inducible factor 1 subunit alpha Homo sapiens 181-191 32877692-0 2020 Elevated Glucose Levels Favor SARS-CoV-2 Infection and Monocyte Response through a HIF-1alpha/Glycolysis-Dependent Axis. Glucose 9-16 hypoxia inducible factor 1 subunit alpha Homo sapiens 83-93 32222493-0 2020 GSK343, an inhibitor of EZH2, mitigates fibrosis and inflammation mediated by HIF-1alpha in human peritoneal mesothelial cells treated with high glucose. Glucose 145-152 hypoxia inducible factor 1 subunit alpha Homo sapiens 78-88 32606855-11 2020 Induction of HIF-1alpha expression by emp may play an essential role in the protection of high glucose-induced proximal renal tubular epithelial cells injury. Glucose 95-102 hypoxia inducible factor 1 subunit alpha Homo sapiens 13-23 32680978-0 2020 Circular RNA circVEGFC accelerates high glucose-induced vascular endothelial cells apoptosis through miR-338-3p/HIF-1alpha/VEGFA axis. Glucose 40-47 hypoxia inducible factor 1 subunit alpha Homo sapiens 112-122 32152275-7 2020 In addition, 1% O2-induced increases in lactate concentration and glucose uptake were also suppressed by HIF1A silencing. Glucose 66-73 hypoxia inducible factor 1 subunit alpha Homo sapiens 105-110 32200037-5 2020 We found that hENT1 reversed GEM-induced drug resistance by inhibiting glycolysis and altering glucose transport mediated by HIF-1alpha in pancreatic cancer. Glucose 95-102 hypoxia inducible factor 1 subunit alpha Homo sapiens 125-135 32158929-3 2020 Enhanced glucose utilization was critically dependent on mitochondrial stress signaling/hypoxia-inducible factor-1alpha representing a therapeutic vulnerability. Glucose 9-16 hypoxia inducible factor 1 subunit alpha Homo sapiens 88-119 32045650-2 2020 The aim of the present study was to examine if hypoxia-inducible factor-1 (HIF-1) might be involved in the regulation of glucose de novo synthesis in kidneys. Glucose 121-128 hypoxia inducible factor 1 subunit alpha Homo sapiens 47-73 32010625-5 2019 We found that both endogenous, glucose-derived lactate and exogenous, lactate supplementation significantly affected the transcription of key oncogenes (MYC, RAS, and PI3KCA), transcription factors (HIF1A and E2F1), tumor suppressors (BRCA1, BRCA2) as well as cell cycle and proliferation genes involved in breast cancer (AKT1, ATM, CCND1, CDK4, CDKN1A, CDK2B) (0.001 < p < 0.05 for all genes). Glucose 31-38 hypoxia inducible factor 1 subunit alpha Homo sapiens 199-204 32241009-7 2020 Increased glucose reabsorption by SGLTs in diabetic subjects generates a high-glucose environment in renal tubulointerstitium, which may impair HIF-1, damage renal erythropoietin-producing cells (REPs) and decrease EPO secretion and erythropoiesis. Glucose 10-17 hypoxia inducible factor 1 subunit alpha Homo sapiens 144-149 32241009-7 2020 Increased glucose reabsorption by SGLTs in diabetic subjects generates a high-glucose environment in renal tubulointerstitium, which may impair HIF-1, damage renal erythropoietin-producing cells (REPs) and decrease EPO secretion and erythropoiesis. Glucose 78-85 hypoxia inducible factor 1 subunit alpha Homo sapiens 144-149 32045650-2 2020 The aim of the present study was to examine if hypoxia-inducible factor-1 (HIF-1) might be involved in the regulation of glucose de novo synthesis in kidneys. Glucose 121-128 hypoxia inducible factor 1 subunit alpha Homo sapiens 75-80 32045650-7 2020 The final conclusion that hypoxia/HIF-1 accelerates the rate of renal glucogenesis via the mechanism engaging activation of PEPCK-C expression might be useful in terms of e.g. diabetes treatment, as it is commonly accepted that under diabetic conditions kidneys and liver seem to be equally important sources of glucose synthesized de novo. Glucose 312-319 hypoxia inducible factor 1 subunit alpha Homo sapiens 34-39 31720731-8 2020 CONCLUSIONS/INTERPRETATION: The conserved pro-survival HIF1alpha-mediated injury-response signalling is activated in beta cells in type 1 diabetes and likely contributes to the relatively slow rate of beta cell loss at the expense of early defective glucose-induced insulin secretion. Glucose 250-257 hypoxia inducible factor 1 subunit alpha Homo sapiens 55-64 31880296-0 2019 miR-206 Inhibits Cell Proliferation and Extracellular Matrix Accumulation by Targeting Hypoxia-Inducible Factor 1-alpha (HIF-1alpha) in Mesangial Cells Treated with High Glucose. Glucose 170-177 hypoxia inducible factor 1 subunit alpha Homo sapiens 121-131 30041062-1 2018 Hypoxia inducible factor-1 (HIF-1) is a transcriptional factor that induces genes involved in glucose metabolism. Glucose 94-101 hypoxia inducible factor 1 subunit alpha Homo sapiens 0-26 31626790-11 2019 SIGNIFICANCE: Taken together these data indicate that HIF-1alpha/PFKFB3/PFK1 regulatory axis is a vital determinant of glucose metabolic reprogramming in hepatocellular carcinoma, which gives new insights into the action of metformin in combatting liver cancer. Glucose 119-126 hypoxia inducible factor 1 subunit alpha Homo sapiens 54-64 31740625-7 2019 MTFR2 can switch glucose metabolism from OXPHS to glycolysis in a HIF1alpha- and HIF2alpha-dependent manner. Glucose 17-24 hypoxia inducible factor 1 subunit alpha Homo sapiens 66-75 31676796-0 2019 Mechanism and Consequences of The Impaired Hif-1alpha Response to Hypoxia in Human Proximal Tubular HK-2 Cells Exposed to High Glucose. Glucose 127-134 hypoxia inducible factor 1 subunit alpha Homo sapiens 43-53 31554283-9 2019 However, the results from the targeted metabolome analyses revealed that HIF1 activity affected neither the consumption of glucose nor the release of ammonium or lactate; however, it significantly inhibited the release of the amino acid alanine. Glucose 123-130 hypoxia inducible factor 1 subunit alpha Homo sapiens 73-77 31214621-8 2019 The effect of glucose on a stable HIF-1A construct with a Pro582Ser mutation was evaluated in vitro. Glucose 14-21 hypoxia inducible factor 1 subunit alpha Homo sapiens 34-40 31078152-0 2019 Ginsenoside compound K inhibits growth of lung cancer cells via HIF-1alpha-mediated glucose metabolism. Glucose 84-91 hypoxia inducible factor 1 subunit alpha Homo sapiens 64-74 30940798-1 2019 HIF-1alpha has a broad impact on tumors, including enhanced utilization of glucose, tumor cell stemness, migration, metastasis and so on. Glucose 75-82 hypoxia inducible factor 1 subunit alpha Homo sapiens 0-10 30848518-4 2019 In addition, high glucose inhibits Axl and hypoxia-inducible factor 1-alpha (HIF-1alpha) protein expression in hypoxia condition. Glucose 18-25 hypoxia inducible factor 1 subunit alpha Homo sapiens 43-75 30848518-4 2019 In addition, high glucose inhibits Axl and hypoxia-inducible factor 1-alpha (HIF-1alpha) protein expression in hypoxia condition. Glucose 18-25 hypoxia inducible factor 1 subunit alpha Homo sapiens 77-87 30733294-5 2019 Our modeling results demonstrate a direct association between the activities of AMPK and HIF-1, master regulators of OXPHOS and glycolysis, respectively, with the activities of three major metabolic pathways: glucose oxidation, glycolysis, and fatty acid oxidation. Glucose 209-216 hypoxia inducible factor 1 subunit alpha Homo sapiens 89-94 30471165-4 2019 Hypoxia Inducible Factor 1 (HIF-1) is a transcription factor involved in the regulation of genes important for cellular adaption to hypoxia and low glucose supply. Glucose 148-155 hypoxia inducible factor 1 subunit alpha Homo sapiens 0-26 30471165-4 2019 Hypoxia Inducible Factor 1 (HIF-1) is a transcription factor involved in the regulation of genes important for cellular adaption to hypoxia and low glucose supply. Glucose 148-155 hypoxia inducible factor 1 subunit alpha Homo sapiens 28-33 30634433-6 2019 In addition, we summarize our own findings revealing that a novel HIF-1-activating factor enhances the antioxidant capacity and resultant radioresistance of cancer cells though reprogramming of the glucose metabolic pathway. Glucose 198-205 hypoxia inducible factor 1 subunit alpha Homo sapiens 66-71 30393198-4 2019 Gain- and loss-of-function assays, a human glucose metabolism array and gene pathway analyses confirm that HIF-1alpha-induced miR-23a~27a~24 cluster collectively regulate glucose metabolic network through regulating various metabolic pathways and targeting multiple tricarboxylic acid cycle (TCA)-related genes. Glucose 43-50 hypoxia inducible factor 1 subunit alpha Homo sapiens 107-117 30082910-4 2019 In addition, ANKDD1A decreases the half-life of HIF1alpha by upregulating FIH1, decreases glucose uptake and lactate production, inhibits glioblastoma multiforme (GBM) autophagy, and induces apoptosis in GBM cells under hypoxia. Glucose 90-97 hypoxia inducible factor 1 subunit alpha Homo sapiens 48-57 30504385-2 2018 Since hypoxia via HIF-1 induces glycolysis, a process essential for malignant melanoma growth/survival, the goal of this study was to analyze the influence of hypoxia on the expression of HIF-1 target genes involved in glucose metabolism. Glucose 219-226 hypoxia inducible factor 1 subunit alpha Homo sapiens 188-193 29772209-1 2018 Hypoxia-inducible factor-1alpha (HIF-1alpha) shifts the metabolism of glucose from highly efficient oxidative phosphorylation to less efficient glycolysis. Glucose 70-77 hypoxia inducible factor 1 subunit alpha Homo sapiens 0-31 29772209-1 2018 Hypoxia-inducible factor-1alpha (HIF-1alpha) shifts the metabolism of glucose from highly efficient oxidative phosphorylation to less efficient glycolysis. Glucose 70-77 hypoxia inducible factor 1 subunit alpha Homo sapiens 33-43 30315965-2 2018 Under hypoxic conditions, HIF-1 is an adaptive system that regulates the transcription of multiple genes associated with growth, angiogenesis, proliferation, glucose transport, metabolism, pH regulation and cell death. Glucose 158-165 hypoxia inducible factor 1 subunit alpha Homo sapiens 26-31 30355156-6 2018 We found that cardiomyocytes cultured in the presence of glucose used primarily aerobic glycolysis and aberrantly upregulated HIF1alpha (hypoxia-inducible factor 1alpha) and its downstream target lactate dehydrogenase A. Glucose 57-64 hypoxia inducible factor 1 subunit alpha Homo sapiens 126-135 30355156-6 2018 We found that cardiomyocytes cultured in the presence of glucose used primarily aerobic glycolysis and aberrantly upregulated HIF1alpha (hypoxia-inducible factor 1alpha) and its downstream target lactate dehydrogenase A. Glucose 57-64 hypoxia inducible factor 1 subunit alpha Homo sapiens 137-168 29894685-0 2018 MiR-182 promotes glucose metabolism by upregulating hypoxia-inducible factor 1alpha in NSCLC cells. Glucose 17-24 hypoxia inducible factor 1 subunit alpha Homo sapiens 52-83 29894685-8 2018 Among a panel of genes controlling glucose metabolism, miR-182 exhibited significantly influence on ENO1, GLUT1, HIF-1alpha, HK1, HK2, LDHA and PDK1, especially HIF-1alpha. Glucose 35-42 hypoxia inducible factor 1 subunit alpha Homo sapiens 113-123 29894685-8 2018 Among a panel of genes controlling glucose metabolism, miR-182 exhibited significantly influence on ENO1, GLUT1, HIF-1alpha, HK1, HK2, LDHA and PDK1, especially HIF-1alpha. Glucose 35-42 hypoxia inducible factor 1 subunit alpha Homo sapiens 161-171 29894685-10 2018 CONCLUSION: MiR-182 promotes glucose metabolism by upregulating HIF-1alpha in NSCLC cells. Glucose 29-36 hypoxia inducible factor 1 subunit alpha Homo sapiens 64-74 31890203-7 2019 Results: Genome-wide ChIP-seq and transcriptome studies revealed that overlapping HIF1- and HIF2-controlled loci were highly enriched for various processes including metabolism, particularly glucose metabolism, but also for chromatin organization, cellular response to stress and G protein-coupled receptor signaling. Glucose 191-198 hypoxia inducible factor 1 subunit alpha Homo sapiens 82-86 31580427-2 2019 We have shown a role for ARNT/HIF1beta in glucose sensing and insulin secretion in vitro and no defects in in vivo glucose homeostasis. Glucose 42-49 hypoxia inducible factor 1 subunit alpha Homo sapiens 30-38 31683709-8 2019 During the development of PM, hypoxia inducible factor-1alpha (HIF-1alpha) plays a key role in activating both aerobic and anaerobic glycolysis, increasing the uptake of glucose, lipid, and glutamine into cancer cells. Glucose 170-177 hypoxia inducible factor 1 subunit alpha Homo sapiens 30-61 31683709-8 2019 During the development of PM, hypoxia inducible factor-1alpha (HIF-1alpha) plays a key role in activating both aerobic and anaerobic glycolysis, increasing the uptake of glucose, lipid, and glutamine into cancer cells. Glucose 170-177 hypoxia inducible factor 1 subunit alpha Homo sapiens 63-73 31683709-9 2019 HIF-1alpha upregulates hexokinase II, phosphoglycerate kinase 1 (PGK1), pyruvate dehydrogenase kinase (PDK), pyruvate kinase muscle isoenzyme 2 (PKM2), lactate dehydrogenase (LDH) and glucose transporters (GLUT) and promotes cytoplasmic glycolysis. Glucose 184-191 hypoxia inducible factor 1 subunit alpha Homo sapiens 0-10 31570448-4 2019 RESULTS: Reprogramming of glucose utilization involving hypoxia-inducible factor 1-alpha (HIF-1alpha) and the extracellular adenosine axis was observed. Glucose 26-33 hypoxia inducible factor 1 subunit alpha Homo sapiens 56-88 31570448-4 2019 RESULTS: Reprogramming of glucose utilization involving hypoxia-inducible factor 1-alpha (HIF-1alpha) and the extracellular adenosine axis was observed. Glucose 26-33 hypoxia inducible factor 1 subunit alpha Homo sapiens 90-100 31146006-9 2019 We conclude that HIF-1 regulates the WSSV-induced glycolysis through induction of glycolytic genes contributing to glucose metabolism in tissues of infected shrimp. Glucose 115-122 hypoxia inducible factor 1 subunit alpha Homo sapiens 17-22 30988076-8 2019 The up-regulated HIF1alpha promoted the glucose uptake and lactate generation of ovarian cancer cells. Glucose 40-47 hypoxia inducible factor 1 subunit alpha Homo sapiens 17-26 31044177-4 2019 Here we show that a parasite-encoded prolyl-isomerase, TaPin1, stabilizes host pyruvate kinase isoform M2 (PKM2) leading to HIF-1alpha-dependent regulation of metabolic enzymes, glucose uptake and transformed phenotypes in parasite-infected cells. Glucose 178-185 hypoxia inducible factor 1 subunit alpha Homo sapiens 124-134 30659228-2 2019 The potent complex induces production of reactive oxygen species (ROS) by higher fatty acid beta-oxidation and down-regulation of glucose transporter-mediated pyruvate dehydrogenase kinase 1 via reduced hypoxia-inducible factor 1alpha. Glucose 130-137 hypoxia inducible factor 1 subunit alpha Homo sapiens 203-234 30003444-7 2019 During hypoxia, addition of glucose further stimulated HIF1alpha expression than by hypoxia alone. Glucose 28-35 hypoxia inducible factor 1 subunit alpha Homo sapiens 55-64 30455857-7 2018 In addition, we also tested the effect of HIF-1alpha siRNA on the high glucose-induced invasive and migratory abilities of BxPC-3 cells in culture. Glucose 71-78 hypoxia inducible factor 1 subunit alpha Homo sapiens 42-52 30455857-12 2018 The expression level of HIF-1alpha in the BxPC-3 cancer cell line increased in response to high glucose and CoCl2 concentrations. Glucose 96-103 hypoxia inducible factor 1 subunit alpha Homo sapiens 24-34 30455857-13 2018 The high glucose-induced invasive ability, migratory capacity and MMP-9 expression were counter-balanced by siRNA specific to HIF-1alpha. Glucose 9-16 hypoxia inducible factor 1 subunit alpha Homo sapiens 126-136 30041062-1 2018 Hypoxia inducible factor-1 (HIF-1) is a transcriptional factor that induces genes involved in glucose metabolism. Glucose 94-101 hypoxia inducible factor 1 subunit alpha Homo sapiens 28-33 29935943-1 2018 Hypothalamic hypoxia-inducible factor-1 (HIF-1) can regulate whole-body energy homeostasis in response to changes in blood glucose, suggesting that it acts as a sensor for systemic energy stores. Glucose 123-130 hypoxia inducible factor 1 subunit alpha Homo sapiens 41-46 29672220-6 2018 We found that: 1) hypoxia blunted the activation of protein synthesis after resistance exercise; 2) hypoxia down-regulated the transcriptional program of autophagy; 3) hypoxia regulated the expression of genes involved in glucose metabolism at rest and the genes involved in myoblast differentiation and fusion and in muscle contraction machinery after exercise; and 4) the hypoxia-inducible factor-1alpha pathway was not activated at the time points studied. Glucose 222-229 hypoxia inducible factor 1 subunit alpha Homo sapiens 374-405 30140083-9 2018 High glucose affected the expression of angiogenic factors in choriocarcinoma cells via the PKCbeta and HIF-1alpha pathways, suggesting their involvement in PE pathogenesis. Glucose 5-12 hypoxia inducible factor 1 subunit alpha Homo sapiens 104-114 29935187-1 2018 Hypoxia-inducible factor-1-alpha (HIF-1alpha) activates the transcription of many genes that code for proteins involved in angiogenesis, glucose metabolism, cell proliferation/survival, and invasion/metastasis. Glucose 