PMID-sentid Pub_year Sent_text comp_official_name comp_offset protein_name organism prot_offset 22865656-6 2012 Here we show that phosphorylation of AKT and AMP-activated kinase (AMPK) is involved in FM19G11-dependent activation of GLUT-4, glucose influx, and consequently in stem cell self-renewal. Glucose 128-135 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 45-65 22865656-6 2012 Here we show that phosphorylation of AKT and AMP-activated kinase (AMPK) is involved in FM19G11-dependent activation of GLUT-4, glucose influx, and consequently in stem cell self-renewal. Glucose 128-135 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 67-71 22771471-10 2012 The role of Fyn inhibition by kazinol E in AMPK-mediated protection of the cell viability and mitochondrial function was strengthened by ectopically expressed Fyn"s reversal of these effects. Kazinol E 30-39 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 43-47 22684842-0 2012 Quercetin enhances hypoxia-mediated apoptosis via direct inhibition of AMPK activity in HCT116 colon cancer. Quercetin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 71-75 22684842-3 2012 Quercetin significantly attenuated tumor growth in an HCT116 cancer xenograft in vivo model with a substantial reduction of AMPK activity. Quercetin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 124-128 22684842-4 2012 In a cell culture system, quercetin more dramatically induced apoptosis of HCT116 cancer cells under hypoxic conditions than normoxic conditions, and this was tightly associated with inhibition of hypoxia-induced AMPK activity. Quercetin 26-35 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 213-217 22684842-5 2012 An in vitro kinase assay demonstrated that quercetin directly inhibits AMPK activity. Quercetin 43-52 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 71-75 22684842-6 2012 Inhibition of AMPK by expressing a dominant-negative form resulted in an increase of apoptosis under hypoxia, and a constitutively active form of AMPK effectively blocked quercetin-induced apoptosis under hypoxia. Quercetin 171-180 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-18 22684842-6 2012 Inhibition of AMPK by expressing a dominant-negative form resulted in an increase of apoptosis under hypoxia, and a constitutively active form of AMPK effectively blocked quercetin-induced apoptosis under hypoxia. Quercetin 171-180 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 146-150 22684842-7 2012 Collectively, our data suggest that quercetin directly inhibits hypoxia-induced AMPK, which plays a protective role against hypoxia. Quercetin 36-45 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 80-84 22509822-5 2012 KEY RESULTS: AMPK was activated by exposure to 3% or 0.2% O(2) for 60 min in cells grown in submerged culture or when fluid (0.1 mL cm(-2) ) was added to the apical surface of cells grown at the air-liquid interface. Superoxides 58-62 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 13-17 22509822-6 2012 Only 0.2% O(2) activated AMPK in cells grown at the air-liquid interface. Superoxides 10-14 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 25-29 22509822-7 2012 AMPK activation was associated with elevation of cellular AMP:ATP ratio and activity of the upstream kinase LKB1. Adenosine Triphosphate 62-65 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 22700795-1 2012 The AMP-activated protein kinase (AMPK) is a serine/threonine protein kinase that acts as a sensor of cellular energy status switch regulating several systems including glucose and lipid metabolism. Glucose 169-176 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 4-32 22700795-1 2012 The AMP-activated protein kinase (AMPK) is a serine/threonine protein kinase that acts as a sensor of cellular energy status switch regulating several systems including glucose and lipid metabolism. Glucose 169-176 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 34-38 22771471-11 2012 In conclusion, kazinols as multi-prenylated polyphenols possess increased antioxidant and cytoprotective activity, which depends on the activation of LKB1-AMPK pathway downstream of Fyn inhibition. kazinols 15-23 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 155-159 23019413-5 2012 Phosphorylation of adenosine monophosphate (AMP)-activated protein kinase alpha1 (AMPKalpha1) was increased by both drugs, which promoted cell survival, as indicated by results obtained using AMPK inhibitor compound C and AMPK activator 5-aminoimidazole-4-carboxamide 1-beta-d-ribofuranoside. Adenosine Monophosphate 19-42 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 82-92 22889215-5 2012 AMPK senses bioenergetic fluctuations in cells and works in concert with LKB1 to maintain cellular energy homeostasis by promoting catabolic pathways of ATP production and limiting processes that consume ATP. Adenosine Triphosphate 153-156 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 22889215-5 2012 AMPK senses bioenergetic fluctuations in cells and works in concert with LKB1 to maintain cellular energy homeostasis by promoting catabolic pathways of ATP production and limiting processes that consume ATP. Adenosine Triphosphate 204-207 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 23019413-5 2012 Phosphorylation of adenosine monophosphate (AMP)-activated protein kinase alpha1 (AMPKalpha1) was increased by both drugs, which promoted cell survival, as indicated by results obtained using AMPK inhibitor compound C and AMPK activator 5-aminoimidazole-4-carboxamide 1-beta-d-ribofuranoside. Adenosine Monophosphate 19-42 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 82-86 23019413-5 2012 Phosphorylation of adenosine monophosphate (AMP)-activated protein kinase alpha1 (AMPKalpha1) was increased by both drugs, which promoted cell survival, as indicated by results obtained using AMPK inhibitor compound C and AMPK activator 5-aminoimidazole-4-carboxamide 1-beta-d-ribofuranoside. Adenosine Monophosphate 19-42 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 192-196 22713505-2 2012 The protein adipose triglyceride lipase (ATGL) is a key regulator of triacylglycerol lipolysis and whole body energy metabolism at rest and during exercise, and ATGL activity is reported to be enhanced by 5"-AMP-activated protein kinase (AMPK)-mediated phosphorylation at Ser(406) in mice. Triglycerides 69-84 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 238-242 23019413-5 2012 Phosphorylation of adenosine monophosphate (AMP)-activated protein kinase alpha1 (AMPKalpha1) was increased by both drugs, which promoted cell survival, as indicated by results obtained using AMPK inhibitor compound C and AMPK activator 5-aminoimidazole-4-carboxamide 1-beta-d-ribofuranoside. Adenosine Monophosphate 44-47 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 82-92 23019413-5 2012 Phosphorylation of adenosine monophosphate (AMP)-activated protein kinase alpha1 (AMPKalpha1) was increased by both drugs, which promoted cell survival, as indicated by results obtained using AMPK inhibitor compound C and AMPK activator 5-aminoimidazole-4-carboxamide 1-beta-d-ribofuranoside. Adenosine Monophosphate 44-47 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 82-86 23019413-5 2012 Phosphorylation of adenosine monophosphate (AMP)-activated protein kinase alpha1 (AMPKalpha1) was increased by both drugs, which promoted cell survival, as indicated by results obtained using AMPK inhibitor compound C and AMPK activator 5-aminoimidazole-4-carboxamide 1-beta-d-ribofuranoside. Adenosine Monophosphate 44-47 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 192-196 23019413-5 2012 Phosphorylation of adenosine monophosphate (AMP)-activated protein kinase alpha1 (AMPKalpha1) was increased by both drugs, which promoted cell survival, as indicated by results obtained using AMPK inhibitor compound C and AMPK activator 5-aminoimidazole-4-carboxamide 1-beta-d-ribofuranoside. acadesine 237-291 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 82-92 23019413-5 2012 Phosphorylation of adenosine monophosphate (AMP)-activated protein kinase alpha1 (AMPKalpha1) was increased by both drugs, which promoted cell survival, as indicated by results obtained using AMPK inhibitor compound C and AMPK activator 5-aminoimidazole-4-carboxamide 1-beta-d-ribofuranoside. acadesine 237-291 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 82-86 23019413-6 2012 This is in good agreement with previous reports, where AMPKalpha1 was demonstrated to represent an important factor for the sensitivity to cisplatin in colon and ovarian cancers, most likely by induction of autophagy. Cisplatin 139-148 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 55-65 23019413-7 2012 Thus, AMPKalpha1 constitutes a potential target to be exploited for chemotherapeutic treatment of SCLC to circumvent resistance to metal-based compounds. Metals 131-136 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 6-16 22860996-8 2012 Using Western blotting, we observed that allicin decreased the level of cytoplasmic p53, the PI3K/mTOR signaling pathway, and the level of Bcl-2 and increased the expression of AMPK/TSC2 and Beclin-1 signaling pathways in Hep G2 cells. allicin 41-48 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 177-181 22706202-4 2012 Depletion of elevated CAV1 led to AMPK activation followed by a p53-dependent G1 cell-cycle arrest and autophagy, suggesting that elevated CAV1 may contribute to ATP generation. Adenosine Triphosphate 162-165 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 34-38 22713505-2 2012 The protein adipose triglyceride lipase (ATGL) is a key regulator of triacylglycerol lipolysis and whole body energy metabolism at rest and during exercise, and ATGL activity is reported to be enhanced by 5"-AMP-activated protein kinase (AMPK)-mediated phosphorylation at Ser(406) in mice. Serine 272-275 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 238-242 22713505-4 2012 We investigated whether the phosphorylation of ATGL Ser(404) (corresponding to murine Ser(406)) was increased during exercise in human skeletal muscle and with pharmacological AMPK activation in myotubes in vitro. Serine 52-55 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 176-180 22442140-1 2012 Focus on "A novel inverse relationship between metformin-triggered AMPK-SIRT1 signaling and p53 protein abundance in high glucose-exposed HepG2 cells". Metformin 47-56 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 67-71 22442140-1 2012 Focus on "A novel inverse relationship between metformin-triggered AMPK-SIRT1 signaling and p53 protein abundance in high glucose-exposed HepG2 cells". Glucose 122-129 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 67-71 22659145-7 2012 In addition, resveratrol stimulated the activity of Ampk and SirT1. Resveratrol 13-24 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 52-56 22692960-6 2012 2-DG-treated ALL cells exhibit upregulation of P-AMPK, P-Akt, and induction of ER stress/UPR markers (IRE1alpha, GRP78, P-eIF2alpha, and CHOP), which correlate with PARP cleavage and apoptosis. Deoxyglucose 0-4 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 49-53 22692960-7 2012 In addition, we find that pharmacologic and genetic Akt inhibition upregulates P-AMPK, downregulates UPR, and sensitizes ALL cells to remarkably low doses of 2-DG (0.5 mmol/L), inducing 85% cell death and overcoming the relative resistance of T-ALL. Deoxyglucose 158-162 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 81-85 22670709-0 2012 Activation of AMPK by pterostilbene suppresses lipogenesis and cell-cycle progression in p53 positive and negative human prostate cancer cells. pterostilbene 22-35 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-18 22670709-5 2012 In this study, we found that pterostilbene activated AMPK in both p53 positive and negative human prostate cancer cells. pterostilbene 29-42 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 53-57 22673193-0 2012 Silencing of Twist1 sensitizes NSCLC cells to cisplatin via AMPK-activated mTOR inhibition. Cisplatin 46-55 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 60-64 22673193-3 2012 Silencing of Twist1 triggered ATP depletion, leading to AMP-activated protein kinase (AMPK)-activated mammalian target of rapamycin (mTOR) inhibition in NSCLC cells. Adenosine Triphosphate 30-33 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 86-90 22673193-8 2012 In conclusion, silencing of Twist1 sensitizes lung cancer cells to cisplatin via stimulating AMPK-induced mTOR inhibition, leading to a reduction in Mcl-1 protein. Cisplatin 67-76 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 93-97 22330070-10 2012 We also showed that inhibition of PKCtheta by rottlerin or dominant negative PKCtheta reduced AMPK-mediated transcriptional activation of NF-AT and AP-1 in activated Jurkat cells. rottlerin 46-55 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 94-98 22670709-6 2012 Pterostilbene-activated AMPK decreased the activity and/or expression of lipogenic enzymes, such as fatty acid synthase (FASN) and acetyl-CoA carboxylase (ACC). pterostilbene 0-13 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 24-28 22717640-1 2012 The AMP-activated protein kinase (AMPK) is a pivotal serine/threonine kinase participating in the regulation of glucose, lipid as well as protein metabolism and maintenance of energy homeostasis. Glucose 112-119 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 4-32 22717640-1 2012 The AMP-activated protein kinase (AMPK) is a pivotal serine/threonine kinase participating in the regulation of glucose, lipid as well as protein metabolism and maintenance of energy homeostasis. Glucose 112-119 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 34-38 22717640-3 2012 In addition, the widely used antidiabetic metformin also exerts its anti-inflammatory effects through activating AMPK. Metformin 42-51 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 113-117 22311299-0 2012 Glucagon-like peptide 1 (GLP-1) can reverse AMP-activated protein kinase (AMPK) and S6 kinase (P70S6K) activities induced by fluctuations in glucose levels in hypothalamic areas involved in feeding behaviour. Glucose 141-148 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 44-72 22451512-0 2012 Deficiency in AMPK attenuates ethanol-induced cardiac contractile dysfunction through inhibition of autophagosome formation. Ethanol 30-37 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-18 22451512-5 2012 Ethanol exposure triggered glucose intolerance and compromised cardiac contraction accompanied by increased phosphorylation of AMPK and ACC as well as autophagosome accumulation (increased LC3II and p62), the effects of which were attenuated or mitigated by AMPK deficiency or inhibition. Ethanol 0-7 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 127-131 22451512-10 2012 CONCLUSION: In summary, these data suggest that ethanol exposure may trigger myocardial dysfunction through a mechanism associated with AMPK-mTORC1-ULK1-mediated autophagy. Ethanol 48-55 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 136-140 22370477-9 2012 LKB1 was recruited to the immunologic synapse, and induction of autophagy in DC required inhibition of mammalian target of rapamycine signaling by the LKB1-AMP activated protein kinase (AMPK) pathway. rapamycine 123-133 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 151-184 22370477-9 2012 LKB1 was recruited to the immunologic synapse, and induction of autophagy in DC required inhibition of mammalian target of rapamycine signaling by the LKB1-AMP activated protein kinase (AMPK) pathway. rapamycine 123-133 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 186-190 22467681-3 2012 Rosiglitazone stimulated adipose tissue mTOR complex 1 and AMPK and induced TAG-derived lipid uptake (136%), LPL mRNA/activity (2- to 6-fold), and fat accretion in subcutaneous (but not visceral) white adipose tissue (WAT; 50%) and in brown adipose tissue (BAT; 266%). Rosiglitazone 0-13 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 59-63 22389381-2 2012 Recent studies showed that the antidiabetic agent metformin decreases proliferation of cancer cells through 5"-AMP-activated protein kinase (AMPK)-dependent inhibition of mTOR. Metformin 50-59 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 141-145 22389381-9 2012 Metformin-inducible AMPK activation was noted only in TT cells. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 20-24 22244860-0 2012 Aspirin prevents resistin-induced endothelial dysfunction by modulating AMPK, ROS, and Akt/eNOS signaling. Aspirin 0-7 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 72-76 22244860-3 2012 We investigated whether aspirin mitigates resistin-induced endothelial dysfunction via modulation of reactive oxygen species (ROS) generation and explored the role that AMP-activated protein kinase (AMPK), a negative regulator of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, plays in the suppressive effects of aspirin on resistin-induced endothelial dysfunction. NAD 230-263 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 199-203 22311299-0 2012 Glucagon-like peptide 1 (GLP-1) can reverse AMP-activated protein kinase (AMPK) and S6 kinase (P70S6K) activities induced by fluctuations in glucose levels in hypothalamic areas involved in feeding behaviour. Glucose 141-148 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 74-78 22311299-2 2012 The brain activity of metabolic sensors such as AMP-activated protein kinase (AMPK) responds to changes in glucose levels. Glucose 107-114 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 48-76 22311299-2 2012 The brain activity of metabolic sensors such as AMP-activated protein kinase (AMPK) responds to changes in glucose levels. Glucose 107-114 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 78-82 22311299-5 2012 Therefore, we investigated the coordinated effects of glucose and GLP-1 on the expression and activity of AMPK and p70S6K in the areas involved in the control of feeding. Glucose 54-61 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 106-110 24298863-12 2012 Our results revealed that the activation of AMPK and S6K in VMH y LH occur in response to the changes of glucose concentrations or in the changes in the nutritional state, as well as GLP-1/exendin-4 act by counteracting the activation/inactivation of these kinases, which support a modulating role of these peptides on the kinases. Glucose 105-112 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 44-48 22274626-4 2012 By repressing a variety of genes involved in cholesterol export and fatty acid oxidation, including ABCA1, CROT, CPT1, HADHB and PRKAA1, miR-33a/b act in concert with their host genes to boost cellular sterol levels. Cholesterol 45-56 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 135-141 22274626-4 2012 By repressing a variety of genes involved in cholesterol export and fatty acid oxidation, including ABCA1, CROT, CPT1, HADHB and PRKAA1, miR-33a/b act in concert with their host genes to boost cellular sterol levels. Fatty Acids 68-78 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 135-141 22274626-4 2012 By repressing a variety of genes involved in cholesterol export and fatty acid oxidation, including ABCA1, CROT, CPT1, HADHB and PRKAA1, miR-33a/b act in concert with their host genes to boost cellular sterol levels. Sterols 50-56 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 135-141 21939670-0 2012 The adenosine derivative 2",3",5"-tri-O-acetyl-N6-(3-hydroxylaniline) adenosine activates AMPK and regulates lipid metabolism in vitro and in vivo. Adenosine 4-13 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 90-94 21939670-0 2012 The adenosine derivative 2",3",5"-tri-O-acetyl-N6-(3-hydroxylaniline) adenosine activates AMPK and regulates lipid metabolism in vitro and in vivo. 2",3",5"-tri-o-acetyl-n6-(3-hydroxylaniline) adenosine 25-79 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 90-94 21939670-1 2012 AIMS: Our overall objective was to investigate the effect of the adenosine derivative 2",3",5"-tri-O-acetyl-N6-(3-hydroxylaniline) adenosine (WS010117) on AMP-activated protein kinase (AMPK) activation and lipid metabolism and to also assess the underlying mechanisms involved in these processes. Adenosine 65-74 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 155-183 21939670-1 2012 AIMS: Our overall objective was to investigate the effect of the adenosine derivative 2",3",5"-tri-O-acetyl-N6-(3-hydroxylaniline) adenosine (WS010117) on AMP-activated protein kinase (AMPK) activation and lipid metabolism and to also assess the underlying mechanisms involved in these processes. Adenosine 65-74 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 185-189 21939670-1 2012 AIMS: Our overall objective was to investigate the effect of the adenosine derivative 2",3",5"-tri-O-acetyl-N6-(3-hydroxylaniline) adenosine (WS010117) on AMP-activated protein kinase (AMPK) activation and lipid metabolism and to also assess the underlying mechanisms involved in these processes. 2",3",5"-tri-o-acetyl-n6-(3-hydroxylaniline) adenosine 86-140 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 155-183 21939670-1 2012 AIMS: Our overall objective was to investigate the effect of the adenosine derivative 2",3",5"-tri-O-acetyl-N6-(3-hydroxylaniline) adenosine (WS010117) on AMP-activated protein kinase (AMPK) activation and lipid metabolism and to also assess the underlying mechanisms involved in these processes. 2",3",5"-tri-o-acetyl-n6-(3-hydroxylaniline) adenosine 86-140 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 185-189 21939670-1 2012 AIMS: Our overall objective was to investigate the effect of the adenosine derivative 2",3",5"-tri-O-acetyl-N6-(3-hydroxylaniline) adenosine (WS010117) on AMP-activated protein kinase (AMPK) activation and lipid metabolism and to also assess the underlying mechanisms involved in these processes. ws010117 142-150 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 155-183 21939670-1 2012 AIMS: Our overall objective was to investigate the effect of the adenosine derivative 2",3",5"-tri-O-acetyl-N6-(3-hydroxylaniline) adenosine (WS010117) on AMP-activated protein kinase (AMPK) activation and lipid metabolism and to also assess the underlying mechanisms involved in these processes. ws010117 142-150 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 185-189 21939670-6 2012 WS010117-induced AMPK activation was essentially abolished by treatment with compound C, and the addition of WS010117 did not alter the intracellular AMP:ATP ratio. ws010117 0-8 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 17-21 21939670-7 2012 In HeLa cells endogenously lacking LKB1, WS010117-mediated AMPK activation was not impaired, even following co-treatment with STO-609, a selective inhibitor of Ca(2+)/calmodulin-dependent protein kinase kinase (CaMKK). ws010117 41-49 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 59-63 22564965-1 2012 In this study we show that diindolylmethane (DIM) induces autophagy in ovarian cancer cells by regulating endoplasmic reticulum (ER) stress and AMPK. 3,3'-diindolylmethane 27-43 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 144-148 22564965-10 2012 DIM treatment increased the cytosolic calcium levels which lead to the activation of AMPK in our model. Calcium 38-45 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 85-89 22564965-11 2012 Chelating cytosolic calcium with BAPT-AM abrogated not only the phosphorylation of AMPK but also prevented DIM induced autophagy. Calcium 20-27 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 83-87 22564965-11 2012 Chelating cytosolic calcium with BAPT-AM abrogated not only the phosphorylation of AMPK but also prevented DIM induced autophagy. bapt-am 33-40 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 83-87 21971952-0 2012 Ginsenoside Re lowers blood glucose and lipid levels via activation of AMP-activated protein kinase in HepG2 cells and high-fat diet fed mice. Ginsenosides 0-11 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 83-111 22536280-6 2012 PRKAA1, HSPA8, and LSM6, which were related to fatty acid metabolism and the I-kappaB kinase/NF-kappaB cascade, were significant biomarkers of the TCM heat-pattern of RA. Fatty Acids 47-57 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-6 23118742-2 2012 Metabolic status plays an important role in the regulation of FGF21, and we therefore examined whether metformin, an indirect AMPK-activator, regulates FGF21 expression in hepatocytes. Metformin 103-112 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 126-130 23118742-6 2012 This effect was blocked by addition of the AMPK-inhibitor Compound C. The study shows that metformin is a potent inducer of hepatic FGF21 expression and that the effect of metformin seems to be mediated through AMPK activation. Metformin 91-100 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 43-47 23118742-6 2012 This effect was blocked by addition of the AMPK-inhibitor Compound C. The study shows that metformin is a potent inducer of hepatic FGF21 expression and that the effect of metformin seems to be mediated through AMPK activation. Metformin 172-181 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 43-47 23118742-6 2012 This effect was blocked by addition of the AMPK-inhibitor Compound C. The study shows that metformin is a potent inducer of hepatic FGF21 expression and that the effect of metformin seems to be mediated through AMPK activation. Metformin 172-181 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 211-215 21971952-8 2012 In conclusion, the current study suggest that ginsenoside Re improves hyperglycemia and hyperlipidemia through activation of AMPK, and confers beneficial effects on type 2 diabetic patients with insulin resistance and dyslipidemia. Ginsenosides 46-57 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 125-129 23029387-0 2012 Lovastatin induces multiple stress pathways including LKB1/AMPK activation that regulate its cytotoxic effects in squamous cell carcinoma cells. Lovastatin 0-10 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 59-63 22343549-8 2012 Metformin treatment blocked ghrelin-induced activation of hypothalamic AMPK/ACC/Raptor and restored mTOR activity without affecting S6K phosphorylation. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 71-75 22343549-9 2012 Metformin also reduced food consumption induced by the AMPK activator AICAR while the ghrelin-triggered food intake was inhibited by the mTOR activator L-leucine. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 55-59 22343549-10 2012 CONCLUSION: Metformin could reduce food intake by preventing ghrelin-induced AMPK signalling and mTOR inhibition in the hypotalamus. Metformin 12-21 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 77-81 23155420-0 2012 Cross regulation of sirtuin 1, AMPK, and PPARgamma in conjugated linoleic acid treated adipocytes. Linoleic Acid 65-78 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 31-35 23155420-1 2012 Trans-10, cis-12 conjugated linoleic acid (t10c12 CLA) reduces triglyceride (TG) levels in adipocytes through multiple pathways, with AMP-activated protein kinase (AMPK) generally facilitating, and peroxisome proliferator-activated receptor gamma (PPARgamma) generally opposing these reductions. Linoleic Acid 28-41 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 134-162 23155420-1 2012 Trans-10, cis-12 conjugated linoleic acid (t10c12 CLA) reduces triglyceride (TG) levels in adipocytes through multiple pathways, with AMP-activated protein kinase (AMPK) generally facilitating, and peroxisome proliferator-activated receptor gamma (PPARgamma) generally opposing these reductions. Linoleic Acid 28-41 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 164-168 23029387-3 2012 METHODOLOGY/PRINCIPAL FINDINGS: In this study, we evaluated the effects of lovastatin on the activity of the LKB1/AMPK pathway that is activated upon cellular energy shortage and can interact with the above pathways. Lovastatin 75-85 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 114-118 23029387-4 2012 In the squamous cell carcinoma (SCC) cell lines SCC9 and SCC25, lovastatin treatment (1-25 microM, 24 hrs) induced LKB1 and AMPK activation similar to metformin (1-10 mM, 24 hrs), a known inducer of this pathway. Lovastatin 64-74 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 124-128 23029387-5 2012 Lovastatin treatment impaired mitochondrial function and also decreased cellular ADP/ATP ratios, common triggers of LKB1/AMPK activation. Lovastatin 0-10 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 121-125 23029387-10 2012 CONCLUSION/SIGNIFICANCE: Thus, targeting multiple metabolic stress pathways including the LKB1/AMPK pathway enhances lovastatin"s ability to synergize with gefitinib in SCC cells. Lovastatin 117-127 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 95-99 22363791-7 2012 SESN2 overexpression was achieved using a Flag-tagged SESN2 expression vector or a stably-integrated tetracycline-inducible system, which also increased AMPKalpha1 and AMPKbeta1 subunit phosphorylation, and co-localized with phosphorylated AMPKalpha-Thr127 in the cytoplasm. Tetracycline 101-113 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 153-163 22359576-1 2012 AMPK, a master metabolic switch, mediates the observed increase of glucose uptake in locomotory muscle of mammals during exercise. Glucose 67-74 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 22359576-2 2012 AMPK is activated by changes in the intracellular AMP:ATP ratio when ATP consumption is stimulated by contractile activity but also by AICAR and metformin, compounds that increase glucose transport in mammalian muscle cells. Adenosine Triphosphate 54-57 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 22359576-2 2012 AMPK is activated by changes in the intracellular AMP:ATP ratio when ATP consumption is stimulated by contractile activity but also by AICAR and metformin, compounds that increase glucose transport in mammalian muscle cells. Adenosine Triphosphate 69-72 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 22359576-2 2012 AMPK is activated by changes in the intracellular AMP:ATP ratio when ATP consumption is stimulated by contractile activity but also by AICAR and metformin, compounds that increase glucose transport in mammalian muscle cells. AICA ribonucleotide 135-140 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 22359576-2 2012 AMPK is activated by changes in the intracellular AMP:ATP ratio when ATP consumption is stimulated by contractile activity but also by AICAR and metformin, compounds that increase glucose transport in mammalian muscle cells. Metformin 145-154 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 22359576-2 2012 AMPK is activated by changes in the intracellular AMP:ATP ratio when ATP consumption is stimulated by contractile activity but also by AICAR and metformin, compounds that increase glucose transport in mammalian muscle cells. Glucose 180-187 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 22359576-5 2012 We show that AICAR and metformin significantly stimulated glucose uptake (1.6 and 1.3 fold, respectively) and that Compound C completely abrogated the stimulatory effects of the AMPK activators on glucose uptake. AICA ribonucleotide 13-18 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 178-182 22359576-5 2012 We show that AICAR and metformin significantly stimulated glucose uptake (1.6 and 1.3 fold, respectively) and that Compound C completely abrogated the stimulatory effects of the AMPK activators on glucose uptake. Glucose 58-65 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 178-182 22359576-5 2012 We show that AICAR and metformin significantly stimulated glucose uptake (1.6 and 1.3 fold, respectively) and that Compound C completely abrogated the stimulatory effects of the AMPK activators on glucose uptake. Glucose 197-204 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 178-182 22359576-7 2012 Moreover, exposure of trout myotubes to AICAR and metformin resulted in an increase in AMPK activity (3.8 and 3 fold, respectively). Metformin 50-59 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 87-91 22359576-8 2012 We also provide evidence suggesting that stimulation of glucose uptake by AMPK activators in trout myotubes may take place, at least in part, by increasing the cell surface and mRNA levels of trout GLUT4. Glucose 56-63 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 74-78 21918180-8 2011 Thus, phenformin and resveratrol caused a strong activation of AMPK in the cytoplasm, whereas the effect was less pronounced in nuclei. Phenformin 6-16 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 63-67 22359576-10 2012 Therefore, we provide evidence, for the first time in non-mammalian vertebrates, suggesting a potentially important role of AMPK in stimulating glucose uptake and utilization in the skeletal muscle of fish. Glucose 144-151 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 124-128 22001597-0 2011 ICAM-1 and AMPK regulate cell detachment and apoptosis by N-methyl-N"-nitro-N-nitrosoguanidine, a widely spread environmental chemical, in human hormone-refractory prostate cancers. Methylnitronitrosoguanidine 58-94 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 11-15 22532801-3 2012 We found that the energy regulator AMPK, which potently inhibits fatty acid synthesis, restricts infection of the Bunyavirus, Rift Valley Fever Virus (RVFV), an important re-emerging arthropod-borne human pathogen for which there are no effective vaccines or therapeutics. Fatty Acids 65-75 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 35-39 22532801-5 2012 Furthermore, we found that AMPK is activated during RVFV infection, leading to the phosphorylation and inhibition of acetyl-CoA carboxylase, the first rate-limiting enzyme in fatty acid synthesis. Fatty Acids 175-185 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 27-31 22532801-7 2012 This restriction could be bypassed by treatment with the fatty acid palmitate, demonstrating that AMPK restricts RVFV infection through its inhibition of fatty acid biosynthesis. fatty acid palmitate 57-77 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 98-102 22532801-7 2012 This restriction could be bypassed by treatment with the fatty acid palmitate, demonstrating that AMPK restricts RVFV infection through its inhibition of fatty acid biosynthesis. Fatty Acids 57-67 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 98-102 22532801-9 2012 Therefore, AMPK is an important component of the cell intrinsic immune response that restricts infection through a novel mechanism involving the inhibition of fatty acid metabolism. Fatty Acids 159-169 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 11-15 22119190-2 2011 Carbonyl cyanide m-chlorophenylhydrazone (CCCP), a mitochondrial uncoupler, leads to AMPK activation and Parkin-dependent mitophagy, respectively. Carbonyl Cyanide m-Chlorophenyl Hydrazone 0-40 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 85-89 22119190-2 2011 Carbonyl cyanide m-chlorophenylhydrazone (CCCP), a mitochondrial uncoupler, leads to AMPK activation and Parkin-dependent mitophagy, respectively. Carbonyl Cyanide m-Chlorophenyl Hydrazone 42-46 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 85-89 22119190-5 2011 Using wild type (WT) and AMPKalpha1/alpha2 double knockout (DKO) MEFs, we observed that CCCP promotes endogenous LC3 lipidation and formation of RFP-LC3 puncta, indicating autophagosome or autolysosome, in an AMPK-independent manner. Carbonyl Cyanide m-Chlorophenyl Hydrazone 88-92 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 25-35 22119190-5 2011 Using wild type (WT) and AMPKalpha1/alpha2 double knockout (DKO) MEFs, we observed that CCCP promotes endogenous LC3 lipidation and formation of RFP-LC3 puncta, indicating autophagosome or autolysosome, in an AMPK-independent manner. Carbonyl Cyanide m-Chlorophenyl Hydrazone 88-92 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 25-29 21918180-8 2011 Thus, phenformin and resveratrol caused a strong activation of AMPK in the cytoplasm, whereas the effect was less pronounced in nuclei. Resveratrol 21-32 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 63-67 21947382-7 2011 Accordingly, metformin only increased AMPKalpha1 activity in human hepatocytes, although both AMPKalpha isoforms were activated in rat hepatocytes. Metformin 13-22 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 38-48 21344388-8 2011 Curcumin reversed Tat-mediated reduction in AMPK activation and downstream acetyl-CoA carboxylase (ACC) activation. Curcumin 0-8 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 44-48 21344388-9 2011 Collectively, our data provide new insights into understanding of the molecular mechanisms of curcumin inhibited Tat-regulated transcription, suggesting that targeting AMPK/HDAC1/NFkappaB pathway could serve as new anti-HIV-1 agents. Curcumin 94-102 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 168-172 22249159-7 2011 The potential for future clinical-translational applications of AMPK activators such as AICAR, metformin and resveratrol for the treatment of chronic myelogenous leukemia (CML) and Ph+ acute lymphoblastic leukemia (ALL) are discussed. Metformin 95-104 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 64-68 22249159-7 2011 The potential for future clinical-translational applications of AMPK activators such as AICAR, metformin and resveratrol for the treatment of chronic myelogenous leukemia (CML) and Ph+ acute lymphoblastic leukemia (ALL) are discussed. Resveratrol 109-120 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 64-68 21689749-5 2011 Results demonstrate that estradiol causes a dose-dependent decrease in LKB1 transcript and protein expression and consistent with this, a significant decrease in the phosphorylation of the LKB1 target AMPK (P <= 0.05). Estradiol 25-34 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 201-205 21836066-0 2011 C1q/TNF-related proteins, a family of novel adipokines, induce vascular relaxation through the adiponectin receptor-1/AMPK/eNOS/nitric oxide signaling pathway. Nitric Oxide 128-140 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 118-122 21945951-2 2011 A reduced supply of energy at the cellular level leads to an increased concentration of AMP, which, in turn, results in LKB1-mediated activation of the AMPK kinase. Adenosine Monophosphate 88-91 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 152-156 21750268-0 2011 Homocysteine suppresses lipolysis in adipocytes by activating the AMPK pathway. Homocysteine 0-12 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 66-70 21896783-0 2011 IRE1-dependent activation of AMPK in response to nitric oxide. Nitric Oxide 49-61 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 29-33 21896783-3 2011 Nitric oxide is a potent activator of AMP-activated protein kinase (AMPK), and AMPK participates in the cellular defense against nitric oxide-mediated damage in pancreatic beta-cells. Nitric Oxide 0-12 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 38-66 21896783-3 2011 Nitric oxide is a potent activator of AMP-activated protein kinase (AMPK), and AMPK participates in the cellular defense against nitric oxide-mediated damage in pancreatic beta-cells. Nitric Oxide 0-12 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 68-72 21896783-3 2011 Nitric oxide is a potent activator of AMP-activated protein kinase (AMPK), and AMPK participates in the cellular defense against nitric oxide-mediated damage in pancreatic beta-cells. Nitric Oxide 129-141 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 79-83 21896783-4 2011 In this study, the mechanism of AMPK activation by nitric oxide was explored. Nitric Oxide 51-63 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 32-36 21896783-7 2011 Nitric oxide-induced AMPK phosphorylation and subsequent signaling to AMPK substrates, including Raptor, acetyl coenzyme A carboxylase, and PGC-1alpha, is attenuated in IRE1alpha-deficient cells. Nitric Oxide 0-12 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 21-25 21896783-7 2011 Nitric oxide-induced AMPK phosphorylation and subsequent signaling to AMPK substrates, including Raptor, acetyl coenzyme A carboxylase, and PGC-1alpha, is attenuated in IRE1alpha-deficient cells. Nitric Oxide 0-12 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 70-74 21896783-8 2011 The endoribonuclease activity of IRE1 appears to be required for AMPK activation in response to nitric oxide. Nitric Oxide 96-108 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 65-69 21896783-9 2011 In addition to nitric oxide, stimulation of IRE1 endoribonuclease activity with the flavonol quercetin leads to IRE1-dependent AMPK activation. Nitric Oxide 15-27 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 127-131 21896783-9 2011 In addition to nitric oxide, stimulation of IRE1 endoribonuclease activity with the flavonol quercetin leads to IRE1-dependent AMPK activation. 3-hydroxyflavone 84-92 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 127-131 21896783-9 2011 In addition to nitric oxide, stimulation of IRE1 endoribonuclease activity with the flavonol quercetin leads to IRE1-dependent AMPK activation. Quercetin 93-102 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 127-131 21873433-2 2011 We hypothesized that gene silencing of NT5 enzymes to increase the intracellular availability of AMP would increase AMP-activated protein kinase (AMPK) activity and metabolism. Adenosine Monophosphate 97-100 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 116-144 21873433-2 2011 We hypothesized that gene silencing of NT5 enzymes to increase the intracellular availability of AMP would increase AMP-activated protein kinase (AMPK) activity and metabolism. Adenosine Monophosphate 97-100 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 146-150 21873433-4 2011 Using siRNA to silence NT5C2 expression in cultured human myotubes, we observed a 2-fold increase in the AMP/ATP ratio, a 2.4-fold increase in AMPK phosphorylation (Thr(172)), and a 2.8-fold increase in acetyl-CoA carboxylase phosphorylation (Ser(79)) (p < 0.05). Threonine 165-168 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 143-147 22012398-8 2011 Notably, miR-33 antagonism in this non-human primate model also increased the expression of miR-33 target genes involved in fatty acid oxidation (CROT, CPT1A, HADHB and PRKAA1) and reduced the expression of genes involved in fatty acid synthesis (SREBF1, FASN, ACLY and ACACA), resulting in a marked suppression of the plasma levels of very-low-density lipoprotein (VLDL)-associated triglycerides, a finding that has not previously been observed in mice. Fatty Acids 124-134 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 169-175 21750268-8 2011 However, Hcy increased phosphorylation levels of AMP-activated protein kinase (AMPK) and its downstream enzyme acetyl-CoA carboxylase. Homocysteine 9-12 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 49-77 21750268-8 2011 However, Hcy increased phosphorylation levels of AMP-activated protein kinase (AMPK) and its downstream enzyme acetyl-CoA carboxylase. Homocysteine 9-12 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 79-83 21750268-9 2011 Compound C, an AMPK inhibitor, abolished Hcy-induced reduction of glycerol and FFA release under both basal and isoproterenol-stimulated conditions. Homocysteine 41-44 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 15-19 21750268-9 2011 Compound C, an AMPK inhibitor, abolished Hcy-induced reduction of glycerol and FFA release under both basal and isoproterenol-stimulated conditions. Glycerol 66-74 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 15-19 21750268-10 2011 Furthermore, AMPKalpha1 siRNA reversed Hcy-inhibited glycerol release. Homocysteine 39-42 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 13-23 21750268-10 2011 Furthermore, AMPKalpha1 siRNA reversed Hcy-inhibited glycerol release. Glycerol 53-61 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 13-23 21750268-13 2011 These results show that Hcy inhibits lipolysis through a pathway that involves AMPK activation. Homocysteine 24-27 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 79-83 21680893-4 2011 PMVECs selectively express the AMPKalpha1 catalytic subunit, pharmacological and short hairpin RNA-mediated inhibition of which attenuates Ca(2+) entry in these cells induced by the inflammatory Ca(2+)-signaling mimetic thapsigargin. Thapsigargin 220-232 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 31-41 21338323-6 2011 AMPKalpha1 is involved in metformin-induced HSL phosphorylation at Ser-552. Metformin 26-35 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-10 21338323-6 2011 AMPKalpha1 is involved in metformin-induced HSL phosphorylation at Ser-552. Serine 67-70 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-10 21831529-0 2011 Spermidine may decrease ER stress in pancreatic beta cells and may reduce apoptosis via activating AMPK dependent autophagy pathway. Spermidine 0-10 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 99-103 21831529-10 2011 Hence either inhibition of mTOR or activation of AMPK by spermidine will play two crucial roles, first being the activation of autophagy and secondly the reduction of endoplasmic reticulum stress which will reduce beta cell death by apoptosis and thus can be a novel therapeutic candidate in the treatment of insulin resistance in type 2 diabetes and preserving pancreatic beta cell mass. Spermidine 57-67 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 49-53 21717584-1 2011 It has been reported that metformin, a biguanide derivative widely used in type II diabetic patients, has antitumor activities in some cancers by activation of AMP-activated protein kinase (AMPK). Metformin 26-35 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 160-188 21884681-1 2011 We found that a natural product, Sanguinarine, directly interacts with AMPK and enhances its enzymatic activity. sanguinarine 33-45 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 71-75 21884681-2 2011 Cell-based assays confirmed that cellular AMPK and the downstream acetyl-CoA carboxylase (ACC) were phosphorylated after Sanguinarine treatment. sanguinarine 121-133 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 42-46 21884681-3 2011 Sanguinarine was shown to exclusively activate AMPK holoenzymes containing alpha1gamma1 complexes, and it activated both beta1- and beta2-containing isotypes of AMPK. sanguinarine 0-12 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 47-51 21884681-3 2011 Sanguinarine was shown to exclusively activate AMPK holoenzymes containing alpha1gamma1 complexes, and it activated both beta1- and beta2-containing isotypes of AMPK. sanguinarine 0-12 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 161-165 21884681-4 2011 Furthermore, a docking study suggested that Sanguinarine binds AMPK at the cleft between the beta and gamma domains whereas the physiological activator, AMP, binds at the well-characterized gamma domain pocket. sanguinarine 44-56 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 63-67 21884681-5 2011 In summary, we report that Sanguinarine is a novel, direct activator of AMPK that binds by a unique allosteric mechanism different from that of the natural AMPK ligand, AMP, and other known AMPK activators. sanguinarine 27-39 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 72-76 21884681-5 2011 In summary, we report that Sanguinarine is a novel, direct activator of AMPK that binds by a unique allosteric mechanism different from that of the natural AMPK ligand, AMP, and other known AMPK activators. sanguinarine 27-39 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 156-160 21884681-5 2011 In summary, we report that Sanguinarine is a novel, direct activator of AMPK that binds by a unique allosteric mechanism different from that of the natural AMPK ligand, AMP, and other known AMPK activators. sanguinarine 27-39 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 156-160 21907923-2 2011 Reduced AMPK levels lead to diminished expression of the DMT1 iron transporter, and the resulting cytosolic iron deficiency activates the iron regulatory proteins, IRP1 and IRP2, and increases expression of the hypoxia inducible factor HIF-1alpha, but not HIF-2alpha. Iron 108-112 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 8-12 21168492-7 2011 In parallel, IGF-II increases phosphorylation of AKT and p70S6K, while metformin increases AMPK phosphorylation and decreases p70S6K phosphorylation. Metformin 71-80 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 91-95 21168492-8 2011 The effects of metformin on PR A/B and p70S6K are partially reversed by an AMPK inhibitor. Metformin 15-24 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 75-79 21602475-1 2011 The AMP-activated protein kinase (AMPK) is known to increase cardiac insulin sensitivity on glucose uptake. Glucose 92-99 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 4-32 21602475-1 2011 The AMP-activated protein kinase (AMPK) is known to increase cardiac insulin sensitivity on glucose uptake. Glucose 92-99 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 34-38 21602475-6 2011 The stimulation of glucose uptake by AMPK activators and insulin correlated with AMPK and protein kinase B (PKB/Akt) activation, respectively. Glucose 19-26 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 37-41 21602475-6 2011 The stimulation of glucose uptake by AMPK activators and insulin correlated with AMPK and protein kinase B (PKB/Akt) activation, respectively. Glucose 19-26 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 81-85 21602475-8 2011 Together, insulin and AMPK activators acted synergistically to induce PKB/Akt overactivation, AS160 overphosphorylation, and glucose uptake overstimulation. Glucose 125-132 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 22-26 21602475-11 2011 Mimicking AMPK activators in the presence of insulin, rapamycin inhibited p70S6K and reduced IRS-1 phosphorylation on serine, resulting in the overphosphorylation of PKB/Akt and AS160. Sirolimus 54-63 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 10-14 21602475-11 2011 Mimicking AMPK activators in the presence of insulin, rapamycin inhibited p70S6K and reduced IRS-1 phosphorylation on serine, resulting in the overphosphorylation of PKB/Akt and AS160. Serine 118-124 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 10-14 21602475-13 2011 In conclusion, although the insulin-sensitizing effect of AMPK on PKB/Akt is explained by the inhibition of the insulin-induced negative feedback loop, its effect on glucose uptake is independent of this mechanism. Glucose 166-173 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 58-62 21907923-1 2011 Inactivation of the TCA cycle enzyme, fumarate hydratase (FH), drives a metabolic shift to aerobic glycolysis in FH-deficient kidney tumors and cell lines from patients with hereditary leiomyomatosis renal cell cancer (HLRCC), resulting in decreased levels of AMP-activated kinase (AMPK) and p53 tumor suppressor, and activation of the anabolic factors, acetyl-CoA carboxylase and ribosomal protein S6. Trichloroacetic Acid 20-23 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 260-280 21907923-1 2011 Inactivation of the TCA cycle enzyme, fumarate hydratase (FH), drives a metabolic shift to aerobic glycolysis in FH-deficient kidney tumors and cell lines from patients with hereditary leiomyomatosis renal cell cancer (HLRCC), resulting in decreased levels of AMP-activated kinase (AMPK) and p53 tumor suppressor, and activation of the anabolic factors, acetyl-CoA carboxylase and ribosomal protein S6. Trichloroacetic Acid 20-23 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 282-286 21907923-2 2011 Reduced AMPK levels lead to diminished expression of the DMT1 iron transporter, and the resulting cytosolic iron deficiency activates the iron regulatory proteins, IRP1 and IRP2, and increases expression of the hypoxia inducible factor HIF-1alpha, but not HIF-2alpha. Iron 62-66 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 8-12 21717584-1 2011 It has been reported that metformin, a biguanide derivative widely used in type II diabetic patients, has antitumor activities in some cancers by activation of AMP-activated protein kinase (AMPK). Metformin 26-35 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 190-194 21717584-1 2011 It has been reported that metformin, a biguanide derivative widely used in type II diabetic patients, has antitumor activities in some cancers by activation of AMP-activated protein kinase (AMPK). Biguanides 39-48 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 160-188 21717584-1 2011 It has been reported that metformin, a biguanide derivative widely used in type II diabetic patients, has antitumor activities in some cancers by activation of AMP-activated protein kinase (AMPK). Biguanides 39-48 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 190-194 21717584-5 2011 Metformin also induced the phosphorylation of AMPK (T172) in a time-dependent manner. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 46-50 21717584-6 2011 Mammalian target of rapamycin complex 1 (mTORC1), which is negatively regulated by AMPK and plays a central role in cell growth and proliferation, was inhibited by metformin, as manifested by dephosphorylation of its downstream targets 40S ribosomal S6 kinase 1 (S6K1) (T389), the eukaryotic translation initiation factor 4E (eIF4E)-binding protein 1 (4E-BP1) (T37/46) and S6 (S235/236) in C666-1 cells. Metformin 164-173 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 83-87 21570709-2 2011 Glucose deprivation results in diminished intracellular ATP; this is counteracted by AMPK activation during energy deficiency to restore ATP levels. Adenosine Triphosphate 56-59 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 85-89 21570709-2 2011 Glucose deprivation results in diminished intracellular ATP; this is counteracted by AMPK activation during energy deficiency to restore ATP levels. Adenosine Triphosphate 137-140 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 85-89 21570709-13 2011 Because ovarian cancer cells are dependent upon glucose for growth and survival, treatment with AMPK activators that mimic glucose deprivation may result in broad clinical benefits to ovarian cancer patients. Glucose 48-55 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 96-100 21994478-4 2011 Treatment with cilostazol increased HO-1 expression and phosphorylation of AMPK in a dose- and time-dependent manner. Cilostazol 15-25 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 75-79 21994478-0 2011 Cilostazol Inhibits Vascular Smooth Muscle Cell Proliferation and Reactive Oxygen Species Production through Activation of AMP-activated Protein Kinase Induced by Heme Oxygenase-1. Cilostazol 0-10 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 123-151 21994478-5 2011 Cilostazol also significantly decreased platelet-derived growth factor (PDGF)-induced VSMC proliferation and ROS production by activating AMPK induced by HO-1. Cilostazol 0-10 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 138-142 21994478-5 2011 Cilostazol also significantly decreased platelet-derived growth factor (PDGF)-induced VSMC proliferation and ROS production by activating AMPK induced by HO-1. vsmc 86-90 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 138-142 21994478-6 2011 Pharmacological and genetic inhibition of HO-1 and AMPK blocked the cilostazol-induced inhibition of cell proliferation and ROS production.These data suggest that cilostazol-induced HO-1 expression and AMPK activation might attenuate PDGF-induced VSMC proliferation and ROS production. Cilostazol 68-78 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 51-55 21994478-6 2011 Pharmacological and genetic inhibition of HO-1 and AMPK blocked the cilostazol-induced inhibition of cell proliferation and ROS production.These data suggest that cilostazol-induced HO-1 expression and AMPK activation might attenuate PDGF-induced VSMC proliferation and ROS production. Cilostazol 68-78 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 202-206 21994478-6 2011 Pharmacological and genetic inhibition of HO-1 and AMPK blocked the cilostazol-induced inhibition of cell proliferation and ROS production.These data suggest that cilostazol-induced HO-1 expression and AMPK activation might attenuate PDGF-induced VSMC proliferation and ROS production. Reactive Oxygen Species 124-127 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 51-55 21994478-6 2011 Pharmacological and genetic inhibition of HO-1 and AMPK blocked the cilostazol-induced inhibition of cell proliferation and ROS production.These data suggest that cilostazol-induced HO-1 expression and AMPK activation might attenuate PDGF-induced VSMC proliferation and ROS production. Cilostazol 163-173 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 51-55 21994478-6 2011 Pharmacological and genetic inhibition of HO-1 and AMPK blocked the cilostazol-induced inhibition of cell proliferation and ROS production.These data suggest that cilostazol-induced HO-1 expression and AMPK activation might attenuate PDGF-induced VSMC proliferation and ROS production. Cilostazol 163-173 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 202-206 21994478-6 2011 Pharmacological and genetic inhibition of HO-1 and AMPK blocked the cilostazol-induced inhibition of cell proliferation and ROS production.These data suggest that cilostazol-induced HO-1 expression and AMPK activation might attenuate PDGF-induced VSMC proliferation and ROS production. Reactive Oxygen Species 270-273 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 51-55 21602274-5 2011 The present study investigated whether LPA could induce AMPK activation and whether this process was associated with cell migration in ovarian cancer cells. lysophosphatidic acid 39-42 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 56-60 21602274-6 2011 We found that LPA led to a striking increase in AMPK phosphorylation in pathways involving the phospholipase C-beta3 (PLC-beta3) and calcium/calmodulin-dependent protein kinase kinase beta (CaMKKbeta) in SKOV3 ovarian cancer cells. lysophosphatidic acid 14-17 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 48-52 21602274-7 2011 siRNA-mediated knockdown of AMPKalpha1, PLC-beta3, or (CaMKKbeta) impaired the stimulatory effects of LPA on cell migration. lysophosphatidic acid 102-105 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 28-38 21602274-8 2011 Furthermore, we found that knockdown of AMPKalpha1 abrogated LPA-induced activation of the small GTPase RhoA and ezrin/radixin/moesin proteins regulating membrane dynamics as membrane-cytoskeleton linkers. lysophosphatidic acid 61-64 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 40-50 21602274-10 2011 Taken together, our results suggest that activation of AMPK by LPA induces cell migration through the signaling pathway to cytoskeletal dynamics and increases tumor metastasis in ovarian cancer. lysophosphatidic acid 63-66 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 55-59 21572254-2 2011 Besides the discovery of somatic mutations in the LKB1 gene in certain type of cancers, a critical emerging point was that the LKB1/AMPK axis remains generally functional and could be stimulated by pharmacological molecules such as metformin in cancer cells. Metformin 232-241 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 132-136 21460634-4 2011 AMP-activated protein kinase (AMPK), which is activated by LKB1/Strad/Mo25 upon high AMP levels, stimulates autophagy by inhibiting mTORC1. Adenosine Monophosphate 0-3 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-34 21540236-0 2011 Metformin, independent of AMPK, induces mTOR inhibition and cell-cycle arrest through REDD1. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 26-30 21572254-4 2011 Further basic research work should be conducted to elucidate the molecular targets of LKB1/AMPK responsible for its anti-tumor activity in parallel of conducting clinical trials using metformin, AICAR or new AMPK activating agents to explore the potential of the LKB1/AMPK signaling pathway as a new target for anticancer drug development. Metformin 184-193 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 91-95 21460621-3 2011 Our laboratories recently discovered that AMPK associates with, and directly phosphorylates, ULK1 on several sites and this modification is required for ULK1 activation after glucose deprivation. Glucose 175-182 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 42-46 21536037-0 2011 Activation of AMPK by berberine promotes adiponectin multimerization in 3T3-L1 adipocytes. Berberine 22-31 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-18 21536037-4 2011 Berberine activates AMPK. Berberine 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 20-24 21536037-5 2011 Knockdown of AMPKalpha1 abolishes the effect of berberine. Berberine 48-57 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 13-23 21536037-7 2011 Our study suggested that activation of AMPK by berberine promotes adiponectin multimerization. Berberine 47-56 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 39-43 21217782-4 2011 Recently, we have reported that mRNA levels of LITAF and TNF superfamily member 15 (TNFSF15) are upregulated by 5" adenosine monophosphate (AMP)-activated protein kinase (AMPK). Adenosine Monophosphate 112-138 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 171-175 21217782-4 2011 Recently, we have reported that mRNA levels of LITAF and TNF superfamily member 15 (TNFSF15) are upregulated by 5" adenosine monophosphate (AMP)-activated protein kinase (AMPK). Adenosine Monophosphate 140-143 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 171-175 21217782-6 2011 Thus, we show that 5-aminoimidazole-4-carboxamide ribonucleoside (AICAR), a pharmacological activator of AMPK, increases the abundance of LITAF and TNFSF15 in LNCaP and C4-2 prostate cancer cells, which is abrogated by small hairpin RNA (shRNA) or the dominant-negative mutant of AMPK alpha1 subunit. acadesine 19-64 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 105-109 21217782-6 2011 Thus, we show that 5-aminoimidazole-4-carboxamide ribonucleoside (AICAR), a pharmacological activator of AMPK, increases the abundance of LITAF and TNFSF15 in LNCaP and C4-2 prostate cancer cells, which is abrogated by small hairpin RNA (shRNA) or the dominant-negative mutant of AMPK alpha1 subunit. acadesine 19-64 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 280-291 21217782-6 2011 Thus, we show that 5-aminoimidazole-4-carboxamide ribonucleoside (AICAR), a pharmacological activator of AMPK, increases the abundance of LITAF and TNFSF15 in LNCaP and C4-2 prostate cancer cells, which is abrogated by small hairpin RNA (shRNA) or the dominant-negative mutant of AMPK alpha1 subunit. acadesine 66-71 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 105-109 21217782-6 2011 Thus, we show that 5-aminoimidazole-4-carboxamide ribonucleoside (AICAR), a pharmacological activator of AMPK, increases the abundance of LITAF and TNFSF15 in LNCaP and C4-2 prostate cancer cells, which is abrogated by small hairpin RNA (shRNA) or the dominant-negative mutant of AMPK alpha1 subunit. acadesine 66-71 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 280-291 21436046-6 2011 However, we found that application of metformin or AICAR, potent AMPK activators, inhibit axogenesis and axon growth in an AMPK-dependent manner. Metformin 38-47 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 65-69 21459332-1 2011 AMP-activated protein kinase (AMPK) is activated when the AMP/ATP ratio in cells is elevated due to energy stress. Adenosine Monophosphate 0-3 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-34 21459332-1 2011 AMP-activated protein kinase (AMPK) is activated when the AMP/ATP ratio in cells is elevated due to energy stress. Adenosine Triphosphate 62-65 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-34 21459332-4 2011 Interestingly, we found that AMPK activation is confined to the cytosol in response to energy stress but can be observed in both the cytosol and nucleus in response to calcium elevation. Calcium 168-175 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 29-33 21396365-1 2011 The LKB1 and AMPK proteins participate in an energy sensing cascade that responds to depletion of ATP, serving as a master regulator of metabolism that inhibits anabolic processes and stimulates catabolic processes. Adenosine Triphosphate 98-101 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 13-17 21436046-6 2011 However, we found that application of metformin or AICAR, potent AMPK activators, inhibit axogenesis and axon growth in an AMPK-dependent manner. Metformin 38-47 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 123-127 21314123-4 2011 We also found that liver kinase B1 (LKB1)/AMP-activated protein kinase (AMPK) signaling is a critical mediator of alpha-mangostin-induced inhibition of cell growth. mangostin 114-129 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 72-76 21427236-6 2011 On the other hand, HGF-induced LKB1/AMPK activation has been found to play a critical role in controlling Hu antigen R cytosolic localization and endothelial nitric oxide synthase activation, and consequently Cyclin D1 and Cyclin A expressions, and nitric oxide generation, respectively. Nitric Oxide 158-170 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 36-40 21274505-6 2011 Furthermore, activation of p53 and AMPK was detected in etoposide-treated cells and inhibition of AMPK triggered apoptosis through suppression of autophagy. Etoposide 56-65 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 35-39 21274505-9 2011 Moreover, AMPK activation is clearly associated with etoposide-induced autophagy. Etoposide 53-62 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 10-14 21314123-5 2011 Activation of AMPK induces alpha-mangostin-mediated phosphorylation of raptor, which subsequently associates with 14-3-3gamma and results in the loss of mTORC1 activity. mangostin 27-42 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-18 21314123-7 2011 Furthermore, the inhibition of AMPK expression with shRNAs or an inhibitor of AMPK reduced alpha-mangostin-induced autophagy and raptor phosphorylation, supporting the theory that activation of AMPK is beneficial to autophagy. mangostin 91-106 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 31-35 21314123-7 2011 Furthermore, the inhibition of AMPK expression with shRNAs or an inhibitor of AMPK reduced alpha-mangostin-induced autophagy and raptor phosphorylation, supporting the theory that activation of AMPK is beneficial to autophagy. mangostin 91-106 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 78-82 21314123-7 2011 Furthermore, the inhibition of AMPK expression with shRNAs or an inhibitor of AMPK reduced alpha-mangostin-induced autophagy and raptor phosphorylation, supporting the theory that activation of AMPK is beneficial to autophagy. mangostin 91-106 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 78-82 21314123-9 2011 Together, these results suggest a critical role for AMPK activation in the alpha-mangostin-induced autophagy of human glioblastoma cells. mangostin 75-90 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 52-56 21209024-0 2011 Phosphorylation and activation of AMP-activated protein kinase (AMPK) by metformin in the human ovary requires insulin. Metformin 73-82 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 34-62 21209024-0 2011 Phosphorylation and activation of AMP-activated protein kinase (AMPK) by metformin in the human ovary requires insulin. Metformin 73-82 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 64-68 21209024-4 2011 We investigated whether metformin activates AMPK in the human ovary by looking for changes in phosphorylation of AMPK and its downstream target acetyl CoA carboxylase (ACC). Metformin 24-33 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 44-48 21209024-8 2011 The addition of compound C, an inhibitor of AMPK, negated the effect of metformin in the presence of insulin on pAMPK. Metformin 72-81 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 44-48 21258367-6 2011 Under glucose starvation, AMPK promotes autophagy by directly activating Ulk1 through phosphorylation of Ser 317 and Ser 777. Glucose 6-13 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 26-30 21054339-0 2011 Metformin inhibits P-glycoprotein expression via the NF-kappaB pathway and CRE transcriptional activity through AMPK activation. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 112-116 21054339-9 2011 The suppression of MDR1 promoter activity and protein expression was mediated through metformin-induced activation of AMP-activated protein kinase (AMPK). Metformin 86-95 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 118-146 21054339-9 2011 The suppression of MDR1 promoter activity and protein expression was mediated through metformin-induced activation of AMP-activated protein kinase (AMPK). Metformin 86-95 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 148-152 21054339-10 2011 Small interfering RNA methods confirmed that reduction of AMPK levels attenuates the inhibition of MDR1 activation associated with metformin exposure. Metformin 131-140 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 58-62 21054339-11 2011 Furthermore, the inhibitory effects of metformin on MDR1 expression and cAMP-responsive element binding protein (CREB) phosphorylation were reversed by overexpression of a dominant-negative mutant of AMPK. Metformin 39-48 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 200-204 21054339-12 2011 CONCLUSIONS AND IMPLICATIONS: These results suggest that metformin activates AMPK and suppresses MDR1 expression in MCF-7/adr cells by inhibiting the activation of NF-kappaB and CREB. Metformin 57-66 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 77-81 21262957-0 2011 AMPK and Akt determine apoptotic cell death following perturbations of one-carbon metabolism by regulating ER stress in acute lymphoblastic leukemia. Carbon 75-81 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 21262957-3 2011 In addition, the combination of AICAr with antifolates [methotrexate (MTX) or pemetrexed] has been shown to further potentiate AMPK activation and to lead to greater cytotoxicity and growth inhibition in leukemia and other malignant cell types. Methotrexate 56-68 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 127-131 21262957-3 2011 In addition, the combination of AICAr with antifolates [methotrexate (MTX) or pemetrexed] has been shown to further potentiate AMPK activation and to lead to greater cytotoxicity and growth inhibition in leukemia and other malignant cell types. Methotrexate 70-73 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 127-131 21262957-3 2011 In addition, the combination of AICAr with antifolates [methotrexate (MTX) or pemetrexed] has been shown to further potentiate AMPK activation and to lead to greater cytotoxicity and growth inhibition in leukemia and other malignant cell types. Pemetrexed 78-88 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 127-131 21262957-6 2011 Under these conditions, the concomitant inhibition of Akt, a cellular antagonist of AMPK, leads to further upregulation of AMPK activity and alleviates AICAr plus MTX-induced ER stress and apoptosis. Methotrexate 163-166 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 84-88 21262957-7 2011 Therefore, we also show that the concomitant activation of AMPK actually rescues the cells from AICAr plus MTX-induced ER stress and apoptosis. Methotrexate 107-110 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 59-63 21146504-0 2011 The peroxisome proliferator-activated receptor beta/delta (PPARbeta/delta) agonist GW501516 prevents TNF-alpha-induced NF-kappaB activation in human HaCaT cells by reducing p65 acetylation through AMPK and SIRT1. GW 501516 83-91 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 197-201 21146504-9 2011 GW501516 increased AMPK phosphorylation and the subsequent p300 phosphorylation, leading to a marked reduction in the association between p65 and this transcriptional co-activator. GW 501516 0-8 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 19-23 21146504-11 2011 Finally, the reduction in IL-8 mRNA levels following GW501516 treatment in TNF-alpha-stimulated cells was abolished in the presence of the PPARbeta/delta antagonist GSK0660, the AMPK inhibitor compound C and the SIRT1 inhibitor sirtinol, indicating that the effects of GW501516 on NF-kappaB activity were dependent on PPARbeta/delta, AMPK and SIRT1, respectively. GW 501516 53-61 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 178-182 21146504-11 2011 Finally, the reduction in IL-8 mRNA levels following GW501516 treatment in TNF-alpha-stimulated cells was abolished in the presence of the PPARbeta/delta antagonist GSK0660, the AMPK inhibitor compound C and the SIRT1 inhibitor sirtinol, indicating that the effects of GW501516 on NF-kappaB activity were dependent on PPARbeta/delta, AMPK and SIRT1, respectively. GW 501516 53-61 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 334-338 21304820-6 2011 Animals fed the drug metformin, which induces a dietary-restriction like state in animals and activates AMPK in mammalian cell culture, have a higher survival rate when exposed to long-term anoxia. Metformin 21-30 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 104-108 21304820-11 2011 Finally, the capacity for an animal to survive long bouts of severe oxygen deprivation is likely dependent on specific subunits of the heterotrimeric protein AMPK and energy stores such as carbohydrates. Oxygen 68-74 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 158-162 21258367-6 2011 Under glucose starvation, AMPK promotes autophagy by directly activating Ulk1 through phosphorylation of Ser 317 and Ser 777. Serine 105-108 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 26-30 21258367-6 2011 Under glucose starvation, AMPK promotes autophagy by directly activating Ulk1 through phosphorylation of Ser 317 and Ser 777. Serine 117-120 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 26-30 21037234-2 2011 Treatment of human ECs with the AMPK activator 5-aminoimidazole-4-carboxamide-1-beta-d-ribofuranoside (AICAR) stimulated a concentration- and time-dependent increase in HO-1 protein and mRNA expression that was associated with a prominent increase in nuclear factor-erythroid 2-related factor 2 (Nrf2) protein. acadesine 47-101 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 32-36 21123367-4 2011 We found that in LKB1-null A549 lung adenocarcinoma cells, an AMPK activator, metformin, failed to block the nuclear export of PTEN, and the reintroduction of functional LKB1 into these cells restored the metformin-mediated inhibition of the nuclear export of PTEN. Metformin 78-87 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 62-66 21123367-5 2011 In addition, the nuclear export of PTEN was blocked in cells treated with the CaMKK activator ATP, and this inhibition was reversed by the addition of inhibitors of either AMPK (compound C) or CaMKK (STO-609). Adenosine Triphosphate 94-97 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 172-176 21123367-6 2011 Although the nuclear export of PTEN is blocked by metformin in MCF-7 breast cancer cells carrying wild-type LKB1, this inhibition could not be reversed by an AMPK inhibitor, suggesting that LKB1 could regulate the nuclear export of PTEN by bypassing AMPK alpha1/2. Metformin 50-59 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 250-261 21224036-2 2011 In the heart, AMPK coordinates the activation of glucose and fatty acid metabolic pathways to ensure increased production of myocardial ATP when required, such as during cardiac ischemia/reperfusion and hypertrophy, causing an increase in AMPK activity that can be viewed as both protective and maladaptive. Glucose 49-56 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-18 21037234-4 2011 Induction of HO-1 by AICAR was blocked by the AMPK inhibitor compound C, the adenosine kinase inhibitor 5"-iodotubercidin, and by silencing AMPK-alpha(1/2) and was mimicked by the AMPK activator A-769662 and by infecting ECs with an adenovirus expressing constitutively active AMPK-alpha(1). acadesine 21-26 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 140-144 21224036-2 2011 In the heart, AMPK coordinates the activation of glucose and fatty acid metabolic pathways to ensure increased production of myocardial ATP when required, such as during cardiac ischemia/reperfusion and hypertrophy, causing an increase in AMPK activity that can be viewed as both protective and maladaptive. Glucose 49-56 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 239-243 21037234-2 2011 Treatment of human ECs with the AMPK activator 5-aminoimidazole-4-carboxamide-1-beta-d-ribofuranoside (AICAR) stimulated a concentration- and time-dependent increase in HO-1 protein and mRNA expression that was associated with a prominent increase in nuclear factor-erythroid 2-related factor 2 (Nrf2) protein. acadesine 103-108 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 32-36 21224036-2 2011 In the heart, AMPK coordinates the activation of glucose and fatty acid metabolic pathways to ensure increased production of myocardial ATP when required, such as during cardiac ischemia/reperfusion and hypertrophy, causing an increase in AMPK activity that can be viewed as both protective and maladaptive. Fatty Acids 61-71 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-18 21037234-6 2011 Finally, activation of AMPK inhibited cytokine-mediated EC death, and this was prevented by the HO inhibitor tin protoporphyrin-IX or by silencing HO-1 expression. tin protoporphyrin IX 109-130 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 23-27 21224036-2 2011 In the heart, AMPK coordinates the activation of glucose and fatty acid metabolic pathways to ensure increased production of myocardial ATP when required, such as during cardiac ischemia/reperfusion and hypertrophy, causing an increase in AMPK activity that can be viewed as both protective and maladaptive. Fatty Acids 61-71 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 239-243 21037234-4 2011 Induction of HO-1 by AICAR was blocked by the AMPK inhibitor compound C, the adenosine kinase inhibitor 5"-iodotubercidin, and by silencing AMPK-alpha(1/2) and was mimicked by the AMPK activator A-769662 and by infecting ECs with an adenovirus expressing constitutively active AMPK-alpha(1). acadesine 21-26 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 46-50 21224036-2 2011 In the heart, AMPK coordinates the activation of glucose and fatty acid metabolic pathways to ensure increased production of myocardial ATP when required, such as during cardiac ischemia/reperfusion and hypertrophy, causing an increase in AMPK activity that can be viewed as both protective and maladaptive. Adenosine Triphosphate 136-139 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-18 21224036-2 2011 In the heart, AMPK coordinates the activation of glucose and fatty acid metabolic pathways to ensure increased production of myocardial ATP when required, such as during cardiac ischemia/reperfusion and hypertrophy, causing an increase in AMPK activity that can be viewed as both protective and maladaptive. Adenosine Triphosphate 136-139 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 239-243 21037234-4 2011 Induction of HO-1 by AICAR was blocked by the AMPK inhibitor compound C, the adenosine kinase inhibitor 5"-iodotubercidin, and by silencing AMPK-alpha(1/2) and was mimicked by the AMPK activator A-769662 and by infecting ECs with an adenovirus expressing constitutively active AMPK-alpha(1). acadesine 21-26 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 140-144 21037234-4 2011 Induction of HO-1 by AICAR was blocked by the AMPK inhibitor compound C, the adenosine kinase inhibitor 5"-iodotubercidin, and by silencing AMPK-alpha(1/2) and was mimicked by the AMPK activator A-769662 and by infecting ECs with an adenovirus expressing constitutively active AMPK-alpha(1). acadesine 21-26 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 140-144 21325824-7 2011 Adenosine or AICAR disrupted mitochondrial membrane potentials, and the effect was inhibited by knocking-down AMPKalpha1 and/or AMPKalpha2, expressing dominant negative mutant AMPKalpha2 or mutant Bcl-X(L) lacking Ser/Thr phosphorylation sites. Adenosine 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 110-120 21670525-3 2011 (Compositae) (PEASL) on glucose production through AMP-activated protein kinase (AMPK) activation in human HepG2 cells. Glucose 24-31 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 51-79 21670525-3 2011 (Compositae) (PEASL) on glucose production through AMP-activated protein kinase (AMPK) activation in human HepG2 cells. Glucose 24-31 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 81-85 21670525-4 2011 PEASL significantly inhibited glucose production in a concentration-dependent manner, and this effect was reversed in the presence of compound C, a selective AMPK inhibitor. Glucose 30-37 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 158-162 21670525-11 2011 This indicates that PEASL inhibited glucose production via the AMPK-GSK-CREB pathway in HepG2 cells, and these effects appeared to be capable of revealing anti-diabetic mechanism of PEASL in HepG2 cells. Glucose 36-43 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 63-67 21325824-7 2011 Adenosine or AICAR disrupted mitochondrial membrane potentials, and the effect was inhibited by knocking-down AMPKalpha1 and/or AMPKalpha2, expressing dominant negative mutant AMPKalpha2 or mutant Bcl-X(L) lacking Ser/Thr phosphorylation sites. Serine 214-217 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 110-120 21325824-7 2011 Adenosine or AICAR disrupted mitochondrial membrane potentials, and the effect was inhibited by knocking-down AMPKalpha1 and/or AMPKalpha2, expressing dominant negative mutant AMPKalpha2 or mutant Bcl-X(L) lacking Ser/Thr phosphorylation sites. Threonine 218-221 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 110-120 21031461-7 2011 PJ34 suppressed PARP1 activation and prevented the high-glucose-induced suppression of SIRT1 and AMP-activated protein kinase (AMPK) activity, which was similar to its effect on the restoration of intracellular nicotinamide adenine dinucleotide (NAD) content. Glucose 56-63 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 97-125 21031461-7 2011 PJ34 suppressed PARP1 activation and prevented the high-glucose-induced suppression of SIRT1 and AMP-activated protein kinase (AMPK) activity, which was similar to its effect on the restoration of intracellular nicotinamide adenine dinucleotide (NAD) content. Glucose 56-63 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 127-131 21031461-10 2011 These data suggest that high-glucose-induced PARP1 activation might play a role in glucose toxicity by down-regulating SIRT1 and AMPK activity through NAD depletion and resulting in insulin insensitivity. Glucose 29-36 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 129-133 21031461-10 2011 These data suggest that high-glucose-induced PARP1 activation might play a role in glucose toxicity by down-regulating SIRT1 and AMPK activity through NAD depletion and resulting in insulin insensitivity. NAD 151-154 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 129-133 20948309-3 2010 Activation of AMPK by AICAR resulted in potent suppressive effects on RCC growth, while combinations of AICAR with statins were potent inducers of apoptosis in such cells. AICA ribonucleotide 22-27 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-18 21150275-10 2010 Inhibition of AMPK, either pharmacologic or via siRNA, protects control HeLa cells from death in low glucose. Glucose 101-108 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-18 21042741-8 2010 Our results indicated that anthocyanins significantly decreased phospho-mTOR comparable to rapamycin, a synthetic mTOR inhibitor, and this inhibitory effect of anthocyanins on mTOR was completely abrogated by inactivating AMPKalpha1. Anthocyanins 160-172 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 222-232 20810185-12 2010 Following alcohol consumption, autophagy is decreased in liver cells, likely due to a decrease in intracellular 5"-AMP-activated protein kinase (AMPk) and due to an alteration in vesicle transport in hepatocytes. Alcohols 10-17 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 145-149 21042741-10 2010 For the first time we have found anthocyanins as novel AMPKalpha1 activators, and in conditions of AMPKalpha1 inactivation, anthocyanins lost their ability to inhibit mTOR in HT-29 colon cancer cells. Anthocyanins 33-45 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 55-65 21042741-0 2010 Anthocyanins are novel AMPKalpha1 stimulators that suppress tumor growth by inhibiting mTOR phosphorylation. Anthocyanins 0-12 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 23-33 21042741-10 2010 For the first time we have found anthocyanins as novel AMPKalpha1 activators, and in conditions of AMPKalpha1 inactivation, anthocyanins lost their ability to inhibit mTOR in HT-29 colon cancer cells. Anthocyanins 124-136 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 55-65 21042741-6 2010 We have investigated the mTOR inhibitory effect of anthocyanins through the activation of AMPK. Anthocyanins 51-63 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 90-94 21042741-7 2010 In this study, anthocyanins were applied to colon cancer cells and tumor-bearing xenograft models to investigate their anti-proliferative and pro-apoptotic effects, and elucidate the mechanisms that link AMP-activated protein kinase (AMPK) alpha1 activation to the survival signal of mTOR. Anthocyanins 15-27 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 204-232 21042741-10 2010 For the first time we have found anthocyanins as novel AMPKalpha1 activators, and in conditions of AMPKalpha1 inactivation, anthocyanins lost their ability to inhibit mTOR in HT-29 colon cancer cells. Anthocyanins 124-136 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 99-109 21042741-7 2010 In this study, anthocyanins were applied to colon cancer cells and tumor-bearing xenograft models to investigate their anti-proliferative and pro-apoptotic effects, and elucidate the mechanisms that link AMP-activated protein kinase (AMPK) alpha1 activation to the survival signal of mTOR. Anthocyanins 15-27 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 234-238 21042741-11 2010 The activation of AMPKalpha1, and the deactivation of mTOR and Akt were observed in anthocyanins-treated tumor-bearing xenograft models. Anthocyanins 84-96 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 18-28 21042741-8 2010 Our results indicated that anthocyanins significantly decreased phospho-mTOR comparable to rapamycin, a synthetic mTOR inhibitor, and this inhibitory effect of anthocyanins on mTOR was completely abrogated by inactivating AMPKalpha1. Anthocyanins 27-39 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 222-232 21042741-12 2010 The results from this study suggest that there is a complex interaction between AMPKalpha1 and mTOR signaling, and anthocyanins are powerful AMPKalpha1 activators that inhibit cancer cell growth by inhibiting mTOR phosphorylation. Anthocyanins 115-127 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 80-90 21042741-12 2010 The results from this study suggest that there is a complex interaction between AMPKalpha1 and mTOR signaling, and anthocyanins are powerful AMPKalpha1 activators that inhibit cancer cell growth by inhibiting mTOR phosphorylation. Anthocyanins 115-127 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 141-151 20570728-10 2010 First, the activation of AMPK by GD was much stronger in C4-2 cells than in LNCaP cells, and the robustness of AMPK activation was correlated favorably with cell viability. Gadolinium 33-35 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 25-29 22043210-3 2010 The activated AMPK is a heterotrimeric protein, separated into a catalytic alpha - subunit (63kDa), a regulating beta - subunit (38kDa) and a gamma - subunit (38kDa), which is allosterically adjusted by adenosine triphosphate (ATP) and adenosine monophosphate (AMP). Adenosine Triphosphate 203-225 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-18 22043210-3 2010 The activated AMPK is a heterotrimeric protein, separated into a catalytic alpha - subunit (63kDa), a regulating beta - subunit (38kDa) and a gamma - subunit (38kDa), which is allosterically adjusted by adenosine triphosphate (ATP) and adenosine monophosphate (AMP). Adenosine Triphosphate 227-230 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-18 22043210-3 2010 The activated AMPK is a heterotrimeric protein, separated into a catalytic alpha - subunit (63kDa), a regulating beta - subunit (38kDa) and a gamma - subunit (38kDa), which is allosterically adjusted by adenosine triphosphate (ATP) and adenosine monophosphate (AMP). Adenosine Monophosphate 236-259 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-18 22043210-4 2010 The actual binding of AMP to the gamma - subunit is the step which activates AMPK. Adenosine Monophosphate 22-25 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 77-81 22043210-6 2010 The AMPK cascade represents a sensitive system, activated by cellular stresses that deplete ATP and acts as an indicator of intracellular ATP/AMP. Adenosine Triphosphate 92-95 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 4-8 22043210-6 2010 The AMPK cascade represents a sensitive system, activated by cellular stresses that deplete ATP and acts as an indicator of intracellular ATP/AMP. Adenosine Triphosphate 138-141 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 4-8 22043210-7 2010 In the context of cellular stressors (i.e. hypoxia, pressure overload, hypertrophy or ATP deficiency) the increasing levels of AMP promote allosteric activation and phosphorylation of AMPK. Adenosine Triphosphate 86-89 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 184-188 22043210-7 2010 In the context of cellular stressors (i.e. hypoxia, pressure overload, hypertrophy or ATP deficiency) the increasing levels of AMP promote allosteric activation and phosphorylation of AMPK. Adenosine Monophosphate 127-130 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 184-188 22043210-8 2010 As the concentration of AMP begins to increase, ATP competitively inhibits further phosphorylation of AMPK. Adenosine Monophosphate 24-27 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 102-106 22043210-8 2010 As the concentration of AMP begins to increase, ATP competitively inhibits further phosphorylation of AMPK. Adenosine Triphosphate 48-51 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 102-106 20639120-5 2010 Furthermore, AMPK inhibitor compound c inhibits H(2)O(2)-induced Raptor (S792) phosphorylation and reverses H(2)O(2)-induced dephosphorylation of mTORC1 downstream targets p70-S6K1 (T389), S6 (S235/236) and 4E-BP1 (T37/46). Hydrogen Peroxide 108-116 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 13-17 20639120-8 2010 Moreover, inhibition of PP2A and AMPK partially rescued cells from H(2)O(2)-induced cell death. Hydrogen Peroxide 67-75 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 33-37 20816671-6 2010 Suppression of metformin-induced AMP-activated protein kinase (AMPK) activity by AMPKalpha1 silencing, however, reduced metformin-associated GLUT-4 expression and stimulation of glucose uptake. Metformin 15-24 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 63-67 20816671-6 2010 Suppression of metformin-induced AMP-activated protein kinase (AMPK) activity by AMPKalpha1 silencing, however, reduced metformin-associated GLUT-4 expression and stimulation of glucose uptake. Metformin 15-24 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 81-91 20816671-6 2010 Suppression of metformin-induced AMP-activated protein kinase (AMPK) activity by AMPKalpha1 silencing, however, reduced metformin-associated GLUT-4 expression and stimulation of glucose uptake. Metformin 120-129 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 63-67 20816671-6 2010 Suppression of metformin-induced AMP-activated protein kinase (AMPK) activity by AMPKalpha1 silencing, however, reduced metformin-associated GLUT-4 expression and stimulation of glucose uptake. Metformin 120-129 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 81-91 20816671-6 2010 Suppression of metformin-induced AMP-activated protein kinase (AMPK) activity by AMPKalpha1 silencing, however, reduced metformin-associated GLUT-4 expression and stimulation of glucose uptake. Glucose 178-185 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 63-67 20816671-6 2010 Suppression of metformin-induced AMP-activated protein kinase (AMPK) activity by AMPKalpha1 silencing, however, reduced metformin-associated GLUT-4 expression and stimulation of glucose uptake. Glucose 178-185 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 81-91 20816671-8 2010 In conclusion, activation of AMPKalpha1 without impairment of cell respiration is crucial for metformin-mediated increase in GLUT-4 protein content and glucose uptake in human adipocytes. Metformin 94-103 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 29-39 20816671-8 2010 In conclusion, activation of AMPKalpha1 without impairment of cell respiration is crucial for metformin-mediated increase in GLUT-4 protein content and glucose uptake in human adipocytes. Glucose 152-159 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 29-39 20709802-2 2010 Herein, we show that the deleterious effects of iron dextran on liver function and iron deposition were significantly reversed by adiponectin gene therapy, which was accompanied by AMP-activated protein kinase (AMPK) phosphorylation and heme oxygenase (HO)-1 induction. Iron-Dextran Complex 48-60 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 181-209 20709802-2 2010 Herein, we show that the deleterious effects of iron dextran on liver function and iron deposition were significantly reversed by adiponectin gene therapy, which was accompanied by AMP-activated protein kinase (AMPK) phosphorylation and heme oxygenase (HO)-1 induction. Iron-Dextran Complex 48-60 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 211-215 20709802-2 2010 Herein, we show that the deleterious effects of iron dextran on liver function and iron deposition were significantly reversed by adiponectin gene therapy, which was accompanied by AMP-activated protein kinase (AMPK) phosphorylation and heme oxygenase (HO)-1 induction. Iron 48-52 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 181-209 20709802-2 2010 Herein, we show that the deleterious effects of iron dextran on liver function and iron deposition were significantly reversed by adiponectin gene therapy, which was accompanied by AMP-activated protein kinase (AMPK) phosphorylation and heme oxygenase (HO)-1 induction. Iron 48-52 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 211-215 20639120-4 2010 In HEK293 cells hydrogen peroxide (H(2)O(2)) stimulates phosphorylation of AMP-activated kinase (AMPK) (T172) and Raptor (S792), enhances association of activated AMPK with Raptor. Hydrogen Peroxide 16-33 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 97-101 20639120-4 2010 In HEK293 cells hydrogen peroxide (H(2)O(2)) stimulates phosphorylation of AMP-activated kinase (AMPK) (T172) and Raptor (S792), enhances association of activated AMPK with Raptor. Hydrogen Peroxide 16-33 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 163-167 20639120-4 2010 In HEK293 cells hydrogen peroxide (H(2)O(2)) stimulates phosphorylation of AMP-activated kinase (AMPK) (T172) and Raptor (S792), enhances association of activated AMPK with Raptor. Hydrogen Peroxide 35-43 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 97-101 20639120-4 2010 In HEK293 cells hydrogen peroxide (H(2)O(2)) stimulates phosphorylation of AMP-activated kinase (AMPK) (T172) and Raptor (S792), enhances association of activated AMPK with Raptor. Hydrogen Peroxide 35-43 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 163-167 20639120-5 2010 Furthermore, AMPK inhibitor compound c inhibits H(2)O(2)-induced Raptor (S792) phosphorylation and reverses H(2)O(2)-induced dephosphorylation of mTORC1 downstream targets p70-S6K1 (T389), S6 (S235/236) and 4E-BP1 (T37/46). Hydrogen Peroxide 48-56 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 13-17 20570728-12 2010 The activation of AMPK by GD was functional, as demonstrated by appropriate phosphorylation changes of mTOR and mTOR downstream substrates. Gadolinium 26-28 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 18-22 20854376-0 2010 Metformin action on AMP-activated protein kinase: a translational research approach to understanding a potential new therapeutic target. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 20-48 20593161-12 2010 Liraglutide-induced enhancement of nitric oxide production and suppression of NF-kappaB activation were attenuated by the AMP-activated protein kinase (AMPK) inhibitor compound C or AMPK (also known as PRKAA1) small interfering RNA. Nitric Oxide 35-47 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 182-186 20593161-12 2010 Liraglutide-induced enhancement of nitric oxide production and suppression of NF-kappaB activation were attenuated by the AMP-activated protein kinase (AMPK) inhibitor compound C or AMPK (also known as PRKAA1) small interfering RNA. Nitric Oxide 35-47 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 202-208 20593161-13 2010 Indeed, liraglutide induced phosphorylation of AMPK, which occurs through a signalling pathway independent of cyclic AMP. Cyclic AMP 110-120 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 47-51 20854376-3 2010 It has recently been proposed that metformin-mediated stimulation of hepatic AMP-activated protein kinase (AMPK) underlies the hypoglycaemic effects of metformin. Metformin 35-44 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 77-105 20854376-3 2010 It has recently been proposed that metformin-mediated stimulation of hepatic AMP-activated protein kinase (AMPK) underlies the hypoglycaemic effects of metformin. Metformin 35-44 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 107-111 20854376-3 2010 It has recently been proposed that metformin-mediated stimulation of hepatic AMP-activated protein kinase (AMPK) underlies the hypoglycaemic effects of metformin. Metformin 152-161 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 77-105 20854376-3 2010 It has recently been proposed that metformin-mediated stimulation of hepatic AMP-activated protein kinase (AMPK) underlies the hypoglycaemic effects of metformin. Metformin 152-161 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 107-111 20811725-0 2010 2-Arylthiazolidine-4-carboxylic acid amides (ATCAA) target dual pathways in cancer cells: 5"-AMP-activated protein kinase (AMPK)/mTOR and PI3K/Akt/mTOR pathways. 2-arylthiazolidine-4-carboxylic acid amides 0-43 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 123-127 20811725-8 2010 Determination of intracellular ATP and AMP concentrations revealed that ATCAA-10 activated AMPK by altering the intracellular AMP/ATP ratio. Adenosine Triphosphate 31-34 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 91-95 20811725-8 2010 Determination of intracellular ATP and AMP concentrations revealed that ATCAA-10 activated AMPK by altering the intracellular AMP/ATP ratio. Adenosine Monophosphate 39-42 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 91-95 20811725-8 2010 Determination of intracellular ATP and AMP concentrations revealed that ATCAA-10 activated AMPK by altering the intracellular AMP/ATP ratio. Adenosine Triphosphate 130-133 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 91-95 20686348-4 2010 Treatment of the cells with AICAR (5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside), an AMPK activator, reduced the methylmercury toxicity. acadesine 28-33 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 95-99 20890104-3 2010 Our research into mechanisms of TSC2 regulation helped uncover a pathway upstream of TSC2 that is regulated by cytoplasmic ATM in response to ROS initiated by ATM activation of LKB1 and AMPK. ros 142-145 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 186-190 20531298-6 2010 Recently, it became clear that the energy sensor, AMP-activated kinase (AMPK) translates the effects of energy stress into altered Sirt1 activity by regulating the intracellular level of its co-substrate nicotinamide adenine dinucleotide (NAD)(+). NAD 204-237 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 50-70 20531298-6 2010 Recently, it became clear that the energy sensor, AMP-activated kinase (AMPK) translates the effects of energy stress into altered Sirt1 activity by regulating the intracellular level of its co-substrate nicotinamide adenine dinucleotide (NAD)(+). NAD 204-237 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 72-76 21165328-0 2010 Losartan Inhibits Vascular Smooth Muscle Cell Proliferation through Activation of AMP-Activated Protein Kinase. Losartan 0-8 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 82-110 21165328-2 2010 We hypothesized that losartan may prevent cell proliferation by activating AMP-activated protein kinase (AMPK) in VSMCs. Losartan 21-29 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 75-103 21165328-2 2010 We hypothesized that losartan may prevent cell proliferation by activating AMP-activated protein kinase (AMPK) in VSMCs. Losartan 21-29 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 105-109 21165328-2 2010 We hypothesized that losartan may prevent cell proliferation by activating AMP-activated protein kinase (AMPK) in VSMCs. vsmcs 114-119 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 75-103 21165328-2 2010 We hypothesized that losartan may prevent cell proliferation by activating AMP-activated protein kinase (AMPK) in VSMCs. vsmcs 114-119 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 105-109 21165328-5 2010 Losartan dose- and time-dependently increased the phosphorylation of AMPK and its downstream target, acetyl-CoA carboxylase (ACC) in VSMCs. Losartan 0-8 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 69-73 21165328-6 2010 Losartan also significantly decreased the Ang II- or 15% FBS-induced VSMC proliferation by inhibiting the expression of cell cycle associated proteins, such as p-Rb, cyclin D, and cyclin E. Compound C, a specific inhibitor of AMPK, or AMPK siRNA blocked the losartan-induced inhibition of cell proliferation and the G(0)/G(1) cell cycle arrest. Losartan 0-8 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 226-230 21165328-6 2010 Losartan also significantly decreased the Ang II- or 15% FBS-induced VSMC proliferation by inhibiting the expression of cell cycle associated proteins, such as p-Rb, cyclin D, and cyclin E. Compound C, a specific inhibitor of AMPK, or AMPK siRNA blocked the losartan-induced inhibition of cell proliferation and the G(0)/G(1) cell cycle arrest. Losartan 0-8 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 235-239 21165328-7 2010 These data suggest that losartan-induced AMPK activation might attenuate Ang II-induced VSMC proliferation through the inhibition of cell cycle progression. Losartan 24-32 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 41-45 20531298-6 2010 Recently, it became clear that the energy sensor, AMP-activated kinase (AMPK) translates the effects of energy stress into altered Sirt1 activity by regulating the intracellular level of its co-substrate nicotinamide adenine dinucleotide (NAD)(+). NAD 239-242 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 50-70 20531298-6 2010 Recently, it became clear that the energy sensor, AMP-activated kinase (AMPK) translates the effects of energy stress into altered Sirt1 activity by regulating the intracellular level of its co-substrate nicotinamide adenine dinucleotide (NAD)(+). NAD 239-242 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 72-76 20686348-4 2010 Treatment of the cells with AICAR (5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside), an AMPK activator, reduced the methylmercury toxicity. acadesine 35-89 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 95-99 20599696-2 2010 AMPK inhibits ACCbeta activity, lowering malonyl-CoA levels and promoting mitochondrial fatty acid beta-oxidation. Malonyl Coenzyme A 41-52 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 20599696-2 2010 AMPK inhibits ACCbeta activity, lowering malonyl-CoA levels and promoting mitochondrial fatty acid beta-oxidation. Fatty Acids 88-98 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 20559023-0 2010 The combination of metformin and 2-deoxyglucose inhibits autophagy and induces AMPK-dependent apoptosis in prostate cancer cells. Metformin 19-28 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 79-83 20647762-7 2010 MiR-451 levels are regulated by glucose; under conditions of abundant energy miR-451 expression is high, and the suppression of AMPK signaling allows cells to maintain elevated proliferation rates via unrestrained mTOR activation. Glucose 32-39 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 128-132 20647762-8 2010 Under conditions of glucose withdrawal, miR-451 downregulation is necessary for AMPK pathway activation, leading to suppressed proliferation rates, increased cell survival and migration. Glucose 20-27 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 80-84 20458181-0 2010 AMPK- and p62/SQSTM1-dependent autophagy mediate resveratrol-induced cell death in chronic myelogenous leukemia. Resveratrol 49-60 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 20559023-0 2010 The combination of metformin and 2-deoxyglucose inhibits autophagy and induces AMPK-dependent apoptosis in prostate cancer cells. Deoxyglucose 33-47 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 79-83 20585398-0 2010 Bryostatin modulates latent HIV-1 infection via PKC and AMPK signaling but inhibits acute infection in a receptor independent manner. Bryostatins 0-10 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 56-60 20458181-1 2010 Resveratrol (RSV) is an attractive candidate for cancer therapy via its ability to intervene at different levels in the AMPK/mTOR pathway. Resveratrol 0-11 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 120-124 20458181-1 2010 Resveratrol (RSV) is an attractive candidate for cancer therapy via its ability to intervene at different levels in the AMPK/mTOR pathway. Resveratrol 13-16 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 120-124 20458181-2 2010 Indeed, RSV is unique in its capacity to inhibit both mTOR and S6 kinase and to activate AMPK. Resveratrol 8-11 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 89-93 20458181-3 2010 Our recent data reveals that RSV triggered autophagic cell death (ACD) in Chronic Myelogenous Leukemia (CML) cells, via both AMPK activation and JNK-mediated p62/SQSTM1 expression. Resveratrol 29-32 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 125-129 20458181-4 2010 Here we discuss how Resveratrol can mediate ACD in CML cells and the possibility of utilizing the AMPK/mTOR and JNK/p62 pathways via Resveratrol to combat CML and other hematopoietic malignancies. Resveratrol 133-144 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 98-102 20217115-5 2010 Thirty minutes after the control sprint, Ser(485)-AMPKalpha1/Ser(491)-AMPKalpha2 phosphorylation was reduced by 33% coinciding with increased Thr(172)-AMPKalpha phosphorylation (both, P < 0.05). Serine 41-44 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 50-60 20217115-5 2010 Thirty minutes after the control sprint, Ser(485)-AMPKalpha1/Ser(491)-AMPKalpha2 phosphorylation was reduced by 33% coinciding with increased Thr(172)-AMPKalpha phosphorylation (both, P < 0.05). Serine 61-64 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 50-60 20217115-5 2010 Thirty minutes after the control sprint, Ser(485)-AMPKalpha1/Ser(491)-AMPKalpha2 phosphorylation was reduced by 33% coinciding with increased Thr(172)-AMPKalpha phosphorylation (both, P < 0.05). Threonine 142-145 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 50-60 20442269-4 2010 Under hypertonic conditions in human red blood cells (RBCs) incubated with 0.3 M sucrose, NKCC1 activity increased as measured by bumetanide-sensitive (86)Rb(+) uptake and AMPK was activated. Sucrose 81-88 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 172-176 20442269-6 2010 AMPK activation by osmotic shrinkage of mouse RBCs was abrogated by 10 microM STO-609 CaMKKbeta inhibitor, but incubation with STO-609 did not affect the increase in (86)Rb(+) uptake induced by hyperosmolarity. STO 609 78-85 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 19728147-5 2010 This effect of NGF-induced viability promotion to glucose starvation can be suppressed by Compound C, a specific inhibitor of AMPK. Glucose 50-57 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 126-130 19728147-6 2010 Meanwhile, western blot analysis showed that AMPKalpha1/alpha2 Thr172 phosphorylation level in HeLa cells was up-regulated after NGF treatment under glucose starvation, and Compound C was able to reduce the AMPKalpha1/alpha2 Thr172 phosphorylation level which was up-regulated by NGF in HeLa cells. Glucose 149-156 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 45-55 20083342-0 2010 Induction of apoptosis by quercetin is mediated through AMPKalpha1/ASK1/p38 pathway. Quercetin 26-35 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 56-66 20083342-5 2010 Interestingly, AMP-activated protein kinase (AMPK) seemed to be a critical controller of quercetin-regulated ASK1/p38 activation. Quercetin 89-98 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 45-49 20083342-7 2010 Thus, we suggested that quercetin-exerted apoptotic effects involve ROS/AMPKalpha1/ASK1/p38 signaling pathway, and AMPKalpha1 is a necessary element for apoptotic event induced by ASK1. Quercetin 24-33 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 72-82 28157435-0 2010 The combination of metformin and 2 deoxyglucose inhibits autophagy and induces AMPK-dependent apoptosis in prostate cancer cells. Metformin 19-28 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 79-83 28157435-0 2010 The combination of metformin and 2 deoxyglucose inhibits autophagy and induces AMPK-dependent apoptosis in prostate cancer cells. Deoxyglucose 33-47 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 79-83 20421294-0 2010 Macrophage alpha1 AMP-activated protein kinase (alpha1AMPK) antagonizes fatty acid-induced inflammation through SIRT1. Fatty Acids 72-82 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 18-46 20421294-4 2010 Activating AMPK signaling in macrophages by 5-aminoimidazole-4-carboxamide-1-beta4-ribofuranoside or constitutively active alpha1AMPK (CA-alpha1) significantly inhibits; although inhibiting alpha1AMPK by short hairpin RNA knock-down or dominant-negative alpha1AMPK (DN-alpha1) increases LPS- and FFA-induced tumor necrosis factor alpha expression. 5-aminoimidazole-4-carboxamide-1-beta4-ribofuranoside 44-97 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 11-15 20421294-5 2010 Chromatin immunoprecipitation and luciferase reporter assays show that activation of AMPK by CA-alpha1 in macrophages significantly inhibits LPS- or FFA-induced NF-kappaB signaling. Fatty Acids, Nonesterified 149-152 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 85-89 20421294-6 2010 More importantly, in a macrophage-adipocyte co-culture system, we find that inactivation of macrophage AMPK signaling inhibits adipocyte insulin signaling and glucose uptake. Glucose 159-166 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 103-107 20421294-7 2010 Activation of AMPK by CA-alpha1 increases the SIRT1 activator NAD(+) content and SIRT1 expression in macrophages. NAD 62-68 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-18 20585398-6 2010 Bryostatin specifically modulated novel PKC (nPKC) involving stress induced AMP Kinase (AMPK) inasmuch as an inhibitor of AMPK, compound C partially ablated the viral reactivation effect. Bryostatins 0-10 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 76-86 20585398-6 2010 Bryostatin specifically modulated novel PKC (nPKC) involving stress induced AMP Kinase (AMPK) inasmuch as an inhibitor of AMPK, compound C partially ablated the viral reactivation effect. Bryostatins 0-10 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 88-92 20585398-6 2010 Bryostatin specifically modulated novel PKC (nPKC) involving stress induced AMP Kinase (AMPK) inasmuch as an inhibitor of AMPK, compound C partially ablated the viral reactivation effect. Bryostatins 0-10 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 122-126 20349036-0 2010 Nitric oxide increases cyclic GMP levels, AMP-activated protein kinase (AMPK)alpha1-specific activity and glucose transport in human skeletal muscle. Nitric Oxide 0-12 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 42-70 20164123-3 2010 In Akt-independent mTORC1 inhibition in selenium-treated colon cancer cells, adenosine monophosphate-activated protein kinase (AMPK) alpha(1) was crucial for suppression of mTORC1 activity. Selenium 40-48 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 127-131 20164123-5 2010 The importance of the AMPKalpha(1)-mTORC1 pathway in mediating the antiproliferative action of selenium was examined in xenograft tumors, and the suppression of mTORC1 as well as Akt was concomitant with an increase in AMPKalpha(1) activity. Selenium 95-103 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 22-33 20164123-5 2010 The importance of the AMPKalpha(1)-mTORC1 pathway in mediating the antiproliferative action of selenium was examined in xenograft tumors, and the suppression of mTORC1 as well as Akt was concomitant with an increase in AMPKalpha(1) activity. Selenium 95-103 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 22-34 20164123-6 2010 These findings suggest that the antiproliferative effect of selenium is mediated by an Akt-independent AMPKalpha(1)/mTORC1 pathway or by the Akt/tuberous sclerosis complex 2 /mTORC1 pathway. Selenium 60-68 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 103-115 20114074-8 2010 Importantly, using AMPK-alpha1(-/-)alpha2(-/-) MEFs we show that thapsigargin application triggers autophagy in the absence of AMPK and does not involve complete mTOR inhibition, as detected by p70S6K phosphorylation. Thapsigargin 65-77 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 19-30 20114074-8 2010 Importantly, using AMPK-alpha1(-/-)alpha2(-/-) MEFs we show that thapsigargin application triggers autophagy in the absence of AMPK and does not involve complete mTOR inhibition, as detected by p70S6K phosphorylation. Thapsigargin 65-77 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 19-23 20114074-9 2010 In addition, STO-609-mediated CaMKK-alpha/beta inhibition decreased the level of thapsigargin-induced autophagy only in AMPK-positive cells. Thapsigargin 81-93 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 120-124 20114074-10 2010 We suggest that apart from reported AMPK-dependent regulation of autophagic degradation, an AMPK-independent pathway triggers Ca(2+)-mediated autophagy, involving the PI(3)P-effector protein WIPI-1 and LC3. 1,2-dipalmitoyl-sn-glycero-3-phospho-(1'D-myo-inositol-3'-phosphate) 167-173 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 92-96 20349036-0 2010 Nitric oxide increases cyclic GMP levels, AMP-activated protein kinase (AMPK)alpha1-specific activity and glucose transport in human skeletal muscle. Nitric Oxide 0-12 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 72-76 20349036-9 2010 Consistent with this, spermine NONOate increased AMP-activated protein kinase (AMPK)-alpha1-associated activity (1.7-fold, p < 0.05). spermine nitric oxide complex 22-38 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 49-77 20349036-9 2010 Consistent with this, spermine NONOate increased AMP-activated protein kinase (AMPK)-alpha1-associated activity (1.7-fold, p < 0.05). spermine nitric oxide complex 22-38 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 79-83 20349036-11 2010 Spermine NONOate also elicited a concomitant increase in AMPK and acetyl-CoA carboxylase phosphorylation. spermine nitric oxide complex 0-16 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 57-61 20349036-13 2010 CONCLUSIONS/INTERPRETATION: Pharmacological treatment of skeletal muscle with spermine NONOate increases glucose transport via insulin-independent signalling pathways involving increased intracellular cGMP levels and AMPK-alpha1-associated activity. spermine nitric oxide complex 78-94 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 217-228 20349036-13 2010 CONCLUSIONS/INTERPRETATION: Pharmacological treatment of skeletal muscle with spermine NONOate increases glucose transport via insulin-independent signalling pathways involving increased intracellular cGMP levels and AMPK-alpha1-associated activity. Glucose 105-112 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 217-228 19896469-2 2010 AMP-activated protein kinase (AMPK) is an evolutionarily conserved key regulator of cellular energy homeostasis that protects the cell from energy depletion and stress by activating several biochemical pathways that lead to the conservation, as well as generation, of ATP. Adenosine Triphosphate 268-271 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-28 20513425-5 2010 mTORC1 inhibition during glucose deprivation decreased AMPK activation and allowed ATP to remain high, which was both necessary and sufficient for protection. Glucose 25-32 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 55-59 20444419-3 2010 It is thought that agents that increase the cellular AMP/ATP ratio, such as the antidiabetic biguanides metformin and phenformin, inhibit mTORC1 through AMPK activation of TSC1/2-dependent or -independent mechanisms. Adenosine Monophosphate 53-56 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 153-157 20444419-3 2010 It is thought that agents that increase the cellular AMP/ATP ratio, such as the antidiabetic biguanides metformin and phenformin, inhibit mTORC1 through AMPK activation of TSC1/2-dependent or -independent mechanisms. Adenosine Triphosphate 57-60 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 153-157 20444419-3 2010 It is thought that agents that increase the cellular AMP/ATP ratio, such as the antidiabetic biguanides metformin and phenformin, inhibit mTORC1 through AMPK activation of TSC1/2-dependent or -independent mechanisms. Biguanides 93-103 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 153-157 20444419-3 2010 It is thought that agents that increase the cellular AMP/ATP ratio, such as the antidiabetic biguanides metformin and phenformin, inhibit mTORC1 through AMPK activation of TSC1/2-dependent or -independent mechanisms. Metformin 104-113 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 153-157 20444419-3 2010 It is thought that agents that increase the cellular AMP/ATP ratio, such as the antidiabetic biguanides metformin and phenformin, inhibit mTORC1 through AMPK activation of TSC1/2-dependent or -independent mechanisms. Phenformin 118-128 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 153-157 20444419-5 2010 Consistent with these observations, in two distinct preclinical models of cancer and diabetes, metformin acts to suppress mTORC1 signaling in an AMPK-independent manner. Metformin 95-104 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 145-149 20919451-0 2010 Induction of phospho-Thr-172 AMPK in 3T3-L1 adipocytes exposed to cold or treated with anisomycin, mithramycin A, and ionic compounds. Threonine 21-24 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 29-33 20919451-0 2010 Induction of phospho-Thr-172 AMPK in 3T3-L1 adipocytes exposed to cold or treated with anisomycin, mithramycin A, and ionic compounds. Anisomycin 87-97 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 29-33 20919451-0 2010 Induction of phospho-Thr-172 AMPK in 3T3-L1 adipocytes exposed to cold or treated with anisomycin, mithramycin A, and ionic compounds. mithramycin A 99-112 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 29-33 20919451-3 2010 We examined the level of phospho-Thr-172 AMPK (an active form of AMPK, a known energy-state sensor) in L1 adipocytes exposed to different temperatures of 4-37 degrees C or stressors, including chemical inhibitors and activators. Threonine 33-36 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 41-45 20919451-3 2010 We examined the level of phospho-Thr-172 AMPK (an active form of AMPK, a known energy-state sensor) in L1 adipocytes exposed to different temperatures of 4-37 degrees C or stressors, including chemical inhibitors and activators. Threonine 33-36 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 65-69 20142804-8 2010 Our findings suggest that AMPK inhibitors may be exploited for prevention of H(2)O(2)-induced neurodegenerative diseases. Hydrogen Peroxide 77-85 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 26-30 20103737-2 2010 When a cell"s energy state is diminished, AMPK activation restores energy balance by stimulating catabolic processes that generate ATP and downregulating anabolic processes that consume ATP but are not acutely needed for survival. Adenosine Triphosphate 131-134 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 42-46 20103737-2 2010 When a cell"s energy state is diminished, AMPK activation restores energy balance by stimulating catabolic processes that generate ATP and downregulating anabolic processes that consume ATP but are not acutely needed for survival. Adenosine Triphosphate 186-189 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 42-46 19830459-3 2010 In addition, we showed that thapsigargin treatment activated AMPK and autophagy in a HIF-1-dependent manner. Thapsigargin 28-40 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 61-65 19896469-2 2010 AMP-activated protein kinase (AMPK) is an evolutionarily conserved key regulator of cellular energy homeostasis that protects the cell from energy depletion and stress by activating several biochemical pathways that lead to the conservation, as well as generation, of ATP. Adenosine Triphosphate 268-271 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-34 20133456-9 2010 An in vivo study showed that prolonged 5-aminoimidazole-4-carboxamide ribonucleoside (AICAR)-induced AMPK activation increases uncoupling protein 1 expression and induces an accumulation of brown adipocytes in white adipose tissue (WAT), as revealed by immunohistology. acadesine 39-84 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 101-105 20190133-0 2010 SIRT1 takes a backseat to AMPK in the regulation of insulin sensitivity by resveratrol. Resveratrol 75-86 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 26-30 20133456-9 2010 An in vivo study showed that prolonged 5-aminoimidazole-4-carboxamide ribonucleoside (AICAR)-induced AMPK activation increases uncoupling protein 1 expression and induces an accumulation of brown adipocytes in white adipose tissue (WAT), as revealed by immunohistology. acadesine 86-91 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 101-105 19928762-5 2010 The suppression of nonessential energy expenditure by activated AMPK along with the CR mimetic and antiproliferative properties of resveratrol has led us to hypothesize that resveratrol activity might have an important role in the activation of AMPK. Resveratrol 174-185 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 64-68 20170512-12 2010 CONCLUSIONS: 4-Hydroxytamoxifen and dexamethasone up-regulated translation initiation of p27 by down-regulating 4E-BP1 phosphorylated at Ser65 and this down-regulation seemed to be mediated by upstream RTKs/PI3K/Akt/AMPK/mTOR protein kinase signaling pathways. hydroxytamoxifen 13-31 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 216-220 20170512-12 2010 CONCLUSIONS: 4-Hydroxytamoxifen and dexamethasone up-regulated translation initiation of p27 by down-regulating 4E-BP1 phosphorylated at Ser65 and this down-regulation seemed to be mediated by upstream RTKs/PI3K/Akt/AMPK/mTOR protein kinase signaling pathways. Dexamethasone 36-49 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 216-220 20222801-2 2010 AMPK activation stimulates fatty acid oxidation, enhances insulin sensitivity, alleviates hyperglycemia and hyperlipidemia, and inhibits proinflammatory changes. Fatty Acids 27-37 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 20222801-7 2010 In keeping with in vitro studies, recent epidemiological studies indicate that the incidence of cancer is reduced in Type 2 diabetes treated with metformin, an AMPK activator. Metformin 146-155 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 160-164 19928762-0 2010 Resveratrol modulates tumor cell proliferation and protein translation via SIRT1-dependent AMPK activation. Resveratrol 0-11 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 91-95 19928762-5 2010 The suppression of nonessential energy expenditure by activated AMPK along with the CR mimetic and antiproliferative properties of resveratrol has led us to hypothesize that resveratrol activity might have an important role in the activation of AMPK. Resveratrol 174-185 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 245-249 19928762-6 2010 Here, we show that resveratrol activated AMPK in both ER-positive and ER-negative breast cancer cells. Resveratrol 19-30 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 41-45 19928762-8 2010 Moreover, we also found that AMPK activity mediated by resveratrol in cancer cells was due to inducing the expression of Sirtuin type 1 (SIRT1) via elevation in the cellular NAD(+)/NADH in ER-positive cells. Resveratrol 55-66 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 29-33 19928762-8 2010 Moreover, we also found that AMPK activity mediated by resveratrol in cancer cells was due to inducing the expression of Sirtuin type 1 (SIRT1) via elevation in the cellular NAD(+)/NADH in ER-positive cells. NAD 174-180 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 29-33 19928762-8 2010 Moreover, we also found that AMPK activity mediated by resveratrol in cancer cells was due to inducing the expression of Sirtuin type 1 (SIRT1) via elevation in the cellular NAD(+)/NADH in ER-positive cells. NAD 181-185 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 29-33 19928762-11 2010 Targeting SIRT1/AMPK signaling by resveratrol may have potential therapeutic implications for cancer and age-related diseases. Resveratrol 34-45 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 16-20 20118562-0 2010 Ginsenoside Rg1 suppresses hepatic glucose production via AMP-activated protein kinase in HepG2 cells. Ginsenosides 0-11 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 58-86 20103647-0 2010 Resveratrol promotes autophagic cell death in chronic myelogenous leukemia cells via JNK-mediated p62/SQSTM1 expression and AMPK activation. Resveratrol 0-11 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 124-128 20103647-5 2010 RSV also stimulated AMPK, thereby inhibiting the mTOR pathway. Resveratrol 0-3 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 20-24 20103647-6 2010 AMPK knockdown or mTOR overexpression impaired RSV-induced autophagy but not JNK activation. Resveratrol 47-50 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 20103647-8 2010 We concluded that RSV triggered autophagic cell death in CML cells via both JNK-mediated p62 overexpression and AMPK activation. Resveratrol 18-21 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 112-116 19940154-9 2010 We conclude that many of the reported biological effects of cordycepin are likely to be due to its effects on mTOR and AMPK signaling. cordycepin 60-70 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 119-123 20118562-0 2010 Ginsenoside Rg1 suppresses hepatic glucose production via AMP-activated protein kinase in HepG2 cells. Glucose 35-42 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 58-86 20118562-2 2010 In this study, we found the inhibitory effect of Rg(1) on hepatic glucose production through AMP-activated protein kinase (AMPK) activation in HepG2 cells. Glucose 66-73 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 93-121 20118562-2 2010 In this study, we found the inhibitory effect of Rg(1) on hepatic glucose production through AMP-activated protein kinase (AMPK) activation in HepG2 cells. Glucose 66-73 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 123-127 20118562-6 2010 Taken together, our results demonstrated the suppressive effect of Rg(1) on hepatic glucose production via LKB1-AMPK-FoxO1 pathway in HepG2 human hepatoma cells. Glucose 84-91 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 112-116 20180761-2 2010 The activation of AMPK can lead to an increase of glucose uptake into muscle, decreased gluconeogenesis in liver, increased fatty acid oxidation in muscle and liver, decreased fatty acid synthesis in liver and adipose tissue, and increase mitochondrial biogenesis. Glucose 50-57 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 18-22 20139613-5 2010 Therefore, we investigated whether 95% ethanol eluate (EE), an active part of ASL, would attenuate hepatic lipid accumulation in human HepG2 cells by activating AMP-activated protein kinase (AMPK). Ethanol 39-46 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 191-195 20180761-2 2010 The activation of AMPK can lead to an increase of glucose uptake into muscle, decreased gluconeogenesis in liver, increased fatty acid oxidation in muscle and liver, decreased fatty acid synthesis in liver and adipose tissue, and increase mitochondrial biogenesis. Fatty Acids 124-134 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 18-22 20180761-2 2010 The activation of AMPK can lead to an increase of glucose uptake into muscle, decreased gluconeogenesis in liver, increased fatty acid oxidation in muscle and liver, decreased fatty acid synthesis in liver and adipose tissue, and increase mitochondrial biogenesis. Fatty Acids 176-186 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 18-22 19720090-6 2009 SIRT1 activator resveratrol reversed Tat-mediated reduction in AMPK activation and downstream ACC activation; while SIRT1 inhibitor nicotinamide or knockdown of SIRT1 by siRNA potentiated Tat-mediated reduction in AMPK activation and downstream ACC activation. Resveratrol 16-27 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 63-67 19818790-1 2009 AMPKalpha is a subunit of AMP-activated protein kinase (AMPK), a heterotrimeric enzyme that works as a fuel sensor activated in response to the depletion of cellular ATP. Adenosine Triphosphate 166-169 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 26-54 19818790-1 2009 AMPKalpha is a subunit of AMP-activated protein kinase (AMPK), a heterotrimeric enzyme that works as a fuel sensor activated in response to the depletion of cellular ATP. Adenosine Triphosphate 166-169 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 19720090-6 2009 SIRT1 activator resveratrol reversed Tat-mediated reduction in AMPK activation and downstream ACC activation; while SIRT1 inhibitor nicotinamide or knockdown of SIRT1 by siRNA potentiated Tat-mediated reduction in AMPK activation and downstream ACC activation. Resveratrol 16-27 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 214-218 19720090-6 2009 SIRT1 activator resveratrol reversed Tat-mediated reduction in AMPK activation and downstream ACC activation; while SIRT1 inhibitor nicotinamide or knockdown of SIRT1 by siRNA potentiated Tat-mediated reduction in AMPK activation and downstream ACC activation. Niacinamide 132-144 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 214-218 19671840-1 2009 The protein complex AMP-activated protein kinase (AMPK) is believed to play an important role in the regulation of skeletal muscle glucose and lipid metabolism. Glucose 131-138 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 20-48 19815529-1 2009 AMP-activated protein kinase (AMPK) senses changes in the intracellular AMP/ATP ratio, switching off energy-consuming processes and switching on catabolic pathways in response to energy depletion. Adenosine Monophosphate 0-3 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-34 19815529-1 2009 AMP-activated protein kinase (AMPK) senses changes in the intracellular AMP/ATP ratio, switching off energy-consuming processes and switching on catabolic pathways in response to energy depletion. Adenosine Triphosphate 76-79 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-28 19815529-1 2009 AMP-activated protein kinase (AMPK) senses changes in the intracellular AMP/ATP ratio, switching off energy-consuming processes and switching on catabolic pathways in response to energy depletion. Adenosine Triphosphate 76-79 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-34 19815529-2 2009 Here, we show that AMPK down-regulates rRNA synthesis under glucose restriction by phosphorylating the RNA polymerase I (Pol I)-associated transcription factor TIF-IA at a single serine residue (Ser-635). Glucose 60-67 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 19-23 19815529-2 2009 Here, we show that AMPK down-regulates rRNA synthesis under glucose restriction by phosphorylating the RNA polymerase I (Pol I)-associated transcription factor TIF-IA at a single serine residue (Ser-635). Serine 179-185 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 19-23 19815529-2 2009 Here, we show that AMPK down-regulates rRNA synthesis under glucose restriction by phosphorylating the RNA polymerase I (Pol I)-associated transcription factor TIF-IA at a single serine residue (Ser-635). Serine 195-198 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 19-23 19815529-4 2009 Mutation of Ser-635 compromises down-regulation of Pol I transcription in response to low energy supply, supporting that activation of AMPK adapts rRNA synthesis to nutrient availability and the cellular energy status. Serine 12-15 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 135-139 19651772-4 2009 Mutation of the corresponding AMPK alpha-subunit residues (Val-219 and Phe-223) to glutamate reduced the tendency of the kinase to form higher order homo-oligomers, as was determined by the following three independent techniques in vitro: (i) small angle x-ray scattering, (ii) surface plasmon resonance spectroscopy, and (iii) two-dimensional blue native/SDS-PAGE. Valine 59-62 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-34 19651772-4 2009 Mutation of the corresponding AMPK alpha-subunit residues (Val-219 and Phe-223) to glutamate reduced the tendency of the kinase to form higher order homo-oligomers, as was determined by the following three independent techniques in vitro: (i) small angle x-ray scattering, (ii) surface plasmon resonance spectroscopy, and (iii) two-dimensional blue native/SDS-PAGE. Phenylalanine 71-74 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-34 19651772-4 2009 Mutation of the corresponding AMPK alpha-subunit residues (Val-219 and Phe-223) to glutamate reduced the tendency of the kinase to form higher order homo-oligomers, as was determined by the following three independent techniques in vitro: (i) small angle x-ray scattering, (ii) surface plasmon resonance spectroscopy, and (iii) two-dimensional blue native/SDS-PAGE. Glutamic Acid 83-92 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-34 19651772-4 2009 Mutation of the corresponding AMPK alpha-subunit residues (Val-219 and Phe-223) to glutamate reduced the tendency of the kinase to form higher order homo-oligomers, as was determined by the following three independent techniques in vitro: (i) small angle x-ray scattering, (ii) surface plasmon resonance spectroscopy, and (iii) two-dimensional blue native/SDS-PAGE. Sodium Dodecyl Sulfate 356-359 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-34 19651772-9 2009 Importantly, activation of mutant AMPK by LKB1 was restored by exchanging the corresponding and conserved hydrophobic alphaG-helix residues of LKB1 (Ile-260 and Phe-264) to positively charged amino acids. Isoleucine 149-152 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 34-38 19651772-9 2009 Importantly, activation of mutant AMPK by LKB1 was restored by exchanging the corresponding and conserved hydrophobic alphaG-helix residues of LKB1 (Ile-260 and Phe-264) to positively charged amino acids. Phenylalanine 161-164 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 34-38 19671840-10 2009 Furthermore, our results indicate a role for gamma3-containing AMPK complexes in downregulation of insulin-stimulated nonoxidative glucose metabolism possibly through inhibition of glycogen synthase activity. Glucose 131-138 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 63-67 19671840-1 2009 The protein complex AMP-activated protein kinase (AMPK) is believed to play an important role in the regulation of skeletal muscle glucose and lipid metabolism. Glucose 131-138 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 50-54 19560442-0 2009 FATP1 mediates fatty acid-induced activation of AMPK in 3T3-L1 adipocytes. Fatty Acids 15-25 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 48-52 19639604-7 2009 Intriguingly, though activation of AMPK by 0.3 and 1.0 mM AICAR synergized IGF-1-induced Akt activation, the expression of UL was not attenuated, but strengthened by AMPK activation. acadesine 58-63 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 35-39 19563826-2 2009 Recently, it was found that dithiolethione compounds had the activities to prevent or treat fibrosis, insulin resistance, and mitochondrial protective effects in the liver by a mechanism involving AMP-activated protein kinase (AMPK) and/or 70-kDa ribosomal protein S6 kinase 1 (S6K1). dithiolethione 28-42 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 197-225 19563826-2 2009 Recently, it was found that dithiolethione compounds had the activities to prevent or treat fibrosis, insulin resistance, and mitochondrial protective effects in the liver by a mechanism involving AMP-activated protein kinase (AMPK) and/or 70-kDa ribosomal protein S6 kinase 1 (S6K1). dithiolethione 28-42 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 227-231 19563826-5 2009 This review focuses on the interaction between oltipraz and the AMPK-mTOR-S6K1 pathway, which regulates genes that confer hepatocyte protection from intoxication, disrupted energy metabolism, and inflammation. oltipraz 47-55 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 64-68 19560442-2 2009 FATP-dependent production of AMP was evaluated using FATP4 proteoliposomes, and fatty acid-dependent activation of AMP-activated protein kinase (AMPK) was assessed in 3T3-L1 adipocytes. Fatty Acids 80-90 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 115-143 19560442-2 2009 FATP-dependent production of AMP was evaluated using FATP4 proteoliposomes, and fatty acid-dependent activation of AMP-activated protein kinase (AMPK) was assessed in 3T3-L1 adipocytes. Fatty Acids 80-90 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 145-149 19560442-3 2009 Insulin-stimulated fatty acid influx (palmitate or arachidonate) into cultured adipocytes resulted in an increase in the phosphorylation of AMPK and its downstream target acetyl-CoA carboxylase. Fatty Acids 19-29 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 140-144 19560442-3 2009 Insulin-stimulated fatty acid influx (palmitate or arachidonate) into cultured adipocytes resulted in an increase in the phosphorylation of AMPK and its downstream target acetyl-CoA carboxylase. Palmitates 38-47 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 140-144 19560442-3 2009 Insulin-stimulated fatty acid influx (palmitate or arachidonate) into cultured adipocytes resulted in an increase in the phosphorylation of AMPK and its downstream target acetyl-CoA carboxylase. Arachidonic Acid 51-63 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 140-144 19560442-4 2009 Consistent with the activation of AMPK, palmitate uptake into 3T3-L1 adipocytes resulted in an increase in intracellular [AMP]/[ATP]. Palmitates 40-49 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 34-38 19560442-4 2009 Consistent with the activation of AMPK, palmitate uptake into 3T3-L1 adipocytes resulted in an increase in intracellular [AMP]/[ATP]. Adenosine Triphosphate 128-131 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 34-38 19560442-5 2009 The fatty acid-induced increase in AMPK activation was attenuated in a cell line expressing shRNA targeting FATP1. Fatty Acids 4-14 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 35-39 19560442-6 2009 Taken together, these results demonstrate that, in adipocytes, insulin-stimulated fatty acid influx mediated by FATP1 regulates AMPK and provides a potential regulatory mechanism for balancing de novo production of fatty acids from glucose metabolism with influx of preformed fatty acids via phosphorylation of acetyl-CoA carboxylase. Fatty Acids 82-92 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 128-132 19560442-6 2009 Taken together, these results demonstrate that, in adipocytes, insulin-stimulated fatty acid influx mediated by FATP1 regulates AMPK and provides a potential regulatory mechanism for balancing de novo production of fatty acids from glucose metabolism with influx of preformed fatty acids via phosphorylation of acetyl-CoA carboxylase. Fatty Acids 215-226 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 128-132 19560442-6 2009 Taken together, these results demonstrate that, in adipocytes, insulin-stimulated fatty acid influx mediated by FATP1 regulates AMPK and provides a potential regulatory mechanism for balancing de novo production of fatty acids from glucose metabolism with influx of preformed fatty acids via phosphorylation of acetyl-CoA carboxylase. Glucose 232-239 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 128-132 19560442-6 2009 Taken together, these results demonstrate that, in adipocytes, insulin-stimulated fatty acid influx mediated by FATP1 regulates AMPK and provides a potential regulatory mechanism for balancing de novo production of fatty acids from glucose metabolism with influx of preformed fatty acids via phosphorylation of acetyl-CoA carboxylase. Fatty Acids 276-287 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 128-132 19491292-4 2009 Treating C(2)C(12) myoblast cultures with 1 mM 5-aminoimidazole-4-carboxamide 1-beta-D-ribonucleoside (AICAR) for up to 24 h induced AMPK phosphorylation. 5-aminoimidazole-4-carboxamide 1-beta-d-ribonucleoside 47-101 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 133-137 19491377-3 2009 Among various transcriptional regulators, the hepatic SIRT1 (sirtuin 1)-AMPK (AMPK-activated kinase) signaling system represents a central target for the action of ethanol in the liver. Ethanol 164-171 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 72-76 19359389-6 2009 siRNA-mediated down-regulation of AMPKalpha1, but not AMPKalpha2, abolished leptin-induced Akt-Ser(473) phosphorylation, eNOS-Ser(1177) phosphorylation, eNOS activation, and cGMP accumulation. Serine 95-98 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 34-44 19359389-6 2009 siRNA-mediated down-regulation of AMPKalpha1, but not AMPKalpha2, abolished leptin-induced Akt-Ser(473) phosphorylation, eNOS-Ser(1177) phosphorylation, eNOS activation, and cGMP accumulation. Serine 126-129 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 34-44 19359389-6 2009 siRNA-mediated down-regulation of AMPKalpha1, but not AMPKalpha2, abolished leptin-induced Akt-Ser(473) phosphorylation, eNOS-Ser(1177) phosphorylation, eNOS activation, and cGMP accumulation. Cyclic GMP 174-178 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 34-44 19491377-3 2009 Among various transcriptional regulators, the hepatic SIRT1 (sirtuin 1)-AMPK (AMPK-activated kinase) signaling system represents a central target for the action of ethanol in the liver. Ethanol 164-171 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 78-82 19803431-0 2009 [Role of AMPK in glucose and lipid metabolisms]. Glucose 17-24 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 9-13 19629071-3 2009 AMPK regulates lipid, cholesterol and glucose metabolism in specialized metabolic tissues, such as liver, muscle and adipose tissue. Cholesterol 22-33 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 19414597-8 2009 In addition, LKB1 nucleocytoplasmic transport and AMPK activation in response to peroxynitrite are markedly reduced by pharmacological inhibition of CRM1, which normally facilitates nuclear export of LKB1-STRAD complexes. Peroxynitrous Acid 81-94 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 50-54 19442239-3 2009 Mitochondrial ROS (reactive oxygen species), generated as a result of the interaction between nitric oxide and mitochondrial cytochrome c oxidase, activate AMPKalpha1 in HUVECs (human umbilical-vein endothelial cells) at a low oxygen concentration (i.e. 3%). Reactive Oxygen Species 14-17 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 156-166 19442239-3 2009 Mitochondrial ROS (reactive oxygen species), generated as a result of the interaction between nitric oxide and mitochondrial cytochrome c oxidase, activate AMPKalpha1 in HUVECs (human umbilical-vein endothelial cells) at a low oxygen concentration (i.e. 3%). Reactive Oxygen Species 19-42 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 156-166 19442239-3 2009 Mitochondrial ROS (reactive oxygen species), generated as a result of the interaction between nitric oxide and mitochondrial cytochrome c oxidase, activate AMPKalpha1 in HUVECs (human umbilical-vein endothelial cells) at a low oxygen concentration (i.e. 3%). Oxygen 28-34 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 156-166 19442239-3 2009 Mitochondrial ROS (reactive oxygen species), generated as a result of the interaction between nitric oxide and mitochondrial cytochrome c oxidase, activate AMPKalpha1 in HUVECs (human umbilical-vein endothelial cells) at a low oxygen concentration (i.e. 3%). Nitric Oxide 94-106 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 156-166 19442239-7 2009 In addition, we show that silencing AMPKalpha1 in cells results in a reduced mitochondrial and eNOS (endothelial NO synthase) content, reduced cell proliferation, increased accumulation of ROS and apoptosis. Reactive Oxygen Species 189-192 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 36-46 19202357-7 2009 Consistent with this idea, AMPK-deficient cells that are less able to deal with bioenergetic stress are also more sensitive to ceramide than wild-type cells. Ceramides 127-135 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 27-31 19494326-2 2009 Metformin is the most widely used drug for diabetes and mediates its action via activating AMP-activated protein kinase (AMPK). Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 91-119 19347029-1 2009 AMP-activated protein kinase (AMPK) serves as a fuel-sensing enzyme that is activated by binding of AMP and subsequent phophorylation by upstream kinases such as the tumor suppressor LKB1, when cells sense an increase in the ratio of AMP to ATP. Adenosine Monophosphate 0-3 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-34 19347029-1 2009 AMP-activated protein kinase (AMPK) serves as a fuel-sensing enzyme that is activated by binding of AMP and subsequent phophorylation by upstream kinases such as the tumor suppressor LKB1, when cells sense an increase in the ratio of AMP to ATP. Adenosine Monophosphate 30-33 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-28 19347029-1 2009 AMP-activated protein kinase (AMPK) serves as a fuel-sensing enzyme that is activated by binding of AMP and subsequent phophorylation by upstream kinases such as the tumor suppressor LKB1, when cells sense an increase in the ratio of AMP to ATP. Adenosine Triphosphate 241-244 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-28 19347029-1 2009 AMP-activated protein kinase (AMPK) serves as a fuel-sensing enzyme that is activated by binding of AMP and subsequent phophorylation by upstream kinases such as the tumor suppressor LKB1, when cells sense an increase in the ratio of AMP to ATP. Adenosine Triphosphate 241-244 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-34 19347029-2 2009 Acute activation of AMPK stimulates fatty acid oxidation to generate more ATP and simultaneously inhibits ATP-consuming processes including fatty acid and protein syntheses, thereby preserving energy for acute cell-surviving program, whereas chronic activation leads to inhibition of cell growth. Fatty Acids 36-46 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 20-24 19347029-2 2009 Acute activation of AMPK stimulates fatty acid oxidation to generate more ATP and simultaneously inhibits ATP-consuming processes including fatty acid and protein syntheses, thereby preserving energy for acute cell-surviving program, whereas chronic activation leads to inhibition of cell growth. Adenosine Triphosphate 74-77 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 20-24 19347029-2 2009 Acute activation of AMPK stimulates fatty acid oxidation to generate more ATP and simultaneously inhibits ATP-consuming processes including fatty acid and protein syntheses, thereby preserving energy for acute cell-surviving program, whereas chronic activation leads to inhibition of cell growth. Adenosine Triphosphate 106-109 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 20-24 19347029-2 2009 Acute activation of AMPK stimulates fatty acid oxidation to generate more ATP and simultaneously inhibits ATP-consuming processes including fatty acid and protein syntheses, thereby preserving energy for acute cell-surviving program, whereas chronic activation leads to inhibition of cell growth. Fatty Acids 140-150 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 20-24 19347029-7 2009 Conversely, treatment of the C4-2 cells with 5-aminoimidazole-4-carboxamide 1-D-ribonucleoside (AICAR), a prototypical AMPK activator, caused opposite changes. 5-aminoimidazole-4-carboxamide 1-d-ribonucleoside 45-94 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 119-123 19347029-7 2009 Conversely, treatment of the C4-2 cells with 5-aminoimidazole-4-carboxamide 1-D-ribonucleoside (AICAR), a prototypical AMPK activator, caused opposite changes. acadesine 96-101 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 119-123 19494326-2 2009 Metformin is the most widely used drug for diabetes and mediates its action via activating AMP-activated protein kinase (AMPK). Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 121-125 19494326-4 2009 Furthermore, the AMPK activity and lipids alterations (total phospholipids and in free fatty acids) were restored by metformin treatment in the CNS of treated EAE animals, suggesting the possible involvement of AMPK. Metformin 117-126 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 17-21 19494326-4 2009 Furthermore, the AMPK activity and lipids alterations (total phospholipids and in free fatty acids) were restored by metformin treatment in the CNS of treated EAE animals, suggesting the possible involvement of AMPK. Metformin 117-126 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 211-215 19494326-5 2009 Metformin activated AMPK in macrophages and thereby inhibited biosynthesis of phospholipids as well as neutral lipids and also down-regulated the expression of endotoxin (LPS)-induced proinflammatory cytokines and their mediators (iNOS and cyclooxygenase 2). Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 20-24 19448692-0 2009 Role of the AMP-activated protein kinase in regulating fatty acid metabolism during exercise. Fatty Acids 55-65 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 12-40 19448692-4 2009 In this review, studies examining the role of AMPK as a regulator of fatty acid metabolism in both adipose tissue and skeletal muscle during exercise will be discussed. Fatty Acids 69-79 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 46-50 19448692-6 2009 In skeletal muscle, exercise-induced activation of AMPK is associated with increases in fatty acid uptake, phosphorylation of HSL, and increased fatty acid oxidation, which is thought to occur via the acetyl-CoA carboxylase-malony-CoA-CPT-1 signalling axis. Fatty Acids 88-98 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 51-55 19448692-6 2009 In skeletal muscle, exercise-induced activation of AMPK is associated with increases in fatty acid uptake, phosphorylation of HSL, and increased fatty acid oxidation, which is thought to occur via the acetyl-CoA carboxylase-malony-CoA-CPT-1 signalling axis. Fatty Acids 145-155 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 51-55 19239414-2 2009 Activated AMPK stimulates the production of ATP by regulating key steps in both glucose and fatty acid metabolism. Adenosine Triphosphate 44-47 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 10-14 19239414-2 2009 Activated AMPK stimulates the production of ATP by regulating key steps in both glucose and fatty acid metabolism. Glucose 80-87 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 10-14 19239414-2 2009 Activated AMPK stimulates the production of ATP by regulating key steps in both glucose and fatty acid metabolism. Fatty Acids 92-102 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 10-14 19239414-8 2009 Mutations in the regulatory gamma2 subunit of AMPK lead to an inherited syndrome of hypertrophic cardiomyopathy and ventricular pre-excitation, which appears to be due to intracellular glycogen accumulation. Glycogen 185-193 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 46-50 19245651-0 2009 AMP-activated protein kinase--a sensor of glycogen as well as AMP and ATP? Glycogen 42-50 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-28 19245651-0 2009 AMP-activated protein kinase--a sensor of glycogen as well as AMP and ATP? Adenosine Triphosphate 70-73 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-28 19245651-1 2009 The classical role of the AMP-activated protein kinase (AMPK) is to act as a sensor of the immediate availability of cellular energy, by monitoring the concentrations of AMP and ATP. Adenosine Monophosphate 26-29 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 56-60 19245651-1 2009 The classical role of the AMP-activated protein kinase (AMPK) is to act as a sensor of the immediate availability of cellular energy, by monitoring the concentrations of AMP and ATP. Adenosine Triphosphate 178-181 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 26-54 19245651-1 2009 The classical role of the AMP-activated protein kinase (AMPK) is to act as a sensor of the immediate availability of cellular energy, by monitoring the concentrations of AMP and ATP. Adenosine Triphosphate 178-181 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 56-60 19245651-2 2009 However, the beta subunits of AMPK contain a glycogen-binding domain, and in this review we develop the hypothesis that this is a regulatory domain that allows AMPK to act as a sensor of the status of cellular reserves of energy in the form of glycogen. Glycogen 45-53 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-34 19245651-2 2009 However, the beta subunits of AMPK contain a glycogen-binding domain, and in this review we develop the hypothesis that this is a regulatory domain that allows AMPK to act as a sensor of the status of cellular reserves of energy in the form of glycogen. Glycogen 45-53 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 160-164 19245651-2 2009 However, the beta subunits of AMPK contain a glycogen-binding domain, and in this review we develop the hypothesis that this is a regulatory domain that allows AMPK to act as a sensor of the status of cellular reserves of energy in the form of glycogen. Glycogen 244-252 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-34 19245651-2 2009 However, the beta subunits of AMPK contain a glycogen-binding domain, and in this review we develop the hypothesis that this is a regulatory domain that allows AMPK to act as a sensor of the status of cellular reserves of energy in the form of glycogen. Glycogen 244-252 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 160-164 19245651-3 2009 We argue that the pool of AMPK that is bound to the glycogen particle is in an active state when glycogen particles are fully synthesized, causing phosphorylation of glycogen synthase at site 2 and providing a feedback inhibition of further extension of the outer chains of glycogen. Glycogen 52-60 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 26-30 19245651-3 2009 We argue that the pool of AMPK that is bound to the glycogen particle is in an active state when glycogen particles are fully synthesized, causing phosphorylation of glycogen synthase at site 2 and providing a feedback inhibition of further extension of the outer chains of glycogen. Glycogen 97-105 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 26-30 19245651-3 2009 We argue that the pool of AMPK that is bound to the glycogen particle is in an active state when glycogen particles are fully synthesized, causing phosphorylation of glycogen synthase at site 2 and providing a feedback inhibition of further extension of the outer chains of glycogen. Glycogen 97-105 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 26-30 19245651-4 2009 However, when glycogen becomes depleted, the glycogen-bound pool of AMPK becomes inhibited due to binding to alpha1-->6-linked branch points exposed by the action of phosphorylase and/or debranching enzyme. Glycogen 14-22 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 68-72 19245651-4 2009 However, when glycogen becomes depleted, the glycogen-bound pool of AMPK becomes inhibited due to binding to alpha1-->6-linked branch points exposed by the action of phosphorylase and/or debranching enzyme. Glycogen 45-53 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 68-72 19245652-7 2009 This adaptive response involves AMPK activation by the initial ATP drop, which elevates cell surface GLUT4 and glucose uptake. Adenosine Triphosphate 63-66 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 32-36 19245652-7 2009 This adaptive response involves AMPK activation by the initial ATP drop, which elevates cell surface GLUT4 and glucose uptake. Glucose 111-118 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 32-36 19245652-10 2009 Given that energy stress is a component of muscle contraction, and that contraction activates AMPK and raises cytosolic calcium, we hypothesize that the increase in glucose uptake during contraction may also involve a reduction in GLUT4 endocytosis. Glucose 165-172 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 94-98 19265677-5 2009 Energy status information triggered by glucose is transmitted via hypothalamic signaling intermediaries, i.e. AMPK and malonyl-CoA, to the orexigenic/anorexigenic neuropeptide system that determines hunger and energy expenditure. Glucose 39-46 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 110-114 19265677-6 2009 The central metabolism of glucose by the glycolytic pathway generates ATP which produces a compensatory decrease in AMP level and AMPK activity. Glucose 26-33 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 130-134 19265677-6 2009 The central metabolism of glucose by the glycolytic pathway generates ATP which produces a compensatory decrease in AMP level and AMPK activity. Adenosine Triphosphate 70-73 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 130-134 19265677-11 2009 Thus, fructose has the opposite effect of glucose on the AMPK/malonyl-CoA signaling system and thereby, feeding behavior. Fructose 6-14 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 57-61 19265677-11 2009 Thus, fructose has the opposite effect of glucose on the AMPK/malonyl-CoA signaling system and thereby, feeding behavior. Glucose 42-49 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 57-61 19261894-6 2009 Interestingly, pharmacological activation of AMPK with AICAR (5-aminoimidazole-4-carboxamide riboside) alone also increased GLUT3 surface expression, with a hyperpolarization of Delta psi(m) evident in many neurons. acadesine 55-60 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 45-49 19171932-0 2009 AMP-activated protein kinase phosphorylates R5/PTG, the glycogen targeting subunit of the R5/PTG-protein phosphatase 1 holoenzyme, and accelerates its down-regulation by the laforin-malin complex. Glycogen 56-64 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-28 19171932-5 2009 We have also mapped the major phosphorylation sites of R5/PTG by mass spectrometry analysis, observing that phosphorylation of Ser-8 and Ser-268 increased upon activation of AMPK. Serine 127-130 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 174-178 19171932-5 2009 We have also mapped the major phosphorylation sites of R5/PTG by mass spectrometry analysis, observing that phosphorylation of Ser-8 and Ser-268 increased upon activation of AMPK. Serine 137-140 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 174-178 19171932-7 2009 We now demonstrate that phosphorylation of R5/PTG at Ser-8 by AMPK accelerates its laforin/malin-dependent ubiquitination and subsequent proteasomal degradation, which results in a decrease of its glycogenic activity. Serine 53-56 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 62-66 19171932-8 2009 Thus, our results define a novel role of AMPK in glycogen homeostasis. Glycogen 49-57 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 41-45 20195491-7 2009 Whereas all the three approaches tested inhibited TXNIP through the glycolytic pathway, DHEA acted by inhibiting G6PD and resveratrol through the activation of AMPK. Dehydroepiandrosterone 88-92 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 160-164 19261894-0 2009 Regulation of glucose transporter 3 surface expression by the AMP-activated protein kinase mediates tolerance to glutamate excitation in neurons. Glutamic Acid 113-122 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 62-90 19261894-5 2009 However, a significant increase only in GLUT3 surface expression was identified 30 min after excitation, with this high surface expression remaining significantly above control levels in many neurons for up to 4 h. Glutamate excitation induced a rapid alteration in the AMP:ATP ratio that was associated with the activation of the AMP-activated protein kinase (AMPK). Glutamic Acid 215-224 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 331-359 19261894-5 2009 However, a significant increase only in GLUT3 surface expression was identified 30 min after excitation, with this high surface expression remaining significantly above control levels in many neurons for up to 4 h. Glutamate excitation induced a rapid alteration in the AMP:ATP ratio that was associated with the activation of the AMP-activated protein kinase (AMPK). Glutamic Acid 215-224 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 361-365 19261894-5 2009 However, a significant increase only in GLUT3 surface expression was identified 30 min after excitation, with this high surface expression remaining significantly above control levels in many neurons for up to 4 h. Glutamate excitation induced a rapid alteration in the AMP:ATP ratio that was associated with the activation of the AMP-activated protein kinase (AMPK). Adenosine Monophosphate 270-273 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 331-359 19261894-5 2009 However, a significant increase only in GLUT3 surface expression was identified 30 min after excitation, with this high surface expression remaining significantly above control levels in many neurons for up to 4 h. Glutamate excitation induced a rapid alteration in the AMP:ATP ratio that was associated with the activation of the AMP-activated protein kinase (AMPK). Adenosine Monophosphate 270-273 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 361-365 19261894-6 2009 Interestingly, pharmacological activation of AMPK with AICAR (5-aminoimidazole-4-carboxamide riboside) alone also increased GLUT3 surface expression, with a hyperpolarization of Delta psi(m) evident in many neurons. acadesine 62-101 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 45-49 19262472-3 2009 Although the chemical reagent 5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside (AICAR) has been used to stimulate AMPK activity, AICAR has been associated with several nonspecific reactions. acadesine 30-84 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 120-124 19182950-0 2009 Compound K, intestinal metabolite of ginsenoside, attenuates hepatic lipid accumulation via AMPK activation in human hepatoma cells. Ginsenosides 37-48 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 92-96 19182950-11 2009 Taken together, AMPK mediates CK induced suppression and activation of SREBP1c and PPAR-alpha, respectively, and these effects seem to be one of antidiabetic and/or antihyperlipidemic mechanisms of CK in insulin-resistant HepG2 human hepatoma cells. ginsenoside M1 30-32 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 16-20 19182950-11 2009 Taken together, AMPK mediates CK induced suppression and activation of SREBP1c and PPAR-alpha, respectively, and these effects seem to be one of antidiabetic and/or antihyperlipidemic mechanisms of CK in insulin-resistant HepG2 human hepatoma cells. ginsenoside M1 198-200 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 16-20 19139632-4 2009 We recently demonstrated that hydrogen peroxide (H(2)O(2)) induces autophagy through a novel autophagy signaling mechanism linking PARP-1 activation to the LKB1-AMP-activated protein kinase (AMPK)-mammalian target of rapamycin (mTOR) pathway. Hydrogen Peroxide 30-47 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 156-189 19139632-4 2009 We recently demonstrated that hydrogen peroxide (H(2)O(2)) induces autophagy through a novel autophagy signaling mechanism linking PARP-1 activation to the LKB1-AMP-activated protein kinase (AMPK)-mammalian target of rapamycin (mTOR) pathway. Hydrogen Peroxide 30-47 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 191-195 19139632-4 2009 We recently demonstrated that hydrogen peroxide (H(2)O(2)) induces autophagy through a novel autophagy signaling mechanism linking PARP-1 activation to the LKB1-AMP-activated protein kinase (AMPK)-mammalian target of rapamycin (mTOR) pathway. Hydrogen Peroxide 49-57 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 156-189 19139632-4 2009 We recently demonstrated that hydrogen peroxide (H(2)O(2)) induces autophagy through a novel autophagy signaling mechanism linking PARP-1 activation to the LKB1-AMP-activated protein kinase (AMPK)-mammalian target of rapamycin (mTOR) pathway. Hydrogen Peroxide 49-57 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 191-195 19170765-1 2009 Glutamine : fructose-6-phosphate amidotransferase 1 (GFAT1) was identified as a protein phosphorylated in glucose-deprived cells by immunoprecipitation using the anti-phospho Akt substrates (PAS) antibody, which recognizes the phosphorylation motif site by AMP-activated protein kinase (AMPK), followed by mass fingerprinting analysis. Glucose 106-113 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 257-285 19170765-1 2009 Glutamine : fructose-6-phosphate amidotransferase 1 (GFAT1) was identified as a protein phosphorylated in glucose-deprived cells by immunoprecipitation using the anti-phospho Akt substrates (PAS) antibody, which recognizes the phosphorylation motif site by AMP-activated protein kinase (AMPK), followed by mass fingerprinting analysis. Glucose 106-113 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 287-291 19170765-2 2009 Glucose depletion-induced phosphorylation of endogenous GFAT was potentiated by 2-deoxyglucose (2-DG), an AMPK activator, and the 2-DG-stimulated phosphorylation of FLAG-tagged GFAT1 in transfected cells was suppressed by Compound C, an AMPK inhibitor. Glucose 0-7 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 106-110 19170765-2 2009 Glucose depletion-induced phosphorylation of endogenous GFAT was potentiated by 2-deoxyglucose (2-DG), an AMPK activator, and the 2-DG-stimulated phosphorylation of FLAG-tagged GFAT1 in transfected cells was suppressed by Compound C, an AMPK inhibitor. Glucose 0-7 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 237-241 19170765-2 2009 Glucose depletion-induced phosphorylation of endogenous GFAT was potentiated by 2-deoxyglucose (2-DG), an AMPK activator, and the 2-DG-stimulated phosphorylation of FLAG-tagged GFAT1 in transfected cells was suppressed by Compound C, an AMPK inhibitor. Deoxyglucose 96-100 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 237-241 19170765-2 2009 Glucose depletion-induced phosphorylation of endogenous GFAT was potentiated by 2-deoxyglucose (2-DG), an AMPK activator, and the 2-DG-stimulated phosphorylation of FLAG-tagged GFAT1 in transfected cells was suppressed by Compound C, an AMPK inhibitor. Deoxyglucose 130-134 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 237-241 19052260-9 2009 Finally, treating NuLi monolayers with the membrane permeant AMPK activator 5-aminoimidazole-4-carboxamide-1-beta-d-ribofuranoside (AICAR) caused a significant decrease of the KCa3.1-mediated short-circuit currents, an effect reversible by coincubation with the AMPK inhibitor Compound C. These observations argue for a regulation of KCa3.1 by AMPK in a functional epithelium through protein/protein interactions involving the gamma1-subunit of AMPK. Aminoimidazole Carboxamide 76-106 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 61-65 19052260-9 2009 Finally, treating NuLi monolayers with the membrane permeant AMPK activator 5-aminoimidazole-4-carboxamide-1-beta-d-ribofuranoside (AICAR) caused a significant decrease of the KCa3.1-mediated short-circuit currents, an effect reversible by coincubation with the AMPK inhibitor Compound C. These observations argue for a regulation of KCa3.1 by AMPK in a functional epithelium through protein/protein interactions involving the gamma1-subunit of AMPK. Aminoimidazole Carboxamide 76-106 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 262-266 19052260-9 2009 Finally, treating NuLi monolayers with the membrane permeant AMPK activator 5-aminoimidazole-4-carboxamide-1-beta-d-ribofuranoside (AICAR) caused a significant decrease of the KCa3.1-mediated short-circuit currents, an effect reversible by coincubation with the AMPK inhibitor Compound C. These observations argue for a regulation of KCa3.1 by AMPK in a functional epithelium through protein/protein interactions involving the gamma1-subunit of AMPK. Aminoimidazole Carboxamide 76-106 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 262-266 19052260-9 2009 Finally, treating NuLi monolayers with the membrane permeant AMPK activator 5-aminoimidazole-4-carboxamide-1-beta-d-ribofuranoside (AICAR) caused a significant decrease of the KCa3.1-mediated short-circuit currents, an effect reversible by coincubation with the AMPK inhibitor Compound C. These observations argue for a regulation of KCa3.1 by AMPK in a functional epithelium through protein/protein interactions involving the gamma1-subunit of AMPK. Aminoimidazole Carboxamide 76-106 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 262-266 19052260-9 2009 Finally, treating NuLi monolayers with the membrane permeant AMPK activator 5-aminoimidazole-4-carboxamide-1-beta-d-ribofuranoside (AICAR) caused a significant decrease of the KCa3.1-mediated short-circuit currents, an effect reversible by coincubation with the AMPK inhibitor Compound C. These observations argue for a regulation of KCa3.1 by AMPK in a functional epithelium through protein/protein interactions involving the gamma1-subunit of AMPK. 1-beta-d-ribofuranoside 107-130 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 61-65 19052260-9 2009 Finally, treating NuLi monolayers with the membrane permeant AMPK activator 5-aminoimidazole-4-carboxamide-1-beta-d-ribofuranoside (AICAR) caused a significant decrease of the KCa3.1-mediated short-circuit currents, an effect reversible by coincubation with the AMPK inhibitor Compound C. These observations argue for a regulation of KCa3.1 by AMPK in a functional epithelium through protein/protein interactions involving the gamma1-subunit of AMPK. 1-beta-d-ribofuranoside 107-130 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 262-266 19052260-9 2009 Finally, treating NuLi monolayers with the membrane permeant AMPK activator 5-aminoimidazole-4-carboxamide-1-beta-d-ribofuranoside (AICAR) caused a significant decrease of the KCa3.1-mediated short-circuit currents, an effect reversible by coincubation with the AMPK inhibitor Compound C. These observations argue for a regulation of KCa3.1 by AMPK in a functional epithelium through protein/protein interactions involving the gamma1-subunit of AMPK. 1-beta-d-ribofuranoside 107-130 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 262-266 19052260-9 2009 Finally, treating NuLi monolayers with the membrane permeant AMPK activator 5-aminoimidazole-4-carboxamide-1-beta-d-ribofuranoside (AICAR) caused a significant decrease of the KCa3.1-mediated short-circuit currents, an effect reversible by coincubation with the AMPK inhibitor Compound C. These observations argue for a regulation of KCa3.1 by AMPK in a functional epithelium through protein/protein interactions involving the gamma1-subunit of AMPK. 1-beta-d-ribofuranoside 107-130 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 262-266 19052260-9 2009 Finally, treating NuLi monolayers with the membrane permeant AMPK activator 5-aminoimidazole-4-carboxamide-1-beta-d-ribofuranoside (AICAR) caused a significant decrease of the KCa3.1-mediated short-circuit currents, an effect reversible by coincubation with the AMPK inhibitor Compound C. These observations argue for a regulation of KCa3.1 by AMPK in a functional epithelium through protein/protein interactions involving the gamma1-subunit of AMPK. acadesine 132-137 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 61-65 19052260-9 2009 Finally, treating NuLi monolayers with the membrane permeant AMPK activator 5-aminoimidazole-4-carboxamide-1-beta-d-ribofuranoside (AICAR) caused a significant decrease of the KCa3.1-mediated short-circuit currents, an effect reversible by coincubation with the AMPK inhibitor Compound C. These observations argue for a regulation of KCa3.1 by AMPK in a functional epithelium through protein/protein interactions involving the gamma1-subunit of AMPK. acadesine 132-137 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 262-266 19052260-9 2009 Finally, treating NuLi monolayers with the membrane permeant AMPK activator 5-aminoimidazole-4-carboxamide-1-beta-d-ribofuranoside (AICAR) caused a significant decrease of the KCa3.1-mediated short-circuit currents, an effect reversible by coincubation with the AMPK inhibitor Compound C. These observations argue for a regulation of KCa3.1 by AMPK in a functional epithelium through protein/protein interactions involving the gamma1-subunit of AMPK. acadesine 132-137 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 262-266 19052260-9 2009 Finally, treating NuLi monolayers with the membrane permeant AMPK activator 5-aminoimidazole-4-carboxamide-1-beta-d-ribofuranoside (AICAR) caused a significant decrease of the KCa3.1-mediated short-circuit currents, an effect reversible by coincubation with the AMPK inhibitor Compound C. These observations argue for a regulation of KCa3.1 by AMPK in a functional epithelium through protein/protein interactions involving the gamma1-subunit of AMPK. acadesine 132-137 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 262-266 19170765-3 2009 The 2-DG induced phosphorylation of GFAT1 was attenuated by the introduction of the kinase-negative mutant of AMPK, and the phosphorylation was observed in the cells expressing the constitutively active mutant of AMPK even in the absence of 2-DG. Deoxyglucose 4-8 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 110-114 19170765-3 2009 The 2-DG induced phosphorylation of GFAT1 was attenuated by the introduction of the kinase-negative mutant of AMPK, and the phosphorylation was observed in the cells expressing the constitutively active mutant of AMPK even in the absence of 2-DG. Deoxyglucose 4-8 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 213-217 19170765-3 2009 The 2-DG induced phosphorylation of GFAT1 was attenuated by the introduction of the kinase-negative mutant of AMPK, and the phosphorylation was observed in the cells expressing the constitutively active mutant of AMPK even in the absence of 2-DG. Deoxyglucose 241-245 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 213-217 19262472-3 2009 Although the chemical reagent 5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside (AICAR) has been used to stimulate AMPK activity, AICAR has been associated with several nonspecific reactions. acadesine 86-91 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 120-124 18703532-0 2009 Cilostazol inhibits cytokine-induced nuclear factor-kappaB activation via AMP-activated protein kinase activation in vascular endothelial cells. Cilostazol 0-10 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 74-102 19032940-7 2009 FASN release might represent a previously unrecognized mechanism through which AMPK monitor and restores cellular energy state in response to increasing AMP/ATP ratios. Adenosine Triphosphate 157-160 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 79-83 18854318-3 2009 Although some studies suggest that LKB1 is constitutively active and is not rate-limiting for activation of AMPK, others have suggested that phosphorylation of Ser-431 is necessary to allow LKB1 to phosphorylate and activate AMPK and other downstream kinases. Serine 160-163 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 225-229 18703532-7 2009 RNA interference of AMPK alpha 1 or the AMPK inhibitor compound C attenuated cilostazol-induced inhibition of NF-kappaB activation by TNFalpha. Cilostazol 77-87 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 20-32 18703532-7 2009 RNA interference of AMPK alpha 1 or the AMPK inhibitor compound C attenuated cilostazol-induced inhibition of NF-kappaB activation by TNFalpha. Cilostazol 77-87 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 20-24 18703532-8 2009 CONCLUSION: In the light of these findings, we suggest that cilostazol might attenuate the cytokine-induced expression of adhesion molecule genes by inhibiting NF-kappaB following AMPK activation. Cilostazol 60-70 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 180-184 19071085-1 2009 We examined in HepG2 cells whether glucose-induced changes in AMP-activated protein kinase (AMPK) activity could be mediated by SIRT1, an NAD(+)-dependent histone/protein deacetylase that has been linked to the increase in longevity caused by caloric restriction. Glucose 35-42 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 62-90 19071085-1 2009 We examined in HepG2 cells whether glucose-induced changes in AMP-activated protein kinase (AMPK) activity could be mediated by SIRT1, an NAD(+)-dependent histone/protein deacetylase that has been linked to the increase in longevity caused by caloric restriction. Glucose 35-42 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 92-96 19071085-1 2009 We examined in HepG2 cells whether glucose-induced changes in AMP-activated protein kinase (AMPK) activity could be mediated by SIRT1, an NAD(+)-dependent histone/protein deacetylase that has been linked to the increase in longevity caused by caloric restriction. NAD 138-144 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 62-90 19071085-1 2009 We examined in HepG2 cells whether glucose-induced changes in AMP-activated protein kinase (AMPK) activity could be mediated by SIRT1, an NAD(+)-dependent histone/protein deacetylase that has been linked to the increase in longevity caused by caloric restriction. NAD 138-144 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 92-96 19071085-2 2009 Incubation with 25 vs. 5mM glucose for 6h concurrently diminished the phosphorylation of AMPK (Thr 172) and ACC (Ser 79), increased lactate release, and decreased the abundance and activity of SIRT1. Glucose 27-34 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 89-93 19071085-2 2009 Incubation with 25 vs. 5mM glucose for 6h concurrently diminished the phosphorylation of AMPK (Thr 172) and ACC (Ser 79), increased lactate release, and decreased the abundance and activity of SIRT1. Threonine 95-98 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 89-93 19071085-3 2009 In contrast, incubation with pyruvate (0.1 and 1mM) for 2h increased AMPK phosphorylation and SIRT1 abundance and activity. Pyruvic Acid 29-37 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 69-73 19071085-3 2009 In contrast, incubation with pyruvate (0.1 and 1mM) for 2h increased AMPK phosphorylation and SIRT1 abundance and activity. Deuterium 56-58 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 69-73 19071085-4 2009 The putative SIRT1 activators resveratrol and quercetin also increased AMPK phosphorylation. Resveratrol 30-41 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 71-75 19071085-4 2009 The putative SIRT1 activators resveratrol and quercetin also increased AMPK phosphorylation. Quercetin 46-55 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 71-75 19071085-6 2009 Collectively, these findings raise the possibility that glucose-induced changes in AMPK are linked to alterations in SIRT1 abundance and activity and possibly cellular redox state. Glucose 56-63 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 83-87 19106626-7 2009 Mechanistically, metformin-induced suppression of HER2 overexpression appears to occur via direct (AMPK-independent) inhibition of p70S6K1 activity. Metformin 17-26 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 99-103 18703532-2 2009 We hypothesized that cilostazol may prevent inflammatory cytokine induced-nuclear factor (NF)-kappaB activation by activating AMP-activated protein kinase (AMPK) in vascular endothelial cells. Cilostazol 21-31 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 126-154 18703532-2 2009 We hypothesized that cilostazol may prevent inflammatory cytokine induced-nuclear factor (NF)-kappaB activation by activating AMP-activated protein kinase (AMPK) in vascular endothelial cells. Cilostazol 21-31 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 156-160 18703532-3 2009 METHODS AND RESULTS: Cilostazol was observed to activate AMPK and its downstream target, acetyl-CoA carboxylase, in human umbilical vein endothelial cells (HUVEC). Cilostazol 21-31 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 57-61 18703532-4 2009 Phosphorylation of AMPK with cilostazol was not affected by co-treatment with an adenylate cyclase inhibitor, SQ 22536, and a cell-permeable cAMP analogue, pCTP-cAMP, did not induce AMPK phosphorylation and had no effect on cilostazol-induced AMPK phosphorylation, suggesting that cilostazol-induced AMPK activation occurs through a signalling pathway independent of cyclic AMP. Cilostazol 29-39 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 19-23 18703532-4 2009 Phosphorylation of AMPK with cilostazol was not affected by co-treatment with an adenylate cyclase inhibitor, SQ 22536, and a cell-permeable cAMP analogue, pCTP-cAMP, did not induce AMPK phosphorylation and had no effect on cilostazol-induced AMPK phosphorylation, suggesting that cilostazol-induced AMPK activation occurs through a signalling pathway independent of cyclic AMP. Cyclic AMP 161-165 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 19-23 18703532-4 2009 Phosphorylation of AMPK with cilostazol was not affected by co-treatment with an adenylate cyclase inhibitor, SQ 22536, and a cell-permeable cAMP analogue, pCTP-cAMP, did not induce AMPK phosphorylation and had no effect on cilostazol-induced AMPK phosphorylation, suggesting that cilostazol-induced AMPK activation occurs through a signalling pathway independent of cyclic AMP. Cilostazol 224-234 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 19-23 18703532-4 2009 Phosphorylation of AMPK with cilostazol was not affected by co-treatment with an adenylate cyclase inhibitor, SQ 22536, and a cell-permeable cAMP analogue, pCTP-cAMP, did not induce AMPK phosphorylation and had no effect on cilostazol-induced AMPK phosphorylation, suggesting that cilostazol-induced AMPK activation occurs through a signalling pathway independent of cyclic AMP. Cilostazol 224-234 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 19-23 18703532-4 2009 Phosphorylation of AMPK with cilostazol was not affected by co-treatment with an adenylate cyclase inhibitor, SQ 22536, and a cell-permeable cAMP analogue, pCTP-cAMP, did not induce AMPK phosphorylation and had no effect on cilostazol-induced AMPK phosphorylation, suggesting that cilostazol-induced AMPK activation occurs through a signalling pathway independent of cyclic AMP. Cyclic AMP 367-377 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 19-23 18502715-0 2008 AMPK activator, AICAR, inhibits palmitate-induced apoptosis in osteoblast. AICA ribonucleotide 16-21 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 19057188-7 2009 Leucine has been shown to modulate the activity of the energy and nutrient sensor pathways controlled by AMPK and mTOR in the hypothalamus. Leucine 0-7 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 105-109 19029811-5 2008 When ATP levels decrease, AMPK is activated to boost ATP production and to inhibit ATP usage, thus restoring energy balance. Adenosine Triphosphate 5-8 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 26-30 19029811-5 2008 When ATP levels decrease, AMPK is activated to boost ATP production and to inhibit ATP usage, thus restoring energy balance. Adenosine Triphosphate 53-56 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 26-30 19029811-5 2008 When ATP levels decrease, AMPK is activated to boost ATP production and to inhibit ATP usage, thus restoring energy balance. Adenosine Triphosphate 53-56 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 26-30 18544643-7 2008 Activation of either the AMPK or calcineurin pathway can also enhance the glycogen storage capacity and insulin sensitivity in skeletal muscle. Glycogen 74-82 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 25-29 18719597-2 2008 Studied extensively in liver and skeletal muscle, AMPK is phosphorylated and activated by LKB1 in response to increasing AMP/ATP ratios, which occur in a variety of settings including hypoxia, nutrient starvation and redox imbalance. Adenosine Triphosphate 125-128 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 50-54 18719601-6 2008 In certain cells, AMPK is activated in response to elevation of cytosolic Ca2+ via phosphorylation of Thr-172 by calmodulin-dependent kinase kinase-beta (CaMKKbeta). Threonine 102-105 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 18-22 18719601-8 2008 Two existing classes of antidiabetic drugs, that is, biguanides (for example, metformin) and the thiazolidinediones (for example, rosiglitazone), both act (at least in part) by activation of AMPK. Biguanides 53-63 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 191-195 18719601-8 2008 Two existing classes of antidiabetic drugs, that is, biguanides (for example, metformin) and the thiazolidinediones (for example, rosiglitazone), both act (at least in part) by activation of AMPK. Metformin 78-87 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 191-195 18719601-8 2008 Two existing classes of antidiabetic drugs, that is, biguanides (for example, metformin) and the thiazolidinediones (for example, rosiglitazone), both act (at least in part) by activation of AMPK. Thiazolidinediones 97-115 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 191-195 18719601-8 2008 Two existing classes of antidiabetic drugs, that is, biguanides (for example, metformin) and the thiazolidinediones (for example, rosiglitazone), both act (at least in part) by activation of AMPK. Rosiglitazone 130-143 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 191-195 19888214-1 2009 Highly conserved among eukaryotic cells, the AMP-activated kinase (AMPK) is a central regulator of carbon metabolism. Carbon 99-105 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 67-71 18693249-1 2008 In endothelial cells, the AMP-activated protein kinase (AMPK) is stimulated by sheer stress or growth factors that stimulate release of nitric oxide (NO). Nitric Oxide 136-148 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 56-60 18693249-3 2008 Exposure of human umbilical vein endothelial cells (HUVECs) to NO donors caused an increase in phosphorylation of both Thr-172 of AMPK and Ser-1177 of endothelial nitric oxide synthase, a downstream enzyme of AMPK. Threonine 119-122 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 130-134 18693249-7 2008 Exposure of HUVECs or isolated mice aortas to either calcium ionophore A23187 or bradykinin significantly increased AMPK Thr-172 phosphorylation, which was abolished by N-nitro-L-arginine methyl ester, an inhibitor of nitric oxide synthase. Calcium 53-60 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 116-120 18693249-7 2008 Exposure of HUVECs or isolated mice aortas to either calcium ionophore A23187 or bradykinin significantly increased AMPK Thr-172 phosphorylation, which was abolished by N-nitro-L-arginine methyl ester, an inhibitor of nitric oxide synthase. Calcimycin 71-77 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 116-120 18693249-7 2008 Exposure of HUVECs or isolated mice aortas to either calcium ionophore A23187 or bradykinin significantly increased AMPK Thr-172 phosphorylation, which was abolished by N-nitro-L-arginine methyl ester, an inhibitor of nitric oxide synthase. Threonine 121-124 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 116-120 18693249-7 2008 Exposure of HUVECs or isolated mice aortas to either calcium ionophore A23187 or bradykinin significantly increased AMPK Thr-172 phosphorylation, which was abolished by N-nitro-L-arginine methyl ester, an inhibitor of nitric oxide synthase. n-nitro-l-arginine methyl ester 169-200 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 116-120 18693249-8 2008 Finally, A23187- or bradykinin-enhanced AMPK activation was significantly greater in aortas from wild type mice than those in the aortas of endothelial nitric oxide synthase knock-out mice. Calcimycin 9-15 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 40-44 18599796-8 2008 Furthermore, lovastatin promoted the activation of AMPK and eNOS, the expression of EC markers, tube formation, adhesion, and in vivo vasculogenesis of EPCs, which could be blocked by treatment with Compound C. CONCLUSIONS: The activation of eNOS by AMPK during EPC differentiation provides a novel mechanism for the pleiotropic effects of statins in benefiting the cardiovascular system. Lovastatin 13-23 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 51-55 18599796-8 2008 Furthermore, lovastatin promoted the activation of AMPK and eNOS, the expression of EC markers, tube formation, adhesion, and in vivo vasculogenesis of EPCs, which could be blocked by treatment with Compound C. CONCLUSIONS: The activation of eNOS by AMPK during EPC differentiation provides a novel mechanism for the pleiotropic effects of statins in benefiting the cardiovascular system. Lovastatin 13-23 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 250-254 18502715-0 2008 AMPK activator, AICAR, inhibits palmitate-induced apoptosis in osteoblast. Palmitates 32-41 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 18502715-3 2008 The AMPK activator, AICAR, has been shown to inhibit palmitate-induced apoptosis. Palmitates 53-62 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 4-8 18502715-9 2008 Constitutively-active AMPK also inhibited palmitate-induced apoptosis. Palmitates 42-51 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 22-26 18502715-14 2008 These results suggest that palmitate induces apoptosis in osteoblasts through the impaired activation of ERK, and the activation of AMPK inhibits palmitate-induced apoptosis by activating ERK. Palmitates 146-155 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 132-136 17896107-13 2008 In the absence of hypoxanthine, the AMP/ATP ratio in PC-3 cells increased by 38% and was accompanied by a modest increase in the level of phosphorylated AMPK; no increase was observed in the presence of hypoxanthine where the AMP/ATP ratio increased by approximately 10%. Adenosine Monophosphate 36-39 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 153-157 17896107-14 2008 Under these same culture conditions, the AMP/ATP ratio in DU145 cells in the absence of hypoxanthine increased by 60% and was accompanied by a large increase in phosphorylated AMPK. Adenosine Monophosphate 41-44 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 176-180 17896107-14 2008 Under these same culture conditions, the AMP/ATP ratio in DU145 cells in the absence of hypoxanthine increased by 60% and was accompanied by a large increase in phosphorylated AMPK. Adenosine Triphosphate 45-48 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 176-180 17896107-18 2008 Activation of the AMPK signaling pathway in drug-treated PC-3 and DU145 cells is cell line dependent and independent of the AMP/ATP ratio. Adenosine Triphosphate 128-131 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 18-22 18436530-2 2008 Here we demonstrate that the muscarinic receptor agonist carbachol activates AMPKalpha1-containing complexes in the human SH-SY5Y cell line via a mechanism specific for the AMPK upstream kinase, Ca(2+)/calmodulin-dependent protein kinase kinase beta. Carbachol 57-66 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 77-87 18436530-2 2008 Here we demonstrate that the muscarinic receptor agonist carbachol activates AMPKalpha1-containing complexes in the human SH-SY5Y cell line via a mechanism specific for the AMPK upstream kinase, Ca(2+)/calmodulin-dependent protein kinase kinase beta. Carbachol 57-66 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 77-81 18369362-3 2008 METHODS AND RESULTS: Treatment of human umbilical vein endothelial cells (HUVECs) with cilostazol resulted in time-dependent activation of AMPK, as monitored by phosphorylation of AMPK and its down-stream target, acetyl-CoA carboxylase (ACC). Cilostazol 87-97 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 139-143 18321858-4 2008 Based on PT1-docked AMPK alpha1 subunit structure model and different mutations, we found PT1 might interact with Glu-96 and Lys-156 residues near the autoinhibitory domain and directly relieve autoinhibition. Glutamic Acid 114-117 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 20-31 18321858-4 2008 Based on PT1-docked AMPK alpha1 subunit structure model and different mutations, we found PT1 might interact with Glu-96 and Lys-156 residues near the autoinhibitory domain and directly relieve autoinhibition. Lysine 125-128 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 20-31 18321858-5 2008 Further studies using L6 myotubes showed that the phosphorylation of AMPK and its downstream substrate, acetyl-CoA carboxylase, were dose-dependently and time-dependently increased by PT1 with-out an increase in cellular AMP:ATP ratio. Adenosine Triphosphate 225-228 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 69-73 18177481-7 2008 The importance of AMPK in cardiovascular functions is best demonstrated by recent studies showing that widely used drugs, including statins, metformin and rosiglitazone, execute cardiovascular protective effects at least partly through the activation of AMPK. Metformin 141-150 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 18-22 18177481-7 2008 The importance of AMPK in cardiovascular functions is best demonstrated by recent studies showing that widely used drugs, including statins, metformin and rosiglitazone, execute cardiovascular protective effects at least partly through the activation of AMPK. Metformin 141-150 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 254-258 18177481-7 2008 The importance of AMPK in cardiovascular functions is best demonstrated by recent studies showing that widely used drugs, including statins, metformin and rosiglitazone, execute cardiovascular protective effects at least partly through the activation of AMPK. Rosiglitazone 155-168 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 18-22 18177481-7 2008 The importance of AMPK in cardiovascular functions is best demonstrated by recent studies showing that widely used drugs, including statins, metformin and rosiglitazone, execute cardiovascular protective effects at least partly through the activation of AMPK. Rosiglitazone 155-168 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 254-258 18508608-3 2008 Specifically, the role of LKB1 and phosphatase PP2C in nucleotide-dependent activation of AMPK, and ionized calcium in CaMKK-dependent activation of AMPK in working muscle is discussed. Calcium 108-115 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 149-153 18508608-5 2008 Currently, during intensive contraction, activation of alpha2-AMPK seems mainly to rely on AMP accumulating from ATP-hydrolysis whereas calcium signaling may have some importance during more gentle contraction conditions. Adenosine Triphosphate 113-116 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 62-66 18387000-2 2008 Blood glucose-lowering Type 2 diabetes drugs also induce LKB1 to activate AMPK, indicating that these compounds could be used to suppress growth of tumour cells. Blood Glucose 0-13 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 74-78 18387000-5 2008 In contrast, activating the AMPK pathway by administration of metformin, phenformin or A-769662 to PTEN(+/-) mice significantly delayed tumour onset. Metformin 62-71 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 28-32 18387000-5 2008 In contrast, activating the AMPK pathway by administration of metformin, phenformin or A-769662 to PTEN(+/-) mice significantly delayed tumour onset. Phenformin 73-83 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 28-32 18387000-9 2008 Most importantly, our results demonstrate the potential of AMPK activators, such as clinically approved metformin, as anticancer agents, which will suppress tumour development by triggering a physiological signalling pathway that potently inhibits cell growth. Metformin 104-113 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 59-63 18477450-0 2008 Glucose restriction inhibits skeletal myoblast differentiation by activating SIRT1 through AMPK-mediated regulation of Nampt. Glucose 0-7 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 91-95 18477450-4 2008 Glucose restriction (GR) impaired differentiation of skeletal myoblasts and was associated with activation of the AMP-activated protein kinase (AMPK). Glucose 0-7 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 114-142 18477450-4 2008 Glucose restriction (GR) impaired differentiation of skeletal myoblasts and was associated with activation of the AMP-activated protein kinase (AMPK). Glucose 0-7 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 144-148 18477450-5 2008 Activated AMPK was required to promote GR-induced transcription of the NAD+ biosynthetic enzyme Nampt. NAD 71-75 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 10-14 18439900-1 2008 AMPK is a highly conserved sensor of cellular energy status that is activated under conditions of low intracellular ATP. Adenosine Triphosphate 116-119 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 18439900-5 2008 We report here that AMPK directly phosphorylates the mTOR binding partner raptor on two well-conserved serine residues, and this phosphorylation induces 14-3-3 binding to raptor. Serine 103-109 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 20-24 18369362-3 2008 METHODS AND RESULTS: Treatment of human umbilical vein endothelial cells (HUVECs) with cilostazol resulted in time-dependent activation of AMPK, as monitored by phosphorylation of AMPK and its down-stream target, acetyl-CoA carboxylase (ACC). Cilostazol 87-97 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 180-184 18184747-5 2008 We also observed a significant increase in AMPK levels up on SIRT1 inhibition under glucose limiting conditions. Glucose 84-91 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 43-47 18063581-5 2008 The 2-DG-induced phosphorylation of GBF1 was suppressed by Compound C, an AMPK inhibitor, and by the overexpression of the kinase-negative AMPK. Deoxyglucose 4-8 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 74-78 18250273-9 2008 Finally, inhibition of PKC-zeta abolished metformin-enhanced coimmunoprecipitation of LKB1 with both AMPKalpha1 and AMPKalpha2. Metformin 42-51 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 101-111 18079111-0 2008 AMP-activated protein kinase subunit interactions: beta1:gamma1 association requires beta1 Thr-263 and Tyr-267. Threonine 91-94 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-28 18079111-0 2008 AMP-activated protein kinase subunit interactions: beta1:gamma1 association requires beta1 Thr-263 and Tyr-267. Tyrosine 103-106 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-28 18079111-1 2008 AMP-activated protein kinase (AMPK) plays multiple roles in the body"s overall metabolic balance and response to exercise, nutritional stress, hormonal stimulation, and the glucose-lowering drugs metformin and rosiglitazone. Glucose 173-180 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-28 18079111-1 2008 AMP-activated protein kinase (AMPK) plays multiple roles in the body"s overall metabolic balance and response to exercise, nutritional stress, hormonal stimulation, and the glucose-lowering drugs metformin and rosiglitazone. Glucose 173-180 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-34 18079111-1 2008 AMP-activated protein kinase (AMPK) plays multiple roles in the body"s overall metabolic balance and response to exercise, nutritional stress, hormonal stimulation, and the glucose-lowering drugs metformin and rosiglitazone. Metformin 196-205 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-28 18079111-1 2008 AMP-activated protein kinase (AMPK) plays multiple roles in the body"s overall metabolic balance and response to exercise, nutritional stress, hormonal stimulation, and the glucose-lowering drugs metformin and rosiglitazone. Metformin 196-205 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-34 18079111-1 2008 AMP-activated protein kinase (AMPK) plays multiple roles in the body"s overall metabolic balance and response to exercise, nutritional stress, hormonal stimulation, and the glucose-lowering drugs metformin and rosiglitazone. Rosiglitazone 210-223 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-28 18079111-1 2008 AMP-activated protein kinase (AMPK) plays multiple roles in the body"s overall metabolic balance and response to exercise, nutritional stress, hormonal stimulation, and the glucose-lowering drugs metformin and rosiglitazone. Rosiglitazone 210-223 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-34 18063581-5 2008 The 2-DG-induced phosphorylation of GBF1 was suppressed by Compound C, an AMPK inhibitor, and by the overexpression of the kinase-negative AMPK. Deoxyglucose 4-8 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 139-143 18063581-6 2008 Analysis using the deletion and point mutants identified Thr(1337) as the 2-DG-induced phosphorylation site in GBF1, which is phosphorylated by AMPK in vitro. Threonine 57-60 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 144-148 18063581-6 2008 Analysis using the deletion and point mutants identified Thr(1337) as the 2-DG-induced phosphorylation site in GBF1, which is phosphorylated by AMPK in vitro. Deoxyglucose 74-78 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 144-148 18063581-9 2008 The expression of the kinase-negative AMPK and the GBF1 mutant replacing Thr(1337) by Ala prevented the 2-DG-induced Golgi disassembly. Deoxyglucose 104-108 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 38-42 18063581-10 2008 These results indicate that GBF1 is a novel AMPK substrate and that the AMPK-mediated phosphorylation of GBF1 at Thr(1337) has a critical role, presumably by attenuating the function of GBF1, in the disassembly of the Golgi apparatus induced under stress conditions that lower the intracellular ATP concentration. Threonine 113-116 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 44-48 18063581-10 2008 These results indicate that GBF1 is a novel AMPK substrate and that the AMPK-mediated phosphorylation of GBF1 at Thr(1337) has a critical role, presumably by attenuating the function of GBF1, in the disassembly of the Golgi apparatus induced under stress conditions that lower the intracellular ATP concentration. Threonine 113-116 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 72-76 18063581-10 2008 These results indicate that GBF1 is a novel AMPK substrate and that the AMPK-mediated phosphorylation of GBF1 at Thr(1337) has a critical role, presumably by attenuating the function of GBF1, in the disassembly of the Golgi apparatus induced under stress conditions that lower the intracellular ATP concentration. Adenosine Triphosphate 295-298 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 44-48 18063581-10 2008 These results indicate that GBF1 is a novel AMPK substrate and that the AMPK-mediated phosphorylation of GBF1 at Thr(1337) has a critical role, presumably by attenuating the function of GBF1, in the disassembly of the Golgi apparatus induced under stress conditions that lower the intracellular ATP concentration. Adenosine Triphosphate 295-298 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 72-76 17995453-6 2008 In HEK-293 cells, LY294002 inhibits phosphorylation of Thr596 of TBC1D1, and promotes phosphorylation of AMPK and Ser237 of TBC1D1. 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one 18-26 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 105-109 17936912-0 2008 Physiological glucose is critical for optimized neuronal viability and AMPK responsiveness in vitro. Glucose 14-21 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 71-75 17919121-0 2008 Polyamines modulate the subcellular localization of RNA-binding protein HuR through AMP-activated protein kinase-regulated phosphorylation and acetylation of importin alpha1. Polyamines 0-10 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 84-112 17919121-3 2008 Here, we provide evidence showing that polyamines modulate subcellular localization of HuR through AMPK-regulated phosphorylation and acetylation of Impalpha1 (importin alpha1) in IECs. Polyamines 39-49 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 99-103 17919121-4 2008 Decreased levels of cellular polyamines as a result of inhibiting ODC (ornithine decarboxylase) with DFMO (D,L-alpha-difluoromethylornithine) repressed AMPK activity and reduced Impalpha1 levels, whereas increased levels of polyamines as a result of ODC overexpression induced both AMPK and Impalpha1 levels. Polyamines 29-39 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 152-156 17919121-4 2008 Decreased levels of cellular polyamines as a result of inhibiting ODC (ornithine decarboxylase) with DFMO (D,L-alpha-difluoromethylornithine) repressed AMPK activity and reduced Impalpha1 levels, whereas increased levels of polyamines as a result of ODC overexpression induced both AMPK and Impalpha1 levels. Polyamines 29-39 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 282-286 17919121-4 2008 Decreased levels of cellular polyamines as a result of inhibiting ODC (ornithine decarboxylase) with DFMO (D,L-alpha-difluoromethylornithine) repressed AMPK activity and reduced Impalpha1 levels, whereas increased levels of polyamines as a result of ODC overexpression induced both AMPK and Impalpha1 levels. Eflornithine 101-105 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 152-156 17919121-4 2008 Decreased levels of cellular polyamines as a result of inhibiting ODC (ornithine decarboxylase) with DFMO (D,L-alpha-difluoromethylornithine) repressed AMPK activity and reduced Impalpha1 levels, whereas increased levels of polyamines as a result of ODC overexpression induced both AMPK and Impalpha1 levels. Eflornithine 101-105 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 282-286 17919121-4 2008 Decreased levels of cellular polyamines as a result of inhibiting ODC (ornithine decarboxylase) with DFMO (D,L-alpha-difluoromethylornithine) repressed AMPK activity and reduced Impalpha1 levels, whereas increased levels of polyamines as a result of ODC overexpression induced both AMPK and Impalpha1 levels. Eflornithine 107-140 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 152-156 17919121-4 2008 Decreased levels of cellular polyamines as a result of inhibiting ODC (ornithine decarboxylase) with DFMO (D,L-alpha-difluoromethylornithine) repressed AMPK activity and reduced Impalpha1 levels, whereas increased levels of polyamines as a result of ODC overexpression induced both AMPK and Impalpha1 levels. Eflornithine 107-140 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 282-286 17919121-5 2008 AMPK activation by overexpression of the AMPK gene increased Impalpha1 but reduced the cytoplasmic levels of HuR in control and polyamine-deficient cells. Polyamines 128-137 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 17919121-5 2008 AMPK activation by overexpression of the AMPK gene increased Impalpha1 but reduced the cytoplasmic levels of HuR in control and polyamine-deficient cells. Polyamines 128-137 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 41-45 17919121-8 2008 These results indicate that polyamine-mediated AMPK activation triggers HuR nuclear import through phosphorylation and acetylation of Impalpha1 in IECs and that polyamine depletion increases cytoplasmic levels of HuR as a result of inactivation of the AMPK-driven Impalpha1 pathway. Polyamines 28-37 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 47-51 17919121-8 2008 These results indicate that polyamine-mediated AMPK activation triggers HuR nuclear import through phosphorylation and acetylation of Impalpha1 in IECs and that polyamine depletion increases cytoplasmic levels of HuR as a result of inactivation of the AMPK-driven Impalpha1 pathway. Polyamines 28-37 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 252-256 17919121-8 2008 These results indicate that polyamine-mediated AMPK activation triggers HuR nuclear import through phosphorylation and acetylation of Impalpha1 in IECs and that polyamine depletion increases cytoplasmic levels of HuR as a result of inactivation of the AMPK-driven Impalpha1 pathway. Polyamines 161-170 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 252-256 18089792-6 2007 Deguelin induced activation of AMP-activated protein kinase (AMPK) and inactivation of Akt. deguelin 0-8 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 61-65 17971295-11 2007 Moreover, we observed that ROS is an important upstream signal for AMPK activation during ginsenoside Rh2 treatment. ros 27-30 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 67-71 18089792-7 2007 Overexpression of constitutively active Akt abolished deguelin-induced modulation of AMPK activity and survivin expression. deguelin 54-62 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 85-89 18402338-6 2007 AMPK also participates in glycolysis regulation, glucose uptake, lipid oxidation, fatty acid synthesis, cholesterol synthesis and gluconeogenesis, and it has been considered as a possible target enzyme in the treatment of some diseases such as obesity, type 2 diabetes and hepatic steatosis. Fatty Acids 82-92 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 17720960-0 2007 Theaflavins attenuate hepatic lipid accumulation through activating AMPK in human HepG2 cells. theaflavin 0-11 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 68-72 17720960-5 2007 Furthermore, theaflavins also inhibited acetyl-coenzyme A carboxylase activities by stimulating AMP-activated protein kinase (AMPK) through the LKB1 and reactive oxygen species pathways. theaflavin 13-24 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 96-124 17720960-5 2007 Furthermore, theaflavins also inhibited acetyl-coenzyme A carboxylase activities by stimulating AMP-activated protein kinase (AMPK) through the LKB1 and reactive oxygen species pathways. theaflavin 13-24 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 126-130 17720960-5 2007 Furthermore, theaflavins also inhibited acetyl-coenzyme A carboxylase activities by stimulating AMP-activated protein kinase (AMPK) through the LKB1 and reactive oxygen species pathways. Reactive Oxygen Species 153-176 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 96-124 17720960-5 2007 Furthermore, theaflavins also inhibited acetyl-coenzyme A carboxylase activities by stimulating AMP-activated protein kinase (AMPK) through the LKB1 and reactive oxygen species pathways. Reactive Oxygen Species 153-176 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 126-130 17720960-6 2007 These observations support the idea that AMPK is a critical component of decreased hepatic lipid accumulation by theaflavin treatments. theaflavin 113-123 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 41-45 18402338-1 2007 The adenine monophosphate (AMP) activated protein kinase (AMPK), is a heterotrimeric complex that is activated by an increase in the AMP/ATP ratio, and is considered to be a cellular energy sensor that contributes to regulate energy balance and caloric intake. Adenosine Monophosphate 27-30 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 58-62 17962330-2 2007 The AMPK system is activated under conditions of cellular stress, indicated by an increase in the AMP/ATP ratio, as observed, e.g. in muscles during contractile activity. Adenosine Triphosphate 102-105 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 4-8 17962330-4 2007 However, recently it has become apparent that AMPK in mammals is also regulated by humoral substances, e.g. catecholamines. Catecholamines 108-122 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 46-50 17997341-5 2007 AMPK is activated by rising AMP and falling ATP. Adenosine Triphosphate 44-47 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 17997341-7 2007 AMPK system is a regulator of energy balance that, once activated by low energy status, switches on ATP-producing catabolic pathways (such as fatty acid oxidation and glycolysis), and switches off ATP-consuming anabolic pathways (such as lipogenesis), both by short-term effect on phosphorylation of regulatory proteins and by long-term effect on gene expression. Adenosine Triphosphate 100-103 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 17997341-7 2007 AMPK system is a regulator of energy balance that, once activated by low energy status, switches on ATP-producing catabolic pathways (such as fatty acid oxidation and glycolysis), and switches off ATP-consuming anabolic pathways (such as lipogenesis), both by short-term effect on phosphorylation of regulatory proteins and by long-term effect on gene expression. Fatty Acids 142-152 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 17997341-7 2007 AMPK system is a regulator of energy balance that, once activated by low energy status, switches on ATP-producing catabolic pathways (such as fatty acid oxidation and glycolysis), and switches off ATP-consuming anabolic pathways (such as lipogenesis), both by short-term effect on phosphorylation of regulatory proteins and by long-term effect on gene expression. Adenosine Triphosphate 197-200 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 17997341-9 2007 AMPK is robustly activated during skeletal muscle contraction and myocardial ischaemia playing a role in glucose transport and fatty acid oxidation. Glucose 105-112 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 17997341-9 2007 AMPK is robustly activated during skeletal muscle contraction and myocardial ischaemia playing a role in glucose transport and fatty acid oxidation. Fatty Acids 127-137 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 17997341-10 2007 In liver, activation of AMPK results in enhanced fatty acid oxidation as well as decreased glucose production. Fatty Acids 49-59 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 24-28 17997341-10 2007 In liver, activation of AMPK results in enhanced fatty acid oxidation as well as decreased glucose production. Glucose 91-98 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 24-28 17997341-11 2007 Moreover, the AMPK system is one of the probable targets for the anti-diabetic drugs biguanides and thiazolidinediones. Biguanides 85-95 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-18 17997341-11 2007 Moreover, the AMPK system is one of the probable targets for the anti-diabetic drugs biguanides and thiazolidinediones. Thiazolidinediones 100-118 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-18 17983576-2 2007 Three new papers providing structural information on mammalian and yeast AMPK homologs give insights into the binding of the regulatory nucleotides AMP and ATP and how mutations are associated with cardiac glycogen storage disorders. Adenosine Triphosphate 156-159 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 73-77 18402338-1 2007 The adenine monophosphate (AMP) activated protein kinase (AMPK), is a heterotrimeric complex that is activated by an increase in the AMP/ATP ratio, and is considered to be a cellular energy sensor that contributes to regulate energy balance and caloric intake. Adenosine Triphosphate 137-140 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 58-62 18402338-2 2007 AMPK is activated by LKB1 hinase and it can phophorylate several enzymes involved in anabolism to prevent further ATP consumption, and induces some catabolic enzymes to increase ATP generation. Adenosine Triphosphate 114-117 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 18402338-2 2007 AMPK is activated by LKB1 hinase and it can phophorylate several enzymes involved in anabolism to prevent further ATP consumption, and induces some catabolic enzymes to increase ATP generation. Adenosine Triphosphate 178-181 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 18402338-6 2007 AMPK also participates in glycolysis regulation, glucose uptake, lipid oxidation, fatty acid synthesis, cholesterol synthesis and gluconeogenesis, and it has been considered as a possible target enzyme in the treatment of some diseases such as obesity, type 2 diabetes and hepatic steatosis. Glucose 49-56 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 18402338-6 2007 AMPK also participates in glycolysis regulation, glucose uptake, lipid oxidation, fatty acid synthesis, cholesterol synthesis and gluconeogenesis, and it has been considered as a possible target enzyme in the treatment of some diseases such as obesity, type 2 diabetes and hepatic steatosis. Cholesterol 104-115 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 17687000-0 2007 Ca2+/calmodulin-dependent protein kinase kinase is involved in AMP-activated protein kinase activation by alpha-lipoic acid in C2C12 myotubes. Thioctic Acid 106-123 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 63-91 17687000-8 2007 Treatment of ALA increased the intracellular Ca(2+) concentration measured by fura-2 fluorescent microscopy (P < 0.05), showing that ALA may activate AMPK through enhancing Ca(2+)/calmodulin-dependent protein kinase kinase (CaMKK) signaling. Thioctic Acid 13-16 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 153-157 17687000-8 2007 Treatment of ALA increased the intracellular Ca(2+) concentration measured by fura-2 fluorescent microscopy (P < 0.05), showing that ALA may activate AMPK through enhancing Ca(2+)/calmodulin-dependent protein kinase kinase (CaMKK) signaling. Fura-2 78-84 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 153-157 17687000-2 2007 ALA stimulates glucose uptake and increases insulin sensitivity by the activation of AMP-activated protein kinase (AMPK) in skeletal muscle, but the underlying mechanism for AMPK activation is unknown. Thioctic Acid 0-3 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 85-113 17687000-8 2007 Treatment of ALA increased the intracellular Ca(2+) concentration measured by fura-2 fluorescent microscopy (P < 0.05), showing that ALA may activate AMPK through enhancing Ca(2+)/calmodulin-dependent protein kinase kinase (CaMKK) signaling. Thioctic Acid 136-139 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 153-157 17687000-2 2007 ALA stimulates glucose uptake and increases insulin sensitivity by the activation of AMP-activated protein kinase (AMPK) in skeletal muscle, but the underlying mechanism for AMPK activation is unknown. Thioctic Acid 0-3 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 115-119 17687000-9 2007 Indeed, chelation of intracellular free Ca(2+) by loading cells with 25 microM BAPTA-AM for 30 min abolished the ALA-induced activation of AMPK and, in turn, phosphorylation of ACC at Ser(79). 1,2-bis(2-aminophenoxy)ethane N,N,N',N'-tetraacetic acid acetoxymethyl ester 79-87 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 139-143 17687000-3 2007 Here, we investigated the mechanism through which ALA activates AMPK in C2C12 myotubes. Thioctic Acid 50-53 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 64-68 17687000-9 2007 Indeed, chelation of intracellular free Ca(2+) by loading cells with 25 microM BAPTA-AM for 30 min abolished the ALA-induced activation of AMPK and, in turn, phosphorylation of ACC at Ser(79). Thioctic Acid 113-116 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 139-143 17687000-4 2007 Incubation of C2C12 myotubes with 200 and 500 microM ALA increased the activity and phosphorylation of the AMPK alpha-subunit at Thr(172). Thioctic Acid 53-56 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 107-111 17687000-4 2007 Incubation of C2C12 myotubes with 200 and 500 microM ALA increased the activity and phosphorylation of the AMPK alpha-subunit at Thr(172). Threonine 129-132 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 107-111 17687000-10 2007 Furthermore, inhibition of CaMKK using its selective inhibitor, STO-609, abolished ALA-stimulated AMPK activation, with an accompanied reduction of ACC phosphorylation at Ser(79). STO 609 64-71 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 98-102 17687000-10 2007 Furthermore, inhibition of CaMKK using its selective inhibitor, STO-609, abolished ALA-stimulated AMPK activation, with an accompanied reduction of ACC phosphorylation at Ser(79). Thioctic Acid 83-86 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 98-102 17687000-5 2007 Phosphorylation of the AMPK substrate, acetyl CoA carboxylase (ACC), at Ser(79) was also increased. Serine 72-75 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 23-27 17687000-11 2007 In addition, ALA treatment increased the association of AMPK with CaMKK. Thioctic Acid 13-16 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 56-60 17603555-1 2007 BACKGROUND AND PURPOSE: AMP-activated protein kinase (AMPK) is activated by metformin, phenformin, and the AMP mimetic, 5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside (AICAR). Metformin 76-85 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 54-58 17687000-12 2007 To further show the role of CaMKK in AMPK activation, short interfering RNA was used to silence CaMKK, which abolished the ALA-induced AMPK activation. Thioctic Acid 123-126 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 37-41 17687000-12 2007 To further show the role of CaMKK in AMPK activation, short interfering RNA was used to silence CaMKK, which abolished the ALA-induced AMPK activation. Thioctic Acid 123-126 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 135-139 17687000-13 2007 These data show that CaMKK is the kinase responsible for ALA-induced AMPK activation in C2C12 myotubes. Thioctic Acid 57-60 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 69-73 17878409-3 2007 Enter LKB1, a kinase that is a tumor suppressor and that is an upstream activator of the adenosine monophosphate (AMP)-activated protein kinase (AMPK), a key sensor of cellular energy status. Adenosine Monophosphate 89-112 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 145-149 17635921-0 2007 Nicotine-induced activation of AMP-activated protein kinase inhibits fatty acid synthase in 3T3L1 adipocytes: a role for oxidant stress. Nicotine 0-8 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 31-59 17635921-2 2007 The objective of this study was to investigate the role of AMPK in nicotine-induced lipogenesis and lipolysis in 3T3L1 adipocytes. Nicotine 67-75 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 59-63 17635921-4 2007 The effects of nicotine on FAS activity were accompanied by phosphorylation of both AMPK (Thr(172)) and acetyl-CoA carboxylase (ACC; Ser(79)). Nicotine 15-23 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 84-88 17635921-4 2007 The effects of nicotine on FAS activity were accompanied by phosphorylation of both AMPK (Thr(172)) and acetyl-CoA carboxylase (ACC; Ser(79)). Threonine 90-93 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 84-88 17635921-5 2007 Nicotine-induced AMPK phosphorylation appeared to be mediated by reactive oxygen species based on the finding that nicotine significantly increased superoxide anions and 3-nitrotyrosine-positive proteins, exogenous peroxynitrite (ONOO(-)) mimicked the effects of nicotine on AMPK, and N-acetylcysteine (NAC) abolished nicotine-enhanced AMPK phosphorylation. Nicotine 0-8 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 17-21 17635921-5 2007 Nicotine-induced AMPK phosphorylation appeared to be mediated by reactive oxygen species based on the finding that nicotine significantly increased superoxide anions and 3-nitrotyrosine-positive proteins, exogenous peroxynitrite (ONOO(-)) mimicked the effects of nicotine on AMPK, and N-acetylcysteine (NAC) abolished nicotine-enhanced AMPK phosphorylation. Nicotine 0-8 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 275-279 17635921-5 2007 Nicotine-induced AMPK phosphorylation appeared to be mediated by reactive oxygen species based on the finding that nicotine significantly increased superoxide anions and 3-nitrotyrosine-positive proteins, exogenous peroxynitrite (ONOO(-)) mimicked the effects of nicotine on AMPK, and N-acetylcysteine (NAC) abolished nicotine-enhanced AMPK phosphorylation. Nicotine 0-8 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 275-279 17635921-5 2007 Nicotine-induced AMPK phosphorylation appeared to be mediated by reactive oxygen species based on the finding that nicotine significantly increased superoxide anions and 3-nitrotyrosine-positive proteins, exogenous peroxynitrite (ONOO(-)) mimicked the effects of nicotine on AMPK, and N-acetylcysteine (NAC) abolished nicotine-enhanced AMPK phosphorylation. Reactive Oxygen Species 65-88 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 17-21 17635921-5 2007 Nicotine-induced AMPK phosphorylation appeared to be mediated by reactive oxygen species based on the finding that nicotine significantly increased superoxide anions and 3-nitrotyrosine-positive proteins, exogenous peroxynitrite (ONOO(-)) mimicked the effects of nicotine on AMPK, and N-acetylcysteine (NAC) abolished nicotine-enhanced AMPK phosphorylation. Reactive Oxygen Species 65-88 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 275-279 17635921-5 2007 Nicotine-induced AMPK phosphorylation appeared to be mediated by reactive oxygen species based on the finding that nicotine significantly increased superoxide anions and 3-nitrotyrosine-positive proteins, exogenous peroxynitrite (ONOO(-)) mimicked the effects of nicotine on AMPK, and N-acetylcysteine (NAC) abolished nicotine-enhanced AMPK phosphorylation. Reactive Oxygen Species 65-88 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 275-279 17635921-5 2007 Nicotine-induced AMPK phosphorylation appeared to be mediated by reactive oxygen species based on the finding that nicotine significantly increased superoxide anions and 3-nitrotyrosine-positive proteins, exogenous peroxynitrite (ONOO(-)) mimicked the effects of nicotine on AMPK, and N-acetylcysteine (NAC) abolished nicotine-enhanced AMPK phosphorylation. Nicotine 115-123 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 17-21 17635921-5 2007 Nicotine-induced AMPK phosphorylation appeared to be mediated by reactive oxygen species based on the finding that nicotine significantly increased superoxide anions and 3-nitrotyrosine-positive proteins, exogenous peroxynitrite (ONOO(-)) mimicked the effects of nicotine on AMPK, and N-acetylcysteine (NAC) abolished nicotine-enhanced AMPK phosphorylation. Nicotine 115-123 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 275-279 17635921-5 2007 Nicotine-induced AMPK phosphorylation appeared to be mediated by reactive oxygen species based on the finding that nicotine significantly increased superoxide anions and 3-nitrotyrosine-positive proteins, exogenous peroxynitrite (ONOO(-)) mimicked the effects of nicotine on AMPK, and N-acetylcysteine (NAC) abolished nicotine-enhanced AMPK phosphorylation. Nicotine 115-123 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 275-279 17635921-5 2007 Nicotine-induced AMPK phosphorylation appeared to be mediated by reactive oxygen species based on the finding that nicotine significantly increased superoxide anions and 3-nitrotyrosine-positive proteins, exogenous peroxynitrite (ONOO(-)) mimicked the effects of nicotine on AMPK, and N-acetylcysteine (NAC) abolished nicotine-enhanced AMPK phosphorylation. Superoxides 148-165 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 17-21 17635921-5 2007 Nicotine-induced AMPK phosphorylation appeared to be mediated by reactive oxygen species based on the finding that nicotine significantly increased superoxide anions and 3-nitrotyrosine-positive proteins, exogenous peroxynitrite (ONOO(-)) mimicked the effects of nicotine on AMPK, and N-acetylcysteine (NAC) abolished nicotine-enhanced AMPK phosphorylation. 3-nitrotyrosine 170-185 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 17-21 17635921-5 2007 Nicotine-induced AMPK phosphorylation appeared to be mediated by reactive oxygen species based on the finding that nicotine significantly increased superoxide anions and 3-nitrotyrosine-positive proteins, exogenous peroxynitrite (ONOO(-)) mimicked the effects of nicotine on AMPK, and N-acetylcysteine (NAC) abolished nicotine-enhanced AMPK phosphorylation. Peroxynitrous Acid 215-228 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 17-21 17635921-5 2007 Nicotine-induced AMPK phosphorylation appeared to be mediated by reactive oxygen species based on the finding that nicotine significantly increased superoxide anions and 3-nitrotyrosine-positive proteins, exogenous peroxynitrite (ONOO(-)) mimicked the effects of nicotine on AMPK, and N-acetylcysteine (NAC) abolished nicotine-enhanced AMPK phosphorylation. onoo 230-234 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 17-21 17635921-5 2007 Nicotine-induced AMPK phosphorylation appeared to be mediated by reactive oxygen species based on the finding that nicotine significantly increased superoxide anions and 3-nitrotyrosine-positive proteins, exogenous peroxynitrite (ONOO(-)) mimicked the effects of nicotine on AMPK, and N-acetylcysteine (NAC) abolished nicotine-enhanced AMPK phosphorylation. Nicotine 263-271 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 17-21 17635921-5 2007 Nicotine-induced AMPK phosphorylation appeared to be mediated by reactive oxygen species based on the finding that nicotine significantly increased superoxide anions and 3-nitrotyrosine-positive proteins, exogenous peroxynitrite (ONOO(-)) mimicked the effects of nicotine on AMPK, and N-acetylcysteine (NAC) abolished nicotine-enhanced AMPK phosphorylation. Acetylcysteine 285-301 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 17-21 17635921-5 2007 Nicotine-induced AMPK phosphorylation appeared to be mediated by reactive oxygen species based on the finding that nicotine significantly increased superoxide anions and 3-nitrotyrosine-positive proteins, exogenous peroxynitrite (ONOO(-)) mimicked the effects of nicotine on AMPK, and N-acetylcysteine (NAC) abolished nicotine-enhanced AMPK phosphorylation. Acetylcysteine 303-306 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 17-21 17635921-5 2007 Nicotine-induced AMPK phosphorylation appeared to be mediated by reactive oxygen species based on the finding that nicotine significantly increased superoxide anions and 3-nitrotyrosine-positive proteins, exogenous peroxynitrite (ONOO(-)) mimicked the effects of nicotine on AMPK, and N-acetylcysteine (NAC) abolished nicotine-enhanced AMPK phosphorylation. Nicotine 263-271 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 17-21 17635921-6 2007 Inhibition of AMPK using either pharmacologic (insulin, compound C) or genetic means (overexpression of dominant negative AMPK; AMPK-DN) abolished FAS inhibition induced by nicotine or ONOO(-). Nicotine 173-181 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-18 17635921-6 2007 Inhibition of AMPK using either pharmacologic (insulin, compound C) or genetic means (overexpression of dominant negative AMPK; AMPK-DN) abolished FAS inhibition induced by nicotine or ONOO(-). Nicotine 173-181 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 122-126 17635921-6 2007 Inhibition of AMPK using either pharmacologic (insulin, compound C) or genetic means (overexpression of dominant negative AMPK; AMPK-DN) abolished FAS inhibition induced by nicotine or ONOO(-). Nicotine 173-181 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 122-126 17635921-6 2007 Inhibition of AMPK using either pharmacologic (insulin, compound C) or genetic means (overexpression of dominant negative AMPK; AMPK-DN) abolished FAS inhibition induced by nicotine or ONOO(-). onoo 185-189 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-18 17635921-6 2007 Inhibition of AMPK using either pharmacologic (insulin, compound C) or genetic means (overexpression of dominant negative AMPK; AMPK-DN) abolished FAS inhibition induced by nicotine or ONOO(-). onoo 185-189 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 122-126 17635921-6 2007 Inhibition of AMPK using either pharmacologic (insulin, compound C) or genetic means (overexpression of dominant negative AMPK; AMPK-DN) abolished FAS inhibition induced by nicotine or ONOO(-). onoo 185-189 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 122-126 17635921-7 2007 Conversely, activation of AMPK by pharmacologic (nicotine, ONOO(-), metformin, and AICAR) or genetic (overexpression of constitutively active AMPK) means inhibited FAS activity. Nicotine 49-57 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 26-30 17635921-7 2007 Conversely, activation of AMPK by pharmacologic (nicotine, ONOO(-), metformin, and AICAR) or genetic (overexpression of constitutively active AMPK) means inhibited FAS activity. onoo( 59-64 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 26-30 17615159-7 2007 Pharmacological activation of AMPK with 5-aminoimidazole-4-carboxamide-1-beta-4-ribofuranoside upregulated IL-6 mRNA expression, which was blocked by knockdown of AMPK alpha(1) and alpha(2) using small, interfering RNA (siRNA) oligonucleotides. 5-aminoimidazole-4-carboxamide-1-beta-4-ribofuranoside 40-94 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-34 17615159-7 2007 Pharmacological activation of AMPK with 5-aminoimidazole-4-carboxamide-1-beta-4-ribofuranoside upregulated IL-6 mRNA expression, which was blocked by knockdown of AMPK alpha(1) and alpha(2) using small, interfering RNA (siRNA) oligonucleotides. 5-aminoimidazole-4-carboxamide-1-beta-4-ribofuranoside 40-94 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 163-176 17615159-7 2007 Pharmacological activation of AMPK with 5-aminoimidazole-4-carboxamide-1-beta-4-ribofuranoside upregulated IL-6 mRNA expression, which was blocked by knockdown of AMPK alpha(1) and alpha(2) using small, interfering RNA (siRNA) oligonucleotides. Oligonucleotides 227-243 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-34 17615159-7 2007 Pharmacological activation of AMPK with 5-aminoimidazole-4-carboxamide-1-beta-4-ribofuranoside upregulated IL-6 mRNA expression, which was blocked by knockdown of AMPK alpha(1) and alpha(2) using small, interfering RNA (siRNA) oligonucleotides. Oligonucleotides 227-243 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 163-176 17603555-13 2007 Additional pharmacological effects evoked by AICAR and phenformin on I(ouabain), with potential secondary effects on apical Na+ conductance, ENaC activity and monolayer resistance, have important consequences for their use as pharmacological activators of AMPK in cell systems where Na+K+ATPase is an important component. Phenformin 55-65 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 256-260 17635921-7 2007 Conversely, activation of AMPK by pharmacologic (nicotine, ONOO(-), metformin, and AICAR) or genetic (overexpression of constitutively active AMPK) means inhibited FAS activity. onoo( 59-64 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 142-146 17635921-7 2007 Conversely, activation of AMPK by pharmacologic (nicotine, ONOO(-), metformin, and AICAR) or genetic (overexpression of constitutively active AMPK) means inhibited FAS activity. Metformin 68-77 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 26-30 17635921-7 2007 Conversely, activation of AMPK by pharmacologic (nicotine, ONOO(-), metformin, and AICAR) or genetic (overexpression of constitutively active AMPK) means inhibited FAS activity. AICA ribonucleotide 83-88 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 26-30 17635921-8 2007 Notably, AMPK activation increased threonine phosphorylation of FAS, and this effect was blocked by adenovirus encoding dominant negative AMPK. Threonine 35-44 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 9-13 17635921-8 2007 Notably, AMPK activation increased threonine phosphorylation of FAS, and this effect was blocked by adenovirus encoding dominant negative AMPK. Threonine 35-44 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 138-142 17635921-10 2007 Taken together, our results strongly suggest that nicotine, via ONOO(-) activates AMPK, resulting in enhanced threonine phosphorylation and consequent inhibition of FAS. Nicotine 50-58 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 82-86 17635921-10 2007 Taken together, our results strongly suggest that nicotine, via ONOO(-) activates AMPK, resulting in enhanced threonine phosphorylation and consequent inhibition of FAS. onoo(-) 64-71 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 82-86 17635921-10 2007 Taken together, our results strongly suggest that nicotine, via ONOO(-) activates AMPK, resulting in enhanced threonine phosphorylation and consequent inhibition of FAS. Threonine 110-119 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 82-86 17572440-1 2007 Nucleoside diphosphate kinase A (NDPK-A) regulates the alpha1 isoform of the AMP-activated protein kinase (AMPK alpha1) selectively, independent of [AMP] and surrounding [ATP], by a process termed substrate channelling. Adenosine Monophosphate 77-80 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 107-118 17603555-1 2007 BACKGROUND AND PURPOSE: AMP-activated protein kinase (AMPK) is activated by metformin, phenformin, and the AMP mimetic, 5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside (AICAR). Phenformin 87-97 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 54-58 17603555-1 2007 BACKGROUND AND PURPOSE: AMP-activated protein kinase (AMPK) is activated by metformin, phenformin, and the AMP mimetic, 5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside (AICAR). Adenosine Monophosphate 24-27 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 54-58 17603555-1 2007 BACKGROUND AND PURPOSE: AMP-activated protein kinase (AMPK) is activated by metformin, phenformin, and the AMP mimetic, 5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside (AICAR). acadesine 120-174 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 54-58 17603555-5 2007 AMPK activity was measured as the amount of radiolabelled phosphate transferred to the SAMS peptide. Phosphates 58-67 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 17603555-7 2007 KEY RESULTS: Phenformin, AICAR and metformin increased AMPK (alpha1) activity and decreased I(amiloride). Phenformin 13-23 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 55-67 17603555-7 2007 KEY RESULTS: Phenformin, AICAR and metformin increased AMPK (alpha1) activity and decreased I(amiloride). Metformin 35-44 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 55-67 17603555-8 2007 The AMPK inhibitor Compound C prevented the action of metformin and AICAR but not phenformin. Metformin 54-63 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 4-8 17332429-6 2007 GD-induced autophagy coincided with activation of AMP-activated protein kinase (AMPK) and inactivation of mTOR (mammalian target of rapamycin). Gadolinium 0-2 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 50-78 17617726-1 2007 In skeletal muscle, AMP-activated protein kinase (AMPK) is a metabolic master switch regulating glucose and lipid metabolism. Glucose 96-103 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 20-48 17617726-1 2007 In skeletal muscle, AMP-activated protein kinase (AMPK) is a metabolic master switch regulating glucose and lipid metabolism. Glucose 96-103 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 50-54 17617726-3 2007 The present study was designed to examine the effect of 5-aminoimidazole-4-carboxamide-1-beta-D-ribonucleoside (AICAR)-induced AMPK signaling on effector mechanisms of myofibrillar protein degradation and the expression of atrophy-related genes (atrogin-1/MAFbx, MuRF1, proteasome C2 subunit, calpains, cathepsin B, and caspase-3) in C2C12 myotubes. 5-aminoimidazole-4-carboxamide-1-beta-d-ribonucleoside 56-110 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 127-131 17617726-3 2007 The present study was designed to examine the effect of 5-aminoimidazole-4-carboxamide-1-beta-D-ribonucleoside (AICAR)-induced AMPK signaling on effector mechanisms of myofibrillar protein degradation and the expression of atrophy-related genes (atrogin-1/MAFbx, MuRF1, proteasome C2 subunit, calpains, cathepsin B, and caspase-3) in C2C12 myotubes. acadesine 112-117 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 127-131 17289170-7 2007 Accordingly, the AMPK activator AICAR elevated cellular ATP levels and produced effects on NTS1 function that were opposite to those for the metabolic inhibitors. Adenosine Triphosphate 56-59 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 17-21 17513706-1 2007 Activation of AMP-activated protein kinase (AMPK) in rodent muscle by exercise, metformin, 5-aminoimidazole-4-carboxamide 1-beta-d-ribofuranoside (AICAR), and adiponectin increases glucose uptake. Metformin 80-89 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 44-48 17513706-1 2007 Activation of AMP-activated protein kinase (AMPK) in rodent muscle by exercise, metformin, 5-aminoimidazole-4-carboxamide 1-beta-d-ribofuranoside (AICAR), and adiponectin increases glucose uptake. acadesine 91-145 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 44-48 17513706-1 2007 Activation of AMP-activated protein kinase (AMPK) in rodent muscle by exercise, metformin, 5-aminoimidazole-4-carboxamide 1-beta-d-ribofuranoside (AICAR), and adiponectin increases glucose uptake. Glucose 181-188 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 44-48 17332429-6 2007 GD-induced autophagy coincided with activation of AMP-activated protein kinase (AMPK) and inactivation of mTOR (mammalian target of rapamycin). Gadolinium 0-2 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 80-84 17332429-7 2007 Inhibition of AMPK by adenine 9-beta-d-arabinofuranoside or dominant negative AMPK significantly reduced GD-induced autophagy, whereas stimulation of autophagy by rapamycin failed to cause an additive effect on GD-induced autophagy, suggesting that activation of AMPK and inhibition of mTOR mediate GD-induced autophagy. Vidarabine 22-56 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-18 17332429-7 2007 Inhibition of AMPK by adenine 9-beta-d-arabinofuranoside or dominant negative AMPK significantly reduced GD-induced autophagy, whereas stimulation of autophagy by rapamycin failed to cause an additive effect on GD-induced autophagy, suggesting that activation of AMPK and inhibition of mTOR mediate GD-induced autophagy. Gadolinium 105-107 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-18 17332429-7 2007 Inhibition of AMPK by adenine 9-beta-d-arabinofuranoside or dominant negative AMPK significantly reduced GD-induced autophagy, whereas stimulation of autophagy by rapamycin failed to cause an additive effect on GD-induced autophagy, suggesting that activation of AMPK and inhibition of mTOR mediate GD-induced autophagy. Gadolinium 105-107 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 78-82 17332429-7 2007 Inhibition of AMPK by adenine 9-beta-d-arabinofuranoside or dominant negative AMPK significantly reduced GD-induced autophagy, whereas stimulation of autophagy by rapamycin failed to cause an additive effect on GD-induced autophagy, suggesting that activation of AMPK and inhibition of mTOR mediate GD-induced autophagy. Gadolinium 105-107 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 78-82 17332429-7 2007 Inhibition of AMPK by adenine 9-beta-d-arabinofuranoside or dominant negative AMPK significantly reduced GD-induced autophagy, whereas stimulation of autophagy by rapamycin failed to cause an additive effect on GD-induced autophagy, suggesting that activation of AMPK and inhibition of mTOR mediate GD-induced autophagy. Gadolinium 211-213 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-18 17332429-7 2007 Inhibition of AMPK by adenine 9-beta-d-arabinofuranoside or dominant negative AMPK significantly reduced GD-induced autophagy, whereas stimulation of autophagy by rapamycin failed to cause an additive effect on GD-induced autophagy, suggesting that activation of AMPK and inhibition of mTOR mediate GD-induced autophagy. Gadolinium 211-213 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-18 17332438-4 2007 AMPK is generally quiescent under normal conditions but is activated in response to hormonal signals and stresses sufficient to produce an increase in AMP/ATP ratio, such as hypoglycemia, strenuous exercise, anoxia, and ischemia. Adenosine Triphosphate 155-158 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 17270342-7 2007 AEA inhibited the effect of AM251 on AMPKalpha1 mRNA levels in myotubes from lean and obese subjects (P<0.05); the dose-response curve was shifted to the left in the obese. anandamide 0-3 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 37-47 17332438-5 2007 Once active, muscle AMPK enhances uptake and oxidative metabolism of fatty acids as well as increases glucose transport and glycolysis. Fatty Acids 69-80 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 20-24 17332438-5 2007 Once active, muscle AMPK enhances uptake and oxidative metabolism of fatty acids as well as increases glucose transport and glycolysis. Glucose 102-109 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 20-24 17237771-2 2007 We present evidence that the cyclin-dependent kinase inhibitor p27(Kip1), is phosphorylated at Thr 198 downstream of the Peutz-Jeghers syndrome protein-AMP-activated protein kinase (LKB1-AMPK) energy-sensing pathway, thereby increasing p27 stability and directly linking sensing of nutrient concentration and bioenergetics to cell-cycle progression. Threonine 95-98 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 187-191 17237771-5 2007 Thus LKB1-AMPK pathway-dependent phosphorylation of p27 at Thr 198 stabilizes p27 and permits cells to survive growth factor withdrawal and metabolic stress through autophagy. Threonine 59-62 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 10-14 17088252-7 2007 An autoinhibitory structural model of human AMPK alpha1-(1-335) was constructed and revealed that Val-298 interacts with Leu-328 through hydrophobic bonding at a distance of about 4 A and may stabilize the autoinhibitory conformation. Leucine 121-124 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 44-55 17116308-4 2007 AMPK, a central regulator of cellular energy homeostasis, responds to high cellular AMP/ATP ratios by promoting energy producing pathways and inhibiting energy consuming biosynthetic pathways. Adenosine Triphosphate 88-91 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 17116308-7 2007 This pseudosubstrate inhibition of AMPK by LiRP proteins reduced the AMP stimulation of AMPK in vitro and caused the inhibited state of the kinase to kinetically resemble the basal, unstimulated state of AMPK, providing potential insight into the molecular mechanisms of AMP stimulation of AMPK. Adenosine Monophosphate 35-38 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 88-92 17116308-7 2007 This pseudosubstrate inhibition of AMPK by LiRP proteins reduced the AMP stimulation of AMPK in vitro and caused the inhibited state of the kinase to kinetically resemble the basal, unstimulated state of AMPK, providing potential insight into the molecular mechanisms of AMP stimulation of AMPK. Adenosine Monophosphate 35-38 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 88-92 17116308-7 2007 This pseudosubstrate inhibition of AMPK by LiRP proteins reduced the AMP stimulation of AMPK in vitro and caused the inhibited state of the kinase to kinetically resemble the basal, unstimulated state of AMPK, providing potential insight into the molecular mechanisms of AMP stimulation of AMPK. Adenosine Monophosphate 35-38 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 88-92 17116308-7 2007 This pseudosubstrate inhibition of AMPK by LiRP proteins reduced the AMP stimulation of AMPK in vitro and caused the inhibited state of the kinase to kinetically resemble the basal, unstimulated state of AMPK, providing potential insight into the molecular mechanisms of AMP stimulation of AMPK. Adenosine Monophosphate 69-72 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 35-39 17116308-7 2007 This pseudosubstrate inhibition of AMPK by LiRP proteins reduced the AMP stimulation of AMPK in vitro and caused the inhibited state of the kinase to kinetically resemble the basal, unstimulated state of AMPK, providing potential insight into the molecular mechanisms of AMP stimulation of AMPK. Adenosine Monophosphate 69-72 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 88-92 17116308-7 2007 This pseudosubstrate inhibition of AMPK by LiRP proteins reduced the AMP stimulation of AMPK in vitro and caused the inhibited state of the kinase to kinetically resemble the basal, unstimulated state of AMPK, providing potential insight into the molecular mechanisms of AMP stimulation of AMPK. Adenosine Monophosphate 69-72 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 88-92 17116308-7 2007 This pseudosubstrate inhibition of AMPK by LiRP proteins reduced the AMP stimulation of AMPK in vitro and caused the inhibited state of the kinase to kinetically resemble the basal, unstimulated state of AMPK, providing potential insight into the molecular mechanisms of AMP stimulation of AMPK. Adenosine Monophosphate 69-72 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 88-92 17088252-7 2007 An autoinhibitory structural model of human AMPK alpha1-(1-335) was constructed and revealed that Val-298 interacts with Leu-328 through hydrophobic bonding at a distance of about 4 A and may stabilize the autoinhibitory conformation. Valine 98-101 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 44-55 17097050-3 2006 Inhibition of AMPK by compound C, a specific inhibitor of AMPK or small interfering RNA of AMPKalpha1 suppressed IL-2 production in Jurkat T cells and peripheral blood lymphocytes stimulated with PMA plus ionomycin (PMA/Io) or with monoclonal anti-CD3 plus anti-CD28. Tetradecanoylphorbol Acetate 196-199 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-18 17008367-7 2006 Regulation of malonyl-CoA levels by AMPK does not seem to work as a master on-off switch, but rather as a modulator of fatty acid import. Malonyl Coenzyme A 14-25 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 36-40 17008367-7 2006 Regulation of malonyl-CoA levels by AMPK does not seem to work as a master on-off switch, but rather as a modulator of fatty acid import. Fatty Acids 119-129 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 36-40 16870829-0 2007 Potentiation of insulin-stimulated glucose transport by the AMP-activated protein kinase. Glucose 35-42 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 60-88 16870829-1 2007 Data from the use of activators and inhibitors of the AMP-activated protein kinase (AMPK) suggest that AMPK increases sensitivity of glucose transport to stimulation by insulin in muscle cells. Glucose 133-140 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 54-82 16870829-1 2007 Data from the use of activators and inhibitors of the AMP-activated protein kinase (AMPK) suggest that AMPK increases sensitivity of glucose transport to stimulation by insulin in muscle cells. Glucose 133-140 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 84-88 16870829-1 2007 Data from the use of activators and inhibitors of the AMP-activated protein kinase (AMPK) suggest that AMPK increases sensitivity of glucose transport to stimulation by insulin in muscle cells. Glucose 133-140 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 103-107 16870829-3 2007 Compared with control (Ad-green fluorescent protein), Ad-AMPK-CA increased the ability of insulin to stimulate glucose transport. Glucose 111-118 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 57-61 16870829-5 2007 Exposure of cells to 5-aminoimidazole-4-carboxamide-1beta-D-ribofuranoside (an AMPK activator) increased insulin action in uninfected myotubes and myotubes transduced with green fluorescent protein but not in Ad-AMPK-DN-infected myotubes. acadesine 21-74 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 79-83 16870829-6 2007 In Ad-AMPK-CA-transduced cells, serine phosphorylation of insulin receptor substrate 1 was decreased at a mammalian target of rapamycin (or p70 S6 kinase) target site that has been reported to be associated with insulin resistance. Serine 32-38 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 6-10 17652779-1 2007 AMP-activated protein kinase (AMPK) is an energy sensing/signaling protein that, when activated, increases ATP production by stimulating glucose uptake and fatty acid oxidation while at the same time inhibiting ATP = consuming processes such as protein synthesis. Adenosine Triphosphate 107-110 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-28 17652779-1 2007 AMP-activated protein kinase (AMPK) is an energy sensing/signaling protein that, when activated, increases ATP production by stimulating glucose uptake and fatty acid oxidation while at the same time inhibiting ATP = consuming processes such as protein synthesis. Adenosine Triphosphate 107-110 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-34 17652779-1 2007 AMP-activated protein kinase (AMPK) is an energy sensing/signaling protein that, when activated, increases ATP production by stimulating glucose uptake and fatty acid oxidation while at the same time inhibiting ATP = consuming processes such as protein synthesis. Glucose 137-144 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-28 17652779-1 2007 AMP-activated protein kinase (AMPK) is an energy sensing/signaling protein that, when activated, increases ATP production by stimulating glucose uptake and fatty acid oxidation while at the same time inhibiting ATP = consuming processes such as protein synthesis. Glucose 137-144 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-34 17652779-1 2007 AMP-activated protein kinase (AMPK) is an energy sensing/signaling protein that, when activated, increases ATP production by stimulating glucose uptake and fatty acid oxidation while at the same time inhibiting ATP = consuming processes such as protein synthesis. Fatty Acids 156-166 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-28 17652779-1 2007 AMP-activated protein kinase (AMPK) is an energy sensing/signaling protein that, when activated, increases ATP production by stimulating glucose uptake and fatty acid oxidation while at the same time inhibiting ATP = consuming processes such as protein synthesis. Fatty Acids 156-166 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-34 17652779-1 2007 AMP-activated protein kinase (AMPK) is an energy sensing/signaling protein that, when activated, increases ATP production by stimulating glucose uptake and fatty acid oxidation while at the same time inhibiting ATP = consuming processes such as protein synthesis. Adenosine Triphosphate 211-214 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-28 17652779-1 2007 AMP-activated protein kinase (AMPK) is an energy sensing/signaling protein that, when activated, increases ATP production by stimulating glucose uptake and fatty acid oxidation while at the same time inhibiting ATP = consuming processes such as protein synthesis. Adenosine Triphosphate 211-214 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-34 17652779-4 2007 Because AMPK enhances both glucose uptake and fatty acid oxidation in skeletal muscle, it has become a target for prevention and treatment of type 2 diabetes and obesity. Glucose 27-34 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 8-12 17652779-4 2007 Because AMPK enhances both glucose uptake and fatty acid oxidation in skeletal muscle, it has become a target for prevention and treatment of type 2 diabetes and obesity. Fatty Acids 46-56 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 8-12 17135357-4 2007 We report that when S122 on NDPK-A is phosphorylated by AMPK alpha1 in vivo, (i.e., stimulation of AMPK using either metformin or phenformin) initiating the substrate channeling mechanism, the catalytic subunit of CK2 (CK2alpha) is expelled from the complex and translocates to bind NDPK-B, a closely related but independent isoform of NDPK. Metformin 117-126 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 56-67 17135357-4 2007 We report that when S122 on NDPK-A is phosphorylated by AMPK alpha1 in vivo, (i.e., stimulation of AMPK using either metformin or phenformin) initiating the substrate channeling mechanism, the catalytic subunit of CK2 (CK2alpha) is expelled from the complex and translocates to bind NDPK-B, a closely related but independent isoform of NDPK. Metformin 117-126 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 56-60 17135357-4 2007 We report that when S122 on NDPK-A is phosphorylated by AMPK alpha1 in vivo, (i.e., stimulation of AMPK using either metformin or phenformin) initiating the substrate channeling mechanism, the catalytic subunit of CK2 (CK2alpha) is expelled from the complex and translocates to bind NDPK-B, a closely related but independent isoform of NDPK. Phenformin 130-140 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 56-67 17135357-4 2007 We report that when S122 on NDPK-A is phosphorylated by AMPK alpha1 in vivo, (i.e., stimulation of AMPK using either metformin or phenformin) initiating the substrate channeling mechanism, the catalytic subunit of CK2 (CK2alpha) is expelled from the complex and translocates to bind NDPK-B, a closely related but independent isoform of NDPK. Phenformin 130-140 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 56-60 17097050-3 2006 Inhibition of AMPK by compound C, a specific inhibitor of AMPK or small interfering RNA of AMPKalpha1 suppressed IL-2 production in Jurkat T cells and peripheral blood lymphocytes stimulated with PMA plus ionomycin (PMA/Io) or with monoclonal anti-CD3 plus anti-CD28. Tetradecanoylphorbol Acetate 196-199 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 91-101 17097050-3 2006 Inhibition of AMPK by compound C, a specific inhibitor of AMPK or small interfering RNA of AMPKalpha1 suppressed IL-2 production in Jurkat T cells and peripheral blood lymphocytes stimulated with PMA plus ionomycin (PMA/Io) or with monoclonal anti-CD3 plus anti-CD28. Ionomycin 205-214 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-18 17097050-3 2006 Inhibition of AMPK by compound C, a specific inhibitor of AMPK or small interfering RNA of AMPKalpha1 suppressed IL-2 production in Jurkat T cells and peripheral blood lymphocytes stimulated with PMA plus ionomycin (PMA/Io) or with monoclonal anti-CD3 plus anti-CD28. Ionomycin 205-214 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 91-101 17097050-3 2006 Inhibition of AMPK by compound C, a specific inhibitor of AMPK or small interfering RNA of AMPKalpha1 suppressed IL-2 production in Jurkat T cells and peripheral blood lymphocytes stimulated with PMA plus ionomycin (PMA/Io) or with monoclonal anti-CD3 plus anti-CD28. Tetradecanoylphorbol Acetate 216-219 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-18 17097050-3 2006 Inhibition of AMPK by compound C, a specific inhibitor of AMPK or small interfering RNA of AMPKalpha1 suppressed IL-2 production in Jurkat T cells and peripheral blood lymphocytes stimulated with PMA plus ionomycin (PMA/Io) or with monoclonal anti-CD3 plus anti-CD28. Tetradecanoylphorbol Acetate 216-219 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 91-101 17097050-4 2006 We then showed that AMPK inhibition reduced PMA/Io-induced IL-2 mRNA expression and IL-2 promoter activation. Tetradecanoylphorbol Acetate 44-47 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 20-24 16936205-6 2006 Moreover, chemical inhibitors of AMPK and p38 MAPK potently repressed fatty acid oxidation and the induction of PPARalpha target gene expression by adiponectin. Fatty Acids 70-80 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 33-37 16595147-8 2006 Over-expression of PRKAA1 was further confirmed by immunohistochemical staining on 125 paraffin-embedded cervical cancer tissues. Paraffin 87-95 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 19-25 16936205-7 2006 Interestingly, araA, an AMPK inhibitor, prevented the activation of p38 MAPK, whereas SB203580, a p38 MAPK inhibitor, did not affect AMPK activation, suggesting that p38 MAPK is a downstream signaling factor of AMPK. Vidarabine 15-19 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 24-28 16936205-8 2006 Taken together, these results suggest that adiponectin stimulates fatty acid oxidation in muscle cells by the sequential activation of AMPK, p38 MAPK, and PPARalpha. Fatty Acids 66-76 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 135-139 17039396-4 2006 We find that ATP is located within this complex and "fed" from NDPK to AMPK without ever "seeing" bulk solution. Adenosine Triphosphate 13-16 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 71-75 17039396-5 2006 Importantly, the reverse can also happen such that AMPK activity can be made to decline when NDPK-A "steals" ATP from AMPK. Adenosine Triphosphate 109-112 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 51-55 17039396-5 2006 Importantly, the reverse can also happen such that AMPK activity can be made to decline when NDPK-A "steals" ATP from AMPK. Adenosine Triphosphate 109-112 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 118-122 16613876-3 2006 These actions of AMPK appear to be mediated through multiple mechanisms including regulation of the cell cycle and inhibition of protein synthesis, de novo fatty acid synthesis, specifically the generation of mevalonate as well as other products downstream of mevalonate in the cholesterol synthesis pathway. Fatty Acids 156-166 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 17-21 16847342-3 2006 AMP-activated protein kinase (AMPK) is a heterotrimeric protein complex that responds to the cellular energy status by switching off ATP-consuming pathways and switching on ATP-generating pathways when ATP is limiting. Adenosine Triphosphate 133-136 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-34 16847342-3 2006 AMP-activated protein kinase (AMPK) is a heterotrimeric protein complex that responds to the cellular energy status by switching off ATP-consuming pathways and switching on ATP-generating pathways when ATP is limiting. Adenosine Triphosphate 173-176 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-34 16847342-3 2006 AMP-activated protein kinase (AMPK) is a heterotrimeric protein complex that responds to the cellular energy status by switching off ATP-consuming pathways and switching on ATP-generating pathways when ATP is limiting. Adenosine Triphosphate 173-176 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-34 16847342-4 2006 AMPK was first discovered as an activity that inhibited preparations of acetyl coenzyme A carboxylase 1 (ACC1), a regulator of cellular fatty acid synthesis. Fatty Acids 136-146 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 16847342-5 2006 We recently reported that NDPK-A (but not NDPK-B) selectively regulates the alpha1 isoform of AMPK independently of the AMP concentration such that the manipulation of NDPK-A nucleotide trans-phosphorylation activity to generate ATP enhanced the activity of AMPK. Adenosine Triphosphate 229-232 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 94-98 16613876-3 2006 These actions of AMPK appear to be mediated through multiple mechanisms including regulation of the cell cycle and inhibition of protein synthesis, de novo fatty acid synthesis, specifically the generation of mevalonate as well as other products downstream of mevalonate in the cholesterol synthesis pathway. Mevalonic Acid 209-219 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 17-21 16709632-3 2006 AMPK stimulates pathways which increase energy production (glucose transport, fatty acid oxidation) and switches off pathways which consume energy (lipogenesis, protein synthesis, gluconeogenesis). Glucose 59-66 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 16613876-3 2006 These actions of AMPK appear to be mediated through multiple mechanisms including regulation of the cell cycle and inhibition of protein synthesis, de novo fatty acid synthesis, specifically the generation of mevalonate as well as other products downstream of mevalonate in the cholesterol synthesis pathway. Mevalonic Acid 260-270 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 17-21 16709632-3 2006 AMPK stimulates pathways which increase energy production (glucose transport, fatty acid oxidation) and switches off pathways which consume energy (lipogenesis, protein synthesis, gluconeogenesis). Fatty Acids 78-88 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 16613876-3 2006 These actions of AMPK appear to be mediated through multiple mechanisms including regulation of the cell cycle and inhibition of protein synthesis, de novo fatty acid synthesis, specifically the generation of mevalonate as well as other products downstream of mevalonate in the cholesterol synthesis pathway. Cholesterol 278-289 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 17-21 16709632-9 2006 When activated, AMPK limits fatty acid efflux from adipocytes and favours local fatty acid oxidation. Fatty Acids 28-38 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 16-20 16709632-9 2006 When activated, AMPK limits fatty acid efflux from adipocytes and favours local fatty acid oxidation. Fatty Acids 80-90 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 16-20 16771775-8 2006 When GST-TPS5 was expressed in human HEK293 cells, Thr49 was phosphorylated in response to 2-deoxyglucose or phenformin, stimuli that activate the AMPK via the upstream kinase LKB1. Phenformin 109-119 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 147-151 16709632-10 2006 Since fatty acids have a key role in insulin resistance, especially in muscles, activating AMPK in adipose tissue might be found to be beneficial in insulin-resistant states, particularly as AMPK activation also reduces cytokine secretion in adipocytes. Fatty Acids 6-17 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 91-95 16597407-2 2006 AMPK is activated by rising AMP and falling ATP, either by inhibiting ATP production or by accelerating ATP consumption, by a complex mechanism that results in an ultrasensitive response. Adenosine Triphosphate 44-47 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 16678800-0 2006 Critical roles of AMP-activated protein kinase in the carcinogenic metal-induced expression of VEGF and HIF-1 proteins in DU145 prostate carcinoma. Metals 67-72 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 18-46 16678800-3 2006 Recently, we demonstrated that AMP-activated protein kinase (AMPK), which acts as an energy sensor, providing metabolic adaptation effects under ATP-deprived conditions, is critical for the expression of VEGF under oxygen- and glucose-deprived conditions. Adenosine Triphosphate 145-148 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 31-59 16678800-3 2006 Recently, we demonstrated that AMP-activated protein kinase (AMPK), which acts as an energy sensor, providing metabolic adaptation effects under ATP-deprived conditions, is critical for the expression of VEGF under oxygen- and glucose-deprived conditions. Adenosine Triphosphate 145-148 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 61-65 16678800-3 2006 Recently, we demonstrated that AMP-activated protein kinase (AMPK), which acts as an energy sensor, providing metabolic adaptation effects under ATP-deprived conditions, is critical for the expression of VEGF under oxygen- and glucose-deprived conditions. Oxygen 215-221 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 31-59 16678800-3 2006 Recently, we demonstrated that AMP-activated protein kinase (AMPK), which acts as an energy sensor, providing metabolic adaptation effects under ATP-deprived conditions, is critical for the expression of VEGF under oxygen- and glucose-deprived conditions. Oxygen 215-221 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 61-65 16678800-3 2006 Recently, we demonstrated that AMP-activated protein kinase (AMPK), which acts as an energy sensor, providing metabolic adaptation effects under ATP-deprived conditions, is critical for the expression of VEGF under oxygen- and glucose-deprived conditions. Glucose 227-234 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 31-59 16678800-3 2006 Recently, we demonstrated that AMP-activated protein kinase (AMPK), which acts as an energy sensor, providing metabolic adaptation effects under ATP-deprived conditions, is critical for the expression of VEGF under oxygen- and glucose-deprived conditions. Glucose 227-234 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 61-65 16678800-4 2006 As carcinogenic metals are potent VEGF expression inducers, we hypothesized that AMPK would also play a crucial role in metal-induced VEGF expression. Metals 16-21 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 81-85 16678800-5 2006 Here, we present evidence that carcinogenic metals such as arsenite, vanadate, and cobalt, induce AMPK activation and VEGF expression via several different mechanisms, and that AMPK is able to regulate the expression of VEGF mRNA in a hypoxia-inducible factor-1-dependent or -independent manner, depending on the metal applied. arsenite 59-67 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 98-102 16678800-5 2006 Here, we present evidence that carcinogenic metals such as arsenite, vanadate, and cobalt, induce AMPK activation and VEGF expression via several different mechanisms, and that AMPK is able to regulate the expression of VEGF mRNA in a hypoxia-inducible factor-1-dependent or -independent manner, depending on the metal applied. arsenite 59-67 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 177-181 16678800-5 2006 Here, we present evidence that carcinogenic metals such as arsenite, vanadate, and cobalt, induce AMPK activation and VEGF expression via several different mechanisms, and that AMPK is able to regulate the expression of VEGF mRNA in a hypoxia-inducible factor-1-dependent or -independent manner, depending on the metal applied. Vanadates 69-77 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 98-102 16678800-5 2006 Here, we present evidence that carcinogenic metals such as arsenite, vanadate, and cobalt, induce AMPK activation and VEGF expression via several different mechanisms, and that AMPK is able to regulate the expression of VEGF mRNA in a hypoxia-inducible factor-1-dependent or -independent manner, depending on the metal applied. Vanadates 69-77 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 177-181 16678800-5 2006 Here, we present evidence that carcinogenic metals such as arsenite, vanadate, and cobalt, induce AMPK activation and VEGF expression via several different mechanisms, and that AMPK is able to regulate the expression of VEGF mRNA in a hypoxia-inducible factor-1-dependent or -independent manner, depending on the metal applied. Cobalt 83-89 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 98-102 16678800-5 2006 Here, we present evidence that carcinogenic metals such as arsenite, vanadate, and cobalt, induce AMPK activation and VEGF expression via several different mechanisms, and that AMPK is able to regulate the expression of VEGF mRNA in a hypoxia-inducible factor-1-dependent or -independent manner, depending on the metal applied. Cobalt 83-89 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 177-181 16678800-5 2006 Here, we present evidence that carcinogenic metals such as arsenite, vanadate, and cobalt, induce AMPK activation and VEGF expression via several different mechanisms, and that AMPK is able to regulate the expression of VEGF mRNA in a hypoxia-inducible factor-1-dependent or -independent manner, depending on the metal applied. Metals 44-49 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 98-102 16678800-5 2006 Here, we present evidence that carcinogenic metals such as arsenite, vanadate, and cobalt, induce AMPK activation and VEGF expression via several different mechanisms, and that AMPK is able to regulate the expression of VEGF mRNA in a hypoxia-inducible factor-1-dependent or -independent manner, depending on the metal applied. Metals 44-49 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 177-181 16678800-7 2006 Overall, our data suggest that AMPK is a critical regulatory component in metal-induced VEGF expression, which further implies its intrinsic involvement in metal-induced carcinogenesis. Metals 74-79 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 31-35 16678800-7 2006 Overall, our data suggest that AMPK is a critical regulatory component in metal-induced VEGF expression, which further implies its intrinsic involvement in metal-induced carcinogenesis. Metals 156-161 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 31-35 16636195-1 2006 AMP-activated protein kinase (AMPK) is tightly regulated by the cellular AMP:ATP ratio and plays a central role in regulation of energy homeostasis and metabolic stress. Adenosine Monophosphate 0-3 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-34 16636195-1 2006 AMP-activated protein kinase (AMPK) is tightly regulated by the cellular AMP:ATP ratio and plays a central role in regulation of energy homeostasis and metabolic stress. Adenosine Triphosphate 77-80 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-34 16636195-2 2006 Metformin has been shown to activate AMPK. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 37-41 16636195-4 2006 Metformin was observed to activate AMPK, as well as its downstream target, phosphoacetyl coenzyme A carboxylase, in human umbilical vein endothelial cells (HUVECs). Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 35-39 16636195-7 2006 A pharmacological activator of AMPK, 5-amino-4-imidazole carboxamide riboside (AICAR), dose-dependently inhibited TNF-alpha- and interleukin-1beta-induced NF-kappaB reporter gene expression. 5-amino-4-imidazole carboxamide riboside 37-77 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 31-35 16636195-7 2006 A pharmacological activator of AMPK, 5-amino-4-imidazole carboxamide riboside (AICAR), dose-dependently inhibited TNF-alpha- and interleukin-1beta-induced NF-kappaB reporter gene expression. acadesine 79-84 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 31-35 16636195-9 2006 The small interfering RNA for AMPKalpha1 attenuated metformin or AICAR-induced inhibition of NF-kappaB activation by TNF-alpha, suggesting a possible role of AMPK in the regulation of cell inflammation. Metformin 52-61 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-40 16636195-9 2006 The small interfering RNA for AMPKalpha1 attenuated metformin or AICAR-induced inhibition of NF-kappaB activation by TNF-alpha, suggesting a possible role of AMPK in the regulation of cell inflammation. Metformin 52-61 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-34 16636195-9 2006 The small interfering RNA for AMPKalpha1 attenuated metformin or AICAR-induced inhibition of NF-kappaB activation by TNF-alpha, suggesting a possible role of AMPK in the regulation of cell inflammation. acadesine 65-70 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-40 16636195-9 2006 The small interfering RNA for AMPKalpha1 attenuated metformin or AICAR-induced inhibition of NF-kappaB activation by TNF-alpha, suggesting a possible role of AMPK in the regulation of cell inflammation. acadesine 65-70 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-34 16636195-10 2006 In light of these findings, we suggest that metformin attenuates the cytokine-induced expression of proinflammatory and adhesion molecule genes by inhibiting NF-kappaB activation via AMPK activation. Metformin 44-53 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 183-187 16518831-2 2006 Adenosine monophosphate-dependent kinase (AMPK) is a key sensor for cellular homeostasis and is highly sensitive to changes in AMP:ATP ratios. Adenosine Triphosphate 131-134 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 42-46 16518831-6 2006 The AMPK chemical inhibitor, 5-iodotubericidin, effectively repressed the hypoxic induction of VEGF mRNA levels and hypoxia inducible factor-1 dependent transcription. 5-iodotubercidin 29-46 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 4-8 16598851-0 2006 Oral glucose ingestion attenuates exercise-induced activation of 5"-AMP-activated protein kinase in human skeletal muscle. Glucose 5-12 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 65-96 16598851-1 2006 5"-AMP-activated protein kinase (AMPK) has been suggested to be a "metabolic master switch" regulating various aspects of muscle glucose and fat metabolism. Glucose 129-136 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-31 16598851-1 2006 5"-AMP-activated protein kinase (AMPK) has been suggested to be a "metabolic master switch" regulating various aspects of muscle glucose and fat metabolism. Glucose 129-136 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 33-37 16598851-2 2006 In isolated rat skeletal muscle, glucose suppresses the activity of AMPK and in human muscle glycogen loading decreases exercise-induced AMPK activation. Glycogen 93-101 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 137-141 16598851-3 2006 We hypothesized that oral glucose ingestion during exercise would attenuate muscle AMPK activation. Glucose 26-33 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 83-87 16598851-9 2006 Activation of alpha2-AMPK was attenuated in the glucose trial compared to the placebo trial (0.24 +/- 0.07 vs. 0.46 +/- 0.14 pmol mg-1 min-1, P = 0.03), whereas the alpha1-AMPK activity was not different between trials or affected by exercise. Glucose 48-55 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 21-25 16598851-9 2006 Activation of alpha2-AMPK was attenuated in the glucose trial compared to the placebo trial (0.24 +/- 0.07 vs. 0.46 +/- 0.14 pmol mg-1 min-1, P = 0.03), whereas the alpha1-AMPK activity was not different between trials or affected by exercise. Glucose 48-55 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 172-176 16598851-11 2006 We conclude that oral glucose ingestion attenuates the exercise-induced activation of alpha2-AMPK, bringing further support for a fuel-sensing role of AMPK in skeletal muscle. Glucose 22-29 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 93-97 16598851-11 2006 We conclude that oral glucose ingestion attenuates the exercise-induced activation of alpha2-AMPK, bringing further support for a fuel-sensing role of AMPK in skeletal muscle. Glucose 22-29 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 151-155 16597407-2 2006 AMPK is activated by rising AMP and falling ATP, either by inhibiting ATP production or by accelerating ATP consumption, by a complex mechanism that results in an ultrasensitive response. Adenosine Triphosphate 70-73 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 16597407-2 2006 AMPK is activated by rising AMP and falling ATP, either by inhibiting ATP production or by accelerating ATP consumption, by a complex mechanism that results in an ultrasensitive response. Adenosine Triphosphate 70-73 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 16597407-8 2006 Moreover, the AMPK system is one of the probable target for the anti-diabetic drug metformin and rosiglitazone. Metformin 83-92 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-18 16597407-8 2006 Moreover, the AMPK system is one of the probable target for the anti-diabetic drug metformin and rosiglitazone. Rosiglitazone 97-110 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-18 16497986-8 2006 Adenosine-induced phosphorylation of AMPK was not mediated by P1 receptors but required adenosine uptake by equilibrative nucleoside transporters followed by its (intracellular) metabolism to AMP. Adenosine 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 37-41 16497986-8 2006 Adenosine-induced phosphorylation of AMPK was not mediated by P1 receptors but required adenosine uptake by equilibrative nucleoside transporters followed by its (intracellular) metabolism to AMP. Adenosine 88-97 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 37-41 16497986-0 2006 Extracellular nucleotides and adenosine independently activate AMP-activated protein kinase in endothelial cells: involvement of P2 receptors and adenosine transporters. Adenosine 30-39 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 63-91 16505231-0 2006 AMP-activated protein kinase activation by adrenoceptors in L6 skeletal muscle cells: mediation by alpha1-adrenoceptors causing glucose uptake. Glucose 128-135 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-28 16497986-3 2006 We demonstrate that extracellular nucleotides (ATP, ADP, and UTP, but not UDP) and adenosine independently induce phosphorylation and activation of AMPK in human umbilical vein EC (HUVEC) by the mechanism that is not linked to changes in AMP:ATP ratio. Adenosine Triphosphate 47-50 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 148-152 16497986-3 2006 We demonstrate that extracellular nucleotides (ATP, ADP, and UTP, but not UDP) and adenosine independently induce phosphorylation and activation of AMPK in human umbilical vein EC (HUVEC) by the mechanism that is not linked to changes in AMP:ATP ratio. Adenosine Diphosphate 52-55 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 148-152 16497986-3 2006 We demonstrate that extracellular nucleotides (ATP, ADP, and UTP, but not UDP) and adenosine independently induce phosphorylation and activation of AMPK in human umbilical vein EC (HUVEC) by the mechanism that is not linked to changes in AMP:ATP ratio. Uridine Triphosphate 61-64 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 148-152 16497986-3 2006 We demonstrate that extracellular nucleotides (ATP, ADP, and UTP, but not UDP) and adenosine independently induce phosphorylation and activation of AMPK in human umbilical vein EC (HUVEC) by the mechanism that is not linked to changes in AMP:ATP ratio. Adenosine 83-92 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 148-152 16497986-3 2006 We demonstrate that extracellular nucleotides (ATP, ADP, and UTP, but not UDP) and adenosine independently induce phosphorylation and activation of AMPK in human umbilical vein EC (HUVEC) by the mechanism that is not linked to changes in AMP:ATP ratio. Adenosine Triphosphate 242-245 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 148-152 16407220-1 2006 We previously reported the phosphoinositide 3-kinase-dependent activation of the 5"-AMP-activated kinase (AMPK) by peroxynitrite (ONOO-) and hypoxia-reoxygenation in cultured endothelial cells. Peroxynitrous Acid 115-128 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 81-104 16407220-1 2006 We previously reported the phosphoinositide 3-kinase-dependent activation of the 5"-AMP-activated kinase (AMPK) by peroxynitrite (ONOO-) and hypoxia-reoxygenation in cultured endothelial cells. Peroxynitrous Acid 115-128 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 106-110 16407220-1 2006 We previously reported the phosphoinositide 3-kinase-dependent activation of the 5"-AMP-activated kinase (AMPK) by peroxynitrite (ONOO-) and hypoxia-reoxygenation in cultured endothelial cells. oxido nitrite 130-135 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 81-104 16407220-1 2006 We previously reported the phosphoinositide 3-kinase-dependent activation of the 5"-AMP-activated kinase (AMPK) by peroxynitrite (ONOO-) and hypoxia-reoxygenation in cultured endothelial cells. oxido nitrite 130-135 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 106-110 16407220-3 2006 Exposure of bovine aortic endothelial cells to ONOO- significantly increased the phosphorylation of both Thr172 of AMPK and Ser1179 of endothelial nitric-oxide synthase, a known downstream enzyme of AMPK. onoo 47-51 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 115-119 16407220-3 2006 Exposure of bovine aortic endothelial cells to ONOO- significantly increased the phosphorylation of both Thr172 of AMPK and Ser1179 of endothelial nitric-oxide synthase, a known downstream enzyme of AMPK. onoo 47-51 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 199-203 16407220-4 2006 In addition, activation of AMPK by ONOO- was accompanied by increased phosphorylation of protein kinase Czeta (PKCzeta) (Thr410/403) and translocation of cytosolic PKCzeta into the membrane. onoo 35-39 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 27-31 16407220-5 2006 Further, inhibition of PKCzeta abrogated ONOO- -induced AMPK-Thr172 phosphorylation as that of endothelial nitric-oxide synthase. onoo 41-45 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 56-60 16407220-10 2006 Further, direct mutation of Ser428 of LKB1 into alanine, like the kinase-inactive LKB1 mutant, abolished ONOO- -induced AMPK activation. Alanine 48-55 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 120-124 16407220-10 2006 Further, direct mutation of Ser428 of LKB1 into alanine, like the kinase-inactive LKB1 mutant, abolished ONOO- -induced AMPK activation. onoo 105-109 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 120-124 16407220-11 2006 In several cell types originating from human, rat, and mouse, inhibition of PKCzeta significantly attenuated the phosphorylation of both LKB1-Ser428 and AMPK-Thr172 that were enhanced by ONOO-. onoo 187-191 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 153-157 16505231-1 2006 AMP-activated protein kinase (AMPK), which functions as a sensor of cellular energy homeostasis, was phosphorylated after norepinephrine stimulation in L6 skeletal muscle cells. Norepinephrine 122-136 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-28 16505231-1 2006 AMP-activated protein kinase (AMPK), which functions as a sensor of cellular energy homeostasis, was phosphorylated after norepinephrine stimulation in L6 skeletal muscle cells. Norepinephrine 122-136 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-34 16505231-4 2006 We further show that glucose uptake mediated by alpha1- but not by beta-adrenoceptors can be inhibited by AMPK inhibition. Glucose 21-28 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 106-110 16505231-6 2006 These results suggest a novel pathway where alpha1-adrenoceptor activation, independent of protein kinase C, leads to activation of AMPK in skeletal muscle, which contributes to alpha1-adrenoceptor-mediated increases in glucose uptake. Glucose 220-227 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 132-136 16188906-9 2006 AMPK inhibited epinephrine-induced HSL activity in L6 myotubes and was associated with reduced HSL Ser(660) but not Ser(563) phosphorylation. Epinephrine 15-26 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 16188906-9 2006 AMPK inhibited epinephrine-induced HSL activity in L6 myotubes and was associated with reduced HSL Ser(660) but not Ser(563) phosphorylation. Serine 99-102 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 16188906-9 2006 AMPK inhibited epinephrine-induced HSL activity in L6 myotubes and was associated with reduced HSL Ser(660) but not Ser(563) phosphorylation. Serine 116-119 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 16188906-11 2006 Conversely, in 3T3-L1 adipocytes, AMPK activation after epinephrine stimulation did not prevent HSL activity or glycerol release, which coincided with maintenance of HSL Ser(660) phosphorylation. Epinephrine 56-67 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 34-38 16405649-4 2006 Using micropore chemotaxis assays to assess migratory responses of the monocyte-like cell line U937, it was found that the AMPK activators AICAR and phenformin rapidly reduced random migration (chemokinesis) as well as chemotaxis due to stromal cell-derived factor (SDF)1alpha. Phenformin 149-159 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 123-127 16622294-9 2006 Several studies have shown that pharmacologic activation of AMPK increases glucose transport in muscle, independent of the actions of insulin. Glucose 75-82 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 60-64 16622294-10 2006 AMPK activation is also involved in the mechanism of action of metformin and adiponectin. Metformin 63-72 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 16405649-10 2006 Although the effect of AMPK activation was partially reversed by mevalonate, this was not associated with altered subcellular localization of Rho GTPases. Mevalonic Acid 65-75 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 23-27 15928020-3 2005 It was revealed that the stimulation with 5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside (AICAR) and 2,4-dinitrophenol (DNP), known activators of AMPK, promptly accelerates its translocation within 4 min, as was found in the case of insulin stimulation. acadesine 98-103 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 154-158 16380484-0 2006 Activation of AMP-activated protein kinase reduces hyperglycemia-induced mitochondrial reactive oxygen species production and promotes mitochondrial biogenesis in human umbilical vein endothelial cells. Reactive Oxygen Species 87-110 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-42 16380484-4 2006 Treatment with metformin and AICAR inhibited hyperglycemia-induced intracellular and mtROS production, stimulated AMP-activated protein kinase (AMPK) activity, and increased the expression of peroxisome proliferator-activated response-gamma coactivator-1alpha (PGC-1alpha) and manganese superoxide dismutase (MnSOD) mRNAs. Metformin 15-24 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 114-142 16380484-4 2006 Treatment with metformin and AICAR inhibited hyperglycemia-induced intracellular and mtROS production, stimulated AMP-activated protein kinase (AMPK) activity, and increased the expression of peroxisome proliferator-activated response-gamma coactivator-1alpha (PGC-1alpha) and manganese superoxide dismutase (MnSOD) mRNAs. Metformin 15-24 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 144-148 16380484-5 2006 The dominant negative form of AMPKalpha1 diminished the effects of metformin and AICAR on these events, and an overexpression of PGC-1alpha completely blocked the hyperglycemia-induced mtROS production. Metformin 67-76 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-40 16380484-7 2006 Dominant negative-AMPK also reduced the effects of metformin and AICAR on these observations. Metformin 51-60 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 18-22 16380484-8 2006 These results suggest that metformin normalizes hyperglycemia-induced mtROS production by induction of MnSOD and promotion of mitochondrial biogenesis through the activation of AMPK-PGC-1alpha pathway. Metformin 27-36 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 177-181 16686439-7 2006 Thus, metabolic-sensing by AMPK underpins the cell-specific response of O2-sensing cells to hypoxia. Oxygen 72-74 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 27-31 16026327-3 2005 AMPK (AMP-activated protein kinase) is a heterotrimeric protein complex that responds to cellular energy status by switching off ATP-consuming pathways and switching on ATP-generating pathways when ATP is limiting. Adenosine Triphosphate 169-172 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 16026327-4 2005 AMPK was first discovered as an activity that inhibited preparations of ACC1 (acetyl-CoA carboxylase), a regulator of cellular fatty acid synthesis. Fatty Acids 127-137 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 16026327-7 2005 Manipulation of NM23-H1/NDPK A nucleotide transphosphorylation activity to generate ATP (but not GTP) enhances the activity of AMPK towards its specific peptide substrate in vitro and also regulates the phosphorylation of ACC1, an in vivo target for AMPK. Adenosine Triphosphate 84-87 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 127-131 16026327-7 2005 Manipulation of NM23-H1/NDPK A nucleotide transphosphorylation activity to generate ATP (but not GTP) enhances the activity of AMPK towards its specific peptide substrate in vitro and also regulates the phosphorylation of ACC1, an in vivo target for AMPK. Adenosine Triphosphate 84-87 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 250-254 15928020-0 2005 Activators of AMP-activated protein kinase enhance GLUT4 translocation and its glucose transport activity in 3T3-L1 adipocytes. Glucose 79-86 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-42 15928020-1 2005 To determine whether the increase in glucose uptake following AMP-activated protein kinase (AMPK) activation in adipocytes is mediated by accelerated GLUT4 translocation into plasma membrane, we constructed a chimera between GLUT4 and enhanced green fluorescent protein (GLUT4-eGFP) and transferred its cDNA into the nucleus of 3T3-L1 adipocytes. Glucose 37-44 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 62-90 15928020-1 2005 To determine whether the increase in glucose uptake following AMP-activated protein kinase (AMPK) activation in adipocytes is mediated by accelerated GLUT4 translocation into plasma membrane, we constructed a chimera between GLUT4 and enhanced green fluorescent protein (GLUT4-eGFP) and transferred its cDNA into the nucleus of 3T3-L1 adipocytes. Glucose 37-44 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 92-96 15928020-3 2005 It was revealed that the stimulation with 5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside (AICAR) and 2,4-dinitrophenol (DNP), known activators of AMPK, promptly accelerates its translocation within 4 min, as was found in the case of insulin stimulation. acadesine 42-96 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 154-158 16686439-3 2006 We considered the possibility that hypoxia may increase the cellular ATP/AMP ratio, increase the activity of AMP-activated protein kinase (AMPK) and thereby evoke Ca2+ signals in O2-sensing cells. Oxygen 179-181 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 139-143 16686439-4 2006 Co-immunoprecipitation identified alpha1beta2gamma1 as the primary AMPK isozyme in pulmonary arterial smooth muscle, whilst the tissue-specific distribution of AMPK activities and their activation by hypoxia suggested that the AMPK-alpha1 catalytic subunit isoform is key to the regulation of O2-sensing cells. Oxygen 293-295 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 227-238 16686439-6 2006 Consistent with these observations Ca2+ imaging, tension recording and electrophysiology demonstrated that AMPK, like hypoxia, activates each cell type via discrete Ca2+ signalling mechanisms: cyclic ADP-ribose-dependent Ca2+ mobilization from the sarcoplasmic reticulum via ryanodine receptors in pulmonary arterial smooth muscle cells and voltage-gated Ca2+ influx into carotid body glomus cells. cyclic adp 193-203 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 107-111 16686439-6 2006 Consistent with these observations Ca2+ imaging, tension recording and electrophysiology demonstrated that AMPK, like hypoxia, activates each cell type via discrete Ca2+ signalling mechanisms: cyclic ADP-ribose-dependent Ca2+ mobilization from the sarcoplasmic reticulum via ryanodine receptors in pulmonary arterial smooth muscle cells and voltage-gated Ca2+ influx into carotid body glomus cells. Ribose 204-210 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 107-111 16026327-3 2005 AMPK (AMP-activated protein kinase) is a heterotrimeric protein complex that responds to cellular energy status by switching off ATP-consuming pathways and switching on ATP-generating pathways when ATP is limiting. Adenosine Triphosphate 129-132 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 16026327-3 2005 AMPK (AMP-activated protein kinase) is a heterotrimeric protein complex that responds to cellular energy status by switching off ATP-consuming pathways and switching on ATP-generating pathways when ATP is limiting. Adenosine Triphosphate 169-172 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 15928020-3 2005 It was revealed that the stimulation with 5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside (AICAR) and 2,4-dinitrophenol (DNP), known activators of AMPK, promptly accelerates its translocation within 4 min, as was found in the case of insulin stimulation. 2,4-Dinitrophenol 109-126 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 154-158 15928020-3 2005 It was revealed that the stimulation with 5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside (AICAR) and 2,4-dinitrophenol (DNP), known activators of AMPK, promptly accelerates its translocation within 4 min, as was found in the case of insulin stimulation. 2,4-Dinitrophenol 128-131 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 154-158 15928020-5 2005 However, the GLUT4 translocation through AMPK activators AICAR and DNP was not affected by wortmannin. 2,4-Dinitrophenol 67-70 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 41-45 15928020-7 2005 Glucose uptake was significantly increased after addition of AMPK activators AICAR and DNP (P < 0.05). Glucose 0-7 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 61-65 15928020-7 2005 Glucose uptake was significantly increased after addition of AMPK activators AICAR and DNP (P < 0.05). 2,4-Dinitrophenol 87-90 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 61-65 15928020-8 2005 AMPK- and insulin-stimulated glucose uptake were similarly suppressed by wortmannin (P < 0.05-0.01). Glucose 29-36 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 15928020-8 2005 AMPK- and insulin-stimulated glucose uptake were similarly suppressed by wortmannin (P < 0.05-0.01). Wortmannin 73-83 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 15928020-9 2005 In addition, SB-203580 also significantly prevented the enhancement of glucose uptake induced by AMPK and insulin (P < 0.05). SB 203580 13-22 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 97-101 15928020-9 2005 In addition, SB-203580 also significantly prevented the enhancement of glucose uptake induced by AMPK and insulin (P < 0.05). Glucose 71-78 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 97-101 15928020-11 2005 On the other hand, the increase of glucose uptake dependent on AMPK activators AICAR and DNP would be additionally due to enhancement of the intrinsic activity in translocated GLUT4 protein, possibly through a p38 MAPK-dependent mechanism. Glucose 35-42 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 63-67 15919715-0 2005 Phenformin and 5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside (AICAR) activation of AMP-activated protein kinase inhibits transepithelial Na+ transport across H441 lung cells. Phenformin 0-10 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 92-120 15919715-0 2005 Phenformin and 5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside (AICAR) activation of AMP-activated protein kinase inhibits transepithelial Na+ transport across H441 lung cells. acadesine 15-69 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 92-120 15834551-0 2005 Troglitazone causes acute mitochondrial membrane depolarisation and an AMPK-mediated increase in glucose phosphorylation in muscle cells. Troglitazone 0-12 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 71-75 15919715-0 2005 Phenformin and 5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside (AICAR) activation of AMP-activated protein kinase inhibits transepithelial Na+ transport across H441 lung cells. acadesine 71-76 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 92-120 15919715-5 2005 AMPK is an ultra-sensitive cellular energy sensor that monitors energy consumption and down-regulates ATP-consuming processes when activated. Adenosine Triphosphate 102-105 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 15919715-6 2005 The biguanide phenformin has been shown to independently decrease ion transport processes, influence cellular metabolism and activate AMPK. Biguanides 4-13 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 134-138 15919715-6 2005 The biguanide phenformin has been shown to independently decrease ion transport processes, influence cellular metabolism and activate AMPK. Phenformin 14-24 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 134-138 15919715-7 2005 The AMP mimetic drug 5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside (AICAR) also activates AMPK in intact cells. Adenosine Monophosphate 4-7 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 99-103 15919715-7 2005 The AMP mimetic drug 5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside (AICAR) also activates AMPK in intact cells. acadesine 21-75 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 99-103 15919715-7 2005 The AMP mimetic drug 5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside (AICAR) also activates AMPK in intact cells. acadesine 77-82 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 99-103 15919715-9 2005 Phenformin and AICAR increased AMPK activity in H441 cells in a dose-dependent fashion, stimulating the kinase maximally at 5-10 mm (P = 0.001, n = 3) and 2 mm (P < 0.005, n = 3), respectively. Phenformin 0-10 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 31-35 15919715-15 2005 Taken together, these results show that phenformin and AICAR suppress amiloride-sensitive Na+ transport across H441 cells via a pathway that includes activation of AMPK and inhibition of both apical Na+ entry through ENaC and basolateral Na+ extrusion via the Na+,K+-ATPase. Phenformin 40-50 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 164-168 15919715-15 2005 Taken together, these results show that phenformin and AICAR suppress amiloride-sensitive Na+ transport across H441 cells via a pathway that includes activation of AMPK and inhibition of both apical Na+ entry through ENaC and basolateral Na+ extrusion via the Na+,K+-ATPase. Amiloride 70-79 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 164-168 15896711-0 2005 Combination of 5-fluorouracil and genistein induces apoptosis synergistically in chemo-resistant cancer cells through the modulation of AMPK and COX-2 signaling pathways. Fluorouracil 15-29 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 136-140 15896711-0 2005 Combination of 5-fluorouracil and genistein induces apoptosis synergistically in chemo-resistant cancer cells through the modulation of AMPK and COX-2 signaling pathways. Genistein 34-43 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 136-140 15896711-5 2005 The present study focused on the correlation of AMPK and COX-2 in combined cytotoxicity of 5-FU and genistein, since AMPK is known as a primary cellular homeostasis regulator and a possible target molecule of cancer treatment, and COX-2 as cell proliferation and anti-apoptotic molecule. Fluorouracil 91-95 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 48-52 15896711-5 2005 The present study focused on the correlation of AMPK and COX-2 in combined cytotoxicity of 5-FU and genistein, since AMPK is known as a primary cellular homeostasis regulator and a possible target molecule of cancer treatment, and COX-2 as cell proliferation and anti-apoptotic molecule. Fluorouracil 91-95 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 117-121 15896711-5 2005 The present study focused on the correlation of AMPK and COX-2 in combined cytotoxicity of 5-FU and genistein, since AMPK is known as a primary cellular homeostasis regulator and a possible target molecule of cancer treatment, and COX-2 as cell proliferation and anti-apoptotic molecule. Genistein 100-109 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 48-52 15896711-5 2005 The present study focused on the correlation of AMPK and COX-2 in combined cytotoxicity of 5-FU and genistein, since AMPK is known as a primary cellular homeostasis regulator and a possible target molecule of cancer treatment, and COX-2 as cell proliferation and anti-apoptotic molecule. Genistein 100-109 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 117-121 15896711-9 2005 Furthermore, the reactive oxygen species (ROS) was found as an upstream signal for AMPK activation by genistein. Reactive Oxygen Species 17-40 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 83-87 15896711-9 2005 Furthermore, the reactive oxygen species (ROS) was found as an upstream signal for AMPK activation by genistein. Reactive Oxygen Species 42-45 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 83-87 15896711-9 2005 Furthermore, the reactive oxygen species (ROS) was found as an upstream signal for AMPK activation by genistein. Genistein 102-111 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 83-87 15896711-10 2005 These results suggested that the combination of 5-FU and genistein exert a novel chemotherapeutic effect in colon cancers, and AMPK may be a novel regulatory molecule of COX-2 expression, further implying its involvement in cytotoxicity caused by genistein. Genistein 247-256 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 127-131 15806154-4 2005 AMPK is a cellular energy sensor whose activation can both block anabolic pathways such as protein synthesis and activate catabolic reactions such as fatty acid oxidation to maintain cellular bioenergetics. Fatty Acids 150-160 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 15769985-5 2005 In lean myotubes, gAD activates AMPKalpha1 and -alpha2 by increasing Thr172 phosphorylation, an effect associated with increased acetyl-coenzyme A carboxylase (ACCbeta) Ser221 phosphorylation and enhanced rates of fatty acid oxidation, effects similar to those observed after pharmacological AMPK activation by 5-aminoimidazole-4-carboxamide riboside. Fatty Acids 214-224 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 32-54 15769985-5 2005 In lean myotubes, gAD activates AMPKalpha1 and -alpha2 by increasing Thr172 phosphorylation, an effect associated with increased acetyl-coenzyme A carboxylase (ACCbeta) Ser221 phosphorylation and enhanced rates of fatty acid oxidation, effects similar to those observed after pharmacological AMPK activation by 5-aminoimidazole-4-carboxamide riboside. acadesine 311-350 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 32-54 15769985-6 2005 In obese myotubes, the activation of AMPK signaling by gAD at low concentrations (0.1 mug/ml) was blunted, but higher concentrations (0.5 mug/ml) stimulated AMPKalpha1 and -alpha2 activities, AMPK and ACCbeta phosphorylation, and fatty acid oxidation. Fatty Acids 230-240 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 37-41 15769985-9 2005 These data suggest that reduced activation of AMPK by gAD in obese and obese type 2 diabetic subjects is not caused by reduced adiponectin receptor expression but that aspects downstream of the receptor may inhibit AMPK signaling. ganoderic acid D 54-57 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 46-50 15769985-9 2005 These data suggest that reduced activation of AMPK by gAD in obese and obese type 2 diabetic subjects is not caused by reduced adiponectin receptor expression but that aspects downstream of the receptor may inhibit AMPK signaling. ganoderic acid D 54-57 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 215-219 15613684-1 2005 The studies described herein were designed to investigate the effects of 5-aminoimidazole-4-carboxamide-1-beta-D-ribonucleoside (AICAR), an activator of the AMP-activated protein kinase (AMPK), on the translational control of protein synthesis and signaling through the mammalian target of rapamycin (mTOR) in rat liver. 5-aminoimidazole-4-carboxamide-1-beta-d-ribonucleoside 73-127 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 157-185 15613684-1 2005 The studies described herein were designed to investigate the effects of 5-aminoimidazole-4-carboxamide-1-beta-D-ribonucleoside (AICAR), an activator of the AMP-activated protein kinase (AMPK), on the translational control of protein synthesis and signaling through the mammalian target of rapamycin (mTOR) in rat liver. 5-aminoimidazole-4-carboxamide-1-beta-d-ribonucleoside 73-127 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 187-191 15834551-0 2005 Troglitazone causes acute mitochondrial membrane depolarisation and an AMPK-mediated increase in glucose phosphorylation in muscle cells. Glucose 97-104 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 71-75 15834551-8 2005 RESULTS: Troglitazone acutely (in 10 min) reduced the mitochondrial membrane potential in L6GLUT4myc myotubes and robustly stimulated AMPK activity. Troglitazone 9-21 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 134-138 15834551-12 2005 Interestingly, interfering with troglitazone-induced activation of AMPK by decreasing the expression of the enzyme using siRNA inhibited the stimulation of 2-deoxyglucose uptake by the TZD. Troglitazone 32-44 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 67-71 15834551-12 2005 Interestingly, interfering with troglitazone-induced activation of AMPK by decreasing the expression of the enzyme using siRNA inhibited the stimulation of 2-deoxyglucose uptake by the TZD. Deoxyglucose 156-170 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 67-71 15834551-12 2005 Interestingly, interfering with troglitazone-induced activation of AMPK by decreasing the expression of the enzyme using siRNA inhibited the stimulation of 2-deoxyglucose uptake by the TZD. 2,4-thiazolidinedione 185-188 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 67-71 15834551-13 2005 CONCLUSIONS/INTERPRETATION: We propose that troglitazone acutely increases glucose flux in muscle via an AMPK-mediated increase in glucose phosphorylation. Troglitazone 44-56 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 105-109 15834551-13 2005 CONCLUSIONS/INTERPRETATION: We propose that troglitazone acutely increases glucose flux in muscle via an AMPK-mediated increase in glucose phosphorylation. Glucose 75-82 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 105-109 15834551-13 2005 CONCLUSIONS/INTERPRETATION: We propose that troglitazone acutely increases glucose flux in muscle via an AMPK-mediated increase in glucose phosphorylation. Glucose 131-138 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 105-109 15644453-0 2005 Long-chain acyl-CoA esters inhibit phosphorylation of AMP-activated protein kinase at threonine-172 by LKB1/STRAD/MO25. long-chain 0-10 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 54-82 15644453-0 2005 Long-chain acyl-CoA esters inhibit phosphorylation of AMP-activated protein kinase at threonine-172 by LKB1/STRAD/MO25. acyl-coa esters 11-26 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 54-82 15644453-0 2005 Long-chain acyl-CoA esters inhibit phosphorylation of AMP-activated protein kinase at threonine-172 by LKB1/STRAD/MO25. Threonine 86-95 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 54-82 15644453-2 2005 AMPK is thought to be inhibited by glycogen, the major storage form of intracellular carbohydrate. Glycogen 35-43 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 15644453-2 2005 AMPK is thought to be inhibited by glycogen, the major storage form of intracellular carbohydrate. Carbohydrates 85-97 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 15644453-3 2005 We hypothesized that long-chain acyl-CoA esters (LCACEs) might also inhibit AMPK signaling. long-chain acyl-coa esters 21-47 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 76-80 15644453-3 2005 We hypothesized that long-chain acyl-CoA esters (LCACEs) might also inhibit AMPK signaling. lcaces 49-55 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 76-80 15644453-5 2005 We found that LCACEs inhibited phosphorylation of AMPK by the recombinant AMPK kinase (AMPKK) LKB1/STRAD/MO25 in a concentration-dependent manner. lcaces 14-20 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 50-54 15644453-5 2005 We found that LCACEs inhibited phosphorylation of AMPK by the recombinant AMPK kinase (AMPKK) LKB1/STRAD/MO25 in a concentration-dependent manner. lcaces 14-20 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 74-78 15640157-3 2005 AMPK functions as an energy sensor to provide metabolic adaptation under ATP-depleting conditions such as hypoxia and nutritional deprivation. Adenosine Triphosphate 73-76 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 15640157-6 2005 We further show that reactive oxygen species is involved in glucose deprivation-induced AMPK activity in DU145 human prostate carcinomas, and c-Jun amino-terminal kinase acts as an upstream component in AMPK activation cascades under these conditions. Reactive Oxygen Species 21-44 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 88-92 15507450-1 2005 During myocardial ischemia, activation of 5"-AMP-activated protein kinase (AMPK) leads to the stimulation of glycolysis and fatty acid oxidation. Fatty Acids 124-134 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 75-79 15834636-2 2005 AMPK plays a major role in protecting mammalian cells from metabolic stress by switching off biosynthetic pathways that require ATP and switching on ATP-regenerating pathways. Adenosine Triphosphate 128-131 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 15834636-2 2005 AMPK plays a major role in protecting mammalian cells from metabolic stress by switching off biosynthetic pathways that require ATP and switching on ATP-regenerating pathways. Adenosine Triphosphate 149-152 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 15377643-1 2005 AMP-activated kinase (AMPK) is a highly conserved heterotrimeric kinase that functions as a metabolic master switch to coordinate cellular enzymes involved in carbohydrate and fat metabolism that regulate ATP conservation and synthesis. Carbohydrates 159-171 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-20 15377643-1 2005 AMP-activated kinase (AMPK) is a highly conserved heterotrimeric kinase that functions as a metabolic master switch to coordinate cellular enzymes involved in carbohydrate and fat metabolism that regulate ATP conservation and synthesis. Carbohydrates 159-171 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 22-26 15377643-1 2005 AMP-activated kinase (AMPK) is a highly conserved heterotrimeric kinase that functions as a metabolic master switch to coordinate cellular enzymes involved in carbohydrate and fat metabolism that regulate ATP conservation and synthesis. Adenosine Triphosphate 205-208 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-20 15377643-1 2005 AMP-activated kinase (AMPK) is a highly conserved heterotrimeric kinase that functions as a metabolic master switch to coordinate cellular enzymes involved in carbohydrate and fat metabolism that regulate ATP conservation and synthesis. Adenosine Triphosphate 205-208 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 22-26 15377643-2 2005 AMPK is activated by conditions that increase AMP-to-ATP ratio, such as exercise and metabolic stress. Adenosine Triphosphate 53-56 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 15377643-6 2005 AMPK inactivation on return to normal physiological saline was approximately 50% in 1 min and fully recovered by 5 min. Sodium Chloride 52-58 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 15377643-7 2005 Immunoprecipitation of the alpha(1)- and alpha(2)-catalytic subunit followed by immunoblot analysis for [P]Thr(172)-AMPK indicates that alpha(1)-AMPK accounts for all activity. Threonine 107-110 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 116-120 15377643-7 2005 Immunoprecipitation of the alpha(1)- and alpha(2)-catalytic subunit followed by immunoblot analysis for [P]Thr(172)-AMPK indicates that alpha(1)-AMPK accounts for all activity. Threonine 107-110 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 145-149 15377643-10 2005 AMPK activation by N(2)-2DG was associated with a rapid and pronounced reduction in endothelin-induced force and reduced phosphorylation of Akt and Erk 1/2. n(2)-2dg 19-27 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 15009683-1 2004 5-Aminoimidazole-4-carboxamide riboside (AICA riboside; Acadesine) activates AMP-activated protein kinase (AMPK) in intact cells, and is reported to exert protective effects in the mammalian CNS. acadesine 0-39 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 77-105 15297373-0 2004 AMP-activated protein kinase activity is required for vanadate-induced hypoxia-inducible factor 1alpha expression in DU145 cells. Vanadates 54-62 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-28 15297373-5 2004 In the present study, we have examined the biochemical mechanisms of the vanadate-induced HIF-1 activation in cancer cells by primarily focusing on the role of AMP-activated protein kinase (AMPK), which plays an essential role as an energy sensor under ATP-deprived conditions. Vanadates 73-81 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 160-188 15297373-5 2004 In the present study, we have examined the biochemical mechanisms of the vanadate-induced HIF-1 activation in cancer cells by primarily focusing on the role of AMP-activated protein kinase (AMPK), which plays an essential role as an energy sensor under ATP-deprived conditions. Vanadates 73-81 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 190-194 15297373-5 2004 In the present study, we have examined the biochemical mechanisms of the vanadate-induced HIF-1 activation in cancer cells by primarily focusing on the role of AMP-activated protein kinase (AMPK), which plays an essential role as an energy sensor under ATP-deprived conditions. Adenosine Triphosphate 253-256 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 160-188 15297373-5 2004 In the present study, we have examined the biochemical mechanisms of the vanadate-induced HIF-1 activation in cancer cells by primarily focusing on the role of AMP-activated protein kinase (AMPK), which plays an essential role as an energy sensor under ATP-deprived conditions. Adenosine Triphosphate 253-256 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 190-194 15297373-6 2004 We demonstrate that AMPK was rapidly activated in response to vanadate in DU145 human prostate carcinoma, and that its activation preceded HIF-1alpha expression. Vanadates 62-70 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 20-24 15297373-7 2004 Under this condition, inhibition of AMPK by a pharmacological and molecular approach dramatically abolished the vanadate-induced HIF-1alpha expression as well as HIF-1-mediated physiological responses. Vanadates 112-120 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 36-40 15297373-8 2004 Phosphatidylinositol-3 kinase/Akt/mammalian target of rapamycin signaling was also involved in vanadate-induced HIF-1alpha expression, but it was independent of AMPK signaling pathway. Vanadates 95-103 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 161-165 15297373-10 2004 These results suggest that AMPK is a novel and critical component of HIF-1 regulation, further implying its involvement in vanadate-induced carcinogenesis. Vanadates 123-131 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 27-31 15504342-0 2004 AMPK inhibits fatty acid-induced increases in NF-kappaB transactivation in cultured human umbilical vein endothelial cells. Fatty Acids 14-24 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 15504342-1 2004 The fuel sensing enzyme AMP-activated protein kinase (AMPK) enhances processes that generate ATP when stresses such as exercise or glucose deprivation make cells energy deficient. Adenosine Triphosphate 93-96 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 24-52 15504342-1 2004 The fuel sensing enzyme AMP-activated protein kinase (AMPK) enhances processes that generate ATP when stresses such as exercise or glucose deprivation make cells energy deficient. Adenosine Triphosphate 93-96 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 54-58 15504342-2 2004 We report here a novel role of AMPK, to prevent the activation of NF-kappaB in endothelial cells exposed to the fatty acid palmitate or the cytokine TNF-alpha. fatty acid palmitate 112-132 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 31-35 15504342-9 2004 The mechanism responsible for this action, as well as its relevance to the reported anti-atherogenic actions of exercise, metformin, thiazolidinediones, and adiponectin, all of which have been shown to activate AMPK, remains to be determined. Metformin 122-131 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 211-215 15504342-9 2004 The mechanism responsible for this action, as well as its relevance to the reported anti-atherogenic actions of exercise, metformin, thiazolidinediones, and adiponectin, all of which have been shown to activate AMPK, remains to be determined. Thiazolidinediones 133-151 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 211-215 15342649-4 2004 First, AMPK triggered the acetylation of importin alpha1 on Lys(22), a process dependent on the acetylase activity of p300. Lysine 60-63 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 7-11 15342649-5 2004 Second, AMPK phosphorylated importin alpha1 on Ser(105). Serine 47-50 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 8-12 15308678-10 2004 In conclusion, the present study suggests that AMPK phosphorylates HSL on Ser565 in human skeletal muscle during exercise with reduced muscle glycogen. Glycogen 142-150 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 47-51 15235328-8 2004 AMPK signaling is intact, because 5-aminoimidazole-4-carboxamide 1-beta-D-ribonucleoside (AICAR) increased AMPK and acetyl-CoA carboxylase (ACC) phosphorylation to a similar extent in Type 2 diabetic and nondiabetic subjects. 