137-144 hypoxia inducible factor 1 subunit alpha Homo sapiens 0-32 29935187-1 2018 Hypoxia-inducible factor-1-alpha (HIF-1alpha) activates the transcription of many genes that code for proteins involved in angiogenesis, glucose metabolism, cell proliferation/survival, and invasion/metastasis. Glucose 137-144 hypoxia inducible factor 1 subunit alpha Homo sapiens 34-44 30140083-3 2018 We examined whether hypoxia-induced factor-1alpha (HIF-1alpha) and protein kinase Cbeta (PKCbeta) are involved in the regulation of placental angiogenic factors under high-glucose conditions in vitro. Glucose 172-179 hypoxia inducible factor 1 subunit alpha Homo sapiens 51-61 30015875-10 2018 Furthermore, when combined with 2-deoxyglucose (2-DG), the anticancer effect of the Bcl-2 inhibitor ABT737 was greatly potentiated and hypoxia-inducible factor 1alpha (HIF-1alpha) appeared to be closely associated with Bcl-2 family members in the regulation of glucose metabolism. Glucose 39-46 hypoxia inducible factor 1 subunit alpha Homo sapiens 135-166 30015875-10 2018 Furthermore, when combined with 2-deoxyglucose (2-DG), the anticancer effect of the Bcl-2 inhibitor ABT737 was greatly potentiated and hypoxia-inducible factor 1alpha (HIF-1alpha) appeared to be closely associated with Bcl-2 family members in the regulation of glucose metabolism. Glucose 39-46 hypoxia inducible factor 1 subunit alpha Homo sapiens 168-178 29789538-6 2018 Rescue assays suggested that compared with Sal-B treatment group, Akt or hif-1a overexpression attenuated the inhibitory effect of Sal-B on glucose uptake and intracellular lactate level. Glucose 140-147 hypoxia inducible factor 1 subunit alpha Homo sapiens 73-79 29363056-6 2018 Meanwhile, maspin reduced the mRNA and protein levels of hypoxia-inducible factor-1alpha and vascular endothelial growth factor in high glucose-stimulated cells in a dose-dependent manner. Glucose 136-143 hypoxia inducible factor 1 subunit alpha Homo sapiens 57-88 29884183-14 2018 CONCLUSIONS: Taken together, KL is a negative regulator of aerobic glycolysis and KL inhibited glucose metabolism transformation via the ERK/ HIF1alpha axis. Glucose 95-102 hypoxia inducible factor 1 subunit alpha Homo sapiens 142-151 29702094-3 2018 The data suggests that ROS mediated EGFR/MEK/ERK/HIF-1alpha loop is activated in high glucose metabolic samples both in vitro and in vivo: The increasing of HIF-1alpha expression is controlled by activation of EGFR/MEK/ERK pathway in hypoxia condition, HIF-1alpha inhibits excessive release of ROS, the reduction of ROS further activates EGFR to form a positive feedback loop. Glucose 86-93 hypoxia inducible factor 1 subunit alpha Homo sapiens 49-59 29702094-3 2018 The data suggests that ROS mediated EGFR/MEK/ERK/HIF-1alpha loop is activated in high glucose metabolic samples both in vitro and in vivo: The increasing of HIF-1alpha expression is controlled by activation of EGFR/MEK/ERK pathway in hypoxia condition, HIF-1alpha inhibits excessive release of ROS, the reduction of ROS further activates EGFR to form a positive feedback loop. Glucose 86-93 hypoxia inducible factor 1 subunit alpha Homo sapiens 157-167 29702094-3 2018 The data suggests that ROS mediated EGFR/MEK/ERK/HIF-1alpha loop is activated in high glucose metabolic samples both in vitro and in vivo: The increasing of HIF-1alpha expression is controlled by activation of EGFR/MEK/ERK pathway in hypoxia condition, HIF-1alpha inhibits excessive release of ROS, the reduction of ROS further activates EGFR to form a positive feedback loop. Glucose 86-93 hypoxia inducible factor 1 subunit alpha Homo sapiens 157-167 29789538-7 2018 Taken together, our results suggested that Sal-B modulated aberrant glucose metabolism via the PI3K/AKT/HIF-1alpha signaling pathways, which might contribute to the anti-carcinogenic activity of Sal-B. Glucose 68-75 hypoxia inducible factor 1 subunit alpha Homo sapiens 104-114 29121446-2 2018 HIF-1 is a key regulator of adaptive responses to a lack of oxygen that controls glucose metabolism, angiogenesis, proliferation, invasion, and metastasis. Glucose 81-88 hypoxia inducible factor 1 subunit alpha Homo sapiens 0-5 28951244-0 2018 Tyrosines-740/751 of PDGFRbeta contribute to the activation of Akt/Hif1alpha/TGFbeta nexus to drive high glucose-induced glomerular mesangial cell hypertrophy. Glucose 105-112 hypoxia inducible factor 1 subunit alpha Homo sapiens 67-76 28951244-9 2018 siRNAs against Hif1alpha inhibited the high glucose-induced mesangial cell hypertrophy. Glucose 44-51 hypoxia inducible factor 1 subunit alpha Homo sapiens 15-24 28951244-11 2018 We found that inhibition of PDGFRbeta and expression of PDGFRbeta Y740/751F mutant significantly inhibited the high glucose-induced expression of Hif1alpha. Glucose 116-123 hypoxia inducible factor 1 subunit alpha Homo sapiens 146-155 28951244-13 2018 Finally, we show that high glucose-stimulated PDGFRbeta tyrosine phosphorylation at 740/751 residues and the tyrosine kinase activity of the receptor regulate the transforming growth factor-beta (TGFbeta) expression by Hif1alpha. Glucose 27-34 hypoxia inducible factor 1 subunit alpha Homo sapiens 219-228 28951244-14 2018 Thus we define the cell surface PDGFRbeta as a major link between high glucose and its effectors Hif1alpha and TGFbeta for induction of diabetic mesangial cell hypertrophy. Glucose 71-78 hypoxia inducible factor 1 subunit alpha Homo sapiens 97-106 29337249-3 2018 HIF-1 induces genes involved in glucose metabolism and regulates cellular oxygen homeostasis. Glucose 32-39 hypoxia inducible factor 1 subunit alpha Homo sapiens 0-5 29337249-11 2018 Silencing of HIF-1alpha blocked the increase of LDH expression and enzyme activity, along with glucose (all tissues) and lactate (gills and hepatopancreas) concentrations produced by WSSV infection. Glucose 95-102 hypoxia inducible factor 1 subunit alpha Homo sapiens 13-23 28752896-7 2017 Study of the underlying mechanisms suggested that the improved cell survival was regulated by HIF-1-induced metabolic reprogramming including decreased reactive oxygen species, increased intracellular pH, enhanced glucose uptake and increased glycogen synthesis. Glucose 214-221 hypoxia inducible factor 1 subunit alpha Homo sapiens 94-99 29262591-4 2017 We further found that Bevacizumab increases the expression of hypoxic (HIF-1alpha and CAIX) and glycolytic markers (GLUT1 and MCT1), leading to higher glucose uptake and lactate production. Glucose 151-158 hypoxia inducible factor 1 subunit alpha Homo sapiens 71-81 29330794-4 2018 Hypoxia-mediated stabilization of hypoxia-inducible factor-1 alpha (HIF-1alpha) transcription factor leads to altered expression of several glycolytic genes and glucose transporters, which results in increased glucose uptake by tumor cells. Glucose 161-168 hypoxia inducible factor 1 subunit alpha Homo sapiens 34-66 29330794-4 2018 Hypoxia-mediated stabilization of hypoxia-inducible factor-1 alpha (HIF-1alpha) transcription factor leads to altered expression of several glycolytic genes and glucose transporters, which results in increased glucose uptake by tumor cells. Glucose 161-168 hypoxia inducible factor 1 subunit alpha Homo sapiens 68-78 28758418-8 2017 The greatest changes in mRNA expression of HIF-1alpha target genes occurred a month after IHT and coincided with the largest decrease in blood glucose levels. Glucose 143-150 hypoxia inducible factor 1 subunit alpha Homo sapiens 43-53 28263817-9 2017 Interestingly, HIF-1alpha knockdown almost eliminated the cell apoptosis induced by high glucose levels. Glucose 89-96 hypoxia inducible factor 1 subunit alpha Homo sapiens 15-25 28622395-6 2017 This change in the redox ratio was indicative of increased catabolism of glucose in the resistant cells after radiation and was associated with significantly greater protein content of hypoxia-inducible factor 1 ( HIF - 1 ? ), a key promoter of glycolytic metabolism. Glucose 73-80 hypoxia inducible factor 1 subunit alpha Homo sapiens 214-223 28555668-3 2017 A glucose-sensitive signal transduction circuit involving the mTOR complex 1 (mTORC1), HIF1alpha and inducible nitric oxide synthase (iNOS) coordinates DC metabolism and function to limit DC-stimulated T-cell responses. Glucose 2-9 hypoxia inducible factor 1 subunit alpha Homo sapiens 87-96 28263817-11 2017 The results showed that SIRT1 knockdown further promoted high-glucose-induced HIF-1alpha expression, while SIRT1 overexpression significantly inhibited HIF-1alpha level induced by high glucose. Glucose 62-69 hypoxia inducible factor 1 subunit alpha Homo sapiens 78-88 28263817-11 2017 The results showed that SIRT1 knockdown further promoted high-glucose-induced HIF-1alpha expression, while SIRT1 overexpression significantly inhibited HIF-1alpha level induced by high glucose. Glucose 185-192 hypoxia inducible factor 1 subunit alpha Homo sapiens 152-162 27808477-1 2017 AIMS/INTRODUCTION: Given the high prevalence of diabetes and burn injuries worldwide, it is essential to dissect the underlying mechanism of delayed burn wound healing in diabetes patients, especially the high glucose-induced hypoxia-inducible factor 1 (HIF-1)-mediated transcription defects. Glucose 210-217 hypoxia inducible factor 1 subunit alpha Homo sapiens 254-259 28881665-4 2017 HPV-negative cells express HIF1alpha and its downstream mediators of glucose metabolism such as hexokinase II (HKII) and carbonic anhydrase IX (CAIX) at higher levels, while the expression level of cytochrome c oxidase (COX) was noticeably higher in HPV-positive HNSCC. Glucose 69-76 hypoxia inducible factor 1 subunit alpha Homo sapiens 27-36 27808477-11 2017 Finally, we showed that co-overexpression of p300 and CREB rectifies the dissociation of HIF-1alpha-p300-CREB protein complex in chronic high glucose-treated cells. Glucose 142-149 hypoxia inducible factor 1 subunit alpha Homo sapiens 89-99 27808477-8 2017 RESULTS: Chronic high glucose treatment resulted in impaired HIF-1-induced VEGF transcription and CREB exclusion from the nucleus. Glucose 22-29 hypoxia inducible factor 1 subunit alpha Homo sapiens 61-66 28214471-10 2017 Indeed, Che-1 depletion impacted on HIF-1alpha stabilization, thus downregulating the expression of several genes involved in the response to hypoxia and affecting glucose metabolism. Glucose 164-171 hypoxia inducible factor 1 subunit alpha Homo sapiens 36-46 28465657-11 2017 Furthermore, high glucose dramatically increased the levels of pERK (p44), hypoxia-inducible factor (HIF-1alpha), and VEGF. Glucose 18-25 hypoxia inducible factor 1 subunit alpha Homo sapiens 101-111 28465657-13 2017 CONCLUSIONS: Our findings, for the first time, showed that the pleiotropic action of miR-21 induced the expression of pERK, HIF-1alpha, and VEGF in the high glucose condition by simultaneously targeting SPRY1, SMAD7, and PTEN in ARPE-19 cells. Glucose 157-164 hypoxia inducible factor 1 subunit alpha Homo sapiens 124-134 28529605-4 2017 MiR-199a-5p directly targets the 3"-untranslated region (UTR) of hypoxia-inducible factor-1alpha (HIF-1alpha), thereby suppressing glucose uptake, lactate production, cell growth, and expression of HIF-1alpha downstream glycolytic genes of HCC cells. Glucose 131-138 hypoxia inducible factor 1 subunit alpha Homo sapiens 65-96 28529605-4 2017 MiR-199a-5p directly targets the 3"-untranslated region (UTR) of hypoxia-inducible factor-1alpha (HIF-1alpha), thereby suppressing glucose uptake, lactate production, cell growth, and expression of HIF-1alpha downstream glycolytic genes of HCC cells. Glucose 131-138 hypoxia inducible factor 1 subunit alpha Homo sapiens 98-108 28193910-8 2017 Furthermore, knockdown of endogenous HIF-1alpha and HIF-2alpha decreased the LDHA expression even in the hypoxic condition, which was accompanied with a significant decrease in lactate production and glucose utilization (p < 0.01). Glucose 200-207 hypoxia inducible factor 1 subunit alpha Homo sapiens 37-47 27959421-5 2017 In the present review, we discuss the role of HIF-1alpha in glucose uptake, cancer proliferation, cell mobility and chemoresistance in GBM. Glucose 60-67 hypoxia inducible factor 1 subunit alpha Homo sapiens 46-56 27751871-3 2017 We showed recently that transient glucose elevation elicited dose-dependent effects on HSCs through elevated metabolic activity and subsequent reactive oxygen species-mediated induction of Hypoxia-Inducible Factor 1alpha (Hif1alpha). Glucose 34-41 hypoxia inducible factor 1 subunit alpha Homo sapiens 189-220 27751871-3 2017 We showed recently that transient glucose elevation elicited dose-dependent effects on HSCs through elevated metabolic activity and subsequent reactive oxygen species-mediated induction of Hypoxia-Inducible Factor 1alpha (Hif1alpha). Glucose 34-41 hypoxia inducible factor 1 subunit alpha Homo sapiens 222-231 27959421-9 2017 The present review focuses on the strategies through which to target HIF-1alpha and the related downstream genes highlighting their regulatory roles in angiogenesis, apoptosis, migration and glucose metabolism for the development of future GBM therapeutics. Glucose 191-198 hypoxia inducible factor 1 subunit alpha Homo sapiens 69-79 27342248-5 2017 The results showed that glucose uptake rate and lactate release rate were increased in cells under hypoxia and/or radiation condition compared with untreated cells (p < 0.05), while the addition of HIF-1alpha inhibitor decreased these rates in hypoxia + radiation treated cells (p < 0.05). Glucose 24-31 hypoxia inducible factor 1 subunit alpha Homo sapiens 201-211 28028936-5 2017 HIF-1alpha-induced reprogramming of glucose metabolic pathway in A549 cells and the effects of HIF-1 and CAIX on the cytotoxicity of vinorelbine were investigated. Glucose 36-43 hypoxia inducible factor 1 subunit alpha Homo sapiens 0-10 28028936-5 2017 HIF-1alpha-induced reprogramming of glucose metabolic pathway in A549 cells and the effects of HIF-1 and CAIX on the cytotoxicity of vinorelbine were investigated. Glucose 36-43 hypoxia inducible factor 1 subunit alpha Homo sapiens 0-5 28028936-9 2017 Glucose metabolic pathway was shifted from oxidative phosphorylation to glycolysis by inducing HIF-1alpha in A549 cells. Glucose 0-7 hypoxia inducible factor 1 subunit alpha Homo sapiens 95-105 27342248-9 2017 Furthermore, HIF-1alpha might inhibit the promoting effect of radiation on glycolysis in hypoxic MCF-7 cells by regulating the glucose metabolic pathway. Glucose 127-134 hypoxia inducible factor 1 subunit alpha Homo sapiens 13-23 27982118-5 2016 In addition, BRU can also decrease glucose consumption under hypoxia through inhibition of HIF-1 signaling pathway. Glucose 35-42 hypoxia inducible factor 1 subunit alpha Homo sapiens 91-96 27829662-6 2016 Indeed, high glucose increased intracellular ROS levels and HIF-1alpha expression, associated with regulation of BACE1 and Liver X Receptor alpha (LXRalpha). Glucose 13-20 hypoxia inducible factor 1 subunit alpha Homo sapiens 60-70 27789221-3 2016 We therefore investigated the effects of LIG on iron uptake protein transferrin receptor 1, iron exporter protein ferroportin 1, iron storage protein ferritin light chain and also hypoxia inducible factor-1 alpha (HIF-1 alpha) in oxygen-glucose deprivation/reoxygenation (OGD/R)-treated SH-SY5Y cells, using Western blot analysis. Glucose 237-244 hypoxia inducible factor 1 subunit alpha Homo sapiens 180-212 27132509-9 2016 EML4-ALK induced hypoxia-independent but glucose-dependent accumulation of HIF1alpha protein via both transcriptional activation of HIF1alpha mRNA and the phosphatidylinositol 3 kinase-AKT pathway to enhance HIF1alpha protein synthesis. Glucose 41-48 hypoxia inducible factor 1 subunit alpha Homo sapiens 75-84 27132509-9 2016 EML4-ALK induced hypoxia-independent but glucose-dependent accumulation of HIF1alpha protein via both transcriptional activation of HIF1alpha mRNA and the phosphatidylinositol 3 kinase-AKT pathway to enhance HIF1alpha protein synthesis. Glucose 41-48 hypoxia inducible factor 1 subunit alpha Homo sapiens 132-141 27132509-9 2016 EML4-ALK induced hypoxia-independent but glucose-dependent accumulation of HIF1alpha protein via both transcriptional activation of HIF1alpha mRNA and the phosphatidylinositol 3 kinase-AKT pathway to enhance HIF1alpha protein synthesis. Glucose 41-48 hypoxia inducible factor 1 subunit alpha Homo sapiens 132-141 27132509-11 2016 Our data reveal a novel EML4-ALK-HIF1alpha-HK2 cascade to enhance glucose metabolism in EML4-ALK-positive NSCLC. Glucose 66-73 hypoxia inducible factor 1 subunit alpha Homo sapiens 33-42 27829662-0 2016 High glucose upregulates BACE1-mediated Abeta production through ROS-dependent HIF-1alpha and LXRalpha/ABCA1-regulated lipid raft reorganization in SK-N-MC cells. Glucose 5-12 hypoxia inducible factor 1 subunit alpha Homo sapiens 79-89 27829662-9 2016 In conclusion, high glucose upregulates BACE1 expression and activity through HIF-1alpha and LXRalpha/ABCA1-regulated lipid raft reorganization, leading to Abeta production and apoptosis of SK-N-MC. Glucose 20-27 hypoxia inducible factor 1 subunit alpha Homo sapiens 78-88 27895745-1 2016 The present study aimed to examine hypoxia-inducible factor (HIF)-1alpha expression and its association with glucose uptake in invasive breast cancer. Glucose 109-116 hypoxia inducible factor 1 subunit alpha Homo sapiens 35-72 27372381-5 2016 Inflamed tissues are characterized by low levels of oxygen and glucose, a microenvironment that triggers the stabilization of the hypoxia-inducible transcription factor HIF-1alpha. Glucose 63-70 hypoxia inducible factor 1 subunit alpha Homo sapiens 169-179 27385728-3 2016 WHAT IS KNOWN ALREADY: TGF-beta1 induces the metabolic conversion of glucose to lactate via aerobic glycolysis (the "Warburg effect") in the peritoneum of women with endometriosis, through increased expression of the transcription factor hypoxia inducible factor alpha (HIF-1alpha). Glucose 69-76 hypoxia inducible factor 1 subunit alpha Homo sapiens 270-280 27748854-10 2016 Furthermore, HIF-1alpha is involved in glucose uptake and metabolism of ASCs. Glucose 39-46 hypoxia inducible factor 1 subunit alpha Homo sapiens 13-23 26755257-2 2016 The presence of hypoxia (O2 <5%) stabilizes the transcription factor Hif1 and results in numerous cellular adaptations including increased flux of glucose through glycolysis. Glucose 150-157 hypoxia inducible factor 1 subunit alpha Homo sapiens 72-76 27281823-9 2016 In accordance, expression of WT-Spry2, but not 3P/3A-Spry2 results in a decrease in HIF1alpha-sensitive glucose uptake. Glucose 104-111 hypoxia inducible factor 1 subunit alpha Homo sapiens 84-93 26983985-5 2016 The relevance of the HIF-1-mediated characteristic features of cancer cells, such as the production of antioxidants through reprogramming of the glucose metabolic pathway and cell cycle regulation, for tumor radioresistance has also been reviewed. Glucose 145-152 hypoxia inducible factor 1 subunit alpha Homo sapiens 21-26 27189088-1 2016 In severely hypoxic condition, HIF-1alpha-mediated induction of Pdk1 was found to regulate glucose oxidation by preventing the entry of pyruvate into the tricarboxylic cycle. Glucose 91-98 hypoxia inducible factor 1 subunit alpha Homo sapiens 31-41 28174749-2 2016 Hypoxia is known to change tissue pH as a result of anaerobic glucose metabolism through the stabilization of hypoxia-inducible factor-1alpha. Glucose 62-69 hypoxia inducible factor 1 subunit alpha Homo sapiens 110-141 27437226-1 2016 INTRODUCTION: Hypoxia-Inducible Factor 1alpha (HIF-1alpha) is one of the major adaptive responses to hypoxia, regulating the activity of glucose transporter -1 (GLUT-1), responsible for glucose uptake. Glucose 137-144 hypoxia inducible factor 1 subunit alpha Homo sapiens 14-45 27437226-1 2016 INTRODUCTION: Hypoxia-Inducible Factor 1alpha (HIF-1alpha) is one of the major adaptive responses to hypoxia, regulating the activity of glucose transporter -1 (GLUT-1), responsible for glucose uptake. Glucose 137-144 hypoxia inducible factor 1 subunit alpha Homo sapiens 47-57 26372812-8 2015 The nanoparticles inhibited the isoprenoid synthesis and the Ras/ERK1/2-driven activation of HIF-1alpha, decreased the transcription and activity of glycolytic enzymes, the glucose flux through the glycolysis and tricarboxylic acid cycle, the electron flux through the mitochondrial respiratory chain, the synthesis of ATP. Glucose 173-180 hypoxia inducible factor 1 subunit alpha Homo sapiens 93-103 26859576-3 2016 These phenotypic properties include activation of genes regulating glycolysis, glucose transport, acidosis regulators, angiogenesis, all of which are orchestrated through the activation of the transcription factor, HIF1A, which is an independent marker of poor prognosis. Glucose 79-86 hypoxia inducible factor 1 subunit alpha Homo sapiens 215-220 26743088-0 2016 Regulation of glucose metabolism by p62/SQSTM1 through HIF1alpha. Glucose 14-21 hypoxia inducible factor 1 subunit alpha Homo sapiens 55-64 26743088-8 2016 Functionally, HIF1alpha expression is required for p62-induced glucose uptake, lactate production and soft agar colony growth. Glucose 63-70 hypoxia inducible factor 1 subunit alpha Homo sapiens 14-23 26449597-4 2015 The key regulatory component, hypoxia-inducible factor (HIF)-1alpha (HIF-1alpha) was stabilized at 5 h in 5 % oxygen for all three studied regimens, i.e. in glycolytic cells at 5 mM or 25 mM glucose, or in aglycemic (OXPHOS) cells when glucose was replaced by galactose. Glucose 191-198 hypoxia inducible factor 1 subunit alpha Homo sapiens 30-67 26449597-4 2015 The key regulatory component, hypoxia-inducible factor (HIF)-1alpha (HIF-1alpha) was stabilized at 5 h in 5 % oxygen for all three studied regimens, i.e. in glycolytic cells at 5 mM or 25 mM glucose, or in aglycemic (OXPHOS) cells when glucose was replaced by galactose. Glucose 191-198 hypoxia inducible factor 1 subunit alpha Homo sapiens 69-79 26449597-4 2015 The key regulatory component, hypoxia-inducible factor (HIF)-1alpha (HIF-1alpha) was stabilized at 5 h in 5 % oxygen for all three studied regimens, i.e. in glycolytic cells at 5 mM or 25 mM glucose, or in aglycemic (OXPHOS) cells when glucose was replaced by galactose. Glucose 236-243 hypoxia inducible factor 1 subunit alpha Homo sapiens 30-67 26449597-4 2015 The key regulatory component, hypoxia-inducible factor (HIF)-1alpha (HIF-1alpha) was stabilized at 5 h in 5 % oxygen for all three studied regimens, i.e. in glycolytic cells at 5 mM or 25 mM glucose, or in aglycemic (OXPHOS) cells when glucose was replaced by galactose. Glucose 236-243 hypoxia inducible factor 1 subunit alpha Homo sapiens 69-79 26187851-8 2015 Moreover, TRPC6 regulated GLUT1 (also known as SLC2A1) expression in a manner that was dependent on HIF-1alpha accumulation to affect glucose uptake during hypoxia. Glucose 134-141 hypoxia inducible factor 1 subunit alpha Homo sapiens 100-110 26347605-6 2015 TPA-induced mTOR activation in neurons leads to hypoxia-inducible factor 1alpha (HIF-1alpha) accumulation, HIF-1alpha-induced expression and membrane recruitment of the neuronal transporter of glucose GLUT3, and GLUT3-mediated uptake of glucose. Glucose 193-200 hypoxia inducible factor 1 subunit alpha Homo sapiens 107-117 26320552-16 2015 As a consequence, cells switch from aerobic to anaerobic glucose metabolism, which can be prevented by HIF1alpha inhibitor BAY87-2243, Dasatinib, Erlotinib or EGFR siRNA. Glucose 57-64 hypoxia inducible factor 1 subunit alpha Homo sapiens 103-112 26347605-6 2015 TPA-induced mTOR activation in neurons leads to hypoxia-inducible factor 1alpha (HIF-1alpha) accumulation, HIF-1alpha-induced expression and membrane recruitment of the neuronal transporter of glucose GLUT3, and GLUT3-mediated uptake of glucose. Glucose 237-244 hypoxia inducible factor 1 subunit alpha Homo sapiens 107-117 25586174-11 2015 Low and high glucose levels increased (i) ROS generation via NADPH oxidase 4 and mitochondrial membrane destabilization; (ii) HIF-1 activity; (iii) nuclear translocation of the NF-kappaB p65 subunit; and (iv) HIF-1alpha mRNA and protein levels. Glucose 13-20 hypoxia inducible factor 1 subunit alpha Homo sapiens 126-131 26349963-0 2015 Study on the mechanism of HIF1a-SOX9 in glucose-induced cardiomyocyte hypertrophy. Glucose 40-47 hypoxia inducible factor 1 subunit alpha Homo sapiens 26-31 26349963-12 2015 Additionally, the results showed that high glucose (HG, 25mM) treatment increased the expression of hypoxia-inducible factor (HIF)1a. Glucose 43-50 hypoxia inducible factor 1 subunit alpha Homo sapiens 100-132 26349963-14 2015 This study revealed a novel regulatory mechanism of HIF1a-SOX9 in high glucose-induced cardiomyocyte hypertrophy, as well as the related molecular mechanisms. Glucose 71-78 hypoxia inducible factor 1 subunit alpha Homo sapiens 52-57 25877955-11 2015 The co-localization of HIF-1alpha and SUMO was mainly in the nucleus induced by high glucose. Glucose 85-92 hypoxia inducible factor 1 subunit alpha Homo sapiens 23-33 28162281-6 2015 Because of the close relationship between hypoxia, metabolism, mitochondrial function and pluripotency we have analyzed by q RT-PCR the expression of genes involved in the glucose metabolism such as: HK2, LDHA and PDK1; besides other HIF-1alpha target gene. Glucose 172-179 hypoxia inducible factor 1 subunit alpha Homo sapiens 234-244 26021979-0 2015 High glucose and/or high insulin affects HIF-1 signaling by regulating AIP1 in human umbilical vein endothelial cells. Glucose 5-12 hypoxia inducible factor 1 subunit alpha Homo sapiens 41-46 26021979-2 2015 METHODS: We investigated the expression of AIP1 and HIF-1alpha signaling in HUVECs at the levels of mRNA and protein following exposure to 30 mmol/L glucose (high glucose), 1 nmol/L insulin (high insulin), and the combination of the two (high glucose/high insulin). Glucose 149-156 hypoxia inducible factor 1 subunit alpha Homo sapiens 52-62 26021979-7 2015 High glucose, high insulin, and high glucose+high insulin decreased HIF-1alpha expression at the mRNA and protein levels. Glucose 5-12 hypoxia inducible factor 1 subunit alpha Homo sapiens 68-78 26021979-7 2015 High glucose, high insulin, and high glucose+high insulin decreased HIF-1alpha expression at the mRNA and protein levels. Glucose 37-44 hypoxia inducible factor 1 subunit alpha Homo sapiens 68-78 26021979-11 2015 CONCLUSIONS: High glucose increases AIP1 expression and decreases the expression of HIF-1alpha and downstream molecules. Glucose 18-25 hypoxia inducible factor 1 subunit alpha Homo sapiens 84-94 26021979-12 2015 Decreased HIF-1alpha signaling may be regulated by increased AIP1 under high glucose. Glucose 77-84 hypoxia inducible factor 1 subunit alpha Homo sapiens 10-20 25586174-11 2015 Low and high glucose levels increased (i) ROS generation via NADPH oxidase 4 and mitochondrial membrane destabilization; (ii) HIF-1 activity; (iii) nuclear translocation of the NF-kappaB p65 subunit; and (iv) HIF-1alpha mRNA and protein levels. Glucose 13-20 hypoxia inducible factor 1 subunit alpha Homo sapiens 209-219 25586174-13 2015 The HIF-1alpha target, Pgp, was up-regulated at low and high glucose levels, which led to lower cellular accumulation of Pgp substrate, rhodamine123, and greater resistance to DOX. Glucose 61-68 hypoxia inducible factor 1 subunit alpha Homo sapiens 4-14 25830305-3 2015 RNA sequencing (RNAseq) and untargeted metabolomics analyses of samples from TRACK kidneys demonstrate that HIF1alpha activates the transcription of genes that cause increased glucose uptake, glycolysis, and lactate production, as well as a decrease in the flux of pyruvate entering the tricarboxylic acid (TCA) cycle and a decrease in oxidative phosphorylation; these changes are identical to those observed in human ccRCC samples. Glucose 176-183 hypoxia inducible factor 1 subunit alpha Homo sapiens 108-117 25471482-2 2015 Herein, small molecules that inhibit HIF-1alpha protein stability by targeting mitochondrial energy production were screened using the Library of Pharmacologically Active Compounds and cell growth assay in galactose or glucose medium. Glucose 219-226 hypoxia inducible factor 1 subunit alpha Homo sapiens 37-47 25644309-6 2015 In CRC cells, glucose elevated the expression of GLUT1 and AREG as well as the activity of the hypoxia-inducible factor 1 (HIF-1) luciferase reporter promoter. Glucose 14-21 hypoxia inducible factor 1 subunit alpha Homo sapiens 95-121 25644309-6 2015 In CRC cells, glucose elevated the expression of GLUT1 and AREG as well as the activity of the hypoxia-inducible factor 1 (HIF-1) luciferase reporter promoter. Glucose 14-21 hypoxia inducible factor 1 subunit alpha Homo sapiens 123-128 25888489-2 2015 METHODS: Hypoxia inducible factor-1 alpha (HIF-1alpha) protein accumulation in pancreatic cell lines treated with SB202190 alone and in combination with glucose analogs was analyzed by Western blot. Glucose 153-160 hypoxia inducible factor 1 subunit alpha Homo sapiens 9-41 25888489-2 2015 METHODS: Hypoxia inducible factor-1 alpha (HIF-1alpha) protein accumulation in pancreatic cell lines treated with SB202190 alone and in combination with glucose analogs was analyzed by Western blot. Glucose 153-160 hypoxia inducible factor 1 subunit alpha Homo sapiens 43-53 25888489-3 2015 HIF-1alpha transcriptional activity was measured in MIA PaCa-2 cells stably transfected with a hypoxia response element luciferase reporter following treatment with glucose analogs alone, and in combination with SB202190. Glucose 165-172 hypoxia inducible factor 1 subunit alpha Homo sapiens 0-10 25656992-4 2015 Intranuclear Trx-1 enhances the DNA-binding activity of HIF-1alpha via its interaction with and reducing action on Ref-1, resulting in increased expression of glycolysis-related proteins (PDHK1, HKII, and LDHA), glucose uptake, and lactate generation under hypoxia. Glucose 212-219 hypoxia inducible factor 1 subunit alpha Homo sapiens 56-66 25630799-2 2015 Hypoxia-inducible factor-1 alpha (HIF-1alpha) and pyruvate dehydrogenase kinase 4 (PDK4) regulate aerobic glycolysis, while pyruvate dehydrogenase phosphatase 2 (PDP2) promotes glucose oxidation. Glucose 177-184 hypoxia inducible factor 1 subunit alpha Homo sapiens 0-32 25630799-2 2015 Hypoxia-inducible factor-1 alpha (HIF-1alpha) and pyruvate dehydrogenase kinase 4 (PDK4) regulate aerobic glycolysis, while pyruvate dehydrogenase phosphatase 2 (PDP2) promotes glucose oxidation. Glucose 177-184 hypoxia inducible factor 1 subunit alpha Homo sapiens 34-44 25630799-17 2015 PDK4 regulates glucose metabolism, in part, via regulation of HIF-1alpha. Glucose 15-22 hypoxia inducible factor 1 subunit alpha Homo sapiens 62-72 25732824-7 2015 The accumulation of HIF-1alpha, in turn, promotes glycolysis by increasing the uptake of glucose, upregulating expression of glycolytic enzymes under normoxic conditions, and inhibiting oxidative phosphorylation by upregulating NDUFA4L2. Glucose 89-96 hypoxia inducible factor 1 subunit alpha Homo sapiens 20-30 24727894-9 2015 Therefore, introducing delta-catenin mutations is an important milestone in prostate cancer metabolic adaptation by modulating beta-catenin and HIF-1alpha signaling under glucose shortage to amplify its tumor-promoting potential. Glucose 171-178 hypoxia inducible factor 1 subunit alpha Homo sapiens 144-154 25327972-4 2015 First, we performed two different hypoxia-like procedures in hCMEC/D3 cells; namely, exposition of cells to 150 muM deferoxamine or to glucose and oxygen deprivation for 6 h. These two procedures led to hypoxia-inducible factor (HIF)-1alpha and HIF-2alpha proteins accumulation together with a significant induction of the two well-known hypoxia-inducible genes VEGF and GLUT-1. Glucose 135-142 hypoxia inducible factor 1 subunit alpha Homo sapiens 203-240 25502934-6 2015 HIF1alpha expression was positively correlated with the glucose concentration in FTC-133 cells, whereas this expression was inversely correlated in 8305c cells. Glucose 56-63 hypoxia inducible factor 1 subunit alpha Homo sapiens 0-9 25502934-11 2015 Glucose concentration inversely affected HIF1alpha expression and the level of GLUT1 in membrane as well as glucose uptake in FTC-133 and 8305c cells. Glucose 0-7 hypoxia inducible factor 1 subunit alpha Homo sapiens 41-50 27125138-9 2015 Similarly, qPCR analysis of HIF1alpha and GAPDH genes showed very high expression of HIF1alpha at 5.5mM glucose concentration which reduced with increased glucose concentration. Glucose 104-111 hypoxia inducible factor 1 subunit alpha Homo sapiens 28-37 25657648-6 2015 Here, we review how different aspects of metabolism in T cells influence their functions, focusing on the emerging role of key regulators of glucose metabolism such as HIF-1alpha. Glucose 141-148 hypoxia inducible factor 1 subunit alpha Homo sapiens 168-178 25535360-4 2015 In diabetes, HIF-1alpha function is compromised by a high glucose-induced and reactive oxygen species-mediated modification of its coactivator p300, leading to impaired HIF-1alpha transactivation. Glucose 58-65 hypoxia inducible factor 1 subunit alpha Homo sapiens 13-23 25833522-0 2015 The Changes by Hypoxia Inducible Factor-1alpha (HIF-1alpha) on Taurine Uptake in Brain Capillary Endothelial Cells at High Glucose Conditions. Glucose 123-130 hypoxia inducible factor 1 subunit alpha Homo sapiens 15-46 25833522-0 2015 The Changes by Hypoxia Inducible Factor-1alpha (HIF-1alpha) on Taurine Uptake in Brain Capillary Endothelial Cells at High Glucose Conditions. Glucose 123-130 hypoxia inducible factor 1 subunit alpha Homo sapiens 48-58 27125138-9 2015 Similarly, qPCR analysis of HIF1alpha and GAPDH genes showed very high expression of HIF1alpha at 5.5mM glucose concentration which reduced with increased glucose concentration. Glucose 104-111 hypoxia inducible factor 1 subunit alpha Homo sapiens 85-94 27125138-9 2015 Similarly, qPCR analysis of HIF1alpha and GAPDH genes