5-aminoimidazole-4-carboxamide 1-beta-d-ribonucleoside 34-88 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 107-111 15235328-10 2004 Our studies highlight important AMPK-dependent and independent pathways in the regulation of GLUT4 and glucose transport activity in insulin resistant skeletal muscle. Glucose 103-110 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 32-36 15033479-1 2004 5-Aminoimidazole-4-carboxamide ribonucleoside (AICAR) can be used as an experimental tool to activate 5"-AMP-activated protein kinase (AMPK) and has been shown to improve insulin sensitivity. acadesine 0-45 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 135-139 15294043-3 2004 The present paper reviews the evidence, which indicates that the decrease in the levels of high-energy phosphates, leading to activation of AMP kinase (AMPK), and the increase in cytosolic Ca(2+), which activates Ca(2+)/calmodulin-dependent protein kinase (CAMK), are signals that initiate these adaptative responses. Phosphates 103-113 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 140-150 15294043-3 2004 The present paper reviews the evidence, which indicates that the decrease in the levels of high-energy phosphates, leading to activation of AMP kinase (AMPK), and the increase in cytosolic Ca(2+), which activates Ca(2+)/calmodulin-dependent protein kinase (CAMK), are signals that initiate these adaptative responses. Phosphates 103-113 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 152-156 15294043-6 2004 Activating AMPK using 5-aminoimidizole-4-carboxamide-1-beta-D-riboside (AICAR) and increasing cytoplasmic Ca(2+) using caffeine, W7 or ionomycin in L6 myotubes increases the concentration of mitochondrial enzymes and GLUT4 and enhances the binding of NRF-1 and NRF-2 to DNA. 5-aminoimidizole-4-carboxamide-1-beta-d-riboside 22-70 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 11-15 15294043-6 2004 Activating AMPK using 5-aminoimidizole-4-carboxamide-1-beta-D-riboside (AICAR) and increasing cytoplasmic Ca(2+) using caffeine, W7 or ionomycin in L6 myotubes increases the concentration of mitochondrial enzymes and GLUT4 and enhances the binding of NRF-1 and NRF-2 to DNA. acadesine 72-77 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 11-15 15009683-1 2004 5-Aminoimidazole-4-carboxamide riboside (AICA riboside; Acadesine) activates AMP-activated protein kinase (AMPK) in intact cells, and is reported to exert protective effects in the mammalian CNS. acadesine 0-39 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 107-111 15009683-1 2004 5-Aminoimidazole-4-carboxamide riboside (AICA riboside; Acadesine) activates AMP-activated protein kinase (AMPK) in intact cells, and is reported to exert protective effects in the mammalian CNS. acadesine 41-54 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 77-105 15009683-1 2004 5-Aminoimidazole-4-carboxamide riboside (AICA riboside; Acadesine) activates AMP-activated protein kinase (AMPK) in intact cells, and is reported to exert protective effects in the mammalian CNS. acadesine 41-54 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 107-111 15009683-1 2004 5-Aminoimidazole-4-carboxamide riboside (AICA riboside; Acadesine) activates AMP-activated protein kinase (AMPK) in intact cells, and is reported to exert protective effects in the mammalian CNS. acadesine 56-65 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 77-105 15009683-1 2004 5-Aminoimidazole-4-carboxamide riboside (AICA riboside; Acadesine) activates AMP-activated protein kinase (AMPK) in intact cells, and is reported to exert protective effects in the mammalian CNS. acadesine 56-65 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 107-111 15009683-6 2004 We conclude that metabolic stress and AICA riboside both stimulate AMPK activity in mammalian brain, but that AICA riboside has an additional effect, i.e. competition with adenosine for uptake by the nucleoside transporter. acadesine 38-51 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 67-71 14500570-2 2003 Thus, factors that activate AMPK and decrease the concentration of malonyl CoA in peripheral tissues, such as exercise, decrease triglyceride accumulation in the adipocyte and other cells. Triglycerides 129-141 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 28-32 14573616-1 2004 We investigated the importance of the two catalytic alpha-isoforms of the 5"-AMP-activated protein kinase (AMPK) in 5-aminoimidazole-4-carboxamide-1-beta-4-ribofuranoside (AICAR) and contraction-induced glucose uptake in skeletal muscle. 5-aminoimidazole-4-carboxamide-1-beta-4-ribofuranoside 116-170 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 74-105 14573616-1 2004 We investigated the importance of the two catalytic alpha-isoforms of the 5"-AMP-activated protein kinase (AMPK) in 5-aminoimidazole-4-carboxamide-1-beta-4-ribofuranoside (AICAR) and contraction-induced glucose uptake in skeletal muscle. 5-aminoimidazole-4-carboxamide-1-beta-4-ribofuranoside 116-170 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 107-111 14573616-1 2004 We investigated the importance of the two catalytic alpha-isoforms of the 5"-AMP-activated protein kinase (AMPK) in 5-aminoimidazole-4-carboxamide-1-beta-4-ribofuranoside (AICAR) and contraction-induced glucose uptake in skeletal muscle. acadesine 172-177 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 74-105 14573616-1 2004 We investigated the importance of the two catalytic alpha-isoforms of the 5"-AMP-activated protein kinase (AMPK) in 5-aminoimidazole-4-carboxamide-1-beta-4-ribofuranoside (AICAR) and contraction-induced glucose uptake in skeletal muscle. acadesine 172-177 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 107-111 14573616-1 2004 We investigated the importance of the two catalytic alpha-isoforms of the 5"-AMP-activated protein kinase (AMPK) in 5-aminoimidazole-4-carboxamide-1-beta-4-ribofuranoside (AICAR) and contraction-induced glucose uptake in skeletal muscle. Glucose 203-210 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 74-105 14573616-1 2004 We investigated the importance of the two catalytic alpha-isoforms of the 5"-AMP-activated protein kinase (AMPK) in 5-aminoimidazole-4-carboxamide-1-beta-4-ribofuranoside (AICAR) and contraction-induced glucose uptake in skeletal muscle. Glucose 203-210 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 107-111 14573616-11 2004 The results show that alpha2-AMPK is the main donor of basal and AICAR-stimulated AMPK activity and is responsible for AICAR-induced glucose uptake. acadesine 65-70 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 29-33 14573616-11 2004 The results show that alpha2-AMPK is the main donor of basal and AICAR-stimulated AMPK activity and is responsible for AICAR-induced glucose uptake. acadesine 65-70 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 82-86 14573616-11 2004 The results show that alpha2-AMPK is the main donor of basal and AICAR-stimulated AMPK activity and is responsible for AICAR-induced glucose uptake. Glucose 133-140 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 29-33 14707762-5 2004 AMP plays its role by activating the protein-kinase, AMPK, which is a key sensor of cellular energy stress. Adenosine Monophosphate 0-3 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 53-57 14500570-5 2003 AMPK activation in turn increases fatty acid oxidation (by effects on enzymes that govern malonyl CoA synthesis and possibly its degradation) and inhibits triglyceride synthesis. Fatty Acids 34-44 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 14500570-5 2003 AMPK activation in turn increases fatty acid oxidation (by effects on enzymes that govern malonyl CoA synthesis and possibly its degradation) and inhibits triglyceride synthesis. Malonyl Coenzyme A 90-101 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 14500570-5 2003 AMPK activation in turn increases fatty acid oxidation (by effects on enzymes that govern malonyl CoA synthesis and possibly its degradation) and inhibits triglyceride synthesis. Triglycerides 155-167 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 14500570-7 2003 Recent studies suggest that the ability of leptin, adiponectin, 5"-aminoimidazole 4-carboxamide riboside (AICAR), adrenergic agonists, and metformin to diminish adiposity may be mediated, at least in part, by AMPK activation in peripheral tissues. acadesine 64-104 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 209-213 14500570-7 2003 Recent studies suggest that the ability of leptin, adiponectin, 5"-aminoimidazole 4-carboxamide riboside (AICAR), adrenergic agonists, and metformin to diminish adiposity may be mediated, at least in part, by AMPK activation in peripheral tissues. acadesine 106-111 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 209-213 14500570-7 2003 Recent studies suggest that the ability of leptin, adiponectin, 5"-aminoimidazole 4-carboxamide riboside (AICAR), adrenergic agonists, and metformin to diminish adiposity may be mediated, at least in part, by AMPK activation in peripheral tissues. Metformin 139-148 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 209-213 12824177-4 2003 Exposure of bovine aortic endothelial cells (BAEC) to chemically synthesized ONOO- acutely and significantly increased phosphorylation of c-Src, PDK1, AMPK, and its downstream target, acetyl-CoA carboxylase (ACC), without affecting cellular AMP. onoo 77-81 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 151-155 14614828-6 2003 LKB1 shares sequence similarity with Elm1, Pak1, and Tos3, and we demonstrated that LKB1 phosphorylates AMPK on the activation loop threonine (Thr172) within the catalytic subunit and activates AMPK in vitro [9]. Threonine 132-141 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 104-108 14614828-6 2003 LKB1 shares sequence similarity with Elm1, Pak1, and Tos3, and we demonstrated that LKB1 phosphorylates AMPK on the activation loop threonine (Thr172) within the catalytic subunit and activates AMPK in vitro [9]. Threonine 132-141 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 194-198 12937023-5 2003 Activity of alpha1-AMPK (160%) and alpha2-AMPK (145%) was increased at rest in the glycogen-depleted compared with the loaded situation. Glycogen 83-91 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 19-23 12937023-5 2003 Activity of alpha1-AMPK (160%) and alpha2-AMPK (145%) was increased at rest in the glycogen-depleted compared with the loaded situation. Glycogen 83-91 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 42-46 12937023-7 2003 After 60 min of exercise in the glycogen-depleted state, individual values of alpha2-AMPK activity correlated significantly (r = 0.87, P < 0.006) with individual values of IL-6 release as well as with average IL-6 release over the entire 60 min (r = 0.86, P < 0.006). Glycogen 32-40 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 85-89 12937023-9 2003 Alternatively, both AMPK and IL-6 are independent sensors of a low muscle glycogen concentration during exercise. Glycogen 74-82 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 20-24 12824177-8 2003 Moreover, H/R, like ONOO-, significantly increased co-immunoprecipitation of AMPK with c-Src, suggesting that ONOO- favors physical association of AMPK with upstream kinases. onoo 20-24 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 77-81 12824177-8 2003 Moreover, H/R, like ONOO-, significantly increased co-immunoprecipitation of AMPK with c-Src, suggesting that ONOO- favors physical association of AMPK with upstream kinases. onoo 20-24 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 147-151 12824177-8 2003 Moreover, H/R, like ONOO-, significantly increased co-immunoprecipitation of AMPK with c-Src, suggesting that ONOO- favors physical association of AMPK with upstream kinases. onoo 110-114 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 77-81 12824177-8 2003 Moreover, H/R, like ONOO-, significantly increased co-immunoprecipitation of AMPK with c-Src, suggesting that ONOO- favors physical association of AMPK with upstream kinases. onoo 110-114 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 147-151 12824177-9 2003 Taken together, our results indicate a novel pathway by which H/R via ONOO- activates AMPK in a c-Src-mediated, PI 3-kinase-dependent manner, and suggest that ONOO--induced activation of AMPK might thereby regulate metabolic enzymes, such as ACC. r 64-65 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 86-90 12824177-9 2003 Taken together, our results indicate a novel pathway by which H/R via ONOO- activates AMPK in a c-Src-mediated, PI 3-kinase-dependent manner, and suggest that ONOO--induced activation of AMPK might thereby regulate metabolic enzymes, such as ACC. r 64-65 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 187-191 12824177-9 2003 Taken together, our results indicate a novel pathway by which H/R via ONOO- activates AMPK in a c-Src-mediated, PI 3-kinase-dependent manner, and suggest that ONOO--induced activation of AMPK might thereby regulate metabolic enzymes, such as ACC. onoo 70-74 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 86-90 12824177-9 2003 Taken together, our results indicate a novel pathway by which H/R via ONOO- activates AMPK in a c-Src-mediated, PI 3-kinase-dependent manner, and suggest that ONOO--induced activation of AMPK might thereby regulate metabolic enzymes, such as ACC. onoo 70-74 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 187-191 12824177-9 2003 Taken together, our results indicate a novel pathway by which H/R via ONOO- activates AMPK in a c-Src-mediated, PI 3-kinase-dependent manner, and suggest that ONOO--induced activation of AMPK might thereby regulate metabolic enzymes, such as ACC. onoo 159-163 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 86-90 12824177-9 2003 Taken together, our results indicate a novel pathway by which H/R via ONOO- activates AMPK in a c-Src-mediated, PI 3-kinase-dependent manner, and suggest that ONOO--induced activation of AMPK might thereby regulate metabolic enzymes, such as ACC. onoo 159-163 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 187-191 11971761-1 2002 Mammalian AMP-activated protein kinase (AMPK) and yeast SNF1 (sucrose non-fermenting 1) kinase are members of a highly conserved protein kinase family that plays an important role in energy homoeostasis. Sucrose 62-69 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 40-44 12519745-6 2003 Activation of endogenous AMPK with the cell-permeant adenosine analog 5-amino-4-imidazolecarboxamide-1-beta-d-ribofuranoside (AICAR) inhibited forskolin-stimulated CFTR-dependent I(sc) in nonpermeabilized monolayers and monolayers with nystatin permeabilization of the basolateral membrane. Colforsin 143-152 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 25-29 12519745-6 2003 Activation of endogenous AMPK with the cell-permeant adenosine analog 5-amino-4-imidazolecarboxamide-1-beta-d-ribofuranoside (AICAR) inhibited forskolin-stimulated CFTR-dependent I(sc) in nonpermeabilized monolayers and monolayers with nystatin permeabilization of the basolateral membrane. Nystatin 236-244 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 25-29 12519745-8 2003 Finally, overexpression of a kinase-dead mutant AMPK-alpha1 subunit (alpha1-K45R) enhanced forskolin-stimulated I(sc) in polarized T84 monolayers, consistent with a dominant-negative reduction in the inhibition of CFTR by endogenous AMPK. Colforsin 91-100 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 48-59 12519745-8 2003 Finally, overexpression of a kinase-dead mutant AMPK-alpha1 subunit (alpha1-K45R) enhanced forskolin-stimulated I(sc) in polarized T84 monolayers, consistent with a dominant-negative reduction in the inhibition of CFTR by endogenous AMPK. Colforsin 91-100 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 48-52 12427743-8 2003 Pharmacologic activation of AMPK inhibited forskolin-stimulated CFTR short circuit currents in polarized Calu-3 cell monolayers. Colforsin 43-52 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 28-32 12427743-9 2003 In whole-cell patch clamp experiments, the activation of endogenous AMPK either pharmacologically or by the overexpression of an AMPK-activating non-catalytic subunit mutant (AMPK-gamma1-R70Q) dramatically inhibited forskolin-stimulated CFTR conductance in Calu-3 and CFTR-expressing Chinese hamster ovary cells. Colforsin 216-225 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 68-72 12427743-9 2003 In whole-cell patch clamp experiments, the activation of endogenous AMPK either pharmacologically or by the overexpression of an AMPK-activating non-catalytic subunit mutant (AMPK-gamma1-R70Q) dramatically inhibited forskolin-stimulated CFTR conductance in Calu-3 and CFTR-expressing Chinese hamster ovary cells. Colforsin 216-225 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 129-133 12427743-9 2003 In whole-cell patch clamp experiments, the activation of endogenous AMPK either pharmacologically or by the overexpression of an AMPK-activating non-catalytic subunit mutant (AMPK-gamma1-R70Q) dramatically inhibited forskolin-stimulated CFTR conductance in Calu-3 and CFTR-expressing Chinese hamster ovary cells. Colforsin 216-225 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 129-133 12502487-0 2003 Regulation of glycogen synthase by glucose and glycogen: a possible role for AMP-activated protein kinase. Glycogen 14-22 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 77-105 12502487-1 2003 We report here use of human myoblasts in culture to study the relationships between cellular glycogen concentrations and the activities of glycogen synthase (GS) and AMP-activated protein kinase (AMPK). Glycogen 93-101 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 166-194 12502487-1 2003 We report here use of human myoblasts in culture to study the relationships between cellular glycogen concentrations and the activities of glycogen synthase (GS) and AMP-activated protein kinase (AMPK). Glycogen 93-101 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 196-200 12502487-4 2003 When glucose was added to glycogen-depleted cells, a rapid and substantial increase in GS activity was accompanied by inactivation of AMPK back to basal values. Glucose 5-12 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 134-138 12502487-4 2003 When glucose was added to glycogen-depleted cells, a rapid and substantial increase in GS activity was accompanied by inactivation of AMPK back to basal values. Glycogen 26-34 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 134-138 12502487-7 2003 Activation of AMPK by either 5-aminoimidazole-4-carboxamide 1-beta-D-ribofuranoside (AICAR) or hydrogen peroxide was also associated with a decrease in the activity ratio of GS. acadesine 29-83 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-18 12502487-7 2003 Activation of AMPK by either 5-aminoimidazole-4-carboxamide 1-beta-D-ribofuranoside (AICAR) or hydrogen peroxide was also associated with a decrease in the activity ratio of GS. acadesine 85-90 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-18 12502487-7 2003 Activation of AMPK by either 5-aminoimidazole-4-carboxamide 1-beta-D-ribofuranoside (AICAR) or hydrogen peroxide was also associated with a decrease in the activity ratio of GS. Hydrogen Peroxide 95-112 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-18 12502487-9 2003 These data support a role for AMPK in both stimulating glucose uptake and inhibiting GS in intact cells, thus promoting glucose flux through glycolysis. Glucose 55-62 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-34 12502487-9 2003 These data support a role for AMPK in both stimulating glucose uptake and inhibiting GS in intact cells, thus promoting glucose flux through glycolysis. Glucose 120-127 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-34 12413941-5 2002 In the thigh muscle, the alpha AMPK subunits became progressively more phosphorylated on Thr(172) during exercise eliciting a parallel increase in alpha2 but not alpha1 AMPK activity. Threonine 89-92 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 31-35 12519745-6 2003 Activation of endogenous AMPK with the cell-permeant adenosine analog 5-amino-4-imidazolecarboxamide-1-beta-d-ribofuranoside (AICAR) inhibited forskolin-stimulated CFTR-dependent I(sc) in nonpermeabilized monolayers and monolayers with nystatin permeabilization of the basolateral membrane. Adenosine 53-62 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 25-29 12519745-6 2003 Activation of endogenous AMPK with the cell-permeant adenosine analog 5-amino-4-imidazolecarboxamide-1-beta-d-ribofuranoside (AICAR) inhibited forskolin-stimulated CFTR-dependent I(sc) in nonpermeabilized monolayers and monolayers with nystatin permeabilization of the basolateral membrane. 5-amino-4-imidazolecarboxamide-1-beta-d-ribofuranoside 70-124 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 25-29 12519745-6 2003 Activation of endogenous AMPK with the cell-permeant adenosine analog 5-amino-4-imidazolecarboxamide-1-beta-d-ribofuranoside (AICAR) inhibited forskolin-stimulated CFTR-dependent I(sc) in nonpermeabilized monolayers and monolayers with nystatin permeabilization of the basolateral membrane. acadesine 126-131 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 25-29 12409306-3 2003 It has a putative Akt phosphorylation motif at amino acids 595-600, and Ser(600) was found to be phosphorylated by active Akt resulting in the activation of kinase activity toward the SAMS peptide, a consensus AMPK substrate. Serine 72-75 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 210-214 14511394-10 2003 Fourth, the AMPK-activating drugs AICA riboside and phenformin do not activate AMPK in HeLa cells (which lack LKB1), but activation can be restored by stably expressing wild-type, but not catalytically inactive, LKB1. riboside 39-47 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 12-16 14511394-10 2003 Fourth, the AMPK-activating drugs AICA riboside and phenformin do not activate AMPK in HeLa cells (which lack LKB1), but activation can be restored by stably expressing wild-type, but not catalytically inactive, LKB1. Phenformin 52-62 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 12-16 12093363-4 2002 The Drosophila kinase (DmAMPK) was activated by AMP in cell-free assays (albeit to a smaller extent than mammalian AMPK), and by stresses that deplete ATP (oligomycin and hypoxia), as well as by carbohydrate deprivation, in intact cells. Adenosine Triphosphate 151-154 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 25-29 12093363-4 2002 The Drosophila kinase (DmAMPK) was activated by AMP in cell-free assays (albeit to a smaller extent than mammalian AMPK), and by stresses that deplete ATP (oligomycin and hypoxia), as well as by carbohydrate deprivation, in intact cells. Oligomycins 156-166 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 25-29 12093363-4 2002 The Drosophila kinase (DmAMPK) was activated by AMP in cell-free assays (albeit to a smaller extent than mammalian AMPK), and by stresses that deplete ATP (oligomycin and hypoxia), as well as by carbohydrate deprivation, in intact cells. Carbohydrates 195-207 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 25-29 11971761-8 2002 Co-expression of the AMPK trimeric complex in yeast yielded an activity, increased by low glucose, that was similar to native SNF1 kinase. Glucose 90-97 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 21-25 11971761-9 2002 Importantly, expression of AMPK restored growth of a snf1 mutant on raffinose. Raffinose 68-77 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 27-31 11971761-10 2002 Our results provide clues to the regulation of AMPK and SNF1 kinase and demonstrate that, in mammalian cells, there are at least two pathways that can activate AMPK, namely one that involves an increase in the AMP/ATP ratio and one that is independent of this ratio. Adenosine Monophosphate 47-50 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 160-164 11971761-10 2002 Our results provide clues to the regulation of AMPK and SNF1 kinase and demonstrate that, in mammalian cells, there are at least two pathways that can activate AMPK, namely one that involves an increase in the AMP/ATP ratio and one that is independent of this ratio. Adenosine Triphosphate 214-217 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 160-164 11971761-11 2002 In yeast, the glucose signalling pathway is able to activate AMPK, suggesting that the mammalian and yeast kinase pathways are conserved. Glucose 14-21 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 61-65 11994296-0 2002 The Anti-diabetic drugs rosiglitazone and metformin stimulate AMP-activated protein kinase through distinct signaling pathways. Rosiglitazone 24-37 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 62-90 11994296-0 2002 The Anti-diabetic drugs rosiglitazone and metformin stimulate AMP-activated protein kinase through distinct signaling pathways. Metformin 42-51 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 62-90 11994296-1 2002 AMP-activated protein kinase (AMPK) is activated within the cell in response to multiple stresses that increase the intracellular AMP:ATP ratio. Adenosine Monophosphate 0-3 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-34 11334434-3 2001 Several groups have recently hypothesized that exercise increases glucose uptake via an insulin-independent mechanism mediated by the activation of AMP-activated protein kinase (AMPK). Glucose 66-73 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 178-182 11994296-1 2002 AMP-activated protein kinase (AMPK) is activated within the cell in response to multiple stresses that increase the intracellular AMP:ATP ratio. Adenosine Triphosphate 134-137 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-28 11994296-1 2002 AMP-activated protein kinase (AMPK) is activated within the cell in response to multiple stresses that increase the intracellular AMP:ATP ratio. Adenosine Triphosphate 134-137 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-34 11994296-2 2002 Here we show that incubation of muscle cells with the thiazolidinedione, rosiglitazone, leads to a dramatic increase in this ratio with the concomitant activation of AMPK. 2,4-thiazolidinedione 54-71 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 166-170 11994296-2 2002 Here we show that incubation of muscle cells with the thiazolidinedione, rosiglitazone, leads to a dramatic increase in this ratio with the concomitant activation of AMPK. Rosiglitazone 73-86 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 166-170 11994296-3 2002 This finding raises the possibility that a number of the beneficial effects of the thiazolidinediones could be mediated via activation of AMPK. Thiazolidinediones 83-101 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 138-142 11994296-5 2002 In muscle cells, both hyperosmotic stress and the anti-diabetic agent, metformin, activate AMPK in the absence of any increase in the AMP:ATP ratio. Metformin 71-80 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 91-95 12068056-5 2002 Exercise-induced phosphorylation of the in vivo AMPK substrate acetyl CoA carboxylase (ACCbeta; Ser(221)) was higher (P < 0.01) in McArdle patients than in control subjects (18 +/- 3 vs. 10 +/- 1 arbitrary units). Serine 96-99 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 48-52 12068056-9 2002 This was not associated with activity changes of GS kinase 3 or protein phosphatase 1, but the changes in GS activity could be due to changes in activity of AMPK or protein kinase A (PKA) as a negative correlation between either ACCbeta phosphorylation (Ser(221)) or plasma adrenaline and GS activity was observed. Serine 254-257 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 157-161 12068056-9 2002 This was not associated with activity changes of GS kinase 3 or protein phosphatase 1, but the changes in GS activity could be due to changes in activity of AMPK or protein kinase A (PKA) as a negative correlation between either ACCbeta phosphorylation (Ser(221)) or plasma adrenaline and GS activity was observed. Epinephrine 274-284 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 157-161 12068056-11 2002 Furthermore, AMPK may be involved in the regulation of glucose utilization during exercise in humans, although the lack of correlation between individual AMPK activity or ACCbeta phosphorylation (Ser(221)) values and individual glucose utilization during exercise implies that AMPK may not be an essential regulator. Glucose 55-62 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 13-17 12051742-8 2002 In an insulinoma cell line, either low glucose or 5-aminoimidazole-4-carboxamide ribonucleoside (AICAR) treatment leads to activation and T172 phosphorylation of endogenous AMPK. acadesine 50-95 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 173-177 12051742-8 2002 In an insulinoma cell line, either low glucose or 5-aminoimidazole-4-carboxamide ribonucleoside (AICAR) treatment leads to activation and T172 phosphorylation of endogenous AMPK. acadesine 97-102 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 173-177 11522840-1 2001 Plant orthologs of the yeast sucrose non-fermenting (Snf1) kinase and mammalian AMP-activated protein kinase (AMPK) represent an emerging class of important regulators of metabolic and stress signalling. Sucrose 29-36 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 110-114 11112354-1 2000 5"-AMP-activated protein kinase (AMPK) acts as a major regulator of cellular ATP levels and protects cells against stresses that cause ATP depletion. Adenosine Triphosphate 77-80 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 33-37 11112354-1 2000 5"-AMP-activated protein kinase (AMPK) acts as a major regulator of cellular ATP levels and protects cells against stresses that cause ATP depletion. Adenosine Triphosphate 135-138 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 33-37 11018120-14 2000 The in vitro AMP dependency of alpha2-AMPK was significantly greater than that of alpha1-AMPK ( approximately 3- vs. approximately 2-fold). Adenosine Monophosphate 13-16 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 38-42 10642499-3 2000 Threonine-172 within the catalytic subunit (alpha) of AMPK (Thr(172)) was identified as the major site phosphorylated by the AMP-activated protein kinase kinase (AMPKK) in vitro. Threonine 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 125-153 10891387-2 2000 AMPK has emerged as an important signaling intermediary in the regulation of cell metabolism being linked to exercise-induced changes in muscle glucose and fatty acid metabolism. Fatty Acids 156-166 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 10642499-1 2000 The AMP-activated protein kinase (AMPK) cascade is activated by an increase in the AMP/ATP ratio within the cell. Adenosine Monophosphate 4-7 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 34-38 10642499-3 2000 Threonine-172 within the catalytic subunit (alpha) of AMPK (Thr(172)) was identified as the major site phosphorylated by the AMP-activated protein kinase kinase (AMPKK) in vitro. Threonine 0-3 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 54-58 10642499-1 2000 The AMP-activated protein kinase (AMPK) cascade is activated by an increase in the AMP/ATP ratio within the cell. Adenosine Triphosphate 87-90 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 4-32 10642499-3 2000 Threonine-172 within the catalytic subunit (alpha) of AMPK (Thr(172)) was identified as the major site phosphorylated by the AMP-activated protein kinase kinase (AMPKK) in vitro. Threonine 0-3 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 125-153 10642499-1 2000 The AMP-activated protein kinase (AMPK) cascade is activated by an increase in the AMP/ATP ratio within the cell. Adenosine Triphosphate 87-90 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 34-38 10642499-4 2000 We have used site-directed mutagenesis to study the role of phosphorylation of Thr(172) on AMPK activity. Threonine 79-82 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 91-95 10642499-3 2000 Threonine-172 within the catalytic subunit (alpha) of AMPK (Thr(172)) was identified as the major site phosphorylated by the AMP-activated protein kinase kinase (AMPKK) in vitro. Threonine 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 54-58 10642499-11 2000 Furthermore, we provide evidence that phosphorylation of Thr(172) may be involved in the sensitivity of the AMPK complex to AMP. Threonine 57-60 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 108-112 8939604-4 1996 AMPK is activated by the elevation of the cellular AMP:ATP ratio, which occurs during cellular stress in mammalian cells. Adenosine Triphosphate 55-58 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 9224708-1 1997 The AMP-activated protein kinase (AMPK) consists of catalytic alpha and non-catalytic, beta and gamma (38 kDa) subunits and is responsible for acting as a metabolic sensor for AMP levels. Adenosine Monophosphate 4-7 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 34-38 9208914-1 1997 A single entity, the AMP-activated protein kinase (AMPK), phosphorylates and regulates in vivo hydroxymethylglutaryl-CoA reductase and acetyl-CoA carboxylase (key regulatory enzymes of sterol synthesis and fatty acid synthesis, respectively), and probably many additional targets. Sterols 185-191 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 21-49 9208914-1 1997 A single entity, the AMP-activated protein kinase (AMPK), phosphorylates and regulates in vivo hydroxymethylglutaryl-CoA reductase and acetyl-CoA carboxylase (key regulatory enzymes of sterol synthesis and fatty acid synthesis, respectively), and probably many additional targets. Sterols 185-191 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 51-55 9208914-1 1997 A single entity, the AMP-activated protein kinase (AMPK), phosphorylates and regulates in vivo hydroxymethylglutaryl-CoA reductase and acetyl-CoA carboxylase (key regulatory enzymes of sterol synthesis and fatty acid synthesis, respectively), and probably many additional targets. Fatty Acids 206-216 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 21-49 9208914-1 1997 A single entity, the AMP-activated protein kinase (AMPK), phosphorylates and regulates in vivo hydroxymethylglutaryl-CoA reductase and acetyl-CoA carboxylase (key regulatory enzymes of sterol synthesis and fatty acid synthesis, respectively), and probably many additional targets. Fatty Acids 206-216 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 51-55 9208914-2 1997 The kinase is activated by high AMP and low ATP via a complex mechanism, which involves allosteric regulation, promotion of phosphorylation by an upstream protein kinase (AMPK kinase), and inhibition of dephosphorylation. Adenosine Monophosphate 32-35 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 171-175 9208914-2 1997 The kinase is activated by high AMP and low ATP via a complex mechanism, which involves allosteric regulation, promotion of phosphorylation by an upstream protein kinase (AMPK kinase), and inhibition of dephosphorylation. Adenosine Triphosphate 44-47 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 171-175 7913470-6 1994 Mammalian AMPK plays a major role in the control of lipid metabolism and phosphorylating, thereby inactivating both acetyl-CoA carboxylase and 3-hydroxy-3-methylglutaryl-CoA reductase, key regulatory enzymes in the synthesis of fatty acids and cholesterol, respectively. Fatty Acids 228-239 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 10-14 8621499-5 1996 The AMPK beta-subunit, when expressed in bacteria and in mammalian cells, migrates anomalously on SDS gels at an apparent molecular mass of 40 kDa. Sodium Dodecyl Sulfate 98-101 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 4-8 7959015-1 1994 AMP-activated protein kinase (AMPK) phosphorylates and inactivates acetyl-CoA carboxylase and beta-hydroxy beta-methylglutaryl-coenzyme A (HMG-CoA) reductase which are the major enzymes involved in fatty acid and lipid biosyntheses. Fatty Acids 198-208 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-28 7959015-1 1994 AMP-activated protein kinase (AMPK) phosphorylates and inactivates acetyl-CoA carboxylase and beta-hydroxy beta-methylglutaryl-coenzyme A (HMG-CoA) reductase which are the major enzymes involved in fatty acid and lipid biosyntheses. Fatty Acids 198-208 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-34 7959015-7 1994 The hAMPK gene bears homology to a yeast protein kinase-encoding gene (snf1) that regulates carbohydrate metabolism, and also with three other genes encoding SNF1-like kinases from different plant species, namely Arabidopsis thaliana, Hordeum vulgare and Secale cereale. Carbohydrates 92-104 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 4-9 7913470-6 1994 Mammalian AMPK plays a major role in the control of lipid metabolism and phosphorylating, thereby inactivating both acetyl-CoA carboxylase and 3-hydroxy-3-methylglutaryl-CoA reductase, key regulatory enzymes in the synthesis of fatty acids and cholesterol, respectively. Cholesterol 244-255 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 10-14 7913470-11 1994 These results suggest that, in addition to their structural similarity, the role of SNF1 and AMPK in the regulation of fatty acid synthesis has been highly conserved throughout evolution. Fatty Acids 119-129 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 93-97 33772142-0 2022 PPARalpha agonist fenofibrate relieves acquired resistance to gefitinib in non-small cell lung cancer by promoting apoptosis via PPARalpha/AMPK/AKT/FoxO1 pathway. Fenofibrate 18-29 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 139-143 33773207-0 2021 The AMPK modulator metformin as adjunct to methotrexate in patients with rheumatoid arthritis: A proof-of-concept, randomized, double-blind, placebo-controlled trial. Metformin 19-28 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 4-8 33824293-0 2021 AMPK activation by ASP4132 inhibits non-small cell lung cancer cell growth. 4-(4-dimethylaminostyryl)-1-methylpyridinium 19-26 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 33824293-2 2021 ASP4132 is an orally active and highly effective AMPK activator. 4-(4-dimethylaminostyryl)-1-methylpyridinium 0-7 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 49-53 33824293-7 2021 In NSCLC cells ASP4132 activated AMPK signaling, induced AMPKalpha1-ACC phosphorylation and increased AMPK activity. 4-(4-dimethylaminostyryl)-1-methylpyridinium 15-22 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 33-37 33824293-7 2021 In NSCLC cells ASP4132 activated AMPK signaling, induced AMPKalpha1-ACC phosphorylation and increased AMPK activity. 4-(4-dimethylaminostyryl)-1-methylpyridinium 15-22 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 57-67 33824293-7 2021 In NSCLC cells ASP4132 activated AMPK signaling, induced AMPKalpha1-ACC phosphorylation and increased AMPK activity. 4-(4-dimethylaminostyryl)-1-methylpyridinium 15-22 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 57-61 33824293-8 2021 Furthermore, AMPK downstream events, including mTORC1 inhibition, receptor tyrosine kinases (PDGFRalpha and EGFR) degradation, Akt inhibition and autophagy induction, were detected in ASP4132-treated NSCLC cells. 4-(4-dimethylaminostyryl)-1-methylpyridinium 184-191 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 13-17 33824293-9 2021 Importantly, AMPK inactivation by AMPKalpha1 shRNA, knockout (using CRISPR/Cas9 strategy) or dominant negative mutation (T172A) almost reversed ASP4132-induced anti-NSCLC cell activity. 4-(4-dimethylaminostyryl)-1-methylpyridinium 144-151 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 13-17 33824293-9 2021 Importantly, AMPK inactivation by AMPKalpha1 shRNA, knockout (using CRISPR/Cas9 strategy) or dominant negative mutation (T172A) almost reversed ASP4132-induced anti-NSCLC cell activity. 4-(4-dimethylaminostyryl)-1-methylpyridinium 144-151 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 34-44 33824293-10 2021 Conversely, a constitutively active AMPKalpha1 (T172D) mimicked and abolished ASP4132-induced actions in NSCLC cells. 4-(4-dimethylaminostyryl)-1-methylpyridinium 78-85 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 36-46 33824293-12 2021 AMPK activation, mTORC1 inhibition and EGFR-PDGFRalpha degradation as well as Akt inhibition and autophagy induction were detected in ASP4132-treated NSCLC xenograft tumor tissues. 4-(4-dimethylaminostyryl)-1-methylpyridinium 134-141 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 33824293-13 2021 Together, activation of AMPK by ASP4132 potently inhibits NSCLC cell growth in vitro and in vivo. 4-(4-dimethylaminostyryl)-1-methylpyridinium 32-39 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 24-28 33821487-8 2021 It summarises the excess-iron-induced alterations in MSC components, processes and discusses signalling pathways involving ROS, PI3K/AKT, MAPK, p53, AMPK/MFF/DRP1 and Wnt. Iron 25-29 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 149-153 33772142-8 2022 In PC-9/GR, H1975 and H1650 cells, fenofibrate dose-dependently increased the expression of AMPK, FoxO1, and decreased the expression of AKT, which were remarkably weakened by knockdown of PPARalpha. Fenofibrate 35-46 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 92-96 33772142-10 2022 All the results suggest that fenofibrate relieves acquired resistance to gefitinib in NSCLC by promoting apoptosis via regulating PPARalpha/AMPK/AKT/FoxO1 pathway. Fenofibrate 29-40 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 140-144 33823340-11 2021 Also, oridonin increased the ratios of LC3-II/LC3-I and p-AMPK/AMPK, but reduced that of p-AKT/AKT. oridonin 6-14 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 58-62 33823340-11 2021 Also, oridonin increased the ratios of LC3-II/LC3-I and p-AMPK/AMPK, but reduced that of p-AKT/AKT. oridonin 6-14 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 63-67 33816292-0 2021 Targeting ACLY Attenuates Tumor Growth and Acquired Cisplatin Resistance in Ovarian Cancer by Inhibiting the PI3K-AKT Pathway and Activating the AMPK-ROS Pathway. ros 150-153 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 145-149 33816292-15 2021 Knockdown of ACLY alleviated cisplatin resistance, and works synergistically with cisplatin treatment to induce apoptosis in A2780/CDDP cells by inhibiting the PI3K-AKT pathway and activating AMPK-ROS pathway. Cisplatin 82-91 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 192-196 33816292-18 2021 Conclusions: Knockdown of ACLY attenuated cisplatin resistance by inhibiting the PI3K-AKT pathway and activating the AMPK-ROS pathway. Cisplatin 42-51 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 117-121 33816292-18 2021 Conclusions: Knockdown of ACLY attenuated cisplatin resistance by inhibiting the PI3K-AKT pathway and activating the AMPK-ROS pathway. ros 122-125 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 117-121 33799444-0 2021 6-Azauridine Induces Autophagy-Mediated Cell Death via a p53- and AMPK-Dependent Pathway. Azauridine 0-12 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 66-70 33799444-8 2021 In addition, we demonstrated that the cytotoxic effect of 6-AZA was dependent on AMPK and p53. Azauridine 58-63 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 81-85 33772142-0 2022 PPARalpha agonist fenofibrate relieves acquired resistance to gefitinib in non-small cell lung cancer by promoting apoptosis via PPARalpha/AMPK/AKT/FoxO1 pathway. Gefitinib 62-71 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 139-143 33778821-0 2020 [Human dental pulp stem cells conditioned medium protects genioglossus myoblast from cobalt chloride-induced hypoxia injury through AMPK/PGC-1alpha pathway]. cobaltous chloride 85-100 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 132-136 33233708-7 2020 Once absorbed, anthocyanins positively modulate GLUT4 density and function in both skeletal muscle and adipose tissues via the upregulation of AMPK and restoration of insulin sensitivity. Anthocyanins 15-27 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 143-147 33234350-0 2021 Curcumin represses mTORC1 signaling in Caco-2 cells by a two-sided mechanism involving the loss of IRS-1 and activation of AMPK. Curcumin 0-8 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 123-127 33483422-7 2021 Loss of both AMPK and HRI is sufficient to render mTORC1 signaling largely resistant to mitochondrial dysfunction induced by the ATP synthase inhibitor oligomycin as well as the electron transport chain inhibitors piericidin and antimycin. Oligomycins 152-162 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 13-17 33483422-7 2021 Loss of both AMPK and HRI is sufficient to render mTORC1 signaling largely resistant to mitochondrial dysfunction induced by the ATP synthase inhibitor oligomycin as well as the electron transport chain inhibitors piericidin and antimycin. piericidin A 214-224 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 13-17 33483422-7 2021 Loss of both AMPK and HRI is sufficient to render mTORC1 signaling largely resistant to mitochondrial dysfunction induced by the ATP synthase inhibitor oligomycin as well as the electron transport chain inhibitors piericidin and antimycin. antimycin 229-238 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 13-17 33235318-5 2020 LW1564 also significantly decreased overall ATP levels by inhibiting mitochondrial electron transport chain (ETC) complex I and downregulated mammalian target of rapamycin (mTOR) signaling by increasing the AMP/ATP ratio, which increased AMP-activated protein kinase (AMPK) phosphorylation. lw1564 0-6 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 238-266 33235318-5 2020 LW1564 also significantly decreased overall ATP levels by inhibiting mitochondrial electron transport chain (ETC) complex I and downregulated mammalian target of rapamycin (mTOR) signaling by increasing the AMP/ATP ratio, which increased AMP-activated protein kinase (AMPK) phosphorylation. lw1564 0-6 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 268-272 33235318-5 2020 LW1564 also significantly decreased overall ATP levels by inhibiting mitochondrial electron transport chain (ETC) complex I and downregulated mammalian target of rapamycin (mTOR) signaling by increasing the AMP/ATP ratio, which increased AMP-activated protein kinase (AMPK) phosphorylation. Adenosine Monophosphate 207-210 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 238-266 33817229-0 2020 Buformin suppresses osteosarcoma via targeting AMPK signaling pathway. Buformin 0-8 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 47-51 33817229-1 2020 Background: Buformin has been reported to be a powerful anticancer drug by activating the AMPK signal. Buformin 12-20 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 90-94 33817229-10 2020 Phosphorylation of AMPK was upregulated by buformin, while phosphorylation of S6, cyclin D1, and MMP9 were significantly downregulated. Buformin 43-51 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 19-23 33817229-13 2020 Conclusions: Buformin could suppress tumor growth and invasion of osteosarcoma through directly targeting the AMPK signaling pathway. Buformin 13-21 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 110-114 20668229-2 2010 We show in our current study that the LKB1/AMPK/TSC tumor suppressor axis is functional in AML and can be activated by the biguanide molecule metformin, resulting in a specific inhibition of mammalian target of rapamycin (mTOR) catalytic activity. Biguanides 123-132 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 43-47 20668229-2 2010 We show in our current study that the LKB1/AMPK/TSC tumor suppressor axis is functional in AML and can be activated by the biguanide molecule metformin, resulting in a specific inhibition of mammalian target of rapamycin (mTOR) catalytic activity. Metformin 142-151 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 43-47 34854518-1 2022 Akt is usually considered to be a negative regulator of both autophagy and adenosine 5"-monophosphate (AMP)-activated protein kinase (AMPK) signaling. Adenosine 75-84 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 134-138 34854518-1 2022 Akt is usually considered to be a negative regulator of both autophagy and adenosine 5"-monophosphate (AMP)-activated protein kinase (AMPK) signaling. Adenosine Monophosphate 103-106 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 134-138 34854518-2 2022 In the present study, we found that SC66, a pyridine-based allosteric Akt inhibitor, suppressed basal and H2 O2 -induced autophagy concurrent with decreased phosphorylation and activity of AMPK. pyridine 44-52 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 189-193 34592338-15 2022 AFE also efficiently regressed CT26-derived solid tumor in Balb/c mice acting alone or in synergy with 5FU through inducing autophagy as a major mechanism of action as indicated by upregulation of Beclin 1 and phospho-AMPK, and inhibition of phosphor-S6K1 levels in the tumor tissue lysates. Fluorouracil 103-106 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 218-222 34902361-0 2022 Hesperetin derivative-16 attenuates CCl4-induced inflammation and liver fibrosis by activating AMPK/SIRT3 pathway. hesperetin 0-10 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 95-99 34902361-0 2022 Hesperetin derivative-16 attenuates CCl4-induced inflammation and liver fibrosis by activating AMPK/SIRT3 pathway. Carbon Tetrachloride 36-40 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 95-99 34902361-12 2022 Overall, HD-16 attenuated CCl4-induced liver inflammation and fibrosis by activating the AMPK/SIRT3 pathway, and HD-16 may be a potential anti-fibrotic compound in the treatment of liver fibrosis. Carbon Tetrachloride 26-30 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 89-93 34725898-4 2022 Furthermore, treatment of mature 3T3-L1 adipocytes with 20 muM nepetin stimulates glucose uptake through AMPK activation. eupafolin 63-70 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 105-109 33237143-10 2020 Vinpocetine treatment increased AMPK phosphorylation in LPS-stimulated BV2 microglia. vinpocetine 0-11 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 32-36 33237143-11 2020 AMPK inhibition by siRNA blocked the anti-inflammatory effects of vinpocetine induced by LPS in BV2 microglia. vinpocetine 66-77 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 33237143-12 2020 The overall results demonstrate that vinpocetine has anti-inflammatory effects on LPS-stimulated BV2 microglia via inducing phosphorylation of AMPK, suggesting that vinpocetine is a potential therapeutic agent in neuroinflammatory injury. vinpocetine 37-48 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 143-147 33237143-12 2020 The overall results demonstrate that vinpocetine has anti-inflammatory effects on LPS-stimulated BV2 microglia via inducing phosphorylation of AMPK, suggesting that vinpocetine is a potential therapeutic agent in neuroinflammatory injury. vinpocetine 165-176 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 143-147 34747550-5 2022 Numerous NCs exerted their therapeutic effects on DOX-mediated cardiac damage via targeting different signaling pathways, including SIRT1/LKB1/AMPK, SIRT1/PGC-1alpha, SIRT1/NLRP3, and SIRT3/FoxO. Doxorubicin 50-53 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 143-147 34637881-5 2022 We then addressed metformin"s effects on the AMPK-AKT-mTOR-HIFA pathway on two human primary cultures: one from a VHL-mutant PCC and other from a sporadic PCC. Metformin 18-27 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 45-49 34922208-13 2022 CONCLUSION: saRNA-mediated NIS expression acted as a critical role in increasing iodide uptake via AMPK/mTOR pathway in thyroid cancer. Iodides 81-87 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 99-103 34482636-4 2022 Neratinib activated ATM, AMPK, ULK1, and PERK and inactivated mTORC1/2, ERK1/2, eIF2 alpha, and STAT3. neratinib 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 25-29 34964241-8 2022 At the same time, we examined the mitochondrial morphology in tumour cells and found that the size of mitochondria in tumour cells increased under the treatment of TMZ, which originated from the regulation of AMPK on the subcellular localization of Drp1 under the condition of unbalanced energy supply and demand in tumour cells. Temozolomide 164-167 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 209-213 34953496-0 2021 Cordycepin augments the chemosensitivity of osteosarcoma to cisplatin by activating AMPK and suppressing the AKT signaling pathway. Cisplatin 60-69 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 84-88 34953496-13 2021 Mechanistically, we demonstrated that cordycepin enhanced the sensitivity of osteosarcoma cells to cisplatin by activating AMPK and inhibiting the AKT/mTOR signaling pathway. Cisplatin 99-108 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 123-127 34953496-14 2021 CONCLUSIONS: In brief, this study provides comprehensive evidence that cordycepin inhibits osteosarcoma cell growth and invasion and induces osteosarcoma cell apoptosis by activating AMPK and inhibiting the AKT/mTOR signaling pathway and enhances the sensitivity of osteosarcoma cells to cisplatin, suggesting that cordycepin is a promising treatment for osteosarcoma. cordycepin 71-81 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 183-187 34293101-9 2021 Canagliflozin reduced NADPH oxidase activity via AMP kinase (AMPK)/Rac1signalling and improved NOS coupling via increased tetrahydrobiopterin bioavailability ex vivo and in vitro. Canagliflozin 0-13 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 49-59 34293101-9 2021 Canagliflozin reduced NADPH oxidase activity via AMP kinase (AMPK)/Rac1signalling and improved NOS coupling via increased tetrahydrobiopterin bioavailability ex vivo and in vitro. Canagliflozin 0-13 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 61-65 34293101-12 2021 CONCLUSIONS: We demonstrate for the first time that canagliflozin suppresses myocardial NADPH oxidase activity and improves NOS coupling via SGLT1/AMPK/Rac1 signalling, leading to global anti-inflammatory and anti-apoptotic effects in the human myocardium. Canagliflozin 52-65 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 147-151 34992508-0 2021 miR-590-3 and SP1 Promote Neuronal Apoptosis in Patients with Alzheimer"s Disease via AMPK Signaling Pathway. mir-590-3 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 86-90 34788781-0 2021 Phloretin attenuation of hepatic steatosis via an improvement of mitochondrial dysfunction by activating AMPK-dependent signaling pathways in C57BL/6J mice and HepG2 cells. Phloretin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 105-109 34788781-6 2021 This biological activity of phloretin was closely related to its capacity to improve mitochondrial dysfunction, including the promotion of mitochondrial biosynthesis and inhibition of mitochondrial swelling through the AMPK-dependent SIRT1/PGC-1alpha and SIRT3/CypD signaling pathways, respectively. Phloretin 28-37 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 219-223 34788781-7 2021 These results demonstrate that phloretin effectively improves mitochondrial function and ameliorates HFD-induced hepatic steatosis through an AMPK-dependent signaling pathway. Phloretin 31-40 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 142-146 34931132-0 2021 Corrigendum to "Melatonin Attenuates Diabetic Myocardial Microvascular Injury through Activating the AMPK/SIRT1 Signaling Pathway". Melatonin 16-25 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 101-105 34887495-5 2021 Downstream of ADIPOR1 sustained activation of AMPK renders it insensitive to changes in AMP/ATP ratio resulting in defective lipid metabolism, reduced Neuroprotectin D1(NPD1) secretion, lower mitochondrial respiration, and reduced ATP production. Adenosine Triphosphate 231-234 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 46-50 34887495-7 2021 Gene augmentation of L-ORD-iRPE with WT CTRP5 or modulation of AMPK, by metformin, re-sensitize L-ORD-iRPE to changes in cellular energy status alleviating the disease cellular phenotypes. Metformin 72-81 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 63-67 34944670-8 2021 Incubation with the adenosine monophosphate-activated protein kinase (AMPK) inhibitor dorsomorphin significantly attenuated dilator responses (p < 0.001), whereas the SIRT-1 inhibitor EX-527 had no effect. dorsomorphin 86-98 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 20-75 34438030-0 2021 Hypoglycemic effect of astragaloside IV via modulating gut microbiota and regulating AMPK/SIRT1 and PI3K/AKT pathway. astragaloside 23-36 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 85-89 34438030-9 2021 The active role of AS-IV as an anti-diabetic compound by regulating the AMPK/SIRT1 and PI3K/AKT signaling pathways was revealed using a T2DM model and verified through the intervention of inhibitors using insulin-resistance HepG2 cells. astragaloside A 19-24 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 72-76 34926404-8 2021 Finally, meroterpenoids 7, 9, 11, and 15 significantly up-regulate p-AMPK protein expression in normal L6 myotubes cells. meroterpenoids 9-23 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 69-73 33237143-0 2020 Anti-inflammatory effects of vinpocetine in LPS-stimulated microglia via activation of AMPK. vinpocetine 29-40 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 87-91 33237143-9 2020 Furthermore, it was observed that phosphorylation levels of AMPK (Thr-172) decreased in LPS-stimulated BV2 microglia. Threonine 66-69 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 60-64 34548620-6 2022 Mechanistically, cannabinoids imprint tolerogenicity in human DCs by inhibiting NF-kappaB, MAPK and mTOR signalling pathways while inducing AMPK and functional autophagy flux via CB1- and PPARalpha-mediated activation, which drives metabolic rewiring towards increased mitochondrial activity and oxidative phosphorylation. Cannabinoids 17-29 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 140-144 34308769-0 2021 Sulforaphane protects intestinal epithelial cells against lipopolysaccharide-induced injury by activating the AMPK/SIRT1/PGC-1alpha pathway. sulforaphane 0-12 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 110-114 34308769-9 2021 Sulforaphane also upregulated p-AMPK, SIRT1, and PGC-1alpha, whose inhibitors antagonized the compound"s protective effects. sulforaphane 0-12 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 32-36 34656065-0 2021 MK8722, an AMPK activator, inhibiting carcinoma proliferation, invasion and migration in human pancreatic cancer cells. MK-8722 0-6 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 11-15 34656065-1 2021 BACKGROUND: MK8722 is a potent and systemic pan-AMPK activator. MK-8722 12-18 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 48-52 34611764-4 2021 Maternal embryonal leucine zipper kinase (MELK) is a member of the Snf1/AMPK family of serine/threonine-protein kinases involved in various processes such as cell cycle regulation, self-renewal of stem cells, apoptosis, and splicing regulation. Serine 87-93 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 72-76 34520103-0 2021 Fenofibrate inhibits hypoxia-inducible factor-1 alpha and carbonic anhydrase expression through activation of AMP-activated protein kinase/HO-1/Sirt1 pathway in glioblastoma cells. Fenofibrate 0-11 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 110-138 34520103-7 2021 Moreover, fenofibrate-inhibited HIF-1alpha expression is mediated by HO-1 activation in GBM cells through the AMP-activated protein kinase (AMPK) pathway. Fenofibrate 10-21 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 110-138 34520103-7 2021 Moreover, fenofibrate-inhibited HIF-1alpha expression is mediated by HO-1 activation in GBM cells through the AMP-activated protein kinase (AMPK) pathway. Fenofibrate 10-21 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 140-144 34343359-7 2021 LC-MS assay and Seahorse analysis revealed that UC dysregulation(UCD) led to the deceleration of the tricarboxylic acid(TCA) cycle, while excess ammonia caused by CPS1 deficiency activated fatty acid beta-oxidation(FAO) through p-AMPK. Ammonia 145-152 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 230-234 34343359-7 2021 LC-MS assay and Seahorse analysis revealed that UC dysregulation(UCD) led to the deceleration of the tricarboxylic acid(TCA) cycle, while excess ammonia caused by CPS1 deficiency activated fatty acid beta-oxidation(FAO) through p-AMPK. Fatty Acids 189-199 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 230-234 34342160-0 2021 Pterostilbene suppresses oxidative stress and allergic airway inflammation through AMPK/Sirt1 and Nrf2/HO-1 pathways. pterostilbene 0-13 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 83-87 34342160-4 2021 Herein, we aim to explore the pharmacological effects of Pts on oxidative stress and allergic inflammatory response as well as the mechanism involving AMPK/Sirt1 and Nrf2/HO-1 pathways. pterostilbene 57-60 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 151-155 34342160-20 2021 Moreover, we found that Pts promoted the phosphorylation of AMPK in 16HBE, and meanwhile inhibited the increase of ROS induced by LPS. pterostilbene 24-27 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 60-64 34730235-0 2021 Policosanol alleviates hepatic lipid accumulation by regulating bile acids metabolism in C57BL6/mice through AMPK-FXR-TGR5 cross-talk. policosanol 0-11 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 109-113 34730235-0 2021 Policosanol alleviates hepatic lipid accumulation by regulating bile acids metabolism in C57BL6/mice through AMPK-FXR-TGR5 cross-talk. Bile Acids and Salts 64-74 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 109-113 34730235-10 2021 The aforementioned results reveal that the potential mechanism of policosanol in alleviating liver lipid accumulation is to promote BA synthesis and lipolysis through regulating the cross-talk of the AMPK-FXR-TGR5. policosanol 66-77 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 200-204 34730235-10 2021 The aforementioned results reveal that the potential mechanism of policosanol in alleviating liver lipid accumulation is to promote BA synthesis and lipolysis through regulating the cross-talk of the AMPK-FXR-TGR5. Bile Acids and Salts 132-134 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 200-204 34730235-14 2021 This study showed that oral administration of policosanol can significantly reduce triglyceride and cholesterol levels in the liver through affecting AMPK-TGR5-FXR cross-talk, whereas no significant toxicological effect is reported in human and mouse models. policosanol 46-57 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 150-154 34730235-14 2021 This study showed that oral administration of policosanol can significantly reduce triglyceride and cholesterol levels in the liver through affecting AMPK-TGR5-FXR cross-talk, whereas no significant toxicological effect is reported in human and mouse models. Cholesterol 100-111 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 150-154 34666245-0 2021 Trelagliptin ameliorates IL-1beta-impaired chondrocyte function via the AMPK/SOX-9 pathway. trelagliptin 0-12 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 72-76 34666245-10 2021 Mechanistically, we demonstrate that AMPK is required for the amelioration of Trelagliptin on SOX-9- reduction by IL-1beta. trelagliptin 78-90 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 37-41 34725898-4 2022 Furthermore, treatment of mature 3T3-L1 adipocytes with 20 muM nepetin stimulates glucose uptake through AMPK activation. Glucose 82-89 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 105-109 34388483-0 2021 Targeting ROS-AMPK pathway by multiaction Platinum(IV) prodrugs containing hypolipidemic drug bezafibrate. ros 10-13 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-18 34739715-0 2021 Resveratrol Inhibits NLRP3 Inflammasome-Induced Pyroptosis and miR-155 Expression in Microglia Through Sirt1/AMPK Pathway. Resveratrol 0-11 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 109-113 34536608-0 2021 5-Aminolaevulinic acid photodynamic therapy suppresses lipid secretion of primary sebocytes through AMPK/SREBP-1 pathway. Aminolevulinic Acid 0-22 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 100-104 34536608-9 2021 Regulation of ALA-PDT on AMPK/SREBP-1 was evaluated by western blot. Alanine 14-17 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 25-29 34536608-12 2021 We also found that ALA-PDT activated AMPK pathway, down-regulating the expression of SREBP-1 in sebocytes after ALA-PDT. Alanine 19-22 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 37-41 34536608-12 2021 We also found that ALA-PDT activated AMPK pathway, down-regulating the expression of SREBP-1 in sebocytes after ALA-PDT. Alanine 112-115 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 37-41 34536608-13 2021 CONCLUSIONS: These findings elucidate that ALA-PDT suppresses lipid secretion through AMPK/SREBP-1 pathway in treatment of acne vulgaris. Alanine 43-46 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 86-90 34852220-3 2021 CHK1 inhibition also activates ERK and AMPK and increases autophagy, providing a mechanistic basis for increased efficacy of concurrent CHK1 and ERK inhibition and/or autophagy inhibition with chloroquine. Chloroquine 193-204 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 39-43 34837101-0 2021 Metformin inhibits human non-small cell lung cancer by regulating AMPK-CEBPB-PDL1 signaling pathway. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 66-70 34837101-10 2021 Western blotting showed that metformin could regulate the function of NSCLC cells via AMPK-CEBPB-PDL1 signaling. Metformin 29-38 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 86-90 34837101-14 2021 In conclusion, metformin inhibited the proliferation of NSCLC cells and played an anti-tumor role in an AMPK-CEBPB-PDL1 signaling-dependent manner. Metformin 15-24 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 104-108 34817678-8 2022 It details how betaine reinstates alcohol-induced alterations in the expressions and/or activities of protein phosphtase-2A, FOXO1, PPAR-alpha, AMPK, SREBP-1c, fatty acid synthase, diacylglycerol transferase-2, adiponectin and nitric oxide. Betaine 15-22 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 144-148 34817678-8 2022 It details how betaine reinstates alcohol-induced alterations in the expressions and/or activities of protein phosphtase-2A, FOXO1, PPAR-alpha, AMPK, SREBP-1c, fatty acid synthase, diacylglycerol transferase-2, adiponectin and nitric oxide. Alcohols 34-41 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 144-148 34739715-7 2021 Additionally, resveratrol inhibits nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kappaB) signaling and activates AMPK/Sirt1 pathways. Resveratrol 14-25 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 134-138 34739715-9 2021 Then, inhibition of AMPK and Sirt1 pathways has significantly reversed protective effect of resveratrol on miR-155 expression. Resveratrol 92-103 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 20-24 34739715-10 2021 To sum up, our results suggest that resveratrol suppresses the NLRP3 inflammasome and miR-155 expression through AMPK and Sirt1 pathways in microglia. Resveratrol 36-47 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 113-117 34787456-0 2022 The Antimalaria Drug Artesunate Inhibits Porcine Reproductive and Respiratory Syndrome Virus Replication via Activating AMPK and Nrf2/HO-1 Signaling Pathways. Artesunate 21-31 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 120-124 34787456-9 2022 Adenosine phosphate analysis showed that AS activates AMPK via improving AMP/ADP:ATP ratio rather than direct interaction with AMPK. Adenosine 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 54-58 34787456-9 2022 Adenosine phosphate analysis showed that AS activates AMPK via improving AMP/ADP:ATP ratio rather than direct interaction with AMPK. Adenosine Monophosphate 73-76 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 54-58 34787456-9 2022 Adenosine phosphate analysis showed that AS activates AMPK via improving AMP/ADP:ATP ratio rather than direct interaction with AMPK. Adenosine Diphosphate 77-80 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 54-58 34787456-9 2022 Adenosine phosphate analysis showed that AS activates AMPK via improving AMP/ADP:ATP ratio rather than direct interaction with AMPK. Adenosine Triphosphate 81-84 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 54-58 34798200-5 2022 PGC-1alpha activity is regulated by 5"-AMP-activated protein kinase (AMPK), however, only limited experimental data exists on the effect of AMPK activation in the regulation of BCAA catabolism. Amino Acids, Branched-Chain 177-181 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 140-144 34798200-6 2022 The present report examined the effects of the commonly used AMPK activator 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR) on the metabolism and expression of several related targets (including BCAA catabolic enzymes) of cultured myotubes. AICA ribonucleotide 76-121 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 61-65 34798200-12 2022 Together, these experiments demonstrate AICAR/AMPK activation can upregulate BCAA catabolic machinery in a model of skeletal muscle. Amino Acids, Branched-Chain 77-81 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 46-50 34388483-0 2021 Targeting ROS-AMPK pathway by multiaction Platinum(IV) prodrugs containing hypolipidemic drug bezafibrate. Platinum 42-50 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-18 34388483-0 2021 Targeting ROS-AMPK pathway by multiaction Platinum(IV) prodrugs containing hypolipidemic drug bezafibrate. Bezafibrate 94-105 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-18 34388483-6 2021 Mechanism studies revealed that the bezafibrate-conjugated Pt(IV) complex CB, as a representative, could massively accumulate in A549 cells and genomic DNA, induce DNA damage, elevate intracellular ROS levels, perturb mitochondrial transmembrane potentials, activate the cellular metabolic sensor AMPK, and result in profound proliferation inhibition and apoptosis. Platinum 59-61 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 297-301 34829834-0 2021 Regulation of Butyrate-Induced Resistance through AMPK Signaling Pathway in Human Colon Cancer Cells. Butyrates 14-22 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 50-54 34869595-7 2021 Subsequently, the upstream signal of autophagy was analyzed and it was found that Ad-VT reduced the resistance of cells to doxorubicin by reducing the level of mTOR, and then the analysis of the upstream and downstream proteins of mTOR found that Ad-VT increased the sensitivity of MCF-7/ADR cells to adriamycin by activating AMPK-mTOR-eIF4F signaling axis. Doxorubicin 301-311 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 326-330 34829834-7 2021 Activation of AMPK by AICAR treatment in BR colon cancer cells suppressed cell proliferation by inhibiting Akt and mTOR and activating ACC. AICA ribonucleotide 22-27 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-18 34927008-7 2021 Metformin activates the LKB1/AMPK pathway to interact with several intracellular signaling pathways and molecular mechanisms. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 29-33 34718329-6 2021 However, these effects were abolished by pretreatment with ULK1 inhibitor SBI-0206965, autophagy inhibitor chloroquine and enhanced by AMPK activator AICAR. AICA ribonucleotide 150-155 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 135-139 34711685-3 2021 This study aimed to assess whether the up-regulation of SIRT1 induced by 17beta-estradiol (17beta-E2) could promote autophagy and inhibit apoptosis in osteoblasts via the AMPK-mTOR and FOXO3a pathways, respectively. Estradiol 73-89 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 171-175 34711685-3 2021 This study aimed to assess whether the up-regulation of SIRT1 induced by 17beta-estradiol (17beta-E2) could promote autophagy and inhibit apoptosis in osteoblasts via the AMPK-mTOR and FOXO3a pathways, respectively. 17beta-e2 91-100 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 171-175 34711685-5 2021 Up-regulation of SIRT1 induced by 17beta-E2 increased the expression level of LC3, Beclin-1, Bcl-2, p-AMPK, FOXO3a but decreased caspase-3 and p-mTOR expression, and then promoted autophagy and inhibited apoptosis. 17beta-e2 34-43 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 102-106 34711685-8 2021 Taken together, our findings demonstrated that the up-regulation of SIRT1 induced by 17beta-E2 could promote autophagy via the AMPK-mTOR pathway and inhibit apoptosis via the FOXO3a activation in osteoblasts, and SIRT1 might become a more significant target in osteoporosis treatment. 17beta-e2 85-94 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 127-131 34870106-9 2021 Pathway enrichment analysis identified potential targets of miR-328-3p implicated in the AMPK signaling pathway linked to amyloid-beta and tau metabolism in AD. mir-328-3p 60-70 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 89-93 34705188-6 2022 Furthermore, failure in energy production as the key factor in various psychiatric disorders was reversed by apigenin modulating effect on AMPK gene expression. Apigenin 109-117 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 139-143 34705188-9 2022 The surprising results were achieved by raise in COQ10 level, which could regulate the overexpression of the AMPK gene in stressful conditions. coenzyme Q10 49-54 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 109-113 34671066-6 2021 In human ADPKD cells, inducing mitochondrial ROS increased ERK1/2 phosphorylation and decreased AMPK phosphorylation, whereas the converse was observed with increased scavenging of ROS in the mitochondria. ros 45-48 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 96-100 34662721-10 2021 CAPE increased phosphorylation of ERK, JNK, p38, and AMPKalpha1/2 to modulate the GDF15 expressions. caffeic acid phenethyl ester 0-4 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 53-65 34727932-11 2021 Exogenous C14 supplementation to cardiomyocytes led to increased lipid deposition in cardiomyocytes along with the obstacles in adenosine 5"-monophosphate (AMP)-activated protein kinase (AMPK) signaling pathways and affecting fatty acid oxidation. Adenosine 128-137 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 187-191 34727932-11 2021 Exogenous C14 supplementation to cardiomyocytes led to increased lipid deposition in cardiomyocytes along with the obstacles in adenosine 5"-monophosphate (AMP)-activated protein kinase (AMPK) signaling pathways and affecting fatty acid oxidation. Adenosine Monophosphate 156-159 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 187-191 34727932-13 2021 However, this effect was mitigated by the AMPK agonist acadesine. acadesine 55-64 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 42-46 34727932-15 2021 C14 supplementation associated lipid accumulation by inhibiting the AMPK/ACC/CPT1 signaling pathway, aggravated myocardial lipotoxicity, increased apoptosis apart from cardiomyocyte hypertrophy and fibrosis were alleviated by the acadesine. acadesine 230-239 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 68-72 34382905-0 2021 AMPK-activated ULK1 phosphorylates PIKFYVE to drive formation of PtdIns5P-containing autophagosomes during glucose starvation. phosphatidylinositol 5-phosphate 65-73 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 34382905-0 2021 AMPK-activated ULK1 phosphorylates PIKFYVE to drive formation of PtdIns5P-containing autophagosomes during glucose starvation. Glucose 107-114 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 34382905-2 2021 Recently, we described a non-canonical signaling pathway involving the kinases AMPK, ULK1 and PIKFYVE that are induced during glucose starvation, leading to the formation of PtdIns5P-containing autophagosomes, resulting in increased autophagy flux and clearance of autophagy substrates. Glucose 126-133 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 79-83 34382905-2 2021 Recently, we described a non-canonical signaling pathway involving the kinases AMPK, ULK1 and PIKFYVE that are induced during glucose starvation, leading to the formation of PtdIns5P-containing autophagosomes, resulting in increased autophagy flux and clearance of autophagy substrates. phosphatidylinositol 5-phosphate 174-182 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 79-83 34603517-0 2021 Mangiferin inhibits hypoxia/reoxygenation-induced alveolar epithelial cell injury via the SIRT1/AMPK signaling pathway. mangiferin 0-10 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 96-100 34603517-10 2021 In addition, compared with those in the group treated with sirtinol, expression of SIRT1, Bcl-2 and AMPK activity were elevated in MAF-treated H/R-A549 cells, whereas the expression of Bax, cleaved caspase-3 and cleaved caspase-9 was suppressed. sirtinol 59-67 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 100-104 34603517-11 2021 TUNEL analysis of H/R-A549 cells treated with MAF in combination with sirtinol revealed that treatment with sirtinol blocked the SIRT1/AMPK signaling pathway and increased the apoptosis rate compared with the MAF group. mangiferin 46-49 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 135-139 34603517-11 2021 TUNEL analysis of H/R-A549 cells treated with MAF in combination with sirtinol revealed that treatment with sirtinol blocked the SIRT1/AMPK signaling pathway and increased the apoptosis rate compared with the MAF group. sirtinol 70-78 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 135-139 34603517-11 2021 TUNEL analysis of H/R-A549 cells treated with MAF in combination with sirtinol revealed that treatment with sirtinol blocked the SIRT1/AMPK signaling pathway and increased the apoptosis rate compared with the MAF group. sirtinol 108-116 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 135-139 34435315-8 2021 Lastly, the AMPK pathway was observed to be significantly activated in OGD/R-challenged HAVECs by Trelagliptin treatment. havecs 88-94 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 12-16 34435315-8 2021 Lastly, the AMPK pathway was observed to be significantly activated in OGD/R-challenged HAVECs by Trelagliptin treatment. trelagliptin 98-110 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 12-16 34435315-9 2021 After co-administration of the inhibitor of the AMPK pathway, the effects of Trelagliptin on mitochondrial function and metabolic alterations were significantly abolished. trelagliptin 77-89 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 48-52 34435315-10 2021 Taken together, our data indicate that Trelagliptin ameliorated OGD/R-induced mitochondrial disturbance and metabolic changes by activating the AMPK pathway. trelagliptin 39-51 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 144-148 34697150-0 2021 (6)-Gingerol Suppresses Oral Cancer Cell Growth by Inducing the Activation of AMPK and Suppressing the AKT/mTOR Signaling Pathway. gingerol 0-12 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 78-82 34697150-8 2021 Moreover, (6)-gingerol induced the activation of AMPK and suppressed the AKT/mTOR signaling pathway in YD10B and Ca9-22 cells. gingerol 10-22 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 49-53 34697150-9 2021 CONCLUSION: (6)-Gingerol exerts anticancer activity by activating AMPK and suppressing the AKT/mTOR signaling pathway in oral cancer cells. gingerol 12-24 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 66-70 34425254-0 2021 Salsalate reduces atherosclerosis through AMPKbeta1 in mice. salicylsalicylic acid 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 42-51 34425254-2 2021 AMP-activated protein kinase (AMPK) is an alphabetagamma heterotrimer which inhibits macrophage inflammation and the synthesis of fatty acids and cholesterol in the liver through phosphorylation of acetyl-CoA carboxylase (ACC) and HMG-CoA reductase (HMGCR), respectively. Fatty Acids 130-141 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-34 34425254-2 2021 AMP-activated protein kinase (AMPK) is an alphabetagamma heterotrimer which inhibits macrophage inflammation and the synthesis of fatty acids and cholesterol in the liver through phosphorylation of acetyl-CoA carboxylase (ACC) and HMG-CoA reductase (HMGCR), respectively. Cholesterol 146-157 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-34 34425254-3 2021 Salicylate binds to and activates AMPKbeta1 containing heterotrimers, that are highly expressed in both macrophages and liver, but whether salsalate reduces atherosclerosis and the potential importance of AMPK has not been evaluated. Salicylates 0-10 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 34-43 34425254-10 2021 CONCLUSIONS: These data indicate that salsalate suppresses macrophage proliferation and atherosclerosis through an AMPKbeta1-dependent pathways and this may involve the phosphorylation of HMGCR and cholesterol synthesis. salicylsalicylic acid 38-47 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 115-124 34500303-0 2021 Trigonelline induces autophagy to protect mesangial cells in response to high glucose via activating the miR-5189-5p-AMPK pathway. trigonelline 0-12 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 117-121 34829834-8 2021 Taken together, chronic exposure to butyrate increased butyrate resistance in human colon cancer by inducing protective autophagy through the downregulation of AMPK/ACC and activation of Akt/mTOR signaling. Butyrates 36-44 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 160-164 34829834-8 2021 Taken together, chronic exposure to butyrate increased butyrate resistance in human colon cancer by inducing protective autophagy through the downregulation of AMPK/ACC and activation of Akt/mTOR signaling. Butyrates 55-63 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 160-164 34829834-9 2021 Activation of AMPK restored sensitivity to butyrate by the inhibition of Akt/mTOR, suggesting that AMPK could be a therapeutic target for BR colon cancers. Butyrates 43-51 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-18 34829834-9 2021 Activation of AMPK restored sensitivity to butyrate by the inhibition of Akt/mTOR, suggesting that AMPK could be a therapeutic target for BR colon cancers. Butyrates 43-51 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 99-103 34704011-0 2021 Biofunctional magnesium-coated Ti6Al4V scaffolds promote autophagy-dependent apoptosis in osteosarcoma by activating the AMPK/mTOR/ULK1 signaling pathway. Magnesium 14-23 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 121-125 34685438-6 2021 Moreover, our results also demonstrated the antagonized role of 6-shogaol in attenuating the ACM effects on CRC cells through activating AMPK signaling. shogaol 64-73 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 137-141 34685438-7 2021 Overall, the present study elucidated the role of adipocyte-containing microenvironment in 5-FU resistance development of CRC through controlling the SREBP-1 level and further enhanced the concept of clinical application of 6-shogaol and AMPK signaling in CRC therapy. Fluorouracil 91-95 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 238-242 34626114-8 2022 Expression of AMPK and SIRT1 was reduced in gut of 6-month-old fish with poly I:C-treatment, and feeding metformin reversed these declines. Poly I 73-79 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-18 34626114-8 2022 Expression of AMPK and SIRT1 was reduced in gut of 6-month-old fish with poly I:C-treatment, and feeding metformin reversed these declines. Carbon 80-81 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-18 34626114-8 2022 Expression of AMPK and SIRT1 was reduced in gut of 6-month-old fish with poly I:C-treatment, and feeding metformin reversed these declines. Metformin 105-114 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-18 34626114-9 2022 Taken together, the present study suggested that poly I:C-injection led to aging-like phenomena in gut and metformin activated AMPK and SIRT1 to reduce NF-kappaB mediated inflammation and resist oxidative stress via enhanced expression of FoxO3a and PGC-1alpha, and finally delayed gut aging in vertebrates. Poly I 49-55 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 127-131 34626114-9 2022 Taken together, the present study suggested that poly I:C-injection led to aging-like phenomena in gut and metformin activated AMPK and SIRT1 to reduce NF-kappaB mediated inflammation and resist oxidative stress via enhanced expression of FoxO3a and PGC-1alpha, and finally delayed gut aging in vertebrates. Metformin 107-116 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 127-131 34310912-9 2021 Additionally, adenosine 5"-monophosphate (AMP)-activated protein kinase/unc-51-like kinase 1 (AMPK-ULK1) signaling pathway was activated by estrogen treatment, which was abrogated by Esrra-silencing, and AMPK-specific inhibitor Compound C pretreatment could reduce estrogen-induced downregulation of ASIC1a protein. Adenosine 14-23 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 94-103 34479029-2 2021 The anti-diabetic agent metformin (MET) and the aspirin metabolite salicylate (SAL) are shown to activate AMP-activated protein kinase (AMPK), suppress de novo lipogenesis (DNL), the mammalian target of rapamycin (mTOR) pathway and reduce PrCa proliferation in-vitro. Metformin 24-33 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 106-134 34479029-2 2021 The anti-diabetic agent metformin (MET) and the aspirin metabolite salicylate (SAL) are shown to activate AMP-activated protein kinase (AMPK), suppress de novo lipogenesis (DNL), the mammalian target of rapamycin (mTOR) pathway and reduce PrCa proliferation in-vitro. Metformin 24-33 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 136-140 34479029-2 2021 The anti-diabetic agent metformin (MET) and the aspirin metabolite salicylate (SAL) are shown to activate AMP-activated protein kinase (AMPK), suppress de novo lipogenesis (DNL), the mammalian target of rapamycin (mTOR) pathway and reduce PrCa proliferation in-vitro. Aspirin 48-55 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 106-134 34479029-2 2021 The anti-diabetic agent metformin (MET) and the aspirin metabolite salicylate (SAL) are shown to activate AMP-activated protein kinase (AMPK), suppress de novo lipogenesis (DNL), the mammalian target of rapamycin (mTOR) pathway and reduce PrCa proliferation in-vitro. Aspirin 48-55 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 136-140 34479029-2 2021 The anti-diabetic agent metformin (MET) and the aspirin metabolite salicylate (SAL) are shown to activate AMP-activated protein kinase (AMPK), suppress de novo lipogenesis (DNL), the mammalian target of rapamycin (mTOR) pathway and reduce PrCa proliferation in-vitro. Salicylates 67-77 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 106-134 34479029-2 2021 The anti-diabetic agent metformin (MET) and the aspirin metabolite salicylate (SAL) are shown to activate AMP-activated protein kinase (AMPK), suppress de novo lipogenesis (DNL), the mammalian target of rapamycin (mTOR) pathway and reduce PrCa proliferation in-vitro. Salicylates 67-77 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 136-140 34479029-2 2021 The anti-diabetic agent metformin (MET) and the aspirin metabolite salicylate (SAL) are shown to activate AMP-activated protein kinase (AMPK), suppress de novo lipogenesis (DNL), the mammalian target of rapamycin (mTOR) pathway and reduce PrCa proliferation in-vitro. Salicylates 79-82 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 106-134 34479029-2 2021 The anti-diabetic agent metformin (MET) and the aspirin metabolite salicylate (SAL) are shown to activate AMP-activated protein kinase (AMPK), suppress de novo lipogenesis (DNL), the mammalian target of rapamycin (mTOR) pathway and reduce PrCa proliferation in-vitro. Salicylates 79-82 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 136-140 34600475-1 2021 BACKGROUND: Activation of Adenosine 5"-monophosphate-activated protein kinase/Sirtuin1 (AMPK/SIRT1) exerts an effect in alleviating obesity and gut damage. Adenosine 26-35 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 88-92 34600475-2 2021 Sodium nitroprusside (SNP), a nitric oxide (NO) donor, has been reported to activate AMPK. Nitroprusside 0-20 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 85-89 34600475-2 2021 Sodium nitroprusside (SNP), a nitric oxide (NO) donor, has been reported to activate AMPK. Nitric Oxide 30-42 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 85-89 34369843-0 2021 An AMPK-ULK1-PIKFYVE signaling axis for PtdIns5P-dependent autophagy regulation upon glucose starvation. phosphatidylinositol 5-phosphate 40-48 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 3-7 34369843-0 2021 An AMPK-ULK1-PIKFYVE signaling axis for PtdIns5P-dependent autophagy regulation upon glucose starvation. Glucose 85-92 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 3-7 34369843-3 2021 A recent study from Dr. David C. Rubinsztein"s lab showed that ULK1 is activated by AMPK upon glucose starvation, resulting in the phosphorylation of the lipid kinase PIKFYVE on S1548. Glucose 94-101 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 84-88 34284074-7 2021 Moreover, our mechanism researches revealed that the DRD1 signaling induced by A-68930 significantly rescued STZ-induced mitochondrial biogenesis deficit, mitochondrial dysfunction, Abeta overexpression, and tau phosphorylation in mice hippocampus and cortex and SH-SY5Y cells, which may be mediated through stimulating AMPK/PGC-1alpha pathway. A 68930 79-86 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 320-324 34284074-7 2021 Moreover, our mechanism researches revealed that the DRD1 signaling induced by A-68930 significantly rescued STZ-induced mitochondrial biogenesis deficit, mitochondrial dysfunction, Abeta overexpression, and tau phosphorylation in mice hippocampus and cortex and SH-SY5Y cells, which may be mediated through stimulating AMPK/PGC-1alpha pathway. Streptozocin 109-112 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 320-324 34148304-10 2021 Importantly, blockage of AMPK signaling reversed ginkgetin-restored autophagy and its protective efficacy against HG-induced dysfunction in mesangial cells. ginkgetin 49-58 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 25-29 34310912-9 2021 Additionally, adenosine 5"-monophosphate (AMP)-activated protein kinase/unc-51-like kinase 1 (AMPK-ULK1) signaling pathway was activated by estrogen treatment, which was abrogated by Esrra-silencing, and AMPK-specific inhibitor Compound C pretreatment could reduce estrogen-induced downregulation of ASIC1a protein. Adenosine 14-23 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 204-208 34310912-9 2021 Additionally, adenosine 5"-monophosphate (AMP)-activated protein kinase/unc-51-like kinase 1 (AMPK-ULK1) signaling pathway was activated by estrogen treatment, which was abrogated by Esrra-silencing, and AMPK-specific inhibitor Compound C pretreatment could reduce estrogen-induced downregulation of ASIC1a protein. Adenosine Monophosphate 42-45 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 94-103 34310912-9 2021 Additionally, adenosine 5"-monophosphate (AMP)-activated protein kinase/unc-51-like kinase 1 (AMPK-ULK1) signaling pathway was activated by estrogen treatment, which was abrogated by Esrra-silencing, and AMPK-specific inhibitor Compound C pretreatment could reduce estrogen-induced downregulation of ASIC1a protein. Adenosine Monophosphate 42-45 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 204-208 34353734-0 2021 Corrigendum to "Anti-arthritis effect of berberine associated with regulating energy metabolism of macrophages through AMPK/HIF-1alpha pathway". Berberine 41-50 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 119-123 34547240-0 2021 Inositol serves as a natural inhibitor of mitochondrial fission by directly targeting AMPK. Inositol 0-8 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 86-90 34308732-0 2021 Quercetin protects oral mucosal keratinocytes against lipopolysaccharide-induced inflammatory toxicity by suppressing the AKT/AMPK/mTOR pathway. Quercetin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 126-130 34308732-7 2021 Quercetin decreased the production of IL-1beta, IL-6, IL-8, TNF-alpha, iNOS, and COX-2, as well as signal transduction via the Akt/AMPK/mTOR pathway. Quercetin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 131-135 34308732-8 2021 Inhibitors of Akt, AMPK, and mTOR strengthened the anti-apoptotic effects of quercetin, while agonists of Akt, AMPK, or mTOR or Akt overexpression weakened the anti-apoptotic effects. Quercetin 77-86 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 19-23 34308732-9 2021 CONCLUSION: These results indicate that quercetin may have a potential protective effect against the chronic inflammation-related periodontitis via suppressing Akt/AMPK/mTOR pathway. Quercetin 40-49 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 164-168 34663976-4 2021 Concurrently, AMPK phosphorylates PHGDH-Ser55, selectively increasing PHGDH oxidation of malate into oxaloacetate, thus generating NADH. malic acid 89-95 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-18 34663976-4 2021 Concurrently, AMPK phosphorylates PHGDH-Ser55, selectively increasing PHGDH oxidation of malate into oxaloacetate, thus generating NADH. Oxaloacetic Acid 101-113 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-18 34663976-4 2021 Concurrently, AMPK phosphorylates PHGDH-Ser55, selectively increasing PHGDH oxidation of malate into oxaloacetate, thus generating NADH. NAD 131-135 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-18 34339945-12 2021 In vitro study demonstrated that POF effectively alleviated FFA-induced steatosis, oxidative stress, mitochondrial dysfunction and inflammation, and these beneficial effects were attributed to the activation of AMPK signaling pathway and suppression of NF-kappaB signaling pathway. Fatty Acids, Nonesterified 60-63 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 211-215 34679752-4 2021 FRI-1 decreases the maximal oxygen consumption rate (OCR), Deltapsim, NADH, and ATP levels, with a notable increase of mitochondrial reactive oxygen species (ROS) production, promoting AMPK activation with pro-survival effects. Reactive Oxygen Species 158-161 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 185-189 34680144-4 2021 In our previous studies resveratrol treatment of parkin-mutant fibroblasts induced a partial rescue of mitochondrial functions associated with stimulation of the AMPK/SIRT1/PGC-1alpha pathway. Resveratrol 24-35 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 162-166 34680144-7 2021 On this basis we hypothesize that resveratrol-mediated enhancement of the Ca2+ level, fine-tuned by the ER-mitochondria Ca2+ crosstalk, might modulate the pAMPK/AMPK pathway in parkin-mutant fibroblasts. Resveratrol 34-45 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 161-165 34547240-2 2021 Here, we show that inositol is a critical metabolite directly restricting AMPK-dependent mitochondrial fission independently of its classical mode as a precursor for phosphoinositide generation. Inositol 19-27 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 74-78 34547240-3 2021 Inositol decline by IMPA1/2 deficiency elicits AMPK activation and mitochondrial fission without affecting ATP level, whereas inositol accumulation prevents AMPK-dependent mitochondrial fission. Inositol 0-8 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 47-51 34547240-3 2021 Inositol decline by IMPA1/2 deficiency elicits AMPK activation and mitochondrial fission without affecting ATP level, whereas inositol accumulation prevents AMPK-dependent mitochondrial fission. Inositol 0-8 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 157-161 34547240-3 2021 Inositol decline by IMPA1/2 deficiency elicits AMPK activation and mitochondrial fission without affecting ATP level, whereas inositol accumulation prevents AMPK-dependent mitochondrial fission. Inositol 126-134 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 157-161 34547240-4 2021 Metabolic stress or mitochondrial damage causes inositol decline in cells and mice to elicit AMPK-dependent mitochondrial fission. Inositol 48-56 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 93-97 34547240-5 2021 Inositol directly binds to AMPKgamma and competes with AMP for AMPKgamma binding, leading to restriction of AMPK activation and mitochondrial fission. Inositol 0-8 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 108-112 34547240-5 2021 Inositol directly binds to AMPKgamma and competes with AMP for AMPKgamma binding, leading to restriction of AMPK activation and mitochondrial fission. Adenosine Monophosphate 55-58 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 108-112 34547240-6 2021 Our study suggests that the AMP/inositol ratio is a critical determinant for AMPK activation and establishes a model in which AMPK activation requires inositol decline to release AMPKgamma for AMP binding. Adenosine Monophosphate 28-31 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 77-81 34573418-1 2021 Metformin is a widely used antidiabetic drug for the treatment of type 2 diabetes and has been recently demonstrated to possess anti-inflammatory properties via AMPK-mediated modulation of M2 macrophage activation. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 161-165 34547240-6 2021 Our study suggests that the AMP/inositol ratio is a critical determinant for AMPK activation and establishes a model in which AMPK activation requires inositol decline to release AMPKgamma for AMP binding. Adenosine Monophosphate 28-31 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 126-130 34547240-6 2021 Our study suggests that the AMP/inositol ratio is a critical determinant for AMPK activation and establishes a model in which AMPK activation requires inositol decline to release AMPKgamma for AMP binding. Inositol 32-40 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 77-81 34547240-6 2021 Our study suggests that the AMP/inositol ratio is a critical determinant for AMPK activation and establishes a model in which AMPK activation requires inositol decline to release AMPKgamma for AMP binding. Inositol 32-40 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 126-130 34547240-6 2021 Our study suggests that the AMP/inositol ratio is a critical determinant for AMPK activation and establishes a model in which AMPK activation requires inositol decline to release AMPKgamma for AMP binding. Inositol 151-159 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 77-81 34547240-6 2021 Our study suggests that the AMP/inositol ratio is a critical determinant for AMPK activation and establishes a model in which AMPK activation requires inositol decline to release AMPKgamma for AMP binding. Inositol 151-159 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 126-130 34547240-6 2021 Our study suggests that the AMP/inositol ratio is a critical determinant for AMPK activation and establishes a model in which AMPK activation requires inositol decline to release AMPKgamma for AMP binding. Adenosine Monophosphate 193-196 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 77-81 34547240-6 2021 Our study suggests that the AMP/inositol ratio is a critical determinant for AMPK activation and establishes a model in which AMPK activation requires inositol decline to release AMPKgamma for AMP binding. Adenosine Monophosphate 193-196 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 126-130 34547240-7 2021 Hence, AMPK is an inositol sensor, whose inactivation by inositol serves as a mechanism to restrict mitochondrial fission. Inositol 18-26 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 7-11 34547240-7 2021 Hence, AMPK is an inositol sensor, whose inactivation by inositol serves as a mechanism to restrict mitochondrial fission. Inositol 57-65 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 7-11 34540999-9 2021 Pharmaceutical inhibitors, siRNAs for PPARalpha/gamma and AMPKalpha1, and exogenous palmitate impaired the inhibition of emodin. Emodin 121-127 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 58-68 34181935-6 2021 For FAS and ACC (involved in fatty acid metabolism), and CRH, TRH and CNR1 (anorexigenic neuropeptides stimulating energy expenditure) there were indications that their regulation in response to thyroid state might be modulated through AMPK pathways. Fatty Acids 29-39 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 236-240 34510030-0 2021 Betulinic acid induces autophagy-dependent apoptosis via Bmi-1/ROS/AMPK-mTOR-ULK1 axis in human bladder cancer cells. betulinic acid 0-14 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 67-71 34510030-6 2021 Moreover, enhanced AMPK phosphorylation and decreased mTOR and ULK-1 phosphorylation suggested BA activates autophagy via the AMPK/mTOR/ULK1 pathway. betulinic acid 95-97 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 19-23 34510030-6 2021 Moreover, enhanced AMPK phosphorylation and decreased mTOR and ULK-1 phosphorylation suggested BA activates autophagy via the AMPK/mTOR/ULK1 pathway. betulinic acid 95-97 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 126-130 34510030-7 2021 Accordingly, exposure to dorsomorphin (Compound C), an AMPK inhibitor, and AICAR, an AMPK activator, respectively inhibited and stimulated BA-induced autophagy in EJ and T24 cells. dorsomorphin 25-37 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 55-59 34460268-7 2021 Among them, stilbenoids, especially resveratrol, have been well-studied, along with their potential molecular targets, including AMPK, Sirt1, NF-kappaB, PKC, Nrf2, and PPARs. Resveratrol 36-47 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 129-133 34509534-0 2021 Targeting PP2A with lomitapide suppresses colorectal tumorigenesis through the activation of AMPK/Beclin1-mediated autophagy. BMS201038 20-30 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 93-97 34509534-5 2021 Mechanistically, lomitapide stimulated mitochondrial dysfunction-mediated AMPK activation, resulting in increased AMPK phosphorylation and enhanced Beclin1/Atg14/Vps34 interactions, provoking autophagy induction. BMS201038 17-27 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 74-78 34509534-5 2021 Mechanistically, lomitapide stimulated mitochondrial dysfunction-mediated AMPK activation, resulting in increased AMPK phosphorylation and enhanced Beclin1/Atg14/Vps34 interactions, provoking autophagy induction. BMS201038 17-27 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 114-118 34509534-6 2021 Autophagy inhibition or AMPK silencing significantly abrogated lomitapide-induced cell death, indicating the significance of AMPK-regulated autophagy in the antitumor activities of lomitapide. BMS201038 63-73 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 24-28 34509534-6 2021 Autophagy inhibition or AMPK silencing significantly abrogated lomitapide-induced cell death, indicating the significance of AMPK-regulated autophagy in the antitumor activities of lomitapide. BMS201038 63-73 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 125-129 34509534-6 2021 Autophagy inhibition or AMPK silencing significantly abrogated lomitapide-induced cell death, indicating the significance of AMPK-regulated autophagy in the antitumor activities of lomitapide. BMS201038 181-191 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 24-28 34509534-6 2021 Autophagy inhibition or AMPK silencing significantly abrogated lomitapide-induced cell death, indicating the significance of AMPK-regulated autophagy in the antitumor activities of lomitapide. BMS201038 181-191 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 125-129 34576192-11 2021 Metformin and DCA inhibited mTOR complex I signaling through upregulated AMPK-independent REDD1. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 73-77 34576192-11 2021 Metformin and DCA inhibited mTOR complex I signaling through upregulated AMPK-independent REDD1. Dichloroacetic Acid 14-17 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 73-77 34171447-7 2021 Of the few requirements of AMPK-SIRT1 activation, increased eNOS is essential for NED by elevating Nitric oxide (NO) levels. Nitric Oxide 99-111 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 27-31 34584194-7 2021 AMPKalpha1 expression was decreased in all of these cases, suggesting that reducing AMPKalpha1 can be considered an effective method to increase the sensitivity of cancer cells to doxorubicin treatment. Doxorubicin 180-191 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-10 34078001-0 2021 Ferulic acid suppresses interleukin-1beta-induced degeneration of chondrocytes isolated from patients with osteoarthritis through the SIRT1/AMPK/PGC-1alpha signaling pathway. ferulic acid 0-12 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 140-144 34584194-7 2021 AMPKalpha1 expression was decreased in all of these cases, suggesting that reducing AMPKalpha1 can be considered an effective method to increase the sensitivity of cancer cells to doxorubicin treatment. Doxorubicin 180-191 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 84-94 34270958-0 2021 AMPK phosphorylates PPARdelta to mediate its stabilization, promote glucose and glutamine uptake, and inhibit colon tumor growth. Glucose 68-75 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 34270958-0 2021 AMPK phosphorylates PPARdelta to mediate its stabilization, promote glucose and glutamine uptake, and inhibit colon tumor growth. Glutamine 80-89 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 34118361-6 2021 Further, the phosphorylation of liver PI3K/AKT/AMPK/ACC was elevated significantly by AWRK6 treatment. awrk6 86-91 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 47-51 34213784-0 2021 Corosolic acid ameliorates non-alcoholic steatohepatitis induced by high-fat diet and carbon tetrachloride by regulating TGF-beta1/Smad2, NF-kappaB, and AMPK signaling pathways. corosolic acid 0-14 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 153-157 34213784-0 2021 Corosolic acid ameliorates non-alcoholic steatohepatitis induced by high-fat diet and carbon tetrachloride by regulating TGF-beta1/Smad2, NF-kappaB, and AMPK signaling pathways. Carbon Tetrachloride 86-106 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 153-157 34107382-2 2021 Here we report an insulin sensitizer thiazolidinedione Pioglitazone selectively preserves the beta cells against high glucose-induced dysfunction by activation of AMPK and Glutaminase 1 (GLS1) axis. 2,4-thiazolidinedione 37-54 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 163-167 34512368-3 2021 In this review, we focus on summarizing some representative natural active compounds, mainly including curcumin, resveratrol, paclitaxel, Bufalin, and Ursolic acid that may ultimately trigger cancer cell death through the regulation of some key autophagic signaling pathways, such as RAS-RAF-MEK-ERK, PI3K-AKT-mTOR, AMPK, ULK1, Beclin-1, Atg5 and p53. ursolic acid 151-163 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 316-320 34429434-5 2021 Interestingly, distinct from its reported function as an activator of AMPK in tumor cells, the type 2 diabetes drug metformin enhances the membrane dissociation of PD-L1-CD by disrupting the electrostatic interaction, thereby decreasing the cellular abundance of PD-L1. Metformin 116-125 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 70-74 34259310-4 2021 SBI-0206965 (>= 25 muM) modestly inhibited AMPK signalling in C2C12 myotubes, but also inhibited insulin signalling, insulin-mediated/AMPK-independent glucose uptake, and AICA-riboside uptake. Glucose 151-158 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 134-138 34259310-7 2021 We observed that mutation of the gatekeeper methionine to a smaller side chain amino acid (threonine) rendered AMPK and ULK1 resistant to SBI-0206965 inhibition. Methionine 44-54 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 111-115 34259310-7 2021 We observed that mutation of the gatekeeper methionine to a smaller side chain amino acid (threonine) rendered AMPK and ULK1 resistant to SBI-0206965 inhibition. Threonine 91-100 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 111-115 34419936-9 2021 Notably, incubation with the AMPK activator AICAR abolished the pro-survival effect of AC136007.2 upon OGD/R treatment. AICA ribonucleotide 44-49 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 29-33 34419936-9 2021 Notably, incubation with the AMPK activator AICAR abolished the pro-survival effect of AC136007.2 upon OGD/R treatment. ac136007 87-95 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 29-33 34107382-2 2021 Here we report an insulin sensitizer thiazolidinedione Pioglitazone selectively preserves the beta cells against high glucose-induced dysfunction by activation of AMPK and Glutaminase 1 (GLS1) axis. Pioglitazone 55-67 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 163-167 34107382-6 2021 Moreover, the pioglitazone effect on AMPK activation was not dependent on the PPARgamma pathway. Pioglitazone 14-26 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 37-41 34107382-7 2021 Strikingly, chemical inhibition of AMPK signaling or glutaminase-1 inhibition abrogates the pioglitazone effect on the TRAP1-GLS1 axis and GSH/GSSG ratio linked to mitochondrial dysfunction. Pioglitazone 92-104 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 35-39 34107382-7 2021 Strikingly, chemical inhibition of AMPK signaling or glutaminase-1 inhibition abrogates the pioglitazone effect on the TRAP1-GLS1 axis and GSH/GSSG ratio linked to mitochondrial dysfunction. Glutathione 139-142 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 35-39 34107382-7 2021 Strikingly, chemical inhibition of AMPK signaling or glutaminase-1 inhibition abrogates the pioglitazone effect on the TRAP1-GLS1 axis and GSH/GSSG ratio linked to mitochondrial dysfunction. Glutathione Disulfide 143-147 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 35-39 34107382-9 2021 Altogether, these results support the proposal that pioglitazone induced AMPK activation stabilizes a novel interaction of TRAP1/HSP75-GLS1 and its downstream signaling leads to improved beta-cell function and survival under high glucose conditions. Pioglitazone 52-64 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 73-77 34107382-9 2021 Altogether, these results support the proposal that pioglitazone induced AMPK activation stabilizes a novel interaction of TRAP1/HSP75-GLS1 and its downstream signaling leads to improved beta-cell function and survival under high glucose conditions. Glucose 230-237 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 73-77 34323067-7 2021 In OPA-stimulated HepG2 cells, curcumin rectified the dysregulated expression of SLC13A5/ACLY possibly via the AMPK-mTOR signaling pathway. Curcumin 31-39 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 111-115 34376668-3 2021 Here, we show that AMPK reactivation blocks both the glutamine-dependent activation of mTORC1 and glutamoptosis in vitro and in vivo. Glutamine 53-62 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 19-23 34376668-4 2021 We also show that glutamine is used for asparagine synthesis and the GABA shunt to produce ATP and to inhibit AMPK, independently of glutaminolysis. Glutamine 18-27 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 110-114 34376668-4 2021 We also show that glutamine is used for asparagine synthesis and the GABA shunt to produce ATP and to inhibit AMPK, independently of glutaminolysis. gamma-Aminobutyric Acid 69-73 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 110-114 34376668-5 2021 Overall, our results indicate that glutamine metabolism is connected with mTORC1 activation through two parallel pathways: an acute alpha-ketoglutarate-dependent pathway; and a secondary ATP/AMPK-dependent pathway. Glutamine 35-44 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 191-195 34376668-5 2021 Overall, our results indicate that glutamine metabolism is connected with mTORC1 activation through two parallel pathways: an acute alpha-ketoglutarate-dependent pathway; and a secondary ATP/AMPK-dependent pathway. Adenosine Triphosphate 187-190 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 191-195 34422646-0 2021 The Effects of NT-1044, a Novel AMPK Activator, on Endometrial Cancer Cell Proliferation, Apoptosis, Cell Stress and In Vivo Tumor Growth. nt-1044 15-22 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 32-36 34449920-7 2021 Furthermore, L-carnitine, an intermediate of fatty acid degradation, is required for goat brown adipocyte differentiation and thermogenesis through activating AMPK pathway. Carnitine 13-24 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 159-163 34449920-7 2021 Furthermore, L-carnitine, an intermediate of fatty acid degradation, is required for goat brown adipocyte differentiation and thermogenesis through activating AMPK pathway. Fatty Acids 45-55 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 159-163 34584194-0 2021 Melatonin and doxorubicin synergistically enhance apoptosis via autophagy-dependent reduction of AMPKalpha1 transcription in human breast cancer cells. Melatonin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 97-107 34422646-1 2021 Objectives: Anti-diabetic biguanide drugs such as metformin may have anti-tumorigenic effects by behaving as AMPK activators and mTOR inhibitors. Biguanides 26-35 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 109-113 34584194-0 2021 Melatonin and doxorubicin synergistically enhance apoptosis via autophagy-dependent reduction of AMPKalpha1 transcription in human breast cancer cells. Doxorubicin 14-25 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 97-107 34584194-4 2021 In the present study, we found that melatonin synergized with doxorubicin to induce apoptosis of breast cancer cells by decreasing the expression of AMP-activated protein kinase alpha1 (AMPK alpha1), which acts as a critical survival factor for cancer cells. Melatonin 36-45 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 186-197 34422646-1 2021 Objectives: Anti-diabetic biguanide drugs such as metformin may have anti-tumorigenic effects by behaving as AMPK activators and mTOR inhibitors. Metformin 50-59 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 109-113 34584194-4 2021 In the present study, we found that melatonin synergized with doxorubicin to induce apoptosis of breast cancer cells by decreasing the expression of AMP-activated protein kinase alpha1 (AMPK alpha1), which acts as a critical survival factor for cancer cells. Doxorubicin 62-73 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 186-197 34422646-2 2021 Metformin requires organic cation transporters (OCTs) for entry into cells, and NT-1044 is an AMPK activator designed to have greater affinity for two of these transporters, OCT1 and OCT3. nt-1044 80-87 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 94-98 34422646-12 2021 NT-1044 increased phosphorylation of AMPK and decreased phosphorylation of S6, a key downstream target of the mTOR pathway. nt-1044 0-7 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 37-41 34422646-15 2021 Conclusions: NT-1044 suppressed EC cell growth through G1 cell cycle arrest, induction of apoptosis and cellular stress, activation of AMPK and inhibition of the mTOR pathway. nt-1044 13-20 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 135-139 34445125-7 2021 In addition, miR-302 also promoted mitophagy and stimulated Sirt1/AMPK-PGC1alpha pathway thereby preserving mitochondrial function. mir-302 13-20 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 66-70 34212313-0 2021 Hesperetin inhibits foam cell formation and promotes cholesterol efflux in THP-1-derived macrophages by activating LXRalpha signal in an AMPK-dependent manner. hesperetin 0-10 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 137-141 34116103-0 2021 Docosahexaenoic acid promotes the formation of autophagosomes in MCF-7 breast cancer cells through oxidative stress-induced growth inhibitor 1 mediated activation of AMPK/mTOR pathway. Docosahexaenoic Acids 0-20 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 166-170 34212313-8 2021 Furthermore, the hesperetin-induced inhibition of foam cell formation and promotion of cholesterol efflux were decreased by transfection of AMPKalpha1/alpha2 siRNA. hesperetin 17-27 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 140-150 34212313-8 2021 Furthermore, the hesperetin-induced inhibition of foam cell formation and promotion of cholesterol efflux were decreased by transfection of AMPKalpha1/alpha2 siRNA. Cholesterol 87-98 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 140-150 34247189-0 2021 Antifungal agent Terbinafine restrains tumor growth in preclinical models of hepatocellular carcinoma via AMPK-mTOR axis. Terbinafine 17-28 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 106-110 34247189-7 2021 Instead, Terbinafine robustly suppressed the proliferation of HCC cells by inhibiting mTORC1 signaling via activation of AMPK. Terbinafine 9-20 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 121-125 34302034-7 2021 Blocking baseline and IL1beta-enhanced MMP13 by galactose-replacement in human osteoarthritic chondrocyte cultures inversely paralleled increases in markers associated with mitochondrial recovery, phospho-AMPK, and PGC1alpha. Galactose 48-57 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 205-209 34422209-3 2021 We have previously shown that berberine (BBR), an isoquinoline alkaloid isolated from Chinese herbs, was able to protect human RPE cells from H2O2-induced oxidative damage through AMPK activation. Berberine 30-39 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 180-184 34422209-3 2021 We have previously shown that berberine (BBR), an isoquinoline alkaloid isolated from Chinese herbs, was able to protect human RPE cells from H2O2-induced oxidative damage through AMPK activation. Berberine 41-44 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 180-184 34422209-5 2021 Given the essential role of AMPK in autophagy activation, we postulated that BBR may confer protection against H2O2-induced oxidative damage by stimulating AMPK-dependent autophagy. Berberine 77-80 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 28-32 34422209-5 2021 Given the essential role of AMPK in autophagy activation, we postulated that BBR may confer protection against H2O2-induced oxidative damage by stimulating AMPK-dependent autophagy. Berberine 77-80 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 156-160 34116207-0 2021 Brivanib alaninate inhibited dengue virus proliferation through VEGFR2/AMPK pathway. brivanib 0-18 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 71-75 34116207-8 2021 However, this effect could be inhibited by brivanib, which significantly reversed the reduction of AMPK phosphorylation caused by DENV infection, thus improving the cellular lipid environment. brivanib 43-51 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 99-103 34116207-9 2021 Moreover, the antiviral effect of brivanib could be reversed by AMPK inhibitor, Compound C. In addition, oral administration of brivianib (20-50mg/kg/day) clearly improved the survival rate of DENV2 infection, and this effect was abolished in accompanied with Compound C (10 /kg/day). brivanib 34-42 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 64-68 34116207-9 2021 Moreover, the antiviral effect of brivanib could be reversed by AMPK inhibitor, Compound C. In addition, oral administration of brivianib (20-50mg/kg/day) clearly improved the survival rate of DENV2 infection, and this effect was abolished in accompanied with Compound C (10 /kg/day). brivianib 128-137 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 64-68 34373765-11 2021 Therefore, we concluded that zinc regulated the glucose metabolism of the spinal cord and neurons and promoted functional recovery after SCI through the AMPK pathway, which is expected to become a potential treatment strategy for SCI. Glucose 48-55 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 153-157 34260232-0 2021 Theaflavin Promotes Mitochondrial Abundance and Glucose Absorption in Myotubes by Activating the CaMKK2-AMPK Signal Axis via Calcium-Ion Influx. theaflavin 0-10 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 104-108 34260232-0 2021 Theaflavin Promotes Mitochondrial Abundance and Glucose Absorption in Myotubes by Activating the CaMKK2-AMPK Signal Axis via Calcium-Ion Influx. Calcium 125-132 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 104-108 34367466-7 2021 In conclusion, our study reveals that ROS-activated TRPM2 inhibits autophagy by downregulating the AMPK/mTOR pathway, which results in neuronal death induced by cerebral I-R, further supporting that TRPM2 might be a potential drug target for cerebral ischemic injury therapy. Reactive Oxygen Species 38-41 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 99-103 34436421-7 2021 We also showed that metformin"s inhibitory effect on the PHGDH-2HG axis may occur through the regulation of the AMPK-MYC pathway. Metformin 20-29 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 112-116 34212313-0 2021 Hesperetin inhibits foam cell formation and promotes cholesterol efflux in THP-1-derived macrophages by activating LXRalpha signal in an AMPK-dependent manner. Cholesterol 53-64 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 137-141 34212313-5 2021 Hesperetin increased the levels of LXRalpha protein and its targets, including ABCA1, ABCG1, SR-BI, and phosphorylated-AMPK. hesperetin 0-10 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 119-123 34212313-6 2021 Meanwhile, the hesperetin-induced increase in LXRalpha expression was further increased by the AMPK agonist and inhibited by an AMPK inhibitor. hesperetin 15-25 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 95-99 34212313-6 2021 Meanwhile, the hesperetin-induced increase in LXRalpha expression was further increased by the AMPK agonist and inhibited by an AMPK inhibitor. hesperetin 15-25 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 128-132 34212313-7 2021 Meanwhile, hesperetin increased the levels of LXRalpha mRNA and its target genes, all of which were decreased in cells transfected with the AMPKalpha1/alpha2 small interfering RNA (siRNA). hesperetin 11-21 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 140-150 34371919-7 2021 We showed that caffeine (1) altered adenosine receptor expression, (2) changed Akt/AMPK/mTOR signaling pathways, and (3) inhibited STAT1/IL-10 signaling axis in M-MPhis. Caffeine 15-23 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 83-87 34272364-0 2021 Glucose limitation activates AMPK coupled SENP1-Sirt3 signalling in mitochondria for T cell memory development. Glucose 0-7 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 29-33 34272364-6 2021 We also show that the glycolytic intermediate fructose-1,6-bisphosphate (FBP) as a negative regulator suppresses AMPK-mediated activation of the SENP1-Sirt3 axis and reduces memory development. fructose-1,6-diphosphate 46-71 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 113-117 34272364-7 2021 Moreover, glucose limitation reduces FBP production and activates AMPK during T cell memory development. Glucose 10-17 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 66-70 34272364-8 2021 These data show that glucose limitation activates AMPK and the subsequent SENP1-Sirt3 signalling for T cell memory development. Glucose 21-28 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 50-54 34336655-4 2021 PF-06409577 induced AMPK activation, mTORC1 inhibition, autophagy induction, and downregulation of multiple receptor tyrosine kinase inOS cells. PF-6409577 0-11 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 20-24 34336655-8 2021 In conclusion, activation of AMPK by PF-06409577 inhibits OS cell growth. PF-6409577 37-48 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 29-33 34326874-0 2021 Oleanolic Acid Induces Autophagy and Apoptosis via the AMPK-mTOR Signaling Pathway in Colon Cancer. Oleanolic Acid 0-14 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 55-59 34253170-1 2021 BACKGROUND: Although the major anticancer effect of metformin involves AMPK-dependent or AMPK-independent mTORC1 inhibition, the mechanisms of action are still not fully understood. Metformin 52-61 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 71-75 34253170-1 2021 BACKGROUND: Although the major anticancer effect of metformin involves AMPK-dependent or AMPK-independent mTORC1 inhibition, the mechanisms of action are still not fully understood. Metformin 52-61 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 89-93 34305600-0 2021 Geniposide Combined With Notoginsenoside R1 Attenuates Inflammation and Apoptosis in Atherosclerosis via the AMPK/mTOR/Nrf2 Signaling Pathway. geniposide 0-10 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 109-113 34298945-0 2021 Licochalcone D Ameliorates Oxidative Stress-Induced Senescence via AMPK Activation. licochalcone 0-12 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 67-71 34298945-9 2021 Taken together, our findings highlight the antioxidant, anti-senescent, and cardioprotective effects of Lico D and suggest that the activation of AMPK and autophagy ameliorates the oxidative stress-induced senescence. licochalcone D 104-110 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 146-150 34305621-0 2021 Caveolin-1 Alleviates Acetaminophen-Induced Fat Accumulation in Non-Alcoholic Fatty Liver Disease by Enhancing Hepatic Antioxidant Ability via Activating AMPK Pathway. Acetaminophen 22-35 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 154-158 34356319-0 2021 3H-1,2-Dithiole-3-Thione Protects Lens Epithelial Cells against Fructose-Induced Epithelial-Mesenchymal Transition via Activation of AMPK to Eliminate AKR1B1-Induced Oxidative Stress in Diabetes Mellitus. 1,2-dithiol-3-thione 0-24 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 133-137 34305600-0 2021 Geniposide Combined With Notoginsenoside R1 Attenuates Inflammation and Apoptosis in Atherosclerosis via the AMPK/mTOR/Nrf2 Signaling Pathway. notoginsenoside R1 25-43 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 109-113 34305600-6 2021 At the same time, the GN combination could also inhibit the H2O2-induced inflammatory response and apoptosis of human umbilical vein endothelial cells (HUVECs), which is mainly related to the activation of the AMPK/mTOR pathway by GN combination, which in turn induces the activation of Nrf2/HO-1 signal. Hydrogen Peroxide 60-64 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 210-214 34302638-0 2021 Ginsenoside-Rg2 exerts anti-cancer effects through ROS-mediated AMPK activation associated mitochondrial damage and oxidation in MCF-7 cells. ginsenoside Rg2 0-15 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 64-68 34302638-0 2021 Ginsenoside-Rg2 exerts anti-cancer effects through ROS-mediated AMPK activation associated mitochondrial damage and oxidation in MCF-7 cells. Reactive Oxygen Species 51-54 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 64-68 34302638-6 2021 G-Rg2 further activated the ROS-sensor protein, AMPK and downstream targets of AMPK activation, including PGC-1alpha, FOXO1, and IDH2, and downregulated mTOR activation and antioxidant response element-driven luciferase activity. ginsenoside Rg2 0-5 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 48-52 34302638-6 2021 G-Rg2 further activated the ROS-sensor protein, AMPK and downstream targets of AMPK activation, including PGC-1alpha, FOXO1, and IDH2, and downregulated mTOR activation and antioxidant response element-driven luciferase activity. ginsenoside Rg2 0-5 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 79-83 34302638-6 2021 G-Rg2 further activated the ROS-sensor protein, AMPK and downstream targets of AMPK activation, including PGC-1alpha, FOXO1, and IDH2, and downregulated mTOR activation and antioxidant response element-driven luciferase activity. Reactive Oxygen Species 28-31 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 48-52 34302638-6 2021 G-Rg2 further activated the ROS-sensor protein, AMPK and downstream targets of AMPK activation, including PGC-1alpha, FOXO1, and IDH2, and downregulated mTOR activation and antioxidant response element-driven luciferase activity. Reactive Oxygen Species 28-31 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 79-83 34604421-6 2021 By adding receptors antagonists (losartan, AT1R antagonist and PD 123319, AT2R antagonist) and/or signaling modulators for AMPK, Akt/PI3K, p38 and PKC we showed the protective effect was enhanced with losartan and abolished with PD 123319. Losartan 201-209 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 123-127 34162151-5 2021 Furthermore, we demonstrate that melatonin up-regulates the transcription of LINC01512 via the AMPK signalling pathway and that the blockade of AMPK represses LINC01512 expression in Treg and Th17 cells. Melatonin 33-42 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 95-99 34162151-7 2021 Moreover, manipulation of the AMPK/LINC01512/SIRT1 axis via melatonin may be a novel therapeutic approach to reduce inflammation. Melatonin 60-69 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-34 34203724-6 2021 Increased sensitivity to GANT-61 was also found following genetic inactivation of the catalytic subunit of AMPK (AMPKalpha1) or pharmacological inhibition of AMPK by Compound C. Additionally, patient-derived xenografts showing high GLI1 expression lacked activated AMPK, suggesting an important role for this signaling pathway in regulating GLI1 protein levels. GANT 61 25-32 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 113-123 34203724-6 2021 Increased sensitivity to GANT-61 was also found following genetic inactivation of the catalytic subunit of AMPK (AMPKalpha1) or pharmacological inhibition of AMPK by Compound C. Additionally, patient-derived xenografts showing high GLI1 expression lacked activated AMPK, suggesting an important role for this signaling pathway in regulating GLI1 protein levels. GANT 61 25-32 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 158-162 34203724-6 2021 Increased sensitivity to GANT-61 was also found following genetic inactivation of the catalytic subunit of AMPK (AMPKalpha1) or pharmacological inhibition of AMPK by Compound C. Additionally, patient-derived xenografts showing high GLI1 expression lacked activated AMPK, suggesting an important role for this signaling pathway in regulating GLI1 protein levels. GANT 61 25-32 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 265-269 34203724-7 2021 Further, joint targeting of HH and AMPK signaling pathways in T-ALL cells by GANT-61 and Compound C significantly increased the therapeutic response. GANT 61 77-84 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 35-39 34179090-0 2021 Sinomenine Suppresses Development of Hepatocellular Carcinoma Cells via Inhibiting MARCH1 and AMPK/STAT3 Signaling Pathway. sinomenine 0-10 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 94-98 34179090-9 2021 Our results suggested that SIN inhibits proliferation and promotes apoptosis of HCC cells by MARCH1-mediated AMPK/STAT3 signaling pathway. sinomenine 27-30 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 109-113 33929389-0 2021 Metformin attenuates hypoxia-induced endothelial cell injury by activating the AMPK pathway. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 79-83 33929389-10 2021 Following metformin treatment, p-AMPK and p-eNOS expression increased, while p-mTOR expression decreased. Metformin 10-19 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 33-37 33929389-12 2021 In conclusion, metformin can attenuate endothelial injuries and suppress EndMT of HCMECs under hypoxic conditions, owing to its ability to activate the AMPK pathway, increase p-AMPK/t-AMPK, and inhibit mTOR. Metformin 15-24 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 152-156 33929389-12 2021 In conclusion, metformin can attenuate endothelial injuries and suppress EndMT of HCMECs under hypoxic conditions, owing to its ability to activate the AMPK pathway, increase p-AMPK/t-AMPK, and inhibit mTOR. Metformin 15-24 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 177-181 33929389-12 2021 In conclusion, metformin can attenuate endothelial injuries and suppress EndMT of HCMECs under hypoxic conditions, owing to its ability to activate the AMPK pathway, increase p-AMPK/t-AMPK, and inhibit mTOR. Metformin 15-24 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 184-188 34093437-6 2021 Additionally, BQ610 suppressed the ET-3-induced increases in phosphorylation of AMPK, c-JUN, and STAT3 proteins, and pretreatment with specific inhibitors of AMPK, JNK/c-JUN, or JAK/STAT3 prevented the ET-3-induced increases in phosphorylation of AMPK, c-JUN, and STAT3, respectively. BQ 610 14-19 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 80-84 34093169-0 2021 Dapagliflozin Alleviates Hepatic Steatosis by Restoring Autophagy via the AMPK-mTOR Pathway. dapagliflozin 0-13 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 74-78 34749615-4 2021 RSV is thought to have an impressive outcome in colorectal cancer (CRC) treatment through the vital molecules and cancer signaling pathways, including SIRT1, P53, P21, AMPK, ROS, BMP7, COX-2, NO, Caspases, Wnt, TNFs, NF-kappaB, EMT, and pentose phosphate pathway. Resveratrol 0-3 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 168-172 34915755-7 2021 Moreover, Cisplatin-induced activation of mammalian target of rapamycin mTOR and inactivation of AMPK/PI3K/Akt signal pathway, and was coupled with induction of p53 activity and the executioner caspase3 to induce apoptotic renal cell death. Cisplatin 10-19 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 97-101 34093169-10 2021 We demonstrated that dapagliflozin ameliorates hepatic steatosis by decreasing lipogenic enzyme, while inducing fatty acid oxidation enzyme and autophagy, which could be associated with AMPK activation. dapagliflozin 21-34 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 186-190 34093169-11 2021 Moreover, our results indicate that dapagliflozin induces autophagy via the AMPK-mTOR pathway. dapagliflozin 36-49 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 76-80 34093437-6 2021 Additionally, BQ610 suppressed the ET-3-induced increases in phosphorylation of AMPK, c-JUN, and STAT3 proteins, and pretreatment with specific inhibitors of AMPK, JNK/c-JUN, or JAK/STAT3 prevented the ET-3-induced increases in phosphorylation of AMPK, c-JUN, and STAT3, respectively. BQ 610 14-19 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 247-251 34859817-8 2022 Metformin and rapamycin elicited similar effects, which were blocked by pharmacological inhibition of AMPK. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 102-106 34109916-15 2021 CONCLUSION: Pseudo-G-Rh2 could induce protective autophagy in HepG2 cells, at least in part, via AMPK and the PI3K/Akt/mTOR pathway. 3-O-glucopyranosyl-3,12,25-trihydroxydammar-20(22)-ene 12-24 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 97-101 34859817-8 2022 Metformin and rapamycin elicited similar effects, which were blocked by pharmacological inhibition of AMPK. Sirolimus 14-23 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 102-106 35504402-8 2022 The effects of ABZ on AMPK, MAPKs, and ULK induction was also evaluated. Albendazole 15-18 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 22-26 35605453-9 2022 Analysis of AMPK phosphorylation revealed that its activation was decreased in the PBMCs of type 2 diabetic patients, an effect which was reversed, once again, by metformin. Metformin 163-172 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 12-16 35605453-11 2022 These results demonstrate that metformin improves mitochondrial function, restores the levels of ETC complexes, and enhances AMPK activation and mitophagy, suggesting beneficial clinical implications in the treatment of type 2 diabetes. Metformin 31-40 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 125-129 35636015-11 2022 ROS production was significantly promoted and mitochondrial potential was remarkably inhibited when overexpressing TRIM22, thus activating AMPK/mTOR signaling. Reactive Oxygen Species 0-3 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 139-143 35636015-15 2022 In conclusion, our study indicated that TRIM22 inhibits OS progression by promoting proteasomal degradation of NRF2 independent of KEAP1, thereby activating ROS/AMPK/mTOR/Autophagy signaling that leads to autophagic cell death in OS. Reactive Oxygen Species 157-160 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 161-165 35351574-0 2022 Pretreatment of hydroethanolic extract of Dillenia indica L. attenuates oleic acid induced NAFLD in HepG2 cells via modulating SIRT-1/p-LKB-1/AMPK, HMGCR & PPAR-alpha signaling pathways. hydroethanolic extract 16-38 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 142-146 35351574-0 2022 Pretreatment of hydroethanolic extract of Dillenia indica L. attenuates oleic acid induced NAFLD in HepG2 cells via modulating SIRT-1/p-LKB-1/AMPK, HMGCR & PPAR-alpha signaling pathways. Oleic Acid 72-82 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 142-146 35351574-16 2022 CONCLUSION: These results suggest that DI-HET is effective against NAFLD by activation of the SIRT-1/p-LKB-1/AMPK signaling pathway via polyphenols present in the extract. Polyphenols 136-147 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 109-113 35435532-0 2022 Inhibition of miR-130b-3p restores autophagy and attenuates intervertebral disc degeneration through mediating ATG14 and PRKAA1. mir-130b-3p 14-25 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 121-127 35435532-14 2022 Mechanistically, we confirmed that the miR-130b-3p regulated the ATG14 and PRKAA1 directly and the knockdown of the ATG14 or PRKAA1 as well as the treatment of autophagy inhibitor blockaded the autophagic flux and reversed the protective effects of miR-130b-3p inhibition in the TBHP-induced human NP cells. tert-Butylhydroperoxide 279-283 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 75-81 35435532-14 2022 Mechanistically, we confirmed that the miR-130b-3p regulated the ATG14 and PRKAA1 directly and the knockdown of the ATG14 or PRKAA1 as well as the treatment of autophagy inhibitor blockaded the autophagic flux and reversed the protective effects of miR-130b-3p inhibition in the TBHP-induced human NP cells. tert-Butylhydroperoxide 279-283 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 125-131 35231606-1 2022 An AMP-activated kinase (AMPK) signaling pathway is activated during myocardial ischemia and promotes cardiac fatty acid (FA) uptake and oxidation. Fatty Acids 110-120 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 25-29 35274762-0 2022 Dapagliflozin attenuates high glucose-induced endothelial cell apoptosis and inflammation through AMPK/SIRT1 activation. dapagliflozin 0-13 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 98-102 35274762-9 2022 Furthermore, DAPA increased the expression of SIRT1, PGC-1alpha, and increased the phosphorylation levels of AMPK (p-AMPK) in a set of HG conditions in HUVEC cells. dapagliflozin 13-17 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 109-113 35274762-9 2022 Furthermore, DAPA increased the expression of SIRT1, PGC-1alpha, and increased the phosphorylation levels of AMPK (p-AMPK) in a set of HG conditions in HUVEC cells. dapagliflozin 13-17 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 117-121 35274762-10 2022 However, the endothelial protective effects of DAPA were abolished when cells were subjected to the SIRT1 inhibitor (EX-527) and AMPK inhibitor (Compound C). dapagliflozin 47-51 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 129-133 35274762-11 2022 These findings suggest that DAPA can abrogate HG-induced endothelial cell dysfunction by AMPK/SIRT1 pathway up-regulation. dapagliflozin 28-32 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 89-93 35274762-12 2022 Therefore, suggesting that the activation of AMPK/SIRT1 axis by DAPA may be a novel target for the treatment of HG-induced endothelial cell injury. dapagliflozin 64-68 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 45-49 35366490-0 2022 Stachydrine hydrochloride inhibits hepatocellular carcinoma progression via LIF/AMPK axis. Stachydrine hydrochloride 0-25 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 80-84 34124601-3 2021 Here, we find that AMPK agonists, A769662, and Metformin, can inhibit GLI1 activity and synergize with Vismodegib to suppress MB cell growth in vitro and in vivo. Metformin 47-56 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 19-23 34124601-5 2021 This is the first report demonstrating that combining AMPK agonist (Metformin) and SHH pathway inhibitor (Vismodegib) confers synergy for MB treatment and provides an effective chemotherapeutic regimen that can be used to overcome resistance to Vismodegib in SHH-driven cancers. Metformin 68-77 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 54-58 35321842-4 2022 AMPK knock out cells demonstrated significant resistance to cytarabine and doxorubicin both in vitro and in vivo. Cytarabine 60-70 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 35321842-4 2022 AMPK knock out cells demonstrated significant resistance to cytarabine and doxorubicin both in vitro and in vivo. Doxorubicin 75-86 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 35321842-8 2022 Finally, AML cells were sensitized to chemotherapy with the addition of the AMPK activator AICAR. AICA ribonucleotide 91-96 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 76-80 35237909-2 2022 This has been attributed to the activation of AMPK, which differentially regulates the expression of multiple genes involved in cholesterol synthesis and trafficking. Cholesterol 128-139 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 46-50 35341775-0 2022 Metformin alleviates dexamethasone-induced apoptosis by regulating autophagy via AMPK/mTOR/p70S6K in osteoblasts. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 81-85 35341775-0 2022 Metformin alleviates dexamethasone-induced apoptosis by regulating autophagy via AMPK/mTOR/p70S6K in osteoblasts. Dexamethasone 21-34 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 81-85 35341775-12 2022 Treatment with the autophagy inhibitor 3-methyladenine (3-MA) attenuated the effect of metformin on apoptosis, autophagy, and the AMPK/mTOR/p70S6K signaling pathway. 3-methyladenine 39-54 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 130-134 35341775-12 2022 Treatment with the autophagy inhibitor 3-methyladenine (3-MA) attenuated the effect of metformin on apoptosis, autophagy, and the AMPK/mTOR/p70S6K signaling pathway. 3-methyladenine 56-60 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 130-134 35341775-14 2022 Furthermore, sh-AMPK transfection and the mTOR activator MHY1485 impaired metformin-mediated inhibition of osteoblast apoptosis and promotion of autophagy. Metformin 74-83 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 16-20 35341775-15 2022 The AMPK/mTOR/p70S6K signaling pathway plays a role in metformin-mediated apoptosis suppression and autophagy promotion. Metformin 55-64 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 4-8 35341775-16 2022 In conclusion, metformin can alleviate Dex-induced osteoblast apoptosis by inducing autophagy via the AMPK/mTOR/p70S6K pathway. Metformin 15-24 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 102-106 35341775-16 2022 In conclusion, metformin can alleviate Dex-induced osteoblast apoptosis by inducing autophagy via the AMPK/mTOR/p70S6K pathway. Dexamethasone 39-42 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 102-106 35489526-0 2022 Mogrol suppresses lung cancer cell growth by activating AMPK-dependent autophagic death and inducing p53-dependent cell cycle arrest and apoptosis. MOGROL 0-6 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 56-60 35489526-10 2022 Furthermore, mogrol significantly activated AMPK to induce autophagy and autophagic cell death, which could be abrogated by Compound C, an AMPK inhibitor. MOGROL 13-19 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 44-48 35489526-10 2022 Furthermore, mogrol significantly activated AMPK to induce autophagy and autophagic cell death, which could be abrogated by Compound C, an AMPK inhibitor. MOGROL 13-19 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 139-143 35619086-8 2022 The 181T>C and 1222A>G changes were further found to alter OCT-1 structure in silico and affect metformin transport in vitro which was illustrated by their effect on the activation of AMPK, the marker for metformin activity. Metformin 96-105 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 184-188 35489526-12 2022 Our results indicated that mogrol effectively suppressed lung cancer cells in vivo and in vitro by inducing the excessive autophagy and autophagic cell death via activating AMPK signaling pathway, as well as cell cycle arrest and apoptosis via activating p53 pathway. MOGROL 27-33 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 173-177 35619086-8 2022 The 181T>C and 1222A>G changes were further found to alter OCT-1 structure in silico and affect metformin transport in vitro which was illustrated by their effect on the activation of AMPK, the marker for metformin activity. Metformin 205-214 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 184-188 35548952-0 2022 FADS1 overexpression promotes fatty acid synthesis and triacylglycerol accumulation via inhibiting the AMPK/SREBP1 pathway in goat mammary epithelial cells. Triglycerides 55-70 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 103-107 35538807-7 2022 Molecular studies revealed that these plant-derived molecules induced glucose uptake via increasing GLUT-4 expression and/or translocation through insulin signaling pathway, AMPK pathway, PTP1B activity inhibition or acting as partial PPARgamma agonists. Glucose 70-77 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 174-178 35367764-7 2022 Furthermore, results from an RT-qPCR analysis disclosed significant upregulation of AMPK by MACK and ONON treatment. calycosin-7-O-beta-D-glucoside 101-105 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 84-88 35620285-6 2022 Western blotting and DCFH-DA probe assay showed that SBA decreased pAMPK/AMPK and pULK1/ULK1 which associated with autophagy initiation, down-regulated Beclin-1, Atg3, Atg5, Atg7, LC3 II and Bax/Bcl2 ratio, and up-regulated pmTOR/mTOR, SQSTM1/p62 and mitochondrial membrane potential (MMP), reduces intracellular autophagosomes. diacetyldichlorofluorescein 21-28 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 73-77 35620285-8 2022 These data demonstrated that SBA treatment inhibits the autophagy of ARPE-19 through the AMPK/mTOR/ULK1 signaling pathway, and reduced early-stage apoptosis occurred by high glucose. sba 29-32 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 89-93 35524978-0 2022 Antitumor activity of pachymic acid in cervical cancer through inducing endoplasmic reticulum stress, mitochondrial dysfunction, and activating the AMPK pathway. pachymic acid 22-35 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 148-152 35524978-8 2022 Phosphorylation of AMPK and acetyl-CoA carboxylase (ACC) of the AMPK pathway key protein was upregulated in pachymic acid-induced HeLa cells. pachymic acid 108-121 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 19-23 35524978-8 2022 Phosphorylation of AMPK and acetyl-CoA carboxylase (ACC) of the AMPK pathway key protein was upregulated in pachymic acid-induced HeLa cells. pachymic acid 108-121 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 64-68 35524978-10 2022 Therefore, these findings demonstrated that pachymic acid plays an anti-tumor activity in cervical cancer through inducing ER stress, mitochondrial dysfunction, and activating the AMPK pathway. pachymic acid 44-57 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 180-184 35358477-7 2022 Treatment of hepatocytes with VAL increased AMPK phosphorylation and SIRT6 expression. valdecoxib 30-33 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 44-48 35358477-8 2022 siRNA-mediated suppression of AMPK or SIRT6 abolished the effects of VAL on lipid accumulation, lipogenesis, and endoplasmic reticulum (ER) stress in palmitate-treated hepatocytes. valdecoxib 69-72 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-34 35358477-10 2022 Moreover, in vivo AMPK siRNA transfection abolished the effects of VAL on hepatic steatosis and lipid metabolism. valdecoxib 67-70 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 18-22 35358477-11 2022 These results suggest that VAL suppresses ER stress through the AMPK/SIRT6 pathway, thereby attenuating hepatic steatosis under hyperlipidemic conditions. valdecoxib 27-30 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 64-68 35364376-0 2022 The enhanced mitochondrial dysfunction by cantleyoside confines inflammatory response and promotes apoptosis of human HFLS-RA cell line via AMPK/Sirt 1/NF-kappaB pathway activation. Cantleyoside 42-54 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 140-144 35121714-0 2022 Homocysteine Suppresses Autophagy via AMPK-mTOR-TFEB Signaling in Human THP-1 Macrophages. Homocysteine 0-12 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 38-42 35187676-0 2022 Chitosan oligosaccharide attenuates hepatic steatosis in HepG2 cells via the activation of AMP-activated protein kinase. D-Glucosaminide 0-24 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 91-119 35218767-0 2022 Hesperidin attenuates hepatic lipid accumulation in mice fed high-fat diet and oleic acid induced HepG2 via AMPK activation. Hesperidin 0-10 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 108-112 35290519-6 2022 In addition, dietary resveratrol, which has an effective anti-obesity effect, has been shown to promote mitochondrial biosynthesis by activating AMPK/PGC-1alpha axis, as well as to regenerate muscle damaged by obesity. Resveratrol 21-32 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 145-149 35150861-0 2022 Ginsenoside Rd ameliorates high glucose-induced retinal endothelial injury through AMPK-STRT1 interdependence. Ginsenosides 0-11 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 83-87 35150861-6 2022 Besides, Rd strengthened the interaction between AMPK and SIRT1 by increasing NAD+/NADH levels and LKB1 deacetylation in endothelial cells. NAD 78-82 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 49-53 35150861-6 2022 Besides, Rd strengthened the interaction between AMPK and SIRT1 by increasing NAD+/NADH levels and LKB1 deacetylation in endothelial cells. NAD 83-87 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 49-53 35487917-4 2022 Consequently, MDK decreases the activity of LKB1 to dampen both the basal and stress-induced activation of AMPK by glucose starvation or treatment of 2-DG. Glucose 115-122 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 107-111 35487917-4 2022 Consequently, MDK decreases the activity of LKB1 to dampen both the basal and stress-induced activation of AMPK by glucose starvation or treatment of 2-DG. Deoxyglucose 150-154 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 107-111 35485096-8 2022 The inhibitory effect of rosiglitazone on expression of p-Akt/t-Akt, PPARa, p-FoxO1/t-FoxO1, and p-AMPK/t-AMPK was significantly (p<0.01) alleviated in the adipocytes by salicin ether. Rosiglitazone 25-38 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 99-103 35485096-8 2022 The inhibitory effect of rosiglitazone on expression of p-Akt/t-Akt, PPARa, p-FoxO1/t-FoxO1, and p-AMPK/t-AMPK was significantly (p<0.01) alleviated in the adipocytes by salicin ether. Rosiglitazone 25-38 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 106-110 35485096-10 2022 Moreover, the activation of FoxO1/Akt/AMPK was up-regulated and FAS/EBPalpha/aP2/HMG-CoA level inhibited by salicin ether in the adipocytes. salicin 108-115 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 38-42 35462605-7 2022 The role of inositol in cancer is further complicated by its ability to inhibit the master metabolic regulator AMPK, which upon activation can either decrease cell proliferation and metastasis or promote cell survival. Inositol 12-20 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 111-115 34990285-10 2022 Silencing of AMPK in the presence of metformin revealed that metformin could exert its inhibitory effect via AMPK. Metformin 37-46 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 13-17 34990285-10 2022 Silencing of AMPK in the presence of metformin revealed that metformin could exert its inhibitory effect via AMPK. Metformin 37-46 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 109-113 34990285-10 2022 Silencing of AMPK in the presence of metformin revealed that metformin could exert its inhibitory effect via AMPK. Metformin 61-70 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 13-17 34990285-10 2022 Silencing of AMPK in the presence of metformin revealed that metformin could exert its inhibitory effect via AMPK. Metformin 61-70 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 109-113 35405615-13 2022 Capsaicin restored AMPK phosphorylation and IHG-inhibited TRPV1 expression. Capsaicin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 19-23 35405615-15 2022 CONCLUSION: Capsaicin elevates SIRT1 levels through TRPV1/(Ca2+)i/CaMKII/AMPK pathway and suppresses IHG-mediated endothelial cell senescence. Capsaicin 12-21 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 73-77 35187676-7 2022 The inhibition of lipogenesis and the enhancement of fatty acid oxidation induced by COS were all blocked by AMPK antagonist (compound C), showing that the attenuation of hepatic steatosis by COS was dependent on AMPK activation. Fatty Acids 53-63 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 109-113 35187676-7 2022 The inhibition of lipogenesis and the enhancement of fatty acid oxidation induced by COS were all blocked by AMPK antagonist (compound C), showing that the attenuation of hepatic steatosis by COS was dependent on AMPK activation. carbonyl sulfide 85-88 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 109-113 35187676-7 2022 The inhibition of lipogenesis and the enhancement of fatty acid oxidation induced by COS were all blocked by AMPK antagonist (compound C), showing that the attenuation of hepatic steatosis by COS was dependent on AMPK activation. carbonyl sulfide 85-88 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 213-217 35187676-7 2022 The inhibition of lipogenesis and the enhancement of fatty acid oxidation induced by COS were all blocked by AMPK antagonist (compound C), showing that the attenuation of hepatic steatosis by COS was dependent on AMPK activation. carbonyl sulfide 192-195 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 109-113 35187676-7 2022 The inhibition of lipogenesis and the enhancement of fatty acid oxidation induced by COS were all blocked by AMPK antagonist (compound C), showing that the attenuation of hepatic steatosis by COS was dependent on AMPK activation. carbonyl sulfide 192-195 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 213-217 35187676-9 2022 AMPK was also involved in the alleviation of hepatic steatosis by COS. carbonyl sulfide 66-69 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 35218767-0 2022 Hesperidin attenuates hepatic lipid accumulation in mice fed high-fat diet and oleic acid induced HepG2 via AMPK activation. Oleic Acid 79-89 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 108-112 35470752-3 2022 Our recent investigation identified that the connection between glutamine and AMPK is not restricted to glutaminolysis. Glutamine 64-73 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 78-82 35470752-4 2022 Rather, we demonstrated the crucial role of ASNS (asparagine synthetase (glutamine-hydrolyzing)) and the GABA shunt for the metabolic control of the AMPK-MTORC1 axis during glutamine sufficiency. gamma-Aminobutyric Acid 105-109 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 149-153 35461323-0 2022 Asteltoxin inhibits extracellular vesicle production through AMPK/mTOR-mediated activation of lysosome function. asteltoxin 0-10 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 61-65 35461323-6 2022 Asteltoxin attenuated cellular ATP levels and induced AMPK-mediated mTORC1 inactivation. asteltoxin 0-10 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 54-58 35527487-0 2022 (Dihydromyricetin reduces lipid accumulation in LO2 cells via AMPK/mTOR-mediated lipophagy pathway and inhibits HepG2 cell proliferation in vitro). dihydromyricetin 1-17 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 62-66 35527487-9 2022 DMY obviously attenuated high FBS-induced inhibition of autophagosome formation in LO2 cells, up- regulated the mRNA levels of LC3, ATG7, Beclin1 and AMPK, and downregulated p62 and mTOR mRNA levels (P < 0.05 or 0.01). dihydromyricetin 0-3 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 150-154 35527487-11 2022 CONCLUSION: DMY reduces lipid accumulation in LO2 cells by regulating the AMPK/ mTOR-mediated lipophagy pathway and inhibits the proliferation of HepG2 by causing cell cycle arrest and promoting apoptosis. dihydromyricetin 12-15 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 74-78 35457010-7 2022 However, NI-hADSC-CM treatment increased the p-mTORC1, p-mTORC2, p-ULK1, p-Akt, p-ERK1/2, ATG13, and beclin-1 levels and decreased the p-AMPK level and GSK3beta activity in response to ROT-induced toxicity. ni-hadsc-cm 9-20 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 137-141 35121714-6 2022 Furthermore, western blotting showed that Hcy significantly increased the levels of p-mTOR and nuclear TFEB and decreased the levels of p-AMPK and cytoplasmic TFEB. Homocysteine 42-45 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 138-142 35121714-7 2022 These data suggest that Hcy inhibits autophagosome formation in human THP-1 macrophages through the AMPK-mTOR-TFEB signaling pathway. Homocysteine 24-27 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 100-104 35487599-0 2022 EGCG and ECG induce apoptosis and decrease autophagy via the AMPK/mTOR and PI3K/AKT/mTOR pathway in human melanoma cells. epigallocatechin gallate 0-4 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 61-65 34990285-0 2022 Metformin exerts anti-tumor effects via Sonic hedgehog signaling pathway by targeting AMPK in HepG2 cells. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 86-90 34990285-11 2022 Our findings demonstrate that metformin can suppress the migration and invasion of HepG2 cells via AMPK-mediated inhibition of the Shh pathway. Metformin 30-39 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 99-103 35487599-0 2022 EGCG and ECG induce apoptosis and decrease autophagy via the AMPK/mTOR and PI3K/AKT/mTOR pathway in human melanoma cells. epicatechin gallate 9-12 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 61-65 35487599-10 2022 Mechanistically, EGCG and ECG treatments decreased phosphorylated-AMPK (p-AMPK) and increased the ratios of p-PI3K, p-AKT and p-mTOR in melanoma cells. epigallocatechin gallate 17-21 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 66-70 35487599-10 2022 Mechanistically, EGCG and ECG treatments decreased phosphorylated-AMPK (p-AMPK) and increased the ratios of p-PI3K, p-AKT and p-mTOR in melanoma cells. epigallocatechin gallate 17-21 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 74-78 35487599-10 2022 Mechanistically, EGCG and ECG treatments decreased phosphorylated-AMPK (p-AMPK) and increased the ratios of p-PI3K, p-AKT and p-mTOR in melanoma cells. epicatechin gallate 26-29 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 66-70 35487599-10 2022 Mechanistically, EGCG and ECG treatments decreased phosphorylated-AMPK (p-AMPK) and increased the ratios of p-PI3K, p-AKT and p-mTOR in melanoma cells. epicatechin gallate 26-29 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 74-78 35487599-11 2022 Conclusively, EGCG and ECG induced apoptosis via mitochondrial signaling pathway, downregulated autophagy through modulating the AMPK/mTOR and PI3K/AKT/mTOR signaling pathway. epigallocatechin gallate 14-18 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 129-133 35487599-11 2022 Conclusively, EGCG and ECG induced apoptosis via mitochondrial signaling pathway, downregulated autophagy through modulating the AMPK/mTOR and PI3K/AKT/mTOR signaling pathway. epicatechin gallate 23-26 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 129-133 35134563-6 2022 ATP and NADH, derivatives of adenosine, inhibit insulin signaling inside cells by downregulation of activities of AMPK and SIRT1, respectively. Adenosine Triphosphate 0-3 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 114-118 35468677-0 2022 AMPK Signaling Regulates Mitophagy and Mitochondrial ATP Production in Human Trophoblast Cell Line BeWo. Adenosine Triphosphate 53-56 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 35134563-6 2022 ATP and NADH, derivatives of adenosine, inhibit insulin signaling inside cells by downregulation of activities of AMPK and SIRT1, respectively. NAD 8-12 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 114-118 35134563-6 2022 ATP and NADH, derivatives of adenosine, inhibit insulin signaling inside cells by downregulation of activities of AMPK and SIRT1, respectively. Adenosine 29-38 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 114-118 35394351-0 2022 Graphene oxide induces autophagy and apoptosis via ROS-dependent AMPK/mTOR/ULK-1 pathway in colorectal cancer cells. graphene oxide 0-14 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 65-69 35394351-0 2022 Graphene oxide induces autophagy and apoptosis via ROS-dependent AMPK/mTOR/ULK-1 pathway in colorectal cancer cells. Reactive Oxygen Species 51-54 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 65-69 35394351-5 2022 GO treatment resulted in cytotoxicity, reactive oxygen species (ROS) production, apoptosis, autophagy and activation of the AMPK/mTOR/ULK1 signal pathway. graphene oxide 0-2 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 124-128 35394351-6 2022 However, ROS scavenger N-acetylcysteine (NAC) attenuated the above effects and restored the effects of GO on protein expressions related to apoptosis, autophagy and AMPK/mTOR/ULK1 signal pathways. Acetylcysteine 23-39 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 165-169 35433698-7 2022 Furthermore, the biguanide diabetes drug metformin, treatment with which enhances autophagy via AMPK-mediated mTOR inactivation, has been reported to reduce the risk of EC. Metformin 41-50 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 96-100 35394351-6 2022 However, ROS scavenger N-acetylcysteine (NAC) attenuated the above effects and restored the effects of GO on protein expressions related to apoptosis, autophagy and AMPK/mTOR/ULK1 signal pathways. Acetylcysteine 41-44 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 165-169 35394351-7 2022 Conclusion: GO exerts anticancer effects against CRC via ROS-dependent AMPK/mTOR/ULK-1 pathway-related autophagy and apoptosis. Reactive Oxygen Species 57-60 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 71-75 35453311-0 2022 Luteolin Synergistically Enhances Antitumor Activity of Oxaliplatin in Colorectal Carcinoma via AMPK Inhibition. Oxaliplatin 56-67 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 96-100 35468677-2 2022 METHODS: In this study, we investigated three major mitophagy pathways mediated by PRKN, FUNDC1, and BNIP3/BNIP3L in response to AMPK activation by AICAR and knockdown of PRKAA1/2 (AKD) in human trophoblast cell line BeWo and the effect of AKD on mitochondrial membrane potential and ATP production. Adenosine Triphosphate 284-287 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 129-133 35468677-6 2022 CONCLUSIONS: In summary, AMPK signaling stimulates mitophagy in human trophoblast cells via PRKN and FUNDC1 mediated mitophagy pathways and AMPK regulated mitophagy contributes to the maintenance of mitochondrial membrane potential and mitochondrial ATP production. Adenosine Triphosphate 250-253 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 25-29 35468677-6 2022 CONCLUSIONS: In summary, AMPK signaling stimulates mitophagy in human trophoblast cells via PRKN and FUNDC1 mediated mitophagy pathways and AMPK regulated mitophagy contributes to the maintenance of mitochondrial membrane potential and mitochondrial ATP production. Adenosine Triphosphate 250-253 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 140-144 35392289-8 2022 Coffee by-products" bioactive compounds decreased lipid accumulation (23-41%) and fatty acid synthase activity (32-65%) and triggered carnitine palmitoyltransferase-1 activity (1.3 to 1.7-fold) by activating AMPK and SREBP-1c pathways. Carnitine 134-143 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 208-212 35339661-7 2022 Non-obese type 2 Diabetic mice (MKR) were used and treated with a CYP4A-inhibitor (HET0016) or AMPK-activator (Metformin). Metformin 111-120 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 95-99 35414794-7 2022 The metabolic shift further led to the inactivation of AMPK by elevating ATP. Adenosine Triphosphate 73-76 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 55-59 35339661-10 2022 AMPK activation via Metformin restored nerve integrity, reduced ROS production, and regulated autophagy. Metformin 20-29 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 35339661-10 2022 AMPK activation via Metformin restored nerve integrity, reduced ROS production, and regulated autophagy. Reactive Oxygen Species 64-67 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 35149085-8 2022 Moreover, treatment with DIO caused an increase in p-LKB1/LKB1 and p-AMPK/AMPK expressions and a decrease in p-mTOR/mTOR, p-ULK1(Ser757), p-P70S6K and p-4EBP1 expressions. Diosgenin 25-28 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 69-73 35051863-0 2022 The Alzheimer"s disease drug candidate J147 decreases blood plasma fatty acid levels via modulation of AMPK/ACC1 signaling in the liver. Fatty Acids 67-77 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 103-107 35196389-1 2022 Contraction-Mediated Glucose Transport in Skeletal Muscle Is Regulated by a Framework of AMPK, TBC1D1/4, and Rac1. Glucose 21-28 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 89-93 35196392-1 2022 Contraction-Mediated Glucose Transport in Skeletal Muscle Is Regulated by a Framework of AMPK, TBC1D1/4, and Rac1. Glucose 21-28 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 89-93 35149085-8 2022 Moreover, treatment with DIO caused an increase in p-LKB1/LKB1 and p-AMPK/AMPK expressions and a decrease in p-mTOR/mTOR, p-ULK1(Ser757), p-P70S6K and p-4EBP1 expressions. Diosgenin 25-28 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 74-78 35149085-10 2022 In conclusion, our study demonstrated for the first time that DIO protected against kidney injury induced by 3-MCPD through the induction of autophagy via LKB1-AMPK-mTOR pathway and the improvement of mitochondrial fission and fusion. Diosgenin 62-65 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 160-164 35149085-10 2022 In conclusion, our study demonstrated for the first time that DIO protected against kidney injury induced by 3-MCPD through the induction of autophagy via LKB1-AMPK-mTOR pathway and the improvement of mitochondrial fission and fusion. alpha-Chlorohydrin 109-115 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 160-164 35039880-0 2022 (Corrigendum) 3-Bromopyruvate sensitizes human breast cancer cells to TRAIL-induced apoptosis via the phosphorylated AMPK-mediated upregulation of DR5. bromopyruvate 14-29 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 117-121 35178649-5 2022 Resveratrol-treated AML-12 hepatocytes showed reduced ratio of the following key metabolic factors: phosphorylated PP2A to total PP2A (pPP2A/PP2A), pAKT/AKT, pFOXO1/FOXO1 and pAMPK/AMPK, indicating inhibition of AKT and AMPK, but activation of PP2A and FOXO1. Resveratrol 0-11 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 181-185 35007932-0 2022 Creatine nitrate supplementation strengthens energy status and delays glycolysis of broiler muscle via inhibition of LKB1/AMPK pathway. Creatine 0-8 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 122-126 35007932-0 2022 Creatine nitrate supplementation strengthens energy status and delays glycolysis of broiler muscle via inhibition of LKB1/AMPK pathway. Nitrates 9-16 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 122-126 35265264-0 2022 Naringin protects human nucleus pulposus cells against TNF-alpha-induced inflammation, oxidative stress, and loss of cellular homeostasis by enhancing autophagic flux via AMPK/SIRT1 activation. naringin 0-8 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 171-175 35265264-8 2022 These findings indicate that naringin boosts autophagic flux through SIRT1 upregulation via AMPK activation, thus protecting NP cells against inflammatory response, oxidative stress, and impaired cellular homeostasis. naringin 29-37 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 92-96 35178649-5 2022 Resveratrol-treated AML-12 hepatocytes showed reduced ratio of the following key metabolic factors: phosphorylated PP2A to total PP2A (pPP2A/PP2A), pAKT/AKT, pFOXO1/FOXO1 and pAMPK/AMPK, indicating inhibition of AKT and AMPK, but activation of PP2A and FOXO1. Resveratrol 0-11 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 220-224 35018944-0 2022 Ginsenoside CK ameliorates hepatic lipid accumulation via activating the LKB1/AMPK pathway in vitro and in vivo. ginsenoside M1 0-14 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 78-82 35018944-9 2022 Mechanically, ginsenoside CK modulated the expression of factors correlated with lipid synthesis and metabolism in vitro and in vivo via activating the phosphorylation of LKB1 and AMPK. Ginsenosides 14-25 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 180-184 35216170-5 2022 The activity of AMPK can be stimulated with the phytochemical berberine. Berberine 62-71 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 16-20 35018944-11 2022 In summary, ginsenoside CK acts as a LKB1/AMPK agonist to regulate the lipid metabolism and interfere with the progression of NAFLD. Ginsenosides 12-23 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 42-46 35085325-5 2022 Other compounds including etomoxir, triacsin-c, PTB1-IN-3, are known to modulate lipid metabolism or to favor catabolic reactions by activating AMPK. etomoxir 26-34 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 144-148 35121743-7 2022 This metabolic switch further correlated with AMPK mediated inhibition of the prolipogenic factor acetyl coenzyme A carboxylase 1 (ACC1), which is known to initiate fatty acid catabolism. Fatty Acids 165-175 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 46-50 35062059-6 2022 Inducing AMPK signaling promotes glucose in DM that is of importance for ameliorating hyperglycemia. Glucose 33-40 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 9-13 35007761-6 2022 AMPK activator (AICAR) inhibited the changes of p-AMPK, ACC, and FAS expression and elevation of glucose and triglyceride levels induced by BDE-209. decabromobiphenyl ether 140-147 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 50-54 35007761-7 2022 DNA methylation inhibitor (5-Aza-CdR) reversed BDE-209 induced alters of PKA/AMPK/ACC/FAS signaling pathway. Decitabine 27-36 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 77-81 35007761-7 2022 DNA methylation inhibitor (5-Aza-CdR) reversed BDE-209 induced alters of PKA/AMPK/ACC/FAS signaling pathway. decabromobiphenyl ether 47-54 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 77-81 35007761-8 2022 These results demonstrated that BDE-209 could disrupt the glycolipid metabolism by causing PRKACA-1 hypermethylation to regulate the PKA/AMPK signaling pathway in hepatocytes. decabromobiphenyl ether 32-39 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 137-141 35007761-8 2022 These results demonstrated that BDE-209 could disrupt the glycolipid metabolism by causing PRKACA-1 hypermethylation to regulate the PKA/AMPK signaling pathway in hepatocytes. Glycolipids 58-68 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 137-141 35001346-0 2022 Procyanidin A1 alleviates DSS-induced ulcerative colitis via regulating AMPK/mTOR/p70S6K-mediated autophagy. Dextran Sulfate 26-29 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 72-76 35001346-10 2022 Meanwhile, the reduced AMP/ATP ratio, enhanced expression of p-AMPK, and decreased p-p70S6K and p-mTOR levels indicate the activation of AMPK/mTOR/p70S6K signaling pathway. Adenosine Monophosphate 23-26 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 137-141 35001346-10 2022 Meanwhile, the reduced AMP/ATP ratio, enhanced expression of p-AMPK, and decreased p-p70S6K and p-mTOR levels indicate the activation of AMPK/mTOR/p70S6K signaling pathway. Adenosine Triphosphate 27-30 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 137-141 34981417-5 2022 Moreover, by performing a molecular docking analysis, we demonstrated that BCA interacts with AMPK residues and impairs autophagy by regulating the AMPK/ULK1 pathway. biochanin A 75-78 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 94-98 34981417-5 2022 Moreover, by performing a molecular docking analysis, we demonstrated that BCA interacts with AMPK residues and impairs autophagy by regulating the AMPK/ULK1 pathway. biochanin A 75-78 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 148-152 35085325-5 2022 Other compounds including etomoxir, triacsin-c, PTB1-IN-3, are known to modulate lipid metabolism or to favor catabolic reactions by activating AMPK. triacsin C 36-46 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 144-148 35072253-4 2022 The mechanism of the antitumor action of metformin is pleiotropic and involves several signalling pathways, including AMPK/mTOR (mitogen activated protein kinase/mammalian target rapamycin), STAT3 (signal transducer and activator of transcription) and numerous factors: NF-KB (nuclear factor kappa), HIF-1 alpha (hypoxia inducible factor 1), IGF-1 (insulin-like growth factor-1), which affect cell proliferation and apoptosis. Metformin 41-50 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 118-122 35075260-10 2022 Low glucose levels increased cellular stress levels, autophagy activity, and enhanced glucose metabolism through the LKB1-AMPK signaling pathway, providing more ATPs to promote wound healing. Glucose 4-11 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 122-126 34709566-9 2022 ISO treatment induced the phosphorylation of AMP-activated protein kinase (AMPK) activation, subsequently the phosphorylation of mammalian target of rapamycin (mTOR) inhibition and peroxisome proliferators-activated receptor alpha (PPARalpha) activation in WT rats, whereas activation of AMPK/mTOR/PPARalpha pathways significantly inhibited in Ucp1-/- rats. Isoproterenol 0-3 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 45-73 34709566-9 2022 ISO treatment induced the phosphorylation of AMP-activated protein kinase (AMPK) activation, subsequently the phosphorylation of mammalian target of rapamycin (mTOR) inhibition and peroxisome proliferators-activated receptor alpha (PPARalpha) activation in WT rats, whereas activation of AMPK/mTOR/PPARalpha pathways significantly inhibited in Ucp1-/- rats. Isoproterenol 0-3 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 75-79 35075260-10 2022 Low glucose levels increased cellular stress levels, autophagy activity, and enhanced glucose metabolism through the LKB1-AMPK signaling pathway, providing more ATPs to promote wound healing. Glucose 86-93 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 122-126 35075260-10 2022 Low glucose levels increased cellular stress levels, autophagy activity, and enhanced glucose metabolism through the LKB1-AMPK signaling pathway, providing more ATPs to promote wound healing. Adenosine Triphosphate 161-165 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 122-126 35162967-0 2022 Quercetin Reduces Lipid Accumulation in a Cell Model of NAFLD by Inhibiting De Novo Fatty Acid Synthesis through the Acetyl-CoA Carboxylase 1/AMPK/PP2A Axis. Quercetin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 142-146 35082605-6 2021 Using the Oli-neuM cell line, we show that GSA-10 promotes Gli2 upregulation, MBP and MAL/OPALIN expression via Smo/AMP-activated Protein Kinase (AMPK) signaling, and efficiently increases the number of axonal contact/ensheathment for each oligodendroglial cell. GSA-10 43-49 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 146-150 35165542-6 2022 LKB1-deficient cancer cells contain an overactive AMPK "energy sensor," which inhibits cellular death and promotes glucose, lipid, and protein synthesis via the mTOR protein complex. Glucose 115-122 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 50-54 35252556-2 2022 In this preclinical study, vorolanib demonstrated competitive binding and inhibitory activities with KDR, PDGFRbeta, FLT3, and C-Kit, and inhibited RET and AMPKalpha1 more weakly than sunitinib, indicating more stringent kinase selectivity. 20,21-epoxyresibufogenin-3-formate 27-36 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 156-166 35053438-7 2022 CAPE induced the ERK/JNK/p38/AMPKalpha1/2 signaling pathways; however, pretreatment with the corresponding inhibitors of MAPK or AMPK1/2 did not inhibit the CAPE effect on MALT1 blocking in PC-3 cells. caffeic acid phenethyl ester 0-4 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 29-41 35162967-0 2022 Quercetin Reduces Lipid Accumulation in a Cell Model of NAFLD by Inhibiting De Novo Fatty Acid Synthesis through the Acetyl-CoA Carboxylase 1/AMPK/PP2A Axis. Fatty Acids 84-94 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 142-146 35162967-8 2022 The high level of ACACA phosphorylation in Que-treated cells was explained by the intervention of AMPK together with the reduction of enzymatic activity of PP2A phosphatase. Quercetin 43-46 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 98-102 35162967-9 2022 Overall, our findings highlight a direct anti-lipogenic effect of Que exerted through inhibition of the DNL pathway by acting on ACACA/AMPK/PP2A axis; thus, suggesting this flavonoid as a promising molecule for the NAFLD treatment. Quercetin 66-69 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 135-139 34525916-5 2022 Data reported for hydroxytyrosol suggest that the activation of the hepatic PPAR-alpha-FGF21-AMPK-PGC-1alpha signaling cascade is associated with fatty acid oxidation enhancement, de novo lipogenesis diminution and recovery of mitochondrial function, a contention that is supported by the actions of several polyphenols on specific components of this signaling pathway. 3,4-dihydroxyphenylethanol 18-32 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 93-97 34525916-5 2022 Data reported for hydroxytyrosol suggest that the activation of the hepatic PPAR-alpha-FGF21-AMPK-PGC-1alpha signaling cascade is associated with fatty acid oxidation enhancement, de novo lipogenesis diminution and recovery of mitochondrial function, a contention that is supported by the actions of several polyphenols on specific components of this signaling pathway. Fatty Acids 146-156 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 93-97 34525916-5 2022 Data reported for hydroxytyrosol suggest that the activation of the hepatic PPAR-alpha-FGF21-AMPK-PGC-1alpha signaling cascade is associated with fatty acid oxidation enhancement, de novo lipogenesis diminution and recovery of mitochondrial function, a contention that is supported by the actions of several polyphenols on specific components of this signaling pathway. Polyphenols 308-319 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 93-97 33400820-9 2021 AraA, an AMPK inhibitor, reversed the effects of CTRP6 on TNF-alpha-induced alterations in the levels of SIRT1, miR-34a-5p, Bcl-2, and cleaved caspase 3 in vitro and ex vivo, whereas activating AMPK by AICAR reversed the decrease in SIRT1 expression and increase in miR-34a-5p expression induced by TNF-alpha. Vidarabine 0-4 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 9-13 34969758-0 2022 Eupatilin Suppresses Pancreatic Cancer Cells via Glucose Uptake Inhibition, AMPK Activation, and Cell Cycle Arrest. eupatilin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 76-80 34969758-6 2022 Eupatilin decreased glucose uptake in pancreatic cancer, which led to cell starvation and AMPK activation. eupatilin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 90-94 34969758-6 2022 Eupatilin decreased glucose uptake in pancreatic cancer, which led to cell starvation and AMPK activation. Glucose 20-27 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 90-94 35368865-13 2022 Moreover, the decreased ATP production induced by Drp1 overexpressing activated the AMPK cellular energy stress sensor and enhanced autophagy through the AMPK-ULK1 pathway, which might play a protective role in PA growth. Adenosine Triphosphate 24-27 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 84-88 35368865-13 2022 Moreover, the decreased ATP production induced by Drp1 overexpressing activated the AMPK cellular energy stress sensor and enhanced autophagy through the AMPK-ULK1 pathway, which might play a protective role in PA growth. Adenosine Triphosphate 24-27 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 154-158 33945864-0 2021 Aconitine induces mitochondrial energy metabolism dysfunction through inhibition of AMPK signaling and interference with mitochondrial dynamics in SH-SY5Y cells. Aconitine 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 84-88 33945864-6 2021 Phosphorylation of AMPK was significantly reduced in aconitine-treated SH-SY5Y cells. Aconitine 53-62 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 19-23 33945864-7 2021 The AMPK activator AIACR pretreatment effectively promoted ATP production to ameliorate mitochondrial energy metabolism disorder caused by aconitine. Adenosine Triphosphate 59-62 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 4-8 33945864-7 2021 The AMPK activator AIACR pretreatment effectively promoted ATP production to ameliorate mitochondrial energy metabolism disorder caused by aconitine. Aconitine 139-148 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 4-8 33945864-10 2021 These results suggest that aconitine induces mitochondrial energy metabolism dysfunction in SH-SY5Y cells, which may involve the inhibition of AMPK signaling and abnormal mitochondrial dynamics. Aconitine 27-36 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 143-147 33400820-9 2021 AraA, an AMPK inhibitor, reversed the effects of CTRP6 on TNF-alpha-induced alterations in the levels of SIRT1, miR-34a-5p, Bcl-2, and cleaved caspase 3 in vitro and ex vivo, whereas activating AMPK by AICAR reversed the decrease in SIRT1 expression and increase in miR-34a-5p expression induced by TNF-alpha. Vidarabine 0-4 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 194-198 33639357-0 2021 Ghrelin protects against rotenone-induced cytotoxicity: Involvement of mitophagy and the AMPK/SIRT1/PGC1alpha pathway. Ghrelin 0-7 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 89-93 33788127-1 2021 OBJECTIVE: To investigate the efficacy and safety of the AMPK activator AICAR alone or in combination with decitabine on myelodysplastic syndromes (MDS). AICA ribonucleotide 72-77 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 57-61 33549532-8 2021 Analysis of protein expression demonstrated that 2-DG treatment induced an activation of AMPK (elevated pAMPK/AMPK ratio), increased mitochondrial fusion (mitofusins 1 and 2) and decreased fission (Drp1) proteins. Deoxyglucose 49-53 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 89-93 33549532-8 2021 Analysis of protein expression demonstrated that 2-DG treatment induced an activation of AMPK (elevated pAMPK/AMPK ratio), increased mitochondrial fusion (mitofusins 1 and 2) and decreased fission (Drp1) proteins. Deoxyglucose 49-53 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 104-114 33125640-0 2021 Icaritin Inhibits Skin Fibrosis through Regulating AMPK and Wnt/beta-catenin Signaling. icaritin 0-8 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 51-55 33639357-0 2021 Ghrelin protects against rotenone-induced cytotoxicity: Involvement of mitophagy and the AMPK/SIRT1/PGC1alpha pathway. Rotenone 25-33 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 89-93 33639357-8 2021 Additionally, we investigated that ghrelin activated the AMPK/SIRT1/PGC1alpha pathway and pharmacological inhibition of AMPK and SIRT1 abolished the cytoprotection of ghrelin, decreased the level of mitophagy, and PINK1/Parkin mitochondrial translocation. Ghrelin 35-42 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 57-61 33639357-8 2021 Additionally, we investigated that ghrelin activated the AMPK/SIRT1/PGC1alpha pathway and pharmacological inhibition of AMPK and SIRT1 abolished the cytoprotection of ghrelin, decreased the level of mitophagy, and PINK1/Parkin mitochondrial translocation. Ghrelin 167-174 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 120-124 33639357-9 2021 Taken together, our findings suggested that mitophagy and AMPK/SIRT1/PGC1alpha pathways were related to the cytoprotection of ghrelin. Ghrelin 126-133 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 58-62 34050352-8 2021 Interestingly, we also found that the expression of AMPK and GCN2 was significantly up-regulated in the endometrium of women with RM, and the same expression trend was also observed in the human endometrial stromal cells cultured in glutamine deprivation medium. Glutamine 233-242 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 52-56 34050207-8 2021 Upon exploring the mechanism of hypertonic stress on eNOS O-GlcNAc activity and function, we found that hypertonic stress can upregulate the expression of O-linked N-acetylglucosamine (GlcNAc) transferase (OGT), which is dependent on AMPK. o-glcnac 58-66 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 234-238 34050207-9 2021 When AMPK was knocked out, the upregulation of OGT expression and increased O-GlcNAc modifications induced by hypertonic stress were reversed. o-glcnac 76-84 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 5-9 34027849-5 2021 Moreover, chronic excess alcohol consumption may result in gut microbiota dysbiosis and autophagy-induced hyperammonemia, initiating the upregulation of muscle protein breakdown and downregulation of MPS via activation of myostatin, AMPK, and REDD1, and deactivation of IGF-1. Alcohols 25-32 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 233-237 33891090-0 2021 Resveratrol induces AMPK and mTOR signaling inhibition-mediated autophagy and apoptosis in multiple myeloma cells. Resveratrol 0-11 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 20-24 34019608-4 2021 A special fraction, SLs, was found to significantly increase the viability of EtOH-treated cells and attenuated EtOH-induced apoptosis partially via the activation of the AMPK/SIRT1 signaling pathway. Ethanol 112-116 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 171-175 34010493-14 2021 Knockdown of SLC45A4 reduced glucose uptake and ATP production which led to activation of autophagy via AMPK/ULK1 pathway. Glucose 29-36 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 104-108 33749723-4 2021 Patient cells had a complex I deficiency that resulted in an increased NADH/NAD+ ratio, diminished TCA cycle activity, a reorganization of one carbon metabolism, and an increased AMP/ATP ratio leading to phosphorylation of AMPK and inhibition of mTORC1. Adenosine Monophosphate 179-182 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 223-227 33749723-4 2021 Patient cells had a complex I deficiency that resulted in an increased NADH/NAD+ ratio, diminished TCA cycle activity, a reorganization of one carbon metabolism, and an increased AMP/ATP ratio leading to phosphorylation of AMPK and inhibition of mTORC1. Adenosine Triphosphate 183-186 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 223-227 33988807-0 2021 Flavonoids modulate AMPK/PGC-1alpha and interconnected pathways toward potential neuroprotective activities. Flavonoids 0-10 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 20-24 33988807-8 2021 In this line, critical role of flavonoids in the upregulation of AMPK/PGC-1alpha pathway seems to pave the road in the treatment of Alzheimer"s disease (AD), Parkinson"s disease (PD), aging, central nervous system (brain/spinal cord) damages, stroke, and other NDDs. Flavonoids 31-41 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 65-69 33988807-9 2021 In the present study, the regulatory role of flavonoids in managing various NDDs has been shown to pass through AMPK/PGC-1alpha signaling pathway. Flavonoids 45-55 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 112-116 33980612-2 2021 To identify genome-wide metabolic-stress regulated genes, we used RNA-Seq in ALL cells treated with AICAR, an AMPK activator. AICA ribonucleotide 100-105 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 110-114 33955148-0 2021 Radiosensitizing effects of curcumin alone or combined with GLUT1 siRNA on laryngeal carcinoma cells through AMPK pathway-induced autophagy. Curcumin 28-36 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 109-113 33788127-3 2021 AMPK agonist AICAR inhibited the proliferation of MDS cell lines (SKM1 and MDS-L) (P < 0.05). AICA ribonucleotide 13-18 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 33655768-0 2021 Impact of hypoxia and AMPK on CFTR-mediated bicarbonate secretion in human cholangiocyte organoids. Bicarbonates 44-55 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 22-26 33094480-9 2021 Small interfering RNA of SEPP1 inhibited TG accumulation by activating adenosine monophosphate activated protein kinase/acetyl-CoA carboxylase (AMPK/ACC), and overexpression of SEPP1 aggravated lipid accumulation and inhibited AMPK/ACC phosphorylation. Thioguanine 41-43 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 144-148 32860006-0 2021 Pyrroloquinoline quinone promotes mitochondrial biogenesis in rotenone-induced Parkinson"s disease model via AMPK activation. PQQ Cofactor 0-24 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 109-113 32860006-0 2021 Pyrroloquinoline quinone promotes mitochondrial biogenesis in rotenone-induced Parkinson"s disease model via AMPK activation. Rotenone 62-70 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 109-113 32860006-9 2021 We conducted Western blot analysis and confirmed that AMPK was activated by PQQ both in PD mice and in rotenone-injured SH-SY5Y cells. Rotenone 103-111 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 54-58 32860006-10 2021 Pretreatment with AMPK inhibitor dorsomorphin (4 muM) significantly attenuated the protective effect and mitochondrial biogenesis by PQQ treatment in rotenone-injured SH-SY5Y cells. dorsomorphin 33-45 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 18-22 32860006-10 2021 Pretreatment with AMPK inhibitor dorsomorphin (4 muM) significantly attenuated the protective effect and mitochondrial biogenesis by PQQ treatment in rotenone-injured SH-SY5Y cells. PQQ Cofactor 133-136 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 18-22 32860006-10 2021 Pretreatment with AMPK inhibitor dorsomorphin (4 muM) significantly attenuated the protective effect and mitochondrial biogenesis by PQQ treatment in rotenone-injured SH-SY5Y cells. Rotenone 150-158 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 18-22 32860006-11 2021 Taken together, PQQ promotes mitochondrial biogenesis in rotenone-injured mice and SH-SY5Y cells via activation of AMPK signaling pathway. PQQ Cofactor 16-19 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 115-119 33742560-2 2021 In addition, the biguanide derivative phenformin exhibits antitumor activity superior to that of the AMPK activator metformin. Metformin 116-125 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 101-105 33377581-9 2021 In sum, Dex activated the PPARdelta-AMPK-PGC-1alpha pathway-mediated autophagy, therefore to inhibit OGD/R-induced cell apoptosis in CMECs. Dexmedetomidine 8-11 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 36-40 33846805-0 2021 PRIMA-1met induces autophagy in colorectal cancer cells through upregulation of the mTOR/AMPK-ULK1-Vps34 signaling cascade. eprenetapopt 0-10 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 89-93 33846805-6 2021 The study indicated that activation of the mTOR/AMPK-ULK1-Vps34 autophagic signaling cascade was key for PRIMA-1met-induced autophagy. eprenetapopt 105-115 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 48-52 33737241-0 2021 Hyperoside relieves particulate matter-induced lung injury by inhibiting AMPK/mTOR-mediated autophagy deregulation. hyperoside 0-10 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 73-77 33737241-6 2021 This cytotoxicity of O-PMs was attenuated by Hyp pretreatment in parallel with downregulation of the expression of autophagy markers, apoptotic proteins, and p-AMPK and upregulation of p-mTOR expression. o-pms 21-26 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 160-164 33737241-10 2021 These findings indicate that Hyp protects against PMs-induced lung injury by suppressing autophagy deregulation and apoptosis through regulation of the AMPK/mTOR pathway. hyperoside 29-32 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 152-156 33737241-10 2021 These findings indicate that Hyp protects against PMs-induced lung injury by suppressing autophagy deregulation and apoptosis through regulation of the AMPK/mTOR pathway. Promethium 50-53 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 152-156 33819767-0 2021 Ginsenoside-Rg2 affects cell growth via regulating ROS-mediated AMPK activation and cell cycle in MCF-7 cells. ginsenoside Rg2 0-15 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 64-68 33819767-0 2021 Ginsenoside-Rg2 affects cell growth via regulating ROS-mediated AMPK activation and cell cycle in MCF-7 cells. Reactive Oxygen Species 51-54 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 64-68 33819767-10 2021 G-Rg2-induced ROS induced G0/G1 cell cycle arrest and AMPK phosphorylation. ginsenoside Rg2 0-5 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 54-58 33819767-12 2021 Immunohistochemistry staining showed that G-Rg2 treatment decreased Rb phosphorylation, while increasing AMPK phosphorylation in tumor tissues. ginsenoside Rg2 42-47 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 105-109 33819767-13 2021 CONCLUSION: G-Rg2 has potential anticancer effects by increasing the ROS-AMPK signaling pathway and inhibiting ERK1/2 and Akt activation-mediated cell proliferation and cell cycle progression in MCF-7 BC cells. ginsenoside Rg2 12-17 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 73-77 33819767-13 2021 CONCLUSION: G-Rg2 has potential anticancer effects by increasing the ROS-AMPK signaling pathway and inhibiting ERK1/2 and Akt activation-mediated cell proliferation and cell cycle progression in MCF-7 BC cells. Reactive Oxygen Species 69-72 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 73-77 32791889-13 2021 Metformin treatment decreased the FRO- or SW1736-CM-induced STAT3 phosphorylation by AMPK phosphorylation. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 85-89 33709560-0 2021 Quercetin induces pro-apoptotic autophagy via SIRT1/AMPK signaling pathway in human lung cancer cell lines A549 and H1299 in vitro. Quercetin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 52-56 33709560-14 2021 CONCLUSIONS: Quercetin-induced autophagy contributes to apoptosis in A549 and H1299 lung cancer cells, which involved the SIRT1/AMPK signaling pathway. Quercetin 13-22 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 128-132 33995638-15 2021 A MTFR2-protein interaction network revealed a potential direct protein interaction between MTFR2 and protein kinase adenosine-monophosphate-activated catalytic subunit alpha 1 (PRKAA1), and their potential binding site was predicted in a molecular docking model. Adenosine 117-126 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 178-184 33886150-9 2021 Moreover, cotreating the cells with metformin (30 mM) and pitavastatin (10 muM) could preserve mitochondrial function, activate AMPK, and inhibit PI3K/mTOR than treatment with metformin or pitavastatin alone. Metformin 36-45 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 128-132 33886150-9 2021 Moreover, cotreating the cells with metformin (30 mM) and pitavastatin (10 muM) could preserve mitochondrial function, activate AMPK, and inhibit PI3K/mTOR than treatment with metformin or pitavastatin alone. pitavastatin 58-70 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 128-132 33886150-10 2021 These findings clearly indicated that metformin plus pitavastatin had a synergistic anticancer effect on pancreatic cancer cells, potentially caused due to the activation of AMPK and inhibition of PI3K/mTOR signaling. Metformin 38-47 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 174-178 33044023-8 2021 Furthermore, we found that exenatide activates the AMPK-SKP2-CARM1 and AMPK-mTOR signaling pathways, which likely lead to exenatide"s effects on activating TFE3. Exenatide 27-36 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 51-55 33044023-8 2021 Furthermore, we found that exenatide activates the AMPK-SKP2-CARM1 and AMPK-mTOR signaling pathways, which likely lead to exenatide"s effects on activating TFE3. Exenatide 27-36 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 71-75 33044023-8 2021 Furthermore, we found that exenatide activates the AMPK-SKP2-CARM1 and AMPK-mTOR signaling pathways, which likely lead to exenatide"s effects on activating TFE3. Exenatide 122-131 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 51-55 33044023-8 2021 Furthermore, we found that exenatide activates the AMPK-SKP2-CARM1 and AMPK-mTOR signaling pathways, which likely lead to exenatide"s effects on activating TFE3. Exenatide 122-131 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 71-75 33888740-4 2021 In this sense, Metformin (MET), an FDA-approved drug used for the treatment of type 2 diabetes, has shown an anti-DENV effect in vitro by activating AMPK and reducing HMGCR activity. Metformin 15-24 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 149-153 33879068-8 2021 These modules are primarily involved in the metabolic processes of prostaglandin transport processes, regulating DNA recombination and AMPK signal transduction. Prostaglandins 67-80 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 135-139 33872672-5 2021 Increased ROS levels can regulate autophagy through several different pathways, such as activation of the AMPK signalling cascade and ULK1 complex, Atg4 oxidation, disruption of the Bcl-2/Beclin-1 interaction, and alteration of mitochondrial homeostasis leading to mitophagy. Reactive Oxygen Species 10-13 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 106-110 33843441-7 2021 Furthermore, we showed that ROS originating from mitochondria (mtROS) probably activated the AMPK-ULK1 axis to trigger ferritinophagy. Reactive Oxygen Species 28-31 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 93-97 33898327-0 2021 Camptothecin Inhibits Neddylation to Activate the Protective Autophagy Through NF-kappaB/AMPK/mTOR/ULK1 Axis in Human Esophageal Cancer Cells. Camptothecin 0-12 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 89-93 33898327-7 2021 Furthermore, CPT induced the generation of ROS to modulate the AMPK/mTOR/ULK1 axis to finally promote protective autophagy. ros 43-46 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 63-67 33749503-5 2021 AMPK phosphorylation and MTOR dephosphorylation were also detected, and block of AMPK activity by the AMPK inhibitor dorsomorphin could reverse SQSTM1 degradation and LC3-II formation. dorsomorphin 117-129 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 33749503-5 2021 AMPK phosphorylation and MTOR dephosphorylation were also detected, and block of AMPK activity by the AMPK inhibitor dorsomorphin could reverse SQSTM1 degradation and LC3-II formation. dorsomorphin 117-129 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 81-85 33749503-5 2021 AMPK phosphorylation and MTOR dephosphorylation were also detected, and block of AMPK activity by the AMPK inhibitor dorsomorphin could reverse SQSTM1 degradation and LC3-II formation. dorsomorphin 117-129 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 81-85 33886150-10 2021 These findings clearly indicated that metformin plus pitavastatin had a synergistic anticancer effect on pancreatic cancer cells, potentially caused due to the activation of AMPK and inhibition of PI3K/mTOR signaling. pitavastatin 53-65 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 174-178 33916835-6 2021 The reduction of protein O-GlcNAcylation was associated with the development of insulin resistance, induced by overfeeding (i.e., defective insulin signaling and reduced mitochondrial activity), which promoted the dysregulation of the hexosamine biosynthetic pathway (HBP) flux, through the AMPK-driven reduction of GFAT1 activation. Hexosamines 235-245 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 291-295 33609560-0 2021 Fangchinoline exerts anticancer effects on colorectal cancer by inducing autophagy via regulation AMPK/mTOR/ULK1 pathway. fangchinoline 0-13 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 98-102 33097833-4 2021 Mechanistically, ferroptosis inducers (erastin, sorafenib, and sulfasalazine) activated AMPK/SREBP1 signaling pathway through iron-dependent ferritinophagy, which in turn inhibited BCAT2 transcription. Sorafenib 48-57 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 88-92 33349646-0 2021 Aldolase is a sensor for both low and high glucose, linking to AMPK and mTORC1. Glucose 43-50 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 63-67 33097833-4 2021 Mechanistically, ferroptosis inducers (erastin, sorafenib, and sulfasalazine) activated AMPK/SREBP1 signaling pathway through iron-dependent ferritinophagy, which in turn inhibited BCAT2 transcription. Sulfasalazine 63-76 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 88-92 33502468-6 2021 Our results revealed that AMPK acutely inhibits the stimulatory effects of LH/PKA on progesterone production without reducing levels of STAR, CYP11A1 and HSD3B proteins. Progesterone 85-97 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 26-30 33502468-7 2021 Exogenous cholesterol reversed the negative effects of AMPK on LH-stimulated steroidogenesis, suggesting that AMPK regulates cholesterol availability in luteal cells. Cholesterol 10-21 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 55-59 33502468-7 2021 Exogenous cholesterol reversed the negative effects of AMPK on LH-stimulated steroidogenesis, suggesting that AMPK regulates cholesterol availability in luteal cells. Cholesterol 10-21 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 110-114 33502468-7 2021 Exogenous cholesterol reversed the negative effects of AMPK on LH-stimulated steroidogenesis, suggesting that AMPK regulates cholesterol availability in luteal cells. Cholesterol 125-136 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 55-59 33502468-7 2021 Exogenous cholesterol reversed the negative effects of AMPK on LH-stimulated steroidogenesis, suggesting that AMPK regulates cholesterol availability in luteal cells. Cholesterol 125-136 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 110-114 33502468-11 2021 The findings indicate that LH and AMPK exert opposite post-translational modifications of HSL, presumptively regulating cholesterol availability for steroidogenesis. Cholesterol 120-131 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 34-38 33444643-0 2021 Resveratrol: Change of SIRT 1 and AMPK signaling pattern during the aging process. Resveratrol 0-11 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 34-38 33097833-4 2021 Mechanistically, ferroptosis inducers (erastin, sorafenib, and sulfasalazine) activated AMPK/SREBP1 signaling pathway through iron-dependent ferritinophagy, which in turn inhibited BCAT2 transcription. Iron 126-130 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 88-92 33789726-0 2021 Glioblastoma stem cell (GSC)-derived PD-L1-containing exosomes activates AMPK/ULK1 pathway mediated autophagy to increase temozolomide-resistance in glioblastoma. Temozolomide 122-134 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 73-77 33789726-2 2021 In the present study, we reported that GSCs derived programmed death-ligand 1 (PD-L1) containing exosomes activated AMPK/ULK1 pathway mediated protective autophagy enhanced TMZ-resistance in GBM in vitro and in vivo. Temozolomide 173-176 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 116-120 33789726-5 2021 In addition, PD-L1-ex activated AMPK/ULK1 pathway to induce autophagy in TMZ treated GBM cells, and the inhibitors for AMPK (compound C) and ULK1 (SBI-0206965) promoted cell apoptosis in GBM cells co-treated with PD-L1-ex and high-dose TMZ. Temozolomide 73-76 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 32-36 33867841-10 2021 Knockdown STIM1 with siRNA or pharmacological inhibition of SOCE attenuated DIM induced apoptosis and autophagy by inhibiting p-AMPK mediated ER stress pathway. 3,3'-diindolylmethane 76-79 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 128-132 33444643-3 2021 The objective this study was to verify in an oxidative stress environment in Human Mononuclear cells from Middle aged and Elderly donors, the existence of a change in the SIRT1 and AMPK signaling pattern by RSV. Resveratrol 207-210 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 181-185 33444643-9 2021 RSV has an antioxidant action in both age groups, and that in aging there was a change in the cellular context characterized by the silencing of the AMPK pathway antioxidant character. Resveratrol 0-3 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 149-153 33694332-1 2021 Progressive neuronal injury following ischaemic stroke is associated with glutamate-induced depolarisation, energetic stress and activation of AMP-activated protein kinase (AMPK). Glutamic Acid 74-83 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 143-171 33694332-3 2021 We report a robust induction of microRNA miR-210-3p both in vitro in primary cortical neurons in response to acute AMPK activation and following ischaemic stroke in vivo. mir-210-3p 41-51 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 115-119 33243500-4 2021 Besides, Mo or/and Cd elevated the number of autophagosome and microtubule-associated protein light chain 3 (LC3) puncta, upregulated mRNA levels of Beclin-1, LC3A, LC3B, Atg5 and adenosine 5"-monophosphate (AMP)-activated protein kinase alpha1 (AMPKalpha-1), inhibited Dynein, p62 and mammalian target of rapamycin (mTOR) mRNA levels, increased Beclin-1 and LC3II/LC3I protein levels. Cadmium 19-21 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 246-257 33693699-1 2021 The Snf1-Related Protein Kinase 1 (SnRK1) is the plant homolog of the heterotrimeric AMP-activated Protein Kinase/ Sucrose Non-Fermenting 1 (AMPK/Snf1), which works as a major regulator of growth under nutrient-limiting conditions in eukaryotes. Sucrose 115-122 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 141-145 33705741-8 2021 Additionally, we observed increased expression of the demethylated genes, which are involved in the master signaling pathways, including MAPK-ERK, calcium-AMPK, and type II diabetes mellitus pathways. Calcium 147-154 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 155-159 33664417-4 2021 Caffeine (50 muM) enhanced endothelial migration via activation of cAMP/PKA/AMPK signaling pathway, which was mimicked by cAMP analog 8-Br-cAMP, and blocked by PKA inhibitor H89, adenylate cyclase inhibitor SQ22536 or AMPK inhibitor compound C. Furthermore, caffeine (50 muM) induced significant mitochondrial shortening through the increased phosphorylation of mitochondrial fission protein dynamin-related protein 1 (Drp1) in HUVECs, which increased its activity to regulate mitochondrial fission. Caffeine 0-8 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 76-80 33482179-7 2021 Furthermore, significant upregulation of markers of mitochondrial biogenesis PGC-1alpha, COX IV, TFAM, and phosphorylation of AMPKalpha1 (Ser485) was observed in THP-1 cells and livers of mice treated with Dox in combination with fidarestat. Doxorubicin 206-209 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 126-136 33657393-0 2021 The phytochemical hyperforin triggers thermogenesis in adipose tissue via a Dlat-AMPK signaling axis to curb obesity. hyperforin 18-28 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 81-85 33664417-4 2021 Caffeine (50 muM) enhanced endothelial migration via activation of cAMP/PKA/AMPK signaling pathway, which was mimicked by cAMP analog 8-Br-cAMP, and blocked by PKA inhibitor H89, adenylate cyclase inhibitor SQ22536 or AMPK inhibitor compound C. Furthermore, caffeine (50 muM) induced significant mitochondrial shortening through the increased phosphorylation of mitochondrial fission protein dynamin-related protein 1 (Drp1) in HUVECs, which increased its activity to regulate mitochondrial fission. Caffeine 0-8 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 218-222 33664417-4 2021 Caffeine (50 muM) enhanced endothelial migration via activation of cAMP/PKA/AMPK signaling pathway, which was mimicked by cAMP analog 8-Br-cAMP, and blocked by PKA inhibitor H89, adenylate cyclase inhibitor SQ22536 or AMPK inhibitor compound C. Furthermore, caffeine (50 muM) induced significant mitochondrial shortening through the increased phosphorylation of mitochondrial fission protein dynamin-related protein 1 (Drp1) in HUVECs, which increased its activity to regulate mitochondrial fission. Cyclic AMP 67-71 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 76-80 33664417-4 2021 Caffeine (50 muM) enhanced endothelial migration via activation of cAMP/PKA/AMPK signaling pathway, which was mimicked by cAMP analog 8-Br-cAMP, and blocked by PKA inhibitor H89, adenylate cyclase inhibitor SQ22536 or AMPK inhibitor compound C. Furthermore, caffeine (50 muM) induced significant mitochondrial shortening through the increased phosphorylation of mitochondrial fission protein dynamin-related protein 1 (Drp1) in HUVECs, which increased its activity to regulate mitochondrial fission. Cyclic AMP 67-71 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 218-222 33664417-4 2021 Caffeine (50 muM) enhanced endothelial migration via activation of cAMP/PKA/AMPK signaling pathway, which was mimicked by cAMP analog 8-Br-cAMP, and blocked by PKA inhibitor H89, adenylate cyclase inhibitor SQ22536 or AMPK inhibitor compound C. Furthermore, caffeine (50 muM) induced significant mitochondrial shortening through the increased phosphorylation of mitochondrial fission protein dynamin-related protein 1 (Drp1) in HUVECs, which increased its activity to regulate mitochondrial fission. Cyclic AMP 122-126 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 76-80 33664417-4 2021 Caffeine (50 muM) enhanced endothelial migration via activation of cAMP/PKA/AMPK signaling pathway, which was mimicked by cAMP analog 8-Br-cAMP, and blocked by PKA inhibitor H89, adenylate cyclase inhibitor SQ22536 or AMPK inhibitor compound C. Furthermore, caffeine (50 muM) induced significant mitochondrial shortening through the increased phosphorylation of mitochondrial fission protein dynamin-related protein 1 (Drp1) in HUVECs, which increased its activity to regulate mitochondrial fission. 8-Bromo Cyclic Adenosine Monophosphate 134-143 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 76-80 33664417-4 2021 Caffeine (50 muM) enhanced endothelial migration via activation of cAMP/PKA/AMPK signaling pathway, which was mimicked by cAMP analog 8-Br-cAMP, and blocked by PKA inhibitor H89, adenylate cyclase inhibitor SQ22536 or AMPK inhibitor compound C. Furthermore, caffeine (50 muM) induced significant mitochondrial shortening through the increased phosphorylation of mitochondrial fission protein dynamin-related protein 1 (Drp1) in HUVECs, which increased its activity to regulate mitochondrial fission. 9-(tetrahydro-2-furyl)-adenine 207-214 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 76-80 33664417-4 2021 Caffeine (50 muM) enhanced endothelial migration via activation of cAMP/PKA/AMPK signaling pathway, which was mimicked by cAMP analog 8-Br-cAMP, and blocked by PKA inhibitor H89, adenylate cyclase inhibitor SQ22536 or AMPK inhibitor compound C. Furthermore, caffeine (50 muM) induced significant mitochondrial shortening through the increased phosphorylation of mitochondrial fission protein dynamin-related protein 1 (Drp1) in HUVECs, which increased its activity to regulate mitochondrial fission. Caffeine 258-266 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 76-80 33664417-7 2021 In a mouse model of hindlimb ischemia, administration of caffeine (0.05% in 200 mL drinking water daily, for 14 days) significantly promoted angiogenesis and perfusion as well as activation of endothelial AMPK signaling in the ischemic hindlimb. Caffeine 57-65 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 205-209 33664417-8 2021 Taken together, caffeine induces mitochondrial fission through cAMP/PKA/AMPK signaling pathway. Caffeine 16-24 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 72-76 33664417-8 2021 Taken together, caffeine induces mitochondrial fission through cAMP/PKA/AMPK signaling pathway. Cyclic AMP 63-67 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 72-76 33159186-4 2021 Here we propose that this increased ROS production not only causes oxidative damage but also ultimately induces an oxidative stress response that reactivates the redox-sensitive AMPK and activates the redox-sensitive stress kinase JNK. Reactive Oxygen Species 36-39 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 178-182 33168978-5 2021 We found that TLAM inhibits phosphofructokinase-1 (PFK1), which in turn activates AMPK-mediated fatty-acid oxidation to promote oxidative phosphorylation, and redirects carbon flow from glycolysis toward the pentose phosphate pathway to reinforce anti-oxidative potential. tlam 14-18 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 82-86 33168978-5 2021 We found that TLAM inhibits phosphofructokinase-1 (PFK1), which in turn activates AMPK-mediated fatty-acid oxidation to promote oxidative phosphorylation, and redirects carbon flow from glycolysis toward the pentose phosphate pathway to reinforce anti-oxidative potential. Fatty Acids 96-106 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 82-86 33168978-5 2021 We found that TLAM inhibits phosphofructokinase-1 (PFK1), which in turn activates AMPK-mediated fatty-acid oxidation to promote oxidative phosphorylation, and redirects carbon flow from glycolysis toward the pentose phosphate pathway to reinforce anti-oxidative potential. Pentosephosphates 208-225 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 82-86 33037751-0 2021 Apple polyphenol extract alleviates lipid accumulation in free-fatty-acid-exposed HepG2 cells via activating autophagy mediated by SIRT1/AMPK signaling. Polyphenols 6-16 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 137-141 33037751-0 2021 Apple polyphenol extract alleviates lipid accumulation in free-fatty-acid-exposed HepG2 cells via activating autophagy mediated by SIRT1/AMPK signaling. Fatty Acids, Nonesterified 58-73 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 137-141 33632157-0 2021 Blockage of AMPK-ULK1 pathway mediated autophagy promotes cell apoptosis to increase doxorubicin sensitivity in breast cancer (BC) cells: an in vitro study. Doxorubicin 85-96 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 12-16 33630415-4 2022 In diabetes and obesity, KPTCs are exposed to nutrient overload, including glucose, free-fatty acids (FFAs) and amino acids (AAs), which dysregulate nutrient and energy sensing by mTORC1 and AMPK, with subsequent induction of tubular injury, inflammation and fibrosis. Glucose 75-82 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 191-195 33630415-4 2022 In diabetes and obesity, KPTCs are exposed to nutrient overload, including glucose, free-fatty acids (FFAs) and amino acids (AAs), which dysregulate nutrient and energy sensing by mTORC1 and AMPK, with subsequent induction of tubular injury, inflammation and fibrosis. Fatty Acids, Nonesterified 84-100 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 191-195 33630415-4 2022 In diabetes and obesity, KPTCs are exposed to nutrient overload, including glucose, free-fatty acids (FFAs) and amino acids (AAs), which dysregulate nutrient and energy sensing by mTORC1 and AMPK, with subsequent induction of tubular injury, inflammation and fibrosis. Fatty Acids, Nonesterified 102-106 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 191-195 33630415-4 2022 In diabetes and obesity, KPTCs are exposed to nutrient overload, including glucose, free-fatty acids (FFAs) and amino acids (AAs), which dysregulate nutrient and energy sensing by mTORC1 and AMPK, with subsequent induction of tubular injury, inflammation and fibrosis. Amino Acids 125-128 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 191-195 33632157-3 2021 In the present study, we identified that inactivation of AMPK-ULK1 signaling cascade mediated protective autophagy sensitized BC cells to doxorubicin in vitro. Doxorubicin 138-149 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 57-61 33758601-10 2021 As suggested in functional annotation analysis, we found an intensive enrichment of these prhRBPs in metabolic pathways, including AMPK, HIF-1 signaling pathway, Glycolysis, and steroid hormone biosynthesis. Steroids 178-185 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 131-135 33593593-3 2021 Here, we highlight recently uncovered mechanisms linking amino acid, glucose, and oxygen levels to autophagy regulation through mTORC1 and AMPK. Oxygen 82-88 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 139-143 33634119-0 2021 Effect of Quercetin on Lipids Metabolism Through Modulating the Gut Microbial and AMPK/PPAR Signaling Pathway in Broilers. Quercetin 10-19 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 82-86 33634119-4 2021 In conclusion, quercetin improved lipid metabolism by modulating gut microbial and AMPK/PPAR signaling pathway in broilers. Quercetin 15-24 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 83-87 33443093-8 2021 Treatment with STO609 also suppressed synphilin-1-induced AMPK phosphorylation, hyperphagia and body weight gain. STO 609 15-21 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 58-62 33535040-4 2021 We show that the serine/threonine kinase LKB1 and one of its substrates, AMPK, regulate cone nuclear positioning. Serine 17-23 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 73-77 33458837-0 2021 The role of AMP-activated protein kinase alpha1-mediated endoplasmic reticulum stress in alleviating the toxic effect of uremic toxin indoxyl sulfate on vascular endothelial cells by Klotho. Indican 134-149 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 12-40 33495519-9 2021 Exendin-4 induced phosphorylation of AMPK and endothelial nitric oxide synthase in HUVECs and arteries. Exenatide 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 37-41 33483906-7 2021 IH-induced autophagic flux peaked at 12-h duration and weakened at 24 h. IH increased the ratio of p-AMPK/AMPK and decreased the ratio of p-mTOR/mTOR, while compound C restored the alteration. Ile-His 0-2 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 101-105 33483906-7 2021 IH-induced autophagic flux peaked at 12-h duration and weakened at 24 h. IH increased the ratio of p-AMPK/AMPK and decreased the ratio of p-mTOR/mTOR, while compound C restored the alteration. Ile-His 0-2 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 106-110 33483906-7 2021 IH-induced autophagic flux peaked at 12-h duration and weakened at 24 h. IH increased the ratio of p-AMPK/AMPK and decreased the ratio of p-mTOR/mTOR, while compound C restored the alteration. Ile-His 73-75 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 101-105 33483906-7 2021 IH-induced autophagic flux peaked at 12-h duration and weakened at 24 h. IH increased the ratio of p-AMPK/AMPK and decreased the ratio of p-mTOR/mTOR, while compound C restored the alteration. Ile-His 73-75 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 106-110 33483906-11 2021 CONCLUSIONS: IH upregulates autophagy through AMPK/mTOR pathway in HUVECs in vitro, which might be protective against endothelial apoptosis and dysfunction caused by IH. Ile-His 13-15 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 46-50 33632157-10 2021 In addition, we proved that high-dose doxorubicin triggered protective autophagy in DR-BC cells by activating AMPK-ULK1 pathway. Doxorubicin 38-49 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 110-114 33632157-11 2021 Functionally, high-dose doxorubicin increased the expression levels of phosphorylated AMPK (p-AMPK) and ULK1 (p-ULK1) to activate AMPK-ULK1 pathway in DR-BC cells, and the inhibitors for AMPK (compound C) and ULK1 (SBI-0206965) blocked autophagy to promote cell death and slow down cell growth in DR-BC cells treated with high-dose doxorubicin. Doxorubicin 24-35 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 86-90 33632157-11 2021 Functionally, high-dose doxorubicin increased the expression levels of phosphorylated AMPK (p-AMPK) and ULK1 (p-ULK1) to activate AMPK-ULK1 pathway in DR-BC cells, and the inhibitors for AMPK (compound C) and ULK1 (SBI-0206965) blocked autophagy to promote cell death and slow down cell growth in DR-BC cells treated with high-dose doxorubicin. Doxorubicin 24-35 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 94-98 33632157-11 2021 Functionally, high-dose doxorubicin increased the expression levels of phosphorylated AMPK (p-AMPK) and ULK1 (p-ULK1) to activate AMPK-ULK1 pathway in DR-BC cells, and the inhibitors for AMPK (compound C) and ULK1 (SBI-0206965) blocked autophagy to promote cell death and slow down cell growth in DR-BC cells treated with high-dose doxorubicin. Doxorubicin 24-35 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 94-98 33632157-11 2021 Functionally, high-dose doxorubicin increased the expression levels of phosphorylated AMPK (p-AMPK) and ULK1 (p-ULK1) to activate AMPK-ULK1 pathway in DR-BC cells, and the inhibitors for AMPK (compound C) and ULK1 (SBI-0206965) blocked autophagy to promote cell death and slow down cell growth in DR-BC cells treated with high-dose doxorubicin. Doxorubicin 24-35 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 94-98 33632157-11 2021 Functionally, high-dose doxorubicin increased the expression levels of phosphorylated AMPK (p-AMPK) and ULK1 (p-ULK1) to activate AMPK-ULK1 pathway in DR-BC cells, and the inhibitors for AMPK (compound C) and ULK1 (SBI-0206965) blocked autophagy to promote cell death and slow down cell growth in DR-BC cells treated with high-dose doxorubicin. Doxorubicin 332-343 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 86-90 33632157-11 2021 Functionally, high-dose doxorubicin increased the expression levels of phosphorylated AMPK (p-AMPK) and ULK1 (p-ULK1) to activate AMPK-ULK1 pathway in DR-BC cells, and the inhibitors for AMPK (compound C) and ULK1 (SBI-0206965) blocked autophagy to promote cell death and slow down cell growth in DR-BC cells treated with high-dose doxorubicin. Doxorubicin 332-343 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 94-98 33632157-11 2021 Functionally, high-dose doxorubicin increased the expression levels of phosphorylated AMPK (p-AMPK) and ULK1 (p-ULK1) to activate AMPK-ULK1 pathway in DR-BC cells, and the inhibitors for AMPK (compound C) and ULK1 (SBI-0206965) blocked autophagy to promote cell death and slow down cell growth in DR-BC cells treated with high-dose doxorubicin. Doxorubicin 332-343 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 94-98 33632157-11 2021 Functionally, high-dose doxorubicin increased the expression levels of phosphorylated AMPK (p-AMPK) and ULK1 (p-ULK1) to activate AMPK-ULK1 pathway in DR-BC cells, and the inhibitors for AMPK (compound C) and ULK1 (SBI-0206965) blocked autophagy to promote cell death and slow down cell growth in DR-BC cells treated with high-dose doxorubicin. Doxorubicin 332-343 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 94-98 33632157-12 2021 CONCLUSIONS: Collectively, our in vitro data indicated that blockage of AMPK-ULK1 signaling cascade mediated protective autophagy might be a promising strategy to increase doxorubicin sensitivity for BC treatment. Doxorubicin 172-183 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 72-76 33387880-0 2021 Bisphenol A promotes autophagy in ovarian granulosa cells by inducing AMPK/mTOR/ULK1 signalling pathway. bisphenol A 0-11 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 70-74 33387880-13 2021 Decreased E2, P4 and AMH level and GCs autophagy could be detected both in-vivo and in-vitro with the activation of AMPK/mTOR/ULK1 signalling pathway. Estradiol 10-12 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 116-120 33387880-13 2021 Decreased E2, P4 and AMH level and GCs autophagy could be detected both in-vivo and in-vitro with the activation of AMPK/mTOR/ULK1 signalling pathway. propiverine 14-16 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 116-120 33387880-14 2021 As being confirmed in KGN cells, phosphorylated AMPK and ULK1 increased while phosphorylated mTOR decreased, and by inhibition autophagy using knockdown of AMPK or 3-MA, adverse effects of BPA exposure in-vitro could be reversed. bisphenol A 189-192 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 156-160 33387880-15 2021 CONCLUSION: BPA exposure might abnormally influence human ovarian functions leading to abnormal folliculogenesis by activation of autophagy in GCs through AMPK/mTOR/ULK1 pathway. bisphenol A 12-15 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 155-159 32563202-6 2021 In particular, we showed that HDAC11 depletion increased mitochondrial fatty acid beta-oxidation through activating the AMPK-ACC pathway and reducing acylcarnitine levels in vivo, thus providing a mechanistic explanation for the improved muscle strength and fatigue resistance. Fatty Acids 71-81 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 120-124 33451752-0 2021 Sestrin2 protects against bavachin induced ER stress through AMPK/mTORC1 signaling pathway in HepG2 cells. bavachin 26-34 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 61-65 33146846-0 2021 Regulation of AKT/AMPK signaling, autophagy and mitigation of apoptosis in Rutin-pretreated SH-SY5Y cells exposed to MPP. Rutin 75-80 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 18-22 33146846-0 2021 Regulation of AKT/AMPK signaling, autophagy and mitigation of apoptosis in Rutin-pretreated SH-SY5Y cells exposed to MPP. mangion-purified polysaccharide (Candida albicans) 117-120 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 18-22 33458837-6 2021 Furthermore, Klotho alleviated the IS toxic effect on HUVECs via promoting AMP-activated protein kinase (AMPK) alpha1 phosphorylation instead of directly upregulating AMPKalpha1, which could be partly blocked by AMPK pathway inhibitor-Compound C. In addition, Klotho also inhibited intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) expression induced by IS. Indican 35-37 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 75-117 33458837-6 2021 Furthermore, Klotho alleviated the IS toxic effect on HUVECs via promoting AMP-activated protein kinase (AMPK) alpha1 phosphorylation instead of directly upregulating AMPKalpha1, which could be partly blocked by AMPK pathway inhibitor-Compound C. In addition, Klotho also inhibited intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) expression induced by IS. Indican 35-37 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 105-109 33500643-0 2021 Empagliflozin Regulates the AdipoR1/p-AMPK/p-ACC Pathway to Alleviate Lipid Deposition in Diabetic Nephropathy. empagliflozin 0-13 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 38-42 33458837-7 2021 Altogether, these results indicated that Klotho can protect HUVECs from IS-induced injury by alleviating AMPKalpha1-mediated endoplasmic reticulum stress. Indican 72-74 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 105-115 33428210-15 2022 Increased fatty acid availability can also increase AMPK activity and this increase PGC-1alpha levels. Fatty Acids 10-20 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 52-56 33520940-7 2020 Furthermore, 12b significantly stimulated the AMPK pathway and restrained the AKT/mTOR pathway in HSC-2 cells. 12b 13-16 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 46-50 33231372-0 2021 Periplocin inhibits the growth of pancreatic cancer by inducing apoptosis via AMPK-mTOR signaling. periplocin 0-10 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 78-82 33323505-7 2021 Absence of PTP-PEST also blocked hypoxia-induced autophagy (LC3 degradation and puncta formation) which was rescued by AMPK activator, metformin (500 microM). Metformin 135-144 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 119-123 33501881-0 2021 CTRP3 protects hippocampal neurons from oxygen-glucose deprivation-induced injury through the AMPK/Nrf2/ARE pathway. Oxygen 40-46 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 94-98 32472997-12 2021 Icaritin induced autophagy through upregulating the phosphorylation of AMPK and ULK1. icaritin 0-8 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 71-75 33332718-6 2021 In human podocytes, NOX4 was predominantly localized to mitochondria and Sal B treatment blocked HG-induced mitochondrial NOX4 derived superoxide generation and thereby ameliorating podocyte apoptosis, which can be abrogated by AMPK knockdown. sal b 73-78 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 228-232 33332718-7 2021 Therefore, our results suggest that Sal B possesses the reno-protective capabilities in part through AMPK-mediated control of NOX4 expression. sal b 36-41 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 101-105 33639076-0 2021 Phyllanthin Averts Oxidative Stress and Neuroinflammation in Cerebral Ischemic-Reperfusion Injury through Modulation of the NF-kappaB and AMPK/Nrf2 Pathways. phyllanthin 0-11 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 138-142 33639076-11 2021 Also, phyllanthin significantly reduced Nrf2 and AMPK levels, with reduced expression of NF-kappaB indicating that cross-talk between the NF-kB and Nrf2 pathways is activated in CIR. phyllanthin 6-17 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 49-53 33231372-11 2021 RESULTS: Periplocin inhibited the proliferation of PANC1 and CFPAC1 cells and induced their apoptosis by activating the AMPK/mTOR pathway and inhibiting p70 S6K. periplocin 9-19 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 120-124 33302416-2 2020 The aims of this study were to determine: (i) the mRNA and protein expression of vaspin and its receptor 78-kDa glucose-regulated (GRP78) in porcine cumulus-oocyte complexes (COCs) by real-time PCR and Western blot analysis, respectively, and their localisation by immunofluorescence; and (ii) the effects of vaspin on in vitro oocyte maturation (IVM) and the involvement of mitogen ERK1/2 (MAP3/1)- and AMPKalpha (PRKAA1)-activated kinases in the studied processes. Glucose 112-119 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 415-421 33231372-13 2021 CONCLUSIONS: Periplocin inhibits human pancreatic cancer cell proliferation and induces their apoptosis by activating the AMPK / mTOR pathway. periplocin 13-23 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 122-126 33375185-9 2020 AMPK pharmacological activation plays a key role, with metformin inhibiting inflammation and improving ED. Metformin 55-64 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 33519472-0 2020 Acacetin Protects Against High Glucose-Induced Endothelial Cells Injury by Preserving Mitochondrial Function via Activating Sirt1/Sirt3/AMPK Signals. acacetin 0-8 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 136-140 33519472-8 2020 These results indicate that vascular endothelial protection of acacetin by activating Sirt1/Sirt3/AMPK signals is likely involved in alleviating diabetes-accelerated atherosclerosis by preserving mitochondrial function, which suggests that acacetin may be a drug candidate for treating cardiovascular disorder in patients with diabetes. acacetin 63-71 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 98-102 33519472-8 2020 These results indicate that vascular endothelial protection of acacetin by activating Sirt1/Sirt3/AMPK signals is likely involved in alleviating diabetes-accelerated atherosclerosis by preserving mitochondrial function, which suggests that acacetin may be a drug candidate for treating cardiovascular disorder in patients with diabetes. acacetin 240-248 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 98-102 33086122-3 2020 The pharmacological activities essentially derive from the capacity of DMC to interact with the protein targets HMGB1 and AMPK. 2',4'-dihydroxy-6'-methoxy-3',5'-dimethylchalcone 71-74 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 122-126 33086122-5 2020 DMC also binds to the AMP site of AMPK to activate phospho-AMPK and then to trigger downstream signals leading to the anti-inflammatory and anti-hyperglycemic effects. 2',4'-dihydroxy-6'-methoxy-3',5'-dimethylchalcone 0-3 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 34-38 33086122-5 2020 DMC also binds to the AMP site of AMPK to activate phospho-AMPK and then to trigger downstream signals leading to the anti-inflammatory and anti-hyperglycemic effects. 2',4'-dihydroxy-6'-methoxy-3',5'-dimethylchalcone 0-3 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 59-63 33086122-5 2020 DMC also binds to the AMP site of AMPK to activate phospho-AMPK and then to trigger downstream signals leading to the anti-inflammatory and anti-hyperglycemic effects. Adenosine Monophosphate 22-25 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 34-38 33086122-5 2020 DMC also binds to the AMP site of AMPK to activate phospho-AMPK and then to trigger downstream signals leading to the anti-inflammatory and anti-hyperglycemic effects. Adenosine Monophosphate 22-25 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 59-63 33086122-6 2020 AMPK activation by DMC reinforces inhibition of HMGB1, to further reduce the release of the alarmin protein, likely contributing to the anticancer effects. 2',4'-dihydroxy-6'-methoxy-3',5'-dimethylchalcone 19-22 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 33086122-7 2020 The characterization of a tight control of DMC over the AMPK-HMGB1 axis not only helps to explain the known activities of DMC but also suggests opportunities to use this chalcone to treat other pathological conditions such as the acute respiratory distress syndrome (which affects patients with COVID-19). 2',4'-dihydroxy-6'-methoxy-3',5'-dimethylchalcone 43-46 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 56-60 33086122-7 2020 The characterization of a tight control of DMC over the AMPK-HMGB1 axis not only helps to explain the known activities of DMC but also suggests opportunities to use this chalcone to treat other pathological conditions such as the acute respiratory distress syndrome (which affects patients with COVID-19). 2',4'-dihydroxy-6'-methoxy-3',5'-dimethylchalcone 122-125 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 56-60 33086122-7 2020 The characterization of a tight control of DMC over the AMPK-HMGB1 axis not only helps to explain the known activities of DMC but also suggests opportunities to use this chalcone to treat other pathological conditions such as the acute respiratory distress syndrome (which affects patients with COVID-19). Chalcone 170-178 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 56-60 33146386-8 2020 Since, NAD+ supplementation reduced the phosphorylation of some AMPK substrates, we hypothesized that the loss of cellular NAD+ after PARP-1 activation may induce an energy stress that activates AMPK. NAD 7-11 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 64-68 33146386-8 2020 Since, NAD+ supplementation reduced the phosphorylation of some AMPK substrates, we hypothesized that the loss of cellular NAD+ after PARP-1 activation may induce an energy stress that activates AMPK. NAD 7-11 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 195-199 33146386-8 2020 Since, NAD+ supplementation reduced the phosphorylation of some AMPK substrates, we hypothesized that the loss of cellular NAD+ after PARP-1 activation may induce an energy stress that activates AMPK. NAD 123-127 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 64-68 33146386-8 2020 Since, NAD+ supplementation reduced the phosphorylation of some AMPK substrates, we hypothesized that the loss of cellular NAD+ after PARP-1 activation may induce an energy stress that activates AMPK. NAD 123-127 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 195-199 33293796-10 2020 Additionally, juglanin increased the activation of the SIRT1/AMPK signaling pathway through the phosphorylation of AMPKalpha. juglanin 14-22 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 61-65 33293796-10 2020 Additionally, juglanin increased the activation of the SIRT1/AMPK signaling pathway through the phosphorylation of AMPKalpha. ampkalpha 115-124 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 61-65 33293796-11 2020 Finally, we performed an AMPK inhibitor experiment, which revealed that the inhibitory effects of juglanin on adipogenesis are mediated through AMPK. juglanin 98-106 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 25-29 33293796-11 2020 Finally, we performed an AMPK inhibitor experiment, which revealed that the inhibitory effects of juglanin on adipogenesis are mediated through AMPK. juglanin 98-106 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 144-148 32985258-0 2020 The effects and mechanisms of isoliquiritigenin loaded nanoliposomes regulated AMPK/mTOR mediated glycolysis in colorectal cancer. isoliquiritigenin 30-47 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 79-83 32985258-2 2020 Herein, we sought to explore the anti-cancer mechanisms of ISL loaded nanoliposomes (ISL-NLs) on AMP-activated protein kinase/mammalian target of rapamycin (AMPK/mTOR) pathways mediated glycolysis. Sirolimus 146-155 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 157-161 32985258-6 2020 Moreover, the AMPK proteins were identified to be up-regulated while the lactic acid production was suppressed by ISL-NLs in the CRC cells, indicating that ISL-NLs had an inhibitory effect on AMPK mediated glycolysis and lactate production. Lactic Acid 73-84 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 192-196 33160989-9 2021 Interestingly, sCLU overexpression promoted autophagy through AMPK/Akt/mTOR signaling pathway leading to cell survival and protection from long exposure serum starvation induced-apoptosis. sclu 15-19 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 62-66 32898504-12 2020 Finally, through the study we demonstrated that the blockage of AMPK activity by Compound C abolished the ameliorative effect of Liraglutide on IL-1beta-induced repressed ATP production and triglyceride accumulation, indicating that the action of Liraglutide was dependent on AMPK activation. Adenosine Triphosphate 171-174 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 64-68 32898504-12 2020 Finally, through the study we demonstrated that the blockage of AMPK activity by Compound C abolished the ameliorative effect of Liraglutide on IL-1beta-induced repressed ATP production and triglyceride accumulation, indicating that the action of Liraglutide was dependent on AMPK activation. Triglycerides 190-202 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 64-68 32862405-11 2020 Exendin-4 treatment was showed to be more significant in 148I/I cells than in 148M/M cells in terms of reducing the intrahepatic fat content, inhibiting SREBP-1c and ER stress-related inflammation, and activating AMPK-ACC lipid oxidation pathway. Exenatide 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 213-217 32243091-0 2020 GPR120 facilitates cholesterol efflux in macrophages through activation of AMPK signaling pathway. Cholesterol 19-30 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 75-79 32243091-5 2020 In addition, GPR120 activation was accompanied with the stimulation of AMPK pathway in macrophages, however, the effect of GPR120 on macrophage cholesterol efflux was largely abolished by AMPK inhibition. Cholesterol 144-155 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 71-75 32243091-5 2020 In addition, GPR120 activation was accompanied with the stimulation of AMPK pathway in macrophages, however, the effect of GPR120 on macrophage cholesterol efflux was largely abolished by AMPK inhibition. Cholesterol 144-155 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 188-192 32243091-7 2020 Because only free cholesterol can be effluxed from macrophages, we found that activation of AMPK could lead to increase both neutral cholesteryl esters hydrolysis by upregulation of neutral cholesterol ester hydrolase (NCEH) expression and acid cholesteryl esters hydrolysis by activation of ULK1. Cholesterol 18-29 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 92-96 32243091-7 2020 Because only free cholesterol can be effluxed from macrophages, we found that activation of AMPK could lead to increase both neutral cholesteryl esters hydrolysis by upregulation of neutral cholesterol ester hydrolase (NCEH) expression and acid cholesteryl esters hydrolysis by activation of ULK1. Cholesterol Esters 133-151 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 92-96 32243091-7 2020 Because only free cholesterol can be effluxed from macrophages, we found that activation of AMPK could lead to increase both neutral cholesteryl esters hydrolysis by upregulation of neutral cholesterol ester hydrolase (NCEH) expression and acid cholesteryl esters hydrolysis by activation of ULK1. acid cholesteryl esters 240-263 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 92-96 32243091-8 2020 In conclusion, these results demonstrated that GPR120 facilitated ABCA1- and ABCG1-mediated cholesterol efflux through activation of PLC/Ca2+ /CaMKK/AMPK signaling pathway, which induced cholesteryl ester hydrolysis and elevated the expression of ABCA1 and ABCG1 in macrophages. Cholesterol 92-103 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 149-153 32986917-7 2020 Finally, the detection of proteins associated with the NF-kappaB/AMPK signaling pathway by western blot suggested that CCAL1 exerts its role on HC-OA cells by activating the NF-kappaB signaling pathway and inhibiting the AMPK signaling pathway, which was verified through the addition of NF-kappaB inhibitor caffeic acid phenethyl ester (CAPE) and AMPK activator 5-aminoimidazole-4carboxamide riboside (AICAR). caffeic acid phenethyl ester 308-336 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 65-69 32986917-7 2020 Finally, the detection of proteins associated with the NF-kappaB/AMPK signaling pathway by western blot suggested that CCAL1 exerts its role on HC-OA cells by activating the NF-kappaB signaling pathway and inhibiting the AMPK signaling pathway, which was verified through the addition of NF-kappaB inhibitor caffeic acid phenethyl ester (CAPE) and AMPK activator 5-aminoimidazole-4carboxamide riboside (AICAR). caffeic acid phenethyl ester 338-342 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 65-69 32986917-7 2020 Finally, the detection of proteins associated with the NF-kappaB/AMPK signaling pathway by western blot suggested that CCAL1 exerts its role on HC-OA cells by activating the NF-kappaB signaling pathway and inhibiting the AMPK signaling pathway, which was verified through the addition of NF-kappaB inhibitor caffeic acid phenethyl ester (CAPE) and AMPK activator 5-aminoimidazole-4carboxamide riboside (AICAR). acadesine 363-401 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 65-69 32986917-7 2020 Finally, the detection of proteins associated with the NF-kappaB/AMPK signaling pathway by western blot suggested that CCAL1 exerts its role on HC-OA cells by activating the NF-kappaB signaling pathway and inhibiting the AMPK signaling pathway, which was verified through the addition of NF-kappaB inhibitor caffeic acid phenethyl ester (CAPE) and AMPK activator 5-aminoimidazole-4carboxamide riboside (AICAR). acadesine 403-408 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 65-69 33078583-12 2020 Remarkably, loss of Nf1 promoted a robust activation of AMPK with a gene expression profile indicative of increased fatty acid catabolism. Fatty Acids 116-126 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 56-60 33457004-0 2020 Propofol activates AMPK to inhibit the growth of HepG2 cells in vitro and hepatocarcinogenesis in xenograft mouse tumor models by inducing autophagy. Propofol 0-8 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 19-23 33457004-2 2020 This study aimed to investigate the anti-tumor effect of propofol on the proliferation, apoptosis, and cell cycle of HCC by regulating adenosine monophosphate-activated protein kinase (AMPK) in vivo and in vitro. Propofol 57-65 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 135-183 33457004-2 2020 This study aimed to investigate the anti-tumor effect of propofol on the proliferation, apoptosis, and cell cycle of HCC by regulating adenosine monophosphate-activated protein kinase (AMPK) in vivo and in vitro. Propofol 57-65 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 185-189 33457004-18 2020 Conclusions: Propofol inhibits the proliferation, apoptosis, and cell cycle of HCC by regulating AMPK in vivo and in vitro. Propofol 13-21 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 97-101 33496141-12 2020 D-gal could not only induce cell aging but also increase LC3II, phosphorylated-AMPK(p-AMPK) and phosphorylated-ULK1(p-ULK1) protein expressions, and activate autophagy-related AMPK-ULK1 signaling pathway. Galactose 0-5 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 79-83 33496141-12 2020 D-gal could not only induce cell aging but also increase LC3II, phosphorylated-AMPK(p-AMPK) and phosphorylated-ULK1(p-ULK1) protein expressions, and activate autophagy-related AMPK-ULK1 signaling pathway. Galactose 0-5 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 86-90 33496141-12 2020 D-gal could not only induce cell aging but also increase LC3II, phosphorylated-AMPK(p-AMPK) and phosphorylated-ULK1(p-ULK1) protein expressions, and activate autophagy-related AMPK-ULK1 signaling pathway. Galactose 0-5 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 86-90 33496141-13 2020 FPS and VE could both improve the changes of LC3II, p-AMPK and p-ULK1 protein expression levels in the HK-2 cells exposed to D-gal. Galactose 125-130 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 54-58 33496141-15 2020 On the whole, for the human proximal renal tubular epithelial cells aging models induced by D-gal, FPS similar to VE, can ameliorate renal cells aging by possibly inhibiting autophagy-related AMPK-ULK1 signaling pathway activation. Galactose 92-97 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 192-196 32985258-6 2020 Moreover, the AMPK proteins were identified to be up-regulated while the lactic acid production was suppressed by ISL-NLs in the CRC cells, indicating that ISL-NLs had an inhibitory effect on AMPK mediated glycolysis and lactate production. Lactic Acid 221-228 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-18 32985258-7 2020 Altogether, these results have provided insights into the mechanism underlying the key role that liposomal ISL played in the multiple inhibition of AMPK and Akt/mTOR mediated glycolysis and lactate generation, which may be regulated as the alternative metabolic pathways of CRC as well as serve as adjuvant therapy for the disease. Lactic Acid 190-197 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 148-152 33219129-6 2021 Mechanistically, we found that ABHD5 elevates intracellular AMP content, which activates AMPK, leading to inhibition of mTORC1. Adenosine Monophosphate 60-63 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 89-93 33240683-0 2020 Four sesquiterpene glycosides from loquat (Eriobotrya japonica) leaf ameliorates palmitic acid-induced insulin resistance and lipid accumulation in HepG2 Cells via AMPK signaling pathway. sesquiterpene glycosides 5-29 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 164-168 33240683-0 2020 Four sesquiterpene glycosides from loquat (Eriobotrya japonica) leaf ameliorates palmitic acid-induced insulin resistance and lipid accumulation in HepG2 Cells via AMPK signaling pathway. Palmitic Acid 81-94 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 164-168 33240683-7 2020 Notably, AMPK inhibitor Compound C (CC) blocked the regulative effects, while AMPK activator AICAR mimicked the effects of SGs in PA-treated insulin-resistant HepG2 cells. Protactinium 130-132 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 78-82 32659400-7 2020 Furthermore, we found that treatment of HBSS-induced HK-2 cells with G-Rb1 resulted in AMPK/mTOR and ERK, p38 MAPKs signaling pathways regulated autophagy inhibition. hbss 40-44 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 87-91 33204156-8 2020 Western blot revealed the expression of p-AMPKalpha1 protein was up-regulated, and the expression of p-mTOR and p-S6K was down-regulated after Baohuoside I treatment. baohuoside 143-153 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 42-52 33224034-0 2020 Alisol A Alleviates Arterial Plaque by Activating AMPK/SIRT1 Signaling Pathway in apoE-Deficient Mice. alisol A 0-8 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 50-54 33224034-6 2020 Alisol A activated the AMPK/SIRT1 signaling pathway and NF-kappaB inhibitor IkappaBalpha in HepG2 cells. alisol A 0-8 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 23-27 32755450-7 2020 Treatment with an ETAR antagonist, such as BQ610, but not ETBR antagonist BQ788, blocked the ET-1-induced increase in cell proliferation and phosphorylated levels of ERK, c-JUN, STAT3, AMPK, and PKCalpha/betaII proteins. BQ 610 43-48 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 185-189 33109551-9 2020 CONCLUSION: AUY922, BIIB021 and SNX5422 induce cytotoxicity by modulating Bim and ERK1/2, AKT and AMPK signaling in thyroid carcinoma cells. 5-(2,4-dihydroxy-5-isopropylphenyl)-4-(4-morpholin-4-ylmethylphenyl)isoxazole-3-carboxylic acid ethylamide 12-18 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 98-102 33243973-5 2020 Using rescue experiments with a brain extracellular extract, and direct measurements, we demonstrate that cytosolic serine starvation controls cell movement by increasing reactive oxygen species formation and decreasing ATP levels, thereby promoting activation of the AMP sensor kinase (AMPK) by phosphorylation. Serine 116-122 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 268-285 33243973-5 2020 Using rescue experiments with a brain extracellular extract, and direct measurements, we demonstrate that cytosolic serine starvation controls cell movement by increasing reactive oxygen species formation and decreasing ATP levels, thereby promoting activation of the AMP sensor kinase (AMPK) by phosphorylation. Serine 116-122 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 287-291 33243973-5 2020 Using rescue experiments with a brain extracellular extract, and direct measurements, we demonstrate that cytosolic serine starvation controls cell movement by increasing reactive oxygen species formation and decreasing ATP levels, thereby promoting activation of the AMP sensor kinase (AMPK) by phosphorylation. Oxygen 180-186 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 287-291 33243973-5 2020 Using rescue experiments with a brain extracellular extract, and direct measurements, we demonstrate that cytosolic serine starvation controls cell movement by increasing reactive oxygen species formation and decreasing ATP levels, thereby promoting activation of the AMP sensor kinase (AMPK) by phosphorylation. Adenosine Triphosphate 220-223 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 287-291 33109551-9 2020 CONCLUSION: AUY922, BIIB021 and SNX5422 induce cytotoxicity by modulating Bim and ERK1/2, AKT and AMPK signaling in thyroid carcinoma cells. 6-chloro-9-(4-methoxy-3,5-dimethylpyridin-2-ylmethyl)-9H-purin-2-ylamine 20-27 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 98-102 33109551-9 2020 CONCLUSION: AUY922, BIIB021 and SNX5422 induce cytotoxicity by modulating Bim and ERK1/2, AKT and AMPK signaling in thyroid carcinoma cells. SNX-5422 32-39 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 98-102 33002460-0 2020 Artesunate induces autophagy dependent apoptosis through upregulating ROS and activating AMPK-mTOR-ULK1 axis in human bladder cancer cells. Artesunate 0-10 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 89-93 33002460-8 2020 Moreover, pretreatment of these cell lines with Acadesine or Dorsomorphin to activate or inhibit the AMPK-mTOR-ULK1 pathway, respectively, also resulting in promotion or suppression in both autophagy and apoptosis. acadesine 48-57 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 101-105 33002460-8 2020 Moreover, pretreatment of these cell lines with Acadesine or Dorsomorphin to activate or inhibit the AMPK-mTOR-ULK1 pathway, respectively, also resulting in promotion or suppression in both autophagy and apoptosis. dorsomorphin 61-73 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 101-105 33002460-9 2020 In the upstream, ROS upregulation triggered by ART initiated AMPK-mTOR-ULK1 axis. ros 17-20 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 61-65 33002460-11 2020 Therefore, this study indicated that Artesunate induces autophagy dependent apoptosis through upregulating ROS and activating AMPK-mTOR-ULK1 pathway in human bladder cancer cells. Artesunate 37-47 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 126-130 33368050-0 2020 Indirubin-3"-Oxime (IDR3O) Inhibits Proliferation of Osteosarcoma Cells in vitro and Tumor Growth in vivo Through AMPK-Activation and PGC-1alpha/TFAM Up-Regulation. indirubin-3'-monoxime 0-18 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 114-118 33368050-4 2020 Treatment of MG63 and Saos-2 cells with IDR3O inhibited proliferation, activated apoptosis and promoted AMPK-activation. mg63 13-17 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 104-108 32898618-5 2020 After that, 5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside (AICAR), exercise mimic chemical that stimulates AMPK level, was also administered to Caco2 cells. acadesine 12-66 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 116-120 32898618-5 2020 After that, 5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside (AICAR), exercise mimic chemical that stimulates AMPK level, was also administered to Caco2 cells. acadesine 68-73 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 116-120 32910998-6 2020 Induction of autophagy occurred following 2.5 to 10 mM 3-MCPD treatment for 24 h via AMPK mediated mTOR signaling pathway. alpha-Chlorohydrin 55-61 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 85-89 33001454-0 2020 Ursolic acid alleviates lipid accumulation by activating the AMPK signaling pathway in vivo and in vitro. ursolic acid 0-12 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 61-65 33001454-7 2020 Of note, these protective effects of UA on a high-fat environment were blocked by the AMPK inhibitor (compound C) in vitro. ursolic acid 37-39 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 86-90 33001454-8 2020 In addition, the molecular docking results suggested that UA could be docked to the AMPK protein as an AMPK activator. ursolic acid 58-60 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 84-88 33001454-8 2020 In addition, the molecular docking results suggested that UA could be docked to the AMPK protein as an AMPK activator. ursolic acid 58-60 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 103-107 33001454-9 2020 These results indicated that UA lowered the lipid content probably via activating the AMPK signaling pathway, thereby inhibiting lipid synthesis and promoting fat decomposition. ursolic acid 29-31 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 86-90 33048307-1 2021 PURPOSE: We earlier reported that Sestrin2 regulates monocyte activation and atherogenic events through AMPK-mTOR nexus under high-glucose and dyslipidemic conditions. Glucose 131-138 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 104-108 33109551-8 2020 AUY922, BIIB021 and SNX5422 increased the protein levels of phospho-AMPK, and decreased those of phospho-ERK1/2, and total and phospho-AKT. 5-(2,4-dihydroxy-5-isopropylphenyl)-4-(4-morpholin-4-ylmethylphenyl)isoxazole-3-carboxylic acid ethylamide 0-6 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 68-72 33109551-8 2020 AUY922, BIIB021 and SNX5422 increased the protein levels of phospho-AMPK, and decreased those of phospho-ERK1/2, and total and phospho-AKT. 6-chloro-9-(4-methoxy-3,5-dimethylpyridin-2-ylmethyl)-9H-purin-2-ylamine 8-15 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 68-72 33109551-8 2020 AUY922, BIIB021 and SNX5422 increased the protein levels of phospho-AMPK, and decreased those of phospho-ERK1/2, and total and phospho-AKT. SNX-5422 20-27 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 68-72 33178328-0 2020 Effect and Comparison of Luteolin and Its Derivative Sodium Luteolin-4"-sulfonate on Adipogenic Differentiation of Human Bone Marrow-Derived Mesenchymal Stem Cells through AMPK-Mediated PPARgamma Signaling. sodium luteolin-4"-sulfonate 53-81 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 172-176 33178328-12 2020 Replacing its 4"-hydroxyl group with sulfonic acid sodium salt diminished its antiadipogenic effect indicating its role in regulating AMPK activation. Sulfonic acid sodium salt 37-62 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 134-138 33086879-0 2021 Fisetin Inhibits Autophagy in HepG2 Cells via PI3K/Akt/mTOR and AMPK Pathway. fisetin 0-7 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 64-68 33086879-7 2021 In the Western blotting analysis, fisetin treatment inhibited the expression of Atg7, Atg16L, mTOR, and pACC and elevated the expression of Atg5, AMPKalpha, AMPKbeta1/2, ACC and Akt. fisetin 34-41 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 157-168 33086879-8 2021 Taken together, the results revealed that fisetin inhibited autophagy by the activation of PI3K/Akt/mTOR and modulation of AMPK signaling pathways. fisetin 42-49 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 123-127 33087848-5 2020 These proteins associate with TBC1D1 via its phosphotyrosine binding (PTB) domains and their interactions with TBC1D1 were unaffected by AMPK activation, distinguishing them from the AMPK regulated interaction between TBC1D1 and AMPKalpha1 complexes. Phosphotyrosine 45-60 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 229-239 33082544-4 2020 By using both molecular and theoretical biological techniques, here we reveal that a delayed negative feedback loop between active AMPK and ULK1 is essential to manage a proper cellular answer after prolonged starvation or rapamycin addition. Sirolimus 223-232 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 131-135 33027994-8 2020 In males, resveratrol enhances testes function and spermatogenesis through activation of the AMPK pathway. Resveratrol 10-21 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 93-97 32663610-12 2020 GlcN-induced lipid accumulation was inhibited by the AMPK activator, AICAR. Glucosamine 0-4 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 53-57 32663610-13 2020 Phosphorylation of AMPK (p-AMPK) was suppressed by GlcN under NG while increased by GlcN under HG. Glucosamine 51-55 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 19-23 32663610-13 2020 Phosphorylation of AMPK (p-AMPK) was suppressed by GlcN under NG while increased by GlcN under HG. Glucosamine 51-55 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 27-31 32663610-13 2020 Phosphorylation of AMPK (p-AMPK) was suppressed by GlcN under NG while increased by GlcN under HG. Glucosamine 84-88 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 19-23 32663610-13 2020 Phosphorylation of AMPK (p-AMPK) was suppressed by GlcN under NG while increased by GlcN under HG. Glucosamine 84-88 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 27-31 32663610-15 2020 Our results collectively suggest that GlcN regulates lipogenesis by sensing the glucose or energy states of normal and excess fuel through AMPK modulation. Glucosamine 38-42 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 139-143 32488849-9 2020 Ascofuranone inhibited IGF-1-induced mTOR phosphorylation and actin cytoskeleton organization via upregulation of AMPK and downregulation of Akt phosphorylation. ascofuranone 0-12 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 114-118 32856615-9 2020 In vitro, epinephrine treatment upregulated PDK4 expression, inhibited AMPK phosphorylation and enhanced IRS1 phosphorylation. Epinephrine 10-21 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 71-75 32768436-0 2020 Glucose restriction delays senescence and promotes proliferation of HUVECs via the AMPK/SIRT1-FOXA3-Beclin1 pathway. Glucose 0-7 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 83-87 32768436-2 2020 On the basis of our previous work and bioinformatics analysis, we hypothesized that glucose restriction can up-regulate autophagy, inhibit senescence and promote proliferation via the AMPK/SIRT1-FOXA3-Beclin1 pathway in human umbilical vein endothelial cells (HUVECs). Glucose 84-91 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 184-188 32768436-4 2020 Furthermore, glucose restriction up-regulated AMPKalpha1, SIRT1, FOXA3 and Beclin1 expression in HUVECs. Glucose 13-20 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 46-56 32768436-5 2020 Additionally, we demonstrated that AMPKalpha1 phosphorylated FOXA3 at S170 and S305 in the cytoplasm and promoted FOXA3 nuclear translocation under glucose restriction. Glucose 148-155 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 35-45 32768436-8 2020 siRNA knock down of AMPKalpha1, SIRT1, FOXA3 or Beclin1 expression impaired the glucose restriction-induced inhibition of senescence, enhanced autophagy, increased migration, and induced proliferation of HUVECs. Glucose 80-87 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 20-30 32768436-9 2020 This study confirmed that glucose restriction can enhance autophagy, inhibit senescence, and enhance proliferation of HUVECs through the AMPK/SIRT1-FOXA3-Beclin1 pathway. Glucose 26-33 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 137-141 32562591-0 2020 4-O-methylascochlorin activates autophagy by activating AMPK and suppressing c-Myc in glioblastoma. 4-O-methylascochlorin 0-21 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 56-60 33048256-14 2021 AMPK activator A769662 reduced IL-6 release. 4-hydroxy-3-(4-(2-hydroxyphenyl)phenyl)-6-oxo-7H-thieno(2,3-b)pyridine-5-carbonitrile 15-22 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 33029288-0 2020 Induction of cytoprotective autophagy by morusin via AMP-activated protein kinase activation in human non-small cell lung cancer cells. morusin 41-48 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 53-81 33029288-4 2020 The role of autophagy and AMP-activated protein kinase (AMPK) was determined by treating NSCLC cells with bafilomycin A1, an autophagy inhibitor, and compound C, an AMPK inhibitor. bafilomycin A1 106-120 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 56-60 33029288-9 2020 Furthermore, we found that AMPK and its downstream acetyl-CoA carboxylase (ACC) were phosphorylated, while mammalian target of rapamycin (mTOR) and its downstream p70S6 kinase (p70S6K) were dephosphorylated by morusin. morusin 210-217 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 27-31 33029288-11 2020 These results suggest that morusin-induced AMPK activation could protect NSCLC cells from apoptosis probably by inducing autophagy. morusin 27-34 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 43-47 33029288-12 2020 CONCLUSIONS: Our findings suggest that combination treatment with morusin and autophagy inhibitor or AMPK inhibitor might enhance the clinical efficacy of morusin for NSCLC. morusin 155-162 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 101-105 32562591-5 2020 Moreover, MAC stimulated AMP-activated protein kinase (AMPK) phosphorylation and suppressed phosphorylation of the mTOR, p70S6K, and 4EBP1. 4-O-methylascochlorin 10-13 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 25-53 32562591-5 2020 Moreover, MAC stimulated AMP-activated protein kinase (AMPK) phosphorylation and suppressed phosphorylation of the mTOR, p70S6K, and 4EBP1. 4-O-methylascochlorin 10-13 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 55-59 32562591-6 2020 The well-known AMPK activator metformin increased LC3-II levels, which were augmented by MAC cotreatment. Metformin 30-39 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 15-19 32562591-6 2020 The well-known AMPK activator metformin increased LC3-II levels, which were augmented by MAC cotreatment. lc3-ii 50-56 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 15-19 32562591-6 2020 The well-known AMPK activator metformin increased LC3-II levels, which were augmented by MAC cotreatment. 4-O-methylascochlorin 89-92 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 15-19 32562591-7 2020 AMPK knockdown decreased LC3-II levels and inhibited MAC activation of autophagy. lc3-ii 25-31 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 32982447-7 2020 In addition, metformin"s effects in the prevention and treatment for GC involve multiple pathways mainly via AMPK and IGF-1R. Metformin 13-22 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 109-113 32989819-10 2021 In addition, exogenous ATP blocked the activation of AMPK and rescued disulfiram-induced cell death. Adenosine Triphosphate 23-26 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 53-57 33041854-5 2020 Whereas, blockage of calcium entry into the mitochondria results in reduced ATP production thereby activates AMPK-mediated pro-survival autophagy. Calcium 21-28 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 109-113 33041854-5 2020 Whereas, blockage of calcium entry into the mitochondria results in reduced ATP production thereby activates AMPK-mediated pro-survival autophagy. Adenosine Triphosphate 76-79 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 109-113 33067969-6 2020 CONCLUSION: Metformin inhibits the proliferation of SKM-1 cells, which may relate with AMPK-induced cell cycle arrest. Metformin 12-21 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 87-91 33042417-7 2020 Furthermore, ATO induced cellular autophagy in cervical cancer cells, which was confirmed by an increase of LC3-I into LC3-II conversion, downregulation of p62 expression, regulation of AMPK and Akt/mTOR pathways. Atorvastatin 13-16 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 186-190 32611235-2 2020 In human macrophages in vitro, heme activates an adenosine monophosphate activated protein kinase / activating transcription factor 1 (AMPK/ATF1) pathway that directs Mhem macrophages through coregulation of heme oxygenase 1 (HMOX1, HO-1) and lipid homeostasis genes. Heme 31-35 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 135-139 32611235-2 2020 In human macrophages in vitro, heme activates an adenosine monophosphate activated protein kinase / activating transcription factor 1 (AMPK/ATF1) pathway that directs Mhem macrophages through coregulation of heme oxygenase 1 (HMOX1, HO-1) and lipid homeostasis genes. Adenosine 49-58 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 135-139 32873793-7 2020 Together, the results of this study highlight the importance of the AMPK/CREB1/GLUT3 pathway for CRC cells to withstand glucose-limiting stress and underscore the therapeutic potential of vitamin C in CRC with high GLUT3 expression. Glucose 120-127 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 68-72 32713306-6 2020 We show how the effects of fluctuating glucose on tumour cells need to be reprogrammed by taking into account the recent history of glucose variations and an AMPK/miR-451 reciprocal feedback loop. Glucose 39-46 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 158-162 32900249-10 2021 CONCLUSION: Collectively, chicoric acid is likely protected against diabetes-induced endothelial dysfunction by activation of the AMPK signaling pathway. chicoric acid 26-39 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 130-134 32911743-0 2020 Metformin Suppresses Cancer Stem Cells through AMPK Activation and Inhibition of Protein Prenylation of the Mevalonate Pathway in Colorectal Cancer. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 47-51 32911743-1 2020 Metformin is a well-known AMPK (AMP-activated protein kinase) activator that suppresses cancer stem cells (CSCs) in some cancers. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 26-30 32911743-1 2020 Metformin is a well-known AMPK (AMP-activated protein kinase) activator that suppresses cancer stem cells (CSCs) in some cancers. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 32-60 32911743-11 2020 Metformin treatment increased p-AMPK and decreased mTOR (pS6) expression; these effects were reversed by addition of mevalonate. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 32-36 32911743-11 2020 Metformin treatment increased p-AMPK and decreased mTOR (pS6) expression; these effects were reversed by addition of mevalonate. Mevalonic Acid 117-127 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 32-36 32911743-15 2020 In conclusion, the CSC-suppressive effect of metformin was associated with AMPK activation and repression of protein prenylation through MVA pathway suppression in colorectal cancer. Metformin 45-54 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 75-79 32526241-0 2020 Berbamine induced AMPK activation regulates mTOR/SREBP-1c axis and Nrf2/ARE pathway to allay lipid accumulation and oxidative stress in steatotic HepG2 cells. berbamine 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 18-22 32526241-3 2020 BBM attenuated intracellular lipid accumulation in oleic-acid exposed HepG2 cells (0.5 mM) by inhibiting fatty acid uptake, lipogenesis, and promoting fatty acid beta-oxidation by activating AMP-activated kinase (AMPK) and peroxisome proliferator-activated receptor (PPAR)-alpha. berbamine 0-3 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 191-211 32526241-3 2020 BBM attenuated intracellular lipid accumulation in oleic-acid exposed HepG2 cells (0.5 mM) by inhibiting fatty acid uptake, lipogenesis, and promoting fatty acid beta-oxidation by activating AMP-activated kinase (AMPK) and peroxisome proliferator-activated receptor (PPAR)-alpha. berbamine 0-3 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 213-217 32526241-3 2020 BBM attenuated intracellular lipid accumulation in oleic-acid exposed HepG2 cells (0.5 mM) by inhibiting fatty acid uptake, lipogenesis, and promoting fatty acid beta-oxidation by activating AMP-activated kinase (AMPK) and peroxisome proliferator-activated receptor (PPAR)-alpha. Oleic Acid 51-61 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 191-211 32526241-3 2020 BBM attenuated intracellular lipid accumulation in oleic-acid exposed HepG2 cells (0.5 mM) by inhibiting fatty acid uptake, lipogenesis, and promoting fatty acid beta-oxidation by activating AMP-activated kinase (AMPK) and peroxisome proliferator-activated receptor (PPAR)-alpha. Oleic Acid 51-61 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 213-217 32526241-4 2020 Berbamine (5 muM) induced AMPK activation (P < 0.001) via LKB1 (Ser-428) and elevated AMP:ATP ratio (P < 0.001). berbamine 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 26-30 32526241-4 2020 Berbamine (5 muM) induced AMPK activation (P < 0.001) via LKB1 (Ser-428) and elevated AMP:ATP ratio (P < 0.001). Serine 64-67 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 26-30 33241029-10 2020 AMPK and mTOR were inactivated with crocin treatment, while PI3K was activated. crocin 36-42 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 33241029-11 2020 These results indicated that crocin might promote autophagy and apoptosis by inactivating AMPK and mTOR signaling. crocin 29-35 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 90-94 33241029-13 2020 Conclusions: Crocin inhibited the progression of cervical cancer in vitro and in vivo, possibly through inactivation of AMPK and mTOR, inhibition of proliferation and invasion, and promotion of autophagy and apoptosis. crocin 13-19 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 120-124 31720741-6 2020 Glutamate reduced starvation-triggered phosphorylation of the energy sensor AMP-activated protein kinase (AMPK) without affecting the activity of mammalian target of rapamycin complex 1, a major negative regulator of autophagy. Glutamic Acid 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 76-104 32883948-0 2020 LKB1-AMPK axis negatively regulates ferroptosis by inhibiting fatty acid synthesis. Fatty Acids 62-72 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 5-9 32900249-0 2021 Chicoric acid attenuates hyperglycemia-induced endothelial dysfunction through AMPK-dependent inhibition of oxidative/nitrative stresses. chicoric acid 0-13 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 79-83 32900249-9 2021 Studies aimed at exploring the underlying mechanisms found that chicoric acid activated the AMP-activated protein kinase (AMPK) signaling pathway to attenuate HG + HF-triggered injury in HUVECs as AMPK inhibitor Compound C or silencing of AMPKalpha1 abolished the beneficial effects of chicoric acid in HUVECs. chicoric acid 64-77 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 92-120 32900249-9 2021 Studies aimed at exploring the underlying mechanisms found that chicoric acid activated the AMP-activated protein kinase (AMPK) signaling pathway to attenuate HG + HF-triggered injury in HUVECs as AMPK inhibitor Compound C or silencing of AMPKalpha1 abolished the beneficial effects of chicoric acid in HUVECs. chicoric acid 64-77 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 122-126 32900249-9 2021 Studies aimed at exploring the underlying mechanisms found that chicoric acid activated the AMP-activated protein kinase (AMPK) signaling pathway to attenuate HG + HF-triggered injury in HUVECs as AMPK inhibitor Compound C or silencing of AMPKalpha1 abolished the beneficial effects of chicoric acid in HUVECs. chicoric acid 64-77 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 197-201 32900249-9 2021 Studies aimed at exploring the underlying mechanisms found that chicoric acid activated the AMP-activated protein kinase (AMPK) signaling pathway to attenuate HG + HF-triggered injury in HUVECs as AMPK inhibitor Compound C or silencing of AMPKalpha1 abolished the beneficial effects of chicoric acid in HUVECs. chicoric acid 64-77 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 239-249 32900249-9 2021 Studies aimed at exploring the underlying mechanisms found that chicoric acid activated the AMP-activated protein kinase (AMPK) signaling pathway to attenuate HG + HF-triggered injury in HUVECs as AMPK inhibitor Compound C or silencing of AMPKalpha1 abolished the beneficial effects of chicoric acid in HUVECs. chicoric acid 286-299 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 92-120 32900249-9 2021 Studies aimed at exploring the underlying mechanisms found that chicoric acid activated the AMP-activated protein kinase (AMPK) signaling pathway to attenuate HG + HF-triggered injury in HUVECs as AMPK inhibitor Compound C or silencing of AMPKalpha1 abolished the beneficial effects of chicoric acid in HUVECs. chicoric acid 286-299 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 122-126 32415699-0 2020 The anti-tumorigenic effect of Ellagic acid in SKOV-3 ovarian cancer cells entails activation of autophagy-mediated by inhibiting Akt and activating AMPK. Ellagic Acid 31-43 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 149-153 32415699-6 2020 Mechanistically, EA decreased levels of p-S6K1 (Thr389 ) and 4EBP-1 (Thr37/46) , two downstream targets of mTORC1, and p-Akt (Thr308 ) but increased levels of AMPK (Thr172 ) and p-raptor (Ser792 ), a natural inhibitor of mTORC1. Ellagic Acid 17-19 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 159-163 32518098-10 2020 CONCLUSIONS: We found that AMPK pathway activation is associated with clinical benefit from treatment with regorafenib in relapsed GBM. regorafenib 107-118 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 27-31 31720741-6 2020 Glutamate reduced starvation-triggered phosphorylation of the energy sensor AMP-activated protein kinase (AMPK) without affecting the activity of mammalian target of rapamycin complex 1, a major negative regulator of autophagy. Glutamic Acid 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 106-110 32574665-0 2020 Combination of luteolin and lycopene effectively protect against the "two-hit" in NAFLD through Sirt1/AMPK signal pathway. Luteolin 15-23 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 102-106 32574665-0 2020 Combination of luteolin and lycopene effectively protect against the "two-hit" in NAFLD through Sirt1/AMPK signal pathway. Lycopene 28-36 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 102-106 31720741-8 2020 Glutamate-mediated transcriptional repression of autophagy was alleviated by overexpression of constitutively active AMPK. Glutamic Acid 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 117-121 31720741-9 2020 Genetic or pharmacological AMPK activation by AMPK overexpression or metformin, as well as genetic or pharmacological autophagy induction by TFEB overexpression or lithium chloride, reduced the sensitivity of nutrient-deprived SH-SY5Y cells to glutamate excitotoxicity. Metformin 69-78 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 27-31 31720741-10 2020 These data indicate that transcriptional inhibition of AMPK-dependent cytoprotective autophagy is involved in glutamate-mediated excitotoxicity during nutrient deprivation in vitro. Glutamic Acid 110-119 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 55-59 32679123-0 2020 Nifedipine-induced AMPK activation alleviates senescence by increasing autophagy and suppressing of Ca2+ levels in vascular smooth muscle cells. Nifedipine 0-10 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 19-23 32679123-7 2020 AMPK inhibition or transfection with AMPK siRNA showed that the anti-senescence effect of nifedipine involved AMPK activation. Nifedipine 90-100 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 32679123-7 2020 AMPK inhibition or transfection with AMPK siRNA showed that the anti-senescence effect of nifedipine involved AMPK activation. Nifedipine 90-100 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 37-41 32679123-7 2020 AMPK inhibition or transfection with AMPK siRNA showed that the anti-senescence effect of nifedipine involved AMPK activation. Nifedipine 90-100 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 37-41 32679123-8 2020 These results suggest nifedipine-inducted AMPK activation suppresses VSMC senescence by regulating autophagic flux and Ca2+ levels. Nifedipine 22-32 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 42-46 32574665-8 2020 SIGNIFICANCE: Thus, luteolin and lycopene in combination can effectively ameliorate "two-hit" in NAFLD through activation of the Sirt1/AMPK pathway. Luteolin 20-28 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 135-139 32574665-8 2020 SIGNIFICANCE: Thus, luteolin and lycopene in combination can effectively ameliorate "two-hit" in NAFLD through activation of the Sirt1/AMPK pathway. Lycopene 33-41 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 135-139 32383028-0 2020 Phenformin inhibits proliferation, invasion, and angiogenesis of cholangiocarcinoma cells via AMPK-mTOR and HIF-1A pathways. Phenformin 0-10 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 94-98 32383028-1 2020 Phenformin (Phen), a potent activator of AMPK, is effective against some resistant cancers. Phenformin 0-10 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 41-45 32383028-1 2020 Phenformin (Phen), a potent activator of AMPK, is effective against some resistant cancers. Phenformin 0-4 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 41-45 32863211-0 2020 Low-protein/high-carbohydrate diet induces AMPK-dependent canonical and non-canonical thermogenesis in subcutaneous adipose tissue. Carbohydrates 17-29 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 43-47 32719535-0 2020 AMPK as a direct sensor of long-chain fatty acyl-CoA esters. fatty acyl-coa esters 38-59 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 32719536-0 2020 Long-chain fatty acyl-CoA esters regulate metabolism via allosteric control of AMPK beta1 isoforms. long-chain fatty acyl-coa esters 0-32 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 79-89 32719536-3 2020 Here we report a new level of regulation wherein LCFA-CoA esters per se allosterically activate AMP-activated protein kinase (AMPK) beta1-containing isoforms to increase fatty acid oxidation through phosphorylation of acetyl-CoA carboxylase. lcfa 49-53 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 96-137 32719536-3 2020 Here we report a new level of regulation wherein LCFA-CoA esters per se allosterically activate AMP-activated protein kinase (AMPK) beta1-containing isoforms to increase fatty acid oxidation through phosphorylation of acetyl-CoA carboxylase. Esters 58-64 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 96-137 32719536-3 2020 Here we report a new level of regulation wherein LCFA-CoA esters per se allosterically activate AMP-activated protein kinase (AMPK) beta1-containing isoforms to increase fatty acid oxidation through phosphorylation of acetyl-CoA carboxylase. Fatty Acids 170-180 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 96-137 32719536-4 2020 Activation of AMPK by LCFA-CoA esters requires the allosteric drug and metabolite site formed between the alpha-subunit kinase domain and the beta-subunit. lcfa-coa esters 22-37 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-18 32719536-6 2020 Thus, LCFA-CoA metabolites act as direct endogenous AMPK beta1-selective activators and promote LCFA oxidation. lcfa 6-10 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 52-62 32464330-0 2020 Chelidonine Selectively Inhibits the Growth of Gefitinib-resistant Non-small Cell Lung Cancer Cells through the EGFR-AMPK Pathway. chelidonine 0-11 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 117-121 32464330-0 2020 Chelidonine Selectively Inhibits the Growth of Gefitinib-resistant Non-small Cell Lung Cancer Cells through the EGFR-AMPK Pathway. Gefitinib 47-56 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 117-121 32464330-5 2020 Proteomics analysis indicated that mitochondrial respiratory chain was significantly inhibited by chelidonine, and inhibitor of AMPK effectively blocked the apoptosis induced by chelidonine. chelidonine 178-189 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 128-132 32086756-9 2020 The results indicated that there was disturbed glucose homeostasis associated with excessive activation of AMPK in endometrium of diabetic pregnant mice. Glucose 47-54 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 107-111 32086756-10 2020 AMPK inhibitor improved the over-activation of AMPK pathway in the endometrium, meanwhile, partially corrected the abnormal glycogen metabolism and improved the implantation. Glycogen 124-132 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 32604037-1 2020 The mitochondrial electron transport chain is a major source of reactive oxygen species (ROS) and is also a target of ROS, with an implied role in the stabilization of hypoxia-inducible factor (HIF) and induction of the AMPK pathway. Reactive Oxygen Species 64-87 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 220-224 32604037-1 2020 The mitochondrial electron transport chain is a major source of reactive oxygen species (ROS) and is also a target of ROS, with an implied role in the stabilization of hypoxia-inducible factor (HIF) and induction of the AMPK pathway. Reactive Oxygen Species 89-92 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 220-224 32604037-1 2020 The mitochondrial electron transport chain is a major source of reactive oxygen species (ROS) and is also a target of ROS, with an implied role in the stabilization of hypoxia-inducible factor (HIF) and induction of the AMPK pathway. Reactive Oxygen Species 118-121 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 220-224 32863211-7 2020 We observed that mitochondrial reactive oxygen species are the upstream molecules controlling AMPK-mediated metabolic rewiring in amino acid-restricted beige adipocytes. Reactive Oxygen Species 31-54 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 94-98 32862503-5 2020 ABSTRACT: We examined the effects of graded muscle glycogen on the subcellular location of AMPK and PGC-1alpha protein content and mRNA expression of genes associated with the regulation of mitochondrial biogenesis and substrate utilisation in human skeletal muscle. Glycogen 51-59 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 91-95 32884949-15 2020 These results indicated that KTZG effectively ameliorated lipid accumulation and hepatic steatosis to prevent NAFLD in high-fat diet-fed rats and FFA-induced HepG2 cells, and this effect was associated with the AMPK/mTOR signaling pathway. ktzg 29-33 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 211-215 32853879-5 2020 Notably, ME1 interference ultimately resulted in adaptive upregulation of mitochondrial IDH2 dependent of AMPK-FoxO1 activation to replenish the NADPH pool and mitigate cytosolic ROS. ros 179-182 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 106-110 32904616-0 2020 AMPK/mTOR/ULK1 Axis-Mediated Pathway Participates in Apoptosis and Autophagy Induction by Oridonin in Colon Cancer DLD-1 Cells. oridonin 90-98 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 32904616-12 2020 Furthermore, oridonin upregulated the expression level of p-AMPK and downregulated the expression levels of p-mTOR, p-ULK1 in the DLD-1 cells in a dose-dependent manner. oridonin 13-21 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 60-64 32904616-14 2020 In addition, outcomes from the in vivo experiments also showed that oridonin treatment significantly repressed tumorigenic growth of DLD-1 cells without any side effects, which was accompanied by the upregulation of p-AMPK, LC3-II, active caspase-3 protein expression levels and the downregulation of p-mTOR and p-ULK1 protein expression levels. oridonin 68-76 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 218-222 32904616-15 2020 Conclusion: This study demonstrated that oridonin induced apoptosis and autophagy of colon cancer DLD-1 cells via regulating the AMPK/mTOR/ULK1 pathway, which indicated that oridonin may be used as a novel therapeutic intervention for patients with colorectal cancer. oridonin 41-49 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 129-133 32904616-15 2020 Conclusion: This study demonstrated that oridonin induced apoptosis and autophagy of colon cancer DLD-1 cells via regulating the AMPK/mTOR/ULK1 pathway, which indicated that oridonin may be used as a novel therapeutic intervention for patients with colorectal cancer. oridonin 174-182 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 129-133 32825760-4 2020 Among the latter, the antidiabetic drug metformin exerts antitumor activity via the activation of AMPK and the subsequent inhibition of mTOR signaling. Metformin 40-49 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 98-102 32815398-3 2021 The regulatory effect of MitoQ on mitochondrial homeostasis is mediated through AMPK and its downstream signaling pathways, including MTOR, SIRT1, Nrf2 and NF-kappaB. mitoquinone 25-30 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 80-84 32674299-5 2020 The most important intermediates by which polyphenols exert their protective effect include Bcl-2, UCP2, SIRT-1, AMPK and JNK1. Polyphenols 42-53 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 113-117 32831652-15 2020 In addition, iron increased the expression of Warburg key enzymes HK2 and Glut1, and affected AMPK/mTORC1 signaling axis. Iron 13-17 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 94-98 32824273-0 2020 Sinensetin Induces Autophagic Cell Death through p53-Related AMPK/mTOR Signaling in Hepatocellular Carcinoma HepG2 Cells. sinensetin 0-10 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 61-65 32826848-10 2020 Restrain of MR activation interrupts LKB1/p-AMPK/PDK4/p-CREB/FOXO1 pathway induced by aldosterone, indicating that aldosterone action on decidualization is mainly dependent on MR stimulation. Aldosterone 86-97 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 44-48 32826848-10 2020 Restrain of MR activation interrupts LKB1/p-AMPK/PDK4/p-CREB/FOXO1 pathway induced by aldosterone, indicating that aldosterone action on decidualization is mainly dependent on MR stimulation. Aldosterone 115-126 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 44-48 32826848-11 2020 Aldosterone biosynthesized in endometrial gland during mid-secretory phase promotes decidualization via activating MR/LKB1/p-AMPK/PDK4/p-CREB/FOXO1 signaling pathway. Aldosterone 0-11 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 125-129 32781739-6 2020 PM extract increased the AMPK and ACC phosphorylation and GLUT4 expression, whose levels were downregulated in FFA-exposed cells. Promethium 0-2 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 25-29 32781739-6 2020 PM extract increased the AMPK and ACC phosphorylation and GLUT4 expression, whose levels were downregulated in FFA-exposed cells. Fatty Acids, Nonesterified 111-114 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 25-29 32781739-11 2020 HFD-fed mice decreased the AMPK and ACC phosphorylation and GLUT4 expression, and increased precursor and mature forms of SREBP-1; these changes were significantly restored by PM extract. pm extract 176-186 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 27-31 32764573-8 2020 In addition, TG2 activation by a calcium ionophore enhanced the phosphorylation of AMPK and FoxO3a and the nuclear translocation of FoxO3a, which was responsible for the increase in MMP-13. Calcium 33-40 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 83-87 31900833-10 2020 Restoration of AMPKalpha1 or FOXP3 expression increased cell survival after treatment with compound C. In conclusion, our results show that compound C suppresses AMPK/TET2 axis-mediated FOXP3 expression and induces autophagy-dependent apoptosis in parental and HQ-selected malignant U937 cells, suggesting that the AMPK/TET2/FOXP3 axis is a promising target for improving AML therapy and attenuating benzene exposure-induced AML progression. Hydroquinones 261-263 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 15-25 31900833-10 2020 Restoration of AMPKalpha1 or FOXP3 expression increased cell survival after treatment with compound C. In conclusion, our results show that compound C suppresses AMPK/TET2 axis-mediated FOXP3 expression and induces autophagy-dependent apoptosis in parental and HQ-selected malignant U937 cells, suggesting that the AMPK/TET2/FOXP3 axis is a promising target for improving AML therapy and attenuating benzene exposure-induced AML progression. Hydroquinones 261-263 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 15-19 31900833-10 2020 Restoration of AMPKalpha1 or FOXP3 expression increased cell survival after treatment with compound C. In conclusion, our results show that compound C suppresses AMPK/TET2 axis-mediated FOXP3 expression and induces autophagy-dependent apoptosis in parental and HQ-selected malignant U937 cells, suggesting that the AMPK/TET2/FOXP3 axis is a promising target for improving AML therapy and attenuating benzene exposure-induced AML progression. Hydroquinones 261-263 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 162-166 31900833-10 2020 Restoration of AMPKalpha1 or FOXP3 expression increased cell survival after treatment with compound C. In conclusion, our results show that compound C suppresses AMPK/TET2 axis-mediated FOXP3 expression and induces autophagy-dependent apoptosis in parental and HQ-selected malignant U937 cells, suggesting that the AMPK/TET2/FOXP3 axis is a promising target for improving AML therapy and attenuating benzene exposure-induced AML progression. Benzene 400-407 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 15-25 31900833-10 2020 Restoration of AMPKalpha1 or FOXP3 expression increased cell survival after treatment with compound C. In conclusion, our results show that compound C suppresses AMPK/TET2 axis-mediated FOXP3 expression and induces autophagy-dependent apoptosis in parental and HQ-selected malignant U937 cells, suggesting that the AMPK/TET2/FOXP3 axis is a promising target for improving AML therapy and attenuating benzene exposure-induced AML progression. Benzene 400-407 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 15-19 31900833-10 2020 Restoration of AMPKalpha1 or FOXP3 expression increased cell survival after treatment with compound C. In conclusion, our results show that compound C suppresses AMPK/TET2 axis-mediated FOXP3 expression and induces autophagy-dependent apoptosis in parental and HQ-selected malignant U937 cells, suggesting that the AMPK/TET2/FOXP3 axis is a promising target for improving AML therapy and attenuating benzene exposure-induced AML progression. Benzene 400-407 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 162-166 32779675-0 2020 Early galactooligosaccharide intervention alters the metabolic profile, improves the antioxidant capacity of mitochondria and activates the AMPK/Nrf2 signaling pathway in suckling piglet liver. 4'-Galactooligosaccharide 6-28 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 140-144 32783662-6 2020 CONCLUSIONS: L-arginine-induced acute pancreatitis modulates TNF-alpha-AMPK axis, IL-10 and other AP biomarkers, which is protected by vitamin E; thus, may offer therapeutic potential in humans. Arginine 13-23 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 71-75 32783662-6 2020 CONCLUSIONS: L-arginine-induced acute pancreatitis modulates TNF-alpha-AMPK axis, IL-10 and other AP biomarkers, which is protected by vitamin E; thus, may offer therapeutic potential in humans. Vitamin E 135-144 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 71-75 32702668-8 2020 When an AMPK inhibitor was added, the anti-inflammatory effect of Deh was blocked. dehydroandrographolide 66-69 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 8-12 32774666-0 2020 Protective Effect of Metformin against Hydrogen Peroxide-Induced Oxidative Damage in Human Retinal Pigment Epithelial (RPE) Cells by Enhancing Autophagy through Activation of AMPK Pathway. Metformin 21-30 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 175-179 32774666-0 2020 Protective Effect of Metformin against Hydrogen Peroxide-Induced Oxidative Damage in Human Retinal Pigment Epithelial (RPE) Cells by Enhancing Autophagy through Activation of AMPK Pathway. Hydrogen Peroxide 39-56 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 175-179 32774666-9 2020 In addition, we showed that metformin could activate the AMPK pathway, whereas both pharmacological and genetic inhibitions of AMPK blocked the autophagy-stimulating and protective effects of metformin. Metformin 28-37 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 57-61 32774666-9 2020 In addition, we showed that metformin could activate the AMPK pathway, whereas both pharmacological and genetic inhibitions of AMPK blocked the autophagy-stimulating and protective effects of metformin. Metformin 192-201 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 127-131 32774666-11 2020 Taken together, these results demonstrate that metformin could protect RPE cells from H2O2-induced oxidative damage by stimulating autophagy via the activation of the AMPK pathway, supporting its potential use in the prevention and treatment of AMD. Metformin 47-56 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 167-171 32692720-7 2020 Pretreatment with selisistat (Sirt1-specific inhibitor) or compound C (AMPK antagonist) significantly reduced the viability and mitochondrial function in H2O2-treated Mst1-silenced RA-FLSs by inhibiting Sirt1 function or Sirt1 expression, respectively. Hydrogen Peroxide 154-158 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 71-75 32692720-9 2020 This suggests the Mst1-AMPK-Sirt1 axis is a potential target for RA therapy. Radium 65-67 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 23-27 33205063-7 2020 We further show that pharmacological treatment of MK-8722 (AMPK activator) and MK-4074 (ACC inhibitor) reduce fibrosis in vivo. MK-8722 50-57 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 59-63 32628492-5 2020 Formicin A inhibited the growth of human triple-negative breast cancer cells by regulating the liver kinase B1-mediated AMPK signaling pathway. Formicin A 0-10 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 120-124 32654534-0 2020 Fish oil and chicoric acid combination protects better against palmitate-induced lipid accumulation via regulating AMPK-mediated SREBP-1/FAS and PPARalpha/UCP2 pathways. Fish Oils 0-8 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 115-119 32654534-0 2020 Fish oil and chicoric acid combination protects better against palmitate-induced lipid accumulation via regulating AMPK-mediated SREBP-1/FAS and PPARalpha/UCP2 pathways. chicoric acid 13-26 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 115-119 32654534-0 2020 Fish oil and chicoric acid combination protects better against palmitate-induced lipid accumulation via regulating AMPK-mediated SREBP-1/FAS and PPARalpha/UCP2 pathways. Palmitates 63-72 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 115-119 32422565-8 2020 Both compounds rapidly activated AMPK, and dorsomorphin (an AMPK inhibitor) abolished ATP production stimulated by these compounds. dorsomorphin 43-55 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 60-64 32422565-8 2020 Both compounds rapidly activated AMPK, and dorsomorphin (an AMPK inhibitor) abolished ATP production stimulated by these compounds. Adenosine Triphosphate 86-89 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 60-64 32422565-9 2020 Moreover, EGCG and RES upregulated the mitochondrial biogenesis factor, PGC-1alpha which is downstream of AMPK activation, and silencing PGC-1alpha blocked their stimulatory effects on ATP production and hFOB differentiation. epigallocatechin gallate 10-14 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 106-110 32422565-9 2020 Moreover, EGCG and RES upregulated the mitochondrial biogenesis factor, PGC-1alpha which is downstream of AMPK activation, and silencing PGC-1alpha blocked their stimulatory effects on ATP production and hFOB differentiation. Adenosine Triphosphate 185-188 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 106-110 32599620-7 2020 CORT treatment upregulated the gene expression of mammalian target of rapamycin, glucocorticoid receptor, AMPKalpha2, neuropeptide Y(NPY), liver kinase B1 (LKB1), AMPKalpha1, and fatty acid synthase in the hypothalamus. Corticosterone 0-4 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 163-173 31558185-4 2020 PRKAA1 downregulation by shRNA or treatment of AMPK inhibitor compound C significantly inhibited proliferation as well as promoted cell cycle arrest and apoptosis of BGC-823 and MKN45 cells. Carbon 71-72 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-6 32353602-8 2020 In addition, AFB1 reduced intracellular ATP levels, whereas Zn supplementation boosted ATP levels and maintained homeostasis and a steady state of cellular energy metabolism by modulating AMPK-ACC phosphorylation levels, while many zinc finger proteins changed after AFB1 treatment. Zinc 60-62 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 188-192 32341017-11 2020 Using specific inhibitors of cellular signaling components, 7alpha,25-dihydroxycholesterol-induced inhibition of lipid accumulation was found to be mediated through Gi/o proteins, p38 MAPKs, PI3K, and AMPK. 7alpha,25-Dihydroxycholesterol 60-90 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 201-205 32541839-0 2020 Iron chelation inhibits mTORC1 signaling involving activation of AMPK and REDD1/Bnip3 pathways. Iron 0-4 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 65-69 32556103-6 2020 Moreover, lowering UA using benzbromarone (a uricosuric agent) or metformin-induced activation of AMPK expression significantly attenuated UA-induced FFA metabolism impairment and adipose beiging suppression, which subsequently alleviated serum FFA elevation and insulin resistance in HUA mice. Metformin 66-75 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 98-102 32556103-7 2020 Taken together, these observations confirm that UA is involved in the aetiology of metabolic abnormalities in adipose tissue by regulating leptin-AMPK pathway,and metformin could lessen HUA-induced serum FFA elevation and insulin resistance by improving adipose tissue function via AMPK activation. Metformin 163-172 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 282-286 32728616-6 2020 On the other hand, metformin-activated AMP-activated protein kinase (AMPK) increased DNA methyltransferase 3A (DNMT3A) activity to increase 5-methylcytosine (5mC) abundance in the TDG promoter. 5-Methylcytosine 140-156 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 39-67 32728616-6 2020 On the other hand, metformin-activated AMP-activated protein kinase (AMPK) increased DNA methyltransferase 3A (DNMT3A) activity to increase 5-methylcytosine (5mC) abundance in the TDG promoter. 5-Methylcytosine 140-156 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 69-73 32728616-8 2020 These findings demonstrate that c-Myc activates, whereas AMPK inhibits, TDG-mediated DNA demethylation of the SREBP1 promoter in insulin-promoted and metformin-suppressed cancer progression, respectively. Metformin 150-159 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 57-61 32606805-0 2020 AMPK alpha1 Downregulates ROS Levels Through Regulating Trx Leading to Dysfunction of Apoptosis in Non-Small Cell Lung Cancer. ros 26-29 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-11 32606805-12 2020 In A549 cells, overexpression of AMPK alpha1 promoted proliferation, suppressed ROS levels and inhibited apoptosis. ros 80-83 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 33-44 32596161-6 2020 Furthermore, treatment with A-769662 (a specific AMPK activator), like NBR2 over-expression, significantly attenuated the malignancy of BHT101 cells while treatment with Compound C (a specific AMPK inhibitor) significantly rescued that NBR2-reduced malignancy of BHT101 cells. 4-hydroxy-3-(4-(2-hydroxyphenyl)phenyl)-6-oxo-7H-thieno(2,3-b)pyridine-5-carbonitrile 28-36 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 49-53 32596161-6 2020 Furthermore, treatment with A-769662 (a specific AMPK activator), like NBR2 over-expression, significantly attenuated the malignancy of BHT101 cells while treatment with Compound C (a specific AMPK inhibitor) significantly rescued that NBR2-reduced malignancy of BHT101 cells. 4-hydroxy-3-(4-(2-hydroxyphenyl)phenyl)-6-oxo-7H-thieno(2,3-b)pyridine-5-carbonitrile 28-36 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 193-197 32527986-0 2020 miR-107 inhibition upregulates CAB39 and activates AMPK-Nrf2 signaling to protect osteoblasts from dexamethasone-induced oxidative injury and cytotoxicity. Dexamethasone 99-112 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 51-55 32527986-9 2020 Further studies demonstrated that antagomiR-107 activated AMPK downstream Nrf2 cascade to inhibit DEX-induced oxidative injury. Dexamethasone 98-101 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 58-62 32527986-11 2020 Collectively, miR-107 inhibition induced CAB39 upregulation and activated AMPK-Nrf2 signaling to protect osteoblasts from DEX-induced oxidative injury and cytotoxicity. Dexamethasone 122-125 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 74-78 32545395-9 2020 In contrast, metformin, an AMPK activator, suppressed H. pylori-induced apoptosis, showing that AMPK activation inhibits H. pylori-induced apoptosis. Metformin 13-22 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 27-31 32545395-9 2020 In contrast, metformin, an AMPK activator, suppressed H. pylori-induced apoptosis, showing that AMPK activation inhibits H. pylori-induced apoptosis. Metformin 13-22 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 96-100 32531951-10 2020 Most importantly, docetaxel sensitivity was restored in stem-like AMPK-transfected cells. Docetaxel 18-27 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 66-70 32535544-7 2020 Specifically, we describe the molecular mechanisms involved in metformin"s effect on gluconeogenesis, its capacity to interfere with major metabolic pathways (AMPK and mTORC1), its action on mitochondria and its antioxidant effects. Metformin 63-72 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 159-163 32529067-8 2020 In addition, niclosamide was found to downregulate mTORC1 via AMPK activation, resulting in a decreased phosphorylation of the downstream substrates of S6K and 4EBP1. Niclosamide 13-24 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 62-66 32529067-11 2020 Our findings, therefore, demonstrated the antiviral mechanism of niclosamide is via the AMPK-mTORC1 pathway, which could be a common therapeutic target for various viruses. Niclosamide 65-76 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 88-92 31840936-10 2020 Decreased GLUT1 protein expression was observed in parallel with increased P-AMPK protein expression in SFC in the presence of metformin (n=4). Metformin 127-136 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 75-81 31840936-14 2020 Furthermore the effect of metformin on pro-inflammatory mechanisms suggests a role for AMPK modifying compounds for treatment of RA. Metformin 26-35 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 87-91 31815524-0 2020 Active Vitamin D activates chondrocyte autophagy to reduce osteoarthritis via mediating the AMPK/mTOR signaling pathway. Vitamin D 7-16 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 92-96 31815524-7 2020 VD treatment elevated p-AMPK/AMPK and decreased p-mTOR/mTOR, and it increased LC3II/LC3I, increased the protein level of Beclin-1, but decreased p62 according to Western blot analysis. Vitamin D 0-2 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 24-28 31815524-7 2020 VD treatment elevated p-AMPK/AMPK and decreased p-mTOR/mTOR, and it increased LC3II/LC3I, increased the protein level of Beclin-1, but decreased p62 according to Western blot analysis. Vitamin D 0-2 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 29-33 31815524-9 2020 Meanwhile, AMPK inhibitor Compound C and autophagy inhibitor 3-methyladenine (3-MA) reversed these changes following VD treatment. 3-methyladenine 78-82 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 11-15 31815524-9 2020 Meanwhile, AMPK inhibitor Compound C and autophagy inhibitor 3-methyladenine (3-MA) reversed these changes following VD treatment. Vitamin D 117-119 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 11-15 31815524-12 2020 This study provided evidence that active VD might activate chondrocyte autophagy to reduce OA inflammation via activating the AMPK/mTOR signaling pathway. Vitamin D 41-43 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 126-130 32156660-6 2020 In this sense, the present study showed that the sub-optimal Sorafenib concentration (10 nM) was associated with activation of caspase-9, AMP-activated protein kinase (AMPK), sustained autophagy, peroxisome proliferator-activated receptor-coactivator 1alpha (PGC-1alpha) and mitochondrial function in HepG2 cells. Sorafenib 61-70 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 138-166 32156660-6 2020 In this sense, the present study showed that the sub-optimal Sorafenib concentration (10 nM) was associated with activation of caspase-9, AMP-activated protein kinase (AMPK), sustained autophagy, peroxisome proliferator-activated receptor-coactivator 1alpha (PGC-1alpha) and mitochondrial function in HepG2 cells. Sorafenib 61-70 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 168-172 32220751-0 2020 Resveratrol prevents benzo(a)pyrene-induced disruption of mitochondrial homeostasis via the AMPK signaling pathway in primary cultured neurons. Resveratrol 0-11 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 92-96 32220751-0 2020 Resveratrol prevents benzo(a)pyrene-induced disruption of mitochondrial homeostasis via the AMPK signaling pathway in primary cultured neurons. Benzo(a)pyrene 21-35 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 92-96 32220751-6 2020 Further, our results indicated that RSV pretreatment enhanced mitochondrial biogenesis via the AMPK/PGC-1alpha pathway and activated mitophagy via the PINK1-Parkin and AMPK/ULK1 pathways, thereby coordinating mitochondrial homeostasis. Resveratrol 36-39 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 95-99 32220751-6 2020 Further, our results indicated that RSV pretreatment enhanced mitochondrial biogenesis via the AMPK/PGC-1alpha pathway and activated mitophagy via the PINK1-Parkin and AMPK/ULK1 pathways, thereby coordinating mitochondrial homeostasis. Resveratrol 36-39 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 168-172 32220751-8 2020 This work provided insights into the role of RSV in preventing BaP-induced primary neuronal apoptosis in the mitochondrial pathway, mainly via regulation of mitochondrial biogenesis and mitophagy through AMPK pathway, thus maintaining the integrity of the mitochondrial network. Resveratrol 45-48 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 204-208 32220751-8 2020 This work provided insights into the role of RSV in preventing BaP-induced primary neuronal apoptosis in the mitochondrial pathway, mainly via regulation of mitochondrial biogenesis and mitophagy through AMPK pathway, thus maintaining the integrity of the mitochondrial network. Benzo(a)pyrene 63-66 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 204-208 32492936-11 2020 Interestingly, at the protein level, chronic fructose treatment favored fasting-like phenotype in human islets, as witnessed by AMPK activation. Fructose 45-53 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 128-132 32398866-8 2020 Alteration of metabolic activity and increased AMP/ATP ratio lead to LKB1-dependent AMPK activation. Adenosine Monophosphate 47-50 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 84-88 32398866-8 2020 Alteration of metabolic activity and increased AMP/ATP ratio lead to LKB1-dependent AMPK activation. Adenosine Triphosphate 51-54 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 84-88 32464299-0 2020 3,5-dicaffeoyl-epi-quinic acid from Atriplex gmelinii enhances the osteoblast differentiation of bone marrow-derived human mesenchymal stromal cells via WnT/BMP signaling and suppresses adipocyte differentiation via AMPK activation. Isochlorogenic acid A 0-30 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 216-220 32464299-14 2020 The adipocyte differentiation inhibitory effect of DCEQA was suggested to arise from its ability to increase AMPK phosphorylation. dceqa 51-56 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 109-113 32184170-7 2020 Submicromolar-concentration As2O3 dose-dependently triggered C2C12 myotube atrophy and increased the protein expressions of atrogenes Atrogin1 and MuRF1 and inhibited the upstream phosphorylated proteins Akt and FoxO1, while As2O3 dose-dependently increased AMPK phosphorylation in myotubes. Arsenic Trioxide 28-33 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 258-262 32245619-0 2020 Humanin attenuates palmitate-induced hepatic lipid accumulation and insulin resistance via AMPK-mediated suppression of the mTOR pathway. Palmitates 19-28 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 91-95 32245619-9 2020 AMPK knockdown by siRNA neutralized the effects of HN on palmitic acid-treated hepatocytes. Palmitic Acid 57-70 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 32245619-10 2020 Collectively, HN prevents palmitate-induced hepatic lipid accumulation, apoptosis, and insulin resistance via AMPK-mediated suppression of the mTOR/SREBP1 pathway, suggesting that it may serve as a potential therapeutic agent in NAFLD treatment. Palmitates 26-35 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 110-114 31558185-4 2020 PRKAA1 downregulation by shRNA or treatment of AMPK inhibitor compound C significantly inhibited proliferation as well as promoted cell cycle arrest and apoptosis of BGC-823 and MKN45 cells. Carbon 71-72 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 47-51 32546967-0 2020 Glycine Improves Ischemic Stroke Through miR-19a-3p/AMPK/GSK-3beta/HO-1 Pathway. Glycine 0-7 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 52-56 32444674-4 2020 These actions depend on metformin-mediated activation of AMP kinase (AMPK). Metformin 24-33 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 57-67 32444674-4 2020 These actions depend on metformin-mediated activation of AMP kinase (AMPK). Metformin 24-33 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 69-73 32444674-7 2020 5-Aminoimidazole-4-carboxamide ribonucleotide (AICAR), an AMPK activator, elicits a similar effect. AICA ribonucleotide 0-45 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 58-62 32444674-7 2020 5-Aminoimidazole-4-carboxamide ribonucleotide (AICAR), an AMPK activator, elicits a similar effect. AICA ribonucleotide 47-52 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 58-62 32444674-11 2020 The transcription factor downstream of AMPK that is relevant to cAMP signaling is CREB; decreased levels of phospho-CREB seem to mediate the observed effects of metformin on NaCT. Cyclic AMP 64-68 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 39-43 32444674-11 2020 The transcription factor downstream of AMPK that is relevant to cAMP signaling is CREB; decreased levels of phospho-CREB seem to mediate the observed effects of metformin on NaCT. Metformin 161-170 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 39-43 32434995-4 2020 Unbiased high-throughput metabolic profiling coupled with in vitro and in vivo flux analyses with isotopically labeled tracers led us to discover that maternal eENT1-dependent adenosine uptake is critical in activating AMPK by controlling the AMP/ATP ratio and its downstream target, bisphosphoglycerate mutase (BPGM); in turn, BPGM mediates 2,3-BPG production, which enhances O2 delivery to maintain placental oxygenation. Adenosine 176-185 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 219-223 32434995-4 2020 Unbiased high-throughput metabolic profiling coupled with in vitro and in vivo flux analyses with isotopically labeled tracers led us to discover that maternal eENT1-dependent adenosine uptake is critical in activating AMPK by controlling the AMP/ATP ratio and its downstream target, bisphosphoglycerate mutase (BPGM); in turn, BPGM mediates 2,3-BPG production, which enhances O2 delivery to maintain placental oxygenation. Adenosine Triphosphate 247-250 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 219-223 32434995-4 2020 Unbiased high-throughput metabolic profiling coupled with in vitro and in vivo flux analyses with isotopically labeled tracers led us to discover that maternal eENT1-dependent adenosine uptake is critical in activating AMPK by controlling the AMP/ATP ratio and its downstream target, bisphosphoglycerate mutase (BPGM); in turn, BPGM mediates 2,3-BPG production, which enhances O2 delivery to maintain placental oxygenation. 2,3-Diphosphoglycerate 342-349 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 219-223 32434995-4 2020 Unbiased high-throughput metabolic profiling coupled with in vitro and in vivo flux analyses with isotopically labeled tracers led us to discover that maternal eENT1-dependent adenosine uptake is critical in activating AMPK by controlling the AMP/ATP ratio and its downstream target, bisphosphoglycerate mutase (BPGM); in turn, BPGM mediates 2,3-BPG production, which enhances O2 delivery to maintain placental oxygenation. Oxygen 377-379 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 219-223 32014500-6 2020 The elevated levels of H2O2 (a biomarker of oxidative stress) and the free radicals (NO and O2 -) reduced the concentration of dominant pathogens and regulated ROS/RNS/AMP-activated protein kinase (AMPK)/mTOR pathway by affecting p-AMPK, Runt-related transcription factor 2 (RUNX2), p-c-Jun N-terminal kinase (JNK)/mammalian target of rapamycin (mTOR), and acetyl-CoA carboxylase 1 (ACC1). Water 23-27 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 161-197 32014500-6 2020 The elevated levels of H2O2 (a biomarker of oxidative stress) and the free radicals (NO and O2 -) reduced the concentration of dominant pathogens and regulated ROS/RNS/AMP-activated protein kinase (AMPK)/mTOR pathway by affecting p-AMPK, Runt-related transcription factor 2 (RUNX2), p-c-Jun N-terminal kinase (JNK)/mammalian target of rapamycin (mTOR), and acetyl-CoA carboxylase 1 (ACC1). Water 23-27 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 199-203 32014500-6 2020 The elevated levels of H2O2 (a biomarker of oxidative stress) and the free radicals (NO and O2 -) reduced the concentration of dominant pathogens and regulated ROS/RNS/AMP-activated protein kinase (AMPK)/mTOR pathway by affecting p-AMPK, Runt-related transcription factor 2 (RUNX2), p-c-Jun N-terminal kinase (JNK)/mammalian target of rapamycin (mTOR), and acetyl-CoA carboxylase 1 (ACC1). Superoxides 25-27 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 161-197 32014500-6 2020 The elevated levels of H2O2 (a biomarker of oxidative stress) and the free radicals (NO and O2 -) reduced the concentration of dominant pathogens and regulated ROS/RNS/AMP-activated protein kinase (AMPK)/mTOR pathway by affecting p-AMPK, Runt-related transcription factor 2 (RUNX2), p-c-Jun N-terminal kinase (JNK)/mammalian target of rapamycin (mTOR), and acetyl-CoA carboxylase 1 (ACC1). Superoxides 25-27 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 199-203 32217192-15 2020 Collectively, these results showed that RS9-mediated activation of POS phagocytosis was mainly ascribed to the enhancement of autophagy via AMPKalpha1 activation. rs9 40-43 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 140-150 32433500-8 2020 Metformin treatment on male diabetic placental explant activated AMPK and stimulated PGC-1alpha expression, concomitant with increased H3K27 acetylation and decreased PGC-1alpha promoter methylation. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 65-69 32518807-7 2020 An AMPK activator, metformin, inhibited FLS proliferation at higher but not lower concentrations, whereas the inhibitor dorsomorphin promoted the proliferation of RA-FLSs. Metformin 19-28 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 3-7 32518807-9 2020 After metformin treatment, expression of interleukin 6 (IL-6), TNF-alpha, and IL-1beta were significantly downregulated in RA-FLSs; however, increased expression of p-AMPK-alpha1, protein kinase A (PKA)-alpha1, and HAPLN1 (hyaluronan and proteoglycan link protein 1) was observed. Metformin 6-15 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 167-178 32393385-6 2020 Reduced AMPK expression by siRNA-mediated knockdown of PRKAA1 and PRKAA2 blocked autophagic flux in EOC spheroids as visualized by fluorescence microscopy using the mCherry-eGFP-LC3B reporter. eoc spheroids 100-113 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 8-12 32393385-6 2020 Reduced AMPK expression by siRNA-mediated knockdown of PRKAA1 and PRKAA2 blocked autophagic flux in EOC spheroids as visualized by fluorescence microscopy using the mCherry-eGFP-LC3B reporter. eoc spheroids 100-113 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 55-61 32393385-7 2020 A complementary approach using pharmacologic agents Compound C and CAMKKbeta inhibitor STO-609 to inhibit AMPK activity both yielded a potent blockade of autophagic flux as well. STO 609 87-94 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 106-110 32393385-8 2020 However, direct activation of AMPK in EOC cells using oligomycin and metformin was insufficient to induce autophagy. Oligomycins 54-64 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-34 32393385-8 2020 However, direct activation of AMPK in EOC cells using oligomycin and metformin was insufficient to induce autophagy. Metformin 69-78 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-34 32397660-0 2020 A Novel Zinc Chelator, 1H10, Ameliorates Experimental Autoimmune Encephalomyelitis by Modulating Zinc Toxicity and AMPK Activation. 