showed very high expression of HIF1alpha at 5.5mM glucose concentration which reduced with increased glucose concentration. Glucose 155-162 hypoxia inducible factor 1 subunit alpha Homo sapiens 28-37 27125138-9 2015 Similarly, qPCR analysis of HIF1alpha and GAPDH genes showed very high expression of HIF1alpha at 5.5mM glucose concentration which reduced with increased glucose concentration. Glucose 155-162 hypoxia inducible factor 1 subunit alpha Homo sapiens 85-94 27125138-11 2015 Thus, these results indicate high HIF1alpha expression in low glucose condition with improved anaerobic glycolysis seems to be one of the key factors in maintaining the quiescent state of CD34+ stem cells. Glucose 62-69 hypoxia inducible factor 1 subunit alpha Homo sapiens 34-43 24997364-4 2014 In cultured cells, melanogenesis also significantly stimulated expression of classical HIF-1-dependent target genes involved in angiogenesis and cellular metabolism, including glucose metabolism and stimulation of activity of key enzymes in the glycolytic pathway. Glucose 176-183 hypoxia inducible factor 1 subunit alpha Homo sapiens 87-92 25801056-10 2015 The knockdown of HIF-1alpha or DEC1 with shRNA construct abrogated the decrease of the CES1 and CES2 expression induced by the insulin in high glucose condition in HepG2 cells. Glucose 143-150 hypoxia inducible factor 1 subunit alpha Homo sapiens 17-27 25336691-9 2014 PDAC cells with enhanced HIF1alpha activity were resistant to lumican-induced inhibition of glucose consumption, lactate production, intracellular ATP, and apoptosis. Glucose 92-99 hypoxia inducible factor 1 subunit alpha Homo sapiens 25-34 25280834-0 2014 Signaling mechanism of protease activated receptor 1-induced proliferation of astrocytes: stabilization of hypoxia inducible factor-1alpha triggers glucose metabolism and accumulation of cyclin D1. Glucose 148-155 hypoxia inducible factor 1 subunit alpha Homo sapiens 107-138 25063250-11 2014 In response to hypoxia stress and oxidative damage in ICP, the placenta activates HIF-1alpha and REDD1, which in turn may up-regulates glucose transport and anaerobic glycolysis. Glucose 135-142 hypoxia inducible factor 1 subunit alpha Homo sapiens 82-92 25222223-2 2014 A high concentration of glucose (HG) was utilized to treat HeLa cells under hypoxic or normoxic conditions, and transcriptional levels of HIF-1, VEGF, and basic fibroblast growth factor (bFGF) were evaluated. Glucose 24-31 hypoxia inducible factor 1 subunit alpha Homo sapiens 138-143 25063250-12 2014 CONCLUSIONS: HIF-1alpha, REDD1 and mTOR may play a significant role in the reaction to hypoxia and oxidative stress and regulate glucose metabolism in the placenta of ICP patients. Glucose 129-136 hypoxia inducible factor 1 subunit alpha Homo sapiens 13-23 24477458-8 2014 Moreover, downregulation of p65/RelA or HIF-1alpha expression in these cells restored normal glucose uptake, lactate production, mitochondrial respiration and glycolytic protein expression. Glucose 93-100 hypoxia inducible factor 1 subunit alpha Homo sapiens 40-50 27774472-5 2014 The HIF1alpha isoform in particular has a strong impact on cellular metabolism, most notably by promoting anaerobic, whilst inhibiting O2-dependent, metabolism of glucose. Glucose 163-170 hypoxia inducible factor 1 subunit alpha Homo sapiens 4-13 24477458-6 2014 TG2/NF-kappaB-induced increase in HIF-1alpha expression was associated with increased glucose uptake, increased lactate production and decreased oxygen consumption by mitochondria. Glucose 86-93 hypoxia inducible factor 1 subunit alpha Homo sapiens 34-44 24658058-6 2014 Moreover, the glucose analog 2-DG and the Hsp90 inhibitor 17-AAG, which destabilizes the HIF-1alpha protein, synergized with IMQ to induce tumor cell apoptosis in vitro and significantly inhibited tumor growth in vivo. Glucose 14-21 hypoxia inducible factor 1 subunit alpha Homo sapiens 89-99 24906151-5 2014 Genetic or pharmacologic inhibition of either ANT2 or HIF-1alpha can prevent or reverse these pathophysiologic events, restoring a state of insulin sensitivity and glucose tolerance. Glucose 164-171 hypoxia inducible factor 1 subunit alpha Homo sapiens 54-64 24584933-0 2014 Steroid receptor coactivator-3 regulates glucose metabolism in bladder cancer cells through coactivation of hypoxia inducible factor 1alpha. Glucose 41-48 hypoxia inducible factor 1 subunit alpha Homo sapiens 108-139 24556689-12 2014 In low glucose, HIF1alpha upregulated expression of sox9 and scleraxis, two critical transcription factors involved in establishing the tenocyte phenotype, and increased collagen synthesis. Glucose 7-14 hypoxia inducible factor 1 subunit alpha Homo sapiens 16-25 24556689-13 2014 The switch from FOXO1-mediated (proapoptosis) to HIF1alpha-mediated (prodifferentiation) transcription occurred at an extracellular glucose concentration of 7 mM, a concentration equivalent to the maximum normal blood glucose concentration. Glucose 132-139 hypoxia inducible factor 1 subunit alpha Homo sapiens 49-58 24556689-13 2014 The switch from FOXO1-mediated (proapoptosis) to HIF1alpha-mediated (prodifferentiation) transcription occurred at an extracellular glucose concentration of 7 mM, a concentration equivalent to the maximum normal blood glucose concentration. Glucose 218-225 hypoxia inducible factor 1 subunit alpha Homo sapiens 49-58 24485121-4 2014 HIF-1alpha is a key regulator of the cellular response to hypoxia and is involved in tumor angiogenesis and cancer cell survival, glucose metabolism, and invasion. Glucose 130-137 hypoxia inducible factor 1 subunit alpha Homo sapiens 0-10 24664750-0 2014 High glucose activates ChREBP-mediated HIF-1alpha and VEGF expression in human RPE cells under normoxia. Glucose 5-12 hypoxia inducible factor 1 subunit alpha Homo sapiens 39-49 24344305-0 2014 JMJD5 regulates PKM2 nuclear translocation and reprograms HIF-1alpha-mediated glucose metabolism. Glucose 78-85 hypoxia inducible factor 1 subunit alpha Homo sapiens 58-68 24664750-2 2014 We aimed to determine if a carbohydrate response element binding protein (ChREBP) plays a role in the transcriptional up-regulation of hypoxia-inducible factor-1alpha (HIF-1alpha) and the downstream VEGF expression in retinal pigment epithelial (RPE) cells exposed to high glucose under normoxic conditions. Glucose 273-280 hypoxia inducible factor 1 subunit alpha Homo sapiens 135-166 24561986-0 2014 The effect of HIF-1alpha on glucose metabolism, growth and apoptosis of pancreatic cancerous cells. Glucose 28-35 hypoxia inducible factor 1 subunit alpha Homo sapiens 14-24 24664750-2 2014 We aimed to determine if a carbohydrate response element binding protein (ChREBP) plays a role in the transcriptional up-regulation of hypoxia-inducible factor-1alpha (HIF-1alpha) and the downstream VEGF expression in retinal pigment epithelial (RPE) cells exposed to high glucose under normoxic conditions. Glucose 273-280 hypoxia inducible factor 1 subunit alpha Homo sapiens 168-178 24664750-7 2014 RESULTS: Immunoblot analyses showed that HIF-1alpha levels were positively related to levels of glucose exposure between 5.6-25 mM in the RPE cells, indicating the induction and stabilization of HIF-1alpha by elevated glucose under normoxic conditions. Glucose 96-103 hypoxia inducible factor 1 subunit alpha Homo sapiens 41-51 24664750-7 2014 RESULTS: Immunoblot analyses showed that HIF-1alpha levels were positively related to levels of glucose exposure between 5.6-25 mM in the RPE cells, indicating the induction and stabilization of HIF-1alpha by elevated glucose under normoxic conditions. Glucose 96-103 hypoxia inducible factor 1 subunit alpha Homo sapiens 195-205 24664750-7 2014 RESULTS: Immunoblot analyses showed that HIF-1alpha levels were positively related to levels of glucose exposure between 5.6-25 mM in the RPE cells, indicating the induction and stabilization of HIF-1alpha by elevated glucose under normoxic conditions. Glucose 218-225 hypoxia inducible factor 1 subunit alpha Homo sapiens 41-51 24664750-7 2014 RESULTS: Immunoblot analyses showed that HIF-1alpha levels were positively related to levels of glucose exposure between 5.6-25 mM in the RPE cells, indicating the induction and stabilization of HIF-1alpha by elevated glucose under normoxic conditions. Glucose 218-225 hypoxia inducible factor 1 subunit alpha Homo sapiens 195-205 24664750-9 2014 Real-time RT-PCR for HIF-1alpha and VEGF and ELISA for VEGF indicated that high glucose is associated with elevated production of HIF-1alpha-induced VEGF, an established inducer of neovascularization, in the RPE cells. Glucose 80-87 hypoxia inducible factor 1 subunit alpha Homo sapiens 21-31 24664750-9 2014 Real-time RT-PCR for HIF-1alpha and VEGF and ELISA for VEGF indicated that high glucose is associated with elevated production of HIF-1alpha-induced VEGF, an established inducer of neovascularization, in the RPE cells. Glucose 80-87 hypoxia inducible factor 1 subunit alpha Homo sapiens 130-140 24664750-11 2014 ChIP analyses suggested a HIF-1alpha gene promoter association with ChREBP under the high glucose condition. Glucose 90-97 hypoxia inducible factor 1 subunit alpha Homo sapiens 26-36 24664750-12 2014 These results imply that RPE cells use cytosolic ChREBP as a glucose sensor to up-regulate HIF-1alpha expression. Glucose 61-68 hypoxia inducible factor 1 subunit alpha Homo sapiens 91-101 24664750-13 2014 CONCLUSION: These results suggest a high glucose-induced, ChREBP-mediated, and normoxic HIF-1alpha activation that may be partially responsible for neovascularization in both diabetic and age-related retinopathy. Glucose 41-48 hypoxia inducible factor 1 subunit alpha Homo sapiens 88-98 23988176-4 2014 HIF-1 controls oxygen delivery, by regulating angiogenesis and vascular remodeling, and oxygen utilization, by regulating glucose metabolism and redox homeostasis. Glucose 122-129 hypoxia inducible factor 1 subunit alpha Homo sapiens 0-5 24862279-4 2014 The uptake of glucose and the glycolytic flux are increased under hypoxic conditions, mostly owing to the upregulation of genes encoding glucose transporters and glycolytic enzymes, a process that depends on hypoxia-inducible factor 1 (HIF-1). Glucose 14-21 hypoxia inducible factor 1 subunit alpha Homo sapiens 208-234 24862279-4 2014 The uptake of glucose and the glycolytic flux are increased under hypoxic conditions, mostly owing to the upregulation of genes encoding glucose transporters and glycolytic enzymes, a process that depends on hypoxia-inducible factor 1 (HIF-1). Glucose 14-21 hypoxia inducible factor 1 subunit alpha Homo sapiens 236-241 24862279-6 2014 In addition, hypoxia induces (1) the HIF-1-dependent expression of BCL2/adenovirus E1B 19-kDa interacting protein 3 (BNIP3) and BNIP3-like (BNIP3L), which trigger mitochondrial autophagy, thereby decreasing the oxidative metabolism of both fatty acids and glucose, and (2) the expression of the sodium-hydrogen exchanger NHE1, which maintains an alkaline intracellular pH. Glucose 256-263 hypoxia inducible factor 1 subunit alpha Homo sapiens 37-42 25006572-1 2013 The hypoxia inducible factor 1 (HIF-1) is a central transcription factor involved in the cellular and molecular adaptation to hypoxia and low glucose supply. Glucose 142-149 hypoxia inducible factor 1 subunit alpha Homo sapiens 4-30 25006572-1 2013 The hypoxia inducible factor 1 (HIF-1) is a central transcription factor involved in the cellular and molecular adaptation to hypoxia and low glucose supply. Glucose 142-149 hypoxia inducible factor 1 subunit alpha Homo sapiens 32-37 24018047-10 2013 Over-expression of a common miRNA (miR-106a) significantly reduced the expression of HIF1alpha and VEGF and prevented high glucose-induced increased permeability. Glucose 123-130 hypoxia inducible factor 1 subunit alpha Homo sapiens 85-94 23872577-10 2013 We also noticed that the oxidative-stress pathway was activated in response to high glucose driven by Hif-1alpha. Glucose 84-91 hypoxia inducible factor 1 subunit alpha Homo sapiens 102-112 23661628-7 2013 Thus, the uptake of glucose and glutamine and utilization of the carbon sources derived from them, coordinated by HIF1alpha and c-Myc, are essential for osteoclast development and bone-resorbing activity through a balanced regulation of the nutrient and energy sensors, mTOR and AMPK. Glucose 20-27 hypoxia inducible factor 1 subunit alpha Homo sapiens 114-123 24221993-0 2013 Resveratrol suppresses cancer cell glucose uptake by targeting reactive oxygen species-mediated hypoxia-inducible factor-1alpha activation. Glucose 35-42 hypoxia inducible factor 1 subunit alpha Homo sapiens 96-127 23857671-6 2013 Furthermore, knockdown of HIF-1 blocked CX3CL1-modified glucose metabolism in pancreatic adenocarcinoma cells. Glucose 56-63 hypoxia inducible factor 1 subunit alpha Homo sapiens 26-31 23857671-7 2013 In conclusion, the CX3CL1/CX3CR1 reprograms glucose metabolism through HIF-1 pathway in pancreatic cancer cells. Glucose 44-51 hypoxia inducible factor 1 subunit alpha Homo sapiens 71-76 23377827-0 2013 Excess glucose induces hypoxia-inducible factor-1alpha in pancreatic cancer cells and stimulates glucose metabolism and cell migration. Glucose 7-14 hypoxia inducible factor 1 subunit alpha Homo sapiens 23-54 23983604-3 2013 In fact, HIF-1alpha and glucose can sometimes influence each other: HIF-1alpha induces the expression of glycolytic enzymes and glucose metabolism affects HIF-1alpha accumulation in some cells. Glucose 24-31 hypoxia inducible factor 1 subunit alpha Homo sapiens 68-78 23983604-3 2013 In fact, HIF-1alpha and glucose can sometimes influence each other: HIF-1alpha induces the expression of glycolytic enzymes and glucose metabolism affects HIF-1alpha accumulation in some cells. Glucose 24-31 hypoxia inducible factor 1 subunit alpha Homo sapiens 68-78 23983604-3 2013 In fact, HIF-1alpha and glucose can sometimes influence each other: HIF-1alpha induces the expression of glycolytic enzymes and glucose metabolism affects HIF-1alpha accumulation in some cells. Glucose 128-135 hypoxia inducible factor 1 subunit alpha Homo sapiens 9-19 23983604-4 2013 Although hyperglycemia upregulates HIF-1alpha signaling in some specific cell types, we emphasize the inhibition of HIF-1alpha by high glucose in this review. Glucose 135-142 hypoxia inducible factor 1 subunit alpha Homo sapiens 116-126 23983604-6 2013 Other explanations for the inhibition of HIF-1alpha by high glucose exist: the increased sensitivity of HIF-1alpha to Von Hippel-Lindau (VHL) machinery, the role of osmolarity and proteasome activity, and the participation of several molecules. Glucose 60-67 hypoxia inducible factor 1 subunit alpha Homo sapiens 41-51 23786679-6 2013 Molecular analysis indicated that hypoxia upregulated glut1 and 6-phosphofructo-2-kinase, key proteins involved in regulating glucose transport and glycolysis, and that these changes were induced by Hypoxia-Inducible factor 1 (HIF1) upregulation and/or AMP-activated protein kinase activation. Glucose 126-133 hypoxia inducible factor 1 subunit alpha Homo sapiens 199-225 23640464-10 2013 Hypoxic cells given glucose showed nuclear translocation of HIF1alpha associated with upregulation of GLUT-1 and GLUT-4 expression, as well as increase of intracellular ATP, pyruvate and lactate levels. Glucose 20-27 hypoxia inducible factor 1 subunit alpha Homo sapiens 60-69 23857671-0 2013 The CX3CL1/CX3CR1 reprograms glucose metabolism through HIF-1 pathway in pancreatic adenocarcinoma. Glucose 29-36 hypoxia inducible factor 1 subunit alpha Homo sapiens 56-61 23911867-9 2013 On the other hand, inhibition of ROS not only attenuated high-glucose-mediated T-cell expression of CXCR4 and HIF-1alpha but also mitigated T-cell HIV entry in a high-glucose milieu. Glucose 62-69 hypoxia inducible factor 1 subunit alpha Homo sapiens 110-120 23911867-10 2013 In our study, high glucose enhanced HIV entry into T cells by increasing expression of CXCR4 and HIF-1alpha. Glucose 19-26 hypoxia inducible factor 1 subunit alpha Homo sapiens 97-107 24116346-9 2013 (18)F-FDG-uptake (SUVmax) is correlated with HIF-1alpha gene expression indicating an association between hypoxia and glucose metabolism in vivo. Glucose 118-125 hypoxia inducible factor 1 subunit alpha Homo sapiens 45-55 23222085-2 2013 The rs11549465 C > T polymorphism in the HIF1A gene, which produces the amino acid substitution Pro582Ser, increases protein stability and transcriptional activity and, therefore, improves glucose metabolism. Glucose 192-199 hypoxia inducible factor 1 subunit alpha Homo sapiens 44-49 23562913-0 2013 Role of HIF1alpha and PKCbeta in mediating the effect of oxygen and glucose in a novel wound assay. Glucose 68-75 hypoxia inducible factor 1 subunit alpha Homo sapiens 8-17 23562913-13 2013 Impaired cell migration mediated by high glucose concentration was restored using an inhibitor of the PKCbetaII pathway which correlated with an increase in the level of HIF1alpha protein. Glucose 41-48 hypoxia inducible factor 1 subunit alpha Homo sapiens 170-179 23377827-2 2013 We have investigated whether excess glucose induces hypoxia-inducible factor-1alpha (HIF-1alpha) and stimulates glucose metabolism and cell migration in pancreatic cancer cells. Glucose 36-43 hypoxia inducible factor 1 subunit alpha Homo sapiens 52-83 23377827-2 2013 We have investigated whether excess glucose induces hypoxia-inducible factor-1alpha (HIF-1alpha) and stimulates glucose metabolism and cell migration in pancreatic cancer cells. Glucose 36-43 hypoxia inducible factor 1 subunit alpha Homo sapiens 85-95 23377827-8 2013 Excess glucose (16.7-22.2mM) increased HIF-1alpha in hypoxic wt-MiaPaCa2 cells. Glucose 7-14 hypoxia inducible factor 1 subunit alpha Homo sapiens 39-49 23377827-14 2013 We conclude that (1) excess glucose increases HIF-1alpha and ATP in hypoxic wt-MiaPaCa2 cells, (2) extracellular glucose and hypoxia regulate glucose metabolisms independent of HIF-1alpha and (3) glucose stimulates cell migration by mechanisms that are both dependent on HIF-1alpha and independent of it. Glucose 28-35 hypoxia inducible factor 1 subunit alpha Homo sapiens 46-56 22961911-2 2013 As a key transcriptional regulator, HIF-1 plays a central role in the adaptation of tumor cells to hypoxia by activating the transcription of targeting genes, which regulate several biological processes including angiogenesis, cell proliferation, survival, glucose metabolism and migration. Glucose 257-264 hypoxia inducible factor 1 subunit alpha Homo sapiens 36-41 22710721-5 2013 Experiments in vitro demonstrated that a decrease in the glucose concentration reduced the transcriptional activity of HIF-1 and expression of a downstream gene for the cell cycle regulator p27(Kip1) even under hypoxic conditions. Glucose 57-64 hypoxia inducible factor 1 subunit alpha Homo sapiens 119-124 23514176-7 2013 mTORC1 regulates glucose metabolism in CTLs through regulating the expression of the transcription factor HIF1alpha (hypoxia-inducible factor 1alpha). Glucose 17-24 hypoxia inducible factor 1 subunit alpha Homo sapiens 106-115 23514176-7 2013 mTORC1 regulates glucose metabolism in CTLs through regulating the expression of the transcription factor HIF1alpha (hypoxia-inducible factor 1alpha). Glucose 17-24 hypoxia inducible factor 1 subunit alpha Homo sapiens 117-148 23514176-8 2013 Strikingly, HIF1alpha functions to couple mTORC1 with a diverse transcriptional programme that extends beyond the control of glucose metabolism to the regulation of multiple key T-cell functions. Glucose 125-132 hypoxia inducible factor 1 subunit alpha Homo sapiens 12-21 23297826-2 2013 The number of HIF-1 and hypoxia-regulated target genes has grown exponentially and includes genes that encode proteins with roles in erythropoiesis, angiogenesis, glycolytic pathway, glucose transport, metastasis, and cell survival. Glucose 183-190 hypoxia inducible factor 1 subunit alpha Homo sapiens 14-19 22750268-3 2012 In the present work, we focused on reviewing the current knowledge about the dysregulation of the proteins/enzymes involved in the key regulatory steps of glucose transport, glycolysis, TCA cycle and glutaminolysis by several oncogenes including c-Myc and hypoxia inducible factor-1 (HIF-1) and tumor suppressor, p53, in cancer cells. Glucose 155-162 hypoxia inducible factor 1 subunit alpha Homo sapiens 256-282 23225732-4 2013 In this in vitro cell model, the protein expressions of Hif-1alpha and angiogenic factors were upregulated by the presence of glucose. Glucose 126-133 hypoxia inducible factor 1 subunit alpha Homo sapiens 56-66 23015148-3 2013 Other investigators reported that HIF-1 promotes cellular glucose uptake by increased expression of GLUT1 and increased glycolysis by increased expression of enzymes such as PDK. Glucose 58-65 hypoxia inducible factor 1 subunit alpha Homo sapiens 34-39 23333395-5 2013 The effects of hypoxia on HIF-1alpha and IL-1beta were potentiated by 5.5 mM glucose, especially after 48 h (p<0.05). Glucose 77-84 hypoxia inducible factor 1 subunit alpha Homo sapiens 26-36 22750268-3 2012 In the present work, we focused on reviewing the current knowledge about the dysregulation of the proteins/enzymes involved in the key regulatory steps of glucose transport, glycolysis, TCA cycle and glutaminolysis by several oncogenes including c-Myc and hypoxia inducible factor-1 (HIF-1) and tumor suppressor, p53, in cancer cells. Glucose 155-162 hypoxia inducible factor 1 subunit alpha Homo sapiens 284-289 21945317-3 2011 The metabolite analysis revealed the contents of glucose, glycine, betaine, phosphocholine, pyruvate and lactate involved in the hypoxia-inducible factor (HIF)-1-dependent glycolytic pathway were significantly lower in cells treated with siARNT2. Glucose 49-56 hypoxia inducible factor 1 subunit alpha Homo sapiens 129-161 22065316-8 2012 Moreover, to promote the upregulation of glucose uptake, the expressions of HIF1alpha and PCNA were induced to 2.6 and 3.3 times higher than that in the normal mucosa. Glucose 41-48 hypoxia inducible factor 1 subunit alpha Homo sapiens 76-85 21970364-2 2012 It has been well elucidated that HIF-1 (hypoxia-inducible factor-1) plays a central role in regulating glucose metabolism under hypoxia; however, the role of HIF-1 in lipid metabolism has not yet been well addressed. Glucose 103-110 hypoxia inducible factor 1 subunit alpha Homo sapiens 33-38 21970364-2 2012 It has been well elucidated that HIF-1 (hypoxia-inducible factor-1) plays a central role in regulating glucose metabolism under hypoxia; however, the role of HIF-1 in lipid metabolism has not yet been well addressed. Glucose 103-110 hypoxia inducible factor 1 subunit alpha Homo sapiens 40-66 21617913-0 2012 HIF-1 is involved in high glucose-induced paracellular permeability of brain endothelial cells. Glucose 26-33 hypoxia inducible factor 1 subunit alpha Homo sapiens 0-5 21617913-3 2012 Here we investigated the role of hypoxia-inducible factor-1 (HIF-1) in high glucose-induced endothelial permeability in vitro using mouse brain microvascular endothelial cells (b.End3). Glucose 76-83 hypoxia inducible factor 1 subunit alpha Homo sapiens 61-66 21617913-4 2012 Our results demonstrated that high glucose (30 mM) upregulated the protein level of HIF-1alpha, the regulatable subunit of HIF-1, and increased the transcriptional activity of HIF-1 in the endothelial cells. Glucose 35-42 hypoxia inducible factor 1 subunit alpha Homo sapiens 84-94 21617913-4 2012 Our results demonstrated that high glucose (30 mM) upregulated the protein level of HIF-1alpha, the regulatable subunit of HIF-1, and increased the transcriptional activity of HIF-1 in the endothelial cells. Glucose 35-42 hypoxia inducible factor 1 subunit alpha Homo sapiens 84-89 21617913-4 2012 Our results demonstrated that high glucose (30 mM) upregulated the protein level of HIF-1alpha, the regulatable subunit of HIF-1, and increased the transcriptional activity of HIF-1 in the endothelial cells. Glucose 35-42 hypoxia inducible factor 1 subunit alpha Homo sapiens 123-128 21617913-6 2012 Upregulating HIF-1 activity by cobalt chloride increased the paracellular permeability of the endothelial cells exposed to normal glucose (5.5 mM). Glucose 130-137 hypoxia inducible factor 1 subunit alpha Homo sapiens 13-18 21617913-7 2012 In contrast, downregulating HIF-1 activity by HIF-1alpha inhibitors and HIF-1alpha specific siRNA ameliorated the increased paracellular permeability and the alterations of distribution pattern of occludin and ZO-1 induced by high glucose. Glucose 231-238 hypoxia inducible factor 1 subunit alpha Homo sapiens 28-33 21617913-7 2012 In contrast, downregulating HIF-1 activity by HIF-1alpha inhibitors and HIF-1alpha specific siRNA ameliorated the increased paracellular permeability and the alterations of distribution pattern of occludin and ZO-1 induced by high glucose. Glucose 231-238 hypoxia inducible factor 1 subunit alpha Homo sapiens 46-56 21617913-7 2012 In contrast, downregulating HIF-1 activity by HIF-1alpha inhibitors and HIF-1alpha specific siRNA ameliorated the increased paracellular permeability and the alterations of distribution pattern of occludin and ZO-1 induced by high glucose. Glucose 231-238 hypoxia inducible factor 1 subunit alpha Homo sapiens 72-82 21617913-8 2012 In addition, high glucose increased expression of vascular endothelial growth factor (VEGF), a downstream gene of HIF-1. Glucose 18-25 hypoxia inducible factor 1 subunit alpha Homo sapiens 114-119 21617913-11 2012 These results strongly indicate that HIF-1 plays an important role in high glucose-induced BBB dysfunction. Glucose 75-82 hypoxia inducible factor 1 subunit alpha Homo sapiens 37-42 21854848-1 2012 The current study was undertaken to address the role of mitochondrial reactive oxygen species (ROS), and hypoxia inducible factor-1 alpha (HIF-1alpha) signaling pathway in the protection against high glucose levels in brain endothelial and NT2 neuron-like cells. Glucose 200-207 hypoxia inducible factor 1 subunit alpha Homo sapiens 105-137 21854848-1 2012 The current study was undertaken to address the role of mitochondrial reactive oxygen species (ROS), and hypoxia inducible factor-1 alpha (HIF-1alpha) signaling pathway in the protection against high glucose levels in brain endothelial and NT2 neuron-like cells. Glucose 200-207 hypoxia inducible factor 1 subunit alpha Homo sapiens 139-149 22894905-8 2012 Similarly, activation of HIF1alpha, but not HIF2alpha, in MDA-MB-231 cells promoted a shift toward aerobic glycolysis, with increased glucose uptake and L-lactate production. Glucose 134-141 hypoxia inducible factor 1 subunit alpha Homo sapiens 25-34 22926943-2 2012 Hif1-alpha regulates angiogenesis, tumour growth, tumour progression, metastatic spread, and glucose metabolism by acting as a transcription factor for relevant genes. Glucose 93-100 hypoxia inducible factor 1 subunit alpha Homo sapiens 0-10 22815500-5 2012 We found that mTOR activation leads to accumulation of the hypoxia-inducible factor-1alpha (HIF-1alpha) and induction and recruitment to the cell membrane of the HIF-1alpha-regulated neuronal transporter of glucose GLUT3. Glucose 207-214 hypoxia inducible factor 1 subunit alpha Homo sapiens 162-172 22676927-7 2012 CONCLUSIONS: FDG uptake was significantly associated with the expression levels of glucose metabolism-related molecules, such as GLUT-1, HK II, and HIF-1alpha, especially in early-stage tumors. Glucose 83-90 hypoxia inducible factor 1 subunit alpha Homo sapiens 148-158 21614571-6 2011 Indeed, destabilisation of HIF-1 by high glucose levels has serious consequences in various organs and tissues, including myocardial collateralisation, wound healing, renal, neural and retinal function, as a result of poor cell and tissue responses to low oxygen. Glucose 41-48 hypoxia inducible factor 1 subunit alpha Homo sapiens 27-32 20813864-3 2010 Inactivation of VHL ubiquitin ligase is associated with normoxic stabilization of hypoxia-inducible factor-1alpha and 2-alpha (HIF-1alpha and HIF-2alpha), transcriptional regulators of tumor angiogenesis, invasion, survival, and glucose utilization. Glucose 229-236 hypoxia inducible factor 1 subunit alpha Homo sapiens 127-137 21709315-0 2011 Pyruvate kinase M2 regulates glucose metabolism by functioning as a coactivator for hypoxia-inducible factor 1 in cancer cells. Glucose 29-36 hypoxia inducible factor 1 subunit alpha Homo sapiens 84-110 21709315-4 2011 Hypoxia-inducible factor 1 (HIF-1) mediates PKM2 gene transcription and glucose reprogramming in cancer cells. Glucose 72-79 hypoxia inducible factor 1 subunit alpha Homo sapiens 0-26 21709315-4 2011 Hypoxia-inducible factor 1 (HIF-1) mediates PKM2 gene transcription and glucose reprogramming in cancer cells. Glucose 72-79 hypoxia inducible factor 1 subunit alpha Homo sapiens 28-33 21404119-7 2011 HIF1 regulates transcription of genes relevant for vascularization, glucose transport and glycolysis, processes that facilitate tumor growth. Glucose 68-75 hypoxia inducible factor 1 subunit alpha Homo sapiens 0-4 21338581-5 2011 It was found that neuronal damage induced by oxygen-glucose deprivation was accompanied by a significant decrease in both HIF-1alpha and HIF-3alpha mRNA levels in CA1 but not CA3 neurons. Glucose 52-59 hypoxia inducible factor 1 subunit alpha Homo sapiens 122-132 21124777-3 2010 In this study, we aimed at identifying the molecular mechanism implicated in destabilization of HIF-1 by high glucose. Glucose 110-117 hypoxia inducible factor 1 subunit alpha Homo sapiens 96-101 21124777-4 2010 In this work, we identified a new molecular mechanism whereby methylglyoxal (MGO), which accumulates in high-glucose conditions, led to a rapid proteasome-dependent degradation of HIF-1alpha under hypoxia. Glucose 109-116 hypoxia inducible factor 1 subunit alpha Homo sapiens 180-190 20711226-1 2010 Since its discovery in early 1990s, hypoxia inducible factor 1 (HIF-1) has been increasingly recognized for its key role in transcriptional control of more than a hundred genes that regulate a wide-spectrum of cellular functional events, including angiogenesis, vasomotor control, glucose and energy metabolism, erythropoiesis, iron homeostasis, pH regulation, cell proliferation and viability. Glucose 281-288 hypoxia inducible factor 1 subunit alpha Homo sapiens 36-62 20578983-2 2010 Hypoxia-inducible factor-1 (HIF-1), a key transcriptional regulator, plays a central role in the adaptation of tumor cells to hypoxia by activating the transcription of genes, which regulate several biological processes including angiogenesis, cell proliferation, survival, glucose metabolism and migration. Glucose 274-281 hypoxia inducible factor 1 subunit alpha Homo sapiens 0-26 20578983-2 2010 Hypoxia-inducible factor-1 (HIF-1), a key transcriptional regulator, plays a central role in the adaptation of tumor cells to hypoxia by activating the transcription of genes, which regulate several biological processes including angiogenesis, cell proliferation, survival, glucose metabolism and migration. Glucose 274-281 hypoxia inducible factor 1 subunit alpha Homo sapiens 28-33 20711226-1 2010 Since its discovery in early 1990s, hypoxia inducible factor 1 (HIF-1) has been increasingly recognized for its key role in transcriptional control of more than a hundred genes that regulate a wide-spectrum of cellular functional events, including angiogenesis, vasomotor control, glucose and energy metabolism, erythropoiesis, iron homeostasis, pH regulation, cell proliferation and viability. Glucose 281-288 hypoxia inducible factor 1 subunit alpha Homo sapiens 64-69 20473281-1 2010 Hypoxia-inducible factor-1alpha is found frequently overexpressed in solid tumors cells, exerting an important role in angiogenesis, glucose metabolism, cell proliferation, survival and invasion. Glucose 133-140 hypoxia inducible factor 1 subunit alpha Homo sapiens 0-31 20621833-0 2010 Glucose is necessary for stabilization of hypoxia-inducible factor-1alpha under hypoxia: contribution of the pentose phosphate pathway to this stabilization. Glucose 0-7 hypoxia inducible factor 1 subunit alpha Homo sapiens 42-73 20621833-5 2010 In conclusion, glucose metabolism through the PPP, but not in glycolysis, plays an important role in the stabilization of HIF-1alpha protein under hypoxic conditions. Glucose 15-22 hypoxia inducible factor 1 subunit alpha Homo sapiens 122-132 20621833-1 2010 In this study, we observed that low glucose or fructose reduces the increase in hypoxia-inducible factor-1alpha (HIF-1alpha) protein under hypoxic conditions. Glucose 36-43 hypoxia inducible factor 1 subunit alpha Homo sapiens 80-111 20621833-1 2010 In this study, we observed that low glucose or fructose reduces the increase in hypoxia-inducible factor-1alpha (HIF-1alpha) protein under hypoxic conditions. Glucose 36-43 hypoxia inducible factor 1 subunit alpha Homo sapiens 113-123 20621833-2 2010 6-Aminonicotinamide (6-AN), an inhibitor of the pentose phosphate pathway (PPP), also inhibited the increase of HIF-1alpha protein under hypoxic conditions, while the reduced protein levels of HIF-1alpha by low glucose were apparently recovered by the addition of MG-132 or NADPH. Glucose 211-218 hypoxia inducible factor 1 subunit alpha Homo sapiens 112-122 20621833-2 2010 6-Aminonicotinamide (6-AN), an inhibitor of the pentose phosphate pathway (PPP), also inhibited the increase of HIF-1alpha protein under hypoxic conditions, while the reduced protein levels of HIF-1alpha by low glucose were apparently recovered by the addition of MG-132 or NADPH. Glucose 211-218 hypoxia inducible factor 1 subunit alpha Homo sapiens 193-203 20368331-6 2010 We assessed the separate involvement of oxygen and glucose in HIF1alpha regulation in differentiated neuroblastoma cells subjected to ischemia. Glucose 51-58 hypoxia inducible factor 1 subunit alpha Homo sapiens 62-71 20368331-7 2010 We report higher transcriptional activity and HIF1alpha expression under oxygen deprivation in the presence of glucose (OD), than in its absence (oxygen and glucose deprivation, OGD). Glucose 111-118 hypoxia inducible factor 1 subunit alpha Homo sapiens 46-55 20228846-6 2010 HIF-1alpha induction resulted in an enhanced rate of glycolysis but with reduced glucose flux through both the tricarboxylic acid cycle and the oxidative arm of the pentose phosphate pathway (PPP). Glucose 81-88 hypoxia inducible factor 1 subunit alpha Homo sapiens 0-10 20037603-7 2010 Our data suggest a novel mechanism in pancreatic cancer cells that links beta-AR and HIF-1alpha signaling under normoxic conditions, with implications for the control of glucose transport, angiogenesis and metastasis. Glucose 170-177 hypoxia inducible factor 1 subunit alpha Homo sapiens 85-95 20184881-2 2010 In tumor cells, high glucose concentrations are known to increase HIF-1alpha expression even under normoxia, presumably by enhancing the concentration of tricarboxylic acid cycle intermediates, while reactions of non-tumor cells are not well defined. Glucose 21-28 hypoxia inducible factor 1 subunit alpha Homo sapiens 66-76 20184881-4 2010 Using cells derived from non-tumor origin, we show that HIF-1alpha accumulation was higher under low compared to high glucose concentrations. Glucose 118-125 hypoxia inducible factor 1 subunit alpha Homo sapiens 56-66 20184881-5 2010 Low glucose allowed mRNA expression of HIF-1 target genes like adrenomedullin. Glucose 4-11 hypoxia inducible factor 1 subunit alpha Homo sapiens 39-44 20184881-6 2010 Transfection of C(2)C(12) cells with a HIF-1alpha oxygen-dependent degradation domaine-GFP fusion protein revealed that prolyl hydroxylase (PHD) activity is impaired at low glucose concentrations, thus stabilizing the fusion protein. Glucose 173-180 hypoxia inducible factor 1 subunit alpha Homo sapiens 39-49 20133848-1 2010 As the result of genetic alterations and tumor hypoxia, many cancer cells avidly take up glucose and generate lactate through lactate dehydrogenase A (LDHA), which is encoded by a target gene of c-Myc and hypoxia-inducible factor (HIF-1). Glucose 89-96 hypoxia inducible factor 1 subunit alpha Homo sapiens 231-236 19942427-1 2010 Hypoxia-inducible factor 1 (HIF-1) plays a key role in the reprogramming of cancer metabolism by activating transcription of genes encoding glucose transporters and glycolytic enzymes, which take up glucose and convert it to lactate; pyruvate dehydrogenase kinase 1, which shunts pyruvate away from the mitochondria; and BNIP3, which triggers selective mitochondrial autophagy. Glucose 140-147 hypoxia inducible factor 1 subunit alpha Homo sapiens 0-26 19942427-1 2010 Hypoxia-inducible factor 1 (HIF-1) plays a key role in the reprogramming of cancer metabolism by activating transcription of genes encoding glucose transporters and glycolytic enzymes, which take up glucose and convert it to lactate; pyruvate dehydrogenase kinase 1, which shunts pyruvate away from the mitochondria; and BNIP3, which triggers selective mitochondrial autophagy. Glucose 140-147 hypoxia inducible factor 1 subunit alpha Homo sapiens 28-33 19762474-2 2009 Hypoxia-inducible factor-1 (HIF-1) can activate expression of a broad range of genes that mediate many of the adaptive responses to decreased oxygen concentration, such as enhanced glucose uptake and formation of new blood vessels. Glucose 181-188 hypoxia inducible factor 1 subunit alpha Homo sapiens 0-26 20306726-5 2009 Products dependent on HIF-1 factor are involved in processes of tumor progression, such as proliferation, glucose metabolism, ph-acidosis, angiogenesis and metastasis. Glucose 106-113 hypoxia inducible factor 1 subunit alpha Homo sapiens 22-27 19924633-6 2010 These data support the existence, in the placenta, of metabolic reprogramming mechanisms, previously documented in tumor cells, whereby HIF-1 stimulates reductions in mitochondrial oxygen consumption at the cost of increased glucose consumption. Glucose 225-232 hypoxia inducible factor 1 subunit alpha Homo sapiens 136-141 19782666-2 2009 Target genes involved in glucose transport are acutely transactivated by HIF-1alpha. Glucose 25-32 hypoxia inducible factor 1 subunit alpha Homo sapiens 73-83 19762474-2 2009 Hypoxia-inducible factor-1 (HIF-1) can activate expression of a broad range of genes that mediate many of the adaptive responses to decreased oxygen concentration, such as enhanced glucose uptake and formation of new blood vessels. Glucose 181-188 hypoxia inducible factor 1 subunit alpha Homo sapiens 28-33 19098000-0 2009 The Akt/mTOR pathway assures the synthesis of HIF-1alpha protein in a glucose- and reoxygenation-dependent manner in irradiated tumors. Glucose 70-77 hypoxia inducible factor 1 subunit alpha Homo sapiens 46-56 19666581-6 2009 This resulted from a high glucose-induced decrease in transactivation by the transcription factor hypoxia-inducible factor-1alpha (HIF-1alpha), which mediates hypoxia-stimulated VEGF expression. Glucose 26-33 hypoxia inducible factor 1 subunit alpha Homo sapiens 98-129 19666581-6 2009 This resulted from a high glucose-induced decrease in transactivation by the transcription factor hypoxia-inducible factor-1alpha (HIF-1alpha), which mediates hypoxia-stimulated VEGF expression. Glucose 26-33 hypoxia inducible factor 1 subunit alpha Homo sapiens 131-141 19254710-2 2009 Central in these processes are the hypoxia-inducible transcription factors, HIF-1 and HIF-2, controlling genes involved in e.g. glucose metabolism and neovascularization. Glucose 128-135 hypoxia inducible factor 1 subunit alpha Homo sapiens 76-81 19098000-6 2009 In vitro experiments confirmed that an increase in glucose availability induced Akt phosphorylation under reoxygenated conditions and consequently up-regulated HIF-1alpha translation. Glucose 51-58 hypoxia inducible factor 1 subunit alpha Homo sapiens 160-170 19098000-8 2009 All of these results indicate that Akt/mTOR-dependent translation of HIF-1alpha plays a critical role in the postirradiation up-regulation of intratumoral HIF-1 activity in response to radiation-induced alterations of glucose and oxygen availability in a solid tumor. Glucose 218-225 hypoxia inducible factor 1 subunit alpha Homo sapiens 69-79 19098000-8 2009 All of these results indicate that Akt/mTOR-dependent translation of HIF-1alpha plays a critical role in the postirradiation up-regulation of intratumoral HIF-1 activity in response to radiation-induced alterations of glucose and oxygen availability in a solid tumor. Glucose 218-225 hypoxia inducible factor 1 subunit alpha Homo sapiens 69-74 19114105-1 2009 The induction of hypoxia-inducible factor 1 (HIF-1) activity, either as a result of intratumoral hypoxia or loss-of-function mutations in the VHL gene, leads to a dramatic reprogramming of cancer cell metabolism involving increased glucose transport into the cell, increased conversion of glucose to pyruvate, and a concomitant decrease in mitochondrial metabolism and mitochondrial mass. Glucose 232-239 hypoxia inducible factor 1 subunit alpha Homo sapiens 17-43 19114105-1 2009 The induction of hypoxia-inducible factor 1 (HIF-1) activity, either as a result of intratumoral hypoxia or loss-of-function mutations in the VHL gene, leads to a dramatic reprogramming of cancer cell metabolism involving increased glucose transport into the cell, increased conversion of glucose to pyruvate, and a concomitant decrease in mitochondrial metabolism and mitochondrial mass. Glucose 232-239 hypoxia inducible factor 1 subunit alpha Homo sapiens 45-50 30754198-0 2008 HIF-1-regulated glucose metabolism in the control of apoptosis signaling. Glucose 16-23 hypoxia inducible factor 1 subunit alpha Homo sapiens 0-5 19671047-2 2009 HIF-1 transactivates genes encoding proteins that are involved in key aspects of the cancer phenotype, including cell immortalization and de-differentiation, stem cell maintenance, genetic instability, glucose uptake and metabolism, pH regulation, autocrine growth/survival, angiogenesis, invasion/metastasis, and resistance to chemotherapy. Glucose 202-209 hypoxia inducible factor 1 subunit alpha Homo sapiens 0-5 18762723-4 2008 A reduced availability of glucose, not amino acids, results in a decrease of the expression of HIF1-dependent genes and HIF-1 alpha protein in response to hypoxia. Glucose 26-33 hypoxia inducible factor 1 subunit alpha Homo sapiens 95-99 18245813-1 2008 Iron depletion improves insulin resistance in patients with nonalcoholic fatty liver disease and diabetes and also stabilizes the hypoxia-inducible factor (HIF)-1, resulting in increased glucose uptake in vitro. Glucose 187-194 hypoxia inducible factor 1 subunit alpha Homo sapiens 130-162 18762723-4 2008 A reduced availability of glucose, not amino acids, results in a decrease of the expression of HIF1-dependent genes and HIF-1 alpha protein in response to hypoxia. Glucose 26-33 hypoxia inducible factor 1 subunit alpha Homo sapiens 120-131 18762723-7 2008 These findings imply that the reduced availability of glucose under hypoxia downregulates HIF-1 in part through the inhibition of HIF-1 alpha mRNA translation, which is occasionally observed in pathophysiological situations such as ischemic diseases. Glucose 54-61 hypoxia inducible factor 1 subunit alpha Homo sapiens 90-95 18762723-7 2008 These findings imply that the reduced availability of glucose under hypoxia downregulates HIF-1 in part through the inhibition of HIF-1 alpha mRNA translation, which is occasionally observed in pathophysiological situations such as ischemic diseases. Glucose 54-61 hypoxia inducible factor 1 subunit alpha Homo sapiens 130-141 21129310-1 2007 BACKGROUND: It has been known that facilitative glucose transporter(GLUT) is the main carrier which intervenes the glucose uptake of cell,and there is a significant correlation between GLUT1 and cancer.The expression of GLUT1 in lung cancer has close relationship with the uptake of 18fluoro-2-deoxyglucose(FDG) of lung cancer,and the expression of GLUT1 is regulated by hypoxia inducible factor-1(HIF-1).The aim of this study is to investigate the relationship among expression of GLUT1,HIF-1alpha and the uptake of FDG in non-small cell lung cancer(NSCLC). Glucose 48-55 hypoxia inducible factor 1 subunit alpha Homo sapiens 371-403 21129310-1 2007 BACKGROUND: It has been known that facilitative glucose transporter(GLUT) is the main carrier which intervenes the glucose uptake of cell,and there is a significant correlation between GLUT1 and cancer.The expression of GLUT1 in lung cancer has close relationship with the uptake of 18fluoro-2-deoxyglucose(FDG) of lung cancer,and the expression of GLUT1 is regulated by hypoxia inducible factor-1(HIF-1).The aim of this study is to investigate the relationship among expression of GLUT1,HIF-1alpha and the uptake of FDG in non-small cell lung cancer(NSCLC). Glucose 48-55 hypoxia inducible factor 1 subunit alpha Homo sapiens 488-498 17875644-1 2007 Hypoxia-inducible factor-1 (HIF-1) is a master regulator of oxygen homeostasis that controls the expression of genes encoding proteins that play key roles in angiogenesis, erythropoiesis, and glucose/energy metabolism. Glucose 192-199 hypoxia inducible factor 1 subunit alpha Homo sapiens 0-26 17875644-1 2007 Hypoxia-inducible factor-1 (HIF-1) is a master regulator of oxygen homeostasis that controls the expression of genes encoding proteins that play key roles in angiogenesis, erythropoiesis, and glucose/energy metabolism. Glucose 192-199 hypoxia inducible factor 1 subunit alpha Homo sapiens 28-33 17785433-7 2007 This study reports the previously unsuspected collaboration between HIF-1 and dysregulated MYC and thereby provides additional insights into the regulation of VEGF and the Warburg effect, which describes the propensity for cancer cells to convert glucose to lactate. Glucose 247-254 hypoxia inducible factor 1 subunit alpha Homo sapiens 68-73 18006690-6 2007 Orexin-mediated activation of HIF-1 results in increased glucose uptake and higher glycolytic activity, as expected from studies of hypoxic cells. Glucose 57-64 hypoxia inducible factor 1 subunit alpha Homo sapiens 30-35 17490410-6 2007 In hypoxia, C. pneumoniae infection had an additive effect on HIF-1alpha stabilization resulting in enhanced glucose uptake during the early phase of infection. Glucose 109-116 hypoxia inducible factor 1 subunit alpha Homo sapiens 62-72 17551816-4 2007 VHL loss-of-function leads, under aerobic conditions, to a HIF-1-dependent reprogramming of glucose and energy metabolism that includes increased glucose uptake, glycolysis, and lactate production accompanied by a reciprocal decrease in respiration. Glucose 92-99 hypoxia inducible factor 1 subunit alpha Homo sapiens 59-64 17762611-5 2007 Furthermore, hypoxia-inducible factor-1alpha has been shown to have very important functions for the regulation of glucose transport, anaerobic energy generation and matrix synthesis by articular chondrocytes. Glucose 115-122 hypoxia inducible factor 1 subunit alpha Homo sapiens 13-44 17609869-1 2007 BACKGROUND AND PURPOSE: The hypoxic accumulation of the transcription factor subunit hypoxia-inducible factor-1alpha (HIF-1alpha), a potential endogenous hypoxia marker and therapeutic target, has recently been shown to strongly depend on glucose availability. Glucose 239-246 hypoxia inducible factor 1 subunit alpha Homo sapiens 85-116 17609869-1 2007 BACKGROUND AND PURPOSE: The hypoxic accumulation of the transcription factor subunit hypoxia-inducible factor-1alpha (HIF-1alpha), a potential endogenous hypoxia marker and therapeutic target, has recently been shown to strongly depend on glucose availability. Glucose 239-246 hypoxia inducible factor 1 subunit alpha Homo sapiens 118-128 17551816-4 2007 VHL loss-of-function leads, under aerobic conditions, to a HIF-1-dependent reprogramming of glucose and energy metabolism that includes increased glucose uptake, glycolysis, and lactate production accompanied by a reciprocal decrease in respiration. Glucose 146-153 hypoxia inducible factor 1 subunit alpha Homo sapiens 59-64 17437992-6 2007 Growth factor-dependent HIF-1alpha expression reprograms the intracellular fate of glucose, resulting in decreased glucose-dependent anabolic synthesis and increased lactate production, an effect that is enhanced when HIF-1alpha protein is stabilized by hypoxia. Glucose 83-90 hypoxia inducible factor 1 subunit alpha Homo sapiens 24-34 17437992-6 2007 Growth factor-dependent HIF-1alpha expression reprograms the intracellular fate of glucose, resulting in decreased glucose-dependent anabolic synthesis and increased lactate production, an effect that is enhanced when HIF-1alpha protein is stabilized by hypoxia. Glucose 83-90 hypoxia inducible factor 1 subunit alpha Homo sapiens 218-228 17437992-6 2007 Growth factor-dependent HIF-1alpha expression reprograms the intracellular fate of glucose, resulting in decreased glucose-dependent anabolic synthesis and increased lactate production, an effect that is enhanced when HIF-1alpha protein is stabilized by hypoxia. Glucose 115-122 hypoxia inducible factor 1 subunit alpha Homo sapiens 24-34 17437992-6 2007 Growth factor-dependent HIF-1alpha expression reprograms the intracellular fate of glucose, resulting in decreased glucose-dependent anabolic synthesis and increased lactate production, an effect that is enhanced when HIF-1alpha protein is stabilized by hypoxia. Glucose 115-122 hypoxia inducible factor 1 subunit alpha Homo sapiens 218-228 17595539-10 2007 With the discovery the oxygen-sensitive transcription factor hypoxia-inducible factor (HIF-1) has come a new understanding of the molecular link between hypoxia and deregulated glucose metabolism. Glucose 177-184 hypoxia inducible factor 1 subunit alpha Homo sapiens 87-92 17009333-4 2007 Preliminary experiments have shown that the effects of HIF-1alpha are dependent on glucose availability. Glucose 83-90 hypoxia inducible factor 1 subunit alpha Homo sapiens 55-65 17043658-8 2007 Moreover, glucose deprivation-induced apoptosis of A204 RMS and A673 ES cells was inhibited under hypoxic conditions in a Hif-1alpha-dependent manner. Glucose 10-17 hypoxia inducible factor 1 subunit alpha Homo sapiens 122-132 17043658-9 2007 As GLUT-1 was induced via Hif-1alpha under hypoxia in A204 RMS and A673 ES, these findings suggest that the Hif-1alpha-mediated increase in glucose uptake plays an important role in conferring apoptosis resistance. Glucose 140-147 hypoxia inducible factor 1 subunit alpha Homo sapiens 26-36 17043658-9 2007 As GLUT-1 was induced via Hif-1alpha under hypoxia in A204 RMS and A673 ES, these findings suggest that the Hif-1alpha-mediated increase in glucose uptake plays an important role in conferring apoptosis resistance. Glucose 140-147 hypoxia inducible factor 1 subunit alpha Homo sapiens 108-118 17404504-0 2007 HIF-1-regulated glucose metabolism: a key to apoptosis resistance? Glucose 16-23 hypoxia inducible factor 1 subunit alpha Homo sapiens 0-5 16979867-2 2007 In this report, we show that Al promotes the translocation of the HIF-1alpha (hypoxia inducible factor) to the nucleus and activates the anaerobic metabolism of D-glucose. Glucose 161-170 hypoxia inducible factor 1 subunit alpha Homo sapiens 66-76 17120749-7 2006 In conclusion, high concentration glucose mainly influence the protein synthesis of HIF-1alpha of RPE cell, and HIF-1alpha protein is able to be accumulated in high concentration glucose. Glucose 179-186 hypoxia inducible factor 1 subunit alpha Homo sapiens 112-122 17120749-8 2006 Under hypoxia, the HIF-1alpha protein induced by high concentration glucose is more stable, and the expression of VEGF is obviously increased. Glucose 68-75 hypoxia inducible factor 1 subunit alpha Homo sapiens 19-29 15749641-2 2005 Among the 70 target genes of HIF-1 known so far, several are involved in angiogenesis, erythropoiesis, cell proliferation, cell viability, and glucose and iron metabolisms. Glucose 143-150 hypoxia inducible factor 1 subunit alpha Homo sapiens 29-34 17120749-0 2006 Up-regulation of HIF-1alpha and VEGF expression by elevated glucose concentration and hypoxia in cultured human retinal pigment epithelial cells. Glucose 60-67 hypoxia inducible factor 1 subunit alpha Homo sapiens 17-27 17120749-4 2006 Although the small amount of HIF-1alpha protein was able to be detected in high glucose group but not in control group, there was no significant difference between the expression of HIF-1alpha mRNA of RPE cells in high glucose group and that of RPE cells in control group. Glucose 80-87 hypoxia inducible factor 1 subunit alpha Homo sapiens 29-39 17120749-7 2006 In conclusion, high concentration glucose mainly influence the protein synthesis of HIF-1alpha of RPE cell, and HIF-1alpha protein is able to be accumulated in high concentration glucose. Glucose 34-41 hypoxia inducible factor 1 subunit alpha Homo sapiens 84-94 16223732-6 2005 We show that inactivation of HIF-1 hydroxylation by glucose-derived 2-oxoacids underlies the prominent basal HIF-1 activity commonly seen in many highly glycolytic cancer cells. Glucose 52-59 hypoxia inducible factor 1 subunit alpha Homo sapiens 29-34 16223732-6 2005 We show that inactivation of HIF-1 hydroxylation by glucose-derived 2-oxoacids underlies the prominent basal HIF-1 activity commonly seen in many highly glycolytic cancer cells. Glucose 52-59 hypoxia inducible factor 1 subunit alpha Homo sapiens 109-114 16223732-7 2005 Since HIF-1 itself promotes glycolytic metabolism, enhancement of HIF-1 by glucose metabolites may constitute a novel feed-forward signaling mechanism involved in malignant progression. Glucose 75-82 hypoxia inducible factor 1 subunit alpha Homo sapiens 6-11 16223732-7 2005 Since HIF-1 itself promotes glycolytic metabolism, enhancement of HIF-1 by glucose metabolites may constitute a novel feed-forward signaling mechanism involved in malignant progression. Glucose 75-82 hypoxia inducible factor 1 subunit alpha Homo sapiens 66-71 16319523-1 2005 HIF-1, a hypoxia inducible transcription factor, plays a pivotal role in the cellular response to hypoxia by activating genes involved in glucose metabolism, vascular remodeling, and erythropoiesis. Glucose 138-145 hypoxia inducible factor 1 subunit alpha Homo sapiens 0-5 15994012-1 2005 Hypoxia inducible factor-1 (HIF-1) is as a key transcriptional mediator of the hypoxic response in eukaryotic cells, regulating the expression of a myriad of genes involved in oxygen transport, glucose uptake and glycolysis and angiogenesis. Glucose 194-201 hypoxia inducible factor 1 subunit alpha Homo sapiens 0-26 15994012-1 2005 Hypoxia inducible factor-1 (HIF-1) is as a key transcriptional mediator of the hypoxic response in eukaryotic cells, regulating the expression of a myriad of genes involved in oxygen transport, glucose uptake and glycolysis and angiogenesis. Glucose 194-201 hypoxia inducible factor 1 subunit alpha Homo sapiens 28-33 16000563-0 2005 Effect of low glutamine/glucose on hypoxia-induced elevation of hypoxia-inducible factor-1alpha in human pancreatic cancer MiaPaCa-2 and human prostatic cancer DU-145 cells. Glucose 24-31 hypoxia inducible factor 1 subunit alpha Homo sapiens 64-95 16000563-4 2005 RESULTS: We observed that low glucose and low glutamine, but not low pyruvate, effectively suppressed the elevation of HIF-1alpha level during hypoxia (0.1-1% oxygen). Glucose 30-37 hypoxia inducible factor 1 subunit alpha Homo sapiens 119-129 16000563-5 2005 Deprivation of glutamine or glucose inhibited the accumulation of HIF-1alpha in the presence of MG-132, a protease inhibitor, regardless of oxygen tensions. Glucose 28-35 hypoxia inducible factor 1 subunit alpha Homo sapiens 66-76 16253768-0 2005 Glucose requirement for hypoxic accumulation of hypoxia-inducible factor-1alpha (HIF-1alpha). Glucose 0-7 hypoxia inducible factor 1 subunit alpha Homo sapiens 48-79 16253768-0 2005 Glucose requirement for hypoxic accumulation of hypoxia-inducible factor-1alpha (HIF-1alpha). Glucose 0-7 hypoxia inducible factor 1 subunit alpha Homo sapiens 81-91 16253768-4 2005 Hypoxic induction of HIF-1alpha protein was strongly dependent on glucose availability and largely abolished at 0.55 mM glucose or less in both cell lines. Glucose 66-73 hypoxia inducible factor 1 subunit alpha Homo sapiens 21-31 16253768-4 2005 Hypoxic induction of HIF-1alpha protein was strongly dependent on glucose availability and largely abolished at 0.55 mM glucose or less in both cell lines. Glucose 120-127 hypoxia inducible factor 1 subunit alpha Homo sapiens 21-31 16136514-9 2005 Recent studies have shown that GLUT1 and GLUT3 are both expressed in chondrocytes and their HIF-1alpha-mediated transcription may be dually stimulated in response to hypoxia and low glucose conditions which in turn promote anaerobic glycolysis in favor of oxidative phosphorylation. Glucose 182-189 hypoxia inducible factor 1 subunit alpha Homo sapiens 92-102 15946479-2 2005 Glucose transporter-1 (Glut1) and hypoxia-inducible factor 1 alpha (HIF-1alpha) enhance glucose metabolism under hypoxia. Glucose 88-95 hypoxia inducible factor 1 subunit alpha Homo sapiens 34-66 15946479-2 2005 Glucose transporter-1 (Glut1) and hypoxia-inducible factor 1 alpha (HIF-1alpha) enhance glucose metabolism under hypoxia. Glucose 88-95 hypoxia inducible factor 1 subunit alpha Homo sapiens 68-78 12914934-1 2003 Hypoxia inducible factor 1 (HIF-1) is a heterodimeric transcriptional complex that plays pivotal role in the regulation of cellular utilization of oxygen as well as glucose and is an essential regulator of angiogenesis in solid tumor and ischemic disorders. Glucose 165-172 hypoxia inducible factor 1 subunit alpha Homo sapiens 0-26 20368827-11 2004 The target genes of HIF-1 are especially related to angiogenesis, cell proliferation and survival, and to glucose and iron metabolism. Glucose 106-113 hypoxia inducible factor 1 subunit alpha Homo sapiens 20-25 15031665-9 2004 The target genes of HIF-1 are especially related to angiogenesis, cell proliferation/survival, and glucose/iron metabolism. Glucose 99-106 hypoxia inducible factor 1 subunit alpha Homo sapiens 20-25 14592787-5 2003 Conversely, the activation of HIF-1alpha associated with iron deficiency may be responsible for the increased glucose tolerance noted in iron-deficient animals; HIF-1alpha promotes efficient glucose uptake and glycolysis - a sensible adaptation to hypoxia - by inducing increased synthesis of glucose transporters and glycolytic enzymes. Glucose 110-117 hypoxia inducible factor 1 subunit alpha Homo sapiens 30-40 14592787-5 2003 Conversely, the activation of HIF-1alpha associated with iron deficiency may be responsible for the increased glucose tolerance noted in iron-deficient animals; HIF-1alpha promotes efficient glucose uptake and glycolysis - a sensible adaptation to hypoxia - by inducing increased synthesis of glucose transporters and glycolytic enzymes. Glucose 191-198 hypoxia inducible factor 1 subunit alpha Homo sapiens 161-171 15315937-3 2004 One of the key mediators of the cell"s response to lowered oxygen environments is hypoxia-inducible-factor-1 (HIF-1), a basic helix-loop-helix transcription factor, which enables cells to adapt to hypoxia by regulating the expression of genes involved in increasing oxygen availability (VEGF, erythropoietin) and enhancing glucose uptake and metabolism (Glut-1, PGK). Glucose 323-330 hypoxia inducible factor 1 subunit alpha Homo sapiens 82-108 15315937-3 2004 One of the key mediators of the cell"s response to lowered oxygen environments is hypoxia-inducible-factor-1 (HIF-1), a basic helix-loop-helix transcription factor, which enables cells to adapt to hypoxia by regulating the expression of genes involved in increasing oxygen availability (VEGF, erythropoietin) and enhancing glucose uptake and metabolism (Glut-1, PGK). Glucose 323-330 hypoxia inducible factor 1 subunit alpha Homo sapiens 110-115 21158113-6 2004 The expression of HIF-1alpha mRNA decreased with the deprivation of both oxygen and glucose, which reversed after the pretreatment of Gin. Glucose 84-91 hypoxia inducible factor 1 subunit alpha Homo sapiens 18-28 15134336-3 2004 Of central importance is the activation of hypoxia-inducible factor-1 (HIF-1), a transcription factor complex that controls the expression of genes the products of which regulate glucose uptake and metabolism, vasotonus and angiogenesis, oxygen capacity of the blood as well as cell growth and death. Glucose 179-186 hypoxia inducible factor 1 subunit alpha Homo sapiens 43-69 15134336-3 2004 Of central importance is the activation of hypoxia-inducible factor-1 (HIF-1), a transcription factor complex that controls the expression of genes the products of which regulate glucose uptake and metabolism, vasotonus and angiogenesis, oxygen capacity of the blood as well as cell growth and death. Glucose 179-186 hypoxia inducible factor 1 subunit alpha Homo sapiens 71-76 12914934-1 2003 Hypoxia inducible factor 1 (HIF-1) is a heterodimeric transcriptional complex that plays pivotal role in the regulation of cellular utilization of oxygen as well as glucose and is an essential regulator of angiogenesis in solid tumor and ischemic disorders. Glucose 165-172 hypoxia inducible factor 1 subunit alpha Homo sapiens 28-33 11818497-1 2002 The heterodimeric hypoxia-inducible factor (HIF)-1 is a transcriptional master regulator of several genes involved in mammalian oxygen homeostasis, including erythropoietin, vascular endothelial growth factor, and factors involved in glucose transport and metabolism. Glucose 234-241 hypoxia inducible factor 1 subunit alpha Homo sapiens 18-50 12558074-4 2003 HIF-1 controls cellular and systemic responses to oxygen availability and coordinates up-regulation of genes involved in many pathways concerned with tumour growth and metabolism including angiogenesis, glucose and energy metabolism, cellular proliferation, differentiation and viability, apoptosis, pH regulation and matrix metabolism. Glucose 203-210 hypoxia inducible factor 1 subunit alpha Homo sapiens 0-5 11859074-1 2002 The serine/threonine kinase Akt/PKB and the oxygen-responsive transcription factor HIF-1 share the ability to induce such processes as angiogenesis, glucose uptake, and glycolysis. Glucose 149-156 hypoxia inducible factor 1 subunit alpha Homo sapiens 83-88 11859074-4 2002 Previous reports suggest that Akt may achieve its effects on angiogenesis and glucose metabolism by stimulating HIF-1 activity. Glucose 78-85 hypoxia inducible factor 1 subunit alpha Homo sapiens 112-117 11829741-1 2002 Hypoxia-inducible factor-1alpha (HIF-1alpha), a member of the transcription family characterized by a basic helix-loop-helix (bHLH) domain and a PAS domain, regulates the transcription of hypoxia-inducible genes involved in erythropoiesis, vascular remodelling and glucose/energy metabolism. Glucose 265-272 hypoxia inducible factor 1 subunit alpha Homo sapiens 0-31 11829741-1 2002 Hypoxia-inducible factor-1alpha (HIF-1alpha), a member of the transcription family characterized by a basic helix-loop-helix (bHLH) domain and a PAS domain, regulates the transcription of hypoxia-inducible genes involved in erythropoiesis, vascular remodelling and glucose/energy metabolism. Glucose 265-272 hypoxia inducible factor 1 subunit alpha Homo sapiens 33-43 11557773-3 2001 Here we report that the distal region of the hepatoma type II hexokinase promoter displays consensus motifs for hypoxia-inducible factor (HIF-1) that overlap E-box sequences known to be related in other gene promoters to glucose response. Glucose 221-228 hypoxia inducible factor 1 subunit alpha Homo sapiens 138-143 11463947-1 2001 Decreased oxygen (O2) levels activate hypoxia-inducible factor (HIF-1) to induce genes involved in glycolysis, glucose transport, erythropoiesis, and angiogenesis. Glucose 111-118 hypoxia inducible factor 1 subunit alpha Homo sapiens 64-69 34651203-15 2022 HIF-1 activation increased IL-1beta and IL-8 in human uroepithelial cells treated with high glucose concentration. Glucose 92-99 hypoxia inducible factor 1 subunit alpha Homo sapiens 0-5 9387095-4 1997 These and other observations suggest that the normal cell responds physiologically to changes in oxygen tension or the availability of glucose by altering glycolysis through the ChoRE, which hypothetically binds c-Myc, HIF-1, or related factors. Glucose 135-142 hypoxia inducible factor 1 subunit alpha Homo sapiens 219-224 9387095-6 1997 We hypothesize that oncogene products either stimulate HIF-1 and related factors or, in the case of c-Myc, directly activate hypoxia/glucose responsive elements in glycolytic enzyme genes to increase the ability of cancer cells to undergo aerobic glycolysis. Glucose 133-140 hypoxia inducible factor 1 subunit alpha Homo sapiens 55-60 34759325-7 2021 Furthermore, in the synovium of the DM OA group and FLSs treated with high glucose, the expression of glucose transporter 1 (GLUT1) and its regulatory factor hypoxia-inducible factor (HIF)-1alpha was increased significantly. Glucose 75-82 hypoxia inducible factor 1 subunit alpha Homo sapiens 158-195 34872812-9 2022 RESULTS: Expression of HIF-1alpha target genes (erythropoietin, VEGF-A, and glucose transporter-1) was reduced by 45% - 95% in experimental diabetic aortas. Glucose 76-83 hypoxia inducible factor 1 subunit alpha Homo sapiens 23-33 34948094-0 2021 Transcription Factor ChREBP Mediates High Glucose-Evoked Increase in HIF-1alpha Content in Epithelial Cells of Renal Proximal Tubules. Glucose 42-49 hypoxia inducible factor 1 subunit alpha Homo sapiens 69-79 34948094-2 2021 The aim of the study was to elucidate the mechanism of high glucose action on HIF-1alpha expression in renal proximal tubule epithelial cells. Glucose 60-67 hypoxia inducible factor 1 subunit alpha Homo sapiens 78-88 34948094-9 2021 It was found that high glucose in HK-2 cells incubated under normoxic conditions: (1) activated transcription of HIF-1 target genes, elevated HIF-1alpha and ChREBP content, and increased the efficacy of ChREBP binding to promoter region of HIF1A gene; and (2), although it lowered NAD+/NADH ratio, it affected neither sirtuin activity nor HIF-1alpha acetylation level. Glucose 23-30 hypoxia inducible factor 1 subunit alpha Homo sapiens 113-118 34948094-9 2021 It was found that high glucose in HK-2 cells incubated under normoxic conditions: (1) activated transcription of HIF-1 target genes, elevated HIF-1alpha and ChREBP content, and increased the efficacy of ChREBP binding to promoter region of HIF1A gene; and (2), although it lowered NAD+/NADH ratio, it affected neither sirtuin activity nor HIF-1alpha acetylation level. Glucose 23-30 hypoxia inducible factor 1 subunit alpha Homo sapiens 142-152 34948094-9 2021 It was found that high glucose in HK-2 cells incubated under normoxic conditions: (1) activated transcription of HIF-1 target genes, elevated HIF-1alpha and ChREBP content, and increased the efficacy of ChREBP binding to promoter region of HIF1A gene; and (2), although it lowered NAD+/NADH ratio, it affected neither sirtuin activity nor HIF-1alpha acetylation level. Glucose 23-30 hypoxia inducible factor 1 subunit alpha Homo sapiens 240-245 34948094-9 2021 It was found that high glucose in HK-2 cells incubated under normoxic conditions: (1) activated transcription of HIF-1 target genes, elevated HIF-1alpha and ChREBP content, and increased the efficacy of ChREBP binding to promoter region of HIF1A gene; and (2), although it lowered NAD+/NADH ratio, it affected neither sirtuin activity nor HIF-1alpha acetylation level. Glucose 23-30 hypoxia inducible factor 1 subunit alpha Homo sapiens 339-349 34948094-10 2021 The stimulatory effect of high glucose on HIF-1alpha expression was not observed upon the knockdown of ChREBP encoding gene. Glucose 31-38 hypoxia inducible factor 1 subunit alpha Homo sapiens 42-52 34948094-11 2021 Experiments on RPTEC and D-RPTEC cells demonstrated that HIF-1alpha content in diabetic proximal tubular cells was lower than that in normal ones but remained high glucose-sensitive, and the latter phenomenon was mediated by ChREBP. Glucose 164-171 hypoxia inducible factor 1 subunit alpha Homo sapiens 57-67 34948094-12 2021 Thus, it is concluded that the mechanism of high glucose-evoked increase in HIF-1alpha content in renal proximal tubule endothelial cells involves activation of ChREBP, indirectly capable of HIF1A gene up-regulation. Glucose 49-56 hypoxia inducible factor 1 subunit alpha Homo sapiens 76-86 34948094-12 2021 Thus, it is concluded that the mechanism of high glucose-evoked increase in HIF-1alpha content in renal proximal tubule endothelial cells involves activation of ChREBP, indirectly capable of HIF1A gene up-regulation. Glucose 49-56 hypoxia inducible factor 1 subunit alpha Homo sapiens 191-196 34820369-9 2021 Inhibitions of HIF1alpha rescues ID1, which compensates the loss of HIF1alpha by the upregulation of GLS2 and glutamine metabolism, thereby switching the metabolic dependency of HIF1alpha -inhibited cells from glucose to glutamine. Glucose 210-217 hypoxia inducible factor 1 subunit alpha Homo sapiens 15-24 34820369-9 2021 Inhibitions of HIF1alpha rescues ID1, which compensates the loss of HIF1alpha by the upregulation of GLS2 and glutamine metabolism, thereby switching the metabolic dependency of HIF1alpha -inhibited cells from glucose to glutamine. Glucose 210-217 hypoxia inducible factor 1 subunit alpha Homo sapiens 68-77 34820369-9 2021 Inhibitions of HIF1alpha rescues ID1, which compensates the loss of HIF1alpha by the upregulation of GLS2 and glutamine metabolism, thereby switching the metabolic dependency of HIF1alpha -inhibited cells from glucose to glutamine. Glucose 210-217 hypoxia inducible factor 1 subunit alpha Homo sapiens 178-187 34992822-16 2021 Conclusions: Our findings suggest that SDH5 deficiency activates HIF-1alpha to promote EMT under high glucose conditions and represents a predictive marker for NSCLC patients with diabetes. Glucose 102-109 hypoxia inducible factor 1 subunit alpha Homo sapiens 65-75 34558885-2 2021 We previously demonstrated that activated hypoxia-inducible factor-1alpha (HIF-1 alpha)/insulin-like growth factor binding protein-3 (IGFBP-3) signaling by reactive oxygen species (ROS)-regulated prolyl hydroxylase domain-containing protein (PHD) is involved in high-glucose (HG)-induced cardiac apoptosis. Glucose 267-274 hypoxia inducible factor 1 subunit alpha Homo sapiens 42-73 34736121-3 2021 M1-activation of macrophages by bacterial lipopolysaccharide (LPS) promotes a paracrine activation of hypoxia-inducible factor-1alpha (HIF1alpha) in brown adipocytes which reduces insulin signaling and glucose uptake, as well as beta-adrenergic sensitivity. Glucose 202-209 hypoxia inducible factor 1 subunit alpha Homo sapiens 102-133 34736121-3 2021 M1-activation of macrophages by bacterial lipopolysaccharide (LPS) promotes a paracrine activation of hypoxia-inducible factor-1alpha (HIF1alpha) in brown adipocytes which reduces insulin signaling and glucose uptake, as well as beta-adrenergic sensitivity. Glucose 202-209 hypoxia inducible factor 1 subunit alpha Homo sapiens 135-144 34558885-2 2021 We previously demonstrated that activated hypoxia-inducible factor-1alpha (HIF-1 alpha)/insulin-like growth factor binding protein-3 (IGFBP-3) signaling by reactive oxygen species (ROS)-regulated prolyl hydroxylase domain-containing protein (PHD) is involved in high-glucose (HG)-induced cardiac apoptosis. Glucose 267-274 hypoxia inducible factor 1 subunit alpha Homo sapiens 75-86 34193173-0 2021 STAT3/HIF-1alpha signaling activation mediates peritoneal fibrosis induced by high glucose. Glucose 83-90 hypoxia inducible factor 1 subunit alpha Homo sapiens 6-16 34196069-10 2021 Mechanistic investigations identified that TEAD4 played a key role as a transcription factor and promoted PKM2 transcription and expression, which further altered the reporter activity of HIF-1alpha and upregulated HIF-1alpha-targeted glycolytic genes glucose transporter-1 and hexokinase II. Glucose 252-259 hypoxia inducible factor 1 subunit alpha Homo sapiens 215-225 34447462-7 2021 By inhibiting HIF-1alpha, miR-18a-5p suppressed aerobic glycolysis in K562/ADM cells, according to the results produced by glucose uptake, lactate production, pyruvate level and ATP synthesis measurement, along with the results obtained from extracellular acidification rate and oxygen consumption rate assays. Glucose 123-130 hypoxia inducible factor 1 subunit alpha Homo sapiens 14-24 34575914-7 2021 Hypoxia activated the HIF-1alpha and downstream molecules including prolyl hydroxylase 3 and glucose transporter-1, whereas paricalcitol attenuated the activation of the HIF-1alpha-dependent molecules and TGF-beta1/Smad signaling pathways in hypoxic pericytes. Glucose 93-100 hypoxia inducible factor 1 subunit alpha Homo sapiens 22-32 34572324-4 2021 By using human endothelial cells and macrophages, we demonstrate that high glucose (HG) induces HIF-1alpha activity and a switch from oxidative metabolism to glycolysis and its principal branches. Glucose 75-82 hypoxia inducible factor 1 subunit alpha Homo sapiens 96-106 34426491-5 2021 Elevated glucose inhibited DNA repair by attenuating hypoxia-inducible factor-1alpha-mediated transcription of NER genes via enhanced 2-ketoglutarate-dependent prolyl hydroxylase (PHD) activity. Glucose 9-16 hypoxia inducible factor 1 subunit alpha Homo sapiens 53-84 34692517-8 2021 High glucose instigated suppression in the intracellular accumulation of anticancer drug doxorubicin and drug-induced chromatin compactness along with declined expression of drug efflux pump MDR-1 and transcription factors and signal transducers governing the survival, aggressiveness, and apoptotic cell death (p53, HIF-1alpha, mTOR, MYC, STAT3). Glucose 5-12 hypoxia inducible factor 1 subunit alpha Homo sapiens 317-327 34479471-4 2021 Our previous studies showed that high-glucose and hypoxic conditions could upregulate HIF-1alpha expression and enhance EC inflammatory injury, independently of the nuclear factor kappa-B (NF-kappaB) pathway. Glucose 38-45 hypoxia inducible factor 1 subunit alpha Homo sapiens 86-96 34479471-9 2021 RESULTS: High glucose and hypoxia up-regulated HIF-1alpha expression, and down-regulated HIF-1alpha decreased the level of inflammation and oxidative stress in HUVECs. Glucose 14-21 hypoxia inducible factor 1 subunit alpha Homo sapiens 47-57 34479471-9 2021 RESULTS: High glucose and hypoxia up-regulated HIF-1alpha expression, and down-regulated HIF-1alpha decreased the level of inflammation and oxidative stress in HUVECs. Glucose 14-21 hypoxia inducible factor 1 subunit alpha Homo sapiens 89-99 34479471-12 2021 Moreover, we observed that HIF-1alpha bound to the promoter of JMJD1A, and the ameliorative effects of si-HIF-1alpha on oxidative stress and inflammatory cytokines in high-glucose and hypoxia-induced HUVECs were reversed by JMJD1A overexpression. Glucose 172-179 hypoxia inducible factor 1 subunit alpha Homo sapiens 27-37 34479471-12 2021 Moreover, we observed that HIF-1alpha bound to the promoter of JMJD1A, and the ameliorative effects of si-HIF-1alpha on oxidative stress and inflammatory cytokines in high-glucose and hypoxia-induced HUVECs were reversed by JMJD1A overexpression. Glucose 172-179 hypoxia inducible factor 1 subunit alpha Homo sapiens 106-116 34479471-16 2021 CONCLUSIONS: These findings provide novel evidence that the HIF-1alpha/JMJD1A signaling pathway is involved in inflammation and oxidative stress in HUVECs induced by high glucose and hypoxia. Glucose 171-178 hypoxia inducible factor 1 subunit alpha Homo sapiens 60-70 34326958-15 2021 Inhibition of HIF-1alpha with siRNA abolished the dcOC-mediated glucose uptake and substantially decreased GLUT1 protein expression. Glucose 64-71 hypoxia inducible factor 1 subunit alpha Homo sapiens 14-24 34193173-9 2021 Furthermore, high glucose-mediated STAT3 activation in mesothelial cells induced the expression of HIF-1alpha and the profibrotic effect of STAT3 signaling was alleviated by siRNA for HIF-1alpha. Glucose 18-25 hypoxia inducible factor 1 subunit alpha Homo sapiens 99-109 34193173-9 2021 Furthermore, high glucose-mediated STAT3 activation in mesothelial cells induced the expression of HIF-1alpha and the profibrotic effect of STAT3 signaling was alleviated by siRNA for HIF-1alpha. Glucose 18-25 hypoxia inducible factor 1 subunit alpha Homo sapiens 184-194 35576836-3 2022 In the hyperglycemic environment caused by abnormal glucose metabolism, hypoxia-inducible factor-1 alpha (HIF-1alpha) enables tumor cells to absorb large amounts of glucose and enhance glycolysis by inducing the expression of glucose transporter type1 (GLUT1) and glycolysis genes, thus promoting tumor cell proliferation and metastasis. Glucose 165-172 hypoxia inducible factor 1 subunit alpha Homo sapiens 72-104 34108057-1 2021 OBJECTIVE: This study aimed to clarify the association between both hypoxia-inducible factor-1alpha and glucose transporter type-1 expression and survival outcome in advanced pharyngeal cancer without human papillomavirus infection. Glucose 104-111 hypoxia inducible factor 1 subunit alpha Homo sapiens 68-99 34178852-2 2021 The aim of this study was investigation of different glucose accessibility conditions on the rate of Warburg effect and its impact on Hypoxia inducible factors-1 alpha (HIF-1 alpha)/vascular endothelium growth factor (VEGF) pathway in breast cancer cells lines. Glucose 53-60 hypoxia inducible factor 1 subunit alpha Homo sapiens 169-180 35576836-3 2022 In the hyperglycemic environment caused by abnormal glucose metabolism, hypoxia-inducible factor-1 alpha (HIF-1alpha) enables tumor cells to absorb large amounts of glucose and enhance glycolysis by inducing the expression of glucose transporter type1 (GLUT1) and glycolysis genes, thus promoting tumor cell proliferation and metastasis. Glucose 165-172 hypoxia inducible factor 1 subunit alpha Homo sapiens 106-116 35576836-13 2022 Furthermore, the downregulation of HK2 and HIF-1alpha caused by SIRT5 knockdown was a high glucose-dependent process, while the downregulation of PKM2 was mediated by a high glucose-independent process. Glucose 91-98 hypoxia inducible factor 1 subunit alpha Homo sapiens 43-53 35412588-4 2022 Mechanistically, IFN-a suppressed HIF1a signaling by inhibiting FosB transcription in HCC cells, resulting in reduced glucose consumption capacity and consequentially establishing the high-glucose microenvironment that fostered transcription of the T cell costimulatory molecule Cd27 via mTOR-FOXM1 signaling in infiltrating CD8+ T cells. Glucose 118-125 hypoxia inducible factor 1 subunit alpha Homo sapiens 34-39 35348849-7 2022 The glucose metabolic shift (the Warburg effect) is mediated by HIF-1. Glucose 4-11 hypoxia inducible factor 1 subunit alpha Homo sapiens 64-69 35415942-13 2022 HIF-1alpha and/or Glut-1 knockout significantly reduced cell viability, glucose uptake and PI3K/Akt/mTOR activity, all of which were induced by hypoxia in the presence of irradiation. Glucose 72-79 hypoxia inducible factor 1 subunit alpha Homo sapiens 0-10 35412588-4 2022 Mechanistically, IFN-a suppressed HIF1a signaling by inhibiting FosB transcription in HCC cells, resulting in reduced glucose consumption capacity and consequentially establishing the high-glucose microenvironment that fostered transcription of the T cell costimulatory molecule Cd27 via mTOR-FOXM1 signaling in infiltrating CD8+ T cells. Glucose 189-196 hypoxia inducible factor 1 subunit alpha Homo sapiens 34-39 35432450-6 2022 Angiogenesis, erythropoiesis, glycolysis regulation, glucose transport, acidosis regulators have all been orchestrated through the activation and stability of a transcription factor termed hypoxia-inducible factor-1 (HIF-1), hence altering crucial Warburg effect activities. Glucose 53-60 hypoxia inducible factor 1 subunit alpha Homo sapiens 189-215 35189090-6 2022 According to the in-depth studies, the abnormal activation of HIF-1alpha/glucose transporters/glycolysis pathway of 5-CQA could be a key molecular mechanism leading to drug resistance of HCC cells. Glucose 73-80 hypoxia inducible factor 1 subunit alpha Homo sapiens 62-72 35088883-0 2022 High-glucose microenvironment promotes perineural invasion of pancreatic cancer via activation of hypoxia inducible factor 1alpha. Glucose 5-12 hypoxia inducible factor 1 subunit alpha Homo sapiens 98-129 35088883-10 2022 In conclusion, a high-glucose microenvironment promotes PNI of PC via activation of HIF1alpha. Glucose 22-29 hypoxia inducible factor 1 subunit alpha Homo sapiens 84-93 35432450-6 2022 Angiogenesis, erythropoiesis, glycolysis regulation, glucose transport, acidosis regulators have all been orchestrated through the activation and stability of a transcription factor termed hypoxia-inducible factor-1 (HIF-1), hence altering crucial Warburg effect activities. Glucose 53-60 hypoxia inducible factor 1 subunit alpha Homo sapiens 217-222 33692685-3 2020 This study aims to explore whether regulating the HIF-1alpha/MIF/AMPK signaling pathway can restore the protective effect and reveal the mechanism of SPostC on cardiomyocyte hypoxia/reoxygenation injury under high glucose conditions. Glucose 214-221 hypoxia inducible factor 1 subunit alpha Homo sapiens 50-60 32551804-3 2021 Presumably, expression of HIF-1a may be reflected by positron emission tomography with 2-deoxy-2 [fluorine-18] fluoro-D-glucose (18F-FDG PET). Glucose 120-127 hypoxia inducible factor 1 subunit alpha Homo sapiens 26-32 33624591-11 2021 Downregulation of HIF-1alpha obviously reversed the effect of UPK1A-AS1 overexpression in promoting glucose consumption, lactate production and HRE luciferase activity. Glucose 100-107 hypoxia inducible factor 1 subunit alpha Homo sapiens 18-28 33754057-17 2021 The in vitro and in vivo findings further demonstrated that high glucose may promote plakoglobin-dependent cooperation of p53 with HIF-1alpha and Smad3, subsequently increasing the expression of TGF-beta1 and the pro-EndMT target genes of the TGF-beta1/Smad signaling pathway in a KLK8-dependent manner. Glucose 65-72 hypoxia inducible factor 1 subunit alpha Homo sapiens 131-141 33649449-4 2021 The o-chlorophenyl derivative 7l (n = 5) indicated the most potent inhibitory effects on HIF-1- and UPR-mediated transcriptional activation (IC50; 1.0 +- 0.1 muM, 7.5 +- 0.1 muM, respectively) and exhibited selective cytotoxicity toward HT29 cells under low glucose condition (IC50; 1.9 +- 0.1 muM). Glucose 258-265 hypoxia inducible factor 1 subunit alpha Homo sapiens 89-94 33649449-5 2021 Additionally, the protein expression of HIF-1alpha induced by hypoxia and of GRP78 and GRP94 induced by glucose starvation was markedly suppressed by the biguanides, thereby inhibiting angiogenesis. Glucose 104-111 hypoxia inducible factor 1 subunit alpha Homo sapiens 40-50 33692685-10 2020 Under high glucose (35 muM), the expression levels of HIF-1alpha and MIF were up-regulated by using agonists, which can significantly increase the level of p-AMPKalpha protein, and the cardioprotective effect of SPostC was restored. Glucose 11-18 hypoxia inducible factor 1 subunit alpha Homo sapiens 54-64 33520443-1 2021 Background: Although the WW-domain-containing oxidoreductase (WWOX)/Hypoxia-inducible factor 1 (HIF1) pathway is a well-known regulator of cellular glucose and energy metabolism in pathophysiological processes, its role in gestational diabetes mellitus (GDM), remains elusive. Glucose 148-155 hypoxia inducible factor 1 subunit alpha Homo sapiens 96-100 33359671-11 2021 HIF-1alpha siRNA also greatly attenuated the inhibitory effect of balanophorin B on HepG2 cells glucose uptake. Glucose 96-103 hypoxia inducible factor 1 subunit alpha Homo sapiens 0-10 33520443-4 2021 Quantitative RT-PCR was performed to determine gene expression profiles of the WWOX/HIF1A-related genes, including those involved in glucose transport (SLC2A1, SLC2A4), glycolytic pathway (HK2, PKM2, PFK, LDHA), Wnt pathway (DVL2, CTNNB1), and inflammatory response (NFKB1). Glucose 133-140 hypoxia inducible factor 1 subunit alpha Homo sapiens 84-89 33401572-7 2021 Recent evidences identified numerous natural flavonoids and their derivatives as inhibitors of HIF-1, associated with the regulation of critical glycolytic components in cancer cells, including pyruvate kinase M2(PKM2), lactate dehydrogenase (LDHA), glucose transporters (GLUTs), hexokinase II (HKII), phosphofructokinase-1 (PFK-1), and pyruvate dehydrogenase kinase (PDK). Glucose 250-257 hypoxia inducible factor 1 subunit alpha Homo sapiens 95-100 33401572-9 2021 Besides, flavonoid effects on glucose metabolism via regulation of HIF-1 activity represent a promising avenue in cancer-related research. Glucose 30-37 hypoxia inducible factor 1 subunit alpha Homo sapiens 67-72