1h10 23-27 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 115-119 32397660-3 2020 Recent studies have demonstrated that AMPK contributes to zinc-induced neurotoxicity and that 1H10, an inhibitor of AMPK, reduces zinc-induced neuronal death and protects against oxidative stress, excitotoxicity, and apoptosis. 1h10 94-98 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 116-120 32397660-10 2020 Therefore, the present study suggests that zinc chelation and AMPK inhibition with 1H10 may have great therapeutic potential for the treatment of multiple sclerosis. 1h10 83-87 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 62-66 32457629-0 2020 Berberine Improves Glucose and Lipid Metabolism in HepG2 Cells Through AMPKalpha1 Activation. Berberine 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 71-81 32457629-10 2020 Conclusion: Our study proves that AMPKalpha1 plays a critical role for BBR to improve glucose and lipid metabolism in HepG2 cells. Glucose 86-93 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 34-44 32382009-0 2020 Vitamin K2 promotes PI3K/AKT/HIF-1alpha-mediated glycolysis that leads to AMPK-dependent autophagic cell death in bladder cancer cells. Vitamin K 2 0-10 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 74-78 32382009-5 2020 Importantly, upon glucose limitation, Vitamin K2-upregulated glycolysis markedly induced metabolic stress, along with AMPK activation and mTORC1 pathway suppression, which subsequently triggered AMPK-dependent autophagic cell death. Glucose 18-25 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 118-122 32382009-5 2020 Importantly, upon glucose limitation, Vitamin K2-upregulated glycolysis markedly induced metabolic stress, along with AMPK activation and mTORC1 pathway suppression, which subsequently triggered AMPK-dependent autophagic cell death. Glucose 18-25 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 195-199 32382009-5 2020 Importantly, upon glucose limitation, Vitamin K2-upregulated glycolysis markedly induced metabolic stress, along with AMPK activation and mTORC1 pathway suppression, which subsequently triggered AMPK-dependent autophagic cell death. Vitamin K 2 38-48 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 118-122 32382009-5 2020 Importantly, upon glucose limitation, Vitamin K2-upregulated glycolysis markedly induced metabolic stress, along with AMPK activation and mTORC1 pathway suppression, which subsequently triggered AMPK-dependent autophagic cell death. Vitamin K 2 38-48 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 195-199 32382009-6 2020 Intriguingly, glucose supplementation profoundly abrogated AMPK activation and rescued bladder cancer cells from Vitamin K2-triggered autophagic cell death. Glucose 14-21 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 59-63 32382009-7 2020 Furthermore, both inhibition of PI3K/AKT/HIF-1alpha and attenuation of glycolysis significantly blocked Vitamin K2-induced AMPK activation and subsequently prevented autophagic cell death. Vitamin K 2 104-114 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 123-127 32382009-8 2020 Collectively, these findings reveal that Vitamin K2 could induce metabolic stress and trigger AMPK-dependent autophagic cell death in bladder cancer cells by PI3K/AKT/HIF-1alpha-mediated glycolysis promotion. Vitamin K 2 41-51 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 94-98 32375255-0 2020 The Metformin Mechanism on Gluconeogenesis and AMPK Activation: The Metabolite Perspective. Metformin 4-13 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 47-51 32375255-4 2020 The activation of AMPK by metformin could be consequent to Complex 1 inhibition and raised AMP through the canonical adenine nucleotide pathway or alternatively by activation of the lysosomal AMPK pool by other mechanisms involving the aldolase substrate fructose 1,6-bisphosphate or perturbations in the lysosomal membrane. Metformin 26-35 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 18-22 32375255-4 2020 The activation of AMPK by metformin could be consequent to Complex 1 inhibition and raised AMP through the canonical adenine nucleotide pathway or alternatively by activation of the lysosomal AMPK pool by other mechanisms involving the aldolase substrate fructose 1,6-bisphosphate or perturbations in the lysosomal membrane. Metformin 26-35 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 192-196 32375255-4 2020 The activation of AMPK by metformin could be consequent to Complex 1 inhibition and raised AMP through the canonical adenine nucleotide pathway or alternatively by activation of the lysosomal AMPK pool by other mechanisms involving the aldolase substrate fructose 1,6-bisphosphate or perturbations in the lysosomal membrane. Adenosine Monophosphate 18-21 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 192-196 32375255-4 2020 The activation of AMPK by metformin could be consequent to Complex 1 inhibition and raised AMP through the canonical adenine nucleotide pathway or alternatively by activation of the lysosomal AMPK pool by other mechanisms involving the aldolase substrate fructose 1,6-bisphosphate or perturbations in the lysosomal membrane. Adenine Nucleotides 117-135 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 18-22 32375255-4 2020 The activation of AMPK by metformin could be consequent to Complex 1 inhibition and raised AMP through the canonical adenine nucleotide pathway or alternatively by activation of the lysosomal AMPK pool by other mechanisms involving the aldolase substrate fructose 1,6-bisphosphate or perturbations in the lysosomal membrane. fructose-1,6-diphosphate 255-280 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 18-22 32156705-0 2020 Metformin limits osteoarthritis development and progression through activation of AMPK signalling. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 82-86 32156705-8 2020 RESULTS: Metformin upregulated phosphorylated and total AMPK expression in articular cartilage tissue. Metformin 9-18 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 56-60 31781983-9 2020 Furthermore, Western blotting analysis showed that ABZ induced the apoptosis in MDA-MB-231 cells via GLUT1/AMPK/P53 signaling pathway. Albendazole 51-54 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 107-111 31916329-10 2020 Enhanced AMPK/SIRT1 signaling may also contribute to the action of SGLT2 inhibitors to interfere with sodium transport mechanisms. Sodium 102-108 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 9-13 31877229-8 2020 Interestingly, the AMPK activator AICAR, the autophagy inducer rapamycin and the demethylation inhibitor difenoconazole negated CD74 ablation-offered benefit against LPS-induced cardiac dysfunction while the SUV39H1 inhibitor chaetocin or methylation inhibitor 5-AzaC ameliorated LPS-induced GFP-LC3B formation and cardiomyocyte contractile dysfunction. Aza Compounds 261-267 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 19-23 32489327-10 2020 Furthermore, mechanistic studies showed that NNMT suppressed the ROS increase, ATP decrease and AMPK-ULK1 pathway activation, resulting in the inhibition of H2O2-induced autophagy in breast cancer cells. Hydrogen Peroxide 157-161 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 96-100 32489327-11 2020 Conclusions: We conclude that NNMT inhibits the autophagy induced by oxidative stress through the ROS-mediated AMPK-ULK1 pathway in breast cancer cells and may protect breast cancer cells against oxidative stress through autophagy suppression. Reactive Oxygen Species 98-101 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 111-115 32219907-7 2020 Target motif analysis of the phosphopeptides increased in PKA-null cells indicates that vasopressin activates one or more members of the AMPK/SNF1-subfamily of basophilic protein kinases. Phosphopeptides 29-44 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 137-141 32067339-5 2020 Here, we will highlight recent findings demonstrating the mechanistic effects through which adiponectin is able to fuel genomic and non-genomic estrogen signalling, inhibiting LKB1/AMPK/mTOR/S6K pathway and switching energy balance. Estrogens 144-152 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 181-185 32179242-0 2020 Non-lethal sonodynamic therapy facilitates the M1-to-M2 transition in advanced atherosclerotic plaques via activating the ROS-AMPK-mTORC1-autophagy pathway. Reactive Oxygen Species 122-125 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 126-130 32179242-4 2020 Further mechanistic studies indicated that NL-SDT enhanced macrophage differentiation toward the M2 phenotype by activating the reactive oxygen species (ROS)-5" AMP-activated protein kinase (AMPK)-mammalian target of rapamycin complex 1 (mTORC1)-autophagy signaling pathway in murine BM-derived M1 macrophages (BMDM1s). nl-sdt 43-49 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 161-189 32179242-4 2020 Further mechanistic studies indicated that NL-SDT enhanced macrophage differentiation toward the M2 phenotype by activating the reactive oxygen species (ROS)-5" AMP-activated protein kinase (AMPK)-mammalian target of rapamycin complex 1 (mTORC1)-autophagy signaling pathway in murine BM-derived M1 macrophages (BMDM1s). nl-sdt 43-49 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 191-195 32179242-4 2020 Further mechanistic studies indicated that NL-SDT enhanced macrophage differentiation toward the M2 phenotype by activating the reactive oxygen species (ROS)-5" AMP-activated protein kinase (AMPK)-mammalian target of rapamycin complex 1 (mTORC1)-autophagy signaling pathway in murine BM-derived M1 macrophages (BMDM1s). Reactive Oxygen Species 128-151 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 161-189 32179242-4 2020 Further mechanistic studies indicated that NL-SDT enhanced macrophage differentiation toward the M2 phenotype by activating the reactive oxygen species (ROS)-5" AMP-activated protein kinase (AMPK)-mammalian target of rapamycin complex 1 (mTORC1)-autophagy signaling pathway in murine BM-derived M1 macrophages (BMDM1s). Reactive Oxygen Species 128-151 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 191-195 32179242-4 2020 Further mechanistic studies indicated that NL-SDT enhanced macrophage differentiation toward the M2 phenotype by activating the reactive oxygen species (ROS)-5" AMP-activated protein kinase (AMPK)-mammalian target of rapamycin complex 1 (mTORC1)-autophagy signaling pathway in murine BM-derived M1 macrophages (BMDM1s). Reactive Oxygen Species 153-156 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 161-189 32179242-4 2020 Further mechanistic studies indicated that NL-SDT enhanced macrophage differentiation toward the M2 phenotype by activating the reactive oxygen species (ROS)-5" AMP-activated protein kinase (AMPK)-mammalian target of rapamycin complex 1 (mTORC1)-autophagy signaling pathway in murine BM-derived M1 macrophages (BMDM1s). Reactive Oxygen Species 153-156 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 191-195 32179242-7 2020 These findings indicate that NL-SDT engages a virtuous cycle that enhances M1-to-M2 polarization, cholesterol efflux, and anti-inflammatory reactions in advanced plaque in vivo and in BMDM1s in vitro by activating the ROS-AMPK-mTORC1-autophagy pathway. Reactive Oxygen Species 218-221 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 222-226 32419825-0 2020 Mogroside V Protects against Hepatic Steatosis in Mice on a High-Fat Diet and LO2 Cells Treated with Free Fatty Acids via AMPK Activation. mogroside V 0-11 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 122-126 32419825-0 2020 Mogroside V Protects against Hepatic Steatosis in Mice on a High-Fat Diet and LO2 Cells Treated with Free Fatty Acids via AMPK Activation. Fatty Acids, Nonesterified 101-117 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 122-126 32419825-7 2020 In addition, in free fatty acids- (FFAs-) incubated LO2 cells MV downregulated de novo lipogenesis and upregulated lipolysis and fatty acid oxidation, thereby attenuating lipid accumulation, which was significantly abrogated by treatment with Compound C, an inhibitor of AMP-activated protein kinase (AMPK). Fatty Acids 21-32 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 271-299 32419825-7 2020 In addition, in free fatty acids- (FFAs-) incubated LO2 cells MV downregulated de novo lipogenesis and upregulated lipolysis and fatty acid oxidation, thereby attenuating lipid accumulation, which was significantly abrogated by treatment with Compound C, an inhibitor of AMP-activated protein kinase (AMPK). Fatty Acids 21-32 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 301-305 32419825-7 2020 In addition, in free fatty acids- (FFAs-) incubated LO2 cells MV downregulated de novo lipogenesis and upregulated lipolysis and fatty acid oxidation, thereby attenuating lipid accumulation, which was significantly abrogated by treatment with Compound C, an inhibitor of AMP-activated protein kinase (AMPK). Fatty Acids 21-31 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 271-299 32419825-7 2020 In addition, in free fatty acids- (FFAs-) incubated LO2 cells MV downregulated de novo lipogenesis and upregulated lipolysis and fatty acid oxidation, thereby attenuating lipid accumulation, which was significantly abrogated by treatment with Compound C, an inhibitor of AMP-activated protein kinase (AMPK). Fatty Acids 21-31 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 301-305 32419825-8 2020 Taken together, these results suggested that MV exerted a pronounced effect upon improving hepatic steatosis through regulating the disequilibrium of lipid metabolism in the liver via an AMPK-dependent pathway, providing a potential lead compound candidate for preventing nonalcoholic fatty liver disease. mogroside V 45-47 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 187-191 33103038-11 2020 Conclusion: Adiponectin attenuated the high-glucose-induced premature senescence of VSMCs via increasing telomerase activity of VSMCs, which was achieved by activation of AMPK/TSC2/mTOR/S6K1 signaling and inhibition of PI3K/Akt/mTOR/S6K1 signaling. Glucose 44-51 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 171-175 32330379-3 2020 We aimed to analyze the protective effects elicited by genistein/estradiol in hepatocytes cultured in NAFLD-like medium on cell viability, triglycerides accumulation, mitochondrial function and oxidative stress and the role of NLRP3 inflammasome, toll like receptors 4 (TLR4), Akt and 5" AMP-activated protein kinase (AMPK)alpha1/2. Genistein 55-64 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 318-331 32420361-0 2020 Catalpol Attenuates Hepatic Steatosis by Regulating Lipid Metabolism via AMP-Activated Protein Kinase Activation. catalpol 0-8 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 73-101 32420361-9 2020 However, the preincubation of the HepG2 cells with compound C (10 muM), an AMPK inhibitor, prevented catalpol-mediated beneficial effects. catalpol 101-109 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 75-79 32420361-10 2020 These findings suggest that catalpol ameliorates hepatic steatosis by suppressing lipogenesis and enhancing fatty acid beta-oxidation in an AMPK-dependent manner. catalpol 28-36 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 140-144 32330121-6 2020 The findings were reproduced in the doxorubicin-induced senescence of young fs-HDF and WI-38 cells via the PKCzeta-LKB1-AMPK signaling pathway, which was regulated by the p53-p21WAF1 pathway when p16INK4a was silenced. Doxorubicin 36-47 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 120-124 32312965-6 2020 We identified that binding of COL11A1 to its receptors, alpha1beta1 integrin and discoidin domain receptor 2 (DDR2), activates Src-Akt-AMPK signaling to increase the expression of both fatty acid synthesis and oxidation enzymes, although DDR2 seems to be the predominant receptor. Fatty Acids 185-195 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 135-139 32312965-8 2020 Taken together, our results suggest that COL11A1 upregulates fatty acid metabolism in ovarian cancer cells in a DDR2-Src-Akt-AMPK dependent manner. Fatty Acids 61-71 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 125-129 32300102-0 2020 MSC-induced lncRNA HCP5 drove fatty acid oxidation through miR-3619-5p/AMPK/PGC1alpha/CEBPB axis to promote stemness and chemo-resistance of gastric cancer. Fatty Acids 30-40 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 71-75 32273511-5 2020 Mechanistically, asparagine and aspartate regulate AMPK-mediated p53 activation by physically binding to LKB1 and oppositely modulating LKB1 activity. Asparagine 17-27 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 51-55 32273511-5 2020 Mechanistically, asparagine and aspartate regulate AMPK-mediated p53 activation by physically binding to LKB1 and oppositely modulating LKB1 activity. Aspartic Acid 32-41 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 51-55 32273511-6 2020 Thus, we found that p53 regulates asparagine metabolism and dictates cell survival by generating an auto-amplification loop via asparagine-aspartate-mediated LKB1-AMPK signalling. Asparagine 34-44 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 163-167 32273511-6 2020 Thus, we found that p53 regulates asparagine metabolism and dictates cell survival by generating an auto-amplification loop via asparagine-aspartate-mediated LKB1-AMPK signalling. Asparagine 128-138 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 163-167 32273511-6 2020 Thus, we found that p53 regulates asparagine metabolism and dictates cell survival by generating an auto-amplification loop via asparagine-aspartate-mediated LKB1-AMPK signalling. Aspartic Acid 139-148 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 163-167 31958198-11 2020 Furthermore, Sestrin2 suppressed impaired trophoblast invasion caused by palmitate, and attenuated palmitate-induced ER stress and inflammation via AMPK/mTORC1 pathways. Palmitates 99-108 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 148-152 31789625-7 2020 We found that microRNA-7 was dramatically upregulated by metformin via AMPK in a dose- and time-dependent manner. Metformin 57-66 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 71-75 31789625-12 2020 Our discovery revealed that metformin, via increasing the expression of microRNA-7 mediated by AMPK, regulates the AKT/mTOR, MAPK/Erk, and NF-kappaB signaling pathways, thereby suppressing A549 cell growth, migration, and invasion. Metformin 28-37 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 95-99 31071273-5 2020 In addition, experiments utilizing pharmacological modulators of adenosine 5"-monophosphate (AMP)-activated protein kinase (AMPK) and liver kinase B1 (LKB1)-deficient HeLa cells demonstrated that these suppressive effects are mediated by the LKB1/AMPK pathway. adenosine 5"-monophosphate 65-91 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 124-128 31071273-5 2020 In addition, experiments utilizing pharmacological modulators of adenosine 5"-monophosphate (AMP)-activated protein kinase (AMPK) and liver kinase B1 (LKB1)-deficient HeLa cells demonstrated that these suppressive effects are mediated by the LKB1/AMPK pathway. adenosine 5"-monophosphate 65-91 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 247-251 31071273-5 2020 In addition, experiments utilizing pharmacological modulators of adenosine 5"-monophosphate (AMP)-activated protein kinase (AMPK) and liver kinase B1 (LKB1)-deficient HeLa cells demonstrated that these suppressive effects are mediated by the LKB1/AMPK pathway. Adenosine Monophosphate 93-96 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 124-128 31071273-5 2020 In addition, experiments utilizing pharmacological modulators of adenosine 5"-monophosphate (AMP)-activated protein kinase (AMPK) and liver kinase B1 (LKB1)-deficient HeLa cells demonstrated that these suppressive effects are mediated by the LKB1/AMPK pathway. Adenosine Monophosphate 93-96 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 247-251 31895870-0 2020 Artemisinin attenuated atherosclerosis in high-fat diet-fed ApoE-/- mice by promoting macrophage autophagy via AMPK/mTOR/ULK1 pathway. Artemisinins 0-11 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 111-115 31877229-8 2020 Interestingly, the AMPK activator AICAR, the autophagy inducer rapamycin and the demethylation inhibitor difenoconazole negated CD74 ablation-offered benefit against LPS-induced cardiac dysfunction while the SUV39H1 inhibitor chaetocin or methylation inhibitor 5-AzaC ameliorated LPS-induced GFP-LC3B formation and cardiomyocyte contractile dysfunction. AICA ribonucleotide 34-39 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 19-23 31705397-12 2020 CONCLUSION: Our data seemed to show that LC attenuate fructose-mediated lipid accumulation through AMPK activation. Fructose 54-62 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 99-103 32060057-1 2020 In response to glucose starvation, AMPK inhibited lipid peroxidation-associated ferroptosis. Glucose 15-22 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 35-39 31895870-5 2020 Moreover, artemisinin promoted AMP activated protein kinase (AMPK) activation, inhibited mammalian target of rapamycin (mTOR) and uncoordinated-51-like kinases 1 (ULK1) phosphorylation, increased LC-3II accumulation and P62 degradation, and thereby enhancing macrophage autophagy. Artemisinins 10-21 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 31-59 31895870-6 2020 Besides, the inhibiting effect of artemisinin on mTOR and ULK1 phosphorylation could be abrogated by AMPK knockdown, suggesting AMPK was the essential target of artemisinin on promoting macrophage autophagy. Artemisinins 34-45 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 101-105 31895870-6 2020 Besides, the inhibiting effect of artemisinin on mTOR and ULK1 phosphorylation could be abrogated by AMPK knockdown, suggesting AMPK was the essential target of artemisinin on promoting macrophage autophagy. Artemisinins 34-45 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 128-132 31895870-6 2020 Besides, the inhibiting effect of artemisinin on mTOR and ULK1 phosphorylation could be abrogated by AMPK knockdown, suggesting AMPK was the essential target of artemisinin on promoting macrophage autophagy. Artemisinins 161-172 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 101-105 31895870-6 2020 Besides, the inhibiting effect of artemisinin on mTOR and ULK1 phosphorylation could be abrogated by AMPK knockdown, suggesting AMPK was the essential target of artemisinin on promoting macrophage autophagy. Artemisinins 161-172 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 128-132 31895870-7 2020 Our study indicated that artemisinin alleviated atherosclerotic lesions by accelerating macrophage autophagy via AMPK/mTOR/ULK1 pathway. Artemisinins 25-36 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 113-117 32206298-0 2020 Sirt6 opposes glycochenodeoxycholate-induced apoptosis of biliary epithelial cells through the AMPK/PGC-1alpha pathway. Glycochenodeoxycholic Acid 14-36 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 95-99 32206298-10 2020 Conclusion: Our data illuminated that Sirt6 ameliorated GCDC-induced HiBEC apoptosis by upregulating PGC-1alpha expression through the AMPK pathway and its deacetylation effect. Glycochenodeoxycholic Acid 56-60 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 135-139 32258129-9 2020 Furthermore, citral suppressed lipogenesis of prostate cancer cells through the activation of AMPK phosphorylation and downregulation of fatty acid synthase (FASN), acetyl coA carboxylase (ACC), 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGR), and sterol regulatory element-binding protein (SREBP1) and apoptosis of PC3 cells by upregulating BAX and downregulating Bcl-2 expression. citral 13-19 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 94-98 32258142-0 2020 Aspirin Improves Nonalcoholic Fatty Liver Disease and Atherosclerosis through Regulation of the PPARdelta-AMPK-PGC-1alpha Pathway in Dyslipidemic Conditions. Aspirin 0-7 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 106-110 32258142-3 2020 The protein levels of biomarkers (PPARdelta, AMPK, and PGC-1alpha) involved in oxidative phosphorylation in both the vascular endothelial and liver cells were elevated by the aspirin in hyperlipidemic condition. Aspirin 175-182 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 45-49 31948761-0 2020 Telmisartan attenuates obesity-induced insulin resistance via suppression of AMPK mediated ER stress. telmisartan 0-11 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 77-81 31948761-5 2020 Furthermore, we showed that Telmisartan suppressed ER stress by activating AMP-activated protein kinase (AMPK) signaling pathway in vivo. telmisartan 28-39 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 75-103 31948761-5 2020 Furthermore, we showed that Telmisartan suppressed ER stress by activating AMP-activated protein kinase (AMPK) signaling pathway in vivo. telmisartan 28-39 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 105-109 31948761-7 2020 Compound C, an AMPK inhibitor, could abolish beneficial effect of Telmisartan on ER stress. telmisartan 66-77 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 15-19 31948761-8 2020 Our data indicated Telmisartan improved obesity-induced insulin resistance through suppression of ER stress by activation of AMPK. telmisartan 19-30 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 125-129 32168879-3 2020 We show that VEGF leads to AMPKalpha1-dependent phosphorylation of Unc-51-like kinase 1 (ULK1) at its serine residue 556 and to the subsequent phosphorylation of the ULK1 substrate ATG14. Serine 102-108 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 27-37 33543028-6 2020 In particular, salicylate was found to potently activate AMPK, a kinase known to inhibit HAS2 activity, and caused a dose-dependent decrease of cell associated (intracellular and membrane-bound) as well as secreted hyaluronan, followed by the down-regulation of HAS2 and the induction of HYAL-2 and CD44 in metastatic breast cancer cells. Salicylates 15-25 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 57-61 31778750-0 2020 Metformin reduces TRPC6 expression through AMPK activation and modulates cytoskeleton dynamics in podocytes under diabetic conditions. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 43-47 31778750-3 2020 AMP-activated protein kinase (AMPK), a key regulator of glucose and fatty acid metabolism, plays a major role in obesity and type 2 diabetes. Glucose 56-63 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-28 31778750-3 2020 AMP-activated protein kinase (AMPK), a key regulator of glucose and fatty acid metabolism, plays a major role in obesity and type 2 diabetes. Glucose 56-63 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-34 31778750-3 2020 AMP-activated protein kinase (AMPK), a key regulator of glucose and fatty acid metabolism, plays a major role in obesity and type 2 diabetes. Fatty Acids 68-78 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-28 31778750-3 2020 AMP-activated protein kinase (AMPK), a key regulator of glucose and fatty acid metabolism, plays a major role in obesity and type 2 diabetes. Fatty Acids 68-78 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-34 31778750-6 2020 Recent studies have suggested that the therapeutic effect of metformin might be mediated by AMPK. Metformin 61-70 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 92-96 31778750-8 2020 In this study, we demonstrated that metformin normalized TRPC6 expression via AMPKalpha1 activation in podocytes exposed to high glucose concentrations. Metformin 36-45 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 78-88 31778750-8 2020 In this study, we demonstrated that metformin normalized TRPC6 expression via AMPKalpha1 activation in podocytes exposed to high glucose concentrations. Glucose 129-136 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 78-88 31778750-9 2020 A quantitative analysis showed that metformin increased the colocalization of TRPC6 and AMPKalpha1 subunits from 42% to 61% in standard glucose (SG) medium and from 29% to 52% in high glucose (HG) medium. Metformin 36-45 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 88-98 31778750-9 2020 A quantitative analysis showed that metformin increased the colocalization of TRPC6 and AMPKalpha1 subunits from 42% to 61% in standard glucose (SG) medium and from 29% to 52% in high glucose (HG) medium. Glucose 136-143 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 88-98 31778750-9 2020 A quantitative analysis showed that metformin increased the colocalization of TRPC6 and AMPKalpha1 subunits from 42% to 61% in standard glucose (SG) medium and from 29% to 52% in high glucose (HG) medium. Glucose 184-191 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 88-98 31778750-11 2020 Moreover, metformin through AMPK activation remodeled cytoskeleton dynamics, and consequently, reduced filtration barrier permeability in diabetic conditions. Metformin 10-19 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 28-32 31895870-5 2020 Moreover, artemisinin promoted AMP activated protein kinase (AMPK) activation, inhibited mammalian target of rapamycin (mTOR) and uncoordinated-51-like kinases 1 (ULK1) phosphorylation, increased LC-3II accumulation and P62 degradation, and thereby enhancing macrophage autophagy. Artemisinins 10-21 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 61-65 31919406-4 2020 The DCA-responsive proteins in AMPK pathway were enriched using proteomic profiling technology. Dichloroacetic Acid 4-7 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 31-35 31919406-5 2020 The effect of DCA on CAB39-AMPK signal pathway was analysed. Dichloroacetic Acid 14-17 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 27-31 31919406-10 2020 DCA could upregulate CAB39 expression, which activates the AMPK/mTOR signalling pathway. Dichloroacetic Acid 0-3 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 59-63 31916911-0 2020 Magnolol Alleviates IL-1beta-Induced Dysfunction of Chondrocytes Through Repression of SIRT1/AMPK/PGC-1alpha Signaling Pathway. magnolol 0-8 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 93-97 31916911-8 2020 We demonstrated that magnolol increased SIRT1/AMPK/PGC-1alpha expression in human chondrocytes. magnolol 21-29 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 46-50 31916911-9 2020 Magnolol could alleviate IL-1beta-induced mitochondrial dysfunction and oxidative stress through SIRT1/AMPK/PGC-1alpha signaling pathway in human chondrocytes. magnolol 0-8 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 103-107 31916911-10 2020 In addition, magnolol maintained the anabolism and catabolism of extracellular matrix balance by SIRT1/AMPK/PGC-1alpha signaling pathway. magnolol 13-21 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 103-107 31916911-12 2020 Magnolol alleviates IL-1beta-induced dysfunction of chondrocytes through repressing SIRT1/AMPK/PGC-1alpha signaling pathway, which provides a potential new therapeutic strategy for human osteoarthritis. magnolol 0-8 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 90-94 31957433-7 2020 Specific suppression of AMPK signaling by AMPKalpha1 siRNA or by AMPK inhibitor compound C significantly attenuated the PB2-induced upregulation of phospho-AMPK, PGC-1alpha, and slow MyHC and downregulation of fast MyHC. phosphorylleucylphenylalanine 148-155 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 42-52 32051337-0 2020 GLUT5-mediated fructose utilization drives lung cancer growth by stimulating fatty acid synthesis and AMPK/mTORC1 signaling. Fructose 15-23 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 102-106 32051337-7 2020 Furthermore, molecular mechanism investigation revealed that GLUT5-mediated fructose utilization was required to suppress AMPK and consequently activate mTORC1 activity to promote LC growth. Fructose 76-84 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 122-126 31957433-0 2020 Procyanidin B2 Promotes Skeletal Slow-Twitch Myofiber Gene Expression through the AMPK Signaling Pathway in C2C12 Myotubes. procyanidin B 0-14 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 82-86 31957433-6 2020 The upstream factors of AMPK, such as phospho-LKB1, NRF1, and CaMKKbeta, and the downstream factors of AMPK, including Sirt1 and PGC-1alpha, were also increased by PB2. phosphorylleucylphenylalanine 38-45 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 24-28 31957433-7 2020 Specific suppression of AMPK signaling by AMPKalpha1 siRNA or by AMPK inhibitor compound C significantly attenuated the PB2-induced upregulation of phospho-AMPK, PGC-1alpha, and slow MyHC and downregulation of fast MyHC. phosphorylleucylphenylalanine 148-155 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 24-28 32191575-0 2020 6-Acetyl-2,2-Dimethylchroman-4-One Isolated from Artemisia princeps Suppresses Adipogenic Differentiation of Human Bone Marrow-Derived Mesenchymal Stromal Cells via Activation of AMPK. 6-acetyl-2,2-dimethylchroman-4-one 0-34 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 179-183 32014016-10 2020 The observed effects of AICAR and NAM were in light of the attenuated mTORC1 activity and increased AMPK activity and autophagy. AICA ribonucleotide 24-29 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 100-104 32014016-10 2020 The observed effects of AICAR and NAM were in light of the attenuated mTORC1 activity and increased AMPK activity and autophagy. Niacinamide 34-37 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 100-104 31874063-0 2020 The insulin-sensitizing mechanism of myo-inositol is associated with AMPK activation and GLUT-4 expression in human endometrial cells exposed to a PCOS environment. Inositol 37-49 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 69-73 31874063-9 2020 Also, MYO restored glucose uptake in cells under PCOS condition through a p-AMPK-dependent mechanism. Glucose 19-26 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 76-80 31746509-0 2020 AMPK and Akt/mTOR signaling pathways participate in glucose-mediated regulation of HBV replication and cellular autophagy. Glucose 52-59 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 31746509-5 2020 At low glucose concentration, AMPK activity was increased and led to ULK1 phosphorylation at Ser 555 and LC3-II accumulation. Glucose 7-14 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-34 31746509-5 2020 At low glucose concentration, AMPK activity was increased and led to ULK1 phosphorylation at Ser 555 and LC3-II accumulation. seryl-seryl-seryl-arginine 93-96 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-34 31746509-7 2020 mTOR inhibition by rapamycin reversed negative effects of high glucose concentrations on HBV replication, suggesting that low glucose concentration promotes HBV replication by stimulating the AMPK/mTOR-ULK1-autophagy axis. Sirolimus 19-28 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 192-196 31746509-7 2020 mTOR inhibition by rapamycin reversed negative effects of high glucose concentrations on HBV replication, suggesting that low glucose concentration promotes HBV replication by stimulating the AMPK/mTOR-ULK1-autophagy axis. Glucose 63-70 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 192-196 31746509-7 2020 mTOR inhibition by rapamycin reversed negative effects of high glucose concentrations on HBV replication, suggesting that low glucose concentration promotes HBV replication by stimulating the AMPK/mTOR-ULK1-autophagy axis. Glucose 126-133 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 192-196 31746509-8 2020 Consistently, we found that glucose transporters (GLUTs) inhibition using phloretin also enhanced HBV replication via increased AMPK/mTOR-ULK1-induced autophagy. Glucose 28-35 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 128-132 31746509-8 2020 Consistently, we found that glucose transporters (GLUTs) inhibition using phloretin also enhanced HBV replication via increased AMPK/mTOR-ULK1-induced autophagy. Phloretin 74-83 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 128-132 31712319-6 2020 Mechanistically, SIRT3 inhibits mitochondrial calcium uniporter (MCU)-mediated mitochondrial calcium overload by reducing the H3K27ac level on the MCU promoter in an AMPK-dependent manner. Calcium 46-53 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 166-170 31712319-6 2020 Mechanistically, SIRT3 inhibits mitochondrial calcium uniporter (MCU)-mediated mitochondrial calcium overload by reducing the H3K27ac level on the MCU promoter in an AMPK-dependent manner. Calcium 93-100 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 166-170 31712319-7 2020 In addition, HFD also inhibits AMPK activity to reduce SIRT3 expression, which could be reversed by capsaicin. Capsaicin 100-109 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 31-35 31930700-5 2020 Phosphorylated AMPK at Thr172 was reduced, and phosphorylated mammalian target of rapamycin (mTOR) was strengthened in the heart of the HFD-fed CTRP9-KO mice compared with the HFD-fed control mice. peptide T amide 23-26 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 15-19 31930700-6 2020 In vitro, AMPK inhibitor compound C significantly abolished the effects of CTRP9 on the inhibition of the apoptotic pathway in palmitate-treated NRCMs. Palmitates 127-136 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 10-14 31881478-0 2020 Hyperoside suppresses hypoxia-induced A549 survival and proliferation through ferrous accumulation via AMPK/HO-1 axis. hyperoside 0-10 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 103-107 32082317-0 2020 Corrigendum: Isovitexin-Mediated Regulation of Microglial Polarization in Lipopolysaccharide-Induced Neuroinflammation via Activation of the CaMKKbeta/AMPK-PGC-1alpha Signaling Axis. isovitexin 13-23 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 151-155 31738958-0 2020 FOXM1 contributes to docetaxel resistance in castration-resistant prostate cancer by inducing AMPK/mTOR-mediated autophagy. Docetaxel 21-30 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 94-98 31738958-7 2020 Mechanistically, FOXM1 targeted AMPK/mTOR to activate the autophagy pathway and altered docetaxel response in CRPC. Docetaxel 88-97 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 32-36 31915322-8 2020 Additionally, intervention of adenosine monophosphate activated protein (AMPK)-mammalian target of rapamycin (mTOR) signaling molecule by the AMPK activator, AICAR, increased p-AMPK and ABCA1 expression, decreased p-mTOR expression and promoted cholesterol efflux, resulting in an obvious reduction in intracellular lipid content. Adenosine 30-39 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 73-77 31915322-8 2020 Additionally, intervention of adenosine monophosphate activated protein (AMPK)-mammalian target of rapamycin (mTOR) signaling molecule by the AMPK activator, AICAR, increased p-AMPK and ABCA1 expression, decreased p-mTOR expression and promoted cholesterol efflux, resulting in an obvious reduction in intracellular lipid content. Adenosine 30-39 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 142-146 31915322-8 2020 Additionally, intervention of adenosine monophosphate activated protein (AMPK)-mammalian target of rapamycin (mTOR) signaling molecule by the AMPK activator, AICAR, increased p-AMPK and ABCA1 expression, decreased p-mTOR expression and promoted cholesterol efflux, resulting in an obvious reduction in intracellular lipid content. Adenosine 30-39 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 142-146 31915322-8 2020 Additionally, intervention of adenosine monophosphate activated protein (AMPK)-mammalian target of rapamycin (mTOR) signaling molecule by the AMPK activator, AICAR, increased p-AMPK and ABCA1 expression, decreased p-mTOR expression and promoted cholesterol efflux, resulting in an obvious reduction in intracellular lipid content. Cholesterol 245-256 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 73-77 31915322-8 2020 Additionally, intervention of adenosine monophosphate activated protein (AMPK)-mammalian target of rapamycin (mTOR) signaling molecule by the AMPK activator, AICAR, increased p-AMPK and ABCA1 expression, decreased p-mTOR expression and promoted cholesterol efflux, resulting in an obvious reduction in intracellular lipid content. Cholesterol 245-256 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 142-146 31915322-8 2020 Additionally, intervention of adenosine monophosphate activated protein (AMPK)-mammalian target of rapamycin (mTOR) signaling molecule by the AMPK activator, AICAR, increased p-AMPK and ABCA1 expression, decreased p-mTOR expression and promoted cholesterol efflux, resulting in an obvious reduction in intracellular lipid content. Cholesterol 245-256 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 142-146 31957433-7 2020 Specific suppression of AMPK signaling by AMPKalpha1 siRNA or by AMPK inhibitor compound C significantly attenuated the PB2-induced upregulation of phospho-AMPK, PGC-1alpha, and slow MyHC and downregulation of fast MyHC. phosphorylleucylphenylalanine 148-155 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 42-46 31957433-7 2020 Specific suppression of AMPK signaling by AMPKalpha1 siRNA or by AMPK inhibitor compound C significantly attenuated the PB2-induced upregulation of phospho-AMPK, PGC-1alpha, and slow MyHC and downregulation of fast MyHC. phosphorylleucylphenylalanine 148-155 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 42-46 31747547-0 2020 Salidroside ameliorates endothelial inflammation and oxidative stress by regulating the AMPK/NF-kappaB/NLRP3 signaling pathway in AGEs-induced HUVECs. rhodioloside 0-11 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 88-92 31747547-10 2020 Importantly, salidroside alleviated endothelial inflammation and oxidative stress by activating AMPK phosphorylation and inhibiting NF-kB p65 and NLRP3 inflammasome activation. rhodioloside 13-24 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 96-100 31747547-13 2020 Our findings suggest that salidroside ameliorates AGEs-induced endothelial inflammation and oxidative stress, partially via the AMPK/NF-kappaB/NLRP3 signaling pathway. rhodioloside 26-37 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 128-132 31901295-0 2020 Corrigendum to "Metformin promotes autophagy in ischemia/reperfusion myocardium via cytoplasmic AMPKalpha1 and nuclear AMPKalpha2 pathways" [Life Sci. Metformin 16-25 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 96-106 31936169-0 2020 Metformin Inhibits Tumor Metastasis through Suppressing Hsp90alpha Secretion in an AMPKalpha1-PKCgamma Dependent Manner. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 83-93 31936169-6 2020 Moreover, we find that metformin inhibits Hsp90alpha secretion in an AMPKalpha1 dependent manner. Metformin 23-32 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 69-79 31936169-8 2020 Collectively, our results illuminate that metformin inhibits tumor metastasis by suppressing Hsp90alpha secretion in an AMPKalpha1 dependent manner. Metformin 42-51 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 120-130 31682805-6 2020 The cytotoxicity of promethazine in these cells was triggered by the activation of AMPK and inhibition of PI3K/AKT/mTOR pathway. Promethazine 20-32 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 83-87 31682805-8 2020 These data highlight targeting autophagy may represent an interesting strategy in CML therapy, and also the antitumor potential of promethazine by acting in AMPK and PI3K/AKT/mTOR signaling pathways. Promethazine 131-143 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 157-161 31515527-2 2020 We previously show that ouabain induces autophagic cell death in human lung cancer cells by regulating AMPK-mediated mTOR and Src-mediated ERK1/2 signaling pathways. Ouabain 24-31 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 103-107 32158203-14 2020 In particular, hsa04750 (inflammatory mediator regulation of TRP channels)-C00469 (ethanol) and hsa04152 (AMPK signaling pathway)-C00389 (quercetin) pairs were found in the metabolite network. Quercetin 138-147 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 106-110 31515527-3 2020 However, whether and how AMPK and Src signaling interacts in ouabain-treated cancer cells remains unclear. Ouabain 61-68 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 25-29 31515527-5 2020 In this study we showed that treatment with ouabain (25 nM) caused simultaneous activation of AMPK and Src signaling pathways in human lung cancer A549 cells and human breast cancer MCF7 cells. Ouabain 44-51 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 94-98 31515527-6 2020 Cotreatment with AMPK inhibitor compound C or siRNA greatly abrogates ouabain-induced Src activation, whereas cotreatment with Src inhibitor PP2 has little effect on ouabain-induced AMPK activity, suggesting that AMPK served as an upstream regulator of the Src signaling pathway. Ouabain 70-77 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 17-21 31515527-7 2020 On the other hand, ouabain treatment greatly depletes ATP production in A549 and MCF7 cells, and supplement of ATP (100 muM) blocked ouabain-induced AMPK activation. Adenosine Triphosphate 111-114 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 149-153 32329643-0 2020 Corosolic Acid Attenuates Hepatic Lipid Accumulation and Inflammatory Response via AMPK/SREBPs and NF-kappaB/MAPK Signaling Pathways. corosolic acid 0-14 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 83-87 31515527-9 2020 Taken together, this study reveals that the altered cancer cell metabolism caused by ouabain may contribute to AMPK activation, as well as its cytotoxicity towards cancer cells. Ouabain 85-92 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 111-115 32219939-8 2020 Dietary DHA supplementation led to upregulation of the expression of AMPK/SIRT1 signaling pathway-related genes, whereas that of inflammatory factor-related genes were downregulated. artenimol 8-11 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 69-73 31626852-4 2020 Following these clues provides a unifying common basis to non-canonical 3-MGAs: constitutive mitochondrial dysfunction induces AMPK activation which, by inhibiting early steps in cholesterol and fatty acid syntheses, pipelines cytoplasmic acetyl-CoA to peroxisomes where a rise in HMG-CoA followed by local dehydration and hydrolysis may lead to 3-MGA yield. Cholesterol 179-190 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 127-131 31626852-4 2020 Following these clues provides a unifying common basis to non-canonical 3-MGAs: constitutive mitochondrial dysfunction induces AMPK activation which, by inhibiting early steps in cholesterol and fatty acid syntheses, pipelines cytoplasmic acetyl-CoA to peroxisomes where a rise in HMG-CoA followed by local dehydration and hydrolysis may lead to 3-MGA yield. Fatty Acids 195-205 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 127-131 31626852-4 2020 Following these clues provides a unifying common basis to non-canonical 3-MGAs: constitutive mitochondrial dysfunction induces AMPK activation which, by inhibiting early steps in cholesterol and fatty acid syntheses, pipelines cytoplasmic acetyl-CoA to peroxisomes where a rise in HMG-CoA followed by local dehydration and hydrolysis may lead to 3-MGA yield. Acetyl Coenzyme A 239-249 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 127-131 31626852-4 2020 Following these clues provides a unifying common basis to non-canonical 3-MGAs: constitutive mitochondrial dysfunction induces AMPK activation which, by inhibiting early steps in cholesterol and fatty acid syntheses, pipelines cytoplasmic acetyl-CoA to peroxisomes where a rise in HMG-CoA followed by local dehydration and hydrolysis may lead to 3-MGA yield. 12-(4'-azido-2'-nitrophenoxy)dodecanoyl-coenzyme A 246-249 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 127-131 31742890-0 2020 Celastrol exerts anti-inflammatory effect in liver fibrosis via activation of AMPK-SIRT3 signalling. celastrol 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 78-82 31512724-0 2020 AMPK subunits harbor largely non-overlapping genetic determinants for body fat mass, glucose- and cholesterol metabolism. Glucose 85-92 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 31512724-0 2020 AMPK subunits harbor largely non-overlapping genetic determinants for body fat mass, glucose- and cholesterol metabolism. Cholesterol 98-109 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 31512724-5 2020 RESULTS: We identified largely non-overlapping SNP sets across four AMPK genes (PRKAA1, PRKAA2, PRKAG2, PRKAG3) associated with adiposity, insulin sensitivity, insulin secretion, blood glucose, total-/LDL-cholesterol or HDL-cholesterol, respectively. Glucose 185-192 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 68-72 31512724-5 2020 RESULTS: We identified largely non-overlapping SNP sets across four AMPK genes (PRKAA1, PRKAA2, PRKAG2, PRKAG3) associated with adiposity, insulin sensitivity, insulin secretion, blood glucose, total-/LDL-cholesterol or HDL-cholesterol, respectively. Cholesterol 205-216 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 68-72 31512724-5 2020 RESULTS: We identified largely non-overlapping SNP sets across four AMPK genes (PRKAA1, PRKAA2, PRKAG2, PRKAG3) associated with adiposity, insulin sensitivity, insulin secretion, blood glucose, total-/LDL-cholesterol or HDL-cholesterol, respectively. Cholesterol 205-216 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 80-86 31512724-5 2020 RESULTS: We identified largely non-overlapping SNP sets across four AMPK genes (PRKAA1, PRKAA2, PRKAG2, PRKAG3) associated with adiposity, insulin sensitivity, insulin secretion, blood glucose, total-/LDL-cholesterol or HDL-cholesterol, respectively. Cholesterol 224-235 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 68-72 31512724-5 2020 RESULTS: We identified largely non-overlapping SNP sets across four AMPK genes (PRKAA1, PRKAA2, PRKAG2, PRKAG3) associated with adiposity, insulin sensitivity, insulin secretion, blood glucose, total-/LDL-cholesterol or HDL-cholesterol, respectively. Cholesterol 224-235 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 80-86 31098946-7 2020 Metformin mainly through AMPK axis can protect different organs against toxicities. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 25-29 31682805-0 2020 AMPK activation induced by promethazine increases NOXA expression and Beclin-1 phosphorylation and drives autophagy-associated apoptosis in chronic myeloid leukemia. Promethazine 27-39 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 31742890-3 2020 This study was to investigate the anti-inflammatory effect of celastrol in liver fibrosis and to further reveal mechanisms of celastrol-induced anti-inflammatory effects with a focus on AMPK-SIRT3 signalling. celastrol 126-135 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 186-190 31742890-8 2020 Besides, we found that celastrol could increase the AMPK phosphorylation. celastrol 23-32 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 52-56 31580898-5 2020 Results show that diiodothyronines in the range of plasma physiological concentrations reduced hepatic lipid accumulation, by modulating the activity of the mTORC1/Raptor complex through an AMPK-mediated mechanism, and stimulated the mTORC2/Rictor complex-activated pathway, leading to the down regulation of the expression of key gluconeogenic genes. Diiodothyronines 18-34 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 190-194 31604003-0 2020 AICAR-induced activation of AMPK inhibits the migration of TSCC cells by targeting ZO-1. AICA ribonucleotide 0-5 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 28-32 31530934-5 2020 We further reveal a previously unrecognized function of AMPKalpha1, which maintains high level of reduced glutathione to keep reduction-oxidation reaction (redox) homeostasis under stress conditions, thus promoting CRC cell survival under metabolic stress in vitro and enhancing tumorigenesis in vivo. Glutathione 106-117 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 56-66 31530934-7 2020 Suppression of AMPKalpha1 by using nano-sized polymeric vector induces a favorable therapeutic effect, especially when in combination with oxaliplatin. Oxaliplatin 139-150 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 15-25 31805502-8 2020 Overall, our data reveal AMPK-triggered phosphorylation of Nrf2 at three serine residues, apparently determining the extent of transactivation of selected target genes. cholecystokinin C-terminal flanking peptide 73-79 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 25-29 31805502-3 2020 Here, MS-based analysis of immunoprecipitated Nrf2 revealed serine 374, 408 and 433 in human Nrf2 to be hyperphosphorylated as a function of activated AMPK. cholecystokinin C-terminal flanking peptide 60-66 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 151-155 31586547-1 2019 The oxidative pentose phosphate pathway (oxiPPP) contributes to cell metabolism through not only the production of metabolic intermediates and reductive NADPH but also inhibition of LKB1-AMPK signaling by ribulose-5-phosphate (Ru-5-P), the product of the third oxiPPP enzyme 6-phosphogluconate dehydrogenase (6PGD). ribulose 5-phosphate 205-225 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 187-191 31805502-4 2020 A direct phosphate-transfer by AMPK to those sites was indicated by in vitro kinase assays with recombinant proteins as well as interaction of AMPK and Nrf2 in cells, evident by co-immunoprecipitation. Phosphates 9-18 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 31-35 31805502-4 2020 A direct phosphate-transfer by AMPK to those sites was indicated by in vitro kinase assays with recombinant proteins as well as interaction of AMPK and Nrf2 in cells, evident by co-immunoprecipitation. Phosphates 9-18 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 143-147 32148244-6 2020 Studies have also shown that hydrogen sulphide (H2S) can activate autophagy through multiple signaling pathways, such as adenylate-activated protein kinase/mammalian target of rapamycin (AMPK/mTOR), phosphoinositide 3 kinase/Akt/mTOR (PI3K/Akt/mTOR), liver kinase B1/STE20 related adapter protein/mouse protein 25 (LKB1/STRAD/MO25) and microRNA-30c (miR-30c), etc. Hydrogen Sulfide 29-46 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 187-191 32148244-6 2020 Studies have also shown that hydrogen sulphide (H2S) can activate autophagy through multiple signaling pathways, such as adenylate-activated protein kinase/mammalian target of rapamycin (AMPK/mTOR), phosphoinositide 3 kinase/Akt/mTOR (PI3K/Akt/mTOR), liver kinase B1/STE20 related adapter protein/mouse protein 25 (LKB1/STRAD/MO25) and microRNA-30c (miR-30c), etc. Hydrogen Sulfide 48-51 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 187-191 31891641-8 2019 Conversely, the AMPK activator AICAR (0.1 and 0.5mM) conferred protection from palmitate mediated-alterations in viability, apoptosis and ER stress, whereas the AMPK inhibitor compound C (20 and 40muM) significantly exacerbated palmitate-mediated damage. AICA ribonucleotide 31-36 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 16-20 31891641-8 2019 Conversely, the AMPK activator AICAR (0.1 and 0.5mM) conferred protection from palmitate mediated-alterations in viability, apoptosis and ER stress, whereas the AMPK inhibitor compound C (20 and 40muM) significantly exacerbated palmitate-mediated damage. Palmitates 79-88 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 16-20 31891641-8 2019 Conversely, the AMPK activator AICAR (0.1 and 0.5mM) conferred protection from palmitate mediated-alterations in viability, apoptosis and ER stress, whereas the AMPK inhibitor compound C (20 and 40muM) significantly exacerbated palmitate-mediated damage. Palmitates 228-237 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 16-20 31586547-0 2019 gamma-6-Phosphogluconolactone, a Byproduct of the Oxidative Pentose Phosphate Pathway, Contributes to AMPK Activation through Inhibition of PP2A. 6-phosphogluconolactone 0-29 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 102-106 31586547-0 2019 gamma-6-Phosphogluconolactone, a Byproduct of the Oxidative Pentose Phosphate Pathway, Contributes to AMPK Activation through Inhibition of PP2A. Pentoses 60-77 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 102-106 31586547-1 2019 The oxidative pentose phosphate pathway (oxiPPP) contributes to cell metabolism through not only the production of metabolic intermediates and reductive NADPH but also inhibition of LKB1-AMPK signaling by ribulose-5-phosphate (Ru-5-P), the product of the third oxiPPP enzyme 6-phosphogluconate dehydrogenase (6PGD). Pentoses 14-31 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 187-191 31852839-0 2019 Compound 13 activates AMPK-Nrf2 signaling to protect neuronal cells from oxygen glucose deprivation-reoxygenation. Glucose 80-87 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 22-26 31674780-0 2019 gamma-Mangostin Ameliorates Free Fatty Acid-Induced Lipid Accumulation via the SIRT1/LKB1/AMPK Pathway in HepG2 and L02 Cells. gamma-mangostin 0-15 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 90-94 31674780-0 2019 gamma-Mangostin Ameliorates Free Fatty Acid-Induced Lipid Accumulation via the SIRT1/LKB1/AMPK Pathway in HepG2 and L02 Cells. Fatty Acids, Nonesterified 28-43 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 90-94 31674780-4 2019 Analysis of the inhibitory effects of gamma-mangostin on lipid accumulation revealed that it downregulated NAFLD-related biochemical parameters and stimulated the SIRT1/LKB1/AMPK pathway. gamma-mangostin 38-53 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 174-178 31381180-0 2019 Phosphoproteomics reveals conserved exercise-stimulated signaling and AMPK regulation of store-operated calcium entry. Calcium 104-111 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 70-74 31614141-0 2019 Trans-10-hydroxy-2-decenoic acid alleviates LPS-induced blood-brain barrier dysfunction by activating the AMPK/PI3K/AKT pathway. 10-hydroxy-2-decenoic acid 0-32 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 106-110 31614141-7 2019 We further illustrated that 10-HDA promoted the activation of the AMPK pathway and the downstream PI3K/AKT pathway. 10-hydroxy-2-decenoic acid 28-34 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 66-70 31614141-8 2019 Compound C (an AMPK inhibitor) and LY294002 (a PI3K inhibitor) markedly reversed the alleviating effect of 10-HDA on the expression of tight junction proteins, indicating that 10-HDA inhibited LPS-induced BBB dysfunction by triggering the activation of the AMPK/PI3K/AKT pathway. Carbon 0-1 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 15-19 31614141-8 2019 Compound C (an AMPK inhibitor) and LY294002 (a PI3K inhibitor) markedly reversed the alleviating effect of 10-HDA on the expression of tight junction proteins, indicating that 10-HDA inhibited LPS-induced BBB dysfunction by triggering the activation of the AMPK/PI3K/AKT pathway. Carbon 0-1 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 257-261 31614141-8 2019 Compound C (an AMPK inhibitor) and LY294002 (a PI3K inhibitor) markedly reversed the alleviating effect of 10-HDA on the expression of tight junction proteins, indicating that 10-HDA inhibited LPS-induced BBB dysfunction by triggering the activation of the AMPK/PI3K/AKT pathway. 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one 35-43 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 257-261 31614141-8 2019 Compound C (an AMPK inhibitor) and LY294002 (a PI3K inhibitor) markedly reversed the alleviating effect of 10-HDA on the expression of tight junction proteins, indicating that 10-HDA inhibited LPS-induced BBB dysfunction by triggering the activation of the AMPK/PI3K/AKT pathway. 10-hydroxy-2-decenoic acid 107-113 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 15-19 31614141-8 2019 Compound C (an AMPK inhibitor) and LY294002 (a PI3K inhibitor) markedly reversed the alleviating effect of 10-HDA on the expression of tight junction proteins, indicating that 10-HDA inhibited LPS-induced BBB dysfunction by triggering the activation of the AMPK/PI3K/AKT pathway. 10-hydroxy-2-decenoic acid 107-113 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 257-261 31614141-8 2019 Compound C (an AMPK inhibitor) and LY294002 (a PI3K inhibitor) markedly reversed the alleviating effect of 10-HDA on the expression of tight junction proteins, indicating that 10-HDA inhibited LPS-induced BBB dysfunction by triggering the activation of the AMPK/PI3K/AKT pathway. 10-hydroxy-2-decenoic acid 176-182 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 15-19 31614141-8 2019 Compound C (an AMPK inhibitor) and LY294002 (a PI3K inhibitor) markedly reversed the alleviating effect of 10-HDA on the expression of tight junction proteins, indicating that 10-HDA inhibited LPS-induced BBB dysfunction by triggering the activation of the AMPK/PI3K/AKT pathway. 10-hydroxy-2-decenoic acid 176-182 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 257-261 31392929-0 2019 The anti-inflammatory function of adenine occurs through AMPK activation and its downstream transcriptional regulation in THP-1 cells. Adenine 34-41 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 57-61 31392929-9 2019 Results also showed that adenine can activate AMPK and its multiple downstream targets. Adenine 25-32 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 46-50 31392929-11 2019 Our data indicate that the anti-inflammatory mechanism of adenine may involve adenine phosphoribosyltransferase-catalyzed intracellular AMP elevation, which stimulates AMPK activation. Adenine 58-65 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 168-172 31392929-11 2019 Our data indicate that the anti-inflammatory mechanism of adenine may involve adenine phosphoribosyltransferase-catalyzed intracellular AMP elevation, which stimulates AMPK activation. Adenosine Monophosphate 136-139 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 168-172 31638409-6 2019 In addition, high glucose reduced AMP-activated protein kinase (AMPK) phosphorylation and retained during the 4 days of the reversal period of culture. Glucose 18-25 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 34-62 31638409-6 2019 In addition, high glucose reduced AMP-activated protein kinase (AMPK) phosphorylation and retained during the 4 days of the reversal period of culture. Glucose 18-25 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 64-68 31638409-7 2019 The effects of resveratrol were abrogated after co-treatment with the SIRT1 inhibitor nicotinamide and the AMPK inhibitor compound C. In conclusion, resveratrol was able to reverse high-glucose-induced inflammation "metabolic memory" of HRVECs by activation of the SIRT1/AMPK/NF-kappaB pathway. resveratrol 15-26 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 107-111 31638409-7 2019 The effects of resveratrol were abrogated after co-treatment with the SIRT1 inhibitor nicotinamide and the AMPK inhibitor compound C. In conclusion, resveratrol was able to reverse high-glucose-induced inflammation "metabolic memory" of HRVECs by activation of the SIRT1/AMPK/NF-kappaB pathway. resveratrol 15-26 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 271-275 31638409-7 2019 The effects of resveratrol were abrogated after co-treatment with the SIRT1 inhibitor nicotinamide and the AMPK inhibitor compound C. In conclusion, resveratrol was able to reverse high-glucose-induced inflammation "metabolic memory" of HRVECs by activation of the SIRT1/AMPK/NF-kappaB pathway. Niacinamide 86-98 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 271-275 31638409-7 2019 The effects of resveratrol were abrogated after co-treatment with the SIRT1 inhibitor nicotinamide and the AMPK inhibitor compound C. In conclusion, resveratrol was able to reverse high-glucose-induced inflammation "metabolic memory" of HRVECs by activation of the SIRT1/AMPK/NF-kappaB pathway. resveratrol 149-160 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 107-111 31638409-7 2019 The effects of resveratrol were abrogated after co-treatment with the SIRT1 inhibitor nicotinamide and the AMPK inhibitor compound C. In conclusion, resveratrol was able to reverse high-glucose-induced inflammation "metabolic memory" of HRVECs by activation of the SIRT1/AMPK/NF-kappaB pathway. resveratrol 149-160 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 271-275 31491460-13 2019 Interestingly, autophagy markers were down regulated in MCF7 cells upon treatment with nicotinamide, an inhibitor of SIRT1 activity and dorsomorphin, a phospho-AMPK inhibitor when treated separately under nitrosative stress. dorsomorphin 136-148 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 160-164 31563593-2 2019 HCT15 cell treatment with DOX resulted in up-regulation of Beclin1, down-regulation of Bcl2, activation of AMPK and JNK, and Akt inactivation, all of which were restored by pretreating with an antioxidant N-acetyl-l-cysteine. Doxorubicin 26-29 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 107-111 31744691-0 2019 Metformin inhibits cell proliferation in SKM-1 cells via AMPK-mediated cell cycle arrest. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 57-61 31744691-8 2019 Metformin promoted the expression of p-AMPK, P53, P21CIP1 and P27KIP1, while inhibited the expression of CDK4 and CyclinD1. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 39-43 31744691-9 2019 AMPK knockdown attenuated the effects of metformin on SKM-1 cells. Metformin 41-50 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 31744691-10 2019 These findings suggested that metformin inhibited proliferation of SKM-1 cells, potentially through an AMPK-mediated cell cycle arrest. Metformin 30-39 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 103-107 31742890-10 2020 In addition, inhibition of AMPK by employing compound C (an AMPK inhibitor) or AMPK1alpha siRNA significantly suppressed SIRT3 expression, suggesting that AMPK was an up-stream protein of SIRT3 in liver fibrosis. Carbon 54-55 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 27-31 31742890-11 2020 We further found that depletion of AMPK significantly attenuated the inhibitory effect of celastrol on inflammation. celastrol 90-99 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 35-39 31742890-12 2020 Collectively, celastrol attenuated liver fibrosis mainly through inhibition of inflammation by activating AMPK-SIRT3 signalling, which makes celastrol be a potential candidate compound in treating or protecting against liver fibrosis. celastrol 14-23 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 106-110 31742890-12 2020 Collectively, celastrol attenuated liver fibrosis mainly through inhibition of inflammation by activating AMPK-SIRT3 signalling, which makes celastrol be a potential candidate compound in treating or protecting against liver fibrosis. celastrol 141-150 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 106-110 31871431-7 2019 In this present study, our results show that NVP-BEZ235 induced autophagy through AMPK/ULK1 pathway in colon cancer cells. dactolisib 45-55 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 82-86 31871431-8 2019 Blocking autophagy by knocking down AMPK or ULK1 inhibited cell proliferation and further promoted NVP-BEZ235 induced apoptosis. dactolisib 99-109 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 36-40 31871431-11 2019 Conclusion: NVP-BEZ235 induced AMPK/ULK1-dependent autophagy. dactolisib 12-22 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 31-35 31557380-10 2019 Metformin led to an increase in AMPK signaling, and a trend for blunted increases in mTORC1 signaling in response to PRT. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 32-36 32042798-8 2019 After intervention of AMPK activity, the proportion of memory T cells in the spleen reduced as compared to the AS group and AS + solvent group; the pro proportion of memory T cells in HFD groups was markedly higher than in the normal group and this increase was more evident in the AS + Compound C than in the AS + A-769662 group. Carbon 287-288 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 22-26 32042798-8 2019 After intervention of AMPK activity, the proportion of memory T cells in the spleen reduced as compared to the AS group and AS + solvent group; the pro proportion of memory T cells in HFD groups was markedly higher than in the normal group and this increase was more evident in the AS + Compound C than in the AS + A-769662 group. 4-hydroxy-3-(4-(2-hydroxyphenyl)phenyl)-6-oxo-7H-thieno(2,3-b)pyridine-5-carbonitrile 315-323 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 22-26 31810927-0 2019 Duloxetine Enhances TRAIL-mediated Apoptosis via AMPK-mediated Inhibition of Autophagy Flux in Lung Cancer Cells. Duloxetine Hydrochloride 0-10 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 49-53 31810927-8 2019 Treatment with duloxetine inhibited AMPK phosphorylation and resulted in increased p62 and microtubule-associated protein 1A/1B light chain 3B-II levels, indicating inhibition of autophagy flux. Duloxetine Hydrochloride 15-25 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 36-40 31841039-1 2019 AMP-activated alpha 1 catalytic subunit (PRKAA1) is one of the subunits of the mammalian 5"-AMP-activated protein kinase (AMPK) playing an important role in maintaining intracellular energy metabolism and associating with the risk of gastric cancer (GC). Adenosine Monophosphate 0-3 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 41-47 31841039-1 2019 AMP-activated alpha 1 catalytic subunit (PRKAA1) is one of the subunits of the mammalian 5"-AMP-activated protein kinase (AMPK) playing an important role in maintaining intracellular energy metabolism and associating with the risk of gastric cancer (GC). Adenosine Monophosphate 0-3 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 122-126 31841039-1 2019 AMP-activated alpha 1 catalytic subunit (PRKAA1) is one of the subunits of the mammalian 5"-AMP-activated protein kinase (AMPK) playing an important role in maintaining intracellular energy metabolism and associating with the risk of gastric cancer (GC). Adenosine Monophosphate 89-95 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 41-47 31841039-1 2019 AMP-activated alpha 1 catalytic subunit (PRKAA1) is one of the subunits of the mammalian 5"-AMP-activated protein kinase (AMPK) playing an important role in maintaining intracellular energy metabolism and associating with the risk of gastric cancer (GC). Adenosine Monophosphate 89-95 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 122-126 31721020-5 2019 However the mRNA expression of adenosine 5"-monophosphate (AMP)-activated protein kinase (AMPK), glucose transporter 4 (GLUT4) and glucose absorption increased to the maximum at concentration of 5 mumol/L then decreased with further increase of DNJ concentration to 10 mumol/L. Adenosine Monophosphate 31-57 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 90-94 31721020-5 2019 However the mRNA expression of adenosine 5"-monophosphate (AMP)-activated protein kinase (AMPK), glucose transporter 4 (GLUT4) and glucose absorption increased to the maximum at concentration of 5 mumol/L then decreased with further increase of DNJ concentration to 10 mumol/L. Adenosine Monophosphate 59-62 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 90-94 31721020-5 2019 However the mRNA expression of adenosine 5"-monophosphate (AMP)-activated protein kinase (AMPK), glucose transporter 4 (GLUT4) and glucose absorption increased to the maximum at concentration of 5 mumol/L then decreased with further increase of DNJ concentration to 10 mumol/L. 1-Deoxynojirimycin 245-248 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 90-94 31795328-3 2019 Over the past 15 years, it has been acknowledged that adenosine monophosphate (AMP)-activated protein kinase (AMPK), a well-known central regulator of energy metabolism, has a reciprocal association with AJCs. Adenosine Monophosphate 54-77 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 110-114 31424537-6 2019 Taken together, it suggested that dietary Mo and Cd might induce autophagy via AMPK/mTOR signaling pathway in duck kidney, and it showed a possible synergistic relationship between the 2 elements. Cadmium 49-51 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 79-83 31795328-3 2019 Over the past 15 years, it has been acknowledged that adenosine monophosphate (AMP)-activated protein kinase (AMPK), a well-known central regulator of energy metabolism, has a reciprocal association with AJCs. Adenosine Monophosphate 79-82 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 110-114 31382115-0 2019 Spinetoram confers its cytotoxic effects by inducing AMPK/mTOR-mediated autophagy and oxidative DNA damage. spinetoram 0-10 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 53-57 31745071-7 2019 PTP1B inhibition directly increased PKM2 Tyr-105 phosphorylation to further result in significant activation of AMPK, which decreased mTOC1 activity and led to inhibition of p70S6K. tyrosyltyrosine 41-44 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 112-116 31382115-6 2019 Intracellular biochemical assay indicated that decrease of mitochondrial membrane potential, LC3-II conversion, accumulation of Beclin-1, degradation of p62 and the changes in the phosphorylation of AMPK, mTOR are contributed to the toxic effects of Spinetoram on HepG2 cells. spinetoram 250-260 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 199-203 31382115-7 2019 These results showed that the cytotoxicity of spinetoram may be associated with the activity of AMPK/mTOR-mediated autophagy pathway. spinetoram 46-56 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 96-100 31382115-9 2019 We conclude that spinetoram has a significant cytotoxic effect by inducing AMPK/mTOR-mediated autophagy and oxidative DNA damage. spinetoram 17-27 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 75-79 31727877-13 2019 Taken together, Lnc-THOR depletion inhibits human glioma cell survival possibly by activating MAGEA6-AMPK signaling. lnc-thor 16-24 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 101-105 31730006-10 2019 Mechanistically, AMPKa1 depletion attenuated these effects of MTX. Methotrexate 62-65 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 17-23 31730006-12 2019 CONCLUSIONS: Taken together, we conclude that MTX exerts protective effects via the AMP-dependent kinase (AMPK)-YAP/TAZ pathway. Methotrexate 46-49 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 84-104 31730006-12 2019 CONCLUSIONS: Taken together, we conclude that MTX exerts protective effects via the AMP-dependent kinase (AMPK)-YAP/TAZ pathway. Methotrexate 46-49 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 106-110 31529536-6 2019 Further, lutein and oxidised lutein augmented the AMPK phosphorylation and activation of mitochondrion signalling molecule TFAM (protein expression) and mRNA expression of PGC-1alpha, TFAM, and NRF1 (responsible for mitochondria biogenesis) along with lowered ROS in HG compared to control and metformin groups. ros 260-263 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 50-54 31529536-6 2019 Further, lutein and oxidised lutein augmented the AMPK phosphorylation and activation of mitochondrion signalling molecule TFAM (protein expression) and mRNA expression of PGC-1alpha, TFAM, and NRF1 (responsible for mitochondria biogenesis) along with lowered ROS in HG compared to control and metformin groups. Metformin 294-303 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 50-54 31494243-6 2019 Tam5R cells also produce significantly higher levels of mitochondrial superoxide but at the same time increase their antioxidant defense (CAT, SOD2) through upregulation of SIRT3 and show phosphorylation of AMPK at Ser 485/491. Serine 215-218 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 207-211 31513784-0 2019 Involvement of E-cadherin/AMPK/mTOR axis in LKB1-induced sensitivity of non-small cell lung cancer to gambogic acid. gambogic acid 102-115 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 26-30 31513784-6 2019 Further studies reveal that GA increases p-AMPK levels through up-regulation of E-cadherin associated with LKB1. gambogic acid 28-30 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 43-47 30926950-10 2019 In cultured HepG2 cells, LNP ligands phosphorylated AMPK and the downstream acetyl-CoA carboxylase and prevented oleic acid-induced intracellular lipid accumulation. Oleic Acid 113-123 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 52-56 31691998-10 2019 Knockdown of Ampka1 markedly reversed the inhibitory effect of berberine on lipid accumulation and mRNA expression of the above genes except Cebpb in porcine adipocytes. Berberine 63-72 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 13-19 31691998-12 2019 These results suggest that berberine inhibits adipogenesis in porcine adipocytes via AMPK-dependent and -independent multiple mechanisms, which would provide an important idea for the reduction of porcine body fat, as well as the prevention and treatment of human obesity. Berberine 27-36 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 85-89 31454158-0 2019 Tomatidine Reduces Palmitate-Induced Lipid Accumulation by Activating AMPK via Vitamin D Receptor-Mediated Signaling in Human HepG2 Hepatocytes. tomatidine 0-10 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 70-74 31454158-0 2019 Tomatidine Reduces Palmitate-Induced Lipid Accumulation by Activating AMPK via Vitamin D Receptor-Mediated Signaling in Human HepG2 Hepatocytes. Palmitates 19-28 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 70-74 31454158-3 2019 METHODS AND RESULTS: It is found that tomatidine, the aglycone of alpha-tomatine abundant in green tomatoes, significantly inhibits palmitate-provoked lipid accumulation and stimulates phosphorylation of AMPK and acetyl-CoA carboxylase 1 (ACC1) in human HepG2 hepatocytes. tomatidine 38-48 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 204-208 31454158-3 2019 METHODS AND RESULTS: It is found that tomatidine, the aglycone of alpha-tomatine abundant in green tomatoes, significantly inhibits palmitate-provoked lipid accumulation and stimulates phosphorylation of AMPK and acetyl-CoA carboxylase 1 (ACC1) in human HepG2 hepatocytes. alpha-tomatine 66-80 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 204-208 31454158-4 2019 The results also indicate that tomatidine can enhance triglyceride turnover and decline in lipogenesis by upregulating adipose triglyceride lipase (ATGL) and downregulating fatty acid synthase (FAS) via the AMPK signaling-dependent regulation of transcription factors, element-binding protein-1c (SREBP-1c) and forkhead box protein O1 (FoxO1). tomatidine 31-41 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 207-211 31454158-5 2019 Furthermore, mechanistic studies demonstrate that tomatidine-stimulated AMPK phosphorylation is due to CaMKKbeta activation in response to an increase in intracellular Ca2+ concentration. tomatidine 50-60 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 72-76 31454158-6 2019 Finally, it is discovered that tomatidine functions as an agonist for vitamin D receptor to elicit AMPK-dependent suppression of lipid accumulation. tomatidine 31-41 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 99-103 31545435-0 2019 Hydrogen sulfide protects against high glucose-induced lipid metabolic disturbances in 3T3-L1 adipocytes via the AMPK signaling pathway. Hydrogen Sulfide 0-16 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 113-117 31545435-0 2019 Hydrogen sulfide protects against high glucose-induced lipid metabolic disturbances in 3T3-L1 adipocytes via the AMPK signaling pathway. Glucose 39-46 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 113-117 31545435-3 2019 The aim of the present study was to investigate if the protective effects of H2S during high glucose (HG)-induced lipid accumulation in 3T3-L1 adipocytes may be mediated by AMP-activated protein kinase (AMPK). hydrogen sulfite 77-80 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 173-201 31545435-3 2019 The aim of the present study was to investigate if the protective effects of H2S during high glucose (HG)-induced lipid accumulation in 3T3-L1 adipocytes may be mediated by AMP-activated protein kinase (AMPK). hydrogen sulfite 77-80 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 203-207 31545435-3 2019 The aim of the present study was to investigate if the protective effects of H2S during high glucose (HG)-induced lipid accumulation in 3T3-L1 adipocytes may be mediated by AMP-activated protein kinase (AMPK). Glucose 93-100 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 173-201 31545435-3 2019 The aim of the present study was to investigate if the protective effects of H2S during high glucose (HG)-induced lipid accumulation in 3T3-L1 adipocytes may be mediated by AMP-activated protein kinase (AMPK). Glucose 93-100 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 203-207 31545435-9 2019 Furthermore, NaHS suppressed HG-induced TG accumulation by activating AMPK. Sodium 13-17 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 70-74 31545435-9 2019 Furthermore, NaHS suppressed HG-induced TG accumulation by activating AMPK. Triglycerides 40-42 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 70-74 31545435-10 2019 Collectively, the findings of the present study suggested that HG induced lipid accumulation in 3T3-L1 adipocytes, and AMPK activation may underlie the lipid-lowering effects of H2S. hydrogen sulfite 178-181 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 119-123 31627130-3 2019 Here, we demonstrate that glucose potentiates E2F1-induced mTORC1 activation by promoting mTORC1 translocation to lysosomes, a process that occurs independently of AMPK activation. Glucose 26-33 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 164-168 31431503-2 2019 5-Aminoimidazole-4-carboxamide ribonucleoside (AICAr), a precursor in purine biosynthesis and a well-established activator of AMP-activated protein kinase (AMPK), induces widespread metabolic alterations and is commonly used for dissecting the role of metabolism in cancer. acadesine 0-45 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 126-154 31431503-2 2019 5-Aminoimidazole-4-carboxamide ribonucleoside (AICAr), a precursor in purine biosynthesis and a well-established activator of AMP-activated protein kinase (AMPK), induces widespread metabolic alterations and is commonly used for dissecting the role of metabolism in cancer. acadesine 0-45 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 156-160 31431503-2 2019 5-Aminoimidazole-4-carboxamide ribonucleoside (AICAr), a precursor in purine biosynthesis and a well-established activator of AMP-activated protein kinase (AMPK), induces widespread metabolic alterations and is commonly used for dissecting the role of metabolism in cancer. purine 70-76 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 126-154 31431503-2 2019 5-Aminoimidazole-4-carboxamide ribonucleoside (AICAr), a precursor in purine biosynthesis and a well-established activator of AMP-activated protein kinase (AMPK), induces widespread metabolic alterations and is commonly used for dissecting the role of metabolism in cancer. purine 70-76 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 156-160 31431503-7 2019 Our results delineate an AMPK-independent effect of AICAr on myeloid leukemia differentiation that involves perturbation of pyrimidine biosynthesis and activation of the DNA damage response network. pyrimidine 124-134 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 25-29 31635305-5 2019 Here, we demonstrated that AMPK deletion induced a delay in tight junction reassembly and relocalization at the plasma membrane during calcium switch, leading to impairments in the establishment of TEER and paracellular permeability. Calcium 135-142 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 27-31 31635305-6 2019 We also showed that 991-induced AMPK activation accelerated the reassembly and reorganization of tight junctions, improved the development of TEER and paracellular permeability after calcium switch. Calcium 183-190 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 32-36 31430456-0 2019 Pinolenic acid ameliorates oleic acid-induced lipogenesis and oxidative stress via AMPK/SIRT1 signaling pathway in HepG2 cells. 5,9,12-octadecatrienoic acid 0-14 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 83-87 31430456-0 2019 Pinolenic acid ameliorates oleic acid-induced lipogenesis and oxidative stress via AMPK/SIRT1 signaling pathway in HepG2 cells. Oleic Acid 27-37 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 83-87 31430456-9 2019 PLA treatment resulted in increasing phosphorylation of AMP-activated protein kinase (AMPK) and peroxisome proliferator-activated receptor-alpha (PPARalpha) expression. 5,9,12-octadecatrienoic acid 0-3 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 56-84 31430456-9 2019 PLA treatment resulted in increasing phosphorylation of AMP-activated protein kinase (AMPK) and peroxisome proliferator-activated receptor-alpha (PPARalpha) expression. 5,9,12-octadecatrienoic acid 0-3 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 86-90 31597941-0 2019 Author Correction: Early Cellular Responses of Prostate Carcinoma Cells to Sepantronium Bromide (YM155) Involve Suppression of mTORC1 by AMPK. YM 155 75-95 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 137-141 31601024-0 2019 The Fast Lane of Hypoxic Adaptation: Glucose Transport Is Modulated via A HIF-Hydroxylase-AMPK-Axis in Jejunum Epithelium. Glucose 37-44 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 90-94 31601024-8 2019 We showed an activation of AMPK under hypoxia and after incubation with DMOG by Western blot. dimethyloxallyl glycine 72-76 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 27-31 31176127-0 2019 Aflatoxin B1 impairs leydig cells through inhibiting AMPK/mTOR-mediated autophagy flux pathway. Aflatoxin B1 0-12 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 53-57 31176127-5 2019 AFB1-induced toxicity in Leydig cells was characterized by inhibiting T-biosynthesis gene expression, reducing Leydig cell number, promoting ROS production, and inducing cell apoptosis via suppressing AMPK/mTOR-mediated autophagy flux pathway. Aflatoxin B1 0-4 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 201-205 31251107-14 2019 Besides, SAL activated PI3K/AKT and AMPK pathways by adjusting miR-138. rhodioloside 9-12 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 36-40 31620247-0 2019 Correction: Metformin sensitizes anticancer effect of dasatinib in head and neck squamous cell carcinoma cells through AMPK-dependent ER stress. Metformin 12-21 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 119-123 31620247-0 2019 Correction: Metformin sensitizes anticancer effect of dasatinib in head and neck squamous cell carcinoma cells through AMPK-dependent ER stress. dasatinib 54-63 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 119-123 31251107-14 2019 Besides, SAL activated PI3K/AKT and AMPK pathways by adjusting miR-138. mir-138 63-70 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 36-40 31251107-15 2019 In conclusions, SAL flattened HG-induced injury in ARPE-19 cells by repression of miR-138 and activating PI3K/AKT and AMPK pathways. rhodioloside 16-19 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 118-122 31251940-9 2019 We showed that Olaparib treatment inhibited nuclear and cytosolic PAR formation, induced NAD+/NADH ratio and consequently boosted SIRT1 and AMPK activity and the downstream transcriptional program leading to increases in OXPHOS. olaparib 15-23 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 140-144 31533227-7 2019 Mechanistically, VAC-treated HMEC-1 cells exhibited higher AMPK phosphorylation, which was attenuated by HG stimulation. Mercury 105-107 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 59-63 31533227-9 2019 In addition, both reactive oxygen species (ROS) scavenger N-acetyl-L-cysteine (NAC) and VAC abolished HG-evoked dephosphorylation of AMPK and eNOS, increased miRNA-34a expression, and decreased NO production. Reactive Oxygen Species 18-41 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 133-137 31533227-9 2019 In addition, both reactive oxygen species (ROS) scavenger N-acetyl-L-cysteine (NAC) and VAC abolished HG-evoked dephosphorylation of AMPK and eNOS, increased miRNA-34a expression, and decreased NO production. Reactive Oxygen Species 43-46 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 133-137 31533227-9 2019 In addition, both reactive oxygen species (ROS) scavenger N-acetyl-L-cysteine (NAC) and VAC abolished HG-evoked dephosphorylation of AMPK and eNOS, increased miRNA-34a expression, and decreased NO production. Acetylcysteine 58-77 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 133-137 31533227-9 2019 In addition, both reactive oxygen species (ROS) scavenger N-acetyl-L-cysteine (NAC) and VAC abolished HG-evoked dephosphorylation of AMPK and eNOS, increased miRNA-34a expression, and decreased NO production. Acetylcysteine 79-82 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 133-137 31533227-10 2019 These results suggest that VAC impedes HG-induced endothelial dysfunction via inhibition of the ROS/AMPK/miRNA-34a/eNOS signaling cascade. Reactive Oxygen Species 96-99 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 100-104 31522191-7 2019 Mechanistically, we showed that trehalose"s autophagy augmentation is mediated by activation and nuclear translocation of TFEB, which may be due to inhibition of Akt and activation of the AMPK-SKP2-CARM1 signaling pathway. Trehalose 32-41 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 188-192 31481524-8 2019 In contrast, mutants impaired in the glucose-mediated repression of genes were 2DG resistant because glucose availability transcriptionally repressed DOG2 by inhibiting signaling mediated by the AMPK ortholog Snf1. Glucose 37-44 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 195-199 31481524-8 2019 In contrast, mutants impaired in the glucose-mediated repression of genes were 2DG resistant because glucose availability transcriptionally repressed DOG2 by inhibiting signaling mediated by the AMPK ortholog Snf1. Deoxyglucose 79-82 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 195-199 31481524-8 2019 In contrast, mutants impaired in the glucose-mediated repression of genes were 2DG resistant because glucose availability transcriptionally repressed DOG2 by inhibiting signaling mediated by the AMPK ortholog Snf1. Glucose 101-108 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 195-199 31480505-9 2019 The aim of this review is to summarize the current knowledge addressing the antidiabetic effects of dietary flavonoids and their underlying molecular mechanisms on selected pathways: Glucose transporter, hepatic enzymes, tyrosine kinase inhibitor, AMPK, PPAR, and NF-kappaB. Flavonoids 108-118 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 248-252 31473186-2 2019 Both metformin and canagliflozin indirectly activate AMPK by inhibiting mitochondrial function, while salsalate is a direct AMPK activator. Metformin 5-14 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 53-57 31597329-3 2019 This study aimed to explore whether the neuroprotective mechanisms of SA were linked to its regulation of AMP-activated protein kinase (AMPK)/mammalian target of rapamycin (mTOR)/autophagy pathway in vivo and in vitro. schizandrin A 70-72 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 136-140 31597329-3 2019 This study aimed to explore whether the neuroprotective mechanisms of SA were linked to its regulation of AMP-activated protein kinase (AMPK)/mammalian target of rapamycin (mTOR)/autophagy pathway in vivo and in vitro. Adenosine Monophosphate 106-109 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 136-140 31473186-2 2019 Both metformin and canagliflozin indirectly activate AMPK by inhibiting mitochondrial function, while salsalate is a direct AMPK activator. Canagliflozin 19-32 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 53-57 31199678-9 2019 These effects were partly abolished in the presence of compound C (an AMPK inhibitor) and ATP and adenosine, and SREBP1c overexpression also could be resistant to the effects of sorafenib, suggesting that the sorafenib-induced reduction in cell viability was mediated by the ATP-AMPK-mTOR-SREBP1 signaling pathway. Sorafenib 209-218 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 70-74 31473186-2 2019 Both metformin and canagliflozin indirectly activate AMPK by inhibiting mitochondrial function, while salsalate is a direct AMPK activator. salicylsalicylic acid 102-111 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 124-128 31473186-4 2019 Although metformin treatment had been shown to attenuate experimental cystic kidney disease, there are concerns that therapeutic AMPK activation in human kidney might require a higher oral metformin dose than can be achieved clinically. Metformin 189-198 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 129-133 31199678-9 2019 These effects were partly abolished in the presence of compound C (an AMPK inhibitor) and ATP and adenosine, and SREBP1c overexpression also could be resistant to the effects of sorafenib, suggesting that the sorafenib-induced reduction in cell viability was mediated by the ATP-AMPK-mTOR-SREBP1 signaling pathway. Sorafenib 209-218 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 279-283 31199678-12 2019 To our knowledge, this is the first evidence that sorafenib disrupts lipogenesis and triggers liver cancer cell death by targeting SCD1 through the ATP-AMPK-mTOR-SREBP1 pathway.-Liu, G., Kuang, S., Cao, R., Wang, J., Peng, Q., Sun, C. Sorafenib kills liver cancer cells by disrupting SCD1-mediated synthesis of monounsaturated fatty acids via the ATP-AMPK-mTOR- SREBP1 signaling pathway. Sorafenib 50-59 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 152-156 31199678-12 2019 To our knowledge, this is the first evidence that sorafenib disrupts lipogenesis and triggers liver cancer cell death by targeting SCD1 through the ATP-AMPK-mTOR-SREBP1 pathway.-Liu, G., Kuang, S., Cao, R., Wang, J., Peng, Q., Sun, C. Sorafenib kills liver cancer cells by disrupting SCD1-mediated synthesis of monounsaturated fatty acids via the ATP-AMPK-mTOR- SREBP1 signaling pathway. Sorafenib 50-59 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 351-355 30187782-1 2019 To compare the stimulation and binding characteristics of adenosine analogs including AMP, IMM-H007, and M1, to AMPK, and to explore the potential mechanism underlying the regulation effect of adenosine analogs on AMPK activity, [gamma-32P]ATP assay, circular dichroism experiments and molecular docking test were performed. Adenosine 58-67 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 112-116 31091354-10 2019 Energy supply to achieve liver PC is met by the combined DHA plus T3 protocol through upregulation of AMPK coupled to peroxisome proliferator-activated receptor-gamma coactivator 1alpha signaling. Docosahexaenoic Acids 57-60 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 102-106 30187782-2 2019 We found that the interactions with Thr86, Thr88, and His150 in site 1 are probably the reason why the affinities of IMM-H007, M1, and adenosine are comparable but their allosteric activation on AMPK varies greatly, partly interpreting the mechanism of AMPK activity regulated by adenosine analogs. Adenosine 135-144 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 195-199 30187782-2 2019 We found that the interactions with Thr86, Thr88, and His150 in site 1 are probably the reason why the affinities of IMM-H007, M1, and adenosine are comparable but their allosteric activation on AMPK varies greatly, partly interpreting the mechanism of AMPK activity regulated by adenosine analogs. Adenosine 135-144 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 253-257 30187782-2 2019 We found that the interactions with Thr86, Thr88, and His150 in site 1 are probably the reason why the affinities of IMM-H007, M1, and adenosine are comparable but their allosteric activation on AMPK varies greatly, partly interpreting the mechanism of AMPK activity regulated by adenosine analogs. Adenosine 280-289 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 195-199 31273790-0 2019 AMPK-SIRT1-independent inhibition of ANGPTL3 gene expression is a potential lipid-lowering mechanism of metformin. Metformin 104-113 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 31273790-6 2019 The role of AMPK-SIRT1 pathway in metformin regulation of ANGPTL3 was determined using pharmacological, RNAi and reporter assays. Metformin 34-43 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 12-16 31273790-8 2019 KEY FINDINGS: Metformin and pharmacological activators of AMPK and SIRT1 inhibited the expression of ANGPTL3 in HepG2 cells. Metformin 14-23 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 58-62 31273790-12 2019 CONCLUSIONS: Metformin inhibits ANGPTL3 expression in the liver in an AMPK-SIRT1-independent manner as a potential mechanism to regulate LPL and lower plasma lipids. Metformin 13-22 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 70-74 31386965-7 2019 Melatonin-mediated inhibition of Ripk3 improved mitochondrial bioenergetics, reduced mitochondria-initiated oxidative damage, sustained mitochondrial dynamics, ameliorated ER stress, normalized calcium recycling, and activated cardioprotective signaling pathways (including AKT, ERK and AMPK) in cardiomyocytes. Melatonin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 287-291 31302203-0 2019 Pregnancy exposure to carbon black nanoparticles exacerbates bleomycin-induced lung fibrosis in offspring via disrupting LKB1-AMPK-ULK1 axis-mediated autophagy. Bleomycin 61-70 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 126-130 31199678-7 2019 Treatment with sorafenib suppressed ATP production, resulting in AMPK activation via phosphorylation. Sorafenib 15-24 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 65-69 31199678-7 2019 Treatment with sorafenib suppressed ATP production, resulting in AMPK activation via phosphorylation. Adenosine Triphosphate 36-39 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 65-69 31202802-10 2019 As a pan PDE inhibitor, rottlerin was also found to activate the AMPK pathway and induce neurodifferentiation in IMR-32 cells, with the effect more efficient in samples co-treated with cAMP activator Forskolin. rottlerin 24-33 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 65-69 31202802-10 2019 As a pan PDE inhibitor, rottlerin was also found to activate the AMPK pathway and induce neurodifferentiation in IMR-32 cells, with the effect more efficient in samples co-treated with cAMP activator Forskolin. Colforsin 200-209 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 65-69 30475650-0 2019 Ginsenoside metabolite compound K induces apoptosis and autophagy in non-small cell lung cancer cells via AMPK-mTOR and JNK pathways. Ginsenosides 0-11 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 106-110 31353224-0 2019 Elevated Exogenous Pyruvate Potentiates Mesodermal Differentiation through Metabolic Modulation and AMPK/mTOR Pathway in Human Embryonic Stem Cells. Pyruvic Acid 19-27 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 100-104 31353224-8 2019 Further study shows that pyruvate increases AMP/ATP ratio, activates AMPK, and modulates the mTOR pathway to enhance mesoderm differentiation. Pyruvic Acid 25-33 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 69-73 31447857-9 2019 In conclusion, our data indicate that an AMPK-NAMPT-NAD+ signaling axis promotes P2Y11 receptor expression during M2 polarization of human macrophages in response to IL-10. NAD 52-56 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 41-45 31324733-0 2019 Capsaicin inhibits the migration and invasion via the AMPK/NF-kappaB signaling pathway in esophagus sequamous cell carcinoma by decreasing matrix metalloproteinase-9 expression. Capsaicin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 54-58 31324733-6 2019 In addition, capsaicin can enhance sirtuin1 (SIRT1) expression, which could activate nuclear factor-kappaB (NF-kappaB) through deacetylation, and activate AMPK inducing the phosphorylation of IkappaBalpha and nuclear localization of NF-kappaB p65. Capsaicin 13-22 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 155-159 31324733-7 2019 Overall, these results revealed that Capsaicin can inhibit the migration and invasion of ESCC cells via the AMPK/NF-kappaB signaling pathway. Capsaicin 37-46 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 108-112 31382550-7 2019 In particular, we describe how ROS impact various signaling pathways of autophagy, including mTORC1-ULK1, AMPK-mTORC1-ULK1, and Keap1-Nrf2-p62, as well as selective autophagy including mitophagy and pexophagy. Reactive Oxygen Species 31-34 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 106-110 31066329-4 2019 IPMK enhances autophagy-related transcription by stimulating AMPK-dependent SIRT1 activation, which mediates the deacetylation of histone 4 lysine 16. Lysine 140-146 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 61-65 31173197-5 2019 Finally, Sal B increased the phosphorylation of AMP kinase (AMPK) and decreased the phosphorylation of mammalian target of rapamycin (mTOR), but had no effect on the phosphorylation of AKT. salvianolic acid B 9-14 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 60-64 30895621-0 2019 Immunomodulatory effect of oleoylethanolamide in dendritic cells via TRPV1/AMPK activation. oleoylethanolamide 27-45 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 75-79 30895621-7 2019 Collectively, the present study suggests that OEA suppresses DCs maturation through the activation of TRPV1/AMPK. oleoylethanolamide 46-49 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 108-112 30475650-9 2019 In conclusion, this study demonstrates that C-K promotes autophagy-mediated apoptosis in NSCLC via AMPK-mTOR and JNK signaling pathways. ginsenoside M1 44-47 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 99-103 31316621-13 2019 This study, to the best of our knowledge, is the first to assess the effects of higenamine on cold-induced vasoconstriction in vivo and its molecular mechanisms on the PI3K/Akt, AMPK/eNOS/nitric oxide, ROS/alpha2C-AR and PTK9 signaling pathways under hypothermia conditions. higenamine 80-90 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 178-182 31173197-5 2019 Finally, Sal B increased the phosphorylation of AMP kinase (AMPK) and decreased the phosphorylation of mammalian target of rapamycin (mTOR), but had no effect on the phosphorylation of AKT. salvianolic acid B 9-14 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 48-58 31242463-6 2019 AMPK inhibition decreased GPER1 accumulation in cells grown in low [D-glucose] while the AMPK-activating compound AICAR increased GPER1 accumulation in cells grown in high [D-glucose] media. Glucose 68-77 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 31242463-6 2019 AMPK inhibition decreased GPER1 accumulation in cells grown in low [D-glucose] while the AMPK-activating compound AICAR increased GPER1 accumulation in cells grown in high [D-glucose] media. Glucose 173-182 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 89-93 31467529-0 2019 Ginsenoside Rg1 Ameliorates Palmitic Acid-Induced Hepatic Steatosis and Inflammation in HepG2 Cells via the AMPK/NF-kappaB Pathway. Ginsenosides 0-11 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 108-112 31467529-0 2019 Ginsenoside Rg1 Ameliorates Palmitic Acid-Induced Hepatic Steatosis and Inflammation in HepG2 Cells via the AMPK/NF-kappaB Pathway. Palmitic Acid 28-41 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 108-112 31467529-10 2019 The present study showed that PA markedly increased the intracellular lipid droplets accumulation and TG levels, but decreased AMPK phosphorylation and the expressions of its downstream lipogenic genes. Palmitic Acid 30-32 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 127-131 31467529-12 2019 In addition, blocking AMPK by using the AMPK inhibitor markedly abolished the G-Rg1-mediated protection against PA-induced lipid deposition in HepG2 cells. Palmitic Acid 112-114 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 22-26 31467529-12 2019 In addition, blocking AMPK by using the AMPK inhibitor markedly abolished the G-Rg1-mediated protection against PA-induced lipid deposition in HepG2 cells. Palmitic Acid 112-114 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 40-44 31534497-12 2019 Another significant finding was that docetaxel treatment repressed KLF5 expression through AMPK/mTOR/p70S6K signaling pathway resulting in increased BECN1, induction of cell autophagy, and promotion of cell survival in castration-resistant prostate cancer cells. Docetaxel 37-46 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 91-95 31402869-0 2019 CTAB Enhances Chemo-Sensitivity Through Activation of AMPK Signaling Cascades in Breast Cancer. Cetrimonium 0-4 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 54-58 31402869-3 2019 In this study, we hypothesized that AMPK as a key metabolic regulator plays a crucial role in regulation of breast cancer drug resistance, which could be alleviated by treatment of CTAB. Cetrimonium 181-185 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 36-40 31402869-4 2019 We observed that CTAB can improve the DOX sensitivity of the breast cancer cells by inhibition of the ATP-dependent drug-efflux pump P-gp complex through activation of the AMPK-HIF-1alpha-P-gp cascades. Cetrimonium 17-21 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 172-176 31402869-4 2019 We observed that CTAB can improve the DOX sensitivity of the breast cancer cells by inhibition of the ATP-dependent drug-efflux pump P-gp complex through activation of the AMPK-HIF-1alpha-P-gp cascades. Doxorubicin 38-41 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 172-176 31402869-4 2019 We observed that CTAB can improve the DOX sensitivity of the breast cancer cells by inhibition of the ATP-dependent drug-efflux pump P-gp complex through activation of the AMPK-HIF-1alpha-P-gp cascades. Adenosine Triphosphate 102-105 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 172-176 31402869-6 2019 Taken together, our results showed that CTAB sensitized drug resistance of breast cancer to DOX chemotherapy by activating AMPK signaling cascades both in vitro and in vivo, suggested that CTAB may be developed as a promising and novel chemosensitizer and chemotherapeutic candidate for breast cancer treatment. Cetrimonium 40-44 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 123-127 31402869-6 2019 Taken together, our results showed that CTAB sensitized drug resistance of breast cancer to DOX chemotherapy by activating AMPK signaling cascades both in vitro and in vivo, suggested that CTAB may be developed as a promising and novel chemosensitizer and chemotherapeutic candidate for breast cancer treatment. Doxorubicin 92-95 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 123-127 31402869-6 2019 Taken together, our results showed that CTAB sensitized drug resistance of breast cancer to DOX chemotherapy by activating AMPK signaling cascades both in vitro and in vivo, suggested that CTAB may be developed as a promising and novel chemosensitizer and chemotherapeutic candidate for breast cancer treatment. Cetrimonium 189-193 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 123-127 31288625-6 2019 Genetic studies of the role of AMPK in mouse cancer suggest that, before disease arises, AMPK acts as a tumour suppressor that protects against cancer, with this protection being further enhanced by AMPK activators such as the biguanide phenformin. Biguanides 227-236 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 31-35 31288625-6 2019 Genetic studies of the role of AMPK in mouse cancer suggest that, before disease arises, AMPK acts as a tumour suppressor that protects against cancer, with this protection being further enhanced by AMPK activators such as the biguanide phenformin. Biguanides 227-236 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 89-93 31288625-6 2019 Genetic studies of the role of AMPK in mouse cancer suggest that, before disease arises, AMPK acts as a tumour suppressor that protects against cancer, with this protection being further enhanced by AMPK activators such as the biguanide phenformin. Biguanides 227-236 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 89-93 31288625-6 2019 Genetic studies of the role of AMPK in mouse cancer suggest that, before disease arises, AMPK acts as a tumour suppressor that protects against cancer, with this protection being further enhanced by AMPK activators such as the biguanide phenformin. Phenformin 237-247 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 31-35 31288625-6 2019 Genetic studies of the role of AMPK in mouse cancer suggest that, before disease arises, AMPK acts as a tumour suppressor that protects against cancer, with this protection being further enhanced by AMPK activators such as the biguanide phenformin. Phenformin 237-247 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 89-93 31288625-6 2019 Genetic studies of the role of AMPK in mouse cancer suggest that, before disease arises, AMPK acts as a tumour suppressor that protects against cancer, with this protection being further enhanced by AMPK activators such as the biguanide phenformin. Phenformin 237-247 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 89-93 31352760-0 2021 Troxerutin attenuates isoproterenol-induced cardiac hypertrophy via the LKB1/AMPK/mTOR pathway. troxerutin 0-10 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 77-81 31352760-0 2021 Troxerutin attenuates isoproterenol-induced cardiac hypertrophy via the LKB1/AMPK/mTOR pathway. Isoproterenol 22-35 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 77-81 31173197-6 2019 In conclusion, the present study revealed that Sal B protects HUVECs from oxidative stress, at least partially by promoting autophagy via activation of the AMPK pathway and downregulation of the mTOR pathway. salvianolic acid B 47-52 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 156-160 31475196-0 2019 Exenatide reduces cardiomyocyte apoptosis by stimulating adiponectin secretion and activating APPL1-AMPK-PPARalpha axis. Exenatide 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 100-104 31341250-11 2019 Interestingly, the preincubation of ML-SA1, by an early activation of AMPK and beclin 1, rescued motor neurons from L-BMAA-induced cell death and reduced the expression of the ER stress marker GRP78. beta-N-methylamino-L-alanine 116-122 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 70-74 31285420-0 2019 4-hydroxyphenylpyruvate dioxygenase promotes lung cancer growth via pentose phosphate pathway (PPP) flux mediated by LKB1-AMPK/HDAC10/G6PD axis. Pentosephosphates 68-85 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 122-126 31353730-5 2019 In addition, VA promoted the expression of p-Nrf2 and HO-1 through LKB1/AMPK signaling pathway, as well as the level of SIRT1 and PGC-1alpha. Vanillic Acid 13-15 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 72-76 31353730-7 2019 These results indicated that AMPK was an important target molecule of VA in the process of alleviating oxidative stress in HUVECs, providing a new potential evidence for vascular protection of anthocyanin in vitro. Anthocyanins 193-204 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 29-33 31353730-9 2019 This study revealed that VA improved oxidative stress in endothelial cells stimulated by palmitic acid by activating AMPK and its downstream proteins. Palmitic Acid 89-102 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 117-121 31079918-0 2019 GSK621 attenuates oxygen glucose deprivation/re-oxygenation-induced myocardial cell injury via AMPK-dependent signaling. Oxygen 18-24 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 95-99 31014671-9 2019 The recuse of the effects of Alox12 depletion using Alox12 metabolites 12S-HETE further confirmed that AMPK and its subsequent inhibition of ACC1 activity and lipid synthesis were the downstream signaling of Alox12 inhibition. 12-Hydroxy-5,8,10,14-eicosatetraenoic Acid 71-79 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 103-107 31189568-9 2019 Incubation of 3T3-L1 cells with MT47-100 selectively inhibited AMPK complexes containing AMPKbeta2 whilst simultaneously inhibiting cellular lipid accumulation as well as cellular levels and secretion of adiponectin. MT47-100 32-40 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 63-67 30851273-0 2019 Metformin reduced NLRP3 inflammasome activity in Ox-LDL stimulated macrophages through adenosine monophosphate activated protein kinase and protein phosphatase 2A. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 87-135 30851273-14 2019 Our data showed Metformin reduced NLRP3 protein expression and NLRP3 inflammasome activation in ox-LDL-stimulated macrophages through AMPK and PP2A. Metformin 16-25 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 134-138 30851273-2 2019 Previous researches showed that metformin activates Adenosine Monophosphate Activated Protein Kinase (AMPK) and Protein Phosphatase 2A (PP2A). Metformin 32-41 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 52-100 30851273-2 2019 Previous researches showed that metformin activates Adenosine Monophosphate Activated Protein Kinase (AMPK) and Protein Phosphatase 2A (PP2A). Metformin 32-41 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 102-106 31100089-10 2019 Catechin also inhibited the activation of NF-kappaB, AMPK, FOXO3a and SIRT1, but increased the phosphorylation level of the above factors. Catechin 0-8 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 53-57 30948787-1 2019 AMPK, a master regulator of metabolic homeostasis, is activated by both AMP-dependent and AMP-independent mechanisms. Adenosine Monophosphate 72-75 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 30948787-3 2019 Here, we show that, depending on the degree of elevation of cellular AMP, distinct compartmentalized pools of AMPK are activated, phosphorylating different sets of targets. Adenosine Monophosphate 69-72 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 110-114 30948787-4 2019 Low glucose activates AMPK exclusively through the AMP-independent, AXIN-based pathway in lysosomes to phosphorylate targets such as ACC1 and SREBP1c, exerting early anti-anabolic and pro-catabolic roles. Glucose 4-11 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 22-26 30948787-4 2019 Low glucose activates AMPK exclusively through the AMP-independent, AXIN-based pathway in lysosomes to phosphorylate targets such as ACC1 and SREBP1c, exerting early anti-anabolic and pro-catabolic roles. axin 68-72 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 22-26 30948787-5 2019 Moderate increases in AMP expand this to activate cytosolic AMPK also in an AXIN-dependent manner. Adenosine Monophosphate 22-25 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 60-64 30948787-5 2019 Moderate increases in AMP expand this to activate cytosolic AMPK also in an AXIN-dependent manner. axin 76-80 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 60-64 30948787-6 2019 In contrast, high concentrations of AMP, arising from severe nutrient stress, activate all pools of AMPK independently of AXIN. Adenosine Monophosphate 36-39 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 100-104 30993829-4 2019 On the one hand, AMPKalpha subunit binds to mitochondria independently of beta subunit and targeting AMPK to mitochondria facilitates oxidative phosphorylation and fatty acid oxidation, and inhibits glycolysis. Fatty Acids 164-174 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 17-21 31191364-0 2019 Irbesartan Ameliorates Lipid Deposition by Enhancing Autophagy via PKC/AMPK/ULK1 Axis in Free Fatty Acid Induced Hepatocytes. Irbesartan 0-10 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 71-75 31191364-7 2019 Irbesartan inhibited PKC and activated AMPK and its downstream effector ULK1, thereby inducing autophagy, decreasing lipid deposition, and restoring mitochondrial function. Irbesartan 0-10 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 39-43 31191364-8 2019 Taken together, irbesartan triggers autophagy via the PKC/AMPK/ULK1 axis to ameliorate the pathological changes in the steatotic hepatocytes. Irbesartan 16-26 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 58-62 31191828-0 2019 Correction: Metformin sensitizes anticancer effect of dasatinib in head and neck squamous cell carcinoma cells through AMPK-dependent ER stress. Metformin 12-21 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 119-123 31191828-0 2019 Correction: Metformin sensitizes anticancer effect of dasatinib in head and neck squamous cell carcinoma cells through AMPK-dependent ER stress. Dasatinib 54-63 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 119-123 31100089-0 2019 Catechin attenuates TNF-alpha induced inflammatory response via AMPK-SIRT1 pathway in 3T3-L1 adipocytes. Catechin 0-8 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 64-68 31077199-0 2019 Metformin regulates lipid metabolism in a canine model of atrial fibrillation through AMPK/PPAR-alpha/VLCAD pathway. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 86-90 31077199-3 2019 MET (Metformin), an AMPK (AMP-activated protein kinase) activator, has been found to be associated with a decreased risk of AF in patients with type 2 diabetes. Metformin 5-14 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 20-24 31077199-3 2019 MET (Metformin), an AMPK (AMP-activated protein kinase) activator, has been found to be associated with a decreased risk of AF in patients with type 2 diabetes. Metformin 5-14 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 26-54 31077199-7 2019 RESULTS: The expression of AMPK increased in the ARP group and significantly increased in the MET+ARP group comparing to the SR group. Strontium 125-127 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 27-31 31077199-12 2019 Metformin reduces lipid accumulation and promotes beta-oxidation of FA in AF models partially through AMPK/PPAR-alpha/VLCAD pathway. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 102-106 30753863-0 2019 Acetaminophen aggravates fat accumulation in NAFLD by inhibiting autophagy via the AMPK/mTOR pathway. Acetaminophen 0-13 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 83-87 30753863-6 2019 Immunohistochemistry analysis showed the intensity of hepatic mTOR was increased and AMPK was decreased in 200 mg/kg APAP treated group. Acetaminophen 117-121 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 85-89 30753863-9 2019 Western blot analysis demonstrated APAP treatment decreased the levels of LC3-II, Beclin1 and AMPK, increased the levels of mTOR and SREBP-1c, but rapamycin treatment significantly reversed these effects of APAP. Acetaminophen 35-39 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 94-98 30753863-10 2019 In conclusion, therapeutic dosages of APAP aggravates fat accumulation in NAFLD, the potential mechanism might be involved in inhibiting autophagy associated with the AMPK/mTOR pathway, and patients with NAFLD should use a lower dose of APAP. Acetaminophen 38-42 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 167-171 30218072-0 2019 Hispidulin induces ER stress-mediated apoptosis in human hepatocellular carcinoma cells in vitro and in vivo by activating AMPK signaling pathway. hispidulin 0-10 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 123-127 30218072-6 2019 Furthermore, we showed that hispidulin-induced apoptosis was mediated by activation of AMPK/mTOR signaling pathway as pretreatment with Compound C, an AMPK inhibitor, or AMPK-targeting siRNA reversed the pro-apoptotic effect of hispidulin. hispidulin 28-38 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 87-91 30218072-6 2019 Furthermore, we showed that hispidulin-induced apoptosis was mediated by activation of AMPK/mTOR signaling pathway as pretreatment with Compound C, an AMPK inhibitor, or AMPK-targeting siRNA reversed the pro-apoptotic effect of hispidulin. hispidulin 28-38 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 151-155 30218072-6 2019 Furthermore, we showed that hispidulin-induced apoptosis was mediated by activation of AMPK/mTOR signaling pathway as pretreatment with Compound C, an AMPK inhibitor, or AMPK-targeting siRNA reversed the pro-apoptotic effect of hispidulin. hispidulin 28-38 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 151-155 31217429-6 2019 This is supported by reduced proliferation of human dermal papilla and predominantly epithelial keratinocytes after incubation with AICAR, the agonist for AMPK signaling which activates PPARGC1a and serves as co-activator of PPARgamma. AICA ribonucleotide 132-137 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 155-159 30975543-13 2019 Sorafenib, through AMPK, blocked the GDNF/AKT survival action without altering the RET apoptotic pathway. Sorafenib 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 19-23 30892786-0 2019 Fucoxanthin Protects against oxLDL-Induced Endothelial Damage via Activating the AMPK-Akt-CREB-PGC1alpha Pathway. fucoxanthin 0-11 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 81-85 30959553-0 2019 Targeting AMP-activated kinase impacts hepatocellular cancer stem cells induced by long-term treatment with sorafenib. Sorafenib 108-117 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 10-30 30959553-7 2019 We report that sorafenib-resistant cells had lower levels of total and phosphorylated AMPK as well as its downstream substrate, ACC, compared with the parental cells. Sorafenib 15-24 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 86-90 30959553-8 2019 Interestingly, AMPK knockdown with siRNA or inhibition with dorsomorphin increased the expression of stem cell markers in parental cells and blocked sorafenib-induced cell death. Sorafenib 149-158 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 15-19 30959553-9 2019 Conversely, the upregulation of AMPK, either by transfection or by pharmacological activation with A-769662, decreased the expression of ALDH1A1, ABCB1A, CD133, Nanog, Oct4, and alpha fetoprotein, and restored sensitivity to sorafenib. Sorafenib 225-234 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 32-36 31105845-7 2019 In this study, we found that AMPK activator metformin suppresses T cell proliferation and inhibits the differentiation of Th1 and Th17 cells while promoting the development of Tregs in vitro in a dose-dependent manner. Metformin 44-53 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 29-33 30738797-0 2019 AMPK: A promising molecular target for combating cisplatin toxicities. Cisplatin 49-58 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 30738797-4 2019 While AMPK activation protects normal tissues against cisplatin-induced toxicities, its impact in cancer is context-dependent and there is no single, uniform role for AMPK. Cisplatin 54-63 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 6-10 30738797-5 2019 On one hand, some report that AMPK activation augments cisplatin-induced apoptosis in cancer, while on the other hand, few reports indicate that AMPK activation rescues cancer cells from the cytotoxicity induced by cisplatin. Cisplatin 55-64 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-34 30738797-5 2019 On one hand, some report that AMPK activation augments cisplatin-induced apoptosis in cancer, while on the other hand, few reports indicate that AMPK activation rescues cancer cells from the cytotoxicity induced by cisplatin. Cisplatin 55-64 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 145-149 30738797-5 2019 On one hand, some report that AMPK activation augments cisplatin-induced apoptosis in cancer, while on the other hand, few reports indicate that AMPK activation rescues cancer cells from the cytotoxicity induced by cisplatin. Cisplatin 215-224 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 145-149 30738797-6 2019 Here we review the most salient signaling pathways regulated by AMPK with an emphasis on their relation to cisplatin toxicity and yet discuss context-dependent functions of AMPK in cancer. Cisplatin 107-116 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 64-68 30950462-0 2019 Zeaxanthin promotes mitochondrial biogenesis and adipocyte browning via AMPKalpha1 activation. Zeaxanthins 0-10 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 72-82 30995468-0 2019 Phenformin, But Not Metformin, Delays Development of T Cell Acute Lymphoblastic Leukemia/Lymphoma via Cell-Autonomous AMPK Activation. Phenformin 0-10 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 118-122 30995468-2 2019 AMPK is activated by biguanides, such as metformin and phenformin, and metformin use in diabetics has been associated with reduced cancer risk. Biguanides 21-31 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 30995468-2 2019 AMPK is activated by biguanides, such as metformin and phenformin, and metformin use in diabetics has been associated with reduced cancer risk. Metformin 41-50 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 30995468-2 2019 AMPK is activated by biguanides, such as metformin and phenformin, and metformin use in diabetics has been associated with reduced cancer risk. Phenformin 55-65 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 30995468-2 2019 AMPK is activated by biguanides, such as metformin and phenformin, and metformin use in diabetics has been associated with reduced cancer risk. Metformin 71-80 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 30995468-5 2019 Oral administration of phenformin, but not metformin, delayed onset and growth of lymphomas, but only when T cells expressed AMPK-alpha1. Phenformin 23-33 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 125-136 30987128-0 2019 Capsaicin Targets Lipogenesis in HepG2 Cells Through AMPK Activation, AKT Inhibition and PPARs Regulation. Capsaicin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 53-57 31114359-0 2019 SLC5A1 promotes growth and proliferation of pancreatic carcinoma via glucose-dependent AMPK/mTOR signaling. Glucose 69-76 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 87-91 31001120-0 2019 Zinc-Doped Copper Oxide Nanocomposites Inhibit the Growth of Pancreatic Cancer by Inducing Autophagy Through AMPK/mTOR Pathway. cupric oxide 11-23 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 109-113 31001120-7 2019 Moreover, in the presence of AMPK activator AMPKinone, the protein level of p-AMPK, p-ULK1, Beclin-1 and LC3-II/LC3-I increased, while the protein expression of p-AMPK, p-ULK1, Beclin-1 and LC3-II/LC3-I decreased in the presence of AMPK inhibitor Compound C. In vivo study using xenograft mice revealed that Zn-CuO NPs significantly inhibited tumor growth with low toxicity. Zinc 308-310 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 29-33 31001120-7 2019 Moreover, in the presence of AMPK activator AMPKinone, the protein level of p-AMPK, p-ULK1, Beclin-1 and LC3-II/LC3-I increased, while the protein expression of p-AMPK, p-ULK1, Beclin-1 and LC3-II/LC3-I decreased in the presence of AMPK inhibitor Compound C. In vivo study using xenograft mice revealed that Zn-CuO NPs significantly inhibited tumor growth with low toxicity. Zinc 308-310 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 44-48 31001120-7 2019 Moreover, in the presence of AMPK activator AMPKinone, the protein level of p-AMPK, p-ULK1, Beclin-1 and LC3-II/LC3-I increased, while the protein expression of p-AMPK, p-ULK1, Beclin-1 and LC3-II/LC3-I decreased in the presence of AMPK inhibitor Compound C. In vivo study using xenograft mice revealed that Zn-CuO NPs significantly inhibited tumor growth with low toxicity. Zinc 308-310 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 44-48 31001120-7 2019 Moreover, in the presence of AMPK activator AMPKinone, the protein level of p-AMPK, p-ULK1, Beclin-1 and LC3-II/LC3-I increased, while the protein expression of p-AMPK, p-ULK1, Beclin-1 and LC3-II/LC3-I decreased in the presence of AMPK inhibitor Compound C. In vivo study using xenograft mice revealed that Zn-CuO NPs significantly inhibited tumor growth with low toxicity. Zinc 308-310 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 44-48 31009513-3 2019 In this work, optimal control theory was applied to regulate intracellular signaling pathways of miR-451-AMPK-mTOR-cell cycle dynamics via glucose and drug intravenous administration infusions. Glucose 139-146 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 105-109 30987128-7 2019 This effect of capsaicin was prevented by dorsomorphin and GW9662, pharmacological inhibitors of AMPK and PPARgamma, respectively. Capsaicin 15-24 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 97-101 30987128-7 2019 This effect of capsaicin was prevented by dorsomorphin and GW9662, pharmacological inhibitors of AMPK and PPARgamma, respectively. dorsomorphin 42-54 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 97-101 30987128-7 2019 This effect of capsaicin was prevented by dorsomorphin and GW9662, pharmacological inhibitors of AMPK and PPARgamma, respectively. 2-chloro-5-nitrobenzanilide 59-65 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 97-101 30987128-8 2019 In addition, capsaicin activated AMPK and inhibited the AKT/mTOR pathway, major regulators of hepatic lipogenesis. Capsaicin 13-22 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 33-37 30902078-0 2019 Correction to: Cryptotanshinone activates AMPK-TSC2 axis leading to inhibition of mTORC1 signaling in cancer cells. cryptotanshinone 15-31 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 42-46 30649496-6 2019 A score formed of the latter SNPs (in ADCY4, CIDEA, GNAS, PDE8B, PRKAA1, PRKAG2) was associated with plasma FFA and glycerol measurements (1.4*10-9 <= P <= 1.2*10-5), visceral adipose tissue mass (P = 0.0326), and proinsulin conversion (P <= 0.0272). Glycerol 116-124 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 65-71 30899201-0 2019 Combination of the natural product capsaicin and docetaxel synergistically kills human prostate cancer cells through the metabolic regulator AMP-activated kinase. Capsaicin 35-44 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 141-161 30899201-0 2019 Combination of the natural product capsaicin and docetaxel synergistically kills human prostate cancer cells through the metabolic regulator AMP-activated kinase. Docetaxel 49-58 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 141-161 30899201-16 2019 In addition, pharmacological inhibition of AMPK with dorsomorphin (compound C) as well as knock down by siRNA of AMPK or its upstream kinase LKB1, abolished the synergy of docetaxel and capsaicin. dorsomorphin 53-65 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 43-47 30841449-8 2019 Conversely, AMPK depletion significantly abolishes the effects of physcion (a selective small-molecule 6PGD inhibitor) in decreasing NADPH/NAD + ratio, growth and survival, confirming the role of AMPK as the relevant upstream activator with 6PGD inhibition in HCC cells. NADP 133-138 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 12-16 30841449-8 2019 Conversely, AMPK depletion significantly abolishes the effects of physcion (a selective small-molecule 6PGD inhibitor) in decreasing NADPH/NAD + ratio, growth and survival, confirming the role of AMPK as the relevant upstream activator with 6PGD inhibition in HCC cells. NAD 139-144 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 12-16 30579288-0 2019 Kazinol U inhibits melanogenesis through the inhibition of tyrosinase-related proteins via AMP kinase activation. kazinol U 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 91-101 30579288-2 2019 Kazinol U has shown cytoprotective effects against cytokine-induced apoptotic cell death and induces AMP kinase (AMPK) activation through LKB1 activation. kazinol U 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 101-111 30579288-2 2019 Kazinol U has shown cytoprotective effects against cytokine-induced apoptotic cell death and induces AMP kinase (AMPK) activation through LKB1 activation. kazinol U 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 113-117 30579288-9 2019 Moreover, kazinol U induced phosphorylation of AMPK and MAPK proteins, which are MITF inhibitors. kazinol U 10-19 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 47-51 30860465-0 2019 One novel curcumin derivative ZYX01 induces autophagy of human non-small lung cancer cells A549 through AMPK/ULK1/Beclin-1 signaling pathway. Curcumin 10-18 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 104-108 30516280-0 2019 Melatonin attenuates myocardial ischemia-reperfusion injury via improving mitochondrial fusion/mitophagy and activating the AMPK-OPA1 signaling pathways. Melatonin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 124-128 30516280-7 2019 Furthermore, we demonstrated that melatonin affected OPA1 stabilization via the AMPK signaling pathway and that blockade of AMPK repressed OPA1 expression and compromised the cardioprotective action of melatonin. Melatonin 34-43 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 80-84 30516280-7 2019 Furthermore, we demonstrated that melatonin affected OPA1 stabilization via the AMPK signaling pathway and that blockade of AMPK repressed OPA1 expression and compromised the cardioprotective action of melatonin. Melatonin 202-211 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 124-128 30516280-9 2019 Moreover, manipulation of the AMPK-OPA1-mitochondrial fusion/mitophagy axis via melatonin may be a novel therapeutic approach to reduce cardiac I/R injury. Melatonin 80-89 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-34 30798915-0 2019 Cellular stress and AMPK links metformin and diverse compounds with accelerated emergence from anesthesia and potential recovery from disorders of consciousness. Metformin 31-40 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 20-24 30798915-5 2019 Additionally, emergence from GA, a passive process that occurs after anesthetic removal, is associated with lower anesthetic concentrations in the brain compared to doses associated with induction of GA. AMPK, an evolutionarily conserved kinase activated by cellular stress (e.g. increases in calcium [Ca2+] and/or reactive oxygen species [ROS], etc.) Calcium 293-300 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 204-208 30798915-5 2019 Additionally, emergence from GA, a passive process that occurs after anesthetic removal, is associated with lower anesthetic concentrations in the brain compared to doses associated with induction of GA. AMPK, an evolutionarily conserved kinase activated by cellular stress (e.g. increases in calcium [Ca2+] and/or reactive oxygen species [ROS], etc.) Reactive Oxygen Species 315-338 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 204-208 30798915-5 2019 Additionally, emergence from GA, a passive process that occurs after anesthetic removal, is associated with lower anesthetic concentrations in the brain compared to doses associated with induction of GA. AMPK, an evolutionarily conserved kinase activated by cellular stress (e.g. increases in calcium [Ca2+] and/or reactive oxygen species [ROS], etc.) Reactive Oxygen Species 340-343 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 204-208 30798915-8 2019 Increases in ROS and Ca2+ play critical roles in neuronal excitation and glutamate, the primary excitatory neurotransmitter in the human brain, activates AMPK in cortical neurons. Reactive Oxygen Species 13-16 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 154-158 30798915-8 2019 Increases in ROS and Ca2+ play critical roles in neuronal excitation and glutamate, the primary excitatory neurotransmitter in the human brain, activates AMPK in cortical neurons. Glutamic Acid 73-82 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 154-158 30798915-9 2019 Nearly every neurotransmitter released from ascending arousal circuits that promote wakefulness, arousal, and consciousness activates AMPK, including acetylcholine, histamine, orexin-A, dopamine, and norepinephrine. Acetylcholine 150-163 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 134-138 30798915-9 2019 Nearly every neurotransmitter released from ascending arousal circuits that promote wakefulness, arousal, and consciousness activates AMPK, including acetylcholine, histamine, orexin-A, dopamine, and norepinephrine. Histamine 165-174 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 134-138 30798915-9 2019 Nearly every neurotransmitter released from ascending arousal circuits that promote wakefulness, arousal, and consciousness activates AMPK, including acetylcholine, histamine, orexin-A, dopamine, and norepinephrine. Dopamine 186-194 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 134-138 30798915-10 2019 Several GAs that are commonly used to induce LOC in human patients also activate AMPK (e.g. propofol, sevoflurane, isoflurane, dexmedetomidine, ketamine, midazolam). Propofol 92-100 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 81-85 30798915-10 2019 Several GAs that are commonly used to induce LOC in human patients also activate AMPK (e.g. propofol, sevoflurane, isoflurane, dexmedetomidine, ketamine, midazolam). Sevoflurane 102-113 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 81-85 30798915-10 2019 Several GAs that are commonly used to induce LOC in human patients also activate AMPK (e.g. propofol, sevoflurane, isoflurane, dexmedetomidine, ketamine, midazolam). Isoflurane 115-125 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 81-85 30798915-10 2019 Several GAs that are commonly used to induce LOC in human patients also activate AMPK (e.g. propofol, sevoflurane, isoflurane, dexmedetomidine, ketamine, midazolam). Dexmedetomidine 127-142 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 81-85 30798915-10 2019 Several GAs that are commonly used to induce LOC in human patients also activate AMPK (e.g. propofol, sevoflurane, isoflurane, dexmedetomidine, ketamine, midazolam). Ketamine 144-152 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 81-85 30798915-10 2019 Several GAs that are commonly used to induce LOC in human patients also activate AMPK (e.g. propofol, sevoflurane, isoflurane, dexmedetomidine, ketamine, midazolam). Midazolam 154-163 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 81-85 30798915-11 2019 Various compounds that accelerate emergence from anesthesia, thus mitigating problematic effects associated with delayed emergence such as delirium, also activate AMPK (e.g. nicotine, caffeine, forskolin, carbachol). Nicotine 174-182 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 163-167 30798915-11 2019 Various compounds that accelerate emergence from anesthesia, thus mitigating problematic effects associated with delayed emergence such as delirium, also activate AMPK (e.g. nicotine, caffeine, forskolin, carbachol). Caffeine 184-192 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 163-167 30798915-11 2019 Various compounds that accelerate emergence from anesthesia, thus mitigating problematic effects associated with delayed emergence such as delirium, also activate AMPK (e.g. nicotine, caffeine, forskolin, carbachol). Colforsin 194-203 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 163-167 30798915-11 2019 Various compounds that accelerate emergence from anesthesia, thus mitigating problematic effects associated with delayed emergence such as delirium, also activate AMPK (e.g. nicotine, caffeine, forskolin, carbachol). Carbachol 205-214 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 163-167 30798915-12 2019 GAs and neurotransmitters also act as preconditioning agents and the GABAA receptor inhibitor bicuculline, which reverses propofol anesthesia, also activates AMPK in cortical neurons. Bicuculline 94-105 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 158-162 30798915-12 2019 GAs and neurotransmitters also act as preconditioning agents and the GABAA receptor inhibitor bicuculline, which reverses propofol anesthesia, also activates AMPK in cortical neurons. Propofol 122-130 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 158-162 30798915-14 2019 Because AMPK activators including metformin and nicotine promote proliferation and differentiation of neural stem cells located in the subventricular zone and the dentate gyrus, AMPK activation may also enhance brain repair and promote potential recovery from disorders of consciousness (i.e. minimally conscious state, vegetative state, coma). Metformin 34-43 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 8-12 30798915-14 2019 Because AMPK activators including metformin and nicotine promote proliferation and differentiation of neural stem cells located in the subventricular zone and the dentate gyrus, AMPK activation may also enhance brain repair and promote potential recovery from disorders of consciousness (i.e. minimally conscious state, vegetative state, coma). Nicotine 48-56 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 8-12 30860465-0 2019 One novel curcumin derivative ZYX01 induces autophagy of human non-small lung cancer cells A549 through AMPK/ULK1/Beclin-1 signaling pathway. zyx01 30-35 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 104-108 30860465-5 2019 We further confirmed the cellular AMPK/ULK1/Beclin-1 signaling pathway in A549 cells after ZYX01 treatment. zyx01 91-96 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 34-38 30860465-7 2019 Current results had confirmed that ZYX01 induced A549 cells autophagy through AMPK/ULK1/Beclin-1 pathway and shed light on the future study on the anti-cancer molecular mechanism. zyx01 35-40 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 78-82 30899201-16 2019 In addition, pharmacological inhibition of AMPK with dorsomorphin (compound C) as well as knock down by siRNA of AMPK or its upstream kinase LKB1, abolished the synergy of docetaxel and capsaicin. Docetaxel 172-181 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 43-47 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 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 80-84 30899201-16 2019 In addition, pharmacological inhibition of AMPK with dorsomorphin (compound C) as well as knock down by siRNA of AMPK or its upstream kinase LKB1, abolished the synergy of docetaxel and capsaicin. Docetaxel 172-181 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 113-117 30899201-16 2019 In addition, pharmacological inhibition of AMPK with dorsomorphin (compound C) as well as knock down by siRNA of AMPK or its upstream kinase LKB1, abolished the synergy of docetaxel and capsaicin. Capsaicin 186-195 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 43-47 30899201-16 2019 In addition, pharmacological inhibition of AMPK with dorsomorphin (compound C) as well as knock down by siRNA of AMPK or its upstream kinase LKB1, abolished the synergy of docetaxel and capsaicin. Capsaicin 186-195 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 113-117 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. Fatty Acids 244-254 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 80-84 30654939-0 2019 Alpha-glucosidase inhibitor 1-Deoxynojirimycin promotes beige remodeling of 3T3-L1 preadipocytes via activating AMPK. 1-Deoxynojirimycin 28-46 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 112-116 30728400-0 2019 The ability to utilise ammonia as nitrogen source is cell type specific and intricately linked to GDH, AMPK and mTORC1. Ammonia 23-30 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 103-107 30899369-0 2019 Metformin induces the M2 macrophage polarization to accelerate the wound healing via regulating AMPK/mTOR/NLRP3 inflammasome singling pathway. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 96-100 30899369-10 2019 Furthermore, blockage of AMPK or activation of mTOR abolished the effects of metformin treatment on depressing NLRP3 inflammasome activation, M2 polarization and improving wound healing. Metformin 77-86 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 25-29 30899369-11 2019 It suggested that the treatment effects of metformin on wound healing were through regulating AMPK/mTOR/NLRP3 inflammasome signaling axis. Metformin 43-52 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 94-98 30899369-12 2019 CONCLUSION: Metformin regulated AMPK/mTOR singling pathway to inhibit NLRP3 inflammasome activation, which boosted M2 macrophage polarization to accelerate the wound healing. Metformin 12-21 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 32-36 30728400-0 2019 The ability to utilise ammonia as nitrogen source is cell type specific and intricately linked to GDH, AMPK and mTORC1. Nitrogen 34-42 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 103-107 30728400-6 2019 Depletion of glutamine promoted a rapid and transient activation of AMPK, whereas, additional ammonia supplementation blocked this starvation-induced AMPK activation. Glutamine 13-22 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 68-72 30728400-6 2019 Depletion of glutamine promoted a rapid and transient activation of AMPK, whereas, additional ammonia supplementation blocked this starvation-induced AMPK activation. Ammonia 94-101 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 150-154 30728400-7 2019 As expected, drug-induced AMPK activation reduced cell proliferation in glutamine-depleted cells supplemented with ammonia. Glutamine 72-81 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 26-30 30728400-7 2019 As expected, drug-induced AMPK activation reduced cell proliferation in glutamine-depleted cells supplemented with ammonia. Ammonia 115-122 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 26-30 30728400-11 2019 The ability of cells to utilise ammonia as a nitrogen source is intricately linked to AMPK, mTORC1 and GDH. Ammonia 32-39 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 86-90 30717766-10 2019 In addition, the AMPK activator metformin remarkably suppressed the growth of PCK1-knockout PLC/PRF/5 cells and inhibited tumor growth in an orthotropic HCC mouse model. Metformin 32-41 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 17-21 30717766-11 2019 CONCLUSION: This study revealed that PCK1 negatively regulates cell cycle progression and hepatoma cell proliferation via the AMPK/p27Kip1 axis and supports a potential therapeutic and protective effect of metformin on HCC. Metformin 206-215 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 126-130 30444033-10 2019 Additionally, VLD promoted the phosphorylation of AMPK and its target acetyl-CoA carboxylase in the setting of high glucose, and AMPK activation led to a decreased expression and activation of Drp1. Glucose 116-123 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 50-54 30362049-0 2019 Sodium butyrate induces autophagy in colorectal cancer cells through LKB1/AMPK signaling. Butyric Acid 0-15 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 74-78 30362049-7 2019 NaB treatment increased the formation of autolysosome and expression of phosphorylated liver kinase B1 (LKB1), AMP-activated protein kinase (AMPK), and acetyl-CoA carboxylase (ACC). nab 0-3 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 111-139 30362049-7 2019 NaB treatment increased the formation of autolysosome and expression of phosphorylated liver kinase B1 (LKB1), AMP-activated protein kinase (AMPK), and acetyl-CoA carboxylase (ACC). nab 0-3 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 141-145 30362049-8 2019 Treatment with compound C (an inhibitor of AMPK) and siRNA-mediated knockdown of AMPK and LKB1 significantly attenuated NaB-induced autophagy in CRC cells. nab 120-123 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 81-85 30362049-9 2019 Collectively, these findings indicated that LKB1 and AMPK are critical for NaB-mediated autophagy and may act as the novel targets for colorectal cancer therapy in the future. nab 75-78 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 53-57 30468782-3 2019 However, whether AMP activated protein kinase (AMPK) contributes to such effects of metformin remains controversial. Metformin 84-93 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 47-51 30468782-5 2019 RESULTS: Metformin treatment induced metabolic reprogramming and reduced the energy state of both Prkaa1 WT and KO MEF cells, as evidenced by suppressed tricarboxylic acid (TCA) cycle, elevated lactate production as well as decreased NAD+/NADH ratio. Metformin 9-18 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 98-104 30468782-8 2019 Similarly, we demonstrated that a commonly used AMPK agonist 5-Aminoimidazole-4-carboxamide ribonucleotide (AICAR) and fetal bovine serum (FBS) starvation, as a common model for energy stress, both led to Ampkalpha-independent metabolism alterations in MEF cells. AICA ribonucleotide 61-106 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 48-52 30468782-8 2019 Similarly, we demonstrated that a commonly used AMPK agonist 5-Aminoimidazole-4-carboxamide ribonucleotide (AICAR) and fetal bovine serum (FBS) starvation, as a common model for energy stress, both led to Ampkalpha-independent metabolism alterations in MEF cells. acadesine 108-113 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 48-52 30468782-8 2019 Similarly, we demonstrated that a commonly used AMPK agonist 5-Aminoimidazole-4-carboxamide ribonucleotide (AICAR) and fetal bovine serum (FBS) starvation, as a common model for energy stress, both led to Ampkalpha-independent metabolism alterations in MEF cells. ampkalpha 205-214 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 48-52 30578887-0 2019 Venlafaxine and carvedilol ameliorate testicular impairment and disrupted spermatogenesis in rheumatoid arthritis by targeting AMPK/ERK and PI3K/AKT/mTOR pathways. Venlafaxine Hydrochloride 0-11 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 127-131 30578887-0 2019 Venlafaxine and carvedilol ameliorate testicular impairment and disrupted spermatogenesis in rheumatoid arthritis by targeting AMPK/ERK and PI3K/AKT/mTOR pathways. Carvedilol 16-26 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 127-131 30578887-11 2019 Together, the present work demonstrates the beneficial effects of venlafaxine and carvedilol in RA testicular dysfunction and impaired spermatogenesis via modulation of AMPK/ERK and PI3K/AKT/mTOR signaling and intervention with the testicular oxidative stress, inflammation and apoptosis. Venlafaxine Hydrochloride 66-77 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 169-173 30578887-11 2019 Together, the present work demonstrates the beneficial effects of venlafaxine and carvedilol in RA testicular dysfunction and impaired spermatogenesis via modulation of AMPK/ERK and PI3K/AKT/mTOR signaling and intervention with the testicular oxidative stress, inflammation and apoptosis. Carvedilol 82-92 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 169-173 30700698-5 2019 Here we pioneeringly elaborated that specific knockdown of cyclinB1 triggered autophagy via AMPK-ULK1-dependent signal pathway through the elevation of ROS, rather than ATP in the cell lines of CNE-1 and CNE-2. ros 152-155 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 92-96 30700698-6 2019 Moreover, ROS scavengers demonstrated that the observed effect of cyclinB1 silencing on AMPK phosphorylation was ROS dependent. ros 10-13 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 88-92 30700698-6 2019 Moreover, ROS scavengers demonstrated that the observed effect of cyclinB1 silencing on AMPK phosphorylation was ROS dependent. ros 113-116 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 88-92 30700011-0 2019 Hypolipogenic Effect of Shikimic Acid Via Inhibition of MID1IP1 and Phosphorylation of AMPK/ACC. Shikimic Acid 24-37 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 87-91 30700011-5 2019 It should be noted that shikimic acid activated phosphorylation of AMP-activated protein kinase (AMPK)/Aacetyl-coenzyme A carboxylase (ACC) and reduced the expression of MID1 Interacting Protein 1 (MID1IP1) in HepG2, Huh7 and 3T3-L1 cells. Shikimic Acid 24-37 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 67-95 30700011-5 2019 It should be noted that shikimic acid activated phosphorylation of AMP-activated protein kinase (AMPK)/Aacetyl-coenzyme A carboxylase (ACC) and reduced the expression of MID1 Interacting Protein 1 (MID1IP1) in HepG2, Huh7 and 3T3-L1 cells. Shikimic Acid 24-37 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 97-101 30700011-8 2019 Taken together, our findings suggest that shikimic acid has hypolipogenic effect in HepG2 and 3T3-L1 cells via phosphorylation of AMPK/ACC and inhibition of MID1IP1 as a potent candidate for prevention or treatment of fatty liver and hyperlipidemia. Shikimic Acid 42-55 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 130-134 30591219-5 2019 Mechanistically, tigecycline specifically inhibits translation by mitochondrial ribosome but not nuclear or cytosolic ribosome, leading to mitochondrial dysfunction, oxidative stress and damage, AMPK activation and inhibition of mTOR signaling in ovarian cancer cells. Tigecycline 17-28 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 195-199 30277819-6 2019 We investigated the regulatory connection between NRF2 and AMPK during oxidative stress induced by tert-butyl hydroperoxide (TBHP) in HEK293T cells and C. elegans. tert-Butylhydroperoxide 99-123 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 59-63 30277819-6 2019 We investigated the regulatory connection between NRF2 and AMPK during oxidative stress induced by tert-butyl hydroperoxide (TBHP) in HEK293T cells and C. elegans. tert-Butylhydroperoxide 125-129 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 59-63 30277819-8 2019 After addition of TBHP, NRF2 and AMPK showed a quick activation; AMPK was later down-regulated, however, while NRF2 level remained high. tert-Butylhydroperoxide 18-22 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 33-37 30277819-8 2019 After addition of TBHP, NRF2 and AMPK showed a quick activation; AMPK was later down-regulated, however, while NRF2 level remained high. tert-Butylhydroperoxide 18-22 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 65-69 30335546-0 2019 STIM2 interacts with AMPK and regulates calcium-induced AMPK activation. Calcium 40-47 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 21-25 30335546-0 2019 STIM2 interacts with AMPK and regulates calcium-induced AMPK activation. Calcium 40-47 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 56-60 30335546-2 2019 LKB1 primarily phosphorylates AMPK after energy stress, whereas calcium-mediated activation of AMPK requires CaMKK2, although the regulatory mechanisms of calcium-mediated AMPK activation remain unclear. Calcium 64-71 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 95-99 30335546-2 2019 LKB1 primarily phosphorylates AMPK after energy stress, whereas calcium-mediated activation of AMPK requires CaMKK2, although the regulatory mechanisms of calcium-mediated AMPK activation remain unclear. Calcium 64-71 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 95-99 30335546-3 2019 Using biochemical, microscopic, and genetic approaches, we demonstrate that the stromal interaction molecule (STIM)2, a calcium sensor, acts as a novel regulator of CaMKK2-AMPK signaling. Calcium 120-127 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 172-176 30335546-4 2019 We reveal that STIM2 interacts with AMPK and CaMKK2 and that the increase in intracellular calcium levels promotes AMPK colocalization and interaction with STIM2. Calcium 91-98 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 115-119 30335546-5 2019 We further show that STIM2 deficiency attenuates calcium-induced but not energy stress-induced AMPK activation, possibly by regulating the CaMKK2-AMPK interaction. Calcium 49-56 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 146-150 30335546-6 2019 Together, our results identify a previously unappreciated mechanism that modulates calcium-mediated AMPK activation.-Chauhan, A. S., Liu, X., Jing, J., Lee, H., Yadav, R. K., Liu, J., Zhou, Y., Gan B. Calcium 83-90 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 100-104 30335546-7 2019 STIM2 interacts with AMPK and regulates calcium-induced AMPK activation. Calcium 40-47 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 21-25 30335546-7 2019 STIM2 interacts with AMPK and regulates calcium-induced AMPK activation. Calcium 40-47 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 56-60 30557609-5 2019 Mechanistically, DHA induced autophagy by regulating the activity of AMPK/mTOR/p70S6k signaling pathway, which accelerated the degradation of ferritin, increased the labile iron pool, promoted the accumulation of cellular ROS and eventually led to ferroptotic cell death. artenimol 17-20 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 69-73 30557609-5 2019 Mechanistically, DHA induced autophagy by regulating the activity of AMPK/mTOR/p70S6k signaling pathway, which accelerated the degradation of ferritin, increased the labile iron pool, promoted the accumulation of cellular ROS and eventually led to ferroptotic cell death. Iron 173-177 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 69-73 30557609-5 2019 Mechanistically, DHA induced autophagy by regulating the activity of AMPK/mTOR/p70S6k signaling pathway, which accelerated the degradation of ferritin, increased the labile iron pool, promoted the accumulation of cellular ROS and eventually led to ferroptotic cell death. ros 222-225 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 69-73 30610735-4 2019 In this regard, evidence suggests that cannabinoids may alter cell metabolism by increasing AMPK activity. Cannabinoids 39-51 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 92-96 30610735-5 2019 In turn, emerging evidence suggests that the activation of AMPK by cannabinoids may mediate an anti-inflammatory effect through a range of processes. Cannabinoids 67-79 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 59-63 30723485-5 2019 SnRK1/AMPK and TOR kinases are both important regulators of cellular metabolism and are controlled to a large extent by the availability of sugars and sugar-phosphates in plants whereas in animals AMP/ATP indirectly translate sugar status. Sugars 140-146 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 6-10 30723485-5 2019 SnRK1/AMPK and TOR kinases are both important regulators of cellular metabolism and are controlled to a large extent by the availability of sugars and sugar-phosphates in plants whereas in animals AMP/ATP indirectly translate sugar status. Sugar Phosphates 151-167 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 6-10 30723485-5 2019 SnRK1/AMPK and TOR kinases are both important regulators of cellular metabolism and are controlled to a large extent by the availability of sugars and sugar-phosphates in plants whereas in animals AMP/ATP indirectly translate sugar status. Adenosine Triphosphate 201-204 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 6-10 30723485-5 2019 SnRK1/AMPK and TOR kinases are both important regulators of cellular metabolism and are controlled to a large extent by the availability of sugars and sugar-phosphates in plants whereas in animals AMP/ATP indirectly translate sugar status. Sugars 140-145 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 6-10 30654529-0 2019 AZD1208, a Pan-Pim Kinase Inhibitor, Has Anti-Growth Effect on 93T449 Human Liposarcoma Cells via Control of the Expression and Phosphorylation of Pim-3, mTOR, 4EBP-1, S6, STAT-3 and AMPK. AZD1208 0-7 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 183-187 30654529-8 2019 In addition, AZD1208 induced a LKB-1-independent AMPK activation, which was crucial for its cytostatic effect, as knock-down of AMPK greatly blocked AZD1208s ability to reduce cell survival. AZD1208 13-20 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 49-53 30654529-8 2019 In addition, AZD1208 induced a LKB-1-independent AMPK activation, which was crucial for its cytostatic effect, as knock-down of AMPK greatly blocked AZD1208s ability to reduce cell survival. AZD1208 13-20 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 128-132 30654529-8 2019 In addition, AZD1208 induced a LKB-1-independent AMPK activation, which was crucial for its cytostatic effect, as knock-down of AMPK greatly blocked AZD1208s ability to reduce cell survival. AZD1208 149-157 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 128-132 30654529-10 2019 Importantly, a central role for Pim-3 in the actions of AZD1208 was confirmed by knock-down, which not only reduced 93T449 cell survival but also led to the inhibition of 4EBP-1, mTOR, eIF-2alpha and STAT-3, along with the activation of AMPK. AZD1208 56-63 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 237-241 30654529-11 2019 In summary, this is the first report demonstrating that AZD1208 inhibits growth of liposarcoma cells and that this activity is mediated through Pim-3 kinase, STAT-3, mTOR, S6 and AMPK expression and phosphorylation pathways. AZD1208 56-63 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 179-183 30468835-8 2019 We also observed a decreased expression of insulin-stimulated phosphorylation of AKT and AMPK after exposure to ENL with PA. Palmitic Acid 121-123 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 89-93 30728400-11 2019 The ability of cells to utilise ammonia as a nitrogen source is intricately linked to AMPK, mTORC1 and GDH. Nitrogen 45-53 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 86-90 31488033-0 2019 Baicalein Induces Autophagy and Apoptosis through AMPK Pathway in Human Glioma Cells. baicalein 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 50-54 30606143-0 2019 Dietary intake of genistein suppresses hepatocellular carcinoma through AMPK-mediated apoptosis and anti-inflammation. Genistein 18-27 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 72-76 30606143-6 2019 Genistein induced phospho-AMPK in total liver extracts, Hep3B cells, and Raw 264.7 cells, and phospho-AMPK promoted apoptosis in liver and Hep3B cells. Genistein 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 26-30 30606143-9 2019 CONCLUSIONS: Genistein-mediated AMPK activation increases hepatocyte apoptosis through energy-dependent caspase pathways, suppresses the inflammatory response in resident liver macrophages by increased cellular respiration, and consequently inhibits the initiation and progression of HCC. Genistein 13-22 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 32-36 31776981-1 2019 AMPK is an evolutionarily conserved serine/threonine-protein kinase that acts as an energy sensor in cells and plays a key role in the upregulation of catabolism and inactivation of anabolism. Serine 36-42 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 31776981-2 2019 Under various physiological and pathological conditions, AMPK can be phosphorylated by an upstream kinase and bind to AMP or ADP rather than ATP, leading to its activation. Adenosine Diphosphate 125-128 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 57-61 31776981-2 2019 Under various physiological and pathological conditions, AMPK can be phosphorylated by an upstream kinase and bind to AMP or ADP rather than ATP, leading to its activation. Adenosine Triphosphate 141-144 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 57-61 31094212-0 2019 beta -Lapachone Regulates Obesity through Modulating Thermogenesis in Brown Adipose Tissue and Adipocytes: Role of AMPK Signaling Pathway. beta-lapachone 0-15 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 115-119 30325018-3 2019 Studies in mice suggest that the AMPK-TBC1D4 signalling axis is important for the increased insulin-stimulated glucose uptake after a single bout of exercise. Glucose 111-118 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 33-37 30571927-9 2019 One was from ROS-dependent activation of ATM via AMPK-ULK1-ATG13-Beclin1/ATG5. ros 13-16 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 49-53 30745824-0 2019 Metformin Promotes the Survival of Random-Pattern Skin Flaps by Inducing Autophagy via the AMPK-mTOR-TFEB signaling pathway. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 91-95 30745824-6 2019 Moreover, metformin also activated the AMPK-mTOR-TFEB signaling pathway in ischemic areas. Metformin 10-19 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 39-43 30745824-7 2019 Inhibitions of AMPK via Compound C (CC) or AMPK shRNA adeno-associated virus (AAV) vector resulted in the downregulation of the AMPK-mTOR-TFEB signaling pathway and autophagy level in metformin-treated flaps. Metformin 184-193 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 15-19 30745824-7 2019 Inhibitions of AMPK via Compound C (CC) or AMPK shRNA adeno-associated virus (AAV) vector resulted in the downregulation of the AMPK-mTOR-TFEB signaling pathway and autophagy level in metformin-treated flaps. Metformin 184-193 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 43-47 30745824-7 2019 Inhibitions of AMPK via Compound C (CC) or AMPK shRNA adeno-associated virus (AAV) vector resulted in the downregulation of the AMPK-mTOR-TFEB signaling pathway and autophagy level in metformin-treated flaps. Metformin 184-193 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 43-47 30648357-0 2019 Omega-3 multiple effects increasing glucocorticoid-induced muscle atrophy: autophagic, AMPK and UPS mechanisms. omega-3 0-7 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 87-91 30648357-7 2019 Conclusion: N-3 supplementation increases muscle atrophy caused by DEXA in an autophagic, AMPK and UPS process. Nitrogen 12-13 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 90-94 30538220-5 2018 Glucose starvation induced progressive autophagy activation in PDA cells via the activation of ROS/AMPK signaling. Glucose 0-7 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 99-103 30538220-5 2018 Glucose starvation induced progressive autophagy activation in PDA cells via the activation of ROS/AMPK signaling. ros 95-98 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 99-103 30372835-13 2018 Compared to the control, Metformin blunted the expression of VEGF subtypes and directed cells to energy status by induction of PRKAA1, PRKAB2, and PRKAG1 genes (p < 0.05). Metformin 25-34 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 127-133 29921885-0 2018 Aescin-induced reactive oxygen species play a pro-survival role in human cancer cells via ATM/AMPK/ULK1-mediated autophagy. Reactive Oxygen Species 15-38 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 94-98 30340831-0 2018 PP2A inhibition by LB-100 protects retinal pigment epithelium cells from UV radiation via activation of AMPK signaling. lb100 19-25 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 104-108 30340831-1 2018 AMP-activated protein kinase (AMPK) signaling activation can inhibit Ultra-violet (UV) radiation (UVR)-induced retinal pigment epithelium (RPE) cell injuries. ultra-violet 69-81 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-34 30340831-2 2018 LB-100 is a novel inhibitor of protein phosphatase 2A (PP2A), the AMPKalpha1 phosphatase. lb100 0-6 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 66-76 30340831-4 2018 LB-100 activated AMPK, nicotinamide adenine dinucleotide phosphate (NADPH) and Nrf2 (NF-E2-related factor 2) signalings, inhibiting UVR-induced oxidative injuries and DNA damage in RPE cells. lb100 0-6 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 17-21 30340831-5 2018 Conversely, AMPK inhibition, by AMPKalpha1-shRNA, -CRISPR/Cas9 knockout or -T172A mutation, almost blocked LB-100-induced RPE cytoprotection against UVR. lb100 107-113 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 12-16 30340831-5 2018 Conversely, AMPK inhibition, by AMPKalpha1-shRNA, -CRISPR/Cas9 knockout or -T172A mutation, almost blocked LB-100-induced RPE cytoprotection against UVR. lb100 107-113 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 32-42 30340831-7 2018 Collectively, these results show that PP2A inhibition by LB-100 protects RPE cells from UVR via activation of AMPK signaling. lb100 57-63 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 110-114 30232152-0 2018 Mitochondria-derived ROS activate AMP-activated protein kinase (AMPK) indirectly. Reactive Oxygen Species 21-24 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 34-62 30232152-0 2018 Mitochondria-derived ROS activate AMP-activated protein kinase (AMPK) indirectly. Reactive Oxygen Species 21-24 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 64-68 30232152-2 2018 Other mitochondrial signals, such as ATP, are sensed by enzymes, including the key metabolic sensor and regulator, AMP-activated protein kinase (AMPK). Adenosine Triphosphate 37-40 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 115-143 30232152-2 2018 Other mitochondrial signals, such as ATP, are sensed by enzymes, including the key metabolic sensor and regulator, AMP-activated protein kinase (AMPK). Adenosine Triphosphate 37-40 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 145-149 30232152-3 2018 AMPK responds to the cellular ATP/AMP and ATP/ADP ratios by matching mitochondrial ATP production to demand. Adenosine Triphosphate 30-33 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 30232152-3 2018 AMPK responds to the cellular ATP/AMP and ATP/ADP ratios by matching mitochondrial ATP production to demand. Adenosine Triphosphate 42-45 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 30232152-3 2018 AMPK responds to the cellular ATP/AMP and ATP/ADP ratios by matching mitochondrial ATP production to demand. Adenosine Diphosphate 46-49 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 30232152-3 2018 AMPK responds to the cellular ATP/AMP and ATP/ADP ratios by matching mitochondrial ATP production to demand. Adenosine Triphosphate 42-45 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 30232152-4 2018 Previous reports proposed that AMPK activity also responds to ROS, by ROS acting on redox-sensitive cysteine residues (Cys-299/Cys-304) on the AMPK alpha subunit. Reactive Oxygen Species 62-65 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 31-35 30232152-4 2018 Previous reports proposed that AMPK activity also responds to ROS, by ROS acting on redox-sensitive cysteine residues (Cys-299/Cys-304) on the AMPK alpha subunit. Reactive Oxygen Species 62-65 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 143-147 30232152-4 2018 Previous reports proposed that AMPK activity also responds to ROS, by ROS acting on redox-sensitive cysteine residues (Cys-299/Cys-304) on the AMPK alpha subunit. Reactive Oxygen Species 70-73 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 31-35 30232152-4 2018 Previous reports proposed that AMPK activity also responds to ROS, by ROS acting on redox-sensitive cysteine residues (Cys-299/Cys-304) on the AMPK alpha subunit. Reactive Oxygen Species 70-73 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 143-147 30232152-4 2018 Previous reports proposed that AMPK activity also responds to ROS, by ROS acting on redox-sensitive cysteine residues (Cys-299/Cys-304) on the AMPK alpha subunit. Cysteine 100-108 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 31-35 30232152-4 2018 Previous reports proposed that AMPK activity also responds to ROS, by ROS acting on redox-sensitive cysteine residues (Cys-299/Cys-304) on the AMPK alpha subunit. Cysteine 100-108 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 143-147 30232152-4 2018 Previous reports proposed that AMPK activity also responds to ROS, by ROS acting on redox-sensitive cysteine residues (Cys-299/Cys-304) on the AMPK alpha subunit. Cysteine 119-122 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 31-35 30232152-4 2018 Previous reports proposed that AMPK activity also responds to ROS, by ROS acting on redox-sensitive cysteine residues (Cys-299/Cys-304) on the AMPK alpha subunit. Cysteine 119-122 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 143-147 30232152-4 2018 Previous reports proposed that AMPK activity also responds to ROS, by ROS acting on redox-sensitive cysteine residues (Cys-299/Cys-304) on the AMPK alpha subunit. Cysteine 127-130 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 31-35 30232152-4 2018 Previous reports proposed that AMPK activity also responds to ROS, by ROS acting on redox-sensitive cysteine residues (Cys-299/Cys-304) on the AMPK alpha subunit. Cysteine 127-130 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 143-147 30232152-5 2018 This suggests an appealing model in which mitochondria fine-tune AMPK activity by both adenine nucleotide-dependent mechanisms and by redox signals. Adenine Nucleotides 87-105 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 65-69 30232152-6 2018 Here we assessed whether physiological levels of ROS directly alter AMPK activity. Reactive Oxygen Species 49-52 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 68-72 30232152-9 2018 Replacing the putative redox-active cysteine residues on AMPK alpha1 with alanines did not alter the response of AMPK to H2O2 In parallel with measurements of AMPK activity, we measured the cell ATP/ADP ratio. Cysteine 36-44 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 57-68 30232152-9 2018 Replacing the putative redox-active cysteine residues on AMPK alpha1 with alanines did not alter the response of AMPK to H2O2 In parallel with measurements of AMPK activity, we measured the cell ATP/ADP ratio. Cysteine 36-44 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 57-61 30232152-10 2018 This allowed us to separate the effects on AMPK activity due to ROS production from those caused by changes in this ratio. Reactive Oxygen Species 64-67 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 43-47 30232152-11 2018 We conclude that AMPK activity in response to redox changes is not due to direct action on AMPK itself, but is a secondary consequence of redox effects on other processes, such as mitochondrial ATP production. Adenosine Triphosphate 194-197 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 17-21 30324559-0 2018 Melatonin Modulates lipid Metabolism in HepG2 Cells Cultured in High Concentrations of Oleic Acid: AMPK Pathway Activation may Play an Important Role. Melatonin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 99-103 30324559-0 2018 Melatonin Modulates lipid Metabolism in HepG2 Cells Cultured in High Concentrations of Oleic Acid: AMPK Pathway Activation may Play an Important Role. Oleic Acid 87-97 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 99-103 30324559-4 2018 Melatonin pretreatment induced phosphorylation of AMP-activated protein kinase (AMPK) and acetyl-CoA carboxylase (ACC), causing their activation and inactivation, respectively. Melatonin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 50-78 30324559-4 2018 Melatonin pretreatment induced phosphorylation of AMP-activated protein kinase (AMPK) and acetyl-CoA carboxylase (ACC), causing their activation and inactivation, respectively. Melatonin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 80-84 30324559-8 2018 The phosphorylation and activation of AMPK may have important roles in inactivating lipid anabolic pathways and activating triglyceride catabolic pathways. Triglycerides 123-135 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 38-42 30316840-0 2018 1,3-Dichloro-2-Propanol inhibits autophagy via P53/AMPK/mTOR pathway in HepG2 cells. 1,3-dichloro-2-propanol 0-23 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 51-55 30316840-7 2018 Use of a specific mTOR inhibitor (rapamycin), a reversible AMPK activator(A-769662) and a selective P53 activator (Nutlin-3a) abolished the ability of 1,3-DCP to inhibit the induction of autophagy. 4-hydroxy-3-(4-(2-hydroxyphenyl)phenyl)-6-oxo-7H-thieno(2,3-b)pyridine-5-carbonitrile 74-82 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 59-63 29745797-6 2018 The energy-sensing pathways, mammalian target of rapamycin, AMPK, and sirtuin-1 have all been implicated in the beneficial effects of CR on longevity and/or physiological function and, as such, have emerged as potential targets for therapeutic intervention as CR mimetics. Chromium 134-136 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 60-64 29745797-6 2018 The energy-sensing pathways, mammalian target of rapamycin, AMPK, and sirtuin-1 have all been implicated in the beneficial effects of CR on longevity and/or physiological function and, as such, have emerged as potential targets for therapeutic intervention as CR mimetics. Chromium 260-262 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 60-64 30247801-6 2018 Mechanisms modulating autophagy found that tigecycline enhanced the phosphorylation of AMPK, but did not decrease the phosphorylation of Akt, to inhibit the phosphorylation of mTOR and its two downstream effectors p70S6K1 and 4E-BP1. Tigecycline 43-54 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 87-91 30348897-5 2018 We found that the treatment of AMPK-specific inhibitor compound C (dorsomorphin dihydrochloride) decreased OATP1A2-mediated uptake of estrone-3-sulfate in a concentration- and time-dependent manner. Dorsomorphin dihydrochloride 67-95 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 31-35 30348897-5 2018 We found that the treatment of AMPK-specific inhibitor compound C (dorsomorphin dihydrochloride) decreased OATP1A2-mediated uptake of estrone-3-sulfate in a concentration- and time-dependent manner. estrone sulfate 134-151 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 31-35 30054562-6 2018 LKB1-AMPK activation in GC cell lines was tumor suppressive, as metformin (an AMPK activator) inhibited GC cell growth in the CAB39L-silenced cells. Metformin 64-73 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 78-82 30251691-6 2018 ALA treatment could increase H2S level, which reduced the autophagy-related index and activation of the 5"-monophosphate-activated protein kinase (AMPK)/mammalian target of rapamycin (mTOR) pathway, thereby protecting vascular function in rats with T2DM. Thioctic Acid 0-3 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 147-151 29688769-1 2018 Adenosine monophosphate-activated protein kinase (AMPK) controls glucose and lipid metabolism and modulates inflammatory responses to maintain metabolic and inflammatory homeostasis during low cellular energy levels. Glucose 65-72 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-48 29688769-1 2018 Adenosine monophosphate-activated protein kinase (AMPK) controls glucose and lipid metabolism and modulates inflammatory responses to maintain metabolic and inflammatory homeostasis during low cellular energy levels. Glucose 65-72 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 50-54 29688769-2 2018 The AMPK activator 5-aminoimidazole-4-carboxamide-1-beta-4-ribofuranoside (AICAR) interferes with inflammatory pathways in skeletal muscle, but the mechanisms are undefined. 5-aminoimidazole-4-carboxamide-1-beta-4-ribofuranoside 19-73 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 4-8 29688769-2 2018 The AMPK activator 5-aminoimidazole-4-carboxamide-1-beta-4-ribofuranoside (AICAR) interferes with inflammatory pathways in skeletal muscle, but the mechanisms are undefined. acadesine 75-80 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 4-8 30251691-6 2018 ALA treatment could increase H2S level, which reduced the autophagy-related index and activation of the 5"-monophosphate-activated protein kinase (AMPK)/mammalian target of rapamycin (mTOR) pathway, thereby protecting vascular function in rats with T2DM. Hydrogen Sulfide 29-32 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 147-151 30251691-8 2018 In cultured VSMCs, high glucose level also reduced H2S level, upregulated the autophagy-related index and activated the AMPK/mTOR pathway, which were reversed by concomitant application of sodium hydrosulfide (NaHS, an H2S donor) or ALA. Glucose 24-31 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 120-124 30251691-8 2018 In cultured VSMCs, high glucose level also reduced H2S level, upregulated the autophagy-related index and activated the AMPK/mTOR pathway, which were reversed by concomitant application of sodium hydrosulfide (NaHS, an H2S donor) or ALA. sodium bisulfide 189-208 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 120-124 30251691-8 2018 In cultured VSMCs, high glucose level also reduced H2S level, upregulated the autophagy-related index and activated the AMPK/mTOR pathway, which were reversed by concomitant application of sodium hydrosulfide (NaHS, an H2S donor) or ALA. sodium bisulfide 210-214 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 120-124 30251691-9 2018 The protective effect of NaHS or ALA was attenuated by rapamycin (an autophagy activator), 5-amino-1-beta-d-ribofuranosyl-imidazole-4-carboxamide (an AMPK activator) or PPG. sodium bisulfide 25-29 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 150-154 30251691-9 2018 The protective effect of NaHS or ALA was attenuated by rapamycin (an autophagy activator), 5-amino-1-beta-d-ribofuranosyl-imidazole-4-carboxamide (an AMPK activator) or PPG. Thioctic Acid 33-36 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 150-154 30251691-9 2018 The protective effect of NaHS or ALA was attenuated by rapamycin (an autophagy activator), 5-amino-1-beta-d-ribofuranosyl-imidazole-4-carboxamide (an AMPK activator) or PPG. acadesine 91-145 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 150-154 30251691-9 2018 The protective effect of NaHS or ALA was attenuated by rapamycin (an autophagy activator), 5-amino-1-beta-d-ribofuranosyl-imidazole-4-carboxamide (an AMPK activator) or PPG. propargylglycine 169-172 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 150-154 30251691-10 2018 In contrast, Compound C (an AMPK inhibitor) enhanced the effect of ALA or NaHS. Thioctic Acid 67-70 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 28-32 30251691-10 2018 In contrast, Compound C (an AMPK inhibitor) enhanced the effect of ALA or NaHS. sodium bisulfide 74-78 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 28-32 30251691-11 2018 ALA may have a protective effect on VSMCs in T2DM by elevating H2S level and downregulating autophagy via the AMPK/mTOR pathway. Thioctic Acid 0-3 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 110-114 30142540-11 2018 RESULTS: High glucose induced the increase of ROS level, activation of TXNIP, but restricted mitochondrial membrane potential and activities of p-AMPK, SOD and CAT, and Trx. Glucose 14-21 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 146-150 30201684-2 2018 AMPK activation increases glucose uptake, lipid oxidation, and mitochondrial biogenesis, leading to enhanced muscle insulin sensitivity and whole-body energy metabolism. Glucose 26-33 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 30266318-0 2018 Camptothecin enhances c-Myc-mediated endoplasmic reticulum stress and leads to autophagy by activating Ca2+-mediated AMPK. Camptothecin 0-12 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 117-121 30266318-6 2018 Ca2+ chelators, ethylene glycol tetraacetic acid and a CaMKII inhibitor, K252a, decreased CPT-induced Beclin-1 and Atg7, and downregulated AMPK phosphorylation, which suggested that CPT-induced Ca2+ release leads to the activation of autophagy through CaMKII-mediated AMPK phosphorylation. Egtazic Acid 16-48 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 139-143 30226553-0 2018 Pterostilbene inhibits nutrient metabolism and induces apoptosis through AMPK activation in multiple myeloma cells. pterostilbene 0-13 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 73-77 30226553-4 2018 It was observed that the administration of PTE induced apoptosis, which was mediated by the increased activation of AMP-activated protein kinase (AMPK). pterostilbene 43-46 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 116-144 30226553-4 2018 It was observed that the administration of PTE induced apoptosis, which was mediated by the increased activation of AMP-activated protein kinase (AMPK). pterostilbene 43-46 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 146-150 30226553-10 2018 Taken together, these data demonstrated that PTE exerts anti-tumor effects on MM cells via AMPK-induced nutrient suppression. pterostilbene 45-48 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 91-95 30301973-1 2018 In the 5th paragraph of the originally published version of this Highlight article, it was incorrectly stated that AMPK is activated by "a high ATP to AMP ratio"; this has now been corrected to a "high AMP to ATP ratio" in the HTML and PDF versions. Adenosine Triphosphate 144-147 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 115-119 30301973-1 2018 In the 5th paragraph of the originally published version of this Highlight article, it was incorrectly stated that AMPK is activated by "a high ATP to AMP ratio"; this has now been corrected to a "high AMP to ATP ratio" in the HTML and PDF versions. Adenosine Monophosphate 151-154 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 115-119 30301973-1 2018 In the 5th paragraph of the originally published version of this Highlight article, it was incorrectly stated that AMPK is activated by "a high ATP to AMP ratio"; this has now been corrected to a "high AMP to ATP ratio" in the HTML and PDF versions. Adenosine Triphosphate 209-212 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 115-119 30125826-0 2018 AMP-activated protein kinase negatively regulates heat treatment-induced lactate secretion in cultured boar sertoli cells. Lactic Acid 73-80 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-28 30125826-5 2018 From 0 to 48 h post-heat stress, lactate secretion was enhanced and reached the maximum level (175% of the control) at 12 h. However, with increased recovery time, the phosphorylation level of AMPK decreased gradually, and reached the minimum level (58% of the control) at 12 h. Compared with heat treatment alone, pretreatment with the AMPK agonist AICAR (2 mmol/L, 2 h) reduced lactate secretion by 42.6%. Lactic Acid 33-40 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 193-197 30125826-5 2018 From 0 to 48 h post-heat stress, lactate secretion was enhanced and reached the maximum level (175% of the control) at 12 h. However, with increased recovery time, the phosphorylation level of AMPK decreased gradually, and reached the minimum level (58% of the control) at 12 h. Compared with heat treatment alone, pretreatment with the AMPK agonist AICAR (2 mmol/L, 2 h) reduced lactate secretion by 42.6%. Lactic Acid 33-40 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 337-341 30125826-5 2018 From 0 to 48 h post-heat stress, lactate secretion was enhanced and reached the maximum level (175% of the control) at 12 h. However, with increased recovery time, the phosphorylation level of AMPK decreased gradually, and reached the minimum level (58% of the control) at 12 h. Compared with heat treatment alone, pretreatment with the AMPK agonist AICAR (2 mmol/L, 2 h) reduced lactate secretion by 42.6%. AICA ribonucleotide 350-355 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 193-197 30125826-5 2018 From 0 to 48 h post-heat stress, lactate secretion was enhanced and reached the maximum level (175% of the control) at 12 h. However, with increased recovery time, the phosphorylation level of AMPK decreased gradually, and reached the minimum level (58% of the control) at 12 h. Compared with heat treatment alone, pretreatment with the AMPK agonist AICAR (2 mmol/L, 2 h) reduced lactate secretion by 42.6%. Lactic Acid 380-387 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 193-197 30125826-7 2018 In addition, AMPK overexpression reduced lactate secretion by 22.5%, significantly decreased the LDH activity, and mRNA and protein expression levels of GLUT3, LDHA, and MCT1. Lactic Acid 41-48 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 13-17 30125826-8 2018 These results showed that AMPK reduces heat-induced lactate secretion by decreasing the expression levels of GLUT3, LDHA and MCT1. Lactic Acid 52-59 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 26-30 30125826-9 2018 The results also suggested that AMPK is a negative regulator of heat treatment-induced lactate secretion in cultured boar Sertoli cells. Lactic Acid 87-94 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 32-36 30378150-0 2018 Perilaldehyde activates AMP-activated protein kinase to suppress the growth of gastric cancer via induction of autophagy. perilaldehyde 0-13 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 24-52 30378150-4 2018 METHODS AND RESULTS: In cultured mouse gastric cancer cell line MFCs and human gastric cancer cell lines GC9811-P, PAH activated AMPK by increasing the Thr172 phosphorylation and activity in a time-/concentration-dependent manner. perillaldehyde 115-118 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 129-133 30378150-5 2018 Furthermore, incubation of MFCs with PAH also increased autophagy as determined by monodansylcadaverine (MDC) staining, which was reversed by AMPK inhibitor compound C. PAH further decreased MFCs cell survival, which was abolished by compound C or autophagy inhibitor 3-Methyladenine (3-MA). perillaldehyde 37-40 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 142-146 30378150-5 2018 Furthermore, incubation of MFCs with PAH also increased autophagy as determined by monodansylcadaverine (MDC) staining, which was reversed by AMPK inhibitor compound C. PAH further decreased MFCs cell survival, which was abolished by compound C or autophagy inhibitor 3-Methyladenine (3-MA). monodansylcadaverine 83-103 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 142-146 30378150-5 2018 Furthermore, incubation of MFCs with PAH also increased autophagy as determined by monodansylcadaverine (MDC) staining, which was reversed by AMPK inhibitor compound C. PAH further decreased MFCs cell survival, which was abolished by compound C or autophagy inhibitor 3-Methyladenine (3-MA). monodansylcadaverine 105-108 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 142-146 30378150-5 2018 Furthermore, incubation of MFCs with PAH also increased autophagy as determined by monodansylcadaverine (MDC) staining, which was reversed by AMPK inhibitor compound C. PAH further decreased MFCs cell survival, which was abolished by compound C or autophagy inhibitor 3-Methyladenine (3-MA). perillaldehyde 169-172 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 142-146 30378150-5 2018 Furthermore, incubation of MFCs with PAH also increased autophagy as determined by monodansylcadaverine (MDC) staining, which was reversed by AMPK inhibitor compound C. PAH further decreased MFCs cell survival, which was abolished by compound C or autophagy inhibitor 3-Methyladenine (3-MA). 3-methyladenine 268-283 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 142-146 30378150-5 2018 Furthermore, incubation of MFCs with PAH also increased autophagy as determined by monodansylcadaverine (MDC) staining, which was reversed by AMPK inhibitor compound C. PAH further decreased MFCs cell survival, which was abolished by compound C or autophagy inhibitor 3-Methyladenine (3-MA). 3-methyladenine 285-289 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 142-146 30378150-8 2018 CONCLUSIONS: PAH increases AMPK phosphorylation and activity to induce gastric cancer cell autophagy to inhibit the growth of gastric cancer. perillaldehyde 13-16 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 27-31 29902460-0 2018 The anti-malarial atovaquone selectively increases chemosensitivity in retinoblastoma via mitochondrial dysfunction-dependent oxidative damage and Akt/AMPK/mTOR inhibition. Atovaquone 18-28 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 151-155 29902460-8 2018 We further demonstrate that atovaquone targets Akt/AMPK/mTOR signaling via inducing mitochondrial dysfunction. Atovaquone 28-38 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 51-55 30222967-6 2018 This role of LKB1 in response to ROS-inducing agents was largely AMPK-dependent. Reactive Oxygen Species 33-36 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 65-69 29572822-0 2018 Methotrexate restores the function of peripheral blood regulatory T cells in psoriasis vulgaris via the CD73/AMPK/mTOR pathway. Methotrexate 0-12 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 109-113 29572822-11 2018 CONCLUSIONS: We speculate that MTX can restore the immunosuppressive function of Tregs through upregulating CD73, activating AMPK and inactivating the mTOR pathway. Methotrexate 31-34 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 125-129 30318520-0 2018 Mutant p53 blocks SESN1/AMPK/PGC-1alpha/UCP2 axis increasing mitochondrial O2- production in cancer cells. Oxygen 75-77 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 24-28 30374107-0 2018 The protective effects of maltol on cisplatin-induced nephrotoxicity through the AMPK-mediated PI3K/Akt and p53 signaling pathways. maltol 26-32 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 81-85 30374107-0 2018 The protective effects of maltol on cisplatin-induced nephrotoxicity through the AMPK-mediated PI3K/Akt and p53 signaling pathways. Cisplatin 36-45 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 81-85 30374107-7 2018 Additionally, maltol restored the reduction of PI3K/Akt and mTOR levels by cisplatin through increasing AMPK expression in cisplatin-treated HEK293 cells. maltol 14-20 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 104-108 30374107-7 2018 Additionally, maltol restored the reduction of PI3K/Akt and mTOR levels by cisplatin through increasing AMPK expression in cisplatin-treated HEK293 cells. Cisplatin 123-132 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 104-108 30374107-9 2018 Overall, maltol may serve as a valuable potential drug to prevent cisplatin-induced nephrotoxicity, and the underlying molecular mechanisms of maltol action may involve intracellular AMPK/PI3K/Akt and p53 signaling pathways. Cisplatin 66-75 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 183-187 30374107-9 2018 Overall, maltol may serve as a valuable potential drug to prevent cisplatin-induced nephrotoxicity, and the underlying molecular mechanisms of maltol action may involve intracellular AMPK/PI3K/Akt and p53 signaling pathways. maltol 143-149 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 183-187 30405404-0 2018 Berberine Attenuated Proliferation, Invasion and Migration by Targeting the AMPK/HNF4alpha/WNT5A Pathway in Gastric Carcinoma. Berberine 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 76-80 30337562-3 2018 Increases in ZMP, accompanied by activation of AMPK and cell growth inhibition, were observed with treatment of LY3213128. AICA ribonucleotide 13-16 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 47-51 30337562-3 2018 Increases in ZMP, accompanied by activation of AMPK and cell growth inhibition, were observed with treatment of LY3213128. ly3213128 112-121 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 47-51 30259865-5 2018 Metformin is shown to negatively regulate PI3K through AMPK induced IRS1 phosphorylation and this brings about a reversal of AKT bistablity in codimension-1 bifurcation diagram from S-shaped, related to cell proliferation in the absence of drug metformin, to Z-shaped, related to apoptosis in the presence of drug metformin. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 55-59 30259865-5 2018 Metformin is shown to negatively regulate PI3K through AMPK induced IRS1 phosphorylation and this brings about a reversal of AKT bistablity in codimension-1 bifurcation diagram from S-shaped, related to cell proliferation in the absence of drug metformin, to Z-shaped, related to apoptosis in the presence of drug metformin. Metformin 245-254 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 55-59 30259865-5 2018 Metformin is shown to negatively regulate PI3K through AMPK induced IRS1 phosphorylation and this brings about a reversal of AKT bistablity in codimension-1 bifurcation diagram from S-shaped, related to cell proliferation in the absence of drug metformin, to Z-shaped, related to apoptosis in the presence of drug metformin. Metformin 314-323 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 55-59 30223924-0 2018 Andrographolide inhibits proliferation and induces apoptosis of nasopharyngeal carcinoma cell line C666-1 through LKB1-AMPK-dependent signaling pathways. andrographolide 0-15 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 119-123 30305866-9 2018 Furthermore, impairment of the antioxidant defense system caused by maternal serine deficiency was mediated by the Akt/AMPK/Sirt1 pathway. Serine 77-83 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 119-123 30009356-0 2018 Correction to: Regulation of SIRT1/AMPK axis is critically involved in gallotannin-induced senescence and impaired autophagy leading to cell death in hepatocellular carcinoma cells. Hydrolyzable Tannins 71-82 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 35-39 30217073-5 2018 In control and AMPKalpha1-depleted human umbilical vein endothelial cells, eNOS phosphorylation on Ser1177 and Thr495 was assessed after AMPK activation with thiopental or ionomycin. Thiopental 158-168 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 15-25 30217073-5 2018 In control and AMPKalpha1-depleted human umbilical vein endothelial cells, eNOS phosphorylation on Ser1177 and Thr495 was assessed after AMPK activation with thiopental or ionomycin. Ionomycin 172-181 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 15-25 30217073-7 2018 The endothelial-specific deletion of the AMPKalpha1 subunit attenuated phenylephrine-mediated contraction in an eNOS- and endothelium-dependent manner. Phenylephrine 71-84 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 41-51 30217073-10 2018 The results of this study indicate that AMPKalpha1 targets the inhibitory phosphorylation Thr495 site in the calmodulin-binding domain of eNOS to attenuate basal NO production and phenylephrine-induced vasoconstriction. Phenylephrine 180-193 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 40-50 29722086-0 2018 Apoptotic effect of lambertianic acid through AMPK/FOXM1 signaling in MDA-MB231 breast cancer cells. lambertianic acid 20-37 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 46-50 29663481-5 2018 Specific inhibition of v-ATPase with bafilomycin and KM91104 induced a down-regulation of the HSC fibrogenic gene profile, which coincided with increased lysosomal pH, decreased pHi, activation of AMPK, reduced proliferation, and lower metabolic activity. bafilomycin 37-48 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 197-201 29663481-5 2018 Specific inhibition of v-ATPase with bafilomycin and KM91104 induced a down-regulation of the HSC fibrogenic gene profile, which coincided with increased lysosomal pH, decreased pHi, activation of AMPK, reduced proliferation, and lower metabolic activity. 3,4-dihydroxy-N'-(2-hydroxybenzylidene)benzohydrazide 53-60 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 197-201 29663481-6 2018 Similarly, pharmacological activation of AMPK by treatment with diflunisal, A769662, and ZLN024 reduced the expression of v-ATPase subunits and profibrogenic markers. Diflunisal 64-74 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 41-45 30037614-7 2018 AMPK is a master metabolic regulator activated by increases in ROS, Ca2+, and/or an AMP(ADP)/ATP ratio increase, etc. Reactive Oxygen Species 63-66 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 30037614-7 2018 AMPK is a master metabolic regulator activated by increases in ROS, Ca2+, and/or an AMP(ADP)/ATP ratio increase, etc. Adenosine Diphosphate 88-91 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 30037614-7 2018 AMPK is a master metabolic regulator activated by increases in ROS, Ca2+, and/or an AMP(ADP)/ATP ratio increase, etc. Adenosine Triphosphate 93-96 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 30037614-10 2018 Cellular stressors that induce TE mobilization (e.g. heat shock) also promote oocyte maturation in an AMPK-dependent manner and the antibiotic ionomycin activates AMPK, promotes TE activation, and induces human oocyte activation, producing normal, healthy children. Ionomycin 143-152 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 163-167 30037614-11 2018 Metformin promotes AMPK-dependent telomerase activation (critical for telomere maintenance) and induces activation of the endonuclease RAG1 (promotes DNA cleavage and transposition) via AMPK. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 19-23 30037614-11 2018 Metformin promotes AMPK-dependent telomerase activation (critical for telomere maintenance) and induces activation of the endonuclease RAG1 (promotes DNA cleavage and transposition) via AMPK. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 186-190 30015975-0 2018 Casticin suppresses the carcinogenesis of small cell lung cancer H446 cells through activation of AMPK/FoxO3a signaling. casticin 0-8 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 98-102 30015975-4 2018 In addition, casticin dose-dependently elevated the phosphorylation levels of AMPK and ACC, and reduced p-FoxO3a expression. casticin 13-21 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 78-82 30015975-7 2018 These findings reveal a novel mechanism for regulating AMPK/FoxO3a signaling in response to casticin, suggesting a new strategy for SCLC therapy by targeting cancer stem-like cells. casticin 92-100 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 55-59 30140075-1 2018 AMP-activated protein kinase (AMPK) regulates autophagy initiation when intracellular ATP level decreases. Adenosine Triphosphate 86-89 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-28 30140075-1 2018 AMP-activated protein kinase (AMPK) regulates autophagy initiation when intracellular ATP level decreases. Adenosine Triphosphate 86-89 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-34 30140075-6 2018 While the treatment of control cells with either compound C or trehalose induces activation of autophagosomes as well as autolysosomes, the treatment of AMPK alpha1 knockout cells with compound C or trehalose induces mainly activation of autophagosomes, but not autolysosomes. Trehalose 199-208 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 153-164 30134922-0 2018 LncRNA ANRIL regulates AML development through modulating the glucose metabolism pathway of AdipoR1/AMPK/SIRT1. Glucose 62-69 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 100-104 30134922-6 2018 Both ANRIL and AdipoR1 knockdown reduced the expression levels of phosphorylation of AMPK and SIRT1, implying a previously unappreciated ANRIL-AdipoR1-AMPK/SIRT1 signaling pathway in regulating cell glucose metabolism and survival in AML. Glucose 199-206 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 85-89 30134922-6 2018 Both ANRIL and AdipoR1 knockdown reduced the expression levels of phosphorylation of AMPK and SIRT1, implying a previously unappreciated ANRIL-AdipoR1-AMPK/SIRT1 signaling pathway in regulating cell glucose metabolism and survival in AML. Glucose 199-206 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 151-155 29147952-10 2018 Moreover, gemigliptin has a synergistic activity with PXD101 in the induction of cell death through involvement of Bcl2 family proteins, xIAP and survivin as well as mediation of Akt and AMPK in thyroid carcinoma cells. LC15-0444 10-21 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 187-191 29732938-0 2018 The protective role of autophagy in nephrotoxicity induced by bismuth nanoparticles through AMPK/mTOR pathway. Bismuth 62-69 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 92-96 30053908-0 2018 Phenformin alone or combined with gefitinib inhibits bladder cancer via AMPK and EGFR pathways. Phenformin 0-10 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 72-76 30053908-0 2018 Phenformin alone or combined with gefitinib inhibits bladder cancer via AMPK and EGFR pathways. Gefitinib 34-43 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 72-76 30053908-6 2018 The potential involvement of AMPK and EGFR pathways in the effects of phenformin and gefitinib was explored using Western blotting. Phenformin 70-80 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 29-33 30053908-6 2018 The potential involvement of AMPK and EGFR pathways in the effects of phenformin and gefitinib was explored using Western blotting. Gefitinib 85-94 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 29-33 29600521-12 2018 Of note, curcumin reduced cyclinD-expression in breast cancer cell treated with thrombin, and activates AMPK in a time-dependent manner. Curcumin 9-17 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 104-108 29600521-13 2018 Also suppression of AMPK abrogated inhibitory effect of phytosomal-curcumin on thrombin-induced cyclin D1 over-expression, suggesting that AMPK is essential for anti-proliferative effect of this agent in breast cancer. Curcumin 67-75 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 20-24 29600521-13 2018 Also suppression of AMPK abrogated inhibitory effect of phytosomal-curcumin on thrombin-induced cyclin D1 over-expression, suggesting that AMPK is essential for anti-proliferative effect of this agent in breast cancer. Curcumin 67-75 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 139-143 29857913-10 2018 AMPK, an evolutionarily conserved kinase activated by increases in intracellular Ca2+, ROS, and/or AMP/ATP ratio increases improves lifespan and healthspan in several model organisms and is essential for T cell activation. ros 87-90 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 29857913-10 2018 AMPK, an evolutionarily conserved kinase activated by increases in intracellular Ca2+, ROS, and/or AMP/ATP ratio increases improves lifespan and healthspan in several model organisms and is essential for T cell activation. Adenosine Triphosphate 103-106 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 29857913-12 2018 AMPK has been found localized in hippocampal CA1 dendrites and glutamate, NMDA, KCl, ionomycin, and BDNF have each been shown to induce AMPK activation in neurons. Glutamic Acid 63-72 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 136-140 29857913-12 2018 AMPK has been found localized in hippocampal CA1 dendrites and glutamate, NMDA, KCl, ionomycin, and BDNF have each been shown to induce AMPK activation in neurons. N-Methylaspartate 74-78 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 29857913-12 2018 AMPK has been found localized in hippocampal CA1 dendrites and glutamate, NMDA, KCl, ionomycin, and BDNF have each been shown to induce AMPK activation in neurons. N-Methylaspartate 74-78 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 136-140 29857913-12 2018 AMPK has been found localized in hippocampal CA1 dendrites and glutamate, NMDA, KCl, ionomycin, and BDNF have each been shown to induce AMPK activation in neurons. Potassium Chloride 80-83 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 29857913-12 2018 AMPK has been found localized in hippocampal CA1 dendrites and glutamate, NMDA, KCl, ionomycin, and BDNF have each been shown to induce AMPK activation in neurons. Potassium Chloride 80-83 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 136-140 29857913-12 2018 AMPK has been found localized in hippocampal CA1 dendrites and glutamate, NMDA, KCl, ionomycin, and BDNF have each been shown to induce AMPK activation in neurons. Ionomycin 85-94 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 29857913-12 2018 AMPK has been found localized in hippocampal CA1 dendrites and glutamate, NMDA, KCl, ionomycin, and BDNF have each been shown to induce AMPK activation in neurons. Ionomycin 85-94 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 136-140 29857913-14 2018 Because both T cell activation and LTP are dependent on intracellular Ca2+ increases and because inhibition of ROS significantly inhibits hippocampal CA1 LTP and T cell activation, it is our hypothesis that AMPK links latent HIV-1 reactivation with hippocampal LTP, learning, and memory. ros 111-114 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 207-211 29733844-7 2018 Furthermore, UVR-induced reactive oxygen species (ROS) production, lipid peroxidation and DNA damage were largely inhibited by the AMPK activator. Reactive Oxygen Species 25-48 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 131-135 29733844-7 2018 Furthermore, UVR-induced reactive oxygen species (ROS) production, lipid peroxidation and DNA damage were largely inhibited by the AMPK activator. Reactive Oxygen Species 50-53 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 131-135 29733844-8 2018 In summary, PF-06409577 inhibits UVR-induced oxidative stress and RPE cell death by activating AMPK signaling. PF-6409577 12-23 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 95-99 29904891-5 2018 Further investigation indicated that KCV could induce cancer cell apoptosis through AMPK-mediated activation of autophagy, and inhibited GR expression in castration-resistant prostate cancer(CRPC). kcv 37-40 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 84-88 29946343-3 2018 Here, we show that the prenylated chalcone, xanthohumol (XN), induces beiging of white adipocytes, stimulates lipolysis, and inhibits adipogenesis of murine 3T3-L1 adipocytes and primary human subcutaneous preadipocytes and these effects are partly mediated by the activation of the AMP-activated protein kinase (AMPK) signaling pathway. Chalcone 34-42 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 283-311 29946343-3 2018 Here, we show that the prenylated chalcone, xanthohumol (XN), induces beiging of white adipocytes, stimulates lipolysis, and inhibits adipogenesis of murine 3T3-L1 adipocytes and primary human subcutaneous preadipocytes and these effects are partly mediated by the activation of the AMP-activated protein kinase (AMPK) signaling pathway. Chalcone 34-42 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 313-317 29946343-3 2018 Here, we show that the prenylated chalcone, xanthohumol (XN), induces beiging of white adipocytes, stimulates lipolysis, and inhibits adipogenesis of murine 3T3-L1 adipocytes and primary human subcutaneous preadipocytes and these effects are partly mediated by the activation of the AMP-activated protein kinase (AMPK) signaling pathway. xanthohumol 44-55 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 283-311 29946343-3 2018 Here, we show that the prenylated chalcone, xanthohumol (XN), induces beiging of white adipocytes, stimulates lipolysis, and inhibits adipogenesis of murine 3T3-L1 adipocytes and primary human subcutaneous preadipocytes and these effects are partly mediated by the activation of the AMP-activated protein kinase (AMPK) signaling pathway. xanthohumol 44-55 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 313-317 29946343-3 2018 Here, we show that the prenylated chalcone, xanthohumol (XN), induces beiging of white adipocytes, stimulates lipolysis, and inhibits adipogenesis of murine 3T3-L1 adipocytes and primary human subcutaneous preadipocytes and these effects are partly mediated by the activation of the AMP-activated protein kinase (AMPK) signaling pathway. xanthohumol 57-59 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 283-311 29946343-3 2018 Here, we show that the prenylated chalcone, xanthohumol (XN), induces beiging of white adipocytes, stimulates lipolysis, and inhibits adipogenesis of murine 3T3-L1 adipocytes and primary human subcutaneous preadipocytes and these effects are partly mediated by the activation of the AMP-activated protein kinase (AMPK) signaling pathway. xanthohumol 57-59 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 313-317 29946343-9 2018 XN activated AMPK and in turn, XN-induced upregulation of UCP1, p-ACC, HSL, and ATGL was downregulated in the presence of dorsomorphin. xanthohumol 0-2 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 13-17 29946343-9 2018 XN activated AMPK and in turn, XN-induced upregulation of UCP1, p-ACC, HSL, and ATGL was downregulated in the presence of dorsomorphin. xanthohumol 31-33 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 13-17 29946343-9 2018 XN activated AMPK and in turn, XN-induced upregulation of UCP1, p-ACC, HSL, and ATGL was downregulated in the presence of dorsomorphin. dorsomorphin 122-134 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 13-17 29946343-12 2018 The anti-obesity effects of XN are partly mediated by AMPK signaling pathway suggesting that XN may have potential therapeutic implications for obesity. xanthohumol 28-30 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 54-58 29946343-12 2018 The anti-obesity effects of XN are partly mediated by AMPK signaling pathway suggesting that XN may have potential therapeutic implications for obesity. xanthohumol 93-95 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 54-58 30002135-2 2018 Surprisingly, we found that, in beta-cells, the AMPK activator 5-amino-4-imidazolecarboxamide ribofuranoside (AICAR) inhibited, rather than stimulated, autophagy. acadesine 63-108 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 48-52 30002135-2 2018 Surprisingly, we found that, in beta-cells, the AMPK activator 5-amino-4-imidazolecarboxamide ribofuranoside (AICAR) inhibited, rather than stimulated, autophagy. acadesine 110-115 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 48-52 28871429-7 2018 Treatment with 2-Cl-Phen increased the expression of phosphorylated AMPK, but Compound C, an AMPK inhibitor, did not influence the expression of c-Myc protein in HT-29 cells. 2-cl-phen 15-24 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 68-72 29786111-0 2018 High glucose suppresses the viability and proliferation of HTR-8/SVneo cells through regulation of the miR-137/PRKAA1/IL-6 axis. Glucose 5-12 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 111-117 29786111-1 2018 The aim of the present study was to investigate the mechanism underlying the high glucose (HG)-associated regulation of HTR-8/SVneo cell viability and proliferation during gestational diabetes mellitus (GDM), and to verify the association of microRNA (miR)-137, protein kinase AMP-activated catalytic subunit alpha1 (PRKAA1) and interlukin-6 (IL-6). Glucose 82-89 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 262-315 29786111-1 2018 The aim of the present study was to investigate the mechanism underlying the high glucose (HG)-associated regulation of HTR-8/SVneo cell viability and proliferation during gestational diabetes mellitus (GDM), and to verify the association of microRNA (miR)-137, protein kinase AMP-activated catalytic subunit alpha1 (PRKAA1) and interlukin-6 (IL-6). Glucose 82-89 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 317-323 29882092-4 2018 We here discuss and analyze data that leads to two possible conclusions: First, although DS and drugs that have some of their therapeutic mechanisms mediated by AMPK activity associated with low ATP levels, some of the associated health problems in vivo and in vitro fertilization/assisted reproductive technologies (IVF/ART) may be better-treated by increasing ATP production using CoQ10 (Ben-Meir et al., Aging Cell 14:887-895, 2015). Adenosine Triphosphate 195-198 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 161-165 29882092-11 2018 AMPK is normally activated by high AMP, commensurate with low ATP, but it was recently shown that if glucose is present inside the cell, AMPK activation by low ATP/high AMP is suppressed (Zhang et al., Nature 548:112-116, 2017). Adenosine Monophosphate 0-3 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 137-141 29882092-11 2018 AMPK is normally activated by high AMP, commensurate with low ATP, but it was recently shown that if glucose is present inside the cell, AMPK activation by low ATP/high AMP is suppressed (Zhang et al., Nature 548:112-116, 2017). Glucose 101-108 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 29882092-11 2018 AMPK is normally activated by high AMP, commensurate with low ATP, but it was recently shown that if glucose is present inside the cell, AMPK activation by low ATP/high AMP is suppressed (Zhang et al., Nature 548:112-116, 2017). Glucose 101-108 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 137-141 29882092-11 2018 AMPK is normally activated by high AMP, commensurate with low ATP, but it was recently shown that if glucose is present inside the cell, AMPK activation by low ATP/high AMP is suppressed (Zhang et al., Nature 548:112-116, 2017). Adenosine Triphosphate 160-163 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 29882092-11 2018 AMPK is normally activated by high AMP, commensurate with low ATP, but it was recently shown that if glucose is present inside the cell, AMPK activation by low ATP/high AMP is suppressed (Zhang et al., Nature 548:112-116, 2017). Adenosine Triphosphate 160-163 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 137-141 29882092-11 2018 AMPK is normally activated by high AMP, commensurate with low ATP, but it was recently shown that if glucose is present inside the cell, AMPK activation by low ATP/high AMP is suppressed (Zhang et al., Nature 548:112-116, 2017). Adenosine Monophosphate 35-38 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 29882092-13 2018 Stress in embryos and stem cells increases AMPK in large stimulation indexes but also direness indexes; the fastest AMPK activation occurs when stem cells are shifted from optimal oxygen to lower or high levels (Yang et al., J Reprod Dev 63:87-94, 2017). Oxygen 180-186 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 116-120 29882092-14 2018 CoQ10 use may be better than risking AMPK-dependent metabolic and developmental toxicity when ATP is depleted and AMPK activated. Adenosine Triphosphate 94-97 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 37-41 29882092-16 2018 Under these conditions, beneficial effects of AMPK on increasing triglyceride and fatty acid and glucose uptake are important, as long as AMPK agonist exposures are not too high or do not occur during developmental windows of sensitivity. Triglycerides 65-77 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 46-50 29882092-16 2018 Under these conditions, beneficial effects of AMPK on increasing triglyceride and fatty acid and glucose uptake are important, as long as AMPK agonist exposures are not too high or do not occur during developmental windows of sensitivity. Fatty Acids 82-92 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 46-50 29882092-16 2018 Under these conditions, beneficial effects of AMPK on increasing triglyceride and fatty acid and glucose uptake are important, as long as AMPK agonist exposures are not too high or do not occur during developmental windows of sensitivity. Glucose 97-104 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 46-50 29967351-7 2018 In a bleomycin model of lung fibrosis in mice, metformin therapeutically accelerates the resolution of well-established fibrosis in an AMPK-dependent manner. Bleomycin 5-14 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 135-139 29967351-7 2018 In a bleomycin model of lung fibrosis in mice, metformin therapeutically accelerates the resolution of well-established fibrosis in an AMPK-dependent manner. Metformin 47-56 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 135-139 30057793-4 2018 To further understand hypoxia-mediated TAp73 regulation, we have focused on the Adenosine monophosphate (AMP)-dependent protein kinase (AMPK) signalling pathway induced by hypoxia. monophosphate 90-103 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 136-140 29974734-0 2018 In Ovo Feeding of Creatine Pyruvate Increases the Glycolysis Pathway, Glucose Transporter Gene Expression, and AMPK Phosphorylation in Breast Muscle of Neonatal Broilers. Creatine pyruvate 18-35 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 111-115 29665353-0 2018 Tripartite motif 31 promotes resistance to anoikis of hepatocarcinoma cells through regulation of p53-AMPK axis. tripartite 0-10 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 102-106 29663499-0 2018 Resveratrol inhibits the proliferation and induces the apoptosis in ovarian cancer cells via inhibiting glycolysis and targeting AMPK/mTOR signaling pathway. Resveratrol 0-11 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 129-133 29663499-4 2018 Exposure to resveratrol increased the expression and activation of AMPK and Caspase 3, and decreased the expression and activation of AMPK downstream kinase mTOR. Resveratrol 12-23 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 67-71 29663499-4 2018 Exposure to resveratrol increased the expression and activation of AMPK and Caspase 3, and decreased the expression and activation of AMPK downstream kinase mTOR. Resveratrol 12-23 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 134-138 29663499-5 2018 Moreover, AMPK inhibitor Compound C significantly abolished the effects of resveratrol on the activation of AMPK and Caspase 3 and the inhibition of mTOR. Resveratrol 75-86 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 10-14 29663499-5 2018 Moreover, AMPK inhibitor Compound C significantly abolished the effects of resveratrol on the activation of AMPK and Caspase 3 and the inhibition of mTOR. Resveratrol 75-86 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 108-112 29915361-5 2018 In stressed (exercised) skeletal muscle, AMPK is activated to cooperate with CREB1 (cAMP response element binding protein-1) and promote glucose metabolism. Glucose 137-144 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 41-45 29577356-6 2018 RESULTS: Increased inhibitory Ser-486/491 AMPKalpha1 /alpha2 phosphorylation, increased AMPKalpha protein expression, decreased AMPKalpha activity, and loss of nuclear AMPKalpha and p-AMPKalpha are associated with prostate cancer progression to metastasis. Serine 30-33 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 42-52 29577356-7 2018 Increased p-Ser-486/491 AMPKalpha1 /alpha2 was also positively correlated with higher Gleason grade and progression to castration-resistance. Serine 12-15 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 24-34 29577356-8 2018 CONCLUSIONS: p-Ser-486/491 AMPKalpha1 /alpha2 is a novel marker of prostate cancer metastasis and castration-resistance. Serine 15-18 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 27-37 29872080-0 2018 Alcohol consumption promotes colorectal carcinoma metastasis via a CCL5-induced and AMPK-pathway-mediated activation of autophagy. Alcohols 0-7 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 84-88 29872080-9 2018 Aforementioned ethanol increases CCL5 secretion, CCL5 activates autophagy through AMPK pathway, and autophagy increases migration was confirmed by experiments with autophagy or AMPK inhibitors. Ethanol 15-22 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 177-181 29400636-0 2018 Buformin suppresses proliferation and invasion via AMPK/S6 pathway in cervical cancer and synergizes with paclitaxel. Buformin 0-8 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 51-55 29400636-7 2018 Consistently, western blotting showed that buformin activated AMPK and suppressed S6, cyclin D1, CDK4, and MMP9. Buformin 43-51 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 62-66 29400636-12 2018 Take together, we are the first to demonstrate that buformin suppresses cellular proliferation and invasion through the AMPK/S6 signaling pathway, which arrests cell cycle and inhibits cellular invasion. Buformin 52-60 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 120-124 29665360-8 2018 Mechanistically, co-administration of PNU-282987 with LY294002 (a PI3K inhibitor), AG490 (a JAK2 inhibitor) or Bcl-2 siRNA, but not compound C (an AMPK inhibitor), reduced Bcl-2 level and prevented the modulation of autophagy afforded by PNU-282987 in H/R cardiomyocytes. N-neopentyl-N-nitrosourea 38-41 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 147-151 29592879-0 2018 Itraconazole-Induced Inhibition on Human Esophageal Cancer Cell Growth Requires AMPK Activation. Itraconazole 0-12 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 80-84 30279304-10 2018 AMPK activator, biguanide metformin, either alone or in combination with other drugs, may selectively modulate signaling pathways, expresses the chemopreventive potential and can be used in current anti-cancer approaches. Biguanides 16-25 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 29592879-3 2018 Itraconazole activated AMPK signaling, which was required for subsequent esophageal cancer cell death. Itraconazole 0-12 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 23-27 29592879-4 2018 Pharmacologic AMPK inhibition, AMPKalpha1 shRNA, or dominant negative mutation (T172A) almost completely abolished itraconazole-induced cytotoxicity against esophageal cancer cells. Itraconazole 115-127 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-18 29592879-5 2018 Significantly, itraconazole induced AMPK-dependent autophagic cell death (but not apoptosis) in esophageal cancer cells. Itraconazole 15-27 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 36-40 29592879-6 2018 Furthermore, AMPK activation by itraconazole induced multiple receptor tyrosine kinases (RTKs: EGFR, PDGFRalpha, and PDGFRbeta), lysosomal translocation, and degradation to inhibit downstream Akt activation. Itraconazole 32-44 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 13-17 29592879-10 2018 AMPK activation, RTK degradation, and Akt inhibition were observed in itraconazole-treated tumors. Itraconazole 70-82 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 29592879-11 2018 Together, itraconazole inhibits esophageal cancer cell growth via activating AMPK signaling. Itraconazole 10-22 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 77-81 29773845-1 2018 5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside (AICAR) is an established pharmacological activator of AMP-activated protein kinase (AMPK). acadesine 0-54 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 110-138 29788929-9 2018 Moreover, we find that resveratrol increases both the levels of microtubule-associated protein 1 light chain 3-II and the number of autophagosomes, and further demonstrate that resveratrol-induced autophagy depends on the LKB1-AMPK-mTOR pathway. Resveratrol 23-34 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 227-231 29788929-9 2018 Moreover, we find that resveratrol increases both the levels of microtubule-associated protein 1 light chain 3-II and the number of autophagosomes, and further demonstrate that resveratrol-induced autophagy depends on the LKB1-AMPK-mTOR pathway. Resveratrol 177-188 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 227-231 29788929-11 2018 CONCLUSIONS: These results suggest that resveratrol induced apoptotic cell death of HL-60 cells depends on the autophagy activated through both the LKB1-AMPK and PI3K/AKT-regulated mTOR signaling pathways. Resveratrol 40-51 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 153-157 29773845-1 2018 5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside (AICAR) is an established pharmacological activator of AMP-activated protein kinase (AMPK). acadesine 0-54 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 140-144 29140707-6 2018 In conclusion, LXRalpha and its target genes are up-regulated by naringenin in an AMPK dependent manner in human macrophages. naringenin 65-75 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 82-86 29872506-8 2018 Moreover, Akt, Erk1/2 and AMPK were major oncogenic pathways altered by TVBs. tvbs 72-76 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 26-30 29754882-0 2018 Activation of AMPK for a Break in Hepatic Lipid Accumulation and Circulating Cholesterol. Cholesterol 77-88 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-18 29546577-1 2018 AIMS: 5-Aminoimidazole-4-carboxamide riboside (AICAR) is an endogenous activator of AMPK, a central regulator of energy homeostasis. acadesine 6-45 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 84-88 29546577-1 2018 AIMS: 5-Aminoimidazole-4-carboxamide riboside (AICAR) is an endogenous activator of AMPK, a central regulator of energy homeostasis. acadesine 47-52 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 84-88 29725013-0 2018 Iron overload promotes mitochondrial fragmentation in mesenchymal stromal cells from myelodysplastic syndrome patients through activation of the AMPK/MFF/Drp1 pathway. Iron 0-4 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 145-149 29725013-5 2018 Reduced ATP phosphorylated AMP-activated protein kinase (AMPK). Adenosine Triphosphate 8-11 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 27-55 29725013-5 2018 Reduced ATP phosphorylated AMP-activated protein kinase (AMPK). Adenosine Triphosphate 8-11 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 57-61 29725013-11 2018 In addition, iron chelation or antioxidant weakened the activity of the AMPK/MFF/Drp1 pathway in MDS-MSCs with IO from several patients, accompanied by attenuation of mitochondrial fragmentation and autophagy. Iron 13-17 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 72-76 29395579-8 2018 Furthermore t-CA-induced Nrf2 translocation is mediated through PKC, AMPK, CKII or ROS signaling cascades. cinnamic acid 12-16 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 69-73 29413962-5 2018 Moreover, we demonstrated that the expression of NF-kappaB, COX-2, IL-8, and MMP-13 were elevated subsequent to inhibition of SIRT1/AMPK/PGC-1alpha/PPAR-gamma pathway by homocysteine, thereby causing detrimental effects on chondrocytes. Homocysteine 170-182 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 132-136 29713279-0 2018 Astragaloside IV Inhibits Triglyceride Accumulation in Insulin-Resistant HepG2 Cells via AMPK-Induced SREBP-1c Phosphorylation. astragaloside 0-13 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 89-93 29413962-0 2018 Homocysteine causes dysfunction of chondrocytes and oxidative stress through repression of SIRT1/AMPK pathway: A possible link between hyperhomocysteinemia and osteoarthritis. Homocysteine 0-12 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 97-101 29413962-3 2018 This study was designed to test whether Hcy caused pro-osteoarthritic changes through modulation of SIRT1 and AMPK. Homocysteine 40-43 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 110-114 29413962-4 2018 Our results showed that administration of Hcy reduced the SIRT1/AMPK/PGC-1alpha signaling in chondrocytes, leading to mitochondrial dysfunction as a result of increased oxidative stress and apoptosis. Homocysteine 42-45 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 64-68 29713279-3 2018 Astragaloside IV (AST-IV) was found to decrease lipid accumulation in hepatocytes by activating AMPK, which is required to regulate lipid metabolism in liver tissue by inducing SREBP-1c phosphorylation. astragaloside 0-13 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 96-100 29896416-0 2018 SIRT3 Protects Rotenone-induced Injury in SH-SY5Y Cells by Promoting Autophagy through the LKB1-AMPK-mTOR Pathway. Rotenone 15-23 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 96-100 29632297-0 2018 Baicalin, a Chinese Herbal Medicine, Inhibits the Proliferation and Migration of Human Non-Small Cell Lung Carcinoma (NSCLC) Cells, A549 and H1299, by Activating the SIRT1/AMPK Signaling Pathway. baicalin 0-8 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 172-176 29632297-2 2018 Activation of the sirtuin 1 gene (SIRT1) and adenosine monophosphate (AMP)-activated protein kinase gene (AMPK), the SIRT1/AMPK signaling pathway, is associated with human malignant tumors. Adenosine Monophosphate 45-68 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 106-110 29632297-2 2018 Activation of the sirtuin 1 gene (SIRT1) and adenosine monophosphate (AMP)-activated protein kinase gene (AMPK), the SIRT1/AMPK signaling pathway, is associated with human malignant tumors. Adenosine Monophosphate 45-68 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 123-127 29632297-2 2018 Activation of the sirtuin 1 gene (SIRT1) and adenosine monophosphate (AMP)-activated protein kinase gene (AMPK), the SIRT1/AMPK signaling pathway, is associated with human malignant tumors. Adenosine Monophosphate 70-73 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 106-110 29632297-2 2018 Activation of the sirtuin 1 gene (SIRT1) and adenosine monophosphate (AMP)-activated protein kinase gene (AMPK), the SIRT1/AMPK signaling pathway, is associated with human malignant tumors. Adenosine Monophosphate 70-73 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 123-127 29632297-11 2018 CONCLUSIONS Baicalin, a flavonoid used in Chinese herbal medicine, inhibited the proliferation and migration of human NSCLC cells, A549 and H1299, by activating the SIRT1/AMPK signaling pathway. baicalin 12-20 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 171-175 29662316-0 2018 Metformin inhibits proliferation and cytotoxicity and induces apoptosis via AMPK pathway in CD19-chimeric antigen receptor-modified T cells. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 76-80 29662316-9 2018 Furthermore, our study revealed that metformin activated AMPK and suppressed mTOR and HIF1alpha expression. Metformin 37-46 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 57-61 29662316-10 2018 By using an AMPK inhibitor, compound C, we demonstrated the crucial roles of AMPK in CD19-CAR T cells when they were treated with metformin. Metformin 130-139 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 12-16 29662316-10 2018 By using an AMPK inhibitor, compound C, we demonstrated the crucial roles of AMPK in CD19-CAR T cells when they were treated with metformin. Metformin 130-139 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 77-81 29662316-12 2018 Conclusion: Taken together, these results indicated that metformin may play an important role in modulating CD19-CAR T cell biological functions in an AMPK-dependent and mTOR/HIF1alpha-independent manner. Metformin 57-66 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 151-155 29896416-12 2018 Together, our findings indicate a novel mechanism by which SIRT3 protects a rotenone-induced PD cell model through the regulation of autophagy, which, in part, is mediated by activation of the LKB1-AMPK-mTOR pathway. Rotenone 76-84 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 198-202 29484444-8 2018 We observed that treatment with cobalt chloride induced autophagy, including the intracellular quality control mechanism, in an AMPK-dependent manner. cobaltous chloride 32-47 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 128-132 29094413-0 2018 Fluoxetine induces autophagic cell death via eEF2K-AMPK-mTOR-ULK complex axis in triple negative breast cancer. Fluoxetine 0-10 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 51-55 29094413-8 2018 The mechanism for Fluoxetine-induced autophagic cell death was associated with inhibition of eEF2K and activation of AMPK-mTOR-ULK complex axis. Fluoxetine 18-28 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 117-121 29242172-2 2018 Curcumin, a traditional Chinese derivative from the rhizomes of Curcuma longa and a well-known AMP-activated protein kinase (AMPK) activator, possess hypocholesterolemic activity, however, the possible link between AMPK and cholesterol is unknown. Curcumin 0-8 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 125-129 29242172-2 2018 Curcumin, a traditional Chinese derivative from the rhizomes of Curcuma longa and a well-known AMP-activated protein kinase (AMPK) activator, possess hypocholesterolemic activity, however, the possible link between AMPK and cholesterol is unknown. Curcumin 0-8 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 215-219 29242172-4 2018 Results showed that curcumin induced AMPK phosphorylation, increased LXRalpha mRNA and protein expression. Curcumin 20-28 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 37-41 29525677-2 2018 Several studies have suggested that dietary antioxidants (such as polyphenols and berberine) may counteract oxidative stress through the involvement of the Sirtuin 1/Adenosine Monophosphate-Activated Protein Kinase (SIRT1/AMPK) pathway. Polyphenols 66-77 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 222-226 29525677-2 2018 Several studies have suggested that dietary antioxidants (such as polyphenols and berberine) may counteract oxidative stress through the involvement of the Sirtuin 1/Adenosine Monophosphate-Activated Protein Kinase (SIRT1/AMPK) pathway. Berberine 82-91 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 222-226 29386287-11 2018 In this study, we found that RSV induces autophagy through a ROS-AMPK signaling axis, which in turn promotes viral infection. Reactive Oxygen Species 61-64 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 65-69 29489344-6 2018 In addition, d-fagomine activated the AMPK signaling pathway through LKB1, increased the expression of SIRT1 and PGC-1alpha, and attenuated the inhibitory effect on SIRT1 and PGC-1alpha activity caused by AMPK and SIRT1 inhibitor. fagomine 13-23 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 38-42 29587684-0 2018 Delphinidin induced protective autophagy via mTOR pathway suppression and AMPK pathway activation in HER-2 positive breast cancer cells. delphinidin 0-11 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 74-78 29587684-8 2018 In addition, delphinidin induced autophagy via suppression of the mTOR signalling pathway and activation of the AMPK signalling pathway in HER-2 positive breast cancer cells. delphinidin 13-24 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 112-116 29587684-9 2018 CONCLUSIONS: Collectively, the results showed that delphinidin induced apoptosis and autophagy in HER-2 positive breast cancer cells and that autophagy was induced via the mTOR and AMPK signalling pathways. delphinidin 51-62 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 181-185 29489344-6 2018 In addition, d-fagomine activated the AMPK signaling pathway through LKB1, increased the expression of SIRT1 and PGC-1alpha, and attenuated the inhibitory effect on SIRT1 and PGC-1alpha activity caused by AMPK and SIRT1 inhibitor. fagomine 13-23 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 205-209 29489344-7 2018 d-Fagomine attenuated high glucose-induced oxidative stress in HUVECs through the AMPK/SIRT1/PGC-1alpha pathway. fagomine 0-10 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 82-86 29489344-7 2018 d-Fagomine attenuated high glucose-induced oxidative stress in HUVECs through the AMPK/SIRT1/PGC-1alpha pathway. Glucose 27-34 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 82-86 29554968-0 2018 Metformin induces autophagy and G0/G1 phase cell cycle arrest in myeloma by targeting the AMPK/mTORC1 and mTORC2 pathways. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 90-94 29554968-10 2018 Metformin activated AMPK and repressed both mTORC1 and mTORC2 signaling pathways in myeloma cells as well as downstream molecular signaling pathways, such as p-4EBP1 and p-AKT. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 20-24 29554968-12 2018 In addition, metformin inhibited myeloma cell growth in an AMPK-dependent manner. Metformin 13-22 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 59-63 29554968-13 2018 The xenograft mouse model further confirmed that metformin inhibited tumor growth by upregulation of AMPK and downregulation of mTOR. Metformin 49-58 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 101-105 29288670-0 2018 The suppressive effects of Britannin (Bri) on human liver cancer through inducing apoptosis and autophagy via AMPK activation regulated by ROS. britannin 27-36 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 110-114 29288670-0 2018 The suppressive effects of Britannin (Bri) on human liver cancer through inducing apoptosis and autophagy via AMPK activation regulated by ROS. Reactive Oxygen Species 139-142 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 110-114 29288670-10 2018 Notably, reducing ROS production by its scavenger, N-acetyl cysteine (NAC), could down-regulate p-AMPK levels, while up-regulate the phosphorylated mechanistic target of rapamycin (p-mTOR) expressions, accompanied with the restored cell viability, as well as the reduced apoptosis and autophagy in Bri-treated liver cancer cells. Reactive Oxygen Species 18-21 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 98-102 29288670-10 2018 Notably, reducing ROS production by its scavenger, N-acetyl cysteine (NAC), could down-regulate p-AMPK levels, while up-regulate the phosphorylated mechanistic target of rapamycin (p-mTOR) expressions, accompanied with the restored cell viability, as well as the reduced apoptosis and autophagy in Bri-treated liver cancer cells. Acetylcysteine 51-68 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 98-102 29288670-10 2018 Notably, reducing ROS production by its scavenger, N-acetyl cysteine (NAC), could down-regulate p-AMPK levels, while up-regulate the phosphorylated mechanistic target of rapamycin (p-mTOR) expressions, accompanied with the restored cell viability, as well as the reduced apoptosis and autophagy in Bri-treated liver cancer cells. Acetylcysteine 70-73 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 98-102 29288670-12 2018 In conclusion, our study illustrated that Bri could induce apoptosis and autophagy by activating AMPK regulated by ROS in liver cancer cells, supplying molecular bases for developing Bri into an effective candidate against liver cancer. Reactive Oxygen Species 115-118 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 97-101 29531259-0 2018 Identification of a novel 2-oxindole fluorinated derivative as in vivo antitumor agent for prostate cancer acting via AMPK activation. 2-oxindole 26-36 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 118-122 29531259-4 2018 This study reports the discovery of a new series of 2-oxindole derivatives whose AMPK modulatory ability, as well as the antitumoral profile in prostate cancer cells, was evaluated. 2-oxindole 52-62 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 81-85 28771713-5 2018 The GPR120 antagonist, AH7614, also blocked the preventive effect of EPA on TNF-alpha-induced decrease of alphaMG uptake and AMPK phosphorylation. AH-7614 23-29 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 125-129 29272251-3 2018 In vivo and in vitro cancer cell culture studies demonstrate that metformin induces both AMPK-dependent and AMPK-independent genes/pathways that result in inhibition of cancer cell growth and migration and induction of apoptosis. Metformin 66-75 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 89-93 29272251-3 2018 In vivo and in vitro cancer cell culture studies demonstrate that metformin induces both AMPK-dependent and AMPK-independent genes/pathways that result in inhibition of cancer cell growth and migration and induction of apoptosis. Metformin 66-75 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 108-112 29510506-0 2018 Resveratrol Inhibits Porcine Intestinal Glucose and Alanine Transport: Potential Roles of Na+/K+-ATPase Activity, Protein Kinase A, AMP-Activated Protein Kinase and the Association of Selected Nutrient Transport Proteins with Detergent Resistant Membranes. Resveratrol 0-11 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 132-160 29593120-0 2018 ROS-mediated activation of AMPK plays a critical role in sulforaphane-induced apoptosis and mitotic arrest in AGS human gastric cancer cells. Reactive Oxygen Species 0-3 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 27-31 29593120-0 2018 ROS-mediated activation of AMPK plays a critical role in sulforaphane-induced apoptosis and mitotic arrest in AGS human gastric cancer cells. sulforaphane 57-69 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 27-31 29593120-4 2018 Sulforaphane concurrently induced phosphorylation of AMPK; however, compound C, an AMPK inhibitor, significantly blocked sulforaphane-induced apoptosis, suggesting that sulforaphane induces apoptosis of AGS cells through the AMPK-dependent pathway. sulforaphane 0-12 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 53-57 29593120-6 2018 Furthermore, sulforaphane provoked the generation of intracellular ROS; especially when ROS production was blocked by antioxidant N-acetylcysteine, both AMPK activation and growth inhibition by sulforaphane were completely abolished. sulforaphane 13-25 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 153-157 29593120-6 2018 Furthermore, sulforaphane provoked the generation of intracellular ROS; especially when ROS production was blocked by antioxidant N-acetylcysteine, both AMPK activation and growth inhibition by sulforaphane were completely abolished. Reactive Oxygen Species 67-70 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 153-157 29593120-6 2018 Furthermore, sulforaphane provoked the generation of intracellular ROS; especially when ROS production was blocked by antioxidant N-acetylcysteine, both AMPK activation and growth inhibition by sulforaphane were completely abolished. Reactive Oxygen Species 88-91 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 153-157 29593120-6 2018 Furthermore, sulforaphane provoked the generation of intracellular ROS; especially when ROS production was blocked by antioxidant N-acetylcysteine, both AMPK activation and growth inhibition by sulforaphane were completely abolished. Acetylcysteine 130-146 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 153-157 29593120-6 2018 Furthermore, sulforaphane provoked the generation of intracellular ROS; especially when ROS production was blocked by antioxidant N-acetylcysteine, both AMPK activation and growth inhibition by sulforaphane were completely abolished. sulforaphane 194-206 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 153-157 29593120-7 2018 Collectively, these findings suggest that sulforaphane inhibited growth of AGS cells, which was mediated by a complex interplay between cellular mechanisms governing redox homeostasis, apoptosis, and cell cycle arrest through an ROS/AMPK-dependent pathway. sulforaphane 42-54 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 233-237 28771713-0 2018 EPA blocks TNF-alpha-induced inhibition of sugar uptake in Caco-2 cells via GPR120 and AMPK. Eicosapentaenoic Acid 0-3 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 87-91 28771713-0 2018 EPA blocks TNF-alpha-induced inhibition of sugar uptake in Caco-2 cells via GPR120 and AMPK. Sugars 43-48 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 87-91 28771713-4 2018 Interestingly, the AMPK inhibitor, Compound C, abolished the ability of EPA to prevent TNF-alpha-induced reduction of sugar uptake and transporter expression. Eicosapentaenoic Acid 72-75 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 19-23 28771713-4 2018 Interestingly, the AMPK inhibitor, Compound C, abolished the ability of EPA to prevent TNF-alpha-induced reduction of sugar uptake and transporter expression. Sugars 118-123 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 19-23 28771713-5 2018 The GPR120 antagonist, AH7614, also blocked the preventive effect of EPA on TNF-alpha-induced decrease of alphaMG uptake and AMPK phosphorylation. Eicosapentaenoic Acid 69-72 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 125-129 28771713-7 2018 EPA prevents the inhibitory effect of TNF-alpha through the involvement of GPR120 and AMPK activation. Eicosapentaenoic Acid 0-3 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 86-90 29432731-7 2018 AMPKalpha1 knockdown (by targeted-shRNAs) or knockout (by CRISPR-Cas-9 KO plasmid) blocked antagomiR-451-induced AMPK activation, and GEC protection against ethanol. Ethanol 157-164 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-10 29432731-7 2018 AMPKalpha1 knockdown (by targeted-shRNAs) or knockout (by CRISPR-Cas-9 KO plasmid) blocked antagomiR-451-induced AMPK activation, and GEC protection against ethanol. Ethanol 157-164 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 29445193-4 2018 Here, we show that in metabolically stressed cancer cells, FoxO3A is recruited to the mitochondria through activation of MEK/ERK and AMPK, which phosphorylate serine 12 and 30, respectively, on FoxO3A N-terminal domain. Serine 159-165 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 133-137 29491429-10 2018 Taken together, our observations indicate that SMG inhibits focal adhesions, leading to inhibition of signaling FAK and RhoA, and the mTORC1 pathway, which results in activation of the AMPK pathway and reduced melanoma cell proliferation and metastasis. N-SUCCINYL METHIONINE 47-50 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 185-189 29552085-0 2018 Nobiletin Inhibits Hepatic Lipogenesis via Activation of AMP-Activated Protein Kinase. nobiletin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 57-85 29552085-6 2018 Nobiletin significantly increased the phosphorylation of AMP-activated protein kinase (AMPK) and acetyl-CoA carboxylase. nobiletin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 57-85 29552085-6 2018 Nobiletin significantly increased the phosphorylation of AMP-activated protein kinase (AMPK) and acetyl-CoA carboxylase. nobiletin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 87-91 29552085-7 2018 Pretreatment with compound C, an AMPK inhibitor, abolished the inhibitory effects of nobiletin on SREBP-1c and FAS expression. nobiletin 85-94 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 33-37 29552085-8 2018 These results suggested that nobiletin might attenuate high glucose-induced lipid accumulation in HepG2 hepatocytes via modulation of AMPK signaling pathway. nobiletin 29-38 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 134-138 29153408-0 2018 AMPK: Sensing Glucose as well as Cellular Energy Status. Glucose 14-21 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 29153408-1 2018 Mammalian AMPK is known to be activated by falling cellular energy status, signaled by rising AMP/ATP and ADP/ATP ratios. Adenosine Triphosphate 98-101 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 10-14 29153408-1 2018 Mammalian AMPK is known to be activated by falling cellular energy status, signaled by rising AMP/ATP and ADP/ATP ratios. Adenosine Diphosphate 106-109 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 10-14 29153408-1 2018 Mammalian AMPK is known to be activated by falling cellular energy status, signaled by rising AMP/ATP and ADP/ATP ratios. Adenosine Triphosphate 110-113 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 10-14 29153408-2 2018 We review recent information about how this occurs but also discuss new studies suggesting that AMPK is able to sense glucose availability independently of changes in adenine nucleotides. Glucose 118-125 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 96-100 29153408-6 2018 Glucose sensing at the lysosome, in which AMPK and other components of the activation complex act antagonistically with another key nutrient sensor, mTORC1, may have been one of the ancestral roles of AMPK. Glucose 0-7 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 42-46 29153408-6 2018 Glucose sensing at the lysosome, in which AMPK and other components of the activation complex act antagonistically with another key nutrient sensor, mTORC1, may have been one of the ancestral roles of AMPK. Glucose 0-7 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 201-205 28943275-6 2018 In addition, mifepristone reduced oxygen consumption and ATP levels and increased AMPK Thr172 phosphorylation. Mifepristone 13-25 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 82-86 28943275-7 2018 The knockdown of AMPK prevented the effects of mifepristone on insulin response. Mifepristone 47-59 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 17-21 28943275-8 2018 CONCLUSIONS: Mifepristone enhanced insulin-stimulated glucose uptake through a mechanism that involves a decrease in mitochondrial function and AMPK activation in skeletal muscle cells. Mifepristone 13-25 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 144-148 28943275-8 2018 CONCLUSIONS: Mifepristone enhanced insulin-stimulated glucose uptake through a mechanism that involves a decrease in mitochondrial function and AMPK activation in skeletal muscle cells. Glucose 54-61 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 144-148 29324976-0 2018 Ginsenoside Rg1 inhibits apoptosis by increasing autophagy via the AMPK/mTOR signaling in serum deprivation macrophages. Ginsenosides 0-11 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 67-71 29277967-5 2018 Additionally, SM1044 also stimulates the de novo synthesis of ceramide, which in turn activates the CaMKK2-AMPK-ULK1 axis, leading to the initiation of autophagy. SM1044 14-20 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 107-111 29277967-5 2018 Additionally, SM1044 also stimulates the de novo synthesis of ceramide, which in turn activates the CaMKK2-AMPK-ULK1 axis, leading to the initiation of autophagy. Ceramides 62-70 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 107-111 29027991-0 2018 N6-isopentenyladenosine dual targeting of AMPK and Rab7 prenylation inhibits melanoma growth through the impairment of autophagic flux. Isopentenyladenosine 0-23 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 42-46 29027991-6 2018 AMPK silencing prevents apoptosis upon iPA treatment, whereas basal autophagosome turnover is still inhibited due to unprenylated Rab7. Isopentenyladenosine 39-42 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 29207101-3 2018 Diosgenin treatment increased the phosphorylation of AMP-activated protein kinase (AMPK) and acetyl-CoA carboxylase (ACC) in HepG2 cells. Diosgenin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 53-81 29207101-3 2018 Diosgenin treatment increased the phosphorylation of AMP-activated protein kinase (AMPK) and acetyl-CoA carboxylase (ACC) in HepG2 cells. Diosgenin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 83-87 29207101-4 2018 Diosgenin significantly inhibited high glucose (HG)-induced triglyceride (TG) accumulation and sterol regulatory element-binding protein-1c (SREBP-1c) mRNA increase in HepG2 cells, which were partially abolished by the AMPK inhibitor compound C. Diosgenin also significantly inhibited the increase of liver X receptor (LXR) alpha mRNA induced by HG or T0901317. Diosgenin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 219-223 28816409-5 2018 Genistein lowered PEPCK-C expression and glucose production in HepG2 cells accompanied with increased in phosphorylation states of AMPK, MEK1/2, ERK1/2, and CRTC2. Genistein 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 131-135 28816409-6 2018 Treatment with the AMPK inhibitor (compound C) enhanced genistein-induced MEK1/2 and ERK1/2 activity indicating a potential cross-talk between the two signaling pathways. Genistein 56-65 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 19-23 28816409-7 2018 In vivo, genistein also reduced fasting glucose levels accompanied with reduced PEPCK-C expression and increased in AMPK and ERK1/2 phosphorylation states in the liver of genistein-treated alloxan-induced diabetic mice. Genistein 9-18 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 116-120 28816409-7 2018 In vivo, genistein also reduced fasting glucose levels accompanied with reduced PEPCK-C expression and increased in AMPK and ERK1/2 phosphorylation states in the liver of genistein-treated alloxan-induced diabetic mice. Genistein 171-180 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 116-120 28816409-7 2018 In vivo, genistein also reduced fasting glucose levels accompanied with reduced PEPCK-C expression and increased in AMPK and ERK1/2 phosphorylation states in the liver of genistein-treated alloxan-induced diabetic mice. Alloxan 189-196 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 116-120 28816409-9 2018 These results indicate that genistein is an effective candidate for preventing T2DM through the modulation of AMPK-CRTC2 and MEK/ERK signaling pathways, which may allow a novel approach to modulate dysfunction in hepatic gluconeogenesis in T2DM. Genistein 28-37 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 110-114 29449537-2 2018 Metformin acts mainly by phosphorylation of AMPK. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 44-48 29449537-10 2018 In addition, in vivo experiments demonstrated that AMPK activation status was negatively related to HCC occurrence and blocking autophagy by chloroquine counteracted the protective effect of AMPK phosphorylation. Chloroquine 141-152 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 191-195 29133590-2 2018 In this study, etoposide activates the alpha1 but not the alpha2 isoform of AMPK, primarily within the nucleus. Etoposide 15-24 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 76-80 28494141-7 2018 Inhibition of LKB1 activity, a common upstream AMPK kinase, markedly reversed metformin-induced AMPK activation, RUNX2 expression and nuclear localization. Metformin 78-87 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 47-51 28494141-7 2018 Inhibition of LKB1 activity, a common upstream AMPK kinase, markedly reversed metformin-induced AMPK activation, RUNX2 expression and nuclear localization. Metformin 78-87 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 96-100 28494141-9 2018 Collectively, functional OCT-expressing iPSC-MSCs responded to metformin by inducing an osteogenic effect in part mediated by the LKB1/AMPK pathway. Metformin 63-72 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 135-139 29133590-4 2018 Intriguingly, Ca2+-dependent activation of AMPK in two different LKB1-null cancer cell lines caused G1-phase cell-cycle arrest, and enhanced cell viability/survival after etoposide treatment, with both effects being abolished by knockout of AMPK-alpha1 and alpha2. Etoposide 171-180 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 43-47 29133590-4 2018 Intriguingly, Ca2+-dependent activation of AMPK in two different LKB1-null cancer cell lines caused G1-phase cell-cycle arrest, and enhanced cell viability/survival after etoposide treatment, with both effects being abolished by knockout of AMPK-alpha1 and alpha2. Etoposide 171-180 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 241-252 29133590-6 2018 These results suggest that AMPK activation protects cells against etoposide by limiting entry into S-phase, where cells would be more vulnerable to genotoxic stress.Implications: These results reveal that the alpha1 isoform of AMPK promotes tumorigenesis by protecting cells against genotoxic stress, which may explain findings that the gene encoding AMPK-alpha1 (but not -alpha2) is amplified in some human cancers. Etoposide 66-75 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 27-31 29133590-6 2018 These results suggest that AMPK activation protects cells against etoposide by limiting entry into S-phase, where cells would be more vulnerable to genotoxic stress.Implications: These results reveal that the alpha1 isoform of AMPK promotes tumorigenesis by protecting cells against genotoxic stress, which may explain findings that the gene encoding AMPK-alpha1 (but not -alpha2) is amplified in some human cancers. Etoposide 66-75 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 227-231 29105398-8 2018 In addition, quercetin supplementation enhanced AMPK level by 12.3% compared with the control group (P<0.05). Quercetin 13-22 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 48-52 29216473-8 2018 Besides inhibition of ERK1/2 phosphorylation, estafiatin also inhibited phosphorylation of p53, AMPKalpha1, CREB, and p27 elicited by TCR activation in Jurkat cells, but it did not bind to any of 95 kinases evaluated. Estafiatin 46-56 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 96-106 29535833-0 2018 Glucagon promotes colon cancer cell growth via regulating AMPK and MAPK pathways. Glucagon 0-8 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 58-62 29535833-7 2018 Molecular assays showed that glucagon acted as an activator of cancer cell growth through deactivation of AMPK and activation of MAPK in a GCGR-dependent manner. Glucagon 29-37 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 106-110 29374159-11 2018 Moreover, AMPKalpha1 knockdown repressed the autophagy and survival of PC cells during hypoglucose, which were promoted by PKM2 knockdown. hypoglucose 87-98 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 10-20 29507591-0 2018 Zanthoxylum ailanthoides Suppresses Oleic Acid-Induced Lipid Accumulation through an Activation of LKB1/AMPK Pathway in HepG2 Cells. Oleic Acid 36-46 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 104-108 28676953-0 2018 Regulation of SIRT1/AMPK axis is critically involved in gallotannin-induced senescence and impaired autophagy leading to cell death in hepatocellular carcinoma cells. Hydrolyzable Tannins 56-67 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 20-24 28676953-7 2018 Interestingly, gallotannin attenuated the expression of SIRT1 and mTOR and activated phosphorylation of AMPK in two HCC cells. Hydrolyzable Tannins 15-26 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 104-108 28676953-8 2018 Furthermore, AMPK activator AICAR significantly enhanced SA-beta-gal activity and antiproliferation induced by gallotannin, while AMPK inhibitor compound C did not in two HCC cells. 2-chloro-10-(4'(N-beta-hydroxyethyl)piperazinyl-1')acetylphenothiazine 57-59 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 13-17 28676953-8 2018 Furthermore, AMPK activator AICAR significantly enhanced SA-beta-gal activity and antiproliferation induced by gallotannin, while AMPK inhibitor compound C did not in two HCC cells. beta-D-galactose 60-68 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 13-17 28676953-11 2018 Overall, these findings highlight evidence that regulation of SIRT1/AMPK is critically involved in gallotannin-induced senescence and impaired autophagy leading to cell death in HCC cells. Hydrolyzable Tannins 99-110 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 68-72 29156518-5 2018 Our results revealed that miR-139-5p inhibited glycolysis by regulating AMP-activated, alpha 1 catalytic subunit (PRKAA1) expression in gastric cancer cells. mir-139-5p 26-36 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 114-120 29156518-5 2018 Our results revealed that miR-139-5p inhibited glycolysis by regulating AMP-activated, alpha 1 catalytic subunit (PRKAA1) expression in gastric cancer cells. Adenosine Monophosphate 72-75 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 114-120 29074724-3 2018 We demonstrate here that glucose deprivation or hypoxia results in the AMPK-mediated phosphorylation of phosphoribosyl pyrophosphate synthetase 1 (PRPS1) S180 and PRPS2 S183, leading to conversion of PRPS hexamers to monomers and thereby inhibiting PRPS1/2 activity, nucleotide synthesis, and nicotinamide adenine dinucleotide (NAD) production. NAD 293-326 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 71-75 29074724-3 2018 We demonstrate here that glucose deprivation or hypoxia results in the AMPK-mediated phosphorylation of phosphoribosyl pyrophosphate synthetase 1 (PRPS1) S180 and PRPS2 S183, leading to conversion of PRPS hexamers to monomers and thereby inhibiting PRPS1/2 activity, nucleotide synthesis, and nicotinamide adenine dinucleotide (NAD) production. NAD 328-331 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 71-75 29074724-6 2018 Our findings highlight the significance of recalibrating tumor cell metabolism by fine-tuning nucleotide and NAD synthesis in tumor growth.Significance: Our findings elucidate an instrumental function of AMPK in direct regulation of nucleic acid and NAD synthesis in tumor cells in response to energy stress. NAD 109-112 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 204-208 29074724-6 2018 Our findings highlight the significance of recalibrating tumor cell metabolism by fine-tuning nucleotide and NAD synthesis in tumor growth.Significance: Our findings elucidate an instrumental function of AMPK in direct regulation of nucleic acid and NAD synthesis in tumor cells in response to energy stress. NAD 250-253 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 204-208 29074724-7 2018 AMPK phosphorylates PRPS1/2, converts PRPS1/2 hexamers to monomers, and inhibits PRPS1/2 activity and subsequent nucleotide and NAD synthesis to maintain tumor cell growth and survival. NAD 128-131 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 29105398-9 2018 CONCLUSIONS: Oral quercetin supplementation improves the metabolic features of PCOS patients by upregulating the expression of adiponectin receptors and AMPK (Registration Number: IRCT2013112515536N1). Quercetin 18-27 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 153-157 30439702-15 2018 CONCLUSION: Lnc-MALAT1 protects human osteoblasts from Dex-induced injuries, possibly via activation of Ppm1e-AMPK signaling. Dexamethasone 55-58 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 110-114 30439702-0 2018 Long Non-Coding RNA MALAT1 Protects Human Osteoblasts from Dexamethasone-Induced Injury via Activation of PPM1E-AMPK Signaling. Dexamethasone 59-72 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 112-116 30439702-12 2018 Treatment of osteoblasts with AMPKalpha1 short hairpin RNA or dominant negative mutation (T172A) abolished LV-MALAT1-induced protection against Dex-induced cytotoxicity. Dexamethasone 144-147 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-40 29635244-13 2018 CONCLUSIONS: MTDH-stimulated cancer resistance to 5-FU may be mediated through autophagy activated by the AMPK/ATG5 pathway in GC. Fluorouracil 50-54 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 106-110 28606032-3 2018 RESULTS: Based on the available scientific literature, metformin suppresses immune responses mainly through its direct effect on the cellular functions of various immune cell types by induction of AMPK and subsequent inhibition of mTORC1, and by inhibition of mitochondrial ROS production. Metformin 55-64 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 197-201 29663879-6 2018 RESULTS: Adenosine Monophosphate (AMP)-Activated Protein Kinase (AMPK) plays an important role in mechanism of action of metformin. Metformin 121-130 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 65-69 29663879-8 2018 The direct effects of metformin include AMPK-independent and AMPK-dependent effects whereas decrease in glucose level, hyperinsulinemia, and Insulin-like Growth Factor 1 (IGF-1) level are considered its indirect effects. Metformin 22-31 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 40-44 29552768-1 2018 PURPOSE: To investigate the expression of sirtuin type 1 (Sirt1) and adenosine 5"-monophosphate (AMP)-activated protein kinase (AMPK) in non-small cell lung cancer (NSCLC), and to explore the mechanism of their functions in NSCLC. adenosine 5"-monophosphate 69-95 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 128-132 29552768-1 2018 PURPOSE: To investigate the expression of sirtuin type 1 (Sirt1) and adenosine 5"-monophosphate (AMP)-activated protein kinase (AMPK) in non-small cell lung cancer (NSCLC), and to explore the mechanism of their functions in NSCLC. Adenosine Monophosphate 97-100 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 128-132 29148173-0 2018 Metformin protects against intestinal barrier dysfunction via AMPKalpha1-dependent inhibition of JNK signalling activation. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 62-72 29148173-7 2018 In addition, metformin suppressed DSS-induced JNK activation, an effect dependent on AMP-activated protein kinase alpha1 (AMPKalpha1) activation. Metformin 13-22 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 85-120 29148173-7 2018 In addition, metformin suppressed DSS-induced JNK activation, an effect dependent on AMP-activated protein kinase alpha1 (AMPKalpha1) activation. Metformin 13-22 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 122-132 29148173-7 2018 In addition, metformin suppressed DSS-induced JNK activation, an effect dependent on AMP-activated protein kinase alpha1 (AMPKalpha1) activation. dss 34-37 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 85-120 29148173-7 2018 In addition, metformin suppressed DSS-induced JNK activation, an effect dependent on AMP-activated protein kinase alpha1 (AMPKalpha1) activation. dss 34-37 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 122-132 29480476-0 2018 Compound C/Dorsomorphin: Its Use and Misuse as an AMPK Inhibitor. dorsomorphin 11-23 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 50-54 29480476-4 2018 The only reagent called dorsomorphin or compound C that is occasionally used as an AMPK inhibitor unfortunately inhibits several other kinases much more potently than AMPK and is therefore highly non-specific. dorsomorphin 24-36 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 83-87 29480476-4 2018 The only reagent called dorsomorphin or compound C that is occasionally used as an AMPK inhibitor unfortunately inhibits several other kinases much more potently than AMPK and is therefore highly non-specific. dorsomorphin 24-36 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 167-171 29480489-1 2018 Recent studies have revealed how AMPK is activated inside the cell and animal tissues: in response to low glucose, AXIN tethers LKB1, by virtue of their constitutive association, to AMPK located on the surface of late endosome/lysosome. Glucose 106-113 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 33-37 29480489-2 2018 Importantly, the lysosomal v-ATPase (vacuolar ATPase)-Ragulator complex, when primed by glucose starvation or concanamycin A, facilitates AXIN/LKB1 to interact with AMPK. concanamycin A 110-124 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 165-169 29480491-2 2018 The function of AMPK can be assayed by analyzing its phosphorylated protein levels in tissues, since AMPK is activated when it is phosphorylated at Thr-172. Threonine 148-151 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 16-20 29480491-2 2018 The function of AMPK can be assayed by analyzing its phosphorylated protein levels in tissues, since AMPK is activated when it is phosphorylated at Thr-172. Threonine 148-151 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 101-105 29480493-3 2018 The example provided herein illustrates the role of AMPK in T lymphocyte survival in response to the mitochondrial poison oligomycin. Oligomycins 122-132 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 52-56 28653238-0 2018 AMPK/NF-kappaB signaling pathway regulated by ghrelin participates in the regulation of HUVEC and THP1 Inflammation. Ghrelin 46-53 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 28653238-6 2018 Furthermore, we found that ghrelin effectively suppressed TNF-alpha-induced inflammatory factors" (including ICAM-1, VCAM-1, MCP-1, and IL-1beta) expression through inhibiting AMPK phosphorylation and p65 expression both in HUVEC and THP-1. Ghrelin 27-34 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 176-180 28653238-8 2018 Our findings suggest that ghrelin may mediate TNF-alpha-induced endothelial inflammation and monocyte adhesion, in part via AMPK/NF-kappaB signaling pathway. Ghrelin 26-33 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 124-128 29273902-0 2018 AMPK-dependent nitric oxide release provides contractile support during hyperosmotic stress. Nitric Oxide 15-27 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 28964787-0 2017 Negative regulation of Sirtuin 1 by AMP-activated protein kinase promotes metformin-induced senescence in hepatocellular carcinoma xenografts. Metformin 74-83 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 36-64 28964787-2 2017 Our previous in vitro studies have demonstrated that a low dose of metformin promoted hepatoma cell senescence instead of apoptosis via activation of AMP-activated protein kinase (AMPK) and inactivation of Sirtuin 1 (SIRT1) deacetylase activity. Metformin 67-76 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 150-178 28964787-2 2017 Our previous in vitro studies have demonstrated that a low dose of metformin promoted hepatoma cell senescence instead of apoptosis via activation of AMP-activated protein kinase (AMPK) and inactivation of Sirtuin 1 (SIRT1) deacetylase activity. Metformin 67-76 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 180-184 28964787-4 2017 We showed here that persistent exposure to a low concentration of metformin led to AMPK activation in a mouse xenograft model of human hepatocellular carcinoma (HCC), resulting in senescence. Metformin 66-75 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 83-87 28964787-5 2017 Intriguingly, AMPK counter-regulated SIRT1 via direct phosphorylation in metformin-mediated senescence in hepatoma cells. Metformin 73-82 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-18 28964787-6 2017 Taken together, these findings suggest that a low dose of metformin could potentially be used as a TIS-inducing therapeutic drug for HCC, and that this occurs by inducing senescence of HCC cells via the AMPK-SIRT1 pathway. Metformin 58-67 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 203-213 29273902-7 2018 HS-induced nNOS and eNOS activation and NO production were also prevented by AMPK inhibition with Dorsomorphin (DORSO). dorsomorphin 98-110 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 77-81 29435120-9 2018 microRNA-135b-mediated silence of Ppm1e could be the key mechanism of AMPK activation by ThIIA. tanshinone 89-94 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 70-74 29259227-5 2017 Identification of DHTS as a C1-Ten inhibitor revealed a new function of C1-Ten in AMPK inhibition, possibly through regulation of IRS-1. dhts 18-22 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 82-86 29259227-6 2017 These findings suggest that C1-Ten inhibition by DHTS could provide a novel therapeutic strategy for insulin resistance-associated metabolic syndrome through dual targeting of IRS-1 and AMPK. dhts 49-53 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 186-190 29233105-0 2017 Salidroside attenuates hypoxia-induced pulmonary arterial smooth muscle cell proliferation and apoptosis resistance by upregulating autophagy through the AMPK-mTOR-ULK1 pathway. rhodioloside 0-11 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 154-158 29233105-14 2017 P-AMPK (Thr 172) and P-ULK1 (Ser 555) of the AMPK-ULK1 pathway were increased in the hypoxia group and were further increased in the salidroside group. Threonine 8-11 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 2-6 29233105-2 2017 Our recent reports have shown that salidroside can exert protective effects against hypoxia-induced pulmonary arterial smooth muscle cell (PASMC) proliferation and apoptosis resistance through the AMPK pathway. rhodioloside 35-46 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 197-201 29233105-14 2017 P-AMPK (Thr 172) and P-ULK1 (Ser 555) of the AMPK-ULK1 pathway were increased in the hypoxia group and were further increased in the salidroside group. Threonine 8-11 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 45-49 29233105-14 2017 P-AMPK (Thr 172) and P-ULK1 (Ser 555) of the AMPK-ULK1 pathway were increased in the hypoxia group and were further increased in the salidroside group. rhodioloside 133-144 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 2-6 29233105-14 2017 P-AMPK (Thr 172) and P-ULK1 (Ser 555) of the AMPK-ULK1 pathway were increased in the hypoxia group and were further increased in the salidroside group. Serine 29-32 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 45-49 29233105-14 2017 P-AMPK (Thr 172) and P-ULK1 (Ser 555) of the AMPK-ULK1 pathway were increased in the hypoxia group and were further increased in the salidroside group. rhodioloside 133-144 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 45-49 29233105-17 2017 Furthermore, P-mTOR (Ser 2448) and P-ULK1 (Ser 757) of the AMPK-mTOR-ULK1 pathway were decreased in the hypoxia group and were further decreased in the salidroside group. Serine 21-24 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 59-63 29233105-17 2017 Furthermore, P-mTOR (Ser 2448) and P-ULK1 (Ser 757) of the AMPK-mTOR-ULK1 pathway were decreased in the hypoxia group and were further decreased in the salidroside group. Serine 43-46 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 59-63 29233105-17 2017 Furthermore, P-mTOR (Ser 2448) and P-ULK1 (Ser 757) of the AMPK-mTOR-ULK1 pathway were decreased in the hypoxia group and were further decreased in the salidroside group. rhodioloside 152-163 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 59-63 29233105-19 2017 CONCLUSIONS: Salidroside might inhibit hypoxia-induced PASMC proliferation and reverse apoptosis resistance via the upregulation of autophagy through both the AMPKalpha1-ULK1 and AMPKalpha1-mTOR-ULK1 pathways. rhodioloside 13-24 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 159-169 29233105-19 2017 CONCLUSIONS: Salidroside might inhibit hypoxia-induced PASMC proliferation and reverse apoptosis resistance via the upregulation of autophagy through both the AMPKalpha1-ULK1 and AMPKalpha1-mTOR-ULK1 pathways. rhodioloside 13-24 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 179-189 29299169-5 2017 Silence of AMPKalpha1, via targeted short hairpin RNAs or CRISPR-Cas9 genome editing, inhibited JLGTE-induced AMPK activation and HepG2 cell apoptosis. jlgte 96-101 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 11-21 28923415-0 2017 Diindolylmethane and its halogenated derivatives induce protective autophagy in human prostate cancer cells via induction of the oncogenic protein AEG-1 and activation of AMP-activated protein kinase (AMPK). 3,3'-diindolylmethane 0-16 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 171-199 28923415-0 2017 Diindolylmethane and its halogenated derivatives induce protective autophagy in human prostate cancer cells via induction of the oncogenic protein AEG-1 and activation of AMP-activated protein kinase (AMPK). 3,3'-diindolylmethane 0-16 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 201-205 28866046-9 2017 AMPKalpha increased significantly in all tested groups and p-AMPK increased significantly after 0.1mM formaldehyde treatment for 48h. Formaldehyde 102-114 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 29094484-0 2017 Degradation of AMPK-alpha1 sensitizes BRAF inhibitor-resistant melanoma cells to arginine deprivation. Arginine 81-89 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 15-26 29299169-5 2017 Silence of AMPKalpha1, via targeted short hairpin RNAs or CRISPR-Cas9 genome editing, inhibited JLGTE-induced AMPK activation and HepG2 cell apoptosis. jlgte 96-101 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 11-15 29299169-8 2017 These results suggest that JLGTE inhibits human hepatocellular carcinoma cells possibly via activating AMPK. jlgte 27-32 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 103-107 29100525-5 2017 Remarkably, a modified variant of AMPKalpha1 (T172Dalpha1) with constitutive low activity most effectively prevents the loss of dopamine neurons, as well as the motor impairments caused by alpha-synuclein accumulation. Dopamine 128-136 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 34-44 29100525-9 2017 CONCLUSIONS: Together, these results indicate that modulating AMPK activity can mitigate alpha-synuclein toxicity in nigral dopamine neurons, which may have implications for the development of neuroprotective treatments against PD. Dopamine 124-132 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 62-66 28940407-4 2017 Although this regulation is dependent on a conserved cysteine residue, the underlying mechanism is different to the redox regulation of animal AMPK and has functional implications for the regulation of the kinase complex in plants under stress conditions. Cysteine 53-61 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 143-147 28707280-0 2017 Multi-regulatory network of ROS: the interconnection of ROS, PGC-1 alpha, and AMPK-SIRT1 during exercise. Reactive Oxygen Species 28-31 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 78-82 28819003-9 2017 Ser485-AMPKalpha1/Ser491-AMPKalpha2 phosphorylation, a known mechanism of Thr172-AMPKalpha phosphorylation inhibition, is increased immediately after sprint exercise in hypoxia, probably by a mechanism independent of ROS.NEW & NOTEWORTHY The glycolytic rate is increased during sprint exercise in severe acute hypoxia. Reactive Oxygen Species 217-220 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 7-17 28819003-9 2017 Ser485-AMPKalpha1/Ser491-AMPKalpha2 phosphorylation, a known mechanism of Thr172-AMPKalpha phosphorylation inhibition, is increased immediately after sprint exercise in hypoxia, probably by a mechanism independent of ROS.NEW & NOTEWORTHY The glycolytic rate is increased during sprint exercise in severe acute hypoxia. Adenosine Monophosphate 226-229 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 7-17 28707280-6 2017 This review mainly focuses on interconnecting role of PGC-1 alpha and AMPK-SIRT1 pathway during exercise and how these proteins are getting tuned by reactive oxygen species in exercise condition. Reactive Oxygen Species 149-172 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 70-74 28755883-0 2017 Metformin: Insights into its anticancer potential with special reference to AMPK dependent and independent pathways. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 76-80 29333122-0 2017 Metformin Enhanced in Vitro Radiosensitivity Associates with G2/M Cell Cycle Arrest and Elevated Adenosine-5"-monophosphate-activated Protein Kinase Levels in Glioblastoma. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 97-148 29333122-7 2017 Induction of a G2/M phase cell cycle block through metformin and combined treatments was observed up to 72 h. These findings were associated with elevated levels of activated AMPK levels in LN229 cells but not in LN18 cells after irradiation, metformin, and temozolomide treatment. Metformin 51-60 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 175-179 29333122-7 2017 Induction of a G2/M phase cell cycle block through metformin and combined treatments was observed up to 72 h. These findings were associated with elevated levels of activated AMPK levels in LN229 cells but not in LN18 cells after irradiation, metformin, and temozolomide treatment. Temozolomide 258-270 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 175-179 29057925-5 2017 2-HG-mediated energy depletion activates AMPK (Threonine 172), blunting protein synthesis and mTOR signaling, culminating in a decline of Mcl-1. Threonine 47-56 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 41-45 29151954-3 2017 In this study, we showed that expression of carnitine palmitoyltransferase 1C (Cpt1c), as a member of the gate-keeper enzymes , which transferring long-chain fatty acids into mitochondria to further oxidation, which is regulated by AMPK promotes papillary thyroid carcinomas cells survival under metabolic stress conditions. long-chain fatty acids 147-169 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 232-236 28687354-2 2017 Adenosine 5"-monophosphate (AMP)-activated protein kinase (AMPK)-mTOR signaling is believed to partially contribute to these anticancer effects, although the mechanism is unclear. adenosine 5"-monophosphate 0-26 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 59-63 28687354-2 2017 Adenosine 5"-monophosphate (AMP)-activated protein kinase (AMPK)-mTOR signaling is believed to partially contribute to these anticancer effects, although the mechanism is unclear. Adenosine Monophosphate 28-31 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 59-63 28687354-3 2017 In this study, we revealed the mechanism underlying the effects of aspirin on AMPK-mTOR signaling, and described a mechanism-based rationale for the use of aspirin in cancer therapy. Aspirin 67-74 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 78-82 28687354-3 2017 In this study, we revealed the mechanism underlying the effects of aspirin on AMPK-mTOR signaling, and described a mechanism-based rationale for the use of aspirin in cancer therapy. Aspirin 156-163 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 78-82 28687354-4 2017 We found that aspirin inhibited mTORC1 signaling through AMPK-dependent and -independent manners. Aspirin 14-21 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 57-61 28687354-5 2017 Aspirin inhibited the AMPK-TSC pathway, thus resulting in the suppression of mTORC1 activity. Aspirin 0-7 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 22-26 28753455-0 2017 Diallyl trisulfide induces apoptosis and mitotic arrest in AGS human gastric carcinoma cells through reactive oxygen species-mediated activation of AMP-activated protein kinase. diallyl trisulfide 0-18 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 148-176 28753455-0 2017 Diallyl trisulfide induces apoptosis and mitotic arrest in AGS human gastric carcinoma cells through reactive oxygen species-mediated activation of AMP-activated protein kinase. Reactive Oxygen Species 101-124 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 148-176 28753455-3 2017 In this study, we investigated the role of ROS on the activation of AMP-activated protein kinase (AMPK) in DATS-induced apoptosis and cell cycle arrest in AGS human gastric carcinoma cells. Reactive Oxygen Species 43-46 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 68-96 28753455-3 2017 In this study, we investigated the role of ROS on the activation of AMP-activated protein kinase (AMPK) in DATS-induced apoptosis and cell cycle arrest in AGS human gastric carcinoma cells. Reactive Oxygen Species 43-46 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 98-102 28753455-3 2017 In this study, we investigated the role of ROS on the activation of AMP-activated protein kinase (AMPK) in DATS-induced apoptosis and cell cycle arrest in AGS human gastric carcinoma cells. diallyl trisulfide 107-111 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 68-96 28753455-3 2017 In this study, we investigated the role of ROS on the activation of AMP-activated protein kinase (AMPK) in DATS-induced apoptosis and cell cycle arrest in AGS human gastric carcinoma cells. diallyl trisulfide 107-111 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 98-102 28753455-6 2017 Furthermore, we found that DATS concurrently induced phosphorylation of AMPK; however, chemical inhibition of AMPK by compound C, an AMPK inhibitor, significantly blocked apoptosis induced by DATS, suggesting that DATS induces cytotoxicity of AGS cells through the AMPK-dependent pathway. diallyl trisulfide 27-31 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 72-76 28753455-6 2017 Furthermore, we found that DATS concurrently induced phosphorylation of AMPK; however, chemical inhibition of AMPK by compound C, an AMPK inhibitor, significantly blocked apoptosis induced by DATS, suggesting that DATS induces cytotoxicity of AGS cells through the AMPK-dependent pathway. diallyl trisulfide 27-31 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 110-114 28753455-6 2017 Furthermore, we found that DATS concurrently induced phosphorylation of AMPK; however, chemical inhibition of AMPK by compound C, an AMPK inhibitor, significantly blocked apoptosis induced by DATS, suggesting that DATS induces cytotoxicity of AGS cells through the AMPK-dependent pathway. diallyl trisulfide 27-31 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 110-114 28753455-6 2017 Furthermore, we found that DATS concurrently induced phosphorylation of AMPK; however, chemical inhibition of AMPK by compound C, an AMPK inhibitor, significantly blocked apoptosis induced by DATS, suggesting that DATS induces cytotoxicity of AGS cells through the AMPK-dependent pathway. diallyl trisulfide 27-31 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 110-114 28753455-6 2017 Furthermore, we found that DATS concurrently induced phosphorylation of AMPK; however, chemical inhibition of AMPK by compound C, an AMPK inhibitor, significantly blocked apoptosis induced by DATS, suggesting that DATS induces cytotoxicity of AGS cells through the AMPK-dependent pathway. diallyl trisulfide 192-196 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 72-76 28753455-6 2017 Furthermore, we found that DATS concurrently induced phosphorylation of AMPK; however, chemical inhibition of AMPK by compound C, an AMPK inhibitor, significantly blocked apoptosis induced by DATS, suggesting that DATS induces cytotoxicity of AGS cells through the AMPK-dependent pathway. diallyl trisulfide 192-196 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 110-114 28753455-6 2017 Furthermore, we found that DATS concurrently induced phosphorylation of AMPK; however, chemical inhibition of AMPK by compound C, an AMPK inhibitor, significantly blocked apoptosis induced by DATS, suggesting that DATS induces cytotoxicity of AGS cells through the AMPK-dependent pathway. diallyl trisulfide 192-196 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 110-114 28753455-6 2017 Furthermore, we found that DATS concurrently induced phosphorylation of AMPK; however, chemical inhibition of AMPK by compound C, an AMPK inhibitor, significantly blocked apoptosis induced by DATS, suggesting that DATS induces cytotoxicity of AGS cells through the AMPK-dependent pathway. diallyl trisulfide 192-196 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 110-114 28753455-6 2017 Furthermore, we found that DATS concurrently induced phosphorylation of AMPK; however, chemical inhibition of AMPK by compound C, an AMPK inhibitor, significantly blocked apoptosis induced by DATS, suggesting that DATS induces cytotoxicity of AGS cells through the AMPK-dependent pathway. diallyl trisulfide 192-196 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 72-76 28753455-6 2017 Furthermore, we found that DATS concurrently induced phosphorylation of AMPK; however, chemical inhibition of AMPK by compound C, an AMPK inhibitor, significantly blocked apoptosis induced by DATS, suggesting that DATS induces cytotoxicity of AGS cells through the AMPK-dependent pathway. diallyl trisulfide 192-196 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 110-114 28753455-6 2017 Furthermore, we found that DATS concurrently induced phosphorylation of AMPK; however, chemical inhibition of AMPK by compound C, an AMPK inhibitor, significantly blocked apoptosis induced by DATS, suggesting that DATS induces cytotoxicity of AGS cells through the AMPK-dependent pathway. diallyl trisulfide 192-196 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 110-114 28753455-6 2017 Furthermore, we found that DATS concurrently induced phosphorylation of AMPK; however, chemical inhibition of AMPK by compound C, an AMPK inhibitor, significantly blocked apoptosis induced by DATS, suggesting that DATS induces cytotoxicity of AGS cells through the AMPK-dependent pathway. diallyl trisulfide 192-196 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 110-114 28753455-7 2017 Moreover, DATS provoked intracellular ROS generation and the loss of mitochondrial membrane potential, and in particular, when ROS production was blocked by antioxidant N-acety-l-cysteine, both AMPK activation and growth inhibition by DATS were completely abolished. diallyl trisulfide 10-14 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 194-198 28753455-7 2017 Moreover, DATS provoked intracellular ROS generation and the loss of mitochondrial membrane potential, and in particular, when ROS production was blocked by antioxidant N-acety-l-cysteine, both AMPK activation and growth inhibition by DATS were completely abolished. Reactive Oxygen Species 127-130 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 194-198 28753455-7 2017 Moreover, DATS provoked intracellular ROS generation and the loss of mitochondrial membrane potential, and in particular, when ROS production was blocked by antioxidant N-acety-l-cysteine, both AMPK activation and growth inhibition by DATS were completely abolished. Acetylcysteine 169-187 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 194-198 28753455-7 2017 Moreover, DATS provoked intracellular ROS generation and the loss of mitochondrial membrane potential, and in particular, when ROS production was blocked by antioxidant N-acety-l-cysteine, both AMPK activation and growth inhibition by DATS were completely abolished. diallyl trisulfide 235-239 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 194-198 28753455-8 2017 Collectively, these findings suggest that DATS inhibited growth of AGS cells, which was mediated by complex interplay between cellular mechanisms governing redox homeostasis, apoptosis, and cell cycle arrest, through a ROS-dependent activation of AMPK pathway. diallyl trisulfide 42-46 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 247-251 28753455-8 2017 Collectively, these findings suggest that DATS inhibited growth of AGS cells, which was mediated by complex interplay between cellular mechanisms governing redox homeostasis, apoptosis, and cell cycle arrest, through a ROS-dependent activation of AMPK pathway. Reactive Oxygen Species 219-222 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 247-251 28849003-8 2017 In addition, the cell cycle-related proteins, including p27, CHK1, cyclin D1, CDK1, p-AMP-activated protein kinase (AMPK) and p-protein kinase B (AKT), were regulated by chrysophanol nanoparticles to prevent human prostate cancer cell progression. chrysophanic acid 170-182 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 84-114 28849003-8 2017 In addition, the cell cycle-related proteins, including p27, CHK1, cyclin D1, CDK1, p-AMP-activated protein kinase (AMPK) and p-protein kinase B (AKT), were regulated by chrysophanol nanoparticles to prevent human prostate cancer cell progression. chrysophanic acid 170-182 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 116-120 28556920-0 2017 AMPK activator acadesine fails to alleviate isoniazid-caused mitochondrial instability in HepG2 cells. acadesine 15-24 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 29655680-0 2018 Panduratin A induces protective autophagy in melanoma via the AMPK and mTOR pathway. panduratin A 0-12 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 62-66 29655680-11 2018 PA-induced autophagy in A375 melanoma cells was found to be mediated through the inhibition of mTOR signaling and activation of AMPK pathway. panduratin A 0-2 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 128-132 29655680-13 2018 CONCLUSION: Taken together, results from the present study suggest that the inhibition of autophagy by targeting mTOR and AMPK could potentiate the cytotoxicity effects of PA on melanoma cells. panduratin A 172-174 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 122-126 29221169-5 2017 LB-100 inhibited PP2A activity and activated AMPK signaling in CRC cells. lb100 0-6 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 45-49 29221169-6 2017 AMPKalpha1 dominant negative mutation, shRNA-mediated knockdown or complete knockout (by CRISPR/Cas9 method) largely attenuated LB-100-induced AMPK activation and HCT-116 cytotoxicity. lb100 128-134 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-10 29221169-6 2017 AMPKalpha1 dominant negative mutation, shRNA-mediated knockdown or complete knockout (by CRISPR/Cas9 method) largely attenuated LB-100-induced AMPK activation and HCT-116 cytotoxicity. lb100 128-134 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 29221169-11 2017 We conclude that targeting PP2A by LB-100 and microRNA-17-92 activates AMPK signaling to inhibit CRC cells. lb100 35-41 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 71-75 29156790-0 2017 Kaempferol induces autophagic cell death of hepatocellular carcinoma cells via activating AMPK signaling. kaempferol 0-10 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 90-94 29156790-2 2017 Kaempferol treatment in HCC cells induced profound AMP-activated protein kinase (AMPK) activation, which led to Ulk1 phosphorylation, mTOR complex 1 inhibition and cell autophagy. kaempferol 0-10 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 51-79 29156790-2 2017 Kaempferol treatment in HCC cells induced profound AMP-activated protein kinase (AMPK) activation, which led to Ulk1 phosphorylation, mTOR complex 1 inhibition and cell autophagy. kaempferol 0-10 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 81-85 29156790-5 2017 AMPK inhibition also largely inhibited Kaempferol-induced cytotoxicity in HCC cells. kaempferol 39-49 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 29156790-7 2017 Kaempferol downregulated melanoma antigen 6, the AMPK ubiquitin ligase, causing AMPKalpha1 stabilization and accumulation. kaempferol 0-10 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 49-53 29156790-7 2017 Kaempferol downregulated melanoma antigen 6, the AMPK ubiquitin ligase, causing AMPKalpha1 stabilization and accumulation. kaempferol 0-10 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 80-90 29156790-8 2017 We conclude that Kaempferol inhibits human HCC cells via activating AMPK signaling. kaempferol 17-27 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 68-72 28755883-4 2017 Metformin inhibits mTORC1 via AMPK dependent and AMPK independent pathways, thereby inhibiting cancer cell growth and development. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-34 28755883-4 2017 Metformin inhibits mTORC1 via AMPK dependent and AMPK independent pathways, thereby inhibiting cancer cell growth and development. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 49-53 28755883-7 2017 Here, we review both AMPK dependent and AMPK independent mechanisms involved in anticancer activity of metformin along with the outcome of preclinical and clinical studies. Metformin 103-112 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 21-25 28755883-7 2017 Here, we review both AMPK dependent and AMPK independent mechanisms involved in anticancer activity of metformin along with the outcome of preclinical and clinical studies. Metformin 103-112 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 40-44 28694192-0 2017 Laminar shear stress suppresses vascular smooth muscle cell proliferation through nitric oxide-AMPK pathway. Nitric Oxide 82-94 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 95-99 28694192-7 2017 The expression of NOS isoforms was increased 1 h after exposure to shear stress, and AMPK phosphorylation started to increase after 2 h. AMPK and LKB1, the upstream kinases of AMPK, phosphorylation were decreased by the non-selective NOS inhibitor l-NAME and the selective iNOS inhibitor aminoguanidine despite exposure to shear stress. NG-Nitroarginine Methyl Ester 248-254 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 85-89 28694192-7 2017 The expression of NOS isoforms was increased 1 h after exposure to shear stress, and AMPK phosphorylation started to increase after 2 h. AMPK and LKB1, the upstream kinases of AMPK, phosphorylation were decreased by the non-selective NOS inhibitor l-NAME and the selective iNOS inhibitor aminoguanidine despite exposure to shear stress. NG-Nitroarginine Methyl Ester 248-254 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 137-141 28694192-7 2017 The expression of NOS isoforms was increased 1 h after exposure to shear stress, and AMPK phosphorylation started to increase after 2 h. AMPK and LKB1, the upstream kinases of AMPK, phosphorylation were decreased by the non-selective NOS inhibitor l-NAME and the selective iNOS inhibitor aminoguanidine despite exposure to shear stress. NG-Nitroarginine Methyl Ester 248-254 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 137-141 28694192-7 2017 The expression of NOS isoforms was increased 1 h after exposure to shear stress, and AMPK phosphorylation started to increase after 2 h. AMPK and LKB1, the upstream kinases of AMPK, phosphorylation were decreased by the non-selective NOS inhibitor l-NAME and the selective iNOS inhibitor aminoguanidine despite exposure to shear stress. pimagedine 288-302 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 85-89 28694192-7 2017 The expression of NOS isoforms was increased 1 h after exposure to shear stress, and AMPK phosphorylation started to increase after 2 h. AMPK and LKB1, the upstream kinases of AMPK, phosphorylation were decreased by the non-selective NOS inhibitor l-NAME and the selective iNOS inhibitor aminoguanidine despite exposure to shear stress. pimagedine 288-302 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 137-141 28694192-7 2017 The expression of NOS isoforms was increased 1 h after exposure to shear stress, and AMPK phosphorylation started to increase after 2 h. AMPK and LKB1, the upstream kinases of AMPK, phosphorylation were decreased by the non-selective NOS inhibitor l-NAME and the selective iNOS inhibitor aminoguanidine despite exposure to shear stress. pimagedine 288-302 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 137-141 28723898-0 2017 Fructose-1,6-bisphosphate and aldolase mediate glucose sensing by AMPK. Glucose 47-54 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 66-70 28874730-4 2017 MPA produced an early and transient drop in the intracellular ATP content related to the inhibition of de novo synthesis of purines, leading to the activation of the energy sensor AMPK. Adenosine Triphosphate 62-65 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 180-184 28874730-4 2017 MPA produced an early and transient drop in the intracellular ATP content related to the inhibition of de novo synthesis of purines, leading to the activation of the energy sensor AMPK. Purines 124-131 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 180-184 28871102-8 2017 In addition, the generated ROS and calcium stimulated AMPK phosphorylation. Reactive Oxygen Species 27-30 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 54-58 28871102-8 2017 In addition, the generated ROS and calcium stimulated AMPK phosphorylation. Calcium 35-42 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 54-58 28828587-0 2017 Tryptanthrin prevents oxidative stress-mediated apoptosis through AMP-activated protein kinase-dependent p38 mitogen-activated protein kinase activation. tryptanthrine 0-12 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 66-94 28828587-5 2017 Mechanistic investigations showed that tryptanthrin increased the phosphorylations of AMP-activated protein kinase (AMPK) and of p38 mitogen-activated protein kinase (p38). tryptanthrine 39-51 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 86-114 28828587-5 2017 Mechanistic investigations showed that tryptanthrin increased the phosphorylations of AMP-activated protein kinase (AMPK) and of p38 mitogen-activated protein kinase (p38). tryptanthrine 39-51 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 116-120 28828587-6 2017 Furthermore, inhibition of AMPK or p38 reduced the ability of tryptanthrin to prevent AA + iron-induced cell death and mitochondrial dysfunction. tryptanthrine 62-74 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 27-31 28828587-6 2017 Furthermore, inhibition of AMPK or p38 reduced the ability of tryptanthrin to prevent AA + iron-induced cell death and mitochondrial dysfunction. Iron 91-95 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 27-31 28828587-7 2017 Transfection experiments using AMPK mutants indicated that p38 phosphorylation by tryptanthrin was dependent on AMPK activation. tryptanthrine 82-94 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 31-35 28828587-7 2017 Transfection experiments using AMPK mutants indicated that p38 phosphorylation by tryptanthrin was dependent on AMPK activation. tryptanthrine 82-94 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 112-116 28828587-10 2017 Thus, these results suggest tryptanthrin has therapeutic potential to protect cells from oxidative injury via AMPK-dependent p38 activation. tryptanthrine 28-40 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 110-114 28700975-6 2017 Detailed study shows that astilbin leads to S phase arrest of the cell cycle by induction of p53 and p21 and activated-AMPK. astilbin 26-34 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 119-123 28411102-0 2017 ZL006 protects spinal cord neurons against ischemia-induced oxidative stress through AMPK-PGC-1alpha-Sirt3 pathway. 4-((3,5-dichloro-2-hydroxybenzyl)amino)-2-hydroxybenzoic acid 0-5 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 85-89 28411102-8 2017 The results of western blot analysis showed that ZL006 increased the activation of AMPK-PGC-1alpha-Sirt3 pathway, and the beneficial effects of ZL006 was partially abolished by AMPK inhibitor and PGC-1alpha knockdown. 4-((3,5-dichloro-2-hydroxybenzyl)amino)-2-hydroxybenzoic acid 49-54 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 83-87 28411102-8 2017 The results of western blot analysis showed that ZL006 increased the activation of AMPK-PGC-1alpha-Sirt3 pathway, and the beneficial effects of ZL006 was partially abolished by AMPK inhibitor and PGC-1alpha knockdown. 4-((3,5-dichloro-2-hydroxybenzyl)amino)-2-hydroxybenzoic acid 144-149 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 83-87 28411102-8 2017 The results of western blot analysis showed that ZL006 increased the activation of AMPK-PGC-1alpha-Sirt3 pathway, and the beneficial effects of ZL006 was partially abolished by AMPK inhibitor and PGC-1alpha knockdown. 4-((3,5-dichloro-2-hydroxybenzyl)amino)-2-hydroxybenzoic acid 144-149 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 177-181 28411102-9 2017 Therefore, our present data showed that, by the AMPK-PGC-1alpha-Sirt3 pathway, ZL006 protects spinal cord neurons against ischemia through reducing mitochondrial oxidative stress to prevent apoptosis. 4-((3,5-dichloro-2-hydroxybenzyl)amino)-2-hydroxybenzoic acid 79-84 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 48-52 28867797-0 2017 Flavonoid-Rich Extract of Paulownia fortunei Flowers Attenuates Diet-Induced Hyperlipidemia, Hepatic Steatosis and Insulin Resistance in Obesity Mice by AMPK Pathway. Flavonoids 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 153-157 28900501-0 2017 Metformin Sensitizes Leukemia Cells to Vincristine via Activation of AMP-activated Protein Kinase. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 69-97 28900501-0 2017 Metformin Sensitizes Leukemia Cells to Vincristine via Activation of AMP-activated Protein Kinase. Vincristine 39-50 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 69-97 28900501-4 2017 It is reported that AMPK is involved in vincristine-induced apoptosis. Vincristine 40-51 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 20-24 28900501-8 2017 We further demonstrated that metformin sensitized leukemia cells to vincristine-induced apoptosis in an AMPK-dependent manner. Metformin 29-38 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 104-108 28900501-8 2017 We further demonstrated that metformin sensitized leukemia cells to vincristine-induced apoptosis in an AMPK-dependent manner. Vincristine 68-79 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 104-108 28900501-9 2017 In addition, knockdown of AMPKalpha1 significantly reduced the effects of metformin on vincristine-induced apoptosis. Metformin 74-83 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 26-36 28900501-9 2017 In addition, knockdown of AMPKalpha1 significantly reduced the effects of metformin on vincristine-induced apoptosis. Vincristine 87-98 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 26-36 28900501-10 2017 Taken together, these results indicate that AMPK activation is critical in metformin effects on vincristine-induced apoptosis and suggest a putative strategy of a combination therapy using metformin and vincristine in treatment of leukemia. Metformin 75-84 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 44-48 28900501-10 2017 Taken together, these results indicate that AMPK activation is critical in metformin effects on vincristine-induced apoptosis and suggest a putative strategy of a combination therapy using metformin and vincristine in treatment of leukemia. Vincristine 96-107 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 44-48 28900501-10 2017 Taken together, these results indicate that AMPK activation is critical in metformin effects on vincristine-induced apoptosis and suggest a putative strategy of a combination therapy using metformin and vincristine in treatment of leukemia. Metformin 189-198 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 44-48 28900501-10 2017 Taken together, these results indicate that AMPK activation is critical in metformin effects on vincristine-induced apoptosis and suggest a putative strategy of a combination therapy using metformin and vincristine in treatment of leukemia. Vincristine 203-214 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 44-48 28723898-2 2017 Glucose deprivation activates AMP-activated protein kinase (AMPK), but it is unclear whether this activation occurs solely via changes in AMP or ADP, the classical activators of AMPK. Adenosine Monophosphate 30-33 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 60-64 28723898-2 2017 Glucose deprivation activates AMP-activated protein kinase (AMPK), but it is unclear whether this activation occurs solely via changes in AMP or ADP, the classical activators of AMPK. Adenosine Diphosphate 145-148 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 178-182 28723898-3 2017 Here, we describe an AMP/ADP-independent mechanism that triggers AMPK activation by sensing the absence of fructose-1,6-bisphosphate (FBP), with AMPK being progressively activated as extracellular glucose and intracellular FBP decrease. Adenosine Monophosphate 21-24 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 65-69 28723898-3 2017 Here, we describe an AMP/ADP-independent mechanism that triggers AMPK activation by sensing the absence of fructose-1,6-bisphosphate (FBP), with AMPK being progressively activated as extracellular glucose and intracellular FBP decrease. Adenosine Monophosphate 21-24 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 145-149 28723898-3 2017 Here, we describe an AMP/ADP-independent mechanism that triggers AMPK activation by sensing the absence of fructose-1,6-bisphosphate (FBP), with AMPK being progressively activated as extracellular glucose and intracellular FBP decrease. Adenosine Diphosphate 25-28 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 65-69 28723898-3 2017 Here, we describe an AMP/ADP-independent mechanism that triggers AMPK activation by sensing the absence of fructose-1,6-bisphosphate (FBP), with AMPK being progressively activated as extracellular glucose and intracellular FBP decrease. Adenosine Diphosphate 25-28 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 145-149 28723898-3 2017 Here, we describe an AMP/ADP-independent mechanism that triggers AMPK activation by sensing the absence of fructose-1,6-bisphosphate (FBP), with AMPK being progressively activated as extracellular glucose and intracellular FBP decrease. Glucose 197-204 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 65-69 28723898-3 2017 Here, we describe an AMP/ADP-independent mechanism that triggers AMPK activation by sensing the absence of fructose-1,6-bisphosphate (FBP), with AMPK being progressively activated as extracellular glucose and intracellular FBP decrease. Glucose 197-204 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 145-149 28723898-7 2017 Importantly, in some cell types AMP/ATP and ADP/ATP ratios remain unchanged during acute glucose starvation, and intact AMP-binding sites on AMPK are not required for AMPK activation. Adenosine Monophosphate 120-123 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 141-145 28723898-8 2017 These results establish that aldolase, as well as being a glycolytic enzyme, is a sensor of glucose availability that regulates AMPK. Glucose 92-99 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 128-132 28450156-5 2017 Of note, under the stressful tumor microenvironment, miR-7 could repress autophagy through up-regulation of LKB1-AMPK-mTOR signaling, and directly targeting the stages of autophagy induction and vesicle elongation to reduce the supply of intracellular glucose to glycolysis metabolism. Glucose 252-259 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 113-117 28445821-4 2017 Several derivatives of 5-aminoimidazole-4-carboxamide-1-beta-d-ribofuranoside (AICAR), an AMP-activated protein kinase (AMPK) activator, were identified as transcriptional activators of the DDT gene. acadesine 23-77 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 90-118 28664915-8 2017 CONCLUSIONS: If validated in a larger cohort of patients, the decreased AMPK-AKT-mTOR activation and phosphorylation of FOXO1 T24/FOXO3 T32 may help identify carboplatin-paclitaxel-resistant EOC patients. Carboplatin 158-169 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 72-76 28664915-8 2017 CONCLUSIONS: If validated in a larger cohort of patients, the decreased AMPK-AKT-mTOR activation and phosphorylation of FOXO1 T24/FOXO3 T32 may help identify carboplatin-paclitaxel-resistant EOC patients. Paclitaxel 170-180 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 72-76 28445821-4 2017 Several derivatives of 5-aminoimidazole-4-carboxamide-1-beta-d-ribofuranoside (AICAR), an AMP-activated protein kinase (AMPK) activator, were identified as transcriptional activators of the DDT gene. acadesine 23-77 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 120-124 28445821-4 2017 Several derivatives of 5-aminoimidazole-4-carboxamide-1-beta-d-ribofuranoside (AICAR), an AMP-activated protein kinase (AMPK) activator, were identified as transcriptional activators of the DDT gene. acadesine 79-84 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 90-118 28445821-4 2017 Several derivatives of 5-aminoimidazole-4-carboxamide-1-beta-d-ribofuranoside (AICAR), an AMP-activated protein kinase (AMPK) activator, were identified as transcriptional activators of the DDT gene. acadesine 79-84 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 120-124 28545687-11 2017 Metformin and trametinib increased phosphorylated AMPK expression in LGSOC lines with combination showing stronger expression. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 50-54 28545687-11 2017 Metformin and trametinib increased phosphorylated AMPK expression in LGSOC lines with combination showing stronger expression. trametinib 14-24 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 50-54 28615457-0 2017 Deconvoluting AMP-activated protein kinase (AMPK) adenine nucleotide binding and sensing. Adenine Nucleotides 50-68 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-42 28615457-0 2017 Deconvoluting AMP-activated protein kinase (AMPK) adenine nucleotide binding and sensing. Adenine Nucleotides 50-68 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 44-48 28615457-2 2017 AMPK senses the ratio of adenine nucleotides (adenylate energy charge) by competitive binding of AMP, ADP, and ATP to three sites (CBS1, CBS3, and CBS4) in its gamma-subunit. Adenine Nucleotides 25-44 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 28615457-2 2017 AMPK senses the ratio of adenine nucleotides (adenylate energy charge) by competitive binding of AMP, ADP, and ATP to three sites (CBS1, CBS3, and CBS4) in its gamma-subunit. Adenosine Diphosphate 102-105 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 28615457-2 2017 AMPK senses the ratio of adenine nucleotides (adenylate energy charge) by competitive binding of AMP, ADP, and ATP to three sites (CBS1, CBS3, and CBS4) in its gamma-subunit. Adenosine Triphosphate 111-114 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 28615457-4 2017 Here, we comprehensively analyze nucleotide binding to wild-type and mutant AMPK protein complexes by quantitative competition assays and by hydrogen-deuterium exchange MS. We also demonstrate that NADPH, in addition to the known AMPK ligand NADH, directly and competitively binds AMPK at the AMP-sensing CBS3 site. Hydrogen 141-149 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 76-80 28615457-4 2017 Here, we comprehensively analyze nucleotide binding to wild-type and mutant AMPK protein complexes by quantitative competition assays and by hydrogen-deuterium exchange MS. We also demonstrate that NADPH, in addition to the known AMPK ligand NADH, directly and competitively binds AMPK at the AMP-sensing CBS3 site. Deuterium 150-159 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 76-80 28615457-4 2017 Here, we comprehensively analyze nucleotide binding to wild-type and mutant AMPK protein complexes by quantitative competition assays and by hydrogen-deuterium exchange MS. We also demonstrate that NADPH, in addition to the known AMPK ligand NADH, directly and competitively binds AMPK at the AMP-sensing CBS3 site. NADP 198-203 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 76-80 28615457-4 2017 Here, we comprehensively analyze nucleotide binding to wild-type and mutant AMPK protein complexes by quantitative competition assays and by hydrogen-deuterium exchange MS. We also demonstrate that NADPH, in addition to the known AMPK ligand NADH, directly and competitively binds AMPK at the AMP-sensing CBS3 site. NAD 242-246 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 76-80 28615457-4 2017 Here, we comprehensively analyze nucleotide binding to wild-type and mutant AMPK protein complexes by quantitative competition assays and by hydrogen-deuterium exchange MS. We also demonstrate that NADPH, in addition to the known AMPK ligand NADH, directly and competitively binds AMPK at the AMP-sensing CBS3 site. Adenosine Monophosphate 76-79 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 230-234 28615457-4 2017 Here, we comprehensively analyze nucleotide binding to wild-type and mutant AMPK protein complexes by quantitative competition assays and by hydrogen-deuterium exchange MS. We also demonstrate that NADPH, in addition to the known AMPK ligand NADH, directly and competitively binds AMPK at the AMP-sensing CBS3 site. Adenosine Monophosphate 76-79 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 230-234 28438603-1 2017 Activation of AMP-activated protein kinase (AMPK) could efficiently protect osteoblasts from dexamethasone (Dex). Dexamethasone 93-106 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 44-48 28744004-5 2017 Moreover, a Sirt1 activator resveratrol stimulated the inhibitory AMPK axis, with reciprocal suppression of the stimulatory PTP1B/Syk axis, thus potently inhibiting anaphylaxis. Resveratrol 28-39 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 66-70 28729704-8 2017 Exogenous GH administration led to a restoration of body weight and length and normalized serum triglycerides by reversing expression of AMPK-alpha1 and its targeted genes SREBP-1c and ACC-1, through increasing H3 acetylation at the promoter of AMPK-alpha1 in SGA in adult period. Triglycerides 96-109 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 137-148 28708087-0 2017 Resveratrol-Induced AMP-Activated Protein Kinase Activation Is Cell-Type Dependent: Lessons from Basic Research for Clinical Application. Resveratrol 0-11 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 20-48 28708087-2 2017 We were the first group to report that the SIRT1 activator resveratrol activates AMP-activated protein kinase (AMPK) (Diabetes 2005; 54: A383), and we think that the variability of this cascade may be responsible for the inconsistency of resveratrol"s effects. Resveratrol 59-70 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 81-109 28708087-2 2017 We were the first group to report that the SIRT1 activator resveratrol activates AMP-activated protein kinase (AMPK) (Diabetes 2005; 54: A383), and we think that the variability of this cascade may be responsible for the inconsistency of resveratrol"s effects. Resveratrol 59-70 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 111-115 28708087-2 2017 We were the first group to report that the SIRT1 activator resveratrol activates AMP-activated protein kinase (AMPK) (Diabetes 2005; 54: A383), and we think that the variability of this cascade may be responsible for the inconsistency of resveratrol"s effects. Resveratrol 238-249 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 81-109 28708087-2 2017 We were the first group to report that the SIRT1 activator resveratrol activates AMP-activated protein kinase (AMPK) (Diabetes 2005; 54: A383), and we think that the variability of this cascade may be responsible for the inconsistency of resveratrol"s effects. Resveratrol 238-249 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 111-115 28708087-3 2017 Our current studies suggest that the effect of SIRT1 activators such as resveratrol may not be solely through activation of SIRT1, but also through an integrated effect of SIRT1-liver kinase B1 (LKB1)-AMPK. Resveratrol 72-83 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 201-205 28708087-4 2017 In this context, resveratrol activates SIRT1 (1) by directly binding to SIRT1; and (2) by increasing NAD+ levels by upregulating the salvage pathway through Nampt activation, an effect mediated by AMPK. Resveratrol 17-28 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 197-201 28708087-7 2017 Despite these findings, detailed mechanisms of how resveratrol activates AMPK have not been reported. Resveratrol 51-62 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 73-77 28708087-9 2017 These results suggest that resveratrol-induced activation of AMPK is not a ubiquitous phenomenon. Resveratrol 27-38 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 61-65 28708087-10 2017 In addition, AMPK-mediated increases in NAD+ in the second mechanism require several ATPs, which may not be available in many pathological conditions. NAD 40-44 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 13-17 28708087-10 2017 In addition, AMPK-mediated increases in NAD+ in the second mechanism require several ATPs, which may not be available in many pathological conditions. Adenosine Triphosphate 85-89 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 13-17 28978086-0 2017 AMPK activation-dependent autophagy compromises oleanolic acid-induced cytotoxicity in human bladder cancer cells. Oleanolic Acid 48-62 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 28978086-5 2017 Moreover, inhibiting autophagy by siRNA to autophagy related 7 (ATG7) or with autophagy inhibitor bafilomycin A1 and 3-methyladenine (3-MA) or AMPK inhibitor dorsomorphin (compound C) promoted OA-induced deaths of bladder cancer cells. dorsomorphin 158-170 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 143-147 28978086-6 2017 In contrast, either autophagy activator rapamycin or AMPK activator acadesine (AICAR) compromised OA-induced anti-cancer effect. acadesine 68-77 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 53-57 28515121-8 2017 Finally, providing specific nutrients (galactose/glucose) to MuSCs directly controlled their fate through the AMPKalpha1/LDH pathway, emphasizing the importance of metabolism in stem cell fate. Galactose 39-48 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 110-120 28515121-8 2017 Finally, providing specific nutrients (galactose/glucose) to MuSCs directly controlled their fate through the AMPKalpha1/LDH pathway, emphasizing the importance of metabolism in stem cell fate. Glucose 49-56 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 110-120 28211632-0 2017 AMP-activated protein kinase (AMPK) activator A-769662 increases intracellular calcium and ATP release from astrocytes in an AMPK-independent manner. Calcium 79-86 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-28 28211632-0 2017 AMP-activated protein kinase (AMPK) activator A-769662 increases intracellular calcium and ATP release from astrocytes in an AMPK-independent manner. Calcium 79-86 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-34 28211632-0 2017 AMP-activated protein kinase (AMPK) activator A-769662 increases intracellular calcium and ATP release from astrocytes in an AMPK-independent manner. Adenosine Triphosphate 91-94 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-28 28211632-0 2017 AMP-activated protein kinase (AMPK) activator A-769662 increases intracellular calcium and ATP release from astrocytes in an AMPK-independent manner. Adenosine Triphosphate 91-94 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-34 28211632-1 2017 AIM: To test the hypothesis that, given the role of AMP-activated protein kinase (AMPK) in regulating intracellular ATP levels, AMPK may alter ATP release from astrocytes, the main sources of extracellular ATP (eATP) within the brain. Adenosine Triphosphate 116-119 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 52-80 28211632-1 2017 AIM: To test the hypothesis that, given the role of AMP-activated protein kinase (AMPK) in regulating intracellular ATP levels, AMPK may alter ATP release from astrocytes, the main sources of extracellular ATP (eATP) within the brain. Adenosine Triphosphate 116-119 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 82-86 28211632-1 2017 AIM: To test the hypothesis that, given the role of AMP-activated protein kinase (AMPK) in regulating intracellular ATP levels, AMPK may alter ATP release from astrocytes, the main sources of extracellular ATP (eATP) within the brain. Adenosine Triphosphate 143-146 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 128-132 28211632-1 2017 AIM: To test the hypothesis that, given the role of AMP-activated protein kinase (AMPK) in regulating intracellular ATP levels, AMPK may alter ATP release from astrocytes, the main sources of extracellular ATP (eATP) within the brain. Adenosine Triphosphate 143-146 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 128-132 28211632-1 2017 AIM: To test the hypothesis that, given the role of AMP-activated protein kinase (AMPK) in regulating intracellular ATP levels, AMPK may alter ATP release from astrocytes, the main sources of extracellular ATP (eATP) within the brain. eatp 211-215 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 128-132 28211632-6 2017 Only A-769662 increased eATP levels, and this was partially blocked by AMPK inhibitor Compound C. A-769662-induced increases in eATP were preserved in AMPK alpha1/alpha2 null MEF cells. eatp 128-132 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 71-75 28211632-6 2017 Only A-769662 increased eATP levels, and this was partially blocked by AMPK inhibitor Compound C. A-769662-induced increases in eATP were preserved in AMPK alpha1/alpha2 null MEF cells. eatp 128-132 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 151-162 28211632-10 2017 A-769662 (>50 muM) enhanced intracellular calcium levels leading to ATP release in an AMPK and purinergic receptor independent pathway. Calcium 45-52 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 89-93 28211632-10 2017 A-769662 (>50 muM) enhanced intracellular calcium levels leading to ATP release in an AMPK and purinergic receptor independent pathway. Adenosine Triphosphate 71-74 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 89-93 28137482-0 2017 Epigallocatechin-3-gallate (EGCG) activates AMPK through the inhibition of glutamate dehydrogenase in muscle and pancreatic ss-cells: A potential beneficial effect in the pre-diabetic state? epigallocatechin gallate 0-26 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 44-48 28137482-0 2017 Epigallocatechin-3-gallate (EGCG) activates AMPK through the inhibition of glutamate dehydrogenase in muscle and pancreatic ss-cells: A potential beneficial effect in the pre-diabetic state? epigallocatechin gallate 28-32 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 44-48 28137482-9 2017 Glutamine/BCH-induced lowering of AMPK phosphorylation did not operate in ssGlud1-/- islets and was similarly prevented by EGCG in control islets, while high glucose systematically inactivated AMPK. Glutamine 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 34-38 28137482-9 2017 Glutamine/BCH-induced lowering of AMPK phosphorylation did not operate in ssGlud1-/- islets and was similarly prevented by EGCG in control islets, while high glucose systematically inactivated AMPK. Glutamine 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 193-197 28137482-9 2017 Glutamine/BCH-induced lowering of AMPK phosphorylation did not operate in ssGlud1-/- islets and was similarly prevented by EGCG in control islets, while high glucose systematically inactivated AMPK. Glucose 158-165 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 193-197 28137482-10 2017 In mouse C2C12 myotubes, like in islets, the inhibition of AMPK following GDH activation with glutamine/BCH was reversed by EGCG. Glutamine 94-103 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 59-63 28137482-10 2017 In mouse C2C12 myotubes, like in islets, the inhibition of AMPK following GDH activation with glutamine/BCH was reversed by EGCG. epigallocatechin gallate 124-128 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 59-63 28659610-9 2017 In vitro incubation of VSMCs with the ARSB inhibitor L-ascorbic acid resulted in marked upregulation of SIRT1 and AMPK. vsmcs 23-28 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 114-118 28659610-9 2017 In vitro incubation of VSMCs with the ARSB inhibitor L-ascorbic acid resulted in marked upregulation of SIRT1 and AMPK. Ascorbic Acid 53-68 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 114-118 29029434-8 2017 Exogenous expression of miR-25-5p silenced PKCzeta to activate AMPK signaling, which inhibited HT-29 cell proliferation. mir-25-5p 24-33 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 63-67 28438603-1 2017 Activation of AMP-activated protein kinase (AMPK) could efficiently protect osteoblasts from dexamethasone (Dex). Dexamethasone 108-111 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 44-48 28526426-0 2017 The effects of troglitazone on AMPK in HepG2 cells. Troglitazone 15-27 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 31-35 28775788-0 2017 Berberine Enhances Chemosensitivity and Induces Apoptosis Through Dose-orchestrated AMPK Signaling in Breast Cancer. Berberine 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 84-88 28775788-4 2017 Berberine, known as AMPK activator, has shown multiple activities including antitumor effect. Berberine 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 20-24 28775788-5 2017 In this study, we investigate the chemosensitive effect of different dosages berberine on drug-resistant human breast cancer MCF-7/MDR cell in vitro and in vivo, and the mechanisms underlying AMPK activation on Doxorubicin (DOX) chemosensitivity. Berberine 77-86 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 192-196 28775788-5 2017 In this study, we investigate the chemosensitive effect of different dosages berberine on drug-resistant human breast cancer MCF-7/MDR cell in vitro and in vivo, and the mechanisms underlying AMPK activation on Doxorubicin (DOX) chemosensitivity. Doxorubicin 211-222 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 192-196 28775788-5 2017 In this study, we investigate the chemosensitive effect of different dosages berberine on drug-resistant human breast cancer MCF-7/MDR cell in vitro and in vivo, and the mechanisms underlying AMPK activation on Doxorubicin (DOX) chemosensitivity. Doxorubicin 224-227 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 192-196 28775788-6 2017 Our results showed that berberine could overcome DOX resistance in dose-orchestrated manner: On one hand, low-dose berberine can enhance DOX sensitivity in drug-resistance breast cancer cells through AMPK-HIF-1alpha-P-gp pathway. Berberine 24-33 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 200-204 28775788-6 2017 Our results showed that berberine could overcome DOX resistance in dose-orchestrated manner: On one hand, low-dose berberine can enhance DOX sensitivity in drug-resistance breast cancer cells through AMPK-HIF-1alpha-P-gp pathway. Berberine 115-124 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 200-204 28775788-6 2017 Our results showed that berberine could overcome DOX resistance in dose-orchestrated manner: On one hand, low-dose berberine can enhance DOX sensitivity in drug-resistance breast cancer cells through AMPK-HIF-1alpha-P-gp pathway. Doxorubicin 137-140 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 200-204 28775788-7 2017 On the other hand, high-dose berberine alone directly induces apoptosis through the AMPK-p53 pathway with the independence of HIF-1alpha expression. Berberine 29-38 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 84-88 28775788-8 2017 Taken together, our findings demonstrate that berberine sensitizes drug-resistant breast cancer to DOX chemotherapy and directly induces apoptosis through the dose-orchestrated AMPK signaling pathway in vitro and in vivo. Berberine 46-55 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 177-181 28526426-2 2017 Thiazolidinediones (TZDs) are a class of anti-diabetic drug known to activate AMPK through increased phosphorylation at Thr172, however there has been no research to date on whether they have any effect on inhibition of AMPK"s lesser known site of inhibition, Ser485/491. Thiazolidinediones 0-18 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 78-82 28526426-2 2017 Thiazolidinediones (TZDs) are a class of anti-diabetic drug known to activate AMPK through increased phosphorylation at Thr172, however there has been no research to date on whether they have any effect on inhibition of AMPK"s lesser known site of inhibition, Ser485/491. Thiazolidinediones 0-18 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 220-224 28526426-2 2017 Thiazolidinediones (TZDs) are a class of anti-diabetic drug known to activate AMPK through increased phosphorylation at Thr172, however there has been no research to date on whether they have any effect on inhibition of AMPK"s lesser known site of inhibition, Ser485/491. Thiazolidinediones 20-24 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 78-82 28526426-2 2017 Thiazolidinediones (TZDs) are a class of anti-diabetic drug known to activate AMPK through increased phosphorylation at Thr172, however there has been no research to date on whether they have any effect on inhibition of AMPK"s lesser known site of inhibition, Ser485/491. Thiazolidinediones 20-24 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 220-224 28526426-5 2017 Incubation with the other TZDs, rosiglitazone and pioglitazone, let to a minor increase in p-AMPK Ser485 phosphorylation as well as AMPK activity; however these findings were significantly less than those of troglitazone under equal conditions. Thiazolidinediones 26-30 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 93-97 28526426-5 2017 Incubation with the other TZDs, rosiglitazone and pioglitazone, let to a minor increase in p-AMPK Ser485 phosphorylation as well as AMPK activity; however these findings were significantly less than those of troglitazone under equal conditions. Thiazolidinediones 26-30 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 132-136 28526426-5 2017 Incubation with the other TZDs, rosiglitazone and pioglitazone, let to a minor increase in p-AMPK Ser485 phosphorylation as well as AMPK activity; however these findings were significantly less than those of troglitazone under equal conditions. Rosiglitazone 32-45 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 93-97 28526426-5 2017 Incubation with the other TZDs, rosiglitazone and pioglitazone, let to a minor increase in p-AMPK Ser485 phosphorylation as well as AMPK activity; however these findings were significantly less than those of troglitazone under equal conditions. Rosiglitazone 32-45 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 132-136 28526426-5 2017 Incubation with the other TZDs, rosiglitazone and pioglitazone, let to a minor increase in p-AMPK Ser485 phosphorylation as well as AMPK activity; however these findings were significantly less than those of troglitazone under equal conditions. Pioglitazone 50-62 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 93-97 28526426-5 2017 Incubation with the other TZDs, rosiglitazone and pioglitazone, let to a minor increase in p-AMPK Ser485 phosphorylation as well as AMPK activity; however these findings were significantly less than those of troglitazone under equal conditions. Pioglitazone 50-62 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 132-136 28526426-6 2017 These data suggest that the effects of troglitazone on AMPK are more complex than previously thought. Troglitazone 39-51 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 55-59 27864418-6 2017 Independent of mTOR signaling, activation of the AMPK (pThr172)/ULK1 (pSer555) pathway was found to be associated with JQ1-induced autophagy in resistant cells. pser555 70-77 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 49-53 28410530-0 2017 Metformin attenuated endotoxin-induced acute myocarditis via activating AMPK. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 72-76 28410530-5 2017 Treatment with metformin promoted the phosphorylation of the catalytic alpha subunit of adenosine 5"-monophosphate-activated protein kinase (AMPKalpha), co-administration of AMPK inhibitor suppressed the stimulatory effects of metformin on AMPKalpha phosphorylation. Metformin 15-24 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 141-145 28410530-5 2017 Treatment with metformin promoted the phosphorylation of the catalytic alpha subunit of adenosine 5"-monophosphate-activated protein kinase (AMPKalpha), co-administration of AMPK inhibitor suppressed the stimulatory effects of metformin on AMPKalpha phosphorylation. Metformin 227-236 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 141-145 28410530-6 2017 Meanwhile, the suppressive effects of metformin on MPO, TNF-alpha, CK-MB and BNP were reversed by the AMPK inhibitor. Metformin 38-47 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 102-106 28410530-7 2017 On the contrary, administration of AMPK activator mimicked the effects of metformin on AMPKalpha phosphorylation, MPO upregulation, CK-MB release and BNP elevation. Metformin 74-83 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 35-39 28410530-8 2017 These evidence suggested that metformin might provide beneficial effects in endotoxin-induced acute myocarditis via activating AMPK-dependent anti-inflammatory mechanism. Metformin 30-39 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 127-131 28656004-0 2017 Berberine Reverses Hypoxia-induced Chemoresistance in Breast Cancer through the Inhibition of AMPK- HIF-1alpha. Berberine 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 94-98 28656004-6 2017 We found that hypoxia increased DOX resistance on breast cancer cells with the AMPK activation. Doxorubicin 32-35 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 79-83 28656004-8 2017 The intriguing fact was that the protein expressions of AMPK and HIF-1alpha were down-regulated by berberine, either low dose or high dose. Berberine 99-108 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 56-60 28656004-9 2017 But the downstream of HIF-1alpha occurred the bifurcation dependent on the dosage of berberine: AMPK-HIF-1alpha-P-gp inactivation played a crucial role on the DOX chemosensitivity of low-dose berberine, while AMPK-HIF-1alpha downregulaton inducing p53 activation led to apoptosis in high-dose berberine. Berberine 85-94 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 96-100 28656004-9 2017 But the downstream of HIF-1alpha occurred the bifurcation dependent on the dosage of berberine: AMPK-HIF-1alpha-P-gp inactivation played a crucial role on the DOX chemosensitivity of low-dose berberine, while AMPK-HIF-1alpha downregulaton inducing p53 activation led to apoptosis in high-dose berberine. Berberine 85-94 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 209-213 28656004-9 2017 But the downstream of HIF-1alpha occurred the bifurcation dependent on the dosage of berberine: AMPK-HIF-1alpha-P-gp inactivation played a crucial role on the DOX chemosensitivity of low-dose berberine, while AMPK-HIF-1alpha downregulaton inducing p53 activation led to apoptosis in high-dose berberine. Doxorubicin 159-162 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 96-100 28656004-9 2017 But the downstream of HIF-1alpha occurred the bifurcation dependent on the dosage of berberine: AMPK-HIF-1alpha-P-gp inactivation played a crucial role on the DOX chemosensitivity of low-dose berberine, while AMPK-HIF-1alpha downregulaton inducing p53 activation led to apoptosis in high-dose berberine. Doxorubicin 159-162 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 209-213 28656004-9 2017 But the downstream of HIF-1alpha occurred the bifurcation dependent on the dosage of berberine: AMPK-HIF-1alpha-P-gp inactivation played a crucial role on the DOX chemosensitivity of low-dose berberine, while AMPK-HIF-1alpha downregulaton inducing p53 activation led to apoptosis in high-dose berberine. Berberine 192-201 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 96-100 28656004-9 2017 But the downstream of HIF-1alpha occurred the bifurcation dependent on the dosage of berberine: AMPK-HIF-1alpha-P-gp inactivation played a crucial role on the DOX chemosensitivity of low-dose berberine, while AMPK-HIF-1alpha downregulaton inducing p53 activation led to apoptosis in high-dose berberine. Berberine 192-201 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 96-100 28487951-0 2017 Berberine activates AMPK to suppress proteolytic processing, nuclear translocation and target DNA binding of SREBP-1c in 3T3-L1 adipocytes. Berberine 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 20-24 28487951-2 2017 In the present study, the fat-reducing mechanisms of berberine (BBR), a natural isoquinoline, was investigated by examining the AMPK-mediated modulation of SREBP-1c in 3T3-L1 adipocytes. Berberine 53-62 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 128-132 28487951-2 2017 In the present study, the fat-reducing mechanisms of berberine (BBR), a natural isoquinoline, was investigated by examining the AMPK-mediated modulation of SREBP-1c in 3T3-L1 adipocytes. Berberine 64-67 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 128-132 28487951-5 2017 Transfection with AMPKalpha1 siRNA, and not control siRNA, inhibited BBR-induced phosphorylation of the 125-kDa SREBP-1c, which confirmed that AMPK was responsible for phosphorylating SREBP-1c. Berberine 69-72 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 18-28 28487951-5 2017 Transfection with AMPKalpha1 siRNA, and not control siRNA, inhibited BBR-induced phosphorylation of the 125-kDa SREBP-1c, which confirmed that AMPK was responsible for phosphorylating SREBP-1c. Berberine 69-72 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 18-22 28487951-7 2017 In addition, BBR-induced suppression of lipogenic gene expression and intracellular fat accumulation were rescued by AMPKalpha1 siRNA transfection. Berberine 13-16 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 117-127 28487951-8 2017 In conclusion, the results of the present study demonstrate that BBR activates AMPK to induce phosphorylation of SREBP-1c, thereby suppressing proteolytic processing, nuclear translocation and target DNA binding of SREBP-1c, which leads to a reduction in lipogenic gene expression and intracellular fat accumulation. Berberine 65-68 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 79-83 28553939-4 2017 LKB1 recruits AMPK to the E-cadherin mechanotransduction complex, thereby stimulating actomyosin contractility, glucose uptake and ATP production. Glucose 112-119 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-18 28553939-4 2017 LKB1 recruits AMPK to the E-cadherin mechanotransduction complex, thereby stimulating actomyosin contractility, glucose uptake and ATP production. Adenosine Triphosphate 131-134 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-18 28561066-1 2017 Autophagy is controlled by AMPK and mTOR, both of which associate with ULK1 and control the production of phosphatidylinositol 3-phosphate (PtdIns3P), a prerequisite for autophagosome formation. phosphatidylinositol 3-phosphate 106-138 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 27-31 28561066-1 2017 Autophagy is controlled by AMPK and mTOR, both of which associate with ULK1 and control the production of phosphatidylinositol 3-phosphate (PtdIns3P), a prerequisite for autophagosome formation. phosphatidylinositol 3-phosphate 140-148 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 27-31 28427181-0 2017 Metformin inhibits ALK1-mediated angiogenesis via activation of AMPK. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 64-68 28427181-4 2017 Thus, we treated human umbilical vein endothelial cells with metformin as well as other pharmacological AMPK activators and showed that activation of AMPK inhibited Smad1/5 phosphorylation and tube formation induced by BMP9. Metformin 61-70 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 150-154 28427181-12 2017 This may offer us a new avenue for the treatment of related diseases using clinically used pharmacological AMPK activators like metformin in combination with other strategies to enhance the treatment efficacy or in the case of anti-VEGF resistance. Metformin 128-137 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 107-111 29069736-0 2017 A novel synthetic derivative of quercetin, 8-trifluoromethyl-3,5,7,3",4"-O-pentamethyl-quercetin, inhibits bladder cancer growth by targeting the AMPK/mTOR signaling pathway. Quercetin 32-41 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 146-150 29069736-0 2017 A novel synthetic derivative of quercetin, 8-trifluoromethyl-3,5,7,3",4"-O-pentamethyl-quercetin, inhibits bladder cancer growth by targeting the AMPK/mTOR signaling pathway. 8-trifluoromethyl-3,5,7,3",4"-o-pentamethyl-quercetin 43-96 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 146-150 29069736-3 2017 In our previous study, we elucidated that quercetin activates AMPK pathway which is the major mechanism for its unique anticancer effect in bladder cancer. Quercetin 42-51 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 62-66 29069736-8 2017 Western blot analysis showed that TFQ possess more potent AMPK activation than Que. 4-(2,2,2-TRIFLUOROETHYL)-L-PHENYLALANINE 34-37 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 58-62 29069736-11 2017 These results demonstrated that the fluorinated quercetin derivative TFQ inhibits bladder cancer cell growth through the AMPK/mTOR pathway. Quercetin 48-57 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 121-125 29069736-11 2017 These results demonstrated that the fluorinated quercetin derivative TFQ inhibits bladder cancer cell growth through the AMPK/mTOR pathway. 4-(2,2,2-TRIFLUOROETHYL)-L-PHENYLALANINE 69-72 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 121-125 28137648-6 2017 Treatment with rosuvastatin alone increased the levels of mTOR-independent/upstream autophagy markers, including Beclin-1 and AMPK. Rosuvastatin Calcium 15-27 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 126-130 28315455-7 2017 While 7,8-DHF treatment and exercise individually mitigated TBI-induced effects, administration of 7,8-DHF concurrently with exercise facilitated memory performance and augmented levels of markers of cell energy metabolism viz., PGC-1alpha, COII and AMPK. 6,7-dihydroxyflavone 99-106 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 250-254 28473727-0 2017 Cryptolepine inhibits melanoma cell growth through coordinated changes in mitochondrial biogenesis, dynamics and metabolic tumor suppressor AMPKalpha1/2-LKB1. cryptolepine 0-12 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 140-150 28473727-5 2017 A decrease in the levels of ATP and mitochondrial mass were associated with activation of the metabolic tumor suppressor AMPKalpha1/2-LKB1, and a reduction in mTOR signaling. Adenosine Triphosphate 28-31 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 121-131 28299793-0 2017 FoxO1-AMPK-ULK1 Regulates Ethanol-Induced Autophagy in Muscle by Enhanced ATG14 Association with the BECN1-PIK3C3 Complex. Ethanol 26-33 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 6-10 28299793-2 2017 EtOH impairs protein synthesis in C2C12 myoblasts via a FoxO1-AMPK-TSC2-mTORC1 pathway and also induces protein degradation. Ethanol 0-4 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 62-66 28299793-3 2017 As the underlying regulatory signaling cascades for these processes are currently poorly defined, we tested the hypothesis that alcohol-induced autophagy is mediated via activation of the PIK3C3 complex that is regulated by FoxO1-AMPK. Alcohols 128-135 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 230-234 28299793-8 2017 EtOH altered ULK1 S555 and S757 phosphorylation in a time- and AMPK-dependent manner. Ethanol 0-4 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 63-67 28299793-12 2017 Reduction of AMPK using siRNA suppressed the stimulatory effect of EtOH on BECN1 S93, BECN1 S14, and PIK3C3 S164 phosphorylation in a time-dependent manner. Ethanol 67-71 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 13-17 28238946-0 2017 Involvement of pregnane X receptor in the suppression of carboxylesterases by metformin in vivo and in vitro, mediated by the activation of AMPK and JNK signaling pathway. Metformin 78-87 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 140-144 28238946-7 2017 Furthermore, metformin significantly suppresses the phosphorylation of AMPK and JNK, and the suppression of carboxylesterases induced by metformin is repeatedly abolished by AMPK inhibitor Compound C and JNK inhibitor SP600125. Metformin 13-22 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 71-75 28238946-7 2017 Furthermore, metformin significantly suppresses the phosphorylation of AMPK and JNK, and the suppression of carboxylesterases induced by metformin is repeatedly abolished by AMPK inhibitor Compound C and JNK inhibitor SP600125. Metformin 13-22 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 174-178 28238946-7 2017 Furthermore, metformin significantly suppresses the phosphorylation of AMPK and JNK, and the suppression of carboxylesterases induced by metformin is repeatedly abolished by AMPK inhibitor Compound C and JNK inhibitor SP600125. Metformin 137-146 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 71-75 28238946-7 2017 Furthermore, metformin significantly suppresses the phosphorylation of AMPK and JNK, and the suppression of carboxylesterases induced by metformin is repeatedly abolished by AMPK inhibitor Compound C and JNK inhibitor SP600125. Metformin 137-146 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 174-178 28238946-7 2017 Furthermore, metformin significantly suppresses the phosphorylation of AMPK and JNK, and the suppression of carboxylesterases induced by metformin is repeatedly abolished by AMPK inhibitor Compound C and JNK inhibitor SP600125. pyrazolanthrone 218-226 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 71-75 28238946-7 2017 Furthermore, metformin significantly suppresses the phosphorylation of AMPK and JNK, and the suppression of carboxylesterases induced by metformin is repeatedly abolished by AMPK inhibitor Compound C and JNK inhibitor SP600125. pyrazolanthrone 218-226 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 174-178 28238946-8 2017 It implies that the activation of AMPK and JNK pathways mediates the suppression of carboxylesterases by metformin. Metformin 105-114 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 34-38 28565878-5 2017 The results indicated that 25 microM ginsenoside Rb3 significantly activated AMPK activity, increased the ratio of p-AMPK/total-AMPK, and had synergistic effects with the activator of AICAR on the activation of AMPK. AICA ribonucleotide 184-189 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 117-121 28565878-5 2017 The results indicated that 25 microM ginsenoside Rb3 significantly activated AMPK activity, increased the ratio of p-AMPK/total-AMPK, and had synergistic effects with the activator of AICAR on the activation of AMPK. AICA ribonucleotide 184-189 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 117-121 28565878-5 2017 The results indicated that 25 microM ginsenoside Rb3 significantly activated AMPK activity, increased the ratio of p-AMPK/total-AMPK, and had synergistic effects with the activator of AICAR on the activation of AMPK. AICA ribonucleotide 184-189 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 117-121 27775072-4 2017 Metformin acts by upregulating microRNA let-7 through AMPK activation, leading to degradation of H19 long noncoding RNA, which normally binds to and inactivates SAHH. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 54-58 28197628-0 2017 Resveratrol-induced autophagy and apoptosis in cisplatin-resistant human oral cancer CAR cells: A key role of AMPK and Akt/mTOR signaling. Resveratrol 0-11 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 110-114 28389629-0 2017 Inhibition of p70 S6 kinase (S6K1) activity by A77 1726, the active metabolite of leflunomide, induces autophagy through TAK1-mediated AMPK and JNK activation. Leflunomide 82-93 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 135-139 28404910-0 2017 Thalidezine, a novel AMPK activator, eliminates apoptosis-resistant cancer cells through energy-mediated autophagic cell death. THALIDEZINE 0-11 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 21-25 28404910-6 2017 Here, we unravelled that the bisbenzylisoquinoline alkaloid thalidezine is a novel direct AMPK activator by using biolayer interferometry analysis and AMPK kinase assays. bisbenzylisoquinoline alkaloid 29-59 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 90-94 28404910-6 2017 Here, we unravelled that the bisbenzylisoquinoline alkaloid thalidezine is a novel direct AMPK activator by using biolayer interferometry analysis and AMPK kinase assays. bisbenzylisoquinoline alkaloid 29-59 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 151-155 28404910-6 2017 Here, we unravelled that the bisbenzylisoquinoline alkaloid thalidezine is a novel direct AMPK activator by using biolayer interferometry analysis and AMPK kinase assays. THALIDEZINE 60-71 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 90-94 28404910-6 2017 Here, we unravelled that the bisbenzylisoquinoline alkaloid thalidezine is a novel direct AMPK activator by using biolayer interferometry analysis and AMPK kinase assays. THALIDEZINE 60-71 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 151-155 28404910-9 2017 Remarkably, thalidezine-induced autophagic cell death in HeLa or apoptosis-resistant DLD-1 BAX-BAK DKO cancer cells was abolished by addition of autophagy inhibitor (3-MA) and AMPK inhibitor (compound C). THALIDEZINE 12-23 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 176-180 28404910-11 2017 Overall, thalidezine is a novel AMPK activator which has great potential to be further developed into a safe and effective intervention for apoptosis- or multidrug-resistant cancers. THALIDEZINE 9-20 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 32-36 28915708-6 2017 Metformin, a well-tolerated anti-diabetic agent, which blocks mitochondria oxidative phosphorylation complex I, became the poster child agent to elicit AMPK activity and tumor suppression. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 152-156 28423712-0 2017 Model-based unsupervised learning informs metformin-induced cell-migration inhibition through an AMPK-independent mechanism in breast cancer. Metformin 42-51 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 97-101 28423712-6 2017 Our functional studies showed that CDC42 was involved in metformin-induced inhibition of cell proliferation and cell migration mediated through an AMPK-independent mechanism. Metformin 57-66 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 147-151 28423712-7 2017 Our results points to 230 genes that might serve as metformin response signatures, which needs to be tested in patients treated with metformin and, further investigation of CDC42 and AMPK-independence"s role in metformin"s anticancer mechanisms. Metformin 52-61 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 183-187 28345916-4 2017 Here, we have performed extensive all-atom molecular dynamics (MD) simulations and shown that the kinase domain (KD) and gamma-subunit come closer resulting in a more compact heterotrimeric AMPK complex in AMP-bound state compared to the ATP-bound state. Adenosine Triphosphate 238-241 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 190-194 28345916-5 2017 The binding of ATP at site 3 of regulatory gamma-subunit allosterically inhibits AMPK by destabilizing different regulatory regions of alpha-subunit: the autoinhibitory domain, the linker region, and the activation loop of the kinase core. Adenosine Triphosphate 15-18 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 81-85 28186975-6 2017 Elastase injection was performed to induce mouse emphysema, and these mice were treated with a specific AMPK activator metformin as well as Compound C. AICAR reduced, whereas Compound C increased CSE-induced increase in IL-8 and IL-6 release and expression of genes involved in cellular senescence. Metformin 119-128 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 104-108 28186975-8 2017 Prophylactic administration of an AMPK activator metformin (50 and 250 mg/kg) reduced while Compound C (4 and 20 mg/kg) aggravated elastase-induced airspace enlargement, inflammatory responses and cellular senescence in mice. Metformin 49-58 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 34-38 28213467-6 2017 Hypoxia is a recognized activator of AMPK, which is known to be expressed in human PASMCs (hPASMCs). pasmcs 83-89 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 37-41 28213467-7 2017 Activation of AMPK by hypoxia has been shown to promote cell survival in PASMCs. pasmcs 73-79 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-18 28358365-0 2017 Madecassic acid, the contributor to the anti-colitis effect of madecassoside, enhances the shift of Th17 toward Treg cells via the PPARgamma/AMPK/ACC1 pathway. madecassic acid 0-15 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 141-145 28358365-0 2017 Madecassic acid, the contributor to the anti-colitis effect of madecassoside, enhances the shift of Th17 toward Treg cells via the PPARgamma/AMPK/ACC1 pathway. madecassoside 63-76 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 141-145 28358365-8 2017 Both compound C and AMPK siRNA inhibited the madecassic acid-mediated downregulation of ACC1 expression and shift of Th17 cells to Treg cells under Th17-polarizing conditions. madecassic acid 45-60 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 20-24 28358365-9 2017 GW9662, T0070907 and PPARgamma siRNA blocked the effect of madecassic acid on AMPK activation, ACC1 expression and shift of Th17 cells to Treg cells. 2-chloro-5-nitrobenzanilide 0-6 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 78-82 28358365-9 2017 GW9662, T0070907 and PPARgamma siRNA blocked the effect of madecassic acid on AMPK activation, ACC1 expression and shift of Th17 cells to Treg cells. madecassic acid 59-74 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 78-82 28358365-12 2017 In conclusion, madecassic acid was the active form of madecassoside in ameliorating colitis by restoring the Th17/Treg balance via regulating the PPARgamma/AMPK/ACC1 pathway. madecassic acid 15-30 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 156-160 28358365-12 2017 In conclusion, madecassic acid was the active form of madecassoside in ameliorating colitis by restoring the Th17/Treg balance via regulating the PPARgamma/AMPK/ACC1 pathway. madecassoside 54-67 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 156-160 28407688-7 2017 ROS scavengers (NAC or MnTBAP) and mPTP blockers (cyclosporin A or sanglifehrin A) blocked NPC-26-induced AMPK activation and attenuated CRC cell death. Reactive Oxygen Species 0-3 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 106-110 28407688-7 2017 ROS scavengers (NAC or MnTBAP) and mPTP blockers (cyclosporin A or sanglifehrin A) blocked NPC-26-induced AMPK activation and attenuated CRC cell death. Cyclosporine 50-63 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 106-110 28407688-7 2017 ROS scavengers (NAC or MnTBAP) and mPTP blockers (cyclosporin A or sanglifehrin A) blocked NPC-26-induced AMPK activation and attenuated CRC cell death. sanglifehrin A 67-81 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 106-110 28161641-0 2017 Neferine reduces cisplatin-induced nephrotoxicity by enhancing autophagy via the AMPK/mTOR signaling pathway. neferine 0-8 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 81-85 28161641-0 2017 Neferine reduces cisplatin-induced nephrotoxicity by enhancing autophagy via the AMPK/mTOR signaling pathway. Cisplatin 17-26 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 81-85 28161641-6 2017 Furthermore, neferine pretreatment activated the AMPK/mTOR pathway; however, pharmacological inhibition of AMPK abolished neferine-mediated autophagy and nephroprotection against cisplatin-induced apoptosis. neferine 13-21 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 49-53 28161641-6 2017 Furthermore, neferine pretreatment activated the AMPK/mTOR pathway; however, pharmacological inhibition of AMPK abolished neferine-mediated autophagy and nephroprotection against cisplatin-induced apoptosis. neferine 122-130 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 107-111 28161641-6 2017 Furthermore, neferine pretreatment activated the AMPK/mTOR pathway; however, pharmacological inhibition of AMPK abolished neferine-mediated autophagy and nephroprotection against cisplatin-induced apoptosis. Cisplatin 179-188 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 107-111 28424433-3 2017 Ceramide synthase 5 (LASS5 or CERS5) gene has function in de novo synthesis of ceramide, and has indirect effect on AMPK gene. Ceramides 79-87 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 116-120 28103582-0 2017 AMPK-autophagy inhibition sensitizes icaritin-induced anti-colorectal cancer cell activity. icaritin 37-45 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 28197628-6 2017 These inhibitors of PI3K class III (3-MA) and AMP-activated protein kinase (AMPK) (compound c) suppressed the autophagic vesicle formation, LC3-II protein levels and autophagy induced by resveratrol. Resveratrol 187-198 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 46-74 28197628-6 2017 These inhibitors of PI3K class III (3-MA) and AMP-activated protein kinase (AMPK) (compound c) suppressed the autophagic vesicle formation, LC3-II protein levels and autophagy induced by resveratrol. Resveratrol 187-198 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 76-80 28197628-8 2017 Resveratrol also enhanced phosphorylation of AMPK and regulated autophagy- and pro-apoptosis-related signals in resveratrol-treated CAR cells. Resveratrol 0-11 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 45-49 28209925-4 2017 Accumulating evidence since has shown that pharmacologic activation of AMPK by Metformin protects the epithelial barrier against multiple environmental and pathological stressful states and suppresses tumorigenesis. Metformin 79-88 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 71-75 28209925-7 2017 Here we review the fundamentals of this specialized signaling pathway that buttresses cell-cell junctions against stress-induced collapse and discuss its pathophysiologic relevance in the context of a variety of diseases, including cancers, diabetes, aging, and the growing list of beneficial effects of the AMPK-activator, Metformin. Metformin 324-333 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 308-312 28337254-4 2017 In times of energy deficit, AMPK is allosterically modified by the binding of increased levels of AMP and ADP, making it a target of specific AMPK kinases (AMPKKs). Adenosine Monophosphate 28-31 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 142-146 28337254-4 2017 In times of energy deficit, AMPK is allosterically modified by the binding of increased levels of AMP and ADP, making it a target of specific AMPK kinases (AMPKKs). Adenosine Diphosphate 106-109 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 28-32 28337254-4 2017 In times of energy deficit, AMPK is allosterically modified by the binding of increased levels of AMP and ADP, making it a target of specific AMPK kinases (AMPKKs). Adenosine Diphosphate 106-109 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 142-146 28337254-8 2017 Biguanides can be used to activate AMPK, but AMPK activity is modified by many different interacting factors; understanding these factors is important in order to control the abnormal growth processes that lead to breast cancer neoplasia. Biguanides 0-10 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 35-39 28337254-9 2017 Fatty acids, estrogens, androgens, adipokines, and another energy sensor, sirtuin-1, alter the phosphorylation and activation of AMPK. Fatty Acids 0-11 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 129-133 28103582-5 2017 Icaritin activated AMP-activated protein kinase (AMPK) signaling in CRC cells, functioning as the upstream signaling for autophagy activation. icaritin 0-8 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 19-47 28103582-5 2017 Icaritin activated AMP-activated protein kinase (AMPK) signaling in CRC cells, functioning as the upstream signaling for autophagy activation. icaritin 0-8 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 49-53 28103582-6 2017 shRNA/siRNA-mediated knockdown of AMPKalpha1inhibited icaritin-induced autophagy activation, but exacerbated CRC cell death. icaritin 54-62 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 34-44 28103582-7 2017 On the other hand, the AMPK activator compound 13 (C13) or the autophagy activator MHY1485 attenuated icaritin-induced cytotoxicity. icaritin 102-110 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 23-27 28103582-9 2017 We conclude that feedback activation of AMPK-autophagy pathway could be a primary resistance factor of icaritin. icaritin 103-111 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 40-44 28063518-7 2017 Finally, the individual administration of berberine, quercetin, ferulic acid, and tyrosol resulted in a statistically significant increase in AMPK activation and mTOR inhibition, whereas their associated administration did not reveal a synergistic effect. Berberine 42-51 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 142-146 28063518-7 2017 Finally, the individual administration of berberine, quercetin, ferulic acid, and tyrosol resulted in a statistically significant increase in AMPK activation and mTOR inhibition, whereas their associated administration did not reveal a synergistic effect. Quercetin 53-62 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 142-146 28063518-7 2017 Finally, the individual administration of berberine, quercetin, ferulic acid, and tyrosol resulted in a statistically significant increase in AMPK activation and mTOR inhibition, whereas their associated administration did not reveal a synergistic effect. ferulic acid 64-76 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 142-146 28063518-7 2017 Finally, the individual administration of berberine, quercetin, ferulic acid, and tyrosol resulted in a statistically significant increase in AMPK activation and mTOR inhibition, whereas their associated administration did not reveal a synergistic effect. 4-hydroxyphenylethanol 82-89 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 142-146 28117414-0 2017 Piperine regulates UCP1 through the AMPK pathway by generating intracellular lactate production in muscle cells. piperine 0-8 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 36-40 28117414-0 2017 Piperine regulates UCP1 through the AMPK pathway by generating intracellular lactate production in muscle cells. Lactic Acid 77-84 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 36-40 28117414-3 2017 Piperine also induced the phosphorylation of AMP-activated protein kinase (AMPK) and its downstream target, acetyl-CoA carboxylase (ACC), while additionally stimulating glucose uptake in an AMPK dependent manner. piperine 0-8 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 45-73 28117414-3 2017 Piperine also induced the phosphorylation of AMP-activated protein kinase (AMPK) and its downstream target, acetyl-CoA carboxylase (ACC), while additionally stimulating glucose uptake in an AMPK dependent manner. piperine 0-8 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 75-79 28117414-3 2017 Piperine also induced the phosphorylation of AMP-activated protein kinase (AMPK) and its downstream target, acetyl-CoA carboxylase (ACC), while additionally stimulating glucose uptake in an AMPK dependent manner. piperine 0-8 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 190-194 28117414-3 2017 Piperine also induced the phosphorylation of AMP-activated protein kinase (AMPK) and its downstream target, acetyl-CoA carboxylase (ACC), while additionally stimulating glucose uptake in an AMPK dependent manner. Glucose 169-176 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 190-194 28117414-4 2017 Piperine also stimulates the p38 mitogen-activated protein kinase (p38 MAPK), an effect that was reversed by pretreatment with compound C, an AMPK inhibitor. piperine 0-8 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 142-146 28117414-7 2017 Knock-down of AMPK blocked piperine-induced UCP1 up-regulation, demonstrating the required role of AMPK in this effect. piperine 27-35 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-18 28117414-7 2017 Knock-down of AMPK blocked piperine-induced UCP1 up-regulation, demonstrating the required role of AMPK in this effect. piperine 27-35 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 99-103 28117414-8 2017 Taken together, these results suggest that piperine leads to benign metabolic effects by activating the AMPK-p38 MAPK signaling pathway and UCP1 expression by activating intracellular lactate production in skeletal muscle. piperine 43-51 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 104-108 27914812-0 2017 Protective effects of gomisin N against hepatic steatosis through AMPK activation. schizandrin B 22-31 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 66-70 27914812-4 2017 In this study, we examined whether GN activates AMP-activated protein kinase (AMPK) and exerts therapeutic effects on liver X receptor (LXR)- or palmitic acid (PA)-induced triglyceride (TG) accumulation in HepG2 cells. schizandrin B 35-37 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 48-76 27914812-4 2017 In this study, we examined whether GN activates AMP-activated protein kinase (AMPK) and exerts therapeutic effects on liver X receptor (LXR)- or palmitic acid (PA)-induced triglyceride (TG) accumulation in HepG2 cells. schizandrin B 35-37 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 78-82 27914812-6 2017 GN stimulated the phosphorylation of AMPK, acetyl-CoA carboxylase (ACC), and sterol regulatory element-binding protein 1c (SREBP1c) in HepG2 cells. schizandrin B 0-2 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 37-41 27914812-9 2017 However, preincubation with compound C, an AMPK inhibitor, prevented GN-mediated effects. schizandrin B 69-71 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 43-47 27914812-11 2017 These findings demonstrate that GN activates the AMPK pathway and ameliorates HFD-induced hepatic steatosis. schizandrin B 32-34 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 49-53 28065882-0 2017 Rescue of mutant rhodopsin traffic by metformin-induced AMPK activation accelerates photoreceptor degeneration. Metformin 38-47 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 56-60 28065882-2 2017 Here, we tested whether the AMPK activator metformin could affect the P23H rhodopsin synthesis and folding. Metformin 43-52 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 28-32 27856330-0 2017 Metformin suppresses adipogenesis through both AMP-activated protein kinase (AMPK)-dependent and AMPK-independent mechanisms. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 47-75 28174693-4 2017 Among the treatments tested, AMPK-activating 5-aminoimidazole-4-carboxamide-ribonucleoside (AICAR) induced monoubiquitination and nuclear foci formation of FANCD2, which are biomarkers of FANCD2 activation. acadesine 45-90 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 29-33 28174693-4 2017 Among the treatments tested, AMPK-activating 5-aminoimidazole-4-carboxamide-ribonucleoside (AICAR) induced monoubiquitination and nuclear foci formation of FANCD2, which are biomarkers of FANCD2 activation. acadesine 92-97 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 29-33 27871897-0 2017 Sauchinone exerts anticancer effects by targeting AMPK signaling in hepatocellular carcinoma cells. sauchinone 0-10 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 50-54 27871897-10 2017 In addition, sauchinone induced the activation of the AMP-activated protein kinase (AMPK) pathway, and compound C (an AMPK inhibitor) blocked the sauchinone-induced mitochondrial dysfunction. sauchinone 13-23 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 54-82 27871897-10 2017 In addition, sauchinone induced the activation of the AMP-activated protein kinase (AMPK) pathway, and compound C (an AMPK inhibitor) blocked the sauchinone-induced mitochondrial dysfunction. sauchinone 13-23 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 84-88 27871897-10 2017 In addition, sauchinone induced the activation of the AMP-activated protein kinase (AMPK) pathway, and compound C (an AMPK inhibitor) blocked the sauchinone-induced mitochondrial dysfunction. sauchinone 146-156 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 118-122 27871897-11 2017 The AMPK activation by sauchinone inhibited the phosphorylation of the mammalian target of rapamycin (mTOR) and its downstream targets, such as ribosomal protein S6 kinase 1 and eIF4E-binding protein 1. sauchinone 23-33 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 4-8 27871897-13 2017 These results provide evidence for sauchinone to be considered as a potent anticancer agent by targeting of the AMPK-mTOR pathway in HCC. sauchinone 35-45 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 112-116 27887947-0 2017 Berberine enhances the AMPK activation and autophagy and mitigates high glucose-induced apoptosis of mouse podocytes. Berberine 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 23-27 27887947-5 2017 Berberine significantly increased the AMPK activation and mitigated high glucose and/or the AMPK inhibitor, compound C-mediated mTOR activation and apoptosis in podocytes. Berberine 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 38-42 27887947-5 2017 Berberine significantly increased the AMPK activation and mitigated high glucose and/or the AMPK inhibitor, compound C-mediated mTOR activation and apoptosis in podocytes. Berberine 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 92-96 27887947-6 2017 Berberine significantly enhanced the AMPK activation and protected from high glucose-induced apoptosis in the AMPK-silencing podocytes. Berberine 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 37-41 27887947-6 2017 Berberine significantly enhanced the AMPK activation and protected from high glucose-induced apoptosis in the AMPK-silencing podocytes. Berberine 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 110-114 27887947-6 2017 Berberine significantly enhanced the AMPK activation and protected from high glucose-induced apoptosis in the AMPK-silencing podocytes. Glucose 77-84 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 110-114 27887947-10 2017 Collectively, berberine enhanced autophagy and protected from high glucose-induced injury in podocytes by promoting the AMPK activation. Berberine 14-23 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 120-124 27196129-7 2017 Furthermore, the anti-invasive activity of arvanil, olvanil and capsaicin was mediated by the AMPK pathway. arvanil 43-50 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 94-98 27196129-7 2017 Furthermore, the anti-invasive activity of arvanil, olvanil and capsaicin was mediated by the AMPK pathway. olvanil 52-59 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 94-98 27196129-7 2017 Furthermore, the anti-invasive activity of arvanil, olvanil and capsaicin was mediated by the AMPK pathway. Capsaicin 64-73 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 94-98 27196129-8 2017 Depletion of AMPK levels by siRNA methodology abrogated the anti-invasive activity of arvanil, olvanil and capsaicin. arvanil 86-93 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 13-17 27196129-8 2017 Depletion of AMPK levels by siRNA methodology abrogated the anti-invasive activity of arvanil, olvanil and capsaicin. olvanil 95-102 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 13-17 27196129-8 2017 Depletion of AMPK levels by siRNA methodology abrogated the anti-invasive activity of arvanil, olvanil and capsaicin. Capsaicin 107-116 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 13-17 27694908-6 2017 In SH-SY5Y cells, THAlpha (1, 10, 20 mug/mL) significantly stimulated PI3K/AKT/mTOR and AMPK/raptor/mTOR signaling-mediated autophagy in the promotion of Abeta clearance as both a PI3K inhibitor and an AMPK indirect activator, and restrained Abeta production as a suppressor against PERK/eIF2alpha-mediated BACE1 expression. thalpha 18-25 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 88-92 27694908-6 2017 In SH-SY5Y cells, THAlpha (1, 10, 20 mug/mL) significantly stimulated PI3K/AKT/mTOR and AMPK/raptor/mTOR signaling-mediated autophagy in the promotion of Abeta clearance as both a PI3K inhibitor and an AMPK indirect activator, and restrained Abeta production as a suppressor against PERK/eIF2alpha-mediated BACE1 expression. thalpha 18-25 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 202-206 28848135-0 2017 Adiponectin Inhibits TNF-alpha-Activated PAI-1 Expression Via the cAMP-PKA-AMPK-NF-kappaB Axis in Human Umbilical Vein Endothelial Cells. Cyclic AMP 66-70 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 75-79 28848135-5 2017 RESULTS: Adp decreased the TNF-alpha-induced upregulation of PAI-1 mRNA and protein expression and suppressed TNF-alpha-induced cAMP-PKA-AMPK inactivation. Cyclic AMP 128-132 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 137-141 28848135-8 2017 CONCLUSIONS: Our data suggest that Adp abrogates TNF-alpha-activated PAI-1 expression by activating cAMP-PKA-AMPK signaling to suppress NF-kB binding to the PAI-1 promoter in HUVECs. Cyclic AMP 100-104 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 109-113 27856330-0 2017 Metformin suppresses adipogenesis through both AMP-activated protein kinase (AMPK)-dependent and AMPK-independent mechanisms. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 77-81 27856330-0 2017 Metformin suppresses adipogenesis through both AMP-activated protein kinase (AMPK)-dependent and AMPK-independent mechanisms. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 97-101 27856330-4 2017 Here we investigate the involvement of the metabolic enzyme, AMP-activated protein kinase (AMPK), in these protective actions of metformin. Metformin 129-138 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 61-89 27856330-4 2017 Here we investigate the involvement of the metabolic enzyme, AMP-activated protein kinase (AMPK), in these protective actions of metformin. Metformin 129-138 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 91-95 27856330-8 2017 Further activation of AMPK in wild type MEFS, with either metformin or the AMPK-specific activator, A769662, was also associated with suppression of adipogenesis. Metformin 58-67 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 22-26 27856330-9 2017 It appears, therefore, that basal AMPK activity is required for adipogenesis and that metformin can inhibit adipogenesis through AMPK-dependent or -independent mechanisms, depending on the cellular context. Metformin 86-95 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 129-133 27878239-1 2017 The AMP-activated protein kinase (AMPK) activator 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR) modulates cellular energy metabolism, and promotes mitochondrial proliferation and apoptosis. AICA ribonucleotide 50-95 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 4-32 27988363-0 2017 In vitro antiglioma action of indomethacin is mediated via AMP-activated protein kinase/mTOR complex 1 signalling pathway. Indomethacin 30-42 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 59-87 27988363-4 2017 Indomethacin increased the phosphorylation of AMPK and its targets Raptor and acetyl-CoA carboxylase (ACC), and reduced the phosphorylation of mTOR and mTOR complex 1 (mTORC1) substrates p70S6 kinase and PRAS40 (Ser183). Indomethacin 0-12 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 46-50 27988363-5 2017 AMPK knockdown by RNA interference, as well as the treatment with the mTORC1 activator leucine, prevented indomethacin-mediated mTORC1 inhibition and cytotoxic action, while AMPK activators metformin and AICAR mimicked the effects of the drug. Indomethacin 106-118 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 27988363-5 2017 AMPK knockdown by RNA interference, as well as the treatment with the mTORC1 activator leucine, prevented indomethacin-mediated mTORC1 inhibition and cytotoxic action, while AMPK activators metformin and AICAR mimicked the effects of the drug. Metformin 190-199 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 27988363-5 2017 AMPK knockdown by RNA interference, as well as the treatment with the mTORC1 activator leucine, prevented indomethacin-mediated mTORC1 inhibition and cytotoxic action, while AMPK activators metformin and AICAR mimicked the effects of the drug. Metformin 190-199 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 174-178 27988363-6 2017 AMPK activation by indomethacin correlated with intracellular ATP depletion and increase in AMP/ATP ratio, and was apparently independent of COX inhibition or the increase in intracellular calcium. Indomethacin 19-31 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 27988363-6 2017 AMPK activation by indomethacin correlated with intracellular ATP depletion and increase in AMP/ATP ratio, and was apparently independent of COX inhibition or the increase in intracellular calcium. Adenosine Triphosphate 62-65 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 27988363-6 2017 AMPK activation by indomethacin correlated with intracellular ATP depletion and increase in AMP/ATP ratio, and was apparently independent of COX inhibition or the increase in intracellular calcium. Adenosine Triphosphate 96-99 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 27988363-6 2017 AMPK activation by indomethacin correlated with intracellular ATP depletion and increase in AMP/ATP ratio, and was apparently independent of COX inhibition or the increase in intracellular calcium. Calcium 189-196 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 27988363-7 2017 Finally, the toxicity of indomethacin towards primary human glioma cells was associated with the activation of AMPK/Raptor/ACC and subsequent suppression of mTORC1/S6K. Indomethacin 25-37 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 111-115 27988363-8 2017 By demonstrating the involvement of AMPK/mTORC1 pathway in the antiglioma action of indomethacin, our results support its further exploration in glioma therapy. Indomethacin 84-96 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 36-40 27878239-1 2017 The AMP-activated protein kinase (AMPK) activator 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR) modulates cellular energy metabolism, and promotes mitochondrial proliferation and apoptosis. AICA ribonucleotide 50-95 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 34-38 27796683-0 2017 Akt/AMPK/mTOR pathway was involved in the autophagy induced by vitamin E succinate in human gastric cancer SGC-7901 cells. alpha-Tocopherol 63-82 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 4-8 28253973-4 2017 However, recent studies have engendered a paradigm shift for how AMPK is activated inside the cell or animal tissues, unraveling that AXIN binds to LKB1 and tethers it to AMPK located on the surface of late endosome and lysosome (hereafter, only lysosome is discussed) in response to glucose starvation. Glucose 284-291 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 65-69 27796683-4 2017 We also observed that VES-induced autophagy was accompanied by the activation of AMP-activated protein kinases (AMPK). alpha-Tocopherol 22-25 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 81-110 27796683-4 2017 We also observed that VES-induced autophagy was accompanied by the activation of AMP-activated protein kinases (AMPK). alpha-Tocopherol 22-25 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 112-116 27762456-0 2017 Hovenia Dulcis Extract Reduces Lipid Accumulation in Oleic Acid-Induced Steatosis of Hep G2 Cells via Activation of AMPK and PPARalpha/CPT-1 Pathway and in Acute Hyperlipidemia Mouse Model. Oleic Acid 53-63 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 116-120 28554169-10 2017 Furthermore, the siRNA or inhibitor targeting FGF21 or AMPK rejected the triglyceride-lowering effect of NHP. Triglycerides 73-85 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 55-59 27754854-15 2017 An alternative pathway by which metformin exerted its action was through downregulation of IGFBP-2 in DU145 and LNCaP cells, independently of AMPK. Metformin 32-41 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 142-146 28033353-8 2016 Blocking AMPK function with AMPK inhibitor, AMPK siRNA or DN-AMPK diminishes the inhibitory effect of 2-DG on ERK, suggesting that 2-DG-induced ERK inhibition is mediated by LKB1/AMPK signaling. Deoxyglucose 102-106 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 9-13 28033353-8 2016 Blocking AMPK function with AMPK inhibitor, AMPK siRNA or DN-AMPK diminishes the inhibitory effect of 2-DG on ERK, suggesting that 2-DG-induced ERK inhibition is mediated by LKB1/AMPK signaling. Deoxyglucose 131-135 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 9-13 28033353-8 2016 Blocking AMPK function with AMPK inhibitor, AMPK siRNA or DN-AMPK diminishes the inhibitory effect of 2-DG on ERK, suggesting that 2-DG-induced ERK inhibition is mediated by LKB1/AMPK signaling. Deoxyglucose 131-135 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 28-32 28033353-8 2016 Blocking AMPK function with AMPK inhibitor, AMPK siRNA or DN-AMPK diminishes the inhibitory effect of 2-DG on ERK, suggesting that 2-DG-induced ERK inhibition is mediated by LKB1/AMPK signaling. Deoxyglucose 131-135 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 28-32 28033353-8 2016 Blocking AMPK function with AMPK inhibitor, AMPK siRNA or DN-AMPK diminishes the inhibitory effect of 2-DG on ERK, suggesting that 2-DG-induced ERK inhibition is mediated by LKB1/AMPK signaling. Deoxyglucose 131-135 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 28-32 28033353-8 2016 Blocking AMPK function with AMPK inhibitor, AMPK siRNA or DN-AMPK diminishes the inhibitory effect of 2-DG on ERK, suggesting that 2-DG-induced ERK inhibition is mediated by LKB1/AMPK signaling. Deoxyglucose 131-135 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 28-32 28033353-10 2016 Conversely, a subset of oncogenic mutants of K-Ras, the main upstream regulator of ERK, blocks 2-DG-induced LKB1/AMPK signaling. Deoxyglucose 95-99 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 113-117 28033353-11 2016 These findings reveal the potential cross-talk between LKB1/AMPK and ERK signaling and help to better understand the mechanism of action of 2-DG. Deoxyglucose 140-144 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 60-64 27989873-11 2016 PGB treatment increased the phosphorylation of AMP-activated protein kinase (AMPK) and subsequently suppressed the AKT/mammalian target of the rapamycin (mTOR) pathway. Prostaglandins B 0-3 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 47-75 27989873-11 2016 PGB treatment increased the phosphorylation of AMP-activated protein kinase (AMPK) and subsequently suppressed the AKT/mammalian target of the rapamycin (mTOR) pathway. Prostaglandins B 0-3 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 77-81 27989873-14 2016 CONCLUSIONS: PGB efficiently induced cancer cell death via autophagy and the modulation of the AMPK/mTOR/AKT and MAPK signaling pathways in A549 cells. Prostaglandins B 13-16 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 95-99 27784766-6 2016 In contrast, VEGF-stimulated AMPKalpha1 Ser487 phosphorylation was sensitive to inhibitors of protein kinase C (PKC) and PKC activation using phorbol esters or overexpression of PKC-stimulated AMPKalpha1 Ser487 phosphorylation. Phorbol Esters 142-156 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 29-39 27784766-8 2016 PKC activation was associated with reduced AMPK activity, as inhibition of PKC increased AMPK activity and phorbol esters inhibited AMPK, an effect lost in cells expressing mutant AMPKalpha1 Ser487Ala. Phorbol Esters 107-121 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 43-47 27784766-8 2016 PKC activation was associated with reduced AMPK activity, as inhibition of PKC increased AMPK activity and phorbol esters inhibited AMPK, an effect lost in cells expressing mutant AMPKalpha1 Ser487Ala. Phorbol Esters 107-121 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 180-190 28003763-0 2016 Isoorientin induces apoptosis, decreases invasiveness, and downregulates VEGF secretion by activating AMPK signaling in pancreatic cancer cells. homoorientin 0-11 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 102-106 28003763-5 2016 Meanwhile, we investigated the activity of the AMP-activated protein kinase (AMPK) signaling pathway after isoorientin treatment, which was forcefully activated by isoorientin, as expected. homoorientin 107-118 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 77-81 28003763-5 2016 Meanwhile, we investigated the activity of the AMP-activated protein kinase (AMPK) signaling pathway after isoorientin treatment, which was forcefully activated by isoorientin, as expected. homoorientin 164-175 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 77-81 28003763-7 2016 Thus, we demonstrated that isoorientin has potential antitumor effects via the AMPK signaling pathway, and isoorientin merits further investigation. homoorientin 27-38 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 79-83 27639899-0 2016 The Anticancer Agent, Di-2-Pyridylketone 4,4-Dimethyl-3-Thiosemicarbazone (Dp44mT), Up-Regulates the AMPK-Dependent Energy Homeostasis Pathway in Cancer Cells. di-2-Pyridyl ketone 22-40 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 101-105 27639899-0 2016 The Anticancer Agent, Di-2-Pyridylketone 4,4-Dimethyl-3-Thiosemicarbazone (Dp44mT), Up-Regulates the AMPK-Dependent Energy Homeostasis Pathway in Cancer Cells. 4,4-dimethyl-3-thiosemicarbazone 41-73 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 101-105 27639899-0 2016 The Anticancer Agent, Di-2-Pyridylketone 4,4-Dimethyl-3-Thiosemicarbazone (Dp44mT), Up-Regulates the AMPK-Dependent Energy Homeostasis Pathway in Cancer Cells. di-2-pyridylketone-4,4-dimethyl-3-thiosemicarbazone 75-81 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 101-105 27639899-1 2016 Adenosine monophosphate-activated protein kinase (AMPK) is a cellular energy sensor that monitors ATP levels. Adenosine Triphosphate 98-101 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 50-54 27639899-4 2016 Therefore, metals (e.g., iron) could play an important role in the regulation of AMPK-dependent pathways. Iron 25-29 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 81-85 27639899-5 2016 Hence, this investigation examined the effect of the iron and copper chelator and potent anti-cancer agent, di-2-pyridylketone 4,4-dimethyl-3-thiosemicarbazone (Dp44mT), on the AMPK-mediated pathway. di-2-Pyridyl ketone 108-126 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 177-181 27639899-5 2016 Hence, this investigation examined the effect of the iron and copper chelator and potent anti-cancer agent, di-2-pyridylketone 4,4-dimethyl-3-thiosemicarbazone (Dp44mT), on the AMPK-mediated pathway. 4,4-dimethyl-3-thiosemicarbazone 127-159 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 177-181 27639899-5 2016 Hence, this investigation examined the effect of the iron and copper chelator and potent anti-cancer agent, di-2-pyridylketone 4,4-dimethyl-3-thiosemicarbazone (Dp44mT), on the AMPK-mediated pathway. di-2-pyridylketone-4,4-dimethyl-3-thiosemicarbazone 161-167 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 177-181 27639899-7 2016 Furthermore, examination of the Dp44mT-metal complexes demonstrated that the effect of Dp44mT on AMPK was due to a dual mechanism: (1) its ability to chelate metal ions; and (2) the generation of reactive oxygen species (ROS). di-2-pyridylketone-4,4-dimethyl-3-thiosemicarbazone 32-38 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 97-101 27639899-7 2016 Furthermore, examination of the Dp44mT-metal complexes demonstrated that the effect of Dp44mT on AMPK was due to a dual mechanism: (1) its ability to chelate metal ions; and (2) the generation of reactive oxygen species (ROS). Metals 39-44 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 97-101 27639899-7 2016 Furthermore, examination of the Dp44mT-metal complexes demonstrated that the effect of Dp44mT on AMPK was due to a dual mechanism: (1) its ability to chelate metal ions; and (2) the generation of reactive oxygen species (ROS). Metals 158-163 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 97-101 27639899-7 2016 Furthermore, examination of the Dp44mT-metal complexes demonstrated that the effect of Dp44mT on AMPK was due to a dual mechanism: (1) its ability to chelate metal ions; and (2) the generation of reactive oxygen species (ROS). Reactive Oxygen Species 196-219 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 97-101 27639899-7 2016 Furthermore, examination of the Dp44mT-metal complexes demonstrated that the effect of Dp44mT on AMPK was due to a dual mechanism: (1) its ability to chelate metal ions; and (2) the generation of reactive oxygen species (ROS). Reactive Oxygen Species 221-224 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 97-101 27639899-11 2016 Together, this AMPK-mediated repair response aims to rescue the loss of metal ions via chelation and the induction of cytotoxic damage mediated by redox cycling of the Dp44mT-metal ion complex. Metals 72-77 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 15-19 27639899-11 2016 Together, this AMPK-mediated repair response aims to rescue the loss of metal ions via chelation and the induction of cytotoxic damage mediated by redox cycling of the Dp44mT-metal ion complex. Metals 175-180 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 15-19 27657826-0 2016 Anti-inflammatory activities of fenoterol through beta-arrestin-2 and inhibition of AMPK and NF-kappaB activation in AICAR-induced THP-1 cells. Fenoterol 32-41 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 84-88 27657826-2 2016 We reported that fenoterol, a beta2-adrenergic receptor (beta2-AR) agonist, inhibited lipopolysaccharide (LPS)-induced AMPK activation and inflammatory cytokine production in THP-1 cells, a monocytic cell line in previous studies. Fenoterol 17-26 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 119-123 27657826-3 2016 5-amino-1-beta-d-ribofuranosyl-imidazole-4-carboxamide (AICAR) is an agonist of AMPK. acadesine 0-54 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 80-84 27657826-3 2016 5-amino-1-beta-d-ribofuranosyl-imidazole-4-carboxamide (AICAR) is an agonist of AMPK. acadesine 56-61 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 80-84 27657826-7 2016 AICAR-induced AMPK activation, NF-kappaB activation and tumor necrosis factor (TNF)-alpha release were reduced by fenoterol. Fenoterol 114-123 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-18 27657826-8 2016 In addition, siRNA-mediated knockdown of beta-arrestin-2 abolished fenoterol"s inhibition of AICAR-induced AMPK activation and TNF-alpha release, thus beta-arrestin-2 mediated the anti-inflammatory effects of fenoterol in AICAR-treated THP-1 cells. Fenoterol 67-76 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 107-111 27657826-8 2016 In addition, siRNA-mediated knockdown of beta-arrestin-2 abolished fenoterol"s inhibition of AICAR-induced AMPK activation and TNF-alpha release, thus beta-arrestin-2 mediated the anti-inflammatory effects of fenoterol in AICAR-treated THP-1 cells. Fenoterol 209-218 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 107-111 27657826-10 2016 These data suggested that fenoterol inhibited AICAR-induced AMPK activation and TNF-alpha release through beta-arrestin-2 in THP-1 cells. Fenoterol 26-35 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 60-64 27657826-10 2016 These data suggested that fenoterol inhibited AICAR-induced AMPK activation and TNF-alpha release through beta-arrestin-2 in THP-1 cells. acadesine 46-51 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 60-64 27636742-0 2016 Metformin inhibits estrogen-dependent endometrial cancer cell growth by activating the AMPK-FOXO1 signal pathway. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 87-91 27636742-4 2016 Metformin treatment suppressed EC cell growth in a time-dependent manner in vitro; this effect was cancelled by cotreatment with an AMPK inhibitor, compound C. Metformin decreased FOXO1 phosphorylation and increased FOXO1 nuclear localization in Ishikawa and HEC-1B cells, with non-significant increase in FOXO1 mRNA expression. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 132-136 27636742-4 2016 Metformin treatment suppressed EC cell growth in a time-dependent manner in vitro; this effect was cancelled by cotreatment with an AMPK inhibitor, compound C. Metformin decreased FOXO1 phosphorylation and increased FOXO1 nuclear localization in Ishikawa and HEC-1B cells, with non-significant increase in FOXO1 mRNA expression. Metformin 160-169 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 132-136 27636742-5 2016 Moreover, compound C blocked the metformin-induced changes of FOXO1 and its phosphorylation protein, suggesting that metformin upregulated FOXO1 activity by AMPK activation. Metformin 33-42 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 157-161 27636742-5 2016 Moreover, compound C blocked the metformin-induced changes of FOXO1 and its phosphorylation protein, suggesting that metformin upregulated FOXO1 activity by AMPK activation. Metformin 117-126 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 157-161 27636742-8 2016 A xenograft mouse model further revealed that metformin suppressed HEC-1B tumor growth, accompanied by downregulated ki-67 and upregulated AMPK phosphorylation and nuclear FOXO1 protein. Metformin 46-55 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 139-143 27636742-9 2016 Taken together, these data provide a novel mechanism of antineoplastic effect for metformin through the regulation of FOXO1, and suggest that the AMPK-FOXO1 pathway may be a therapeutic target to the development of new antineoplastic drugs. Metformin 82-91 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 146-150 27689873-0 2016 Autophagy requires poly(adp-ribosyl)ation-dependent AMPK nuclear export. poly(adp 19-27 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 52-56 27687210-0 2016 Lack of mitochondrial DNA impairs chemical hypoxia-induced autophagy in liver tumor cells through ROS-AMPK-ULK1 signaling dysregulation independently of HIF-1alpha. Reactive Oxygen Species 98-101 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 102-106 27687210-10 2016 In wild-type cells, the antioxidant N-acetylcysteine blocked CoCl2- and DFO-induced AMPK and autophagy activation, but not endoplasmic reticulum stress induced by CoCl2. Acetylcysteine 36-52 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 84-88 27687210-10 2016 In wild-type cells, the antioxidant N-acetylcysteine blocked CoCl2- and DFO-induced AMPK and autophagy activation, but not endoplasmic reticulum stress induced by CoCl2. cobaltous chloride 61-66 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 84-88 27687210-10 2016 In wild-type cells, the antioxidant N-acetylcysteine blocked CoCl2- and DFO-induced AMPK and autophagy activation, but not endoplasmic reticulum stress induced by CoCl2. Deferoxamine 72-75 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 84-88 27419805-0 2016 Hydrogen sulphide exacerbates acute pancreatitis by over-activating autophagy via AMPK/mTOR pathway. Hydrogen Sulfide 0-17 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 82-86 27419805-8 2016 Our findings suggested that H2 S exacerbated taurocholate-induced AP by over-activating autophagy via activation of AMPK and subsequently, inhibition of mTOR. Hydrogen 28-30 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 116-120 27419805-8 2016 Our findings suggested that H2 S exacerbated taurocholate-induced AP by over-activating autophagy via activation of AMPK and subsequently, inhibition of mTOR. Taurocholic Acid 45-57 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 116-120 27733682-0 2016 Activation of AMP-activated Protein Kinase by Metformin Induces Protein Acetylation in Prostate and Ovarian Cancer Cells. Metformin 46-55 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-42 27733682-3 2016 Activation of AMPK occurs when the intracellular AMP/ATP ratio increases and leads to a metabolic switch from anabolism to catabolism. Adenosine Triphosphate 53-56 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-18 27733682-4 2016 AMPK phosphorylates and inhibits acetyl-CoA carboxylase (ACC), which catalyzes carboxylation of acetyl-CoA to malonyl-CoA, the first and rate-limiting reaction in de novo synthesis of fatty acids. Acetyl Coenzyme A 33-43 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 27733682-4 2016 AMPK phosphorylates and inhibits acetyl-CoA carboxylase (ACC), which catalyzes carboxylation of acetyl-CoA to malonyl-CoA, the first and rate-limiting reaction in de novo synthesis of fatty acids. Malonyl Coenzyme A 110-121 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 27733682-4 2016 AMPK phosphorylates and inhibits acetyl-CoA carboxylase (ACC), which catalyzes carboxylation of acetyl-CoA to malonyl-CoA, the first and rate-limiting reaction in de novo synthesis of fatty acids. Fatty Acids 184-195 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 27733682-5 2016 AMPK thus regulates homeostasis of acetyl-CoA, a key metabolite at the crossroads of metabolism, signaling, chromatin structure, and transcription. Acetyl Coenzyme A 35-45 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 27733682-7 2016 Here we show that activation of AMPK with the widely used antidiabetic drug metformin or with the AMP mimetic 5-aminoimidazole-4-carboxamide ribonucleotide increases the inhibitory phosphorylation of ACC and decreases the conversion of acetyl-CoA to malonyl-CoA, leading to increased protein acetylation and altered gene expression in prostate and ovarian cancer cells. Metformin 76-85 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 32-36 27733682-7 2016 Here we show that activation of AMPK with the widely used antidiabetic drug metformin or with the AMP mimetic 5-aminoimidazole-4-carboxamide ribonucleotide increases the inhibitory phosphorylation of ACC and decreases the conversion of acetyl-CoA to malonyl-CoA, leading to increased protein acetylation and altered gene expression in prostate and ovarian cancer cells. AICA ribonucleotide 110-155 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 32-36 27733682-7 2016 Here we show that activation of AMPK with the widely used antidiabetic drug metformin or with the AMP mimetic 5-aminoimidazole-4-carboxamide ribonucleotide increases the inhibitory phosphorylation of ACC and decreases the conversion of acetyl-CoA to malonyl-CoA, leading to increased protein acetylation and altered gene expression in prostate and ovarian cancer cells. Acetyl Coenzyme A 236-246 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 32-36 27733682-7 2016 Here we show that activation of AMPK with the widely used antidiabetic drug metformin or with the AMP mimetic 5-aminoimidazole-4-carboxamide ribonucleotide increases the inhibitory phosphorylation of ACC and decreases the conversion of acetyl-CoA to malonyl-CoA, leading to increased protein acetylation and altered gene expression in prostate and ovarian cancer cells. Malonyl Coenzyme A 250-261 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 32-36 27733682-10 2016 Together, our data indicate that AMPK regulates the availability of nucleocytosolic acetyl-CoA for protein acetylation and that AMPK activators, such as metformin, have the capacity to increase protein acetylation and alter patterns of gene expression, further expanding the plethora of metformin"s physiological effects. Metformin 153-162 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 128-132 27733682-10 2016 Together, our data indicate that AMPK regulates the availability of nucleocytosolic acetyl-CoA for protein acetylation and that AMPK activators, such as metformin, have the capacity to increase protein acetylation and alter patterns of gene expression, further expanding the plethora of metformin"s physiological effects. Metformin 287-296 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 33-37 27733682-10 2016 Together, our data indicate that AMPK regulates the availability of nucleocytosolic acetyl-CoA for protein acetylation and that AMPK activators, such as metformin, have the capacity to increase protein acetylation and alter patterns of gene expression, further expanding the plethora of metformin"s physiological effects. Metformin 287-296 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 128-132 27654259-8 2016 In parallel, the activation of AMPK and suppression of mTOR seemed to play an important role for the effect of metformin in patients with EC. Metformin 111-120 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 31-35 27762456-5 2017 Conversely, AMPK inhibitor compound C blocked the anti-fatty liver effect of HDT to induce AMPK phosphorylation and decrease 3-hydroxy-3-methylglutaryl-CoA reductase and lipid accumulation by oil red O staining in OA-treated Hep G2 cells. oil red O 192-201 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 12-16 27638620-3 2016 To examine whether AMPK regulates bladder cancer cell growth, HTB2 and HT1376 bladder cells were treated with an AMPK activator, 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR). AICA ribonucleotide 129-174 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 113-117 27821173-11 2016 Similarly, all these experiments were replicated in SH-SY5Y cells by silencing AMPK with siRNA, which suggests that AMPK is the key mediator in glutamate-induced neurotoxicity. Glutamic Acid 144-153 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 79-83 27821173-11 2016 Similarly, all these experiments were replicated in SH-SY5Y cells by silencing AMPK with siRNA, which suggests that AMPK is the key mediator in glutamate-induced neurotoxicity. Glutamic Acid 144-153 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 116-120 27637001-8 2016 EPA also promoted the activation of master regulators of mitochondrial biogenesis such as sirtuin 1, PGC1-alpha and AMPK. Eicosapentaenoic Acid 0-3 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 116-120 27492225-0 2016 From the Cover: Autophagy Induction Contributes to Cadmium Toxicity in Mesenchymal Stem Cells via AMPK/FOXO3a/BECN1 Signaling. Cadmium 51-58 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 98-102 27689873-2 2016 In the current study we uncover that Poly(ADP-ribosyl)ation (PARylation), a post-translational modification (PTM) of proteins, accounts for the spatial and temporal regulation of autophagy by modulating AMPK subcellular localisation and activation. poly(adp 37-45 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 203-207 27689873-2 2016 In the current study we uncover that Poly(ADP-ribosyl)ation (PARylation), a post-translational modification (PTM) of proteins, accounts for the spatial and temporal regulation of autophagy by modulating AMPK subcellular localisation and activation. ribosyl) 46-54 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 203-207 27650555-6 2016 Mechanistically, AMPKalpha1 was found to coimmunoprecipitate with CHOP and phosphorylate CHOP at serine 30. Serine 97-103 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 17-27 27650555-11 2016 CONCLUSIONS: Our results indicate that AMPKalpha1 mediates CHOP ubiquitination and proteasomal degradation in macrophages by promoting the phosphorylation of CHOP at serine 30. Serine 166-172 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 39-49 27763549-0 2016 Maternal Betaine Supplementation throughout Gestation and Lactation Modifies Hepatic Cholesterol Metabolic Genes in Weaning Piglets via AMPK/LXR-Mediated Pathway and Histone Modification. Betaine 9-16 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 136-140 27792760-3 2016 When activated, AMPK causes mitochondria to elongate/fuse and proliferate, with mitochondria now producing more ATP and less reactive oxygen species. Adenosine Triphosphate 112-115 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 16-20 27792760-3 2016 When activated, AMPK causes mitochondria to elongate/fuse and proliferate, with mitochondria now producing more ATP and less reactive oxygen species. Reactive Oxygen Species 125-148 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 16-20 27792760-8 2016 Adding AICAR, a specific AMPK activator, at the time of drug exposure prevented and reversed these effects. AICA ribonucleotide 7-12 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 25-29 27792760-11 2016 AMPK activation also stimulated autophagy/mitophagy, most significantly in acetaminophen-treated cells. Acetaminophen 75-88 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 27725120-0 2016 Methylene blue alleviates experimental autoimmune encephalomyelitis by modulating AMPK/SIRT1 signaling pathway and Th17/Treg immune response. Methylene Blue 0-14 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 82-86 27492225-7 2016 Specifically, Cd increased FOXO3a and FOXO1 expression at the mRNA and protein levels, and AMPK was demonstrated to enhance FOXO3a nuclear translocation and transcriptional activity by phosphorylating FOXO3a at specific serine residues (Ser588) in Cd-treated MSCs. Serine 220-226 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 91-95 27492225-7 2016 Specifically, Cd increased FOXO3a and FOXO1 expression at the mRNA and protein levels, and AMPK was demonstrated to enhance FOXO3a nuclear translocation and transcriptional activity by phosphorylating FOXO3a at specific serine residues (Ser588) in Cd-treated MSCs. Cadmium 248-250 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 91-95 27763549-6 2016 These results suggest that gestational and lactational betaine supplementation modulates hepatic gene expression involved in cholesterol metabolism via an AMPK/LXR pathway and histone modification in the weaning offspring. Betaine 55-62 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 155-159 27641099-5 2016 Remarkably, postnatal AMPK activation with AICAR or metformin rescued obesity-induced suppression of brown adipogenesis and thermogenesis. Metformin 52-61 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 22-26 27582546-0 2016 Eupafolin enhances TRAIL-mediated apoptosis through cathepsin S-induced down-regulation of Mcl-1 expression and AMPK-mediated Bim up-regulation in renal carcinoma Caki cells. eupafolin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 112-116 27732831-0 2016 Metformin Activates AMPK through the Lysosomal Pathway. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 20-24 27582546-6 2016 In addition, eupafolin increased Bim expression at the post-translational levels via AMP-activated protein kinase (AMPK)-mediated inhibition of proteasome activity. eupafolin 13-22 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 85-113 27582546-6 2016 In addition, eupafolin increased Bim expression at the post-translational levels via AMP-activated protein kinase (AMPK)-mediated inhibition of proteasome activity. eupafolin 13-22 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 115-119 27499160-2 2016 Hypoxia, a hallmark characteristic of solid tumors, has been linked to an increase in the activity of the ATP-generating AMPK protein. Adenosine Triphosphate 106-109 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 121-125 27490779-7 2016 AMPK was activated by swertiamarin action, thus restoring insulin sensitivity in hepatocytes. swertiamarin 22-34 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 27490779-10 2016 Cumulatively, swertiamarin targets potential metabolic regulators AMPK and PPAR-alpha, through which it regulates hepatic glycemic burden, fat accumulation, insulin resistance and ROS in hepatic steatosis which emphasizes clinical significance of swertiamarin in regulating metabolism and as a suitable candidate for treating NAFLD. swertiamarin 14-26 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 66-70 27602497-8 2016 Since TZD is a ligand for transcription factor PPARgamma and can activate AMPK, we determined their roles on antagonism of GSK3beta. tzd 6-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 74-78 27499160-3 2016 Since Malat1 was recently shown to be upregulated during hypoxia, the objective of this study was to determine the contribution of AMPK in the mechanistic pathways regulating Malat1 expression in low oxygen conditions. Oxygen 200-206 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 131-135 27499160-6 2016 Interestingly, pharmacological stimulation of AMPK increased Malat1 promoter transactivation in 21% O2 conditions, whereas inhibition of either AMPK or its upstream activator CaMKK completely abolished the augmentation of Malat1 under hypoxia. Oxygen 100-102 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 46-50 27899819-6 2016 Further investigation showed that 4-cholesten-3-one promoted ROS generation, which transiently activated AMPKalpha1, increased HIF1alpha expression, reduced Bcl-2 expression and caused autophagy. cholest-4-en-3-one 34-51 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 105-115 27899819-6 2016 Further investigation showed that 4-cholesten-3-one promoted ROS generation, which transiently activated AMPKalpha1, increased HIF1alpha expression, reduced Bcl-2 expression and caused autophagy. ros 61-64 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 105-115 27899819-7 2016 AMPKalpha1 knockdown partly suppressed 4-cholesten-3-one-induced autophagy but, neither prevented 4-cholesten-3-one-induced upregulation of HIF1alpha or downregulation of Bcl-2. cholest-4-en-3-one 39-56 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-10 27343431-3 2016 Pharmacological or genetic activation of AMPK increased mRNA and protein expression of ABCA1 and its transcriptional activator liver X receptor (LXR) alpha, resulting in increased cholesterol efflux to apolipoprotein AI-containing medium. Cholesterol 180-191 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 41-45 27457805-0 2016 Liraglutide ameliorates palmitate-induced endothelial dysfunction through activating AMPK and reversing leptin resistance. Palmitates 24-33 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 85-89 27304906-0 2016 AMPK regulates autophagy by phosphorylating BECN1 at threonine 388. Threonine 53-62 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 27574022-0 2016 The emerging role of AMPK in the regulation of breathing and oxygen supply. Oxygen 61-67 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 21-25 27574022-6 2016 It would appear, therefore, that evolutionary pressures have led to AMPK being utilized to regulate oxygen delivery and thus energy supply to the body in the short, medium and longer term. Oxygen 100-106 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 68-72 27574022-9 2016 Allied to this, AMPK is critical to the control of hypoxic pulmonary vasoconstriction and thus ventilation-perfusion matching at the lungs and may also determine oxygen supply to the foetus by, for example, modulating utero-placental blood flow. Oxygen 162-168 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 16-20 27343431-8 2016 Our data link AMPK activation to an increased cholesterol efflux capacity of macrophages, suggesting an atheroprotective effect of macrophage AMPK. Cholesterol 46-57 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-18 27343431-8 2016 Our data link AMPK activation to an increased cholesterol efflux capacity of macrophages, suggesting an atheroprotective effect of macrophage AMPK. Cholesterol 46-57 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 142-146 27062501-4 2016 AMPK activation by 5-aminoimidazole-4-carboxamide riboside, A769662 or C13 attenuated Kv 1.5 currents in pulmonary arterial myocytes, and this effect was non-additive with respect to Kv 1.5 inhibition by hypoxia and mitochondrial poisons. acadesine 19-58 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 27062501-8 2016 We sought to determine the role in this process of the AMP-activated protein kinase (AMPK), which is intimately coupled to mitochondrial function due to its activation by LKB1-dependent phosphorylation in response to increases in the cellular AMP:ATP and/or ADP:ATP ratios. Adenosine Monophosphate 55-58 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 85-89 27062501-8 2016 We sought to determine the role in this process of the AMP-activated protein kinase (AMPK), which is intimately coupled to mitochondrial function due to its activation by LKB1-dependent phosphorylation in response to increases in the cellular AMP:ATP and/or ADP:ATP ratios. Adenosine Triphosphate 247-250 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 55-83 27062501-8 2016 We sought to determine the role in this process of the AMP-activated protein kinase (AMPK), which is intimately coupled to mitochondrial function due to its activation by LKB1-dependent phosphorylation in response to increases in the cellular AMP:ATP and/or ADP:ATP ratios. Adenosine Triphosphate 247-250 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 85-89 27062501-8 2016 We sought to determine the role in this process of the AMP-activated protein kinase (AMPK), which is intimately coupled to mitochondrial function due to its activation by LKB1-dependent phosphorylation in response to increases in the cellular AMP:ATP and/or ADP:ATP ratios. Adenosine Diphosphate 258-261 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 55-83 27062501-8 2016 We sought to determine the role in this process of the AMP-activated protein kinase (AMPK), which is intimately coupled to mitochondrial function due to its activation by LKB1-dependent phosphorylation in response to increases in the cellular AMP:ATP and/or ADP:ATP ratios. Adenosine Diphosphate 258-261 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 85-89 27062501-8 2016 We sought to determine the role in this process of the AMP-activated protein kinase (AMPK), which is intimately coupled to mitochondrial function due to its activation by LKB1-dependent phosphorylation in response to increases in the cellular AMP:ATP and/or ADP:ATP ratios. Adenosine Triphosphate 262-265 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 55-83 27062501-8 2016 We sought to determine the role in this process of the AMP-activated protein kinase (AMPK), which is intimately coupled to mitochondrial function due to its activation by LKB1-dependent phosphorylation in response to increases in the cellular AMP:ATP and/or ADP:ATP ratios. Adenosine Triphosphate 262-265 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 85-89 27562249-4 2016 Whether pharmacological AMPK activation suppresses SFA-induced inflammation in a human system is unclear. Fatty Acids 51-54 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 24-28 27562249-5 2016 In a setting of hypoxia-potentiated inflammation induced by SFA palmitate, we found that the AMP-mimetic AMPK activator 5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside (AICAR) potently suppressed upregulation of ER stress marker mRNAs and pro-inflammatory cytokines. sfa palmitate 60-73 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 105-109 27562249-5 2016 In a setting of hypoxia-potentiated inflammation induced by SFA palmitate, we found that the AMP-mimetic AMPK activator 5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside (AICAR) potently suppressed upregulation of ER stress marker mRNAs and pro-inflammatory cytokines. Adenosine Monophosphate 93-96 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 105-109 27562249-5 2016 In a setting of hypoxia-potentiated inflammation induced by SFA palmitate, we found that the AMP-mimetic AMPK activator 5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside (AICAR) potently suppressed upregulation of ER stress marker mRNAs and pro-inflammatory cytokines. acadesine 120-174 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 105-109 27449087-7 2016 MMC treatment resulted in an increase in AMPKalpha phosphorylation/activation, indicating AMPK is involved in the cellular response to ICLs. Mitomycin 0-3 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 41-45 27345664-5 2016 Glycan signaling from the extracellular matrix converges on "master" regulators of autophagy including AMPK and mTORC1, thus impacting their localization, activity, and/or expression. Polysaccharides 0-6 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 103-107 27413184-2 2016 Although AMPK is implicated in the regulation of a multitude of ATP-dependent cellular processes, exactly how these processes are controlled by AMPK as well as the identity of AMPK targets and pathways continues to evolve. Adenosine Triphosphate 64-67 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 9-13 27413184-4 2016 Specifically, we show AMPK-dependent Ser(353) phosphorylation of the human MNK1a isoform in cell-free and cellular systems. Serine 37-40 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 22-26 27246478-7 2016 AMPK and CaMKII-dependent signaling pathways were associated with the non-genomic effects of Dex. Dexamethasone 93-96 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 27246478-9 2016 AMPK and CaMKII-mediated Glut4 translocation may play a critical role in GC-induced rapid inhibition of glucose uptake. Glucose 104-111 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 27062501-9 2016 Inhibition of complex I of the mitochondrial electron transport chain using phenformin activated AMPK and inhibited Kv currents in pulmonary arterial myocytes, consistent with previously reported effects of mitochondrial inhibitors. Phenformin 76-86 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 97-101 27062501-10 2016 Myocyte Kv currents were also markedly inhibited upon AMPK activation by A769662, 5-aminoimidazole-4-carboxamide riboside and C13 and by intracellular dialysis from a patch-pipette of activated (thiophosphorylated) recombinant AMPK heterotrimers (alpha2beta2gamma1 or alpha1beta1gamma1). acadesine 82-121 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 54-58 27062501-11 2016 Hypoxia and inhibitors of mitochondrial oxidative phosphorylation reduced AMPK-sensitive K(+) currents, which were also blocked by the selective Kv 1.5 channel inhibitor diphenyl phosphine oxide-1 but unaffected by the presence of the BKCa channel blocker paxilline. triphenylphosphine oxide 170-194 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 74-78 27062501-11 2016 Hypoxia and inhibitors of mitochondrial oxidative phosphorylation reduced AMPK-sensitive K(+) currents, which were also blocked by the selective Kv 1.5 channel inhibitor diphenyl phosphine oxide-1 but unaffected by the presence of the BKCa channel blocker paxilline. paxilline 256-265 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 74-78 27230877-1 2016 PURPOSE: The purpose of the present study is to test whether metformin, aspirin, or diet supplement (DS) BioResponse-3,3"-Diindolylmethane (BR-DIM) can induce AMP-activated protein kinase (AMPK)-dependent potency loss in cultured embryos and whether metformin (Met) + Aspirin (Asa) or BR-DIM causes an AMPK-dependent decrease in embryonic development. Metformin 61-70 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 159-187 27372854-10 2016 Interestingly, AMPK, a master regulator of cell metabolism that is activated thorough the induction of cellular stress (e.g. increase in Ca(2+) concentration, reactive oxygen species generation, increase in AMP/ATP ratio) is essential for oocyte maturation, T cell activation, and mitochondrial function. Reactive Oxygen Species 159-182 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 15-19 27372854-10 2016 Interestingly, AMPK, a master regulator of cell metabolism that is activated thorough the induction of cellular stress (e.g. increase in Ca(2+) concentration, reactive oxygen species generation, increase in AMP/ATP ratio) is essential for oocyte maturation, T cell activation, and mitochondrial function. Adenosine Triphosphate 211-214 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 15-19 26804254-0 2016 AMPK signaling in skeletal muscle during exercise: Role of reactive oxygen and nitrogen species. reactive oxygen and nitrogen species 59-95 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 26804254-5 2016 Directly, RONS may activate or deactivate AMPK by modifying RONS-sensitive residues of the AMPK-alpha subunit. rons 10-14 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 42-46 26804254-5 2016 Directly, RONS may activate or deactivate AMPK by modifying RONS-sensitive residues of the AMPK-alpha subunit. rons 10-14 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 91-95 26804254-6 2016 Indirectly, RONS may activate AMPK by reducing mitochondrial ATP synthesis, leading to an increased AMP:ATP ratio and subsequent Thr(172)-AMPK phosphorylation by the two main AMPK kinases: LKB1 and CaMKKbeta. Adenosine Triphosphate 61-64 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-34 26804254-6 2016 Indirectly, RONS may activate AMPK by reducing mitochondrial ATP synthesis, leading to an increased AMP:ATP ratio and subsequent Thr(172)-AMPK phosphorylation by the two main AMPK kinases: LKB1 and CaMKKbeta. Adenosine Monophosphate 30-33 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 138-142 26804254-6 2016 Indirectly, RONS may activate AMPK by reducing mitochondrial ATP synthesis, leading to an increased AMP:ATP ratio and subsequent Thr(172)-AMPK phosphorylation by the two main AMPK kinases: LKB1 and CaMKKbeta. Adenosine Monophosphate 30-33 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 138-142 26804254-6 2016 Indirectly, RONS may activate AMPK by reducing mitochondrial ATP synthesis, leading to an increased AMP:ATP ratio and subsequent Thr(172)-AMPK phosphorylation by the two main AMPK kinases: LKB1 and CaMKKbeta. Adenosine Triphosphate 104-107 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-34 26804254-6 2016 Indirectly, RONS may activate AMPK by reducing mitochondrial ATP synthesis, leading to an increased AMP:ATP ratio and subsequent Thr(172)-AMPK phosphorylation by the two main AMPK kinases: LKB1 and CaMKKbeta. Threonine 129-132 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-34 26804254-6 2016 Indirectly, RONS may activate AMPK by reducing mitochondrial ATP synthesis, leading to an increased AMP:ATP ratio and subsequent Thr(172)-AMPK phosphorylation by the two main AMPK kinases: LKB1 and CaMKKbeta. Threonine 129-132 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 138-142 26804254-6 2016 Indirectly, RONS may activate AMPK by reducing mitochondrial ATP synthesis, leading to an increased AMP:ATP ratio and subsequent Thr(172)-AMPK phosphorylation by the two main AMPK kinases: LKB1 and CaMKKbeta. Threonine 129-132 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 138-142 26804254-7 2016 In presence of RONS the rate of Thr(172)-AMPK dephosphorylation is reduced. Threonine 32-35 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 41-45 26804254-10 2016 Both too high (hypoxia) and too low (ingestion of antioxidants) RONS levels may lead to Ser(485)-AMPKalpha1/Ser(491)-AMPKalpha2 phosphorylation causing inhibition of Thr(172)-AMPKalpha phosphorylation. rons 64-68 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 97-107 26804254-10 2016 Both too high (hypoxia) and too low (ingestion of antioxidants) RONS levels may lead to Ser(485)-AMPKalpha1/Ser(491)-AMPKalpha2 phosphorylation causing inhibition of Thr(172)-AMPKalpha phosphorylation. Serine 88-91 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 97-107 26804254-10 2016 Both too high (hypoxia) and too low (ingestion of antioxidants) RONS levels may lead to Ser(485)-AMPKalpha1/Ser(491)-AMPKalpha2 phosphorylation causing inhibition of Thr(172)-AMPKalpha phosphorylation. Threonine 166-169 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 97-107 27432584-3 2016 Alcohol has a significant role in alteration of lipid homeostasis, sterol regulatory element-binding proteins (SREBPs) and peroxidase proliferator-activated receptors through AMP-activated protein kinase (AMPK)-dependent mechanism. Alcohols 0-7 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 175-203 27432584-3 2016 Alcohol has a significant role in alteration of lipid homeostasis, sterol regulatory element-binding proteins (SREBPs) and peroxidase proliferator-activated receptors through AMP-activated protein kinase (AMPK)-dependent mechanism. Alcohols 0-7 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 205-209 27230877-6 2016 CONCLUSION: These experimental designs here showed that Met-, Asa-, BR-DIM-, or sorbitol stress-induced rapid potency loss in two-cell embryos is AMPK dependent as suggested by inhibition of Rex1 and/or Oct4 protein loss with an AMPK inhibitor. Sorbitol 80-88 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 229-233 27230877-7 2016 The DS BR-DIM or fertility drugs (e.g., Met + Asa) that are used to enhance maternal metabolism to support fertility can also chronically slow embryo growth and block development in an AMPK-dependent manner. Aspirin 46-49 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 185-189 27141100-2 2016 Increases in AMP:ATP and ADP:ATP ratios, signifying energy deficit, promote allosteric activation and net Thr172 phosphorylation mediated by LKB1, so that the LKB1-AMPK pathway acts as an energy sensor. Adenosine Monophosphate 13-16 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 164-168 27141100-2 2016 Increases in AMP:ATP and ADP:ATP ratios, signifying energy deficit, promote allosteric activation and net Thr172 phosphorylation mediated by LKB1, so that the LKB1-AMPK pathway acts as an energy sensor. Adenosine Triphosphate 17-20 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 164-168 27141100-2 2016 Increases in AMP:ATP and ADP:ATP ratios, signifying energy deficit, promote allosteric activation and net Thr172 phosphorylation mediated by LKB1, so that the LKB1-AMPK pathway acts as an energy sensor. Adenosine Diphosphate 25-28 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 164-168 27141100-2 2016 Increases in AMP:ATP and ADP:ATP ratios, signifying energy deficit, promote allosteric activation and net Thr172 phosphorylation mediated by LKB1, so that the LKB1-AMPK pathway acts as an energy sensor. Adenosine Triphosphate 29-32 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 164-168 27141100-5 2016 In three LKB1-null tumor cell lines, treatment with the Ca(2+) ionophore A23187 caused a G1 arrest that correlated with AMPK activation and Thr172 phosphorylation. Calcimycin 73-79 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 120-124 27230877-1 2016 PURPOSE: The purpose of the present study is to test whether metformin, aspirin, or diet supplement (DS) BioResponse-3,3"-Diindolylmethane (BR-DIM) can induce AMP-activated protein kinase (AMPK)-dependent potency loss in cultured embryos and whether metformin (Met) + Aspirin (Asa) or BR-DIM causes an AMPK-dependent decrease in embryonic development. Metformin 61-70 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 189-193 27230877-1 2016 PURPOSE: The purpose of the present study is to test whether metformin, aspirin, or diet supplement (DS) BioResponse-3,3"-Diindolylmethane (BR-DIM) can induce AMP-activated protein kinase (AMPK)-dependent potency loss in cultured embryos and whether metformin (Met) + Aspirin (Asa) or BR-DIM causes an AMPK-dependent decrease in embryonic development. Metformin 61-70 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 302-306 27230877-1 2016 PURPOSE: The purpose of the present study is to test whether metformin, aspirin, or diet supplement (DS) BioResponse-3,3"-Diindolylmethane (BR-DIM) can induce AMP-activated protein kinase (AMPK)-dependent potency loss in cultured embryos and whether metformin (Met) + Aspirin (Asa) or BR-DIM causes an AMPK-dependent decrease in embryonic development. Aspirin 72-79 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 159-187 27230877-1 2016 PURPOSE: The purpose of the present study is to test whether metformin, aspirin, or diet supplement (DS) BioResponse-3,3"-Diindolylmethane (BR-DIM) can induce AMP-activated protein kinase (AMPK)-dependent potency loss in cultured embryos and whether metformin (Met) + Aspirin (Asa) or BR-DIM causes an AMPK-dependent decrease in embryonic development. 3,3'-diindolylmethane 117-138 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 159-187 27230877-1 2016 PURPOSE: The purpose of the present study is to test whether metformin, aspirin, or diet supplement (DS) BioResponse-3,3"-Diindolylmethane (BR-DIM) can induce AMP-activated protein kinase (AMPK)-dependent potency loss in cultured embryos and whether metformin (Met) + Aspirin (Asa) or BR-DIM causes an AMPK-dependent decrease in embryonic development. 3,3'-diindolylmethane 117-138 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 189-193 27230877-1 2016 PURPOSE: The purpose of the present study is to test whether metformin, aspirin, or diet supplement (DS) BioResponse-3,3"-Diindolylmethane (BR-DIM) can induce AMP-activated protein kinase (AMPK)-dependent potency loss in cultured embryos and whether metformin (Met) + Aspirin (Asa) or BR-DIM causes an AMPK-dependent decrease in embryonic development. 3,3'-diindolylmethane 117-138 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 302-306 27230877-1 2016 PURPOSE: The purpose of the present study is to test whether metformin, aspirin, or diet supplement (DS) BioResponse-3,3"-Diindolylmethane (BR-DIM) can induce AMP-activated protein kinase (AMPK)-dependent potency loss in cultured embryos and whether metformin (Met) + Aspirin (Asa) or BR-DIM causes an AMPK-dependent decrease in embryonic development. br-dim 140-146 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 159-187 27230877-1 2016 PURPOSE: The purpose of the present study is to test whether metformin, aspirin, or diet supplement (DS) BioResponse-3,3"-Diindolylmethane (BR-DIM) can induce AMP-activated protein kinase (AMPK)-dependent potency loss in cultured embryos and whether metformin (Met) + Aspirin (Asa) or BR-DIM causes an AMPK-dependent decrease in embryonic development. br-dim 140-146 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 189-193 27230877-1 2016 PURPOSE: The purpose of the present study is to test whether metformin, aspirin, or diet supplement (DS) BioResponse-3,3"-Diindolylmethane (BR-DIM) can induce AMP-activated protein kinase (AMPK)-dependent potency loss in cultured embryos and whether metformin (Met) + Aspirin (Asa) or BR-DIM causes an AMPK-dependent decrease in embryonic development. br-dim 140-146 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 302-306 27230877-1 2016 PURPOSE: The purpose of the present study is to test whether metformin, aspirin, or diet supplement (DS) BioResponse-3,3"-Diindolylmethane (BR-DIM) can induce AMP-activated protein kinase (AMPK)-dependent potency loss in cultured embryos and whether metformin (Met) + Aspirin (Asa) or BR-DIM causes an AMPK-dependent decrease in embryonic development. Metformin 250-259 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 159-187 27230877-1 2016 PURPOSE: The purpose of the present study is to test whether metformin, aspirin, or diet supplement (DS) BioResponse-3,3"-Diindolylmethane (BR-DIM) can induce AMP-activated protein kinase (AMPK)-dependent potency loss in cultured embryos and whether metformin (Met) + Aspirin (Asa) or BR-DIM causes an AMPK-dependent decrease in embryonic development. Aspirin 268-275 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 159-187 27230877-1 2016 PURPOSE: The purpose of the present study is to test whether metformin, aspirin, or diet supplement (DS) BioResponse-3,3"-Diindolylmethane (BR-DIM) can induce AMP-activated protein kinase (AMPK)-dependent potency loss in cultured embryos and whether metformin (Met) + Aspirin (Asa) or BR-DIM causes an AMPK-dependent decrease in embryonic development. Aspirin 277-280 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 159-187 27230877-1 2016 PURPOSE: The purpose of the present study is to test whether metformin, aspirin, or diet supplement (DS) BioResponse-3,3"-Diindolylmethane (BR-DIM) can induce AMP-activated protein kinase (AMPK)-dependent potency loss in cultured embryos and whether metformin (Met) + Aspirin (Asa) or BR-DIM causes an AMPK-dependent decrease in embryonic development. br-dim 285-291 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 159-187 27230877-6 2016 CONCLUSION: These experimental designs here showed that Met-, Asa-, BR-DIM-, or sorbitol stress-induced rapid potency loss in two-cell embryos is AMPK dependent as suggested by inhibition of Rex1 and/or Oct4 protein loss with an AMPK inhibitor. Aspirin 62-65 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 146-150 27230877-6 2016 CONCLUSION: These experimental designs here showed that Met-, Asa-, BR-DIM-, or sorbitol stress-induced rapid potency loss in two-cell embryos is AMPK dependent as suggested by inhibition of Rex1 and/or Oct4 protein loss with an AMPK inhibitor. Aspirin 62-65 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 229-233 27230877-6 2016 CONCLUSION: These experimental designs here showed that Met-, Asa-, BR-DIM-, or sorbitol stress-induced rapid potency loss in two-cell embryos is AMPK dependent as suggested by inhibition of Rex1 and/or Oct4 protein loss with an AMPK inhibitor. Sorbitol 80-88 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 146-150 27166596-0 2016 Corrigendum to "Ox-Lp(a) transiently induces HUVEC autophagy via an ROS-dependent PAPR-1-LKB1-AMPK-mTOR pathway" [Atherosclerosis 243 (1) (2015) 223-235]. ros 68-71 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 94-98 27444220-1 2016 Energy metabolism, involving the ATP-dependent AMPK-PgC-Ppar pathway impacts metabolic health immensely, in that its impairment can lead to obesity, giving rise to disease. Adenosine Triphosphate 33-36 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 47-51 26849413-6 2016 The FDA approved anti-diabetic drug Metformin, a well-known AMPK activator, induces mitochondrial biogenesis and is documented for its anti-inflammatory role. Metformin 36-45 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 60-64 26849413-7 2016 We observed a dose-dependent activation of AMPKalpha1 in metformin-treated X-ALD patient-derived fibroblasts. Metformin 57-66 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 43-53 26849413-13 2016 Taken together, these results provide proof-of-principle for therapeutic potential of metformin as a useful strategy for correcting the metabolic and inflammatory derangements in X-ALD by targeting AMPK. Metformin 86-95 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 198-202 26849413-15 2016 We document the therapeutic potential of FDA approved drug, Metformin, for X-ALD by targeting AMPK. Metformin 60-69 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 94-98 26849413-18 2016 Metformin-induced Abcd2 levels were dependent on AMPKalpha1, a metabolic and anti-inflammatory gene, recently documented by our laboratory to play a putative role in X-ALD pathology. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 49-59 27020861-0 2016 AMPK Activation and Metabolic Reprogramming by Tamoxifen through Estrogen Receptor-Independent Mechanisms Suggests New Uses for This Therapeutic Modality in Cancer Treatment. Tamoxifen 47-56 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 27147746-7 2016 Accordingly, an AMPK inhibitor, compound C, augmented viral lytic gene expressions and virion productions but an AMPK agonist, 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR), suppressed both. AICA ribonucleotide 127-172 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 113-117 27147746-8 2016 Furthermore, a common diabetes drug, metformin, which carries an AMPK-agonistic activity, drastically inhibited the expression of viral lytic genes and the production of infectious virions, suggesting the use of metformin as a therapeutic agent for KSHV infection and replication. Metformin 37-46 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 65-69 27147746-8 2016 Furthermore, a common diabetes drug, metformin, which carries an AMPK-agonistic activity, drastically inhibited the expression of viral lytic genes and the production of infectious virions, suggesting the use of metformin as a therapeutic agent for KSHV infection and replication. Metformin 212-221 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 65-69 27147746-14 2016 AICAR and metformin, both of which are AMPK agonists currently used in clinics for the treatment of conditions associated with metabolic disorders, inhibit KSHV lytic replication. AICA ribonucleotide 0-5 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 39-43 27147746-14 2016 AICAR and metformin, both of which are AMPK agonists currently used in clinics for the treatment of conditions associated with metabolic disorders, inhibit KSHV lytic replication. Metformin 10-19 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 39-43 27292634-5 2016 A transcriptomic, metabolomic, and phosphoproteomic study revealed that this metabolic switch is mediated by downregulation of HIF1alpha and AKT and upregulation of AMPK, allowing uptake and degradation of fatty acids and ketone bodies. Fatty Acids 206-217 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 165-169 27292634-5 2016 A transcriptomic, metabolomic, and phosphoproteomic study revealed that this metabolic switch is mediated by downregulation of HIF1alpha and AKT and upregulation of AMPK, allowing uptake and degradation of fatty acids and ketone bodies. Ketones 222-228 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 165-169 27325206-5 2016 Biochemical analysis revealed that HSP60 knockdown increased reactive oxygen species (ROS) production that led to AMPK activation, similarly to the complex I inhibitor rotenone-induced AMPK activation. Rotenone 168-176 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 185-189 27072494-0 2016 Exenatide exerts direct protective effects on endothelial cells through the AMPK/Akt/eNOS pathway in a GLP-1 receptor-dependent manner. Exenatide 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 76-80 27072494-11 2016 The effect may be mediated through activation of AMPK/PI3K-Akt/eNOS pathway via a GLP-1R/cAMP-dependent mechanism. Cyclic AMP 89-93 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 49-53 27020861-3 2016 Using combined pharmacologic and genetic knockout approaches, we demonstrate that tamoxifen inhibits oxygen consumption via inhibition of mitochondrial complex I, resulting in an increase in the AMP/ATP ratio and activation of the AMP-activated protein kinase (AMPK) signaling pathway in vitro and in vivo AMPK in turn promotes glycolysis and alters fatty acid metabolism. Tamoxifen 82-91 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 231-259 27020861-3 2016 Using combined pharmacologic and genetic knockout approaches, we demonstrate that tamoxifen inhibits oxygen consumption via inhibition of mitochondrial complex I, resulting in an increase in the AMP/ATP ratio and activation of the AMP-activated protein kinase (AMPK) signaling pathway in vitro and in vivo AMPK in turn promotes glycolysis and alters fatty acid metabolism. Tamoxifen 82-91 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 261-265 27020861-3 2016 Using combined pharmacologic and genetic knockout approaches, we demonstrate that tamoxifen inhibits oxygen consumption via inhibition of mitochondrial complex I, resulting in an increase in the AMP/ATP ratio and activation of the AMP-activated protein kinase (AMPK) signaling pathway in vitro and in vivo AMPK in turn promotes glycolysis and alters fatty acid metabolism. Tamoxifen 82-91 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 306-310 27020861-3 2016 Using combined pharmacologic and genetic knockout approaches, we demonstrate that tamoxifen inhibits oxygen consumption via inhibition of mitochondrial complex I, resulting in an increase in the AMP/ATP ratio and activation of the AMP-activated protein kinase (AMPK) signaling pathway in vitro and in vivo AMPK in turn promotes glycolysis and alters fatty acid metabolism. Oxygen 101-107 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 231-259 27020861-3 2016 Using combined pharmacologic and genetic knockout approaches, we demonstrate that tamoxifen inhibits oxygen consumption via inhibition of mitochondrial complex I, resulting in an increase in the AMP/ATP ratio and activation of the AMP-activated protein kinase (AMPK) signaling pathway in vitro and in vivo AMPK in turn promotes glycolysis and alters fatty acid metabolism. Oxygen 101-107 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 306-310 27020861-3 2016 Using combined pharmacologic and genetic knockout approaches, we demonstrate that tamoxifen inhibits oxygen consumption via inhibition of mitochondrial complex I, resulting in an increase in the AMP/ATP ratio and activation of the AMP-activated protein kinase (AMPK) signaling pathway in vitro and in vivo AMPK in turn promotes glycolysis and alters fatty acid metabolism. Fatty Acids 350-360 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 261-265 27020861-4 2016 We also show that tamoxifen-induced cytotoxicity is modulated by isoform-specific effects of AMPK signaling, in which AMPKalpha1 promotes cell death through inhibition of the mTOR pathway and translation. Tamoxifen 18-27 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 93-97 27020861-4 2016 We also show that tamoxifen-induced cytotoxicity is modulated by isoform-specific effects of AMPK signaling, in which AMPKalpha1 promotes cell death through inhibition of the mTOR pathway and translation. Tamoxifen 18-27 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 118-128 27035650-0 2016 Involvement of mTOR and Regulation by AMPK in Early Iodine Deficiency-Induced Thyroid Microvascular Activation. Iodine 52-58 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 38-42 27035650-8 2016 Activation of AMPK by metformin inhibited ID effects both in vivo and in vitro. Metformin 22-31 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-18 27035650-11 2016 AMPK negatively regulates this pathway, which may account for the transient nature of ID-induced TSH-independent vascular effects under benign conditions. Thyrotropin 97-100 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 27367504-9 2016 CONCLUSIONS: Berberine inhibits modified LDL-induced Muller cell injury by activating the AMPK pathway, and merits further study as an agent for preventing and/or treating DR. Berberine 13-22 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 90-94 26975583-8 2016 Here, we show that inhibition of AMPK by compound C or by shRNA-mediated depletion of LKB1 reduces activation of autophagy by rapamycin in Tsc2-null cells. Sirolimus 126-135 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 33-37 26975583-12 2016 These results indicate that an AMPK/p27 axis is promoting a survival mechanism that could explain in part the relapse of TSC tumors treated with rapamycin, exposing new avenues for designing more efficient treatments for TSC patients. Sirolimus 145-154 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 31-35 27109475-4 2016 The results displayed that the AMPKalpha1 overexpression suppressed lipid accumulation in the cytoplasm, decreased triglyceride levels, maintained the survival of steatotic hepatocyte model with decreased cell apoptosis and increased survival rate. Triglycerides 115-127 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 31-41 27109475-7 2016 Finally, Anisomycin, a frequently-used activator of p38MAPK, reversed the inhibitory effect of pc-AMPKalpha1 on the expression of p-p38MAPK, suggesting that AMPKalpha1 overexpression alleviates inflammatory response through the inactivation of p38MAPK. Anisomycin 9-19 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 98-108 27109475-7 2016 Finally, Anisomycin, a frequently-used activator of p38MAPK, reversed the inhibitory effect of pc-AMPKalpha1 on the expression of p-p38MAPK, suggesting that AMPKalpha1 overexpression alleviates inflammatory response through the inactivation of p38MAPK. Anisomycin 9-19 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 157-167 27184670-11 2016 CONCLUSIONS: Our results demonstrate that RCE regulates hepatic glycogen and lipid metabolism through the AMPK signaling pathway. Glycogen 64-72 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 106-110 27002150-4 2016 Recently, we found that therapeutic metformin concentrations suppressed glucose production in primary hepatocytes through AMPK; activation of the cAMP-PKA pathway negatively regulates AMPK activity by phosphorylating AMPKalpha subunit at Ser-485, which in turn reduces AMPK activity. Metformin 36-45 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 122-126 27002150-4 2016 Recently, we found that therapeutic metformin concentrations suppressed glucose production in primary hepatocytes through AMPK; activation of the cAMP-PKA pathway negatively regulates AMPK activity by phosphorylating AMPKalpha subunit at Ser-485, which in turn reduces AMPK activity. Metformin 36-45 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 184-188 27002150-4 2016 Recently, we found that therapeutic metformin concentrations suppressed glucose production in primary hepatocytes through AMPK; activation of the cAMP-PKA pathway negatively regulates AMPK activity by phosphorylating AMPKalpha subunit at Ser-485, which in turn reduces AMPK activity. Metformin 36-45 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 184-188 27002150-4 2016 Recently, we found that therapeutic metformin concentrations suppressed glucose production in primary hepatocytes through AMPK; activation of the cAMP-PKA pathway negatively regulates AMPK activity by phosphorylating AMPKalpha subunit at Ser-485, which in turn reduces AMPK activity. Glucose 72-79 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 122-126 27002150-4 2016 Recently, we found that therapeutic metformin concentrations suppressed glucose production in primary hepatocytes through AMPK; activation of the cAMP-PKA pathway negatively regulates AMPK activity by phosphorylating AMPKalpha subunit at Ser-485, which in turn reduces AMPK activity. Cyclic AMP 146-150 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 184-188 27002150-4 2016 Recently, we found that therapeutic metformin concentrations suppressed glucose production in primary hepatocytes through AMPK; activation of the cAMP-PKA pathway negatively regulates AMPK activity by phosphorylating AMPKalpha subunit at Ser-485, which in turn reduces AMPK activity. Cyclic AMP 146-150 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 184-188 27002150-6 2016 Expression of the AMPKalpha1(S485A) mutant, which is unable to be phosphorylated by PKA, increased both AMPKalpha activation and the suppression of glucose production in primary hepatocytes treated with metformin. Glucose 148-155 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 18-28 27002150-6 2016 Expression of the AMPKalpha1(S485A) mutant, which is unable to be phosphorylated by PKA, increased both AMPKalpha activation and the suppression of glucose production in primary hepatocytes treated with metformin. Metformin 203-212 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 18-28 27002150-7 2016 Intriguingly, salicylate/aspirin prevents the phosphorylation of AMPKalpha at Ser-485, blocks cAMP-PKA negative regulation of AMPK, and improves metformin resistance. Salicylates 14-24 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 65-69 27002150-7 2016 Intriguingly, salicylate/aspirin prevents the phosphorylation of AMPKalpha at Ser-485, blocks cAMP-PKA negative regulation of AMPK, and improves metformin resistance. Aspirin 25-32 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 65-69 27002150-7 2016 Intriguingly, salicylate/aspirin prevents the phosphorylation of AMPKalpha at Ser-485, blocks cAMP-PKA negative regulation of AMPK, and improves metformin resistance. Serine 78-81 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 65-69 27002150-7 2016 Intriguingly, salicylate/aspirin prevents the phosphorylation of AMPKalpha at Ser-485, blocks cAMP-PKA negative regulation of AMPK, and improves metformin resistance. Cyclic AMP 94-98 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 65-69 27002150-7 2016 Intriguingly, salicylate/aspirin prevents the phosphorylation of AMPKalpha at Ser-485, blocks cAMP-PKA negative regulation of AMPK, and improves metformin resistance. Metformin 145-154 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 65-69 27164138-0 2016 Polyphenol-Rich Propolis Extracts Strengthen Intestinal Barrier Function by Activating AMPK and ERK Signaling. Polyphenols 0-10 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 87-91 27164138-7 2016 Using selective inhibitors, we found that the positive effects of PPE on barrier function were abolished in cells in which AMPK and ERK1/2 signaling were inhibited. ppe 66-69 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 123-127 27164138-9 2016 Overall, these data suggest that PPE strengthens intestinal barrier function by activating AMPK and ERK signaling and provide novel insights into the potential application of propolis for human gut health. ppe 33-36 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 91-95 26924458-0 2016 Genistein-induced LKB1-AMPK activation inhibits senescence of VSMC through autophagy induction. Genistein 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 23-27 26924458-6 2016 Genistein dose- and time-dependently increased the phosphorylation of LKB1 and AMPK in VSMCs. Genistein 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 79-83 26924458-8 2016 Genistein-induced autophagy was inhibited in dominant-negative AMPK-transfected cells, whereas it was accelerated in cells transfected with the constitutively active form of AMPK. Genistein 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 63-67 26924458-8 2016 Genistein-induced autophagy was inhibited in dominant-negative AMPK-transfected cells, whereas it was accelerated in cells transfected with the constitutively active form of AMPK. Genistein 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 174-178 26924458-11 2016 These results suggest that genistein-dependent autophagy diminishes VSMC senescence and genistein may attenuate the VSMC senescence via an LKB1-AMPK-dependent mechanism. Genistein 88-97 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 144-148 27145268-0 2016 mir-101-3p is a key regulator of tumor metabolism in triple negative breast cancer targeting AMPK. mir-101-3p 0-10 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 93-97 27145268-6 2016 Ectopic expression of AMPK improved glucose uptake, glycolysis, proliferation of TNBC cells in vitro and its tumorigenicity in vivo. Glucose 36-43 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 22-26 27145268-9 2016 The expression of AMPK was suppressed by transfection of mir-101-3p in TNBC cells. mir-101 57-64 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 18-22 27145268-10 2016 Over-expression of mir-101-3p or knock-down of AMPK inhibited glucose metabolism and proliferation of TNBC cells in vitro. Glucose 62-69 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 47-51 26942884-3 2016 We have found that pharmacologic stimulation of the Kv11.3 channel with a small molecule activator, NS1643 induced autophagy via activation of an AMPK-dependent signaling pathway in melanoma cell line. 1,3-bis(2-hydroxy-5-trifluoromethylphenyl)urea 100-106 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 146-150 27030036-0 2016 Erratum to: Suppression of c-Myc induces apoptosis via an AMPK/mTOR-dependent pathway by 4-O-methyl-ascochlorin in leukemia cells. 4-O-methylascochlorin 89-111 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 58-62 26922069-0 2016 Suppression of c-Myc induces apoptosis via an AMPK/mTOR-dependent pathway by 4-O-methyl-ascochlorin in leukemia cells. 4-O-methylascochlorin 77-99 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 46-50 26922069-7 2016 Treatment of cells with AICAR (an AMPK activator), rapamycin (an mTOR inhibitor), or mTOR siRNA downregulated c-Myc expression and induced apoptosis to a similar extent to that of MAC. AICA ribonucleotide 24-29 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 34-38 26771234-8 2016 On the other hand, overexpression of Atg5 or AMPK-alpha1 in BR cells can redirect arginine deprivation-induced apoptosis toward autophagy. Arginine 82-90 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 45-56 26894973-4 2016 Both AMPK and PKA were promptly activated after glucose withdrawal. Glucose 48-55 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 5-9 26894973-6 2016 We detected AMPK phosphorylation (AMPKalpha(Ser173)) by PKA, which was increased in glucose starved cells and was associated with diminution of AMPK activation. Glucose 84-91 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 12-16 26894973-6 2016 We detected AMPK phosphorylation (AMPKalpha(Ser173)) by PKA, which was increased in glucose starved cells and was associated with diminution of AMPK activation. Glucose 84-91 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 34-38 26952388-0 2016 Structural basis of allosteric and synergistic activation of AMPK by furan-2-phosphonic derivative C2 binding. furan-2-phosphonic 69-87 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 61-65 27010359-7 2016 We further elucidate a Smo/Lkb1/Ampk axis as the non-canonical Hh pathway used by MP(Hh+) and GSA-10 to inhibit adipocyte differentiation. GSA-10 94-100 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 32-36 26885898-3 2016 In this present study, we confirmed that metformin enhanced SIRT1 and AMPK expression in human umbilical vein endothelial cells (HUVECs). Metformin 41-50 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 70-74 26885898-5 2016 However, silencing SIRT1 and AMPK diminished the protective function of metformin against oxidative injuries. Metformin 72-81 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 29-33 26952388-3 2016 We have determined the crystal structure of AMPK in complex with its activator 5-(5-hydroxyl-isoxazol-3-yl)-furan-2-phosphonic acid (C2), revealing two C2-binding sites in the gamma-subunit distinct from nucleotide sites. 5-(5-hydroxylisoxazol-3-yl)furan-2-phosphonic acid 79-131 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 44-48 26952388-3 2016 We have determined the crystal structure of AMPK in complex with its activator 5-(5-hydroxyl-isoxazol-3-yl)-furan-2-phosphonic acid (C2), revealing two C2-binding sites in the gamma-subunit distinct from nucleotide sites. A(2)C 133-135 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 44-48 26952388-4 2016 C2 acts synergistically with the drug A769662 to activate AMPK alpha1-containing complexes independent of upstream kinases. 4-hydroxy-3-(4-(2-hydroxyphenyl)phenyl)-6-oxo-7H-thieno(2,3-b)pyridine-5-carbonitrile 38-45 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 58-69 26673543-9 2016 These results suggest that the PPAR-gamma agonist pioglitazone prevents NF-kappaB activation in cisplatin nephrotoxicity through a reduction in p65 acetylation via the AMPK-SIRT1/p300 pathway. Pioglitazone 50-62 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 168-172 26804918-5 2016 These data implicate the PGC-1alpha/ERRalpha axis as a core regulatory node of folate cycle metabolism and further suggest that activators of AMPK could be used to modulate this pathway in cancer. Folic Acid 79-85 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 142-146 26673543-0 2016 The peroxisome proliferator-activated receptor gamma agonist pioglitazone prevents NF-kappaB activation in cisplatin nephrotoxicity through the reduction of p65 acetylation via the AMPK-SIRT1/p300 pathway. Pioglitazone 61-73 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 181-185 26689352-0 2016 1,4-Dihydropyridines Active on the SIRT1/AMPK Pathway Ameliorate Skin Repair and Mitochondrial Function and Exhibit Inhibition of Proliferation in Cancer Cells. 1,4-dihydropyridine 0-20 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 41-45 26689352-5 2016 All the effects were reverted by coadministration of compound C (9), an AMPK inhibitor, or of EX-527 (10), a SIRT1 inhibitor, highlighting the involvement of the SIRT1/AMPK pathway in the action of DHPs. 6-chloro-2,3,4,9-tetrahydro-1H-carbazole-1-carboxamide 94-100 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 168-172 26689352-5 2016 All the effects were reverted by coadministration of compound C (9), an AMPK inhibitor, or of EX-527 (10), a SIRT1 inhibitor, highlighting the involvement of the SIRT1/AMPK pathway in the action of DHPs. 1,4-dihydropyridine 198-202 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 168-172 26802022-8 2016 The results demonstrated that metformin activated AMPK and decreased phosphorylation of Akt and Erk. Metformin 30-39 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 50-54 26717043-5 2016 Second, Metformin, a pharmacological AMPK activator and anti-diabetic drug, or ectopic expression of LKB1, diminished expression of Bmi-1 in cancer cells, an event that was reversed by silencing LKB1. Metformin 8-17 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 37-41 26673543-0 2016 The peroxisome proliferator-activated receptor gamma agonist pioglitazone prevents NF-kappaB activation in cisplatin nephrotoxicity through the reduction of p65 acetylation via the AMPK-SIRT1/p300 pathway. Cisplatin 107-116 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 181-185 26673543-9 2016 These results suggest that the PPAR-gamma agonist pioglitazone prevents NF-kappaB activation in cisplatin nephrotoxicity through a reduction in p65 acetylation via the AMPK-SIRT1/p300 pathway. Cisplatin 96-105 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 168-172 26089158-8 2016 We also found that gene silencing of AMPK prevented gAcrp-induced nuclear translocation of FoxO3A in HepG2 and MCF-7 cells. gacrp 52-57 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 37-41 26089158-9 2016 In addition, suppression of AMPK also blocked gAcrp-induced cell cycle arrest and further attenuated gAcrp-induced caspase-3/7 activation, indicating that AMPK signaling plays a pivotal role in both gAcrp-induced cell cycle arrest and apoptosis via acting as an upstream signaling of FoxO3A. gacrp 46-51 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 28-32 26089158-9 2016 In addition, suppression of AMPK also blocked gAcrp-induced cell cycle arrest and further attenuated gAcrp-induced caspase-3/7 activation, indicating that AMPK signaling plays a pivotal role in both gAcrp-induced cell cycle arrest and apoptosis via acting as an upstream signaling of FoxO3A. gacrp 46-51 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 155-159 26089158-9 2016 In addition, suppression of AMPK also blocked gAcrp-induced cell cycle arrest and further attenuated gAcrp-induced caspase-3/7 activation, indicating that AMPK signaling plays a pivotal role in both gAcrp-induced cell cycle arrest and apoptosis via acting as an upstream signaling of FoxO3A. gacrp 101-106 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 28-32 26089158-9 2016 In addition, suppression of AMPK also blocked gAcrp-induced cell cycle arrest and further attenuated gAcrp-induced caspase-3/7 activation, indicating that AMPK signaling plays a pivotal role in both gAcrp-induced cell cycle arrest and apoptosis via acting as an upstream signaling of FoxO3A. gacrp 101-106 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 155-159 26089158-9 2016 In addition, suppression of AMPK also blocked gAcrp-induced cell cycle arrest and further attenuated gAcrp-induced caspase-3/7 activation, indicating that AMPK signaling plays a pivotal role in both gAcrp-induced cell cycle arrest and apoptosis via acting as an upstream signaling of FoxO3A. gacrp 101-106 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 28-32 26089158-9 2016 In addition, suppression of AMPK also blocked gAcrp-induced cell cycle arrest and further attenuated gAcrp-induced caspase-3/7 activation, indicating that AMPK signaling plays a pivotal role in both gAcrp-induced cell cycle arrest and apoptosis via acting as an upstream signaling of FoxO3A. gacrp 101-106 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 155-159 26614120-11 2016 Consistently, pharmacological AMPK activation with 5-aminoimidazole-4-carboxamide riboside (AICAR) in mouse muscle did not affect the LC3-II/LC3-I ratio. acadesine 51-90 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-34 26054542-8 2016 Treatment of Lkb1-deficient cells with an AMP-activated protein kinase (AMPK) agonist (A769662) or a peroxisome proliferative activated receptor alpha agonist (fenofibrate) restored the fatty oxidation defect and reduced apoptosis. 4-hydroxy-3-(4-(2-hydroxyphenyl)phenyl)-6-oxo-7H-thieno(2,3-b)pyridine-5-carbonitrile 87-94 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 42-70 26054542-8 2016 Treatment of Lkb1-deficient cells with an AMP-activated protein kinase (AMPK) agonist (A769662) or a peroxisome proliferative activated receptor alpha agonist (fenofibrate) restored the fatty oxidation defect and reduced apoptosis. 4-hydroxy-3-(4-(2-hydroxyphenyl)phenyl)-6-oxo-7H-thieno(2,3-b)pyridine-5-carbonitrile 87-94 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 72-76 26643070-0 2016 Pioglitazone, a PPARgamma agonist, attenuates PDGF-induced vascular smooth muscle cell proliferation through AMPK-dependent and AMPK-independent inhibition of mTOR/p70S6K and ERK signaling. Pioglitazone 0-12 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 109-113 26643070-0 2016 Pioglitazone, a PPARgamma agonist, attenuates PDGF-induced vascular smooth muscle cell proliferation through AMPK-dependent and AMPK-independent inhibition of mTOR/p70S6K and ERK signaling. Pioglitazone 0-12 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 128-132 26643070-6 2016 In particular, PIO at 30muM concentration activates AMPK to induce raptor phosphorylation, which diminishes PDGF-induced mTOR activity as evidenced by decreased phosphorylation of p70S6K, 4E-BP1, and S6 and increased accumulation of p27(kip1), a cell cycle inhibitor. Pioglitazone 15-18 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 52-56 26643070-8 2016 Downregulation of endogenous AMPK by target-specific siRNA reveals an AMPK-independent effect for PIO inhibition of ERK, which contributes in part to diminutions in cyclin D1 expression and Rb phosphorylation and the suppression of VSMC proliferation. vsmc 232-236 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 29-33 26643070-8 2016 Downregulation of endogenous AMPK by target-specific siRNA reveals an AMPK-independent effect for PIO inhibition of ERK, which contributes in part to diminutions in cyclin D1 expression and Rb phosphorylation and the suppression of VSMC proliferation. vsmc 232-236 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 70-74 26614120-11 2016 Consistently, pharmacological AMPK activation with 5-aminoimidazole-4-carboxamide riboside (AICAR) in mouse muscle did not affect the LC3-II/LC3-I ratio. acadesine 92-97 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-34 26742424-2 2016 Activation of AMPK is associated with increased phosphorylation of the alpha-subunit at threonine 172 (T172) and decreased phosphorylation at serine 485 in AMPKalpha1 and serine 491 in AMPKalpha2 (S485/491). Serine 142-148 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 156-166 26998423-8 2016 CONCLUSION: The present study confirmed the AMPK signaling activation in the doxorubicin-treated osteosarcoma cells, in response to hypoxia, and the chemical upregulation or downregulation of AMPK signaling reduced or increased the chemo-sensitivity of osteosarcoma U2-os cells in vitro. Doxorubicin 77-88 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 44-48 27186419-0 2016 Quercetin induces bladder cancer cells apoptosis by activation of AMPK signaling pathway. Quercetin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 66-70 27186419-10 2016 We are the first to show that quercetin displays potent inhibition on bladder cancer cells via activation of AMPK pathway. Quercetin 30-39 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 109-113 26545901-10 2016 Moreover, the AMPK stimulator 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR) failed to increase AMPK activity in cells expressing the modified N-cadherin, indicating uncoupling of a functional association between AMPK and the cadherin. AICA ribonucleotide 30-75 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-18 26564773-5 2016 We also established fatty acid overload cell model in HepG2 cells to investigate the effect of melatonin on AMP-activated protein kinase (AMPK) activity. Melatonin 95-104 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 108-136 26564773-5 2016 We also established fatty acid overload cell model in HepG2 cells to investigate the effect of melatonin on AMP-activated protein kinase (AMPK) activity. Melatonin 95-104 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 138-142 26545901-10 2016 Moreover, the AMPK stimulator 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR) failed to increase AMPK activity in cells expressing the modified N-cadherin, indicating uncoupling of a functional association between AMPK and the cadherin. AICA ribonucleotide 77-82 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-18 26940341-6 2016 In addition, resveratrol, a known AMPK activator, induced similar G1-S arrests, while lentivirally-transduced WT or constitutively-active AMPKalpha1 retarded the proliferation of WT T cells. Resveratrol 13-24 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 34-38 26100787-0 2016 Testosterone stimulates glucose uptake and GLUT4 translocation through LKB1/AMPK signaling in 3T3-L1 adipocytes. Testosterone 0-12 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 76-80 27149559-0 2016 Resveratrol via activation of LKB1-AMPK signaling suppresses oxidative stress to prevent endothelial dysfunction in diabetic mice. Resveratrol 0-11 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 35-39 27149559-1 2016 BACKGROUND: Resveratrol, a phytoalexin, is reported to activate AMP-activated protein kinase (AMPK) in vascular cells. Resveratrol 12-23 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 94-98 27149559-1 2016 BACKGROUND: Resveratrol, a phytoalexin, is reported to activate AMP-activated protein kinase (AMPK) in vascular cells. phytoalexins 27-38 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 94-98 27149559-2 2016 Whether resveratrol via activation of AMPK improves endothelial dysfunction in diabetes remains unknown. Resveratrol 8-19 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 38-42 27149559-3 2016 Here, we reported that activation of AMPK is required for resveratrol-induced improvement of endothelial function in diabetic mice. Resveratrol 58-69 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 37-41 27149559-5 2016 RESULTS: Exposure of cultured human umbilical vein endothelial cells (HUVECs) to resveratrol activates AMPK by increasing the thr172 phosphorylation and its activities in time/dose-dependent manner. Resveratrol 81-92 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 103-107 27149559-6 2016 Loss function of liver kinase B1 by siRNA or mutant abolished resveratrol-induced AMPK activation. Resveratrol 62-73 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 82-86 27149559-7 2016 Incubation of endothelial cells with high glucose (HG) markedly induced oxidative stress of HUVECs, which was abolished by resveratrol in AMPK-dependent manner. Glucose 42-49 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 138-142 27149559-7 2016 Incubation of endothelial cells with high glucose (HG) markedly induced oxidative stress of HUVECs, which was abolished by resveratrol in AMPK-dependent manner. Resveratrol 123-134 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 138-142 27149559-10 2016 CONCLUSIONS: We conclude that AMPK activation is required for resveratrol to improve endothelial function in diabetic mice. Resveratrol 62-73 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-34 26695692-3 2016 Metformin exerts its anticancer action via a variety of adenosine monophosphate (AMP)-activated protein kinase (AMPK)- dependent and/or AMPK-independent mechanisms. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 112-116 26695692-3 2016 Metformin exerts its anticancer action via a variety of adenosine monophosphate (AMP)-activated protein kinase (AMPK)- dependent and/or AMPK-independent mechanisms. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 136-140 26695692-3 2016 Metformin exerts its anticancer action via a variety of adenosine monophosphate (AMP)-activated protein kinase (AMPK)- dependent and/or AMPK-independent mechanisms. Adenosine Monophosphate 56-79 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 112-116 26695692-3 2016 Metformin exerts its anticancer action via a variety of adenosine monophosphate (AMP)-activated protein kinase (AMPK)- dependent and/or AMPK-independent mechanisms. Adenosine Monophosphate 81-84 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 112-116 26100787-0 2016 Testosterone stimulates glucose uptake and GLUT4 translocation through LKB1/AMPK signaling in 3T3-L1 adipocytes. Glucose 24-31 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 76-80 26100787-10 2016 Testosterone and testosterone-BSA stimulated the phosphorylation of AMPK, LKB1, and CaMKII. Testosterone 0-12 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 68-72 26100787-10 2016 Testosterone and testosterone-BSA stimulated the phosphorylation of AMPK, LKB1, and CaMKII. Testosterone 17-29 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 68-72 26100787-11 2016 The knockdown of LKB1 by siRNA attenuated testosterone- and testosterone-BSA-stimulated AMPK phosphorylation and glucose uptake. Testosterone 42-54 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 88-92 26100787-12 2016 These results indicate that high-dose testosterone and testosterone-BSA increase GLUT4-dependent glucose uptake in 3T3-L1 adipocytes by inducing the LKB1/AMPK signaling pathway. Testosterone 38-50 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 154-158 26100787-12 2016 These results indicate that high-dose testosterone and testosterone-BSA increase GLUT4-dependent glucose uptake in 3T3-L1 adipocytes by inducing the LKB1/AMPK signaling pathway. Glucose 97-104 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 154-158 26105159-1 2016 The activation of AMP-activated protein kinase (AMPK) is known to repress the expression of the insulin gene and glucose-stimulated insulin secretion (GSIS). Glucose 113-120 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 18-46 27812975-0 2016 Regulation of Carbohydrate Metabolism, Lipid Metabolism, and Protein Metabolism by AMPK. Carbohydrates 14-26 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 83-87 27812975-1 2016 This chapter summarizes AMPK function in the regulation of substrate and energy metabolism with the main emphasis on carbohydrate and lipid metabolism, protein turnover, mitochondrial biogenesis, and whole-body energy homeostasis. Carbohydrates 117-129 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 24-28 27812975-3 2016 AMPK mainly promotes glucose and fatty acid catabolism, whereas it prevents protein, glycogen, and fatty acid synthesis. Glucose 21-28 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 27812975-3 2016 AMPK mainly promotes glucose and fatty acid catabolism, whereas it prevents protein, glycogen, and fatty acid synthesis. Fatty Acids 33-43 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 27812975-3 2016 AMPK mainly promotes glucose and fatty acid catabolism, whereas it prevents protein, glycogen, and fatty acid synthesis. Glycogen 85-93 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 27812975-3 2016 AMPK mainly promotes glucose and fatty acid catabolism, whereas it prevents protein, glycogen, and fatty acid synthesis. Fatty Acids 99-109 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 27812977-4 2016 Balancing the oxygen regulatory environment with the demands for energy and need to maintain metabolism during this process places AMPK at the center of maintaining placental cellular homeostasis as it integrates and responds to numerous complex stimuli. Oxygen 14-20 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 131-135 28042296-0 2016 Deferoxamine Suppresses Collagen Cleavage and Protease, Cytokine, and COL10A1 Expression and Upregulates AMPK and Krebs Cycle Genes in Human Osteoarthritic Cartilage. Deferoxamine 0-12 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 105-109 26105159-1 2016 The activation of AMP-activated protein kinase (AMPK) is known to repress the expression of the insulin gene and glucose-stimulated insulin secretion (GSIS). Glucose 113-120 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 48-52 26682233-0 2016 Coenzyme Q10 Attenuates High Glucose-Induced Endothelial Progenitor Cell Dysfunction through AMP-Activated Protein Kinase Pathways. Glucose 29-36 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 93-121 26682233-12 2016 CoQ10 reduced high glucose-induced EPC apoptosis and dysfunction through upregulation of eNOS, HO-1 through the AMPK pathway. Glucose 19-26 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 112-116 27551487-3 2015 We provide evidence that AMPK-p38-PGC-1alpha axis, by regulating energy homeostasis, maintains survival in cancer cells under glucose-limiting conditions. Glucose 126-133 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 25-29 26824050-0 2016 Clopidogrel Protects Endothelium by Hindering TNFalpha-Induced VCAM-1 Expression through CaMKKbeta/AMPK/Nrf2 Pathway. Clopidogrel 0-11 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 99-103 26497305-0 2016 AMPK activator AICAR promotes 5-FU-induced apoptosis in gastric cancer cells. Fluorouracil 30-34 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 26497305-9 2016 Finally, p-AMPK levels were reduced in 5-FU-resistant gastric cancer cells compared to human immortalized gastric epithelial cell line and 5-FU-sensitive gastric cancer cells. Fluorouracil 39-43 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 11-15 26497305-9 2016 Finally, p-AMPK levels were reduced in 5-FU-resistant gastric cancer cells compared to human immortalized gastric epithelial cell line and 5-FU-sensitive gastric cancer cells. Fluorouracil 139-143 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 11-15 26485766-3 2015 Our results showed that the C allele of PRKAA1 rs13361707 increased the GC risk in the study population [CT vs. TT, odds ratio (OR) = 1.72, 95% confidence interval (CI) = 1.40-2.12; CC vs. TT, OR = 2.15, 95%CI = 1.70-2.71; CT/CC vs. TT, OR = 1.86, 95%CI = 1.53-2.26; CC vs.TT/CT, OR = 1.49, 95%CI = 1.24-1.79]. Carbon Tetrachloride 105-107 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 40-46 26715839-0 2015 Autophagy facilitates lung adenocarcinoma resistance to cisplatin treatment by activation of AMPK/mTOR signaling pathway. Cisplatin 56-65 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 93-97 26715839-9 2015 Compared to cisplatin treatment alone, the combination of cisplatin and CQ decreased p-AMPK and increased p-mTOR protein expressions, in addition, the AMPK inhibitor Compound C plus cisplatin downregulated p-AMPK and upregulated p-mTOR as well as depressed LC3B cleavage. Cisplatin 58-67 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 87-91 26715839-9 2015 Compared to cisplatin treatment alone, the combination of cisplatin and CQ decreased p-AMPK and increased p-mTOR protein expressions, in addition, the AMPK inhibitor Compound C plus cisplatin downregulated p-AMPK and upregulated p-mTOR as well as depressed LC3B cleavage. Cisplatin 58-67 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 151-155 26715839-9 2015 Compared to cisplatin treatment alone, the combination of cisplatin and CQ decreased p-AMPK and increased p-mTOR protein expressions, in addition, the AMPK inhibitor Compound C plus cisplatin downregulated p-AMPK and upregulated p-mTOR as well as depressed LC3B cleavage. Cisplatin 58-67 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 151-155 26715839-9 2015 Compared to cisplatin treatment alone, the combination of cisplatin and CQ decreased p-AMPK and increased p-mTOR protein expressions, in addition, the AMPK inhibitor Compound C plus cisplatin downregulated p-AMPK and upregulated p-mTOR as well as depressed LC3B cleavage. Chloroquine 72-74 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 87-91 26715839-9 2015 Compared to cisplatin treatment alone, the combination of cisplatin and CQ decreased p-AMPK and increased p-mTOR protein expressions, in addition, the AMPK inhibitor Compound C plus cisplatin downregulated p-AMPK and upregulated p-mTOR as well as depressed LC3B cleavage. Chloroquine 72-74 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 151-155 26715839-9 2015 Compared to cisplatin treatment alone, the combination of cisplatin and CQ decreased p-AMPK and increased p-mTOR protein expressions, in addition, the AMPK inhibitor Compound C plus cisplatin downregulated p-AMPK and upregulated p-mTOR as well as depressed LC3B cleavage. Chloroquine 72-74 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 151-155 26715839-9 2015 Compared to cisplatin treatment alone, the combination of cisplatin and CQ decreased p-AMPK and increased p-mTOR protein expressions, in addition, the AMPK inhibitor Compound C plus cisplatin downregulated p-AMPK and upregulated p-mTOR as well as depressed LC3B cleavage. Cisplatin 58-67 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 87-91 26715839-9 2015 Compared to cisplatin treatment alone, the combination of cisplatin and CQ decreased p-AMPK and increased p-mTOR protein expressions, in addition, the AMPK inhibitor Compound C plus cisplatin downregulated p-AMPK and upregulated p-mTOR as well as depressed LC3B cleavage. Cisplatin 58-67 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 151-155 26715839-9 2015 Compared to cisplatin treatment alone, the combination of cisplatin and CQ decreased p-AMPK and increased p-mTOR protein expressions, in addition, the AMPK inhibitor Compound C plus cisplatin downregulated p-AMPK and upregulated p-mTOR as well as depressed LC3B cleavage. Cisplatin 58-67 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 151-155 26715839-10 2015 These findings demonstrate that activation of autophagy is a hallmark of cisplatin exposure in human lung adenocarcinoma cells, and that there is a cisplatin-induced autophagic response via activation of the AMPK/mTOR signaling pathway. Cisplatin 148-157 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 208-212 26491018-5 2015 Intriguingly, low glycogen storage and transcription of lactate turnover-related genes in DMRC hepatocytes were recovered by inhibition of AMPK activity. Glycogen 18-26 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 139-143 26491018-5 2015 Intriguingly, low glycogen storage and transcription of lactate turnover-related genes in DMRC hepatocytes were recovered by inhibition of AMPK activity. Lactic Acid 56-63 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 139-143 26491018-6 2015 Thus, AMPK activation led to metabolic changes in terms of glycogen storage and lactate turnover in DMRC hepatocytes. Glycogen 59-67 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 6-10 26491018-6 2015 Thus, AMPK activation led to metabolic changes in terms of glycogen storage and lactate turnover in DMRC hepatocytes. Lactic Acid 80-87 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 6-10 26491018-7 2015 These data demonstrate for the first time that energy depletion may lead to lactic acidosis in the DMRC patient by reduction of lactate uptake via AMPK in liver. dmrc 99-103 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 147-151 26491018-7 2015 These data demonstrate for the first time that energy depletion may lead to lactic acidosis in the DMRC patient by reduction of lactate uptake via AMPK in liver. Lactic Acid 128-135 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 147-151 25858560-4 2015 Deletion of AMPKalpha1 or AMPKalpha2 resulted in activation of STAT1 and in increases in proinflammatory mediators, both of which were attenuated by administration of STAT1 small interfering RNA or fludarabine, a selective STAT1 inhibitor. fludarabine 198-209 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 12-22 26626483-4 2015 Under glucose starvation, but not amino acid starvation, cytoplasmic GAPDH is phosphorylated on Ser122 by activated AMPK. Glucose 6-13 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 116-120 26678339-5 2015 NAD+ depletion activated the intracellular energy sensor AMPK, triggered autophagy, and resulted in cytotoxicity. NAD 0-4 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 57-61 26426570-2 2015 On the other hand, the well-recognized role of AMPK in maintaining ATP homeostasis, through suppression of anabolism and promotion of catabolism, as well as the role of AMPK in neutralizing reactive oxygen species, via maintenance of NADPH-dependent reductive capacity, point to tumour-protective roles in the context of metabolic stress, which is a key feature of many solid tumours. Adenosine Triphosphate 67-70 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 47-51 26426570-2 2015 On the other hand, the well-recognized role of AMPK in maintaining ATP homeostasis, through suppression of anabolism and promotion of catabolism, as well as the role of AMPK in neutralizing reactive oxygen species, via maintenance of NADPH-dependent reductive capacity, point to tumour-protective roles in the context of metabolic stress, which is a key feature of many solid tumours. Reactive Oxygen Species 190-213 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 169-173 26424816-1 2015 AMP-activated protein kinase (AMPK), an important downstream effector of the tumor suppressor liver kinase 1 (LKB1) and pharmacologic target of metformin, is well known to exert a preventive and inhibitory effect on tumorigenesis; however, its role in cancer progression and metastasis has not been well characterized. Metformin 144-153 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-28 26424816-1 2015 AMP-activated protein kinase (AMPK), an important downstream effector of the tumor suppressor liver kinase 1 (LKB1) and pharmacologic target of metformin, is well known to exert a preventive and inhibitory effect on tumorigenesis; however, its role in cancer progression and metastasis has not been well characterized. Metformin 144-153 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-34 26424816-3 2015 Our results showed that activation of AMPK by metformin inhibited TGF-beta-induced Smad2/3 phosphorylation in cancer cells in a dose-dependent manner. Metformin 46-55 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 38-42 27551487-4 2015 Functioning as a molecular switch, AMPK promotes glycolysis by activating PFK2, and facilitates mitochondrial metabolism of non-glucose carbon sources thereby maintaining cellular ATP level. Glucose 128-135 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 35-39 27551487-4 2015 Functioning as a molecular switch, AMPK promotes glycolysis by activating PFK2, and facilitates mitochondrial metabolism of non-glucose carbon sources thereby maintaining cellular ATP level. Carbon 136-142 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 35-39 27551487-4 2015 Functioning as a molecular switch, AMPK promotes glycolysis by activating PFK2, and facilitates mitochondrial metabolism of non-glucose carbon sources thereby maintaining cellular ATP level. Adenosine Triphosphate 180-183 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 35-39 26400185-0 2015 Folic acid supplementation during high-fat diet feeding restores AMPK activation via an AMP-LKB1-dependent mechanism. Folic Acid 0-10 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 65-69 26616021-1 2015 AMP-activated protein kinase (AMPK) inhibits several anabolic pathways such as fatty acid and protein synthesis, and identification of AMPK substrate specificity would be useful to understand its role in particular cellular processes and develop strategies to modulate AMPK activity in a substrate-specific manner. Fatty Acids 79-89 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-34 26486079-5 2015 Inhibition of both AMPK and PERK/CHOP pathways by siRNA or chemical inhibitor could block CGK733-induced p21Waf1/Cip1 expression as well as caspase-3 cleavage. CGK 733 90-96 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 19-23 26400185-9 2015 Consistent with in vivo findings, 5-methyltetrahydrofolate (bioactive form of folate) restored phosphorylation (activation) of both AMPK and LKB1 in palmitic acid-treated HepG2 cells. Folic Acid 52-58 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 132-136 26400185-9 2015 Consistent with in vivo findings, 5-methyltetrahydrofolate (bioactive form of folate) restored phosphorylation (activation) of both AMPK and LKB1 in palmitic acid-treated HepG2 cells. Palmitic Acid 149-162 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 132-136 26400185-10 2015 Activation of AMPK by folic acid might be responsible for AMPK-dependent phosphorylation of HMG-CoA reductase, leading to reduced hepatic cholesterol synthesis during high-fat diet feeding. Folic Acid 22-32 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-18 26400185-10 2015 Activation of AMPK by folic acid might be responsible for AMPK-dependent phosphorylation of HMG-CoA reductase, leading to reduced hepatic cholesterol synthesis during high-fat diet feeding. Folic Acid 22-32 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 58-62 26400185-10 2015 Activation of AMPK by folic acid might be responsible for AMPK-dependent phosphorylation of HMG-CoA reductase, leading to reduced hepatic cholesterol synthesis during high-fat diet feeding. Cholesterol 138-149 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-18 26400185-10 2015 Activation of AMPK by folic acid might be responsible for AMPK-dependent phosphorylation of HMG-CoA reductase, leading to reduced hepatic cholesterol synthesis during high-fat diet feeding. Cholesterol 138-149 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 58-62 26400185-11 2015 These results suggest that folic acid supplementation may improve cholesterol and glucose metabolism by restoration of AMPK activation in the liver. Folic Acid 27-37 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 119-123 26400185-1 2015 AMPK is an endogenous energy sensor that regulates lipid and carbohydrate metabolism. Carbohydrates 61-73 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 26400185-4 2015 The aim of the present study was to investigate the effect of folic acid on hepatic AMPK during high-fat diet feeding and the mechanisms involved. Folic Acid 62-72 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 84-88 26400185-7 2015 Folic acid supplementation restored AMPK phosphorylation (activation) and reduced blood glucose and hepatic cholesterol levels. Folic Acid 0-10 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 36-40 26400185-8 2015 Activation of AMPK by folic acid was mediated through an elevation of its allosteric activator AMP and activation of its upstream kinase, namely, liver kinase B1 (LKB1) in the liver. Folic Acid 22-32 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-18 26400185-9 2015 Consistent with in vivo findings, 5-methyltetrahydrofolate (bioactive form of folate) restored phosphorylation (activation) of both AMPK and LKB1 in palmitic acid-treated HepG2 cells. 5-methyltetrahydrofolate 34-58 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 132-136 26430787-3 2015 Although the precise molecular mechanisms by which metformin affects various cancers have not been fully elucidated, activation of AMPK-dependent and AMPK-independent pathways along with energy metabolism aberration, cell cycle arrest and apoptosis or autophagy induction have emerged as crucial regulators in this process. Metformin 51-60 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 131-135 26471090-0 2015 Saponarin activates AMPK in a calcium-dependent manner and suppresses gluconeogenesis and increases glucose uptake via phosphorylation of CRTC2 and HDAC5. saponarin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 20-24 26471090-0 2015 Saponarin activates AMPK in a calcium-dependent manner and suppresses gluconeogenesis and increases glucose uptake via phosphorylation of CRTC2 and HDAC5. Calcium 30-37 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 20-24 26471090-2 2015 Saponarin suppressed the rate of gluconeogenesis and increased cellular glucose uptake in HepG2 and TE671 cells by regulating AMPK. saponarin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 126-130 26471090-4 2015 Instead, saponarin increased intracellular calcium levels and induced AMPK phosphorylation, which was diminished by co-stimulation with STO-609, an inhibitor of CAMKKbeta. saponarin 9-18 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 70-74 26471090-4 2015 Instead, saponarin increased intracellular calcium levels and induced AMPK phosphorylation, which was diminished by co-stimulation with STO-609, an inhibitor of CAMKKbeta. STO 609 136-143 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 70-74 26471090-6 2015 This nuclear translocation was inhibited by increased phosphorylation of CRTC2 and HDAC5 by saponarin-induced AMPK in HepG2 cells and suppression of CREB and FoxO1 transactivation activities in cells stimulated by saponarin. saponarin 92-101 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 110-114 26544976-0 2015 Activation of AMP-Activated Protein Kinase by Adenine Alleviates TNF-Alpha-Induced Inflammation in Human Umbilical Vein Endothelial Cells. Adenine 46-53 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-42 26544976-2 2015 Previous studies suggest that the anti-inflammatory role of AMPK involves activation by adenine, but the mechanism that allows adenine to produce these effects has not yet been elucidated. Adenine 88-95 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 60-64 26544976-3 2015 In human umbilical vein endothelial cells (HUVECs), adenine was observed to induce the phosphorylation of AMPK in both a time- and dose-dependent manner as well as its downstream target acetyl Co-A carboxylase (ACC). Adenine 52-59 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 106-110 26544976-5 2015 The short hairpin RNA (shRNA) against AMPK alpha1 in HUVECs attenuated the adenine-induced inhibition of NF-kappaB activation in response to TNF-alpha, thereby suggesting that the anti-inflammatory role of adenine is mediated by AMPK. Adenine 75-82 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 38-49 26544976-5 2015 The short hairpin RNA (shRNA) against AMPK alpha1 in HUVECs attenuated the adenine-induced inhibition of NF-kappaB activation in response to TNF-alpha, thereby suggesting that the anti-inflammatory role of adenine is mediated by AMPK. Adenine 75-82 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 38-42 26544976-5 2015 The short hairpin RNA (shRNA) against AMPK alpha1 in HUVECs attenuated the adenine-induced inhibition of NF-kappaB activation in response to TNF-alpha, thereby suggesting that the anti-inflammatory role of adenine is mediated by AMPK. Adenine 206-213 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 38-49 26544976-5 2015 The short hairpin RNA (shRNA) against AMPK alpha1 in HUVECs attenuated the adenine-induced inhibition of NF-kappaB activation in response to TNF-alpha, thereby suggesting that the anti-inflammatory role of adenine is mediated by AMPK. Adenine 206-213 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 38-42 26544976-8 2015 These results suggested that the role of adenine as an AMPK activator is related to catabolism by APRT, which increases the cellular AMP levels to activate AMPK. Adenine 41-48 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 55-59 26544976-8 2015 These results suggested that the role of adenine as an AMPK activator is related to catabolism by APRT, which increases the cellular AMP levels to activate AMPK. Adenine 41-48 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 156-160 26544976-8 2015 These results suggested that the role of adenine as an AMPK activator is related to catabolism by APRT, which increases the cellular AMP levels to activate AMPK. Adenosine Monophosphate 55-58 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 156-160 26440282-4 2015 AMPK deletion significantly delayed leukemogenesis and depleted LICs by reducing the expression of glucose transporter 1 (Glut1), compromising glucose flux, and increasing oxidative stress and DNA damage. Glucose 99-106 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 26497364-3 2015 Metformin triggered AMPKalpha1 activation in macrophage and silencing of AMPKalpha1 partially abrogated the inhibitory effect of metformin in IL-13 induced M2-like polarization. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 20-30 26497364-3 2015 Metformin triggered AMPKalpha1 activation in macrophage and silencing of AMPKalpha1 partially abrogated the inhibitory effect of metformin in IL-13 induced M2-like polarization. Metformin 129-138 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 20-30 26497364-3 2015 Metformin triggered AMPKalpha1 activation in macrophage and silencing of AMPKalpha1 partially abrogated the inhibitory effect of metformin in IL-13 induced M2-like polarization. Metformin 129-138 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 73-83 26497364-4 2015 Administration of AICAR, another activator of AMPK, also blocked the M2-like polarization of macrophages. AICA ribonucleotide 18-23 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 46-50 26497364-8 2015 These findings suggest that metformin is able to block the M2-like polarization of macrophages partially through AMPKalpha1, which plays an important role in metformin inhibited metastasis of Lewis lung cancer. Metformin 28-37 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 113-123 26497364-8 2015 These findings suggest that metformin is able to block the M2-like polarization of macrophages partially through AMPKalpha1, which plays an important role in metformin inhibited metastasis of Lewis lung cancer. Metformin 158-167 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 113-123 26430787-3 2015 Although the precise molecular mechanisms by which metformin affects various cancers have not been fully elucidated, activation of AMPK-dependent and AMPK-independent pathways along with energy metabolism aberration, cell cycle arrest and apoptosis or autophagy induction have emerged as crucial regulators in this process. Metformin 51-60 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 150-154 26201966-15 2015 The finding of IGF-1R elevation in positive PNBs versus p-AMPK elevation in negative PNBs suggests altered metabolic pathway activation precipitated by metformin use. Metformin 152-161 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 58-62 26391455-10 2015 Of note, AMPK inactivation or autophagy inhibition in STK11-proficient cells sensitize SB202190-treated PCa cells to apoptosis. 4-(4-fluorophenyl)-2-(4-hydroxyphenyl)-5-(4-pyridyl)imidazole 87-95 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 9-13 26297911-7 2015 Gemigliptin increased AMP-activated protein kinase (AMPK) phosphorylation and inhibited tumor necrosis factor (TNF) alpha-induced mTOR phosphorylation, SREBP-1 cleavage, lipid accumulation, and LECT2 expression in HepG2 cells; these events were attenuated by an AMPK inhibitor. LC15-0444 0-11 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 22-50 26297911-7 2015 Gemigliptin increased AMP-activated protein kinase (AMPK) phosphorylation and inhibited tumor necrosis factor (TNF) alpha-induced mTOR phosphorylation, SREBP-1 cleavage, lipid accumulation, and LECT2 expression in HepG2 cells; these events were attenuated by an AMPK inhibitor. LC15-0444 0-11 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 52-56 26297911-7 2015 Gemigliptin increased AMP-activated protein kinase (AMPK) phosphorylation and inhibited tumor necrosis factor (TNF) alpha-induced mTOR phosphorylation, SREBP-1 cleavage, lipid accumulation, and LECT2 expression in HepG2 cells; these events were attenuated by an AMPK inhibitor. LC15-0444 0-11 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 262-266 26297911-8 2015 Gemigliptin recovered TNFalpha-induced inhibition of insulin receptor substrate (IRS)-1 and Akt phosphorylation that was abolished in LECT2 knockdown cells or by AMPK inhibition. LC15-0444 0-11 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 162-166 26297911-9 2015 In preliminary in vivo experiments, gemigliptin induced AMPK phosphorylation and inhibited LECT2 expression in liver tissues from HFD-fed mice. LC15-0444 36-47 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 56-60 26297911-11 2015 Gemigliptin might alleviate hepatic steatosis and insulin resistance by inhibiting LECT2 expression by AMPK-dependent and JNK-dependent mechanisms, suggesting a direct protective effect against NAFLD progression. LC15-0444 0-11 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 103-107 26344902-0 2015 Palmitate activates mTOR/p70S6K through AMPK inhibition and hypophosphorylation of raptor in skeletal muscle cells: Reversal by oleate is similar to metformin. Palmitates 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 40-44 26344902-7 2015 Palmitate also inhibited phosphorylation of AMPK, but did not change the phosphorylated levels of mTOR or rictor. Palmitates 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 44-48 26344902-9 2015 To understand this more, we show activation of AMPK by metformin also prevented palmitate-induced changes in the phosphorylations of raptor and p70S6K, confirming that the mTORC1/p70S6K signaling pathway is responsive to AMPK activity. Metformin 55-64 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 47-51 26344902-9 2015 To understand this more, we show activation of AMPK by metformin also prevented palmitate-induced changes in the phosphorylations of raptor and p70S6K, confirming that the mTORC1/p70S6K signaling pathway is responsive to AMPK activity. Metformin 55-64 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 221-225 26344902-9 2015 To understand this more, we show activation of AMPK by metformin also prevented palmitate-induced changes in the phosphorylations of raptor and p70S6K, confirming that the mTORC1/p70S6K signaling pathway is responsive to AMPK activity. Palmitates 80-89 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 47-51 26344902-9 2015 To understand this more, we show activation of AMPK by metformin also prevented palmitate-induced changes in the phosphorylations of raptor and p70S6K, confirming that the mTORC1/p70S6K signaling pathway is responsive to AMPK activity. Palmitates 80-89 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 221-225 26344902-10 2015 By contrast, inhibition of AMPK phosphorylation by Compound C worsened palmitate-induced changes and correspondingly blocked the protective effect of oleate. Palmitates 71-80 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 27-31 26344902-10 2015 By contrast, inhibition of AMPK phosphorylation by Compound C worsened palmitate-induced changes and correspondingly blocked the protective effect of oleate. Oleic Acid 150-156 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 27-31 26344902-12 2015 Our findings indicate that palmitate activates mTORC1/p70S6K signaling by AMPK inhibition and phosphorylation of raptor. Palmitates 27-36 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 74-78 26344902-13 2015 Oleate reverses these effects through a metformin-like facilitation of AMPK. Oleic Acid 0-6 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 71-75 26344902-13 2015 Oleate reverses these effects through a metformin-like facilitation of AMPK. Metformin 40-49 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 71-75 27352350-5 2015 In addition, physcion provoked the generation of reactive oxygen species (ROS) in SGC-7901 cells, while the antioxidant N-acetyl cysteine almost completely blocked physcion-induced AMPK activation and apoptosis. Acetylcysteine 120-137 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 181-185 26337027-1 2015 AMP-activated protein kinase (AMPK) is a cellular energy sensor, which is activated when the intracellular ATP production decreases. Adenosine Triphosphate 107-110 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-28 26337027-1 2015 AMP-activated protein kinase (AMPK) is a cellular energy sensor, which is activated when the intracellular ATP production decreases. Adenosine Triphosphate 107-110 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-34 26337027-11 2015 We found that in chicken embryonic retina, the activation of AMP-activated protein kinase (AMPK) is under circadian control and anti-phase to the retinal ATP rhythm. Adenosine Triphosphate 154-157 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 61-89 26337027-11 2015 We found that in chicken embryonic retina, the activation of AMP-activated protein kinase (AMPK) is under circadian control and anti-phase to the retinal ATP rhythm. Adenosine Triphosphate 154-157 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 91-95 26343941-5 2015 There was also severe mitochondrial damage accompanied by decrease of mitochondria, associated with toxic levels of propionyl CoA as shown by carnitine supplementation studies, which explains the apparently paradoxical mitochondrial diminution in the face of the energy sensor AMPK activation, known to induce mitochondria biogenesis. propionyl-coenzyme A 116-129 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 277-281 26460945-0 2015 Non-canonical Hedgehog/AMPK-Mediated Control of Polyamine Metabolism Supports Neuronal and Medulloblastoma Cell Growth. Polyamines 48-57 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 23-27 26471090-8 2015 In TE671 cells, AMPK phosphorylated HDAC5, which suppressed nuclear penetration and upregulated GLUT4 transcription, leading to enhanced glucose uptake. Glucose 137-144 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 16-20 26471090-9 2015 Collectively, these results suggest that saponarin activates AMPK in a calcium-dependent manner, thus regulating gluconeogenesis and glucose uptake. saponarin 41-50 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 61-65 26471090-9 2015 Collectively, these results suggest that saponarin activates AMPK in a calcium-dependent manner, thus regulating gluconeogenesis and glucose uptake. Calcium 71-78 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 61-65 26471090-9 2015 Collectively, these results suggest that saponarin activates AMPK in a calcium-dependent manner, thus regulating gluconeogenesis and glucose uptake. Glucose 133-140 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 61-65 26460945-3 2015 This process is governed by AMPK, which phosphorylates threonine 173 of the zinc finger protein CNBP in response to Hedgehog activation. Threonine 55-64 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 28-32 26359363-7 2015 In contrast to the cells that express N-cadherin, in N-cadherin deficient cells, metformin plays an anti-tumor role via activation of AMPK. Metformin 81-90 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 134-138 26439622-12 2015 Furthermore, metformin, but not Exendin-4, activated AMPK and induced apoptosis in LNCaP cells. Metformin 13-22 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 53-57 26439622-13 2015 The anti-proliferative effect of metformin was abolished by inhibition or knock down of AMPK. Metformin 33-42 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 88-92 26439622-15 2015 Immunohistochemistry on tumors revealed that the P504S and Ki67 expression decreased by Exendin-4 and/or metformin, and that metformin increased phospho-AMPK expression and the apoptotic cell number. Metformin 125-134 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 153-157 26219912-0 2015 Aspirin Targets SIRT1 and AMPK to Induce Senescence of Colorectal Carcinoma Cells. Aspirin 0-7 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 26-30 26219912-5 2015 In this study, we investigated the effects of aspirin on TIS of human colorectal carcinoma (CRC) cells and show that it occurs via sirtuin 1 (SIRT1) and AMP-activated protein kinase (AMPK), two key regulators of cellular metabolism. Aspirin 46-53 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 153-181 26219912-5 2015 In this study, we investigated the effects of aspirin on TIS of human colorectal carcinoma (CRC) cells and show that it occurs via sirtuin 1 (SIRT1) and AMP-activated protein kinase (AMPK), two key regulators of cellular metabolism. Aspirin 46-53 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 183-187 26219912-6 2015 Aspirin increased the senescence of CRC cells, increased the protein levels of SIRT1, phospho-AMPK (T172), and phospho-acetyl CoA carboxylase (S79), and reduced the cellular level of ATP. Aspirin 0-7 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 94-98 26219912-7 2015 Small-interfering RNA-mediated downregulation or pharmacological inhibition of SIRT1 or AMPK significantly attenuated the aspirin-induced cellular senescence in CRC cells. Aspirin 122-129 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 88-92 26219912-9 2015 Remarkably, SIRT1 knockdown abrogated the aspirin-induced activation of AMPK, and vice versa. Aspirin 42-49 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 72-76 26219912-11 2015 Collectively, these novel findings suggest that aspirin could provide anticancer effects by inducing senescence in human CRC cells through the reciprocal regulation of SIRT1-AMPK pathways. Aspirin 48-55 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 174-178 26652486-10 2015 In conclusion, we defined the metabolic phenotype of human chondrocytes, in which both starvation and steroids depletion induce the activation of PTEN, AMPK and autophagy signaling, concomitant with metabolic reprogramming. Steroids 102-110 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 152-156 26198640-7 2015 Additionally, siRNA-mediated knockdown of endogenous AMPKalpha1 expression showed a reduction of TRAIL-TZD-induced apoptosis, further confirming the participation of AMPK in mediating this apoptosis. tzd 103-106 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 53-63 26198640-7 2015 Additionally, siRNA-mediated knockdown of endogenous AMPKalpha1 expression showed a reduction of TRAIL-TZD-induced apoptosis, further confirming the participation of AMPK in mediating this apoptosis. tzd 103-106 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 53-57 26102194-0 2015 Curcumin enhanced cholesterol efflux by upregulating ABCA1 expression through AMPK-SIRT1-LXRalpha signaling in THP-1 macrophage-derived foam cells. Curcumin 0-8 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 78-82 26116623-0 2015 C6 ceramide dramatically increases vincristine sensitivity both in vivo and in vitro, involving AMP-activated protein kinase-p53 signaling. Ceramides 3-11 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 96-124 26116623-0 2015 C6 ceramide dramatically increases vincristine sensitivity both in vivo and in vitro, involving AMP-activated protein kinase-p53 signaling. Vincristine 35-46 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 96-124 26116623-3 2015 In vitro, C6 and vincristine coadministration induced substantial necrosis and apoptosis in multiple human cancer cell lines, which were accompanied by a profound AMP-activated protein kinase (AMPK) activation, subsequent p53 activation, mTORC1 inactivation and Bcl-2/HIF-1alpha downregulation. Vincristine 17-28 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 163-191 26116623-3 2015 In vitro, C6 and vincristine coadministration induced substantial necrosis and apoptosis in multiple human cancer cell lines, which were accompanied by a profound AMP-activated protein kinase (AMPK) activation, subsequent p53 activation, mTORC1 inactivation and Bcl-2/HIF-1alpha downregulation. Vincristine 17-28 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 193-197 26116623-8 2015 Together, C6 sensitizes vincristine-induced anticancer activity in vivo and in vitro, involving activating AMPK-p53 signaling. Vincristine 24-35 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 107-111 25579456-9 2015 RESULTS: Phospho-AMPK was increased by metformin in all cell lines whilst phospho-Akt and phospho-ERK expressions were decreased in two. Metformin 39-48 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 17-21 26313261-0 2015 8-Chloroadenosine Sensitivity in Renal Cell Carcinoma Is Associated with AMPK Activation and mTOR Pathway Inhibition. 8-chloroadenosine 0-17 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 73-77 26102194-0 2015 Curcumin enhanced cholesterol efflux by upregulating ABCA1 expression through AMPK-SIRT1-LXRalpha signaling in THP-1 macrophage-derived foam cells. Cholesterol 18-29 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 78-82 26102194-4 2015 Curcumin activated AMP-activated protein kinase (AMPK) and SIRT1, and then activated LXRalpha in THP-1 macrophage-derived foam cells. Curcumin 0-8 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 19-47 26102194-4 2015 Curcumin activated AMP-activated protein kinase (AMPK) and SIRT1, and then activated LXRalpha in THP-1 macrophage-derived foam cells. Curcumin 0-8 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 49-53 26102194-5 2015 Inhibiting AMPK/SIRT1 activity by its specific inhibitor or by small interfering RNA could inhibit LXRalpha activation and abolish curcumin-induced ABCA1 expression and cholesterol efflux. Curcumin 131-139 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 11-15 26102194-5 2015 Inhibiting AMPK/SIRT1 activity by its specific inhibitor or by small interfering RNA could inhibit LXRalpha activation and abolish curcumin-induced ABCA1 expression and cholesterol efflux. Cholesterol 169-180 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 11-15 26102194-6 2015 Thus, curcumin enhanced cholesterol efflux by upregulating ABCA1 expression through activating AMPK-SIRT1-LXRalpha signaling in THP-1 macrophage-derived foam cells. Curcumin 6-14 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 95-99 26102194-6 2015 Thus, curcumin enhanced cholesterol efflux by upregulating ABCA1 expression through activating AMPK-SIRT1-LXRalpha signaling in THP-1 macrophage-derived foam cells. Cholesterol 24-35 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 95-99 26139607-12 2015 These results suggest implication of autophagy against BPA-mediated neurodegeneration through involvement of AMPK and mTOR pathways. bisphenol A 55-58 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 109-113 26044878-9 2015 Thereby, (E)-resveratrol, but not Z-TMS, showed potent induction of SHP mRNA levels in an AMPK- and SIRT1-dependent manner, as confirmed by knockdown experiments. Resveratrol 9-24 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 90-94 26061431-8 2015 Our data delineate a novel link between AMPK, the energy sensor, and HIF-1, the major driver of ATP production, indicating that specifically inhibiting HDAC5 may selectively suppress the survival and proliferation of hypoxic tumor cells. Adenosine Triphosphate 96-99 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 40-44 26114447-6 2015 Meanwhile, cAMP, SIRT3 or AMPK inhibitors were treated respectively before incubation with caffeine in oleate-treated HepG2 cells. Caffeine 91-99 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 26-30 26114447-9 2015 Caffeine increased the transformation of ADP to ATP and activated the cAMP/CREB/SIRT3/AMPK/ACC pathway in the liver. Caffeine 0-8 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 86-90 26114447-9 2015 Caffeine increased the transformation of ADP to ATP and activated the cAMP/CREB/SIRT3/AMPK/ACC pathway in the liver. Cyclic AMP 70-74 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 86-90 26114447-10 2015 Nile red staining demonstrated that suppression of cAMP, SIRT3 or AMPK in oleate-treated HepG2 cells counteracted the effect of caffeine. nile red 0-8 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 66-70 26114447-10 2015 Nile red staining demonstrated that suppression of cAMP, SIRT3 or AMPK in oleate-treated HepG2 cells counteracted the effect of caffeine. Caffeine 128-136 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 66-70 26114447-11 2015 Moreover, knocking down SIRT3 could down-regulate AMPK and ACC phosphorylation by caffeine. Caffeine 82-90 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 50-54 26114447-12 2015 These results demonstrate that caffeine could improve HED-induced hepatic steatosis by promoting lipid metabolism via the cAMP/CREB/SIRT3/AMPK/ACC pathway. Caffeine 31-39 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 138-142 26114447-12 2015 These results demonstrate that caffeine could improve HED-induced hepatic steatosis by promoting lipid metabolism via the cAMP/CREB/SIRT3/AMPK/ACC pathway. Cyclic AMP 122-126 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 138-142 26198640-0 2015 Tumor Necrosis Factor-related Apoptosis-inducing Ligand (TRAIL)-Troglitazone-induced Apoptosis in Prostate Cancer Cells Involve AMP-activated Protein Kinase. Troglitazone 64-76 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 128-156 26198640-4 2015 Because TZD is known to activate AMP-activated protein kinase (AMPK), we determined whether AMPK is a molecular target mediating this apoptotic cascade by utilizing PCa cell lines stably overexpressing AMPKalpha1 dominant negative (C4-2-DN) or empty vector (C4-2-EV). tzd 8-11 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 33-61 26198640-4 2015 Because TZD is known to activate AMP-activated protein kinase (AMPK), we determined whether AMPK is a molecular target mediating this apoptotic cascade by utilizing PCa cell lines stably overexpressing AMPKalpha1 dominant negative (C4-2-DN) or empty vector (C4-2-EV). tzd 8-11 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 63-67 26318663-8 2015 Using siRNA against AMPK as well as AMPK deficient cells, autophagy stimulation by 1% O2 was shown to be AMPK-independent. Oxygen 86-88 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 20-24 25993908-11 2015 Moreover, treatment of megakaryocytes with metformin enhanced mitochondrial content and in the same cells metformin enhanced the phosphorylation of the Drp-1 on Ser637 via an AMPKalpha1-dependent mechanism. Metformin 43-52 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 175-185 25993908-11 2015 Moreover, treatment of megakaryocytes with metformin enhanced mitochondrial content and in the same cells metformin enhanced the phosphorylation of the Drp-1 on Ser637 via an AMPKalpha1-dependent mechanism. Metformin 106-115 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 175-185 26313261-11 2015 We thus infer that 8-chloroadenosine may be effective in RCC by activating AMPK and inhibiting the mTOR pathway. 8-chloroadenosine 19-36 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 75-79 26139607-0 2015 Activation of Autophagic Flux against Xenoestrogen Bisphenol-A-induced Hippocampal Neurodegeneration via AMP kinase (AMPK)/Mammalian Target of Rapamycin (mTOR) Pathways. xenoestrogen bisphenol-a 38-62 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 105-115 26139607-0 2015 Activation of Autophagic Flux against Xenoestrogen Bisphenol-A-induced Hippocampal Neurodegeneration via AMP kinase (AMPK)/Mammalian Target of Rapamycin (mTOR) Pathways. xenoestrogen bisphenol-a 38-62 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 117-121 26139607-8 2015 Activation of autophagy against BPA resulted in intracellular energy sensor AMP kinase (AMPK) activation, increased phosphorylation of raptor and acetyl-CoA carboxylase, and decreased phosphorylation of ULK1 (Ser-757), and silencing of AMPK exacerbated BPA neurotoxicity. bisphenol A 32-35 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 76-86 26139607-8 2015 Activation of autophagy against BPA resulted in intracellular energy sensor AMP kinase (AMPK) activation, increased phosphorylation of raptor and acetyl-CoA carboxylase, and decreased phosphorylation of ULK1 (Ser-757), and silencing of AMPK exacerbated BPA neurotoxicity. bisphenol A 32-35 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 88-92 26139607-8 2015 Activation of autophagy against BPA resulted in intracellular energy sensor AMP kinase (AMPK) activation, increased phosphorylation of raptor and acetyl-CoA carboxylase, and decreased phosphorylation of ULK1 (Ser-757), and silencing of AMPK exacerbated BPA neurotoxicity. bisphenol A 32-35 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 236-240 26043699-2 2015 Previously, we found that 8-Cl-cAMP-induced growth inhibition is mediated by AMP-activated protein kinase (AMPK) as well as p38 mitogen-activated protein kinase (p38 MAPK). 8-chloro-cyclic adenosine monophosphate 26-35 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 77-105 26043699-2 2015 Previously, we found that 8-Cl-cAMP-induced growth inhibition is mediated by AMP-activated protein kinase (AMPK) as well as p38 mitogen-activated protein kinase (p38 MAPK). 8-chloro-cyclic adenosine monophosphate 26-35 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 107-111 26043699-3 2015 To identify downstream mediators of the 8-Cl-cAMP signaling, we performed co-immunoprecipitation combined with mass spectrometry using the anti-AMPK or p38 MAPK antibodies. 8-chloro-cyclic adenosine monophosphate 40-49 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 144-148 26088335-6 2015 Further studies revealed that 1 persistently activated adenosine 5"-monophosphate (AMP)-activated protein kinase (AMPK) during differentiation, suggesting that the AMPK may be an upstream mechanism for the effect of 1 on adipogenesis and lipogenesis. adenosine 5"-monophosphate 55-81 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 114-118 26088335-6 2015 Further studies revealed that 1 persistently activated adenosine 5"-monophosphate (AMP)-activated protein kinase (AMPK) during differentiation, suggesting that the AMPK may be an upstream mechanism for the effect of 1 on adipogenesis and lipogenesis. adenosine 5"-monophosphate 55-81 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 164-168 26088335-6 2015 Further studies revealed that 1 persistently activated adenosine 5"-monophosphate (AMP)-activated protein kinase (AMPK) during differentiation, suggesting that the AMPK may be an upstream mechanism for the effect of 1 on adipogenesis and lipogenesis. Adenosine Monophosphate 83-86 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 114-118 26088335-6 2015 Further studies revealed that 1 persistently activated adenosine 5"-monophosphate (AMP)-activated protein kinase (AMPK) during differentiation, suggesting that the AMPK may be an upstream mechanism for the effect of 1 on adipogenesis and lipogenesis. Adenosine Monophosphate 83-86 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 164-168 26050920-11 2015 Metformin influences on AMPK/mTOR cell signaling were evaluated by investigating AKT, AMPK and S6 phosphorylation levels. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 24-28 26050920-11 2015 Metformin influences on AMPK/mTOR cell signaling were evaluated by investigating AKT, AMPK and S6 phosphorylation levels. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 86-90 26313261-5 2015 In time-course experiments, 8-chloroadenosine treatment rapidly activated AMPK, measured by AMPK and ACC phosphorylation, and subsequently caused dephosphorylation of p70S6K and ribosomal protein RPS6 in the sensitive cell lines. 8-chloroadenosine 28-45 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 74-78 26313261-5 2015 In time-course experiments, 8-chloroadenosine treatment rapidly activated AMPK, measured by AMPK and ACC phosphorylation, and subsequently caused dephosphorylation of p70S6K and ribosomal protein RPS6 in the sensitive cell lines. 8-chloroadenosine 28-45 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 92-96 26037398-0 2015 Curcumin inhibits Ec109 cell growth via an AMPK-mediated metabolic switch. Curcumin 0-8 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 43-47 26037398-8 2015 Our results further indicated that the AMPK was required for curcumin-mediated down-regulation of glycolytic enzymes. Curcumin 61-69 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 39-43 26174015-0 2015 Blocking a vicious cycle nNOS/peroxynitrite/AMPK by S-nitrosoglutathione: implication for stroke therapy. S-Nitrosoglutathione 52-72 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 44-48 25943029-7 2015 Incubation with inhibitors of AC (adenylyl cyclase), PRKA, AMPK, SIRT1, or with AC, PRKA, AMPK, or SIRT1 siRNA abolished RSV-mediated autophagy. Resveratrol 121-124 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 59-63 25943029-7 2015 Incubation with inhibitors of AC (adenylyl cyclase), PRKA, AMPK, SIRT1, or with AC, PRKA, AMPK, or SIRT1 siRNA abolished RSV-mediated autophagy. Resveratrol 121-124 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 90-94 25943029-9 2015 CONCLUSION: RSV improved hepatic steatosis partially by inducing autophagy via the cAMP-PRKA-AMPK-SIRT1 signaling pathway, which provides new evidence regarding RSV"s effects on NAFLD treatment. Resveratrol 12-15 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 93-97 25943029-9 2015 CONCLUSION: RSV improved hepatic steatosis partially by inducing autophagy via the cAMP-PRKA-AMPK-SIRT1 signaling pathway, which provides new evidence regarding RSV"s effects on NAFLD treatment. Cyclic AMP 83-87 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 93-97 25943029-9 2015 CONCLUSION: RSV improved hepatic steatosis partially by inducing autophagy via the cAMP-PRKA-AMPK-SIRT1 signaling pathway, which provides new evidence regarding RSV"s effects on NAFLD treatment. Resveratrol 161-164 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 93-97 26190112-4 2015 AMPK is directly responsive to intracellular AMP levels, inhibiting a wide range of cell activities if ATP is low and AMP is high. Adenosine Triphosphate 103-106 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 26190112-4 2015 AMPK is directly responsive to intracellular AMP levels, inhibiting a wide range of cell activities if ATP is low and AMP is high. Adenosine Monophosphate 45-48 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 26190112-7 2015 AMPK phosphorylates GLI1 at serines 102 and 408 and threonine 1074. Serine 28-35 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 26190112-7 2015 AMPK phosphorylates GLI1 at serines 102 and 408 and threonine 1074. Threonine 52-61 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 26190112-8 2015 Mutation of these three sites into alanine prevents phosphorylation by AMPK. Alanine 35-42 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 71-75 26196392-0 2015 Metformin Induced AMPK Activation, G0/G1 Phase Cell Cycle Arrest and the Inhibition of Growth of Esophageal Squamous Cell Carcinomas In Vitro and In Vivo. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 18-22 26196392-4 2015 The findings reported herein show that the anti-proliferative action of metformin on ESCC cell lines is partially mediated by AMPK. Metformin 72-81 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 126-130 26196392-7 2015 Most importantly, the up-regulation of AMPK, p53, p21CIP1, p27KIP1 and the down-regulation of cyclinD1 are involved in the anti-tumor action of metformin in vivo. Metformin 144-153 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 39-43 26196392-9 2015 AMPK, p53, p21CIP1, p27KIP1 and cyclinD1 are involved in the inhibition of tumor growth that is induced by metformin and cell cycle arrest in ESCC. Metformin 107-116 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 26174015-9 2015 GSNO also decreased the activation of AMP Kinase (AMPK) and its upstream kinase LKB1, both of which were activated in IR brain. S-Nitrosoglutathione 0-4 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 38-48 26174015-9 2015 GSNO also decreased the activation of AMP Kinase (AMPK) and its upstream kinase LKB1, both of which were activated in IR brain. S-Nitrosoglutathione 0-4 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 50-54 26174015-10 2015 AMPK has been implicated in nNOS activation via Ser(1412) phosphorylation. Serine 48-51 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 25779083-0 2015 Metformin and caloric restriction induce an AMPK-dependent restoration of mitochondrial dysfunction in fibroblasts from Fibromyalgia patients. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 44-48 25779083-4 2015 AMPK was not phosphorylated in fibroblasts from FM patients and was associated with decreased mitochondrial biogenesis, reduced oxygen consumption, decreased antioxidant enzymes expression levels and mitochondrial dysfunction. Oxygen 128-134 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 25779083-7 2015 In contrast, AMPK activation by metformin or incubation with serum from caloric restricted mice improved the response to moderate oxidative stress and mitochondrial metabolism in FM fibroblasts. Metformin 32-41 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 13-17 26091703-1 2015 Evidence suggests that AMP protein kinase (AMPK) is the main target of the phytochemical resveratrol (RSV) in mammalian cells. Resveratrol 89-100 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 23-41 26091703-1 2015 Evidence suggests that AMP protein kinase (AMPK) is the main target of the phytochemical resveratrol (RSV) in mammalian cells. Resveratrol 89-100 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 43-47 26091703-1 2015 Evidence suggests that AMP protein kinase (AMPK) is the main target of the phytochemical resveratrol (RSV) in mammalian cells. Resveratrol 102-105 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 23-41 26091703-1 2015 Evidence suggests that AMP protein kinase (AMPK) is the main target of the phytochemical resveratrol (RSV) in mammalian cells. Resveratrol 102-105 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 43-47 26091703-3 2015 Herein, we provide evidence indicating that RSV stimulates glycolysis via sucrose non-fermenting 1 gene (SNF1, Saccharomyces cerevisiae orthologous of AMPK). Resveratrol 44-47 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 151-155 26091703-3 2015 Herein, we provide evidence indicating that RSV stimulates glycolysis via sucrose non-fermenting 1 gene (SNF1, Saccharomyces cerevisiae orthologous of AMPK). Sucrose 74-81 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 151-155 26091703-8 2015 Taken together, these findings suggest that SNF1 (AMPK in mammalian systems) is the molecular target of RSV in S. cerevisiae. Resveratrol 104-107 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 50-54 25980607-2 2015 Here, we found that hypoxia induces phosphorylation of ULK1 at Serine-555 by Adenosine 5"-monophosphate (AMP)-activated protein kinase (AMPK). Serine 63-69 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 136-140 25980607-2 2015 Here, we found that hypoxia induces phosphorylation of ULK1 at Serine-555 by Adenosine 5"-monophosphate (AMP)-activated protein kinase (AMPK). adenosine 5"-monophosphate 77-103 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 136-140 25841981-3 2015 The key energy regulator in yeast Snf1 and its mammalian ortholog AMPK have earlier been shown to have similar functions at glucose limited conditions and here we show that they also have analogies when grown with glucose excess. Glucose 124-131 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 66-70 25841981-3 2015 The key energy regulator in yeast Snf1 and its mammalian ortholog AMPK have earlier been shown to have similar functions at glucose limited conditions and here we show that they also have analogies when grown with glucose excess. Glucose 214-221 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 66-70 25841981-5 2015 Strikingly, we demonstrate that Snf1/AMPK-deficient cells remodel their metabolism fueling mitochondria and show glucose and amino acids addiction, a typical hallmark of cancer cells. Glucose 113-120 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 37-41 25957914-0 2015 Downregulation of microRNA-451 in non-alcoholic steatohepatitis inhibits fatty acid-induced proinflammatory cytokine production through the AMPK/AKT pathway. Fatty Acids 73-83 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 140-144 25957914-13 2015 These results provide new insights into the negative regulation of miR-451 in fatty acid-induced inflammation via the AMPK/AKT pathway and demonstrate potential therapeutic applications for miR-451 in preventing the progression from simple steatosis to severely advanced liver disease. Fatty Acids 78-88 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 118-122 26116564-8 2015 Treatment of HT29 and Caco-2 cells with 12-O-tetradecanoylphorbol-13-acetate (TPA) induced an invasive phenotype response along with corresponding increases in ROS production and NOX2 and MMP-7 expression as well as reduced AMPK phosphorylation, which resemble basal conditions of highly invasive human colon cancer cells (SW620 and HCT116). Tetradecanoylphorbol Acetate 40-76 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 224-228 26116564-8 2015 Treatment of HT29 and Caco-2 cells with 12-O-tetradecanoylphorbol-13-acetate (TPA) induced an invasive phenotype response along with corresponding increases in ROS production and NOX2 and MMP-7 expression as well as reduced AMPK phosphorylation, which resemble basal conditions of highly invasive human colon cancer cells (SW620 and HCT116). Tetradecanoylphorbol Acetate 78-81 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 224-228 26116564-9 2015 In addition, inverse regulation between AMPK phosphorylation and NOX2 and MMP-7 expression was observed in HT29 cells treated with different concentrations of exogenous hydrogen peroxide. Hydrogen Peroxide 169-186 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 40-44 26116564-13 2015 CONCLUSIONS: Molecular switch from NOX1 to NOX2 in colon cancer cells induces ROS production and subsequently enhances MMP-7 expression by deactivating AMPK, which otherwise inhibits stimulus-induced autoregulation of ROS and NOX2 gene expression. Reactive Oxygen Species 78-81 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 152-156 26116564-13 2015 CONCLUSIONS: Molecular switch from NOX1 to NOX2 in colon cancer cells induces ROS production and subsequently enhances MMP-7 expression by deactivating AMPK, which otherwise inhibits stimulus-induced autoregulation of ROS and NOX2 gene expression. Reactive Oxygen Species 218-221 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 152-156 26098914-0 2015 AMP-Activated Protein Kinase Interacts with the Peroxisome Proliferator-Activated Receptor Delta to Induce Genes Affecting Fatty Acid Oxidation in Human Macrophages. Fatty Acids 123-133 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-28 26098914-1 2015 AMP-activated protein kinase (AMPK) maintains energy homeostasis by suppressing cellular ATP-consuming processes and activating catabolic, ATP-producing pathways such as fatty acid oxidation (FAO). Adenosine Triphosphate 89-92 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-28 26098914-1 2015 AMP-activated protein kinase (AMPK) maintains energy homeostasis by suppressing cellular ATP-consuming processes and activating catabolic, ATP-producing pathways such as fatty acid oxidation (FAO). Adenosine Triphosphate 89-92 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-34 26098914-1 2015 AMP-activated protein kinase (AMPK) maintains energy homeostasis by suppressing cellular ATP-consuming processes and activating catabolic, ATP-producing pathways such as fatty acid oxidation (FAO). Adenosine Triphosphate 139-142 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-28 26098914-1 2015 AMP-activated protein kinase (AMPK) maintains energy homeostasis by suppressing cellular ATP-consuming processes and activating catabolic, ATP-producing pathways such as fatty acid oxidation (FAO). Adenosine Triphosphate 139-142 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-34 26098914-1 2015 AMP-activated protein kinase (AMPK) maintains energy homeostasis by suppressing cellular ATP-consuming processes and activating catabolic, ATP-producing pathways such as fatty acid oxidation (FAO). Fatty Acids 170-180 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-28 26098914-1 2015 AMP-activated protein kinase (AMPK) maintains energy homeostasis by suppressing cellular ATP-consuming processes and activating catabolic, ATP-producing pathways such as fatty acid oxidation (FAO). Fatty Acids 170-180 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-34 26098914-1 2015 AMP-activated protein kinase (AMPK) maintains energy homeostasis by suppressing cellular ATP-consuming processes and activating catabolic, ATP-producing pathways such as fatty acid oxidation (FAO). fao 192-195 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-28 26098914-1 2015 AMP-activated protein kinase (AMPK) maintains energy homeostasis by suppressing cellular ATP-consuming processes and activating catabolic, ATP-producing pathways such as fatty acid oxidation (FAO). fao 192-195 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-34 25975952-2 2015 Our aim was to examine whether AMP-activated protein kinase (AMPK), a conditional oncogene, rescues the energetic stress and cytotoxicity induced by 2-deoxyglucose (2-DG), a glycolytic inhibitor, and the related mechanisms. Deoxyglucose 149-163 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 31-59 25975952-2 2015 Our aim was to examine whether AMP-activated protein kinase (AMPK), a conditional oncogene, rescues the energetic stress and cytotoxicity induced by 2-deoxyglucose (2-DG), a glycolytic inhibitor, and the related mechanisms. Deoxyglucose 149-163 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 61-65 25975952-2 2015 Our aim was to examine whether AMP-activated protein kinase (AMPK), a conditional oncogene, rescues the energetic stress and cytotoxicity induced by 2-deoxyglucose (2-DG), a glycolytic inhibitor, and the related mechanisms. Deoxyglucose 165-169 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 31-59 25975952-2 2015 Our aim was to examine whether AMP-activated protein kinase (AMPK), a conditional oncogene, rescues the energetic stress and cytotoxicity induced by 2-deoxyglucose (2-DG), a glycolytic inhibitor, and the related mechanisms. Deoxyglucose 165-169 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 61-65 25975952-4 2015 2-DG decreased ATP levels and subsequently activated AMPK, which contribute to intracellular ATP recovery in MCF-7 cells thus exhibiting no apparent cytotoxicity. Deoxyglucose 0-4 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 53-57 25975952-4 2015 2-DG decreased ATP levels and subsequently activated AMPK, which contribute to intracellular ATP recovery in MCF-7 cells thus exhibiting no apparent cytotoxicity. Adenosine Triphosphate 93-96 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 53-57 25975952-5 2015 Compound C, an AMPK inhibitor, further potentiates 2-DG-induced decrease in ATP levels and inhibits their recovery. Deoxyglucose 51-55 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 15-19 25975952-5 2015 Compound C, an AMPK inhibitor, further potentiates 2-DG-induced decrease in ATP levels and inhibits their recovery. Adenosine Triphosphate 76-79 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 15-19 25975952-6 2015 2-DG, via AMPK activation, stimulated cAMP response element-binding protein (CREB) phosphorylation and activity and promoted nuclear peroxisome proliferator-activated receptor gamma coactivator-1-beta (PGC-1beta) and estrogen-related receptor alpha (ERRalpha) protein expression, leading to augmented mitochondrial biogenesis and expression of fatty acid oxidation (FAO) genes including PPARalpha, MCAD, CPT1C, and ACO. Deoxyglucose 0-4 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 10-14 25975952-7 2015 This metabolic adaptation elicited by AMPK counteracts the ATP-depleting and cancer cell-killing effect of 2-DG. Adenosine Triphosphate 59-62 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 38-42 25975952-7 2015 This metabolic adaptation elicited by AMPK counteracts the ATP-depleting and cancer cell-killing effect of 2-DG. Deoxyglucose 107-111 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 38-42 26194078-0 2015 Exendin-4 Inhibits the Expression of SEPP1 and Fetuin-A via Improvement of Palmitic Acid-Induced Endoplasmic Reticulum Stress by AMPK. Palmitic Acid 75-88 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 129-133 26194078-8 2015 In cells treated with the AMPK activator 5-aminoidazole-4-carboxamide ribonucleotide (AICAR), the expression of hepatic SEPP1 and fetuin-A were negatively related by AMPK, which is the target of exendin-4. 5-aminoidazole-4-carboxamide ribonucleotide 41-84 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 26-30 26194078-8 2015 In cells treated with the AMPK activator 5-aminoidazole-4-carboxamide ribonucleotide (AICAR), the expression of hepatic SEPP1 and fetuin-A were negatively related by AMPK, which is the target of exendin-4. 5-aminoidazole-4-carboxamide ribonucleotide 41-84 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 166-170 26194078-8 2015 In cells treated with the AMPK activator 5-aminoidazole-4-carboxamide ribonucleotide (AICAR), the expression of hepatic SEPP1 and fetuin-A were negatively related by AMPK, which is the target of exendin-4. acadesine 86-91 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 26-30 26194078-8 2015 In cells treated with the AMPK activator 5-aminoidazole-4-carboxamide ribonucleotide (AICAR), the expression of hepatic SEPP1 and fetuin-A were negatively related by AMPK, which is the target of exendin-4. acadesine 86-91 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 166-170 26194078-10 2015 CONCLUSION: These data suggest that exendin-4 can attenuate the expression of hepatic SEPP1 and fetuin-A via improvement of PA-induced ER stress by AMPK. Palmitic Acid 124-126 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 148-152 25761413-0 2015 Resveratrol induces brown-like adipocyte formation in white fat through activation of AMP-activated protein kinase (AMPK) alpha1. Resveratrol 0-11 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 116-120 25761413-7 2015 Concomitantly, resveratrol markedly enhanced AMPKalpha1 phosphorylation and differentiated SVC oxygen consumption. Resveratrol 15-26 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 45-55 25761413-8 2015 Such changes were absent in cells lacking AMPKalpha1, showing that AMPKalpha1 is a critical mediator of resveratrol action. Resveratrol 104-115 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 42-52 25761413-8 2015 Such changes were absent in cells lacking AMPKalpha1, showing that AMPKalpha1 is a critical mediator of resveratrol action. Resveratrol 104-115 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 67-77 25761413-10 2015 CONCLUSIONS: Resveratrol induces brown-like adipocyte formation in iWAT via AMPKalpha1 activation and suggest that its beneficial antiobesity effects may be partly due to the browning of WAT and, as a consequence, increased oxygen consumption. Resveratrol 13-24 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 76-86 25891779-0 2015 Metformin attenuates palmitic acid-induced insulin resistance in L6 cells through the AMP-activated protein kinase/sterol regulatory element-binding protein-1c pathway. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 86-114 25891779-0 2015 Metformin attenuates palmitic acid-induced insulin resistance in L6 cells through the AMP-activated protein kinase/sterol regulatory element-binding protein-1c pathway. Palmitic Acid 21-34 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 86-114 25891779-1 2015 AMP-activated protein kinase (AMPK) is an important effector of metformin action on glucose uptake in skeletal muscle cells. Metformin 64-73 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-28 25891779-1 2015 AMP-activated protein kinase (AMPK) is an important effector of metformin action on glucose uptake in skeletal muscle cells. Metformin 64-73 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-34 25891779-1 2015 AMP-activated protein kinase (AMPK) is an important effector of metformin action on glucose uptake in skeletal muscle cells. Glucose 84-91 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-28 25891779-1 2015 AMP-activated protein kinase (AMPK) is an important effector of metformin action on glucose uptake in skeletal muscle cells. Glucose 84-91 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-34 25891779-7 2015 In the PA-treated L6 cells, metformin treatment enhanced AMPK phosphorylation, reduced SREBP-1c expression and increased IRS-1 and Akt protein expression, whereas treatment with compound C blocked the effects of metformin on SREBP-1c expression and the IRS-1 and Akt levels. Palmitic Acid 7-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 57-61 25891779-7 2015 In the PA-treated L6 cells, metformin treatment enhanced AMPK phosphorylation, reduced SREBP-1c expression and increased IRS-1 and Akt protein expression, whereas treatment with compound C blocked the effects of metformin on SREBP-1c expression and the IRS-1 and Akt levels. Metformin 28-37 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 57-61 25891779-8 2015 Moreover, metformin suppressed SREBP-1c promoter activity and promoted glucose uptake through AMPK. Metformin 10-19 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 94-98 25891779-8 2015 Moreover, metformin suppressed SREBP-1c promoter activity and promoted glucose uptake through AMPK. Glucose 71-78 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 94-98 25891779-9 2015 The results from this study demonstrate that metformin ameliorates PA-induced insulin resistance through the activation of AMPK and the suppression of SREBP-1c in skeletal muscle cells. Metformin 45-54 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 123-127 25891779-9 2015 The results from this study demonstrate that metformin ameliorates PA-induced insulin resistance through the activation of AMPK and the suppression of SREBP-1c in skeletal muscle cells. Palmitic Acid 67-69 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 123-127 25428125-4 2015 Activation of AMPK by 5-aminoimidazole-4-carboxamide-1-beta-d-ribofuranoside (AICAR) inhibited high glucose-induced and TGF-beta stimulation of nuclear Smad4. acadesine 22-76 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-18 25428125-4 2015 Activation of AMPK by 5-aminoimidazole-4-carboxamide-1-beta-d-ribofuranoside (AICAR) inhibited high glucose-induced and TGF-beta stimulation of nuclear Smad4. acadesine 78-83 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-18 25428125-4 2015 Activation of AMPK by 5-aminoimidazole-4-carboxamide-1-beta-d-ribofuranoside (AICAR) inhibited high glucose-induced and TGF-beta stimulation of nuclear Smad4. Glucose 100-107 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-18 25751140-6 2015 Moreover, AMPK directly phosphorylates YAP Ser 94, a residue essential for the interaction with TEAD, thus disrupting the YAP-TEAD interaction. Serine 43-46 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 10-14 25930996-0 2015 Fenoterol inhibits LPS-induced AMPK activation and inflammatory cytokine production through beta-arrestin-2 in THP-1 cell line. Fenoterol 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 31-35 25892241-4 2015 We discovered that AMPKalpha1, not AMPKalpha2, was the subunit that preferentially conferred spatial specificity to AMPK, and that inhibition of AMPK activity at the mitochondria was sufficient for triggering cytosolic ATP increase. Adenosine Triphosphate 219-222 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 19-29 25874865-3 2015 We found that both JNK and AMPK were phosphorylated at their activation sites by TNF-alpha, Anisomycin, H2O2 and sorbitol. Anisomycin 92-102 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 27-31 25874865-3 2015 We found that both JNK and AMPK were phosphorylated at their activation sites by TNF-alpha, Anisomycin, H2O2 and sorbitol. Hydrogen Peroxide 104-108 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 27-31 25874865-3 2015 We found that both JNK and AMPK were phosphorylated at their activation sites by TNF-alpha, Anisomycin, H2O2 and sorbitol. Sorbitol 113-121 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 27-31 25874865-4 2015 Interestingly, sorbitol stimulated phosphorylation of AMPK at T172 in LKB1-deficient cells. Sorbitol 15-23 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 54-58 25930996-6 2015 LPS-induced AMPK activation and interleukin 1beta (IL-1beta) release were reduced with fenoterol pretreatment of THP-1 cells. Fenoterol 87-96 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 12-16 25930996-7 2015 SiRNA knockdown of beta-arrestin-2 abolished the fenoterol inhibition of LPS-induced AMPK activation and interleukin 1beta (IL-1beta) release, thus beta-arrestin-2 mediated the anti-inflammatory effects of fenoterol on LPS-treated THP-1 cells. Fenoterol 49-58 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 85-89 25930996-7 2015 SiRNA knockdown of beta-arrestin-2 abolished the fenoterol inhibition of LPS-induced AMPK activation and interleukin 1beta (IL-1beta) release, thus beta-arrestin-2 mediated the anti-inflammatory effects of fenoterol on LPS-treated THP-1 cells. Fenoterol 206-215 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 85-89 25930996-9 2015 These results suggested the beta2-AR agonist fenoterol inhibited LPS-induced AMPK activation and IL-1beta release via beta-arrestin-2 in THP-1 cells. Fenoterol 45-54 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 77-81 25970614-0 2015 Cucurbitacin E Induces Autophagy via Downregulating mTORC1 Signaling and Upregulating AMPK Activity. cucurbitacin E 0-14 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 86-90 25961164-5 2015 Celastrol significantly increased protein phosphorylation of insulin signaling cascades with amplified expression of AMPK protein and attenuated NF-kappaB and PKC theta activation in human skeletal muscle treated with AMA. celastrol 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 117-121 25839176-0 2015 Requirement of AMPK activation for neuronal metabolic-enhancing effects of antidepressant paroxetine. Paroxetine 90-100 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 15-19 25839176-4 2015 Given that AMP-activated protein kinase (AMPK) is a master switch for energy homeostasis, we aimed to determine whether selective serotonin reuptake inhibitor paroxetine enhances energy metabolism by activating AMPK in neuroblastoma cells. Paroxetine 159-169 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 11-39 25839176-4 2015 Given that AMP-activated protein kinase (AMPK) is a master switch for energy homeostasis, we aimed to determine whether selective serotonin reuptake inhibitor paroxetine enhances energy metabolism by activating AMPK in neuroblastoma cells. Paroxetine 159-169 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 41-45 25839176-4 2015 Given that AMP-activated protein kinase (AMPK) is a master switch for energy homeostasis, we aimed to determine whether selective serotonin reuptake inhibitor paroxetine enhances energy metabolism by activating AMPK in neuroblastoma cells. Paroxetine 159-169 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 211-215 25839176-5 2015 We found that paroxetine dose dependently increased mitochondrial biogenesis, which involves the AMPK-peroxisome proliferator-activated receptor-gamma coactivator-1alpha pathway. Paroxetine 14-24 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 97-101 25839176-6 2015 In addition, paroxetine-induced AMPK activation increases glucose uptake and ATP production. Paroxetine 13-23 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 32-36 25839176-6 2015 In addition, paroxetine-induced AMPK activation increases glucose uptake and ATP production. Glucose 58-65 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 32-36 25839176-6 2015 In addition, paroxetine-induced AMPK activation increases glucose uptake and ATP production. Adenosine Triphosphate 77-80 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 32-36 25839176-7 2015 These neurometabolic effects of paroxetine were suppressed by cotreatment with compound C (CC), an AMPK inhibitor. Paroxetine 32-42 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 99-103 25661535-4 2015 Using Western blotting, we demonstrated that gemigliptin efficiently increased the level of AMP-activated protein kinase (AMPK) and Akt phosphorylation in a dose-dependent manner. LC15-0444 45-56 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 92-120 25661535-4 2015 Using Western blotting, we demonstrated that gemigliptin efficiently increased the level of AMP-activated protein kinase (AMPK) and Akt phosphorylation in a dose-dependent manner. LC15-0444 45-56 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 122-126 25661535-8 2015 However, these anti-inflammatory and anti-atherosclerotic effects of gemigliptin in HUVECs and THP-1 cells were significantly reduced after treatment with an AMPK or an Akt inhibitor. LC15-0444 69-80 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 158-162 25661535-9 2015 Our results suggest that gemigliptin efficiently inhibited LPS-induced pro-inflammatory effects in vascular endothelial cells by attenuating NF-kappaB and JNK signaling via Akt/AMPK-dependent mechanisms. LC15-0444 25-36 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 177-181 25867026-7 2015 We show that metformin induces decreased proliferation, cell cycle arrest, autophagy, apoptosis and cell death in vitro with a concomitant activation of AMPK, Redd1 and inhibition of the mTOR pathway. Metformin 13-22 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 153-157 25867026-9 2015 Interestingly, knockdown of AMPK and Redd1 with siRNA partially, but incompletely, abrogates the induction of apoptosis by metformin suggesting both AMPK/Redd1-dependent and -independent effects. Metformin 123-132 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 28-32 25867026-9 2015 Interestingly, knockdown of AMPK and Redd1 with siRNA partially, but incompletely, abrogates the induction of apoptosis by metformin suggesting both AMPK/Redd1-dependent and -independent effects. Metformin 123-132 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 149-153 25760243-5 2015 Moreover, we demonstrate that protein phosphatases are the key mediators of AMPK-dependent effects on T cell death, and inhibition of phosphatase activity by okadaic acid successfully restores T cell survival and function. Okadaic Acid 158-170 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 76-80 25259783-1 2015 The AMP-activated protein kinase (AMPK) is a sensor of energy status that, when activated by metabolic stress, maintains cellular energy homeostasis by switching on catabolic pathways and switching off ATP-consuming processes. Adenosine Triphosphate 202-205 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 4-32 25259783-1 2015 The AMP-activated protein kinase (AMPK) is a sensor of energy status that, when activated by metabolic stress, maintains cellular energy homeostasis by switching on catabolic pathways and switching off ATP-consuming processes. Adenosine Triphosphate 202-205 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 34-38 25581901-5 2015 Additionally, EGCG increased the phsophorylation of eNOS at Ser635 and Ser1179, Akt at Ser473, calmodulin-dependent protein kinase II (CaMKII) at Thr286 and AMP-activated protein kinase (AMPK) at Thr172, all abolished by the TRPV1 antagonist capsazepine. epigallocatechin gallate 14-18 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 157-185 25581901-5 2015 Additionally, EGCG increased the phsophorylation of eNOS at Ser635 and Ser1179, Akt at Ser473, calmodulin-dependent protein kinase II (CaMKII) at Thr286 and AMP-activated protein kinase (AMPK) at Thr172, all abolished by the TRPV1 antagonist capsazepine. epigallocatechin gallate 14-18 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 187-191 25581901-6 2015 EGCG-induced NO production was diminished by pretreatment with LY294002 (an Akt inhibitor), KN62 (a CaMKII inhibitor), and compound C (an AMPK inhibitor). epigallocatechin gallate 0-4 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 138-142 25581901-8 2015 CONCLUSION: EGCG may trigger activation of TRPV1-Ca(2+) signaling, which leads to phosphorylation of Akt, AMPK, and CaMKII; eNOS activation; NO production; and, ultimately, angiogenesis in ECs. epigallocatechin gallate 12-16 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 106-110 25812520-2 2015 This finding may help to explain why the antidiabetic drug metformin, for which AMPK is a key effector, is linked to cancer-protective activity. Metformin 59-68 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 80-84 25732571-0 2015 Yhhu981, a novel compound, stimulates fatty acid oxidation via the activation of AMPK and ameliorates lipid metabolism disorder in ob/ob mice. Yhhu981 0-7 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 81-85 25736509-7 2015 Mammalian AMPK heterotrimers are phosphorylated on the T-loop (pThr175/176) within both catalytic a subunits. pthr175 63-70 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 10-14 25727016-5 2015 Meantime, doxorubicin promoted HMGCR expression and inhibited AMPKalpha1 expression, which was further facilitated by miR-301a overexpression. Doxorubicin 10-21 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 62-72 25713188-7 2015 Restoration of mitochondrial function and superoxide production via activation of AMPK has now been associated with improvement in markers of renal, cardiovascular, and neuronal dysfunction with diabetes. Superoxides 42-52 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 82-86 25713188-8 2015 With this Perspective, approaches that stimulate AMPK and PGC1alpha via exercise, caloric restriction, and medications result in stimulation of mitochondrial oxidative phosphorylation activity, restore physiologic mitochondrial superoxide production, and promote organ healing. Superoxides 228-238 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 49-53 25499441-10 2015 Mangiferin enhanced AMPK phosphorylation and AMPK inhibitor compound C diminished its beneficial effects, indicating the potential role of AMPK in its action. mangiferin 0-10 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 20-24 26120598-5 2015 Induction of autophagic flux, through metformin-mediated AMP-activated protein kinase (AMPK) activation and interruption of mammalian target of rapamycin (mTOR) signaling mitigated the inflammation in experimental arthritis. Metformin 38-47 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 57-85 26120598-5 2015 Induction of autophagic flux, through metformin-mediated AMP-activated protein kinase (AMPK) activation and interruption of mammalian target of rapamycin (mTOR) signaling mitigated the inflammation in experimental arthritis. Metformin 38-47 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 87-91 26120598-6 2015 Further investigation into the effects of metformin suggest that the drug directly activates AMPK and dose-dependently suppressed the release of TNF-alpha, IL-6, and MCP-1 by macrophages while enhancing the release of IL-10 in vitro. Metformin 42-51 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 93-97 25510732-3 2015 To determine the main components in JLDG and to explore the effect of JLDG on autophagy and lipid accumulation in NIT-1 pancreatic beta cells exposed to politic acid (PA) through AMP activated protein kinase (AMPK) signaling pathway. politic acid 153-165 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 209-213 25510732-3 2015 To determine the main components in JLDG and to explore the effect of JLDG on autophagy and lipid accumulation in NIT-1 pancreatic beta cells exposed to politic acid (PA) through AMP activated protein kinase (AMPK) signaling pathway. Protactinium 167-169 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 209-213 25683712-0 2015 HIGD1A Regulates Oxygen Consumption, ROS Production, and AMPK Activity during Glucose Deprivation to Modulate Cell Survival and Tumor Growth. Glucose 78-85 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 57-61 25732571-9 2015 Furthermore, yhhu981 dose-dependently increased the phosphorylation of AMPK and ACC in both C2C12 myotubes and HepG2 cells. Yhhu981 13-20 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 71-75 25732571-10 2015 Compound C, an AMPK inhibitor, blocked fatty acid oxidation in yhhu981-treated C2C12 myotubes and fatty acid synthesis decrease in yhhu981-treated HepG2 cells. Fatty Acids 39-49 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 15-19 25732571-12 2015 CONCLUSION: Yhhu981 is a potent compound that stimulates fatty acid oxidation, and exerts pleiotropic effects on lipid metabolism by activating AMPK. Yhhu981 12-19 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 144-148 25679763-8 2015 This leads to inhibition of autophagy, activation of mTOR signaling, and hypersensitization to AMPK agonists, such as metformin. Metformin 118-127 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 95-99 25670261-0 2015 Ethanol extract of Remotiflori radix induces endoplasmic reticulum stress-mediated cell death through AMPK/mTOR signaling in human prostate cancer cells. Ethanol 0-7 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 102-106 25670261-0 2015 Ethanol extract of Remotiflori radix induces endoplasmic reticulum stress-mediated cell death through AMPK/mTOR signaling in human prostate cancer cells. remotiflori radix 19-36 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 102-106 25354528-0 2015 Glucose and palmitate uncouple AMPK from autophagy in human aortic endothelial cells. Glucose 0-7 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 31-35 25354528-6 2015 Glucose and palmitate diminished AMPK activity and phosphorylation of the uncoordinated-51-like kinase 1 (ULK1) at Ser555, an autophagy-activating site targeted by AMPK. Glucose 0-7 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 33-37 25354528-6 2015 Glucose and palmitate diminished AMPK activity and phosphorylation of the uncoordinated-51-like kinase 1 (ULK1) at Ser555, an autophagy-activating site targeted by AMPK. Glucose 0-7 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 164-168 25354528-6 2015 Glucose and palmitate diminished AMPK activity and phosphorylation of the uncoordinated-51-like kinase 1 (ULK1) at Ser555, an autophagy-activating site targeted by AMPK. Palmitates 12-21 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 33-37 25354528-6 2015 Glucose and palmitate diminished AMPK activity and phosphorylation of the uncoordinated-51-like kinase 1 (ULK1) at Ser555, an autophagy-activating site targeted by AMPK. Palmitates 12-21 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 164-168 25354528-7 2015 5-Aminoimidazole-4-carboxamide-1-beta-d-ribofuranoside (AICAR)-mediated activation of AMPK phosphorylated acetyl-CoA carboxylase, but treatment with AICAR or other AMPK activators (A769662, phenformin) did not restore ULK1 phosphorylation or autophagosome formation. acadesine 0-54 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 86-90 25354528-7 2015 5-Aminoimidazole-4-carboxamide-1-beta-d-ribofuranoside (AICAR)-mediated activation of AMPK phosphorylated acetyl-CoA carboxylase, but treatment with AICAR or other AMPK activators (A769662, phenformin) did not restore ULK1 phosphorylation or autophagosome formation. acadesine 56-61 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 86-90 25354528-7 2015 5-Aminoimidazole-4-carboxamide-1-beta-d-ribofuranoside (AICAR)-mediated activation of AMPK phosphorylated acetyl-CoA carboxylase, but treatment with AICAR or other AMPK activators (A769662, phenformin) did not restore ULK1 phosphorylation or autophagosome formation. acadesine 56-61 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 164-168 25500743-0 2015 Uncoupling AMPK from autophagy: a foe that hinders the beneficial effects of metformin treatment on metabolic syndrome-associated atherosclerosis? Metformin 77-86 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 11-15 25500743-1 2015 Focus on "glucose and palmitate uncouple AMPK from autophagy in human aortic endothelial cells". Glucose 10-17 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 41-45 25743752-0 2015 Aspirin regulates hepatocellular lipid metabolism by activating AMPK signaling pathway. Aspirin 0-7 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 64-68 25511868-0 2015 Apoptolidins A and C activate AMPK in metabolically sensitive cell types and are mechanistically distinct from oligomycin A. apoptolidins a and c 0-20 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-34 25511868-6 2015 Shifts in cellular metabolism in intact cells and the status of the AMP-activated protein kinase (AMPK) stress pathway in response to apoptolidin A were entirely consistent with the actions of an ATP synthase inhibitor. apoptolidin A 134-147 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 68-96 25511868-6 2015 Shifts in cellular metabolism in intact cells and the status of the AMP-activated protein kinase (AMPK) stress pathway in response to apoptolidin A were entirely consistent with the actions of an ATP synthase inhibitor. apoptolidin A 134-147 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 98-102 25511868-8 2015 The apoptolidins induce indirect activation of AMPK and trigger autophagy in sensitive cell types without significant inhibition of mTORC1. apoptolidin 4-16 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 47-51 25496421-0 2015 AMPK-dependent autophagic activation is probably involved in the mechanism of resveratrol exerting therapeutic effects for Alzheimer"s disease. Resveratrol 78-89 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 25607458-4 2015 Activated T cells were found to possess a glucose-sensitive metabolic checkpoint controlled by the energy sensor AMP-activated protein kinase (AMPK) that regulated mRNA translation and glutamine-dependent mitochondrial metabolism to maintain T cell bioenergetics and viability. Glucose 42-49 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 143-147 25607458-4 2015 Activated T cells were found to possess a glucose-sensitive metabolic checkpoint controlled by the energy sensor AMP-activated protein kinase (AMPK) that regulated mRNA translation and glutamine-dependent mitochondrial metabolism to maintain T cell bioenergetics and viability. Glutamine 185-194 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 143-147 25607458-5 2015 T cells lacking AMPKalpha1 displayed reduced mitochondrial bioenergetics and cellular ATP in response to glucose limitation in vitro or pathogenic challenge in vivo. Adenosine Triphosphate 86-89 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 16-26 25607458-5 2015 T cells lacking AMPKalpha1 displayed reduced mitochondrial bioenergetics and cellular ATP in response to glucose limitation in vitro or pathogenic challenge in vivo. Glucose 105-112 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 16-26 26735433-2 2015 The HDAC (histone deacetylase) inhibitor valproic acid (VPA) interacted synergistically with chemotherapeutic agents to trigger lymphoma cell autophagy, which resulted from activation of AMPK (AMP-activated protein kinase) and inhibition of downstream MTOR (mechanistic target of rapamycin [serine/threonine kinase]) signaling. Valproic Acid 41-54 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 187-191 26735433-2 2015 The HDAC (histone deacetylase) inhibitor valproic acid (VPA) interacted synergistically with chemotherapeutic agents to trigger lymphoma cell autophagy, which resulted from activation of AMPK (AMP-activated protein kinase) and inhibition of downstream MTOR (mechanistic target of rapamycin [serine/threonine kinase]) signaling. Valproic Acid 56-59 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 187-191 26735433-3 2015 In an HDAC-independent manner, VPA potentiated the effect of doxorubicin on lymphoma cell autophagy via reduction of cellular inositol 1,4,5 trisphosphate (IP3), blockade of calcium into mitochondria and modulation of PRKAA1/2-MTOR cascade. Doxorubicin 61-72 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 218-224 25591762-3 2015 METHODS: Currently, we conducted this study to investigate the effects of AMPK on high glucose-induced extracellular matrix synthesis and involved intracellular signaling pathway by using western blot in the kidney fibroblast cell line (NRK-49f). Glucose 87-94 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 74-78 25591762-6 2015 High glucose-induced extracellular matrix accumulation and mTOR activation were significantly inhibited by the co-treatment of rAAV-AMPKalpha1(312) (encoding constitutively active AMPKalpha1) whereas activated by r-AAV-AMPKalpha1D157A (encoding dominant negative AMPKalpha1). Glucose 5-12 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 132-142 25591762-6 2015 High glucose-induced extracellular matrix accumulation and mTOR activation were significantly inhibited by the co-treatment of rAAV-AMPKalpha1(312) (encoding constitutively active AMPKalpha1) whereas activated by r-AAV-AMPKalpha1D157A (encoding dominant negative AMPKalpha1). Glucose 5-12 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 180-190 25591762-6 2015 High glucose-induced extracellular matrix accumulation and mTOR activation were significantly inhibited by the co-treatment of rAAV-AMPKalpha1(312) (encoding constitutively active AMPKalpha1) whereas activated by r-AAV-AMPKalpha1D157A (encoding dominant negative AMPKalpha1). Glucose 5-12 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 180-190 26351511-4 2015 An altered lipid metabolism induced by berberine was observed under the inhibition of FASN, AMPK, and ACC in breast cancer cell MCF-7. Berberine 39-48 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 92-96 26351511-6 2015 A robust apoptosis induced by berberine even under the inhibition of AMPK and lipid synthesis was also indicated. Berberine 30-39 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 69-73 25377300-4 2015 In THP-1 cells, AMPKalpha1 was phosphorylated within 1h of menadione (15 muM)-triggered increases in [reactive oxygen species (ROS)]cyto, an effect which was followed by upregulation of PPARgamma and several of its target genes (PGC-1alpha, liver X receptor alpha [LXRalpha] and ATP-binding cassette subfamily A, member 1 [ABCA1]; 24-72 h), with these effects being blunted by co-administration of vitamin C (62.5 muM). Hydrogen 53-55 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 16-26 25377300-4 2015 In THP-1 cells, AMPKalpha1 was phosphorylated within 1h of menadione (15 muM)-triggered increases in [reactive oxygen species (ROS)]cyto, an effect which was followed by upregulation of PPARgamma and several of its target genes (PGC-1alpha, liver X receptor alpha [LXRalpha] and ATP-binding cassette subfamily A, member 1 [ABCA1]; 24-72 h), with these effects being blunted by co-administration of vitamin C (62.5 muM). Vitamin K 3 59-68 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 16-26 25377300-4 2015 In THP-1 cells, AMPKalpha1 was phosphorylated within 1h of menadione (15 muM)-triggered increases in [reactive oxygen species (ROS)]cyto, an effect which was followed by upregulation of PPARgamma and several of its target genes (PGC-1alpha, liver X receptor alpha [LXRalpha] and ATP-binding cassette subfamily A, member 1 [ABCA1]; 24-72 h), with these effects being blunted by co-administration of vitamin C (62.5 muM). Reactive Oxygen Species 102-125 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 16-26 25377300-4 2015 In THP-1 cells, AMPKalpha1 was phosphorylated within 1h of menadione (15 muM)-triggered increases in [reactive oxygen species (ROS)]cyto, an effect which was followed by upregulation of PPARgamma and several of its target genes (PGC-1alpha, liver X receptor alpha [LXRalpha] and ATP-binding cassette subfamily A, member 1 [ABCA1]; 24-72 h), with these effects being blunted by co-administration of vitamin C (62.5 muM). Reactive Oxygen Species 127-130 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 16-26 25377300-4 2015 In THP-1 cells, AMPKalpha1 was phosphorylated within 1h of menadione (15 muM)-triggered increases in [reactive oxygen species (ROS)]cyto, an effect which was followed by upregulation of PPARgamma and several of its target genes (PGC-1alpha, liver X receptor alpha [LXRalpha] and ATP-binding cassette subfamily A, member 1 [ABCA1]; 24-72 h), with these effects being blunted by co-administration of vitamin C (62.5 muM). Ascorbic Acid 398-407 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 16-26 26337566-3 2015 METHODS: The expression of AMPKalpha1, AMPKalpha2 and phosphorylated AMPKalpha (p-AMPKalpha) was determined immunohistochemically in 524 formalin-fixed, paraffin-embedded malignant and premalignant cervical tissues. Formaldehyde 137-145 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 27-37 25256353-8 2015 Suppression of AMPK activity using cAMP-simulating agents rescued the mislocalization of TDP-43 in NSC34 cells and delayed disease progression in TDP-43 transgenic mice. Cyclic AMP 35-39 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 15-19 25743752-8 2015 Thus, we confirmed in this study that aspirin promoted lipid oxidation by upregulating the AMPK signaling pathway. Aspirin 38-45 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 91-95 25512602-8 2015 IL-10 induced phosphorylation of both Tyr(705) and Ser(727) residues of STAT3 in an AMPKalpha1-dependent manner, and these phosphorylation events were blocked by inhibition of Ca(2+)/calmodulin-dependent protein kinase kinase beta, an upstream activator of AMPK, and by the mTORC1 inhibitor rapamycin, respectively. Tyrosine 38-41 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 84-94 25512602-8 2015 IL-10 induced phosphorylation of both Tyr(705) and Ser(727) residues of STAT3 in an AMPKalpha1-dependent manner, and these phosphorylation events were blocked by inhibition of Ca(2+)/calmodulin-dependent protein kinase kinase beta, an upstream activator of AMPK, and by the mTORC1 inhibitor rapamycin, respectively. Tyrosine 38-41 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 84-88 25512602-8 2015 IL-10 induced phosphorylation of both Tyr(705) and Ser(727) residues of STAT3 in an AMPKalpha1-dependent manner, and these phosphorylation events were blocked by inhibition of Ca(2+)/calmodulin-dependent protein kinase kinase beta, an upstream activator of AMPK, and by the mTORC1 inhibitor rapamycin, respectively. Serine 51-54 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 84-94 25512602-8 2015 IL-10 induced phosphorylation of both Tyr(705) and Ser(727) residues of STAT3 in an AMPKalpha1-dependent manner, and these phosphorylation events were blocked by inhibition of Ca(2+)/calmodulin-dependent protein kinase kinase beta, an upstream activator of AMPK, and by the mTORC1 inhibitor rapamycin, respectively. Serine 51-54 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 84-88 26103054-0 2015 Thyroid hormone induction of mitochondrial activity is coupled to mitophagy via ROS-AMPK-ULK1 signaling. Reactive Oxygen Species 80-83 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 84-88 26103054-5 2015 We show that T3 induction of ROS activates CAMKK2 (calcium/calmodulin-dependent protein kinase kinase 2, beta) mediated phosphorylation of PRKAA1/AMPK (5" AMP-activated protein kinase), which in turn phosphorylates ULK1 (unc-51 like autophagy activating kinase 1) leading to its mitochondrial recruitment and initiation of mitophagy. Reactive Oxygen Species 29-32 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 139-145 26103054-5 2015 We show that T3 induction of ROS activates CAMKK2 (calcium/calmodulin-dependent protein kinase kinase 2, beta) mediated phosphorylation of PRKAA1/AMPK (5" AMP-activated protein kinase), which in turn phosphorylates ULK1 (unc-51 like autophagy activating kinase 1) leading to its mitochondrial recruitment and initiation of mitophagy. Reactive Oxygen Species 29-32 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 146-150 26103054-7 2015 These findings demonstrate a novel ROS-AMPK-ULK1 mechanism that couples T3-induced mitochondrial turnover with activity, wherein mitophagy is necessary not only for removing damaged mitochondria but also for sustaining efficient OXPHOS. Reactive Oxygen Species 35-38 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 39-43 25456211-0 2015 AMPK/mTOR-mediated inhibition of survivin partly contributes to metformin-induced apoptosis in human gastric cancer cell. Metformin 64-73 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 25456211-9 2015 AMPK knockdown by siRNA restores metformin-inhibited survivin expression and partially abolishes metformin-induced apoptosis. Metformin 33-42 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 25456211-9 2015 AMPK knockdown by siRNA restores metformin-inhibited survivin expression and partially abolishes metformin-induced apoptosis. Metformin 97-106 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 25456211-12 2015 Xenograft nude mouse experiment also confirmed that AMPK/mTOR-mediated decrease of suvivin is in vivo implicated in metformin-induced apoptosis. Metformin 116-125 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 52-56 25456211-13 2015 Taken together, these evidences suggest that AMPK/mTOR-mediated inhibition of survivin may partly contribute to metformin-induced apoptosis of gastric cancer cell. Metformin 112-121 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 45-49 26065336-0 2015 NBM-T-BMX-OS01, an Osthole Derivative, Sensitizes Human Lung Cancer A549 Cells to Cisplatin through AMPK-Dependent Inhibition of ERK and Akt Pathway. Cisplatin 82-91 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 100-104 26065336-10 2015 In contrast, BMX inhibited the activation of AMPK, and knockdown of AMPK using specific siRNA partially reversed BMX-induced inhibition of ERK and Akt, as well as its synthetic effects on cisplatin induced anticancer activity in A549 cells. Cisplatin 188-197 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 68-72 26065336-11 2015 CONCLUSION: Taken together, this study provides that BMX might modulate cisplatin resistance through AMPK-ERK and AMPK-Akt pathways. Cisplatin 72-81 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 101-105 26065336-11 2015 CONCLUSION: Taken together, this study provides that BMX might modulate cisplatin resistance through AMPK-ERK and AMPK-Akt pathways. Cisplatin 72-81 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 114-118 25941821-3 2015 Improving insulin sensitivity, enhancing GLUT4 translocation, reducing oxidative stress, regulating carbohydrate metabolizing enzymes, activating SIRT1 and AMPK, and decreasing adipogenic genes are some promising mechanisms established until now for resveratrol. Resveratrol 250-261 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 156-160 26411966-1 2015 Increasing epidemiologic evidence suggests that metformin, a well-established AMPK activator and the most favorable first-line anti-diabetic drug, reduces stroke incidence and severity. Metformin 48-57 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 78-82 26411966-4 2015 However, recent studies have consistently suggested that AMPK-mediated microglia/macrophage polarization and angioneurogenesis may play essential roles in metformin-promoted, long-term functional recovery following stroke. Metformin 155-164 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 57-61 26411966-5 2015 The present review summarizes the neuropharmacological actions of metformin in experimental stroke with an emphasis on the recent findings that the cell-specific effects and duration of AMPK activation are critical to the effects of metformin on stroke outcomes. Metformin 233-242 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 186-190 25142777-0 2015 Adamts1 mediates ethanol-induced alterations in collagen and elastin via a FoxO1-sestrin3-AMPK signaling cascade in myocytes. Ethanol 17-24 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 90-94 25142777-10 2015 The AMPK inhibitor compound C blocked the EtOH-induced stimulation of collagen and O-GLcNAc Adamts1 protein. Ethanol 42-46 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 4-8 25142777-11 2015 Changes in AMPK appear linked to FoxO1, since inhibition of FoxO1 blocked the effects of EtOH on AMPK phosphorylation and O-GLcNAc levels. Ethanol 89-93 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 11-15 25142777-11 2015 Changes in AMPK appear linked to FoxO1, since inhibition of FoxO1 blocked the effects of EtOH on AMPK phosphorylation and O-GLcNAc levels. Ethanol 89-93 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 97-101 25131770-11 2015 Metformin, an AMPK activator, more strongly suppressed cell growth in p53-mutant cell lines with inactive SIRT1 than in p53-mutant cell lines with active SIRT1. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-18 25131770-13 2015 Metformin could be a therapeutic drug for HCC in patients with mutated p53, inactivated SIRT1, and AMPK expression. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 99-103 25743752-3 2015 We presently investigated aspirin"s promotion of AMP-activated protein kinase (AMPK) pathway activation in human hepatoma HepG2 cells by examining AMPK expression, the promotion of AMPK activation. Aspirin 26-33 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 49-77 25743752-3 2015 We presently investigated aspirin"s promotion of AMP-activated protein kinase (AMPK) pathway activation in human hepatoma HepG2 cells by examining AMPK expression, the promotion of AMPK activation. Aspirin 26-33 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 79-83 25743752-3 2015 We presently investigated aspirin"s promotion of AMP-activated protein kinase (AMPK) pathway activation in human hepatoma HepG2 cells by examining AMPK expression, the promotion of AMPK activation. Aspirin 26-33 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 147-151 25743752-3 2015 We presently investigated aspirin"s promotion of AMP-activated protein kinase (AMPK) pathway activation in human hepatoma HepG2 cells by examining AMPK expression, the promotion of AMPK activation. Aspirin 26-33 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 147-151 25743752-4 2015 Then we investigated the influence of aspirin-promoted AMPK signaling on fatty acid oxidation in HepG2 cells. Aspirin 38-45 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 55-59 25743752-4 2015 Then we investigated the influence of aspirin-promoted AMPK signaling on fatty acid oxidation in HepG2 cells. Fatty Acids 73-83 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 55-59 25743752-5 2015 The results demonstrated that aspirin treatment did not regulate the expression of AMPK and its downstream target, Acetyl-Coenzyme A Carboxylase (ACC), but activated the AMPK signaling pathway by promoting the phosphorylation of AMPK and ACC. Aspirin 30-37 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 170-174 25743752-5 2015 The results demonstrated that aspirin treatment did not regulate the expression of AMPK and its downstream target, Acetyl-Coenzyme A Carboxylase (ACC), but activated the AMPK signaling pathway by promoting the phosphorylation of AMPK and ACC. Aspirin 30-37 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 170-174 25743752-7 2015 Moreover, the activated AMPK signaling promoted the fatty acid oxidation, by promoting expression of Carnitine palmitoyltransferase I (CPT1) and Medium-Chain Acyl-CoA Dehydrogenase (MCAD) in both mRNA and protein levels. Fatty Acids 52-62 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 24-28 25734181-5 2015 Metformin, an antidiabetic drug, is effective for endometrial cancer through inhibition of the PI3K-Akt-mTOR pathway by activating LKB1-AMPK and reduction of insulin and insulin-like growth factor-1 due to AMPK activation. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 136-140 25734181-5 2015 Metformin, an antidiabetic drug, is effective for endometrial cancer through inhibition of the PI3K-Akt-mTOR pathway by activating LKB1-AMPK and reduction of insulin and insulin-like growth factor-1 due to AMPK activation. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 206-210 25493642-0 2014 Dose-Dependent AMPK-Dependent and Independent Mechanisms of Berberine and Metformin Inhibition of mTORC1, ERK, DNA Synthesis and Proliferation in Pancreatic Cancer Cells. Berberine 60-69 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 15-19 25281642-4 2015 AMPK activity, evaluated as Thr(172) phosphorylation by western blot, is effectively increased by A769662 in spermatozoa. Threonine 28-31 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 25281642-6 2015 Moreover, AMPK activation in spermatozoa incubated in TBM or TCM significantly reduces curvilinear VCL, straight-line VSL and average VAP velocities, which subsequently lead to a significant decrease in the percentage of rapid spermatozoa (VAP > 80 mum/s). Tobramycin 54-57 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 10-14 25281642-9 2015 Sustained (24 h) AMPK activation under TBM or TCM significantly increases both lipid disorganization and phosphatidylserine externalization in the sperm plasma membrane, and diminishes the acrosome membrane integrity. Tobramycin 39-42 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 17-21 25481044-0 2014 Bortezomib induces AMPK-dependent autophagosome formation uncoupled from apoptosis in drug resistant cells. Bortezomib 0-10 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 19-23 25481044-2 2014 Drug sensitive myeloma cells were exposed to bortezomib to generate drug resistant cells that displayed a significant increase in subunits of the energy sensor AMP-activated protein kinase (AMPK). Bortezomib 45-55 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 160-188 25481044-2 2014 Drug sensitive myeloma cells were exposed to bortezomib to generate drug resistant cells that displayed a significant increase in subunits of the energy sensor AMP-activated protein kinase (AMPK). Bortezomib 45-55 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 190-194 25481044-5 2014 Genetic ablation of AMPK activity reduced the bortezomib effect on autophagy. Bortezomib 46-56 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 20-24 25481044-9 2014 In contrast, AICAR, an AMPK activator, enhanced bortezomib-induced cleavage of ATG5 and increased bortezomib-induced killing. AICA ribonucleotide 13-18 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 23-27 25481044-9 2014 In contrast, AICAR, an AMPK activator, enhanced bortezomib-induced cleavage of ATG5 and increased bortezomib-induced killing. Bortezomib 48-58 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 23-27 25481044-9 2014 In contrast, AICAR, an AMPK activator, enhanced bortezomib-induced cleavage of ATG5 and increased bortezomib-induced killing. Bortezomib 98-108 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 23-27 25493642-7 2014 However, at higher concentrations, berberine inhibited mitogenic signaling (mTORC1 and ERK) and DNA synthesis through an AMPK-independent mechanism. Berberine 35-44 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 121-125 25493642-9 2014 We propose that berberine and metformin inhibit mitogenic signaling in PDAC cells through dose-dependent AMPK-dependent and independent pathways. Berberine 16-25 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 105-109 25493642-9 2014 We propose that berberine and metformin inhibit mitogenic signaling in PDAC cells through dose-dependent AMPK-dependent and independent pathways. Metformin 30-39 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 105-109 25493642-0 2014 Dose-Dependent AMPK-Dependent and Independent Mechanisms of Berberine and Metformin Inhibition of mTORC1, ERK, DNA Synthesis and Proliferation in Pancreatic Cancer Cells. Metformin 74-83 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 15-19 25493642-4 2014 Mechanistic studies revealed that berberine decreased mitochondrial membrane potential and intracellular ATP levels and induced potent AMPK activation, as shown by phosphorylation of AMPK alpha subunit at Thr-172 and acetyl-CoA carboxylase (ACC) at Ser79. Berberine 34-43 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 135-139 25493642-4 2014 Mechanistic studies revealed that berberine decreased mitochondrial membrane potential and intracellular ATP levels and induced potent AMPK activation, as shown by phosphorylation of AMPK alpha subunit at Thr-172 and acetyl-CoA carboxylase (ACC) at Ser79. Berberine 34-43 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 183-187 25493642-4 2014 Mechanistic studies revealed that berberine decreased mitochondrial membrane potential and intracellular ATP levels and induced potent AMPK activation, as shown by phosphorylation of AMPK alpha subunit at Thr-172 and acetyl-CoA carboxylase (ACC) at Ser79. Threonine 205-208 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 183-187 25493642-6 2014 Knockdown of alpha1 and alpha2 catalytic subunit expression of AMPK reversed the inhibitory effect produced by treatment with low concentrations of berberine on mTORC1, ERK and DNA synthesis in PDAC cells. Berberine 148-157 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 63-67 25315694-4 2014 Here we show that AMP-activated protein kinase (AMPK) activation by AICAR (5-amino-1-beta-d-ribofuranosyl-imidazole-4-carboxamide) or phenformin induced the ubiquitination of FSP27 and promoted its degradation in 3T3-L1 adipocytes. acadesine 68-73 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 18-46 25503637-8 2014 Agonist induction of AMPK activity with AICAR or metformin increased macroautophagy protein LC3 and normalized p62/SQSTM1 expression and mTOR activity. AICA ribonucleotide 40-45 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 21-25 25503637-8 2014 Agonist induction of AMPK activity with AICAR or metformin increased macroautophagy protein LC3 and normalized p62/SQSTM1 expression and mTOR activity. Metformin 49-58 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 21-25 25456737-5 2014 Metformin-induced activation of the energy-sensor AMPK is well documented, but may not account for all actions of the drug. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 50-54 25456737-6 2014 Here, we summarize current knowledge about the different AMPK-dependent and AMPK-independent mechanisms underlying metformin action. Metformin 115-124 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 57-61 25456737-6 2014 Here, we summarize current knowledge about the different AMPK-dependent and AMPK-independent mechanisms underlying metformin action. Metformin 115-124 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 76-80 25399650-0 2014 Probucol suppresses human glioma cell proliferation in vitro via ROS production and LKB1-AMPK activation. Probucol 0-8 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 89-93 25399650-11 2014 Probucol-induced suppression of U87 cell proliferation could be reversed by pretreatment with tempol (a superoxide dismutase mimetic), MG132 (proteasome inhibitor) or compound C (AMPK inhibitor), or by gene silencing of LKB1, AMPK or p27(Kip1). Probucol 0-8 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 179-183 25399650-11 2014 Probucol-induced suppression of U87 cell proliferation could be reversed by pretreatment with tempol (a superoxide dismutase mimetic), MG132 (proteasome inhibitor) or compound C (AMPK inhibitor), or by gene silencing of LKB1, AMPK or p27(Kip1). Probucol 0-8 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 226-230 25315694-4 2014 Here we show that AMP-activated protein kinase (AMPK) activation by AICAR (5-amino-1-beta-d-ribofuranosyl-imidazole-4-carboxamide) or phenformin induced the ubiquitination of FSP27 and promoted its degradation in 3T3-L1 adipocytes. acadesine 68-73 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 48-52 25315694-4 2014 Here we show that AMP-activated protein kinase (AMPK) activation by AICAR (5-amino-1-beta-d-ribofuranosyl-imidazole-4-carboxamide) or phenformin induced the ubiquitination of FSP27 and promoted its degradation in 3T3-L1 adipocytes. acadesine 75-129 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 18-46 25315694-4 2014 Here we show that AMP-activated protein kinase (AMPK) activation by AICAR (5-amino-1-beta-d-ribofuranosyl-imidazole-4-carboxamide) or phenformin induced the ubiquitination of FSP27 and promoted its degradation in 3T3-L1 adipocytes. acadesine 75-129 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 48-52 25315694-4 2014 Here we show that AMP-activated protein kinase (AMPK) activation by AICAR (5-amino-1-beta-d-ribofuranosyl-imidazole-4-carboxamide) or phenformin induced the ubiquitination of FSP27 and promoted its degradation in 3T3-L1 adipocytes. Phenformin 134-144 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 18-46 25315694-4 2014 Here we show that AMP-activated protein kinase (AMPK) activation by AICAR (5-amino-1-beta-d-ribofuranosyl-imidazole-4-carboxamide) or phenformin induced the ubiquitination of FSP27 and promoted its degradation in 3T3-L1 adipocytes. Phenformin 134-144 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 48-52 25217963-7 2014 In capsaicin-treated cells, levels of phosphorylated AMPK increased, and this effect was abolished by treatment with the AMPK inhibitor, Compound C. Capsaicin enhanced the expression of SIRT1, which can activate the transcription factor NF-kappaB by deacetylation. Capsaicin 149-158 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 53-57 25016296-10 2014 Fisetin treatment to 2-D melanoma cultures resulted in phosphorylation and activation of the multifunctional AMP-activated protein kinase (AMPK) involved in the regulation of diverse cellular processes, including autophagy and apoptosis. fisetin 0-7 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 109-137 25016296-10 2014 Fisetin treatment to 2-D melanoma cultures resulted in phosphorylation and activation of the multifunctional AMP-activated protein kinase (AMPK) involved in the regulation of diverse cellular processes, including autophagy and apoptosis. fisetin 0-7 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 139-143 25016296-11 2014 Silencing of AMPK failed to prevent cell death indicating that fisetin induced cytotoxicity is mediated through both AMPK-dependent and -independent mechanisms. fisetin 63-70 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 117-121 25217963-7 2014 In capsaicin-treated cells, levels of phosphorylated AMPK increased, and this effect was abolished by treatment with the AMPK inhibitor, Compound C. Capsaicin enhanced the expression of SIRT1, which can activate the transcription factor NF-kappaB by deacetylation. Capsaicin 149-158 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 121-125 25217963-9 2014 In addition, capsaicin-activated AMPK induced the phosphorylation of IkappaBalpha and nuclear localization of NF-kappaB p65. Capsaicin 13-22 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 33-37 25217963-11 2014 These findings provide evidence that capsaicin suppresses the migration and invasion of cholangiocarcinoma cells by inhibiting NF-kappaB p65 via the AMPK-SIRT1 and the AMPK-IkappaBalpha signaling pathways, leading to subsequent suppression of MMP-9 expression. Capsaicin 37-46 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 149-153 25217963-11 2014 These findings provide evidence that capsaicin suppresses the migration and invasion of cholangiocarcinoma cells by inhibiting NF-kappaB p65 via the AMPK-SIRT1 and the AMPK-IkappaBalpha signaling pathways, leading to subsequent suppression of MMP-9 expression. Capsaicin 37-46 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 168-172 25450947-7 2014 RESULTS: We show that the high levels of activated AMPK, observed in astrocytic tumours, increase extracellular lipid internalisation and reduce energy expenditure by inhibiting "de novo" fatty acid (FA) synthesis, which allows tumour cells to obtain building blocks and energy to be able to create new organelles and new cells. Fatty Acids 188-198 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 51-55 25172886-6 2014 Instead, feedback signals through AMPK and mechanical stress are likely to account for most of contraction-stimulated glucose transport. Glucose 118-125 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 34-38 25220346-8 2014 We conclude that AMPK activation improves the integrity of the BBB disrupted by LPS through suppressing the induction of NAD(P)H oxidase-derived ROS in HBMECs. Reactive Oxygen Species 145-148 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 17-21 24824502-2 2014 A recently reported crystal structure has illuminated the complex regulatory mechanisms by which AMP and ADP cause activation of AMPK, involving phosphorylation by the upstream kinase LKB1. Adenosine Monophosphate 97-100 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 129-133 24824502-2 2014 A recently reported crystal structure has illuminated the complex regulatory mechanisms by which AMP and ADP cause activation of AMPK, involving phosphorylation by the upstream kinase LKB1. Adenosine Diphosphate 105-108 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 129-133 24824502-3 2014 Once activated by falling cellular energy status, AMPK activates catabolic pathways that generate ATP whilst inhibiting anabolic pathways and other cellular processes that consume ATP. Adenosine Triphosphate 98-101 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 50-54 24824502-3 2014 Once activated by falling cellular energy status, AMPK activates catabolic pathways that generate ATP whilst inhibiting anabolic pathways and other cellular processes that consume ATP. Adenosine Triphosphate 180-183 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 50-54 24824502-6 2014 AMPK-activating drugs reverse many of the metabolic defects associated with insulin resistance, and recent findings suggest that the insulin-sensitizing effects of the widely used antidiabetic drug metformin are mediated by AMPK. Metformin 198-207 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 24824502-6 2014 AMPK-activating drugs reverse many of the metabolic defects associated with insulin resistance, and recent findings suggest that the insulin-sensitizing effects of the widely used antidiabetic drug metformin are mediated by AMPK. Metformin 198-207 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 224-228 24824502-9 2014 Salicylate (the major in vivo metabolite of aspirin) activates AMPK, and this could be responsible for at least some of the anticancer and anti-inflammatory effects of aspirin. Salicylates 0-10 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 63-67 24824502-9 2014 Salicylate (the major in vivo metabolite of aspirin) activates AMPK, and this could be responsible for at least some of the anticancer and anti-inflammatory effects of aspirin. Aspirin 44-51 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 63-67 24824502-9 2014 Salicylate (the major in vivo metabolite of aspirin) activates AMPK, and this could be responsible for at least some of the anticancer and anti-inflammatory effects of aspirin. Aspirin 168-175 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 63-67 25450395-0 2014 Silibinin activates AMP-activated protein kinase to protect neuronal cells from oxygen and glucose deprivation-re-oxygenation. Silybin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 20-48 25450395-0 2014 Silibinin activates AMP-activated protein kinase to protect neuronal cells from oxygen and glucose deprivation-re-oxygenation. Oxygen 80-86 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 20-48 25450395-0 2014 Silibinin activates AMP-activated protein kinase to protect neuronal cells from oxygen and glucose deprivation-re-oxygenation. Glucose 91-98 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 20-48 25450395-5 2014 At the molecular level, silibinin treatment in SH-SY5Y cells and primary cortical neurons led to significant AMP-activated protein kinase (AMPK) signaling activation, detected by phosphorylations of AMPKalpha1, its upstream kinase liver kinase B1 (LKB1) and the downstream target acetyl-CoA Carboxylase (ACC). Silybin 24-33 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 109-137 25450395-5 2014 At the molecular level, silibinin treatment in SH-SY5Y cells and primary cortical neurons led to significant AMP-activated protein kinase (AMPK) signaling activation, detected by phosphorylations of AMPKalpha1, its upstream kinase liver kinase B1 (LKB1) and the downstream target acetyl-CoA Carboxylase (ACC). Silybin 24-33 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 139-143 25450395-5 2014 At the molecular level, silibinin treatment in SH-SY5Y cells and primary cortical neurons led to significant AMP-activated protein kinase (AMPK) signaling activation, detected by phosphorylations of AMPKalpha1, its upstream kinase liver kinase B1 (LKB1) and the downstream target acetyl-CoA Carboxylase (ACC). Silybin 24-33 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 199-209 25450395-6 2014 Pharmacological inhibition or genetic depletion of AMPK alleviated the neuroprotective ability of silibinin against OGD/re-oxygenation. Silybin 98-107 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 51-55 25450395-7 2014 Further, ROS scavenging ability by silibinin was abolished with AMPK inhibition or silencing. Reactive Oxygen Species 9-12 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 64-68 25450395-7 2014 Further, ROS scavenging ability by silibinin was abolished with AMPK inhibition or silencing. Silybin 35-44 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 64-68 25450395-8 2014 While A-769662, the AMPK activator, mimicked silibinin actions and suppressed ROS production and neuronal cell death following OGD/re-oxygenation. Silybin 45-54 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 20-24 25450395-8 2014 While A-769662, the AMPK activator, mimicked silibinin actions and suppressed ROS production and neuronal cell death following OGD/re-oxygenation. Reactive Oxygen Species 78-81 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 20-24 25450395-9 2014 Together, these results show that silibinin-mediated neuroprotection requires activation of AMPK signaling. Silybin 34-43 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 92-96 24186207-7 2014 Our results further indicate that the AMPK-mediated metabolic changes increased intracellular ATP levels and peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1alpha)-mediated mitochondrial biogenesis, affording distinct growth advantages to the prostate cancer cells. Adenosine Triphosphate 94-97 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 38-42 25078626-9 2014 Additionally, calcitriol increased levels of autophagy markers, including LC3, beclin-1, and AMPK. Calcitriol 14-24 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 93-97 25217963-0 2014 Capsaicin suppresses the migration of cholangiocarcinoma cells by down-regulating matrix metalloproteinase-9 expression via the AMPK-NF-kappaB signaling pathway. Capsaicin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 128-132 25217963-7 2014 In capsaicin-treated cells, levels of phosphorylated AMPK increased, and this effect was abolished by treatment with the AMPK inhibitor, Compound C. Capsaicin enhanced the expression of SIRT1, which can activate the transcription factor NF-kappaB by deacetylation. Capsaicin 3-12 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 53-57 25217963-7 2014 In capsaicin-treated cells, levels of phosphorylated AMPK increased, and this effect was abolished by treatment with the AMPK inhibitor, Compound C. Capsaicin enhanced the expression of SIRT1, which can activate the transcription factor NF-kappaB by deacetylation. Capsaicin 3-12 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 121-125 25412667-7 2014 Treatment with 200 mumol/L H2O2tended to up-regulate p53 and to down-regulate SIRT1 and AMPKalpha1, but had no effect on AMPKalpha2 and 14-3-3 sigma expression. h2o2tended 27-37 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 88-98 25412667-8 2014 Pretreatment with TJ-10 inhibited H2O2-induced up-regulation of p53 and enhanced AMPKalpha1 expression. Hydrogen Peroxide 34-38 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 81-91 25123628-0 2014 Alpha-lipoic acid improves high-fat diet-induced hepatic steatosis by modulating the transcription factors SREBP-1, FoxO1 and Nrf2 via the SIRT1/LKB1/AMPK pathway. Thioctic Acid 0-17 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 150-154 25129649-0 2014 Alpha linolenic acid and oleic acid additively down-regulate malignant potential and positively cross-regulate AMPK/S6 axis in OE19 and OE33 esophageal cancer cells. alpha-Linolenic Acid 0-20 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 111-115 25129649-0 2014 Alpha linolenic acid and oleic acid additively down-regulate malignant potential and positively cross-regulate AMPK/S6 axis in OE19 and OE33 esophageal cancer cells. Oleic Acid 25-35 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 111-115 25129649-7 2014 Also, we observed that OA and/or ALA positively cross-regulates the expression levels of AMPK/S6 axis. alpha-Linolenic Acid 33-36 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 89-93 25129649-8 2014 Moreover, OA and ALA up-regulated tumor suppressor genes (p53, p21, and p27) and these effects are abolished by AMPK siRNA administration. alpha-Linolenic Acid 17-20 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 112-116 25294820-6 2014 Mechanistically, silibinin activated AMPK, thereby increasing SREBP1 phosphorylation and inhibiting its nuclear translocation; AMPK inhibition reversed silibinin-mediated decrease in nuclear SREBP1 and lipid accumulation. Silybin 17-26 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 37-41 25294820-6 2014 Mechanistically, silibinin activated AMPK, thereby increasing SREBP1 phosphorylation and inhibiting its nuclear translocation; AMPK inhibition reversed silibinin-mediated decrease in nuclear SREBP1 and lipid accumulation. Silybin 152-161 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 127-131 25089813-0 2014 Activated AMPK explains hypolipidemic effects of sulfated low molecular weight guluronate on HepG2 cells. D-GulA 79-89 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 10-14 25132405-0 2014 Baicalein induces autophagic cell death through AMPK/ULK1 activation and downregulation of mTORC1 complex components in human cancer cells. baicalein 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 48-52 25302702-6 2014 Molecular pathways underlying these effects of resveratrol involve SIRT1, AMPK, Nrf2 and estrogen receptors. Resveratrol 47-58 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 74-78 25065674-0 2014 AMP-activated protein kinase mediates the antioxidant effects of resveratrol through regulation of the transcription factor FoxO1. Resveratrol 65-76 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-28 25065674-4 2014 Recently, several antioxidants have been reported to activate AMPK, although the mechanisms by which AMPK acts to adjust the levels of cellular reactive oxygen species are not fully characterized. Reactive Oxygen Species 144-167 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 101-105 25065674-5 2014 In the present study, we investigated the role of AMPK in mediating resveratrol-induced antioxidant effects and the molecular mechanisms underlying its actions. Resveratrol 68-79 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 50-54 25065674-6 2014 We demonstrate that AMPK activity plays an indispensable role in the operation of the ROS defense system by inducing the expression of the antioxidant enzymes, manganese superoxide dismutase and catalase, in response to resveratrol or the AMPK agonist 5-aminoimidazole-4-carboxamide-1-beta-d-ribonucleotide. Reactive Oxygen Species 86-89 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 20-24 25065674-6 2014 We demonstrate that AMPK activity plays an indispensable role in the operation of the ROS defense system by inducing the expression of the antioxidant enzymes, manganese superoxide dismutase and catalase, in response to resveratrol or the AMPK agonist 5-aminoimidazole-4-carboxamide-1-beta-d-ribonucleotide. Reactive Oxygen Species 86-89 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 239-243 25065674-6 2014 We demonstrate that AMPK activity plays an indispensable role in the operation of the ROS defense system by inducing the expression of the antioxidant enzymes, manganese superoxide dismutase and catalase, in response to resveratrol or the AMPK agonist 5-aminoimidazole-4-carboxamide-1-beta-d-ribonucleotide. Resveratrol 220-231 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 20-24 25065674-6 2014 We demonstrate that AMPK activity plays an indispensable role in the operation of the ROS defense system by inducing the expression of the antioxidant enzymes, manganese superoxide dismutase and catalase, in response to resveratrol or the AMPK agonist 5-aminoimidazole-4-carboxamide-1-beta-d-ribonucleotide. 5-aminoimidazole-4-carboxamide-1-beta-d-ribonucleotide 252-306 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 20-24 25065674-6 2014 We demonstrate that AMPK activity plays an indispensable role in the operation of the ROS defense system by inducing the expression of the antioxidant enzymes, manganese superoxide dismutase and catalase, in response to resveratrol or the AMPK agonist 5-aminoimidazole-4-carboxamide-1-beta-d-ribonucleotide. 5-aminoimidazole-4-carboxamide-1-beta-d-ribonucleotide 252-306 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 239-243 25065674-7 2014 In addition, we identified the mechanism involved in the antioxidant function of AMPK, demonstrating that AMPK directly phosphorylates human FoxO1 (forkhead box O1) at Thr(649) in vitro and increases FoxO1-dependent transcription of manganese superoxide dismutase and catalase. Threonine 168-171 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 81-85 25065674-7 2014 In addition, we identified the mechanism involved in the antioxidant function of AMPK, demonstrating that AMPK directly phosphorylates human FoxO1 (forkhead box O1) at Thr(649) in vitro and increases FoxO1-dependent transcription of manganese superoxide dismutase and catalase. Threonine 168-171 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 106-110 25360075-0 2014 5-aminoimidazole-4-carboxamide Riboside Induces Apoptosis Through AMP-activated Protein Kinase-independent and NADPH Oxidase-dependent Pathways. acadesine 0-39 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 66-94 25360075-2 2014 AICAR treatment increases AMPK-alpha1 phosphorylation, decreases intracellular reactive oxygen species (ROS) levels, and significantly increases Annexin V-positive cells, DNA laddering, and caspase activity in human myeloid cell. AICA ribonucleotide 0-5 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 26-37 25360075-7 2014 Collectively, our results demonstrate that in AICAR-induced apoptosis, intracellular ROS levels are far more relevant than AMPK activation. AICA ribonucleotide 46-51 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 123-127 25402373-6 2014 Metformin induced AMPK phosphorylation in pancreatic BON1 and midgut GOT1 but suppressed AMPK activity in bronchopulmonary NCI-H727. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 18-22 25402373-6 2014 Metformin induced AMPK phosphorylation in pancreatic BON1 and midgut GOT1 but suppressed AMPK activity in bronchopulmonary NCI-H727. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 89-93 25109475-0 2014 Valsartan independent of AT1 receptor inhibits tissue factor, TLR-2 and -4 expression by regulation of Egr-1 through activation of AMPK in diabetic conditions. Valsartan 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 131-135 25109475-6 2014 Valsartan increased AMPK phosphorylation in a concentration and time-dependent manner via activation of LKB1. Valsartan 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 20-24 25109475-8 2014 The reduced expression of Egr-1 by valsartan was reversed by either silencing Egr-1, or compound C, or DN-AMPK-transfected cells. Valsartan 35-44 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 106-110 25109475-13 2014 Taken together, we concluded that valsartan may reduce atherothrombosis in diabetic conditions through AMPK/Egr-1 regulation. Valsartan 34-43 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 103-107 25009141-4 2014 Administration of AMPK activators (AICAR and metformin) significantly blocked hypertrophy, accompanied by enhanced autophagy level in the hearts. Metformin 45-54 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 18-22 25225183-6 2014 We identified significant SNP associations with birth weight near coding regions for two genes involved in oxygen sensing and vascular control, PRKAA1 and EDNRA, respectively. Oxygen 107-113 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 144-150 24965170-0 2014 Resveratrol prevents AngII-induced hypertension via AMPK activation and RhoA/ROCK suppression in mice. Resveratrol 0-11 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 52-56 24965170-2 2014 In cultured human vascular smooth muscle cells (VSMCs), we found that the activation of AMP-activated protein kinase (AMPK) by RSV inhibited angiotensin II (AngII)-induced phosphorylation of myosin phosphatase-targeting subunit 1 (MYPT1) and myosin light chain (MLC). Resveratrol 127-130 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 88-116 24965170-2 2014 In cultured human vascular smooth muscle cells (VSMCs), we found that the activation of AMP-activated protein kinase (AMPK) by RSV inhibited angiotensin II (AngII)-induced phosphorylation of myosin phosphatase-targeting subunit 1 (MYPT1) and myosin light chain (MLC). Resveratrol 127-130 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 118-122 24965170-3 2014 Inversely, AMPK inhibition with RNA interference and compound C, an AMPK inhibitor, abolished the inhibitory effect of RSV on AngII-induced MYPT1 and MLC phosphorylation. Resveratrol 119-122 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 11-15 24965170-3 2014 Inversely, AMPK inhibition with RNA interference and compound C, an AMPK inhibitor, abolished the inhibitory effect of RSV on AngII-induced MYPT1 and MLC phosphorylation. Resveratrol 119-122 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 68-72 24953559-0 2014 AMPK is involved in mediation of erythropoietin influence on metabolic activity and reactive oxygen species production in white adipocytes. Reactive Oxygen Species 84-107 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 24414799-0 2014 Tanshinone II A inhibits tat-induced HIV-1 transactivation through redox-regulated AMPK/Nampt pathway. tanshinone 0-15 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 83-87 24414799-9 2014 Tanshinone II A-evoked Nampt expression was mediated by AMPK signaling pathway. tanshinone 0-15 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 56-60 24414799-10 2014 Tanshinone II A inhibited Tat-induced HIV-1 LTR transactivation dependent on AMPK-Nampt pathway. tanshinone 0-15 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 77-81 24414799-11 2014 Collectively, our data provide new insights into understanding of the molecular mechanisms of tanshinone II A inhibited Tat-regulated transcription, suggesting that targeting AMPK/Nampt/SIRT1 pathway could serve as new anti-HIV-1 agents. tanshinone 94-109 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 175-179 24895169-3 2014 AMPK is a cellular energy sensor that maintains energy homeostasis within the cell and is activated when the AMP/ATP ratio increases. Adenosine Triphosphate 113-116 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 24895169-4 2014 When activated, AMPK increases catabolic processes that increase ATP synthesis and inhibit anabolic processes that require ATP. Adenosine Triphosphate 65-68 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 16-20 24895169-4 2014 When activated, AMPK increases catabolic processes that increase ATP synthesis and inhibit anabolic processes that require ATP. Adenosine Triphosphate 123-126 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 16-20 24619908-0 2014 Inhibition of AMPK/autophagy potentiates parthenolide-induced apoptosis in human breast cancer cells. parthenolide 41-53 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-18 25009658-9 2014 AMPK was activated and histone H2B monoubiquitination and downstream gene transcription were inhibited following metformin treatment in the T47D cells. Metformin 113-122 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 25009658-10 2014 The effect of metformin on T47D cell proliferation was dependent on AMPK activity. Metformin 14-23 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 68-72 25009658-11 2014 It was concluded that metformin can suppress breast cancer cell growth by the activation of AMPK and the inhibition of histone H2B monoubiquitination and downstream gene transcription. Metformin 22-31 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 92-96 25072399-2 2014 Activation of AMP-activated protein kinase (AMPK) pathway has been proposed as mechanism for berberine"s action. Berberine 93-102 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-42 25072399-2 2014 Activation of AMP-activated protein kinase (AMPK) pathway has been proposed as mechanism for berberine"s action. Berberine 93-102 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 44-48 25072399-3 2014 This study aimed to examine whether AMPK activation was necessary for berberine"s glucose-lowering effect. Berberine 70-79 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 36-40 25072399-3 2014 This study aimed to examine whether AMPK activation was necessary for berberine"s glucose-lowering effect. Glucose 82-89 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 36-40 25072399-5 2014 AMPK and acetyl coenzyme A synthetase (ACC) phosphorylation were stimulated by 20 micromol/L berberine. Berberine 93-102 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 25072399-6 2014 Nevertheless, berberine was still effective on stimulating glucose utilization and lactate production, when the AMPK activation was blocked by (1) inhibition of AMPK activity by Compound C, (2) suppression of AMPKalpha expression by siRNA, and (3) blockade of AMPK pathway by adenoviruses containing dominant-negative forms of AMPKalpha1/alpha2. Berberine 14-23 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 112-116 25072399-6 2014 Nevertheless, berberine was still effective on stimulating glucose utilization and lactate production, when the AMPK activation was blocked by (1) inhibition of AMPK activity by Compound C, (2) suppression of AMPKalpha expression by siRNA, and (3) blockade of AMPK pathway by adenoviruses containing dominant-negative forms of AMPKalpha1/alpha2. Berberine 14-23 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 161-165 25072399-6 2014 Nevertheless, berberine was still effective on stimulating glucose utilization and lactate production, when the AMPK activation was blocked by (1) inhibition of AMPK activity by Compound C, (2) suppression of AMPKalpha expression by siRNA, and (3) blockade of AMPK pathway by adenoviruses containing dominant-negative forms of AMPKalpha1/alpha2. Berberine 14-23 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 161-165 25072399-6 2014 Nevertheless, berberine was still effective on stimulating glucose utilization and lactate production, when the AMPK activation was blocked by (1) inhibition of AMPK activity by Compound C, (2) suppression of AMPKalpha expression by siRNA, and (3) blockade of AMPK pathway by adenoviruses containing dominant-negative forms of AMPKalpha1/alpha2. Berberine 14-23 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 327-337 24965170-6 2014 In addition, gene silencing of p190-guanosine triphosphatase-activating protein blocked the effects of RSV-induced AMPK activation on MLC, MYPT1 and RhoA in VSMCs. Resveratrol 103-106 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 115-119 24965170-8 2014 Finally, daily chronic administration of RSVl alleviated hypertension in the experimental model of AngII-induced hypertensive mice, and these effects were accompanied by the activation of AMPK, significantly decreased RhoA activity and phosphorylation levels of MYPT1 and MLC in AngII-treated murine aortic VSMCs. rsvl 41-45 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 188-192 24965170-10 2014 In conclusion, AMPK suppression of the p190-GAP-dependent RhoA/ROCK/MYPT1/MLC pathway contributes to the hypotensive effect of RSV in AngII-treated mice. Resveratrol 127-130 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 15-19 24619908-8 2014 Therefore, our results show that parthenolide activates both apoptosis pathway and AMPK-autophagy survival pathway through the generation of ROS, and that suppression of AMPK or autophagy can potentially enhance the anti-cancer effect of parthenolide on breast cancer cells. parthenolide 33-45 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 83-87 24619908-8 2014 Therefore, our results show that parthenolide activates both apoptosis pathway and AMPK-autophagy survival pathway through the generation of ROS, and that suppression of AMPK or autophagy can potentially enhance the anti-cancer effect of parthenolide on breast cancer cells. parthenolide 238-250 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 170-174 24619908-3 2014 Here, we showed that parthenolide increased reactive oxygen species (ROS), induced cell death, activated AMPK and autophagy, and led to M phase cell cycle arrest in breast cancer cells. parthenolide 21-33 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 105-109 24619908-4 2014 Removal of ROS inhibited all parthenolide-associated events, such as cell death, AMPK activation, autophagy induction, and cell cycle arrest. Reactive Oxygen Species 11-14 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 81-85 24619908-4 2014 Removal of ROS inhibited all parthenolide-associated events, such as cell death, AMPK activation, autophagy induction, and cell cycle arrest. parthenolide 29-41 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 81-85 24619908-6 2014 These observations clearly showed that parthenolide-driven ROS activated AMPK-autophagy pathway. parthenolide 39-51 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 73-77 24619908-6 2014 These observations clearly showed that parthenolide-driven ROS activated AMPK-autophagy pathway. Reactive Oxygen Species 59-62 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 73-77 24619908-7 2014 Furthermore, inhibition of either AMPK or autophagy significantly potentiated parthenolide-induced apoptosis. parthenolide 78-90 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 34-38 24892446-3 2014 METHODS: Expression of components of the AMPK pathway including phosphorylated AMPK (pAMPK), phosphorylated acetyl-Coa carboxylase (pACC) and liver kinase B1 (LKB1) was investigated by immunohistochemistry in 48 colorectal cancers treated with FOLFIRI plus bevacizumab. FOLFIRI regimen 244-251 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 41-45 24895284-5 2014 Ionomycin activated calcium calmodulin kinase II (CaMKII), AMPK, and PKCs, but not Akt. Ionomycin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 59-63 24895284-6 2014 Silencing CaMKIIdelta or AMPKalpha1/alpha2 partly reduced the ionomycin-induced gain in surface GLUT4myc, as did peptidic or small molecule inhibitors of CaMKII (CN21) and AMPK (Compound C). Ionomycin 62-71 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 25-35 24895284-6 2014 Silencing CaMKIIdelta or AMPKalpha1/alpha2 partly reduced the ionomycin-induced gain in surface GLUT4myc, as did peptidic or small molecule inhibitors of CaMKII (CN21) and AMPK (Compound C). Ionomycin 62-71 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 25-29 24895284-9 2014 siRNA-mediated knockdown of CaMKIIdelta or AMPKalpha1/alpha2 partly reversed ionomycin-induced GLUT4myc exocytosis but did not prevent its reduced endocytosis. Ionomycin 77-86 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 43-53 25045295-1 2014 BACKGROUND/AIMS: 5"-Adenosine monophosphate (AMP)-activated protein kinase (AMPK) is a cellular energy sensor that monitors intracellular AMP/adenosine triphosphate (ATP) ratios and is a key regulator of the proliferation and survival of diverse malignant cell types. Adenosine Monophosphate 45-48 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 76-80 25006835-5 2014 Cisplatin induced hyperphosphorylation of p38alpha MAPK and AMPKalpha1, whereas oxoplatin treatment resulted in increased phosphorylation of a large number of signaling proteins involved in stress response/drug resistance, including JNK, GSK-3alpha, AMPKalpha1, src kinases, STATs, CHK-2 and especially focal adhesion kinase (FAK). Cisplatin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 60-70 25006835-5 2014 Cisplatin induced hyperphosphorylation of p38alpha MAPK and AMPKalpha1, whereas oxoplatin treatment resulted in increased phosphorylation of a large number of signaling proteins involved in stress response/drug resistance, including JNK, GSK-3alpha, AMPKalpha1, src kinases, STATs, CHK-2 and especially focal adhesion kinase (FAK). Cisplatin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 250-260 24842158-0 2014 Bortezomib induces protective autophagy through AMP-activated protein kinase activation in cultured pancreatic and colorectal cancer cells. Bortezomib 0-10 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 48-76 24842158-5 2014 Activation of AMP-activated protein kinase (AMPK) was required for bortezomib-induced autophagy induction in PANC-1 and HT-29 cells, and AMPK inhibition by its inhibitor compound C (CC) or RNAi-depletion suppressed bortezomib-induced autophagy, while dramatically enhancing cancer cell apoptosis/cytotoxicity. Bortezomib 67-77 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-42 24842158-5 2014 Activation of AMP-activated protein kinase (AMPK) was required for bortezomib-induced autophagy induction in PANC-1 and HT-29 cells, and AMPK inhibition by its inhibitor compound C (CC) or RNAi-depletion suppressed bortezomib-induced autophagy, while dramatically enhancing cancer cell apoptosis/cytotoxicity. Bortezomib 67-77 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 44-48 24842158-5 2014 Activation of AMP-activated protein kinase (AMPK) was required for bortezomib-induced autophagy induction in PANC-1 and HT-29 cells, and AMPK inhibition by its inhibitor compound C (CC) or RNAi-depletion suppressed bortezomib-induced autophagy, while dramatically enhancing cancer cell apoptosis/cytotoxicity. Bortezomib 215-225 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-42 24842158-5 2014 Activation of AMP-activated protein kinase (AMPK) was required for bortezomib-induced autophagy induction in PANC-1 and HT-29 cells, and AMPK inhibition by its inhibitor compound C (CC) or RNAi-depletion suppressed bortezomib-induced autophagy, while dramatically enhancing cancer cell apoptosis/cytotoxicity. Bortezomib 215-225 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 44-48 24842158-6 2014 Meanwhile, significant AMPK activation and autophagy induction were observed after bortezomib stimulation in primary cultured pancreatic cancer cells derived from a patient"s tumor tissue. Bortezomib 83-93 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 23-27 24842158-8 2014 CONCLUSIONS: In conclusion, our data here suggest that bortezomib induces protective autophagy in pancreatic and colorectal cancer cells through activating AMPK-Ulk1 signalings. Bortezomib 55-65 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 156-160 24842158-9 2014 AMPK or autophagy inhibitors could be developed as an adjunct or chemo-sensitizer for bortezomib. Bortezomib 86-96 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 25045295-1 2014 BACKGROUND/AIMS: 5"-Adenosine monophosphate (AMP)-activated protein kinase (AMPK) is a cellular energy sensor that monitors intracellular AMP/adenosine triphosphate (ATP) ratios and is a key regulator of the proliferation and survival of diverse malignant cell types. Adenosine Triphosphate 142-164 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 76-80 25045295-1 2014 BACKGROUND/AIMS: 5"-Adenosine monophosphate (AMP)-activated protein kinase (AMPK) is a cellular energy sensor that monitors intracellular AMP/adenosine triphosphate (ATP) ratios and is a key regulator of the proliferation and survival of diverse malignant cell types. Adenosine Triphosphate 166-169 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 76-80 25045295-2 2014 In the present study, we investigated the effect of activating AMPK by 5-aminoimidazole-4-carboxamide-ribonucleotide (AICAR) in thyroid cancer cells. AICA ribonucleotide 71-116 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 63-67 24909911-0 2014 Radiosensitization of pancreatic cancer cells by metformin through the AMPK pathway. Metformin 49-58 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 71-75 24909911-8 2014 Examination of the AMPK pathway showed that pharmacological inhibition of AMPK signaling or RNAi of AMPKalpha1 reversed metformin-mediated radiosensitization. Metformin 120-129 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 19-23 24909911-8 2014 Examination of the AMPK pathway showed that pharmacological inhibition of AMPK signaling or RNAi of AMPKalpha1 reversed metformin-mediated radiosensitization. Metformin 120-129 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 74-78 24909911-8 2014 Examination of the AMPK pathway showed that pharmacological inhibition of AMPK signaling or RNAi of AMPKalpha1 reversed metformin-mediated radiosensitization. Metformin 120-129 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 100-110 24909911-9 2014 These studies show that metformin radiosensitization of pancreatic cancer cells at micromolar concentration acts through AMPK and may affect DNA damage signaling. Metformin 24-33 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 121-125 24815694-0 2014 The mammalian AMP-activated protein kinase complex mediates glucose regulation of gene expression in the yeast Saccharomyces cerevisiae. Glucose 60-67 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-42 24815694-4 2014 Phosphorylation of the AMPK alpha1-subunit was glucose-regulated, albeit not by the Glc7-Reg1/2 phosphatase, which performs this function on yeast AMPK/SNF1. Glucose 47-54 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 23-27 24815694-7 2014 Our results demonstrate a remarkable functional conservation of AMPK and that glucose regulation of AMPK may not be mediated by regulatory features of a specific phosphatase. Glucose 78-85 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 100-104 24722377-0 2014 Chalcones suppress fatty acid-induced lipid accumulation through a LKB1/AMPK signaling pathway in HepG2 cells. Chalcones 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 72-76 24722377-0 2014 Chalcones suppress fatty acid-induced lipid accumulation through a LKB1/AMPK signaling pathway in HepG2 cells. Fatty Acids 19-29 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 72-76 24722377-8 2014 Moreover, these chalcones increased phosphorylation of AMP-activated protein kinase (AMPK) and liver kinase B1 (LKB1), upstream regulators of SREBP-1 and PPARalpha. Chalcones 16-25 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 55-83 24722377-8 2014 Moreover, these chalcones increased phosphorylation of AMP-activated protein kinase (AMPK) and liver kinase B1 (LKB1), upstream regulators of SREBP-1 and PPARalpha. Chalcones 16-25 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 85-89 24722377-9 2014 We confirmed that an AMPK inhibitor, compound C, reversed chalcone-induced changes in SREBP-1 and PPARalpha expression in the HepG2 cells. Chalcone 58-66 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 21-25 24799027-0 2014 AKT and AMPK activation after high-fat and high-glucose in vitro treatment of prostate epithelial cells. Glucose 48-55 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 8-12 24799027-4 2014 After 24 h of high-fat alone or associated with high-glucose treatment, there was an increase in AMPK and AKT activation associated to unchanged MTS-cell proliferation. Glucose 53-60 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 97-101 24799027-9 2014 A high-fat medium containing 100 muM of palmitate stimulates proliferation in PNT1A cells by decreasing the activation of AMPK and increasing activation of AKT after longer exposure time. Palmitates 40-49 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 122-126 24762438-7 2014 We revealed that loss of FLCN constitutively activates AMPK, resulting in PGC-1alpha-mediated mitochondrial biogenesis and increased ROS production. ros 133-136 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 55-59 24762438-8 2014 ROS induced HIF transcriptional activity and drove Warburg metabolic reprogramming, coupling AMPK-dependent mitochondrial biogenesis to HIF-dependent metabolic changes. ros 0-3 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 93-97 24573187-4 2014 In addition, apelin-13 dose dependently stimulated the phosphorylation of AMP-activated protein kinase (AMPK) and endothelial nitric oxide synthase (eNOS) at Thr-172 and Ser-1179, respectively. Threonine 158-161 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 74-102 24584901-13 2014 Resveratrol also upregulated the expression of AMPK and Silent information regulator T1 (SIRT1). Resveratrol 0-11 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 47-51 24584901-16 2014 These data suggest that resveratrol inhibits foam cell formation by regulating the expression of MCP-1 and activating the AMPK-SIRT1-PPAR signaling pathway; thus, resveratrol may be a novel therapeutic agent for atherosclerosis. Resveratrol 24-35 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 122-126 24584901-16 2014 These data suggest that resveratrol inhibits foam cell formation by regulating the expression of MCP-1 and activating the AMPK-SIRT1-PPAR signaling pathway; thus, resveratrol may be a novel therapeutic agent for atherosclerosis. Resveratrol 163-174 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 122-126 25046749-4 2014 We found that cordycepin inhibited mTOR complex 1 (mTORC1) activation and down-regulated multiple drug resistant (MDR)/hypoxia-inducible factor 1alpha (HIF-1alpha) expression through activating of AMP-activated protein kinase (AMPK) signaling in gallbladder cancer GBC-SD cells. cordycepin 14-24 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 197-225 25046749-4 2014 We found that cordycepin inhibited mTOR complex 1 (mTORC1) activation and down-regulated multiple drug resistant (MDR)/hypoxia-inducible factor 1alpha (HIF-1alpha) expression through activating of AMP-activated protein kinase (AMPK) signaling in gallbladder cancer GBC-SD cells. cordycepin 14-24 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 227-231 25046749-6 2014 Further, our results showed that co-treatment with a low concentration cordycepin could remarkably enhance the chemosensitivity of GBC-SD cells to gemcitabine and 5-fluorouracil (5-FU), and the mechanism may be attributed to AMPK activation and MDR degradation. Fluorouracil 163-177 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 225-229 25046749-6 2014 Further, our results showed that co-treatment with a low concentration cordycepin could remarkably enhance the chemosensitivity of GBC-SD cells to gemcitabine and 5-fluorouracil (5-FU), and the mechanism may be attributed to AMPK activation and MDR degradation. Fluorouracil 179-183 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 225-229 25046749-7 2014 In summary, cordycepin induces growth inhibition and apoptosis in gallbladder cancer cells via activating AMPK signaling. cordycepin 12-22 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 106-110 24655923-8 2014 More importantly, we show, for the first time, that the AMPK pathway is activated in platelets of patients undergoing major cardiac surgery, in a heparin-sensitive manner. Heparin 146-153 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 56-60 24905518-0 2014 Metformin affects macrophages" phenotype and improves the activity of glutathione peroxidase, superoxide dismutase, catalase and decreases malondialdehyde concentration in a partially AMPK-independent manner in LPS-stimulated human monocytes/macrophages. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 184-188 24905518-11 2014 All the aforementioned results resulted from AMPK activation, but a residual activity of metformin after AMPK blockade was still noticeable even after inhibition of AMPK by compound C. CONCLUSIONS: Authors believe that metformin-based therapy, a cornerstone in diabetes therapy, not only improves the prognosis of diabetics by reducing blood glucose but also by reducing oxidative stress, inflammatory cytokine production and the shift toward alternative activation of macrophages. Metformin 89-98 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 105-109 24905518-11 2014 All the aforementioned results resulted from AMPK activation, but a residual activity of metformin after AMPK blockade was still noticeable even after inhibition of AMPK by compound C. CONCLUSIONS: Authors believe that metformin-based therapy, a cornerstone in diabetes therapy, not only improves the prognosis of diabetics by reducing blood glucose but also by reducing oxidative stress, inflammatory cytokine production and the shift toward alternative activation of macrophages. Metformin 89-98 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 105-109 24905518-11 2014 All the aforementioned results resulted from AMPK activation, but a residual activity of metformin after AMPK blockade was still noticeable even after inhibition of AMPK by compound C. CONCLUSIONS: Authors believe that metformin-based therapy, a cornerstone in diabetes therapy, not only improves the prognosis of diabetics by reducing blood glucose but also by reducing oxidative stress, inflammatory cytokine production and the shift toward alternative activation of macrophages. Metformin 219-228 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 45-49 24905518-11 2014 All the aforementioned results resulted from AMPK activation, but a residual activity of metformin after AMPK blockade was still noticeable even after inhibition of AMPK by compound C. CONCLUSIONS: Authors believe that metformin-based therapy, a cornerstone in diabetes therapy, not only improves the prognosis of diabetics by reducing blood glucose but also by reducing oxidative stress, inflammatory cytokine production and the shift toward alternative activation of macrophages. Metformin 219-228 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 105-109 24905518-11 2014 All the aforementioned results resulted from AMPK activation, but a residual activity of metformin after AMPK blockade was still noticeable even after inhibition of AMPK by compound C. CONCLUSIONS: Authors believe that metformin-based therapy, a cornerstone in diabetes therapy, not only improves the prognosis of diabetics by reducing blood glucose but also by reducing oxidative stress, inflammatory cytokine production and the shift toward alternative activation of macrophages. Metformin 219-228 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 105-109 24858012-0 2014 Metformin induces apoptosis and cell cycle arrest mediated by oxidative stress, AMPK and FOXO3a in MCF-7 breast cancer cells. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 80-84 24858012-8 2014 In MCF-7 cells metformin decreased the activation of IRbeta, Akt and ERK1/2, increased p-AMPK, FOXO3a, p27, Bax and cleaved caspase-3, and decreased phosphorylation of p70S6K and Bcl-2 protein expression. Metformin 15-24 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 89-93 24858012-12 2014 These results show that metformin has an antiproliferative effect associated with cell cycle arrest and apoptosis, which is mediated by oxidative stress, as well as AMPK and FOXO3a activation. Metformin 24-33 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 165-169 24849329-0 2014 Use of metformin alone is not associated with survival outcomes of colorectal cancer cell but AMPK activator AICAR sensitizes anticancer effect of 5-fluorouracil through AMPK activation. Fluorouracil 147-161 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 94-98 24849329-0 2014 Use of metformin alone is not associated with survival outcomes of colorectal cancer cell but AMPK activator AICAR sensitizes anticancer effect of 5-fluorouracil through AMPK activation. Fluorouracil 147-161 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 170-174 24849329-7 2014 Taken together, our results suggest that metformin has not antineoplastic activity for CRC cells as a single agent but AMPK activator AICAR can induce apoptosis and enhance the cytotoxic effect of 5-FU through AMPK activation. Fluorouracil 197-201 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 119-123 24849329-7 2014 Taken together, our results suggest that metformin has not antineoplastic activity for CRC cells as a single agent but AMPK activator AICAR can induce apoptosis and enhance the cytotoxic effect of 5-FU through AMPK activation. Fluorouracil 197-201 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 210-214 24904600-1 2014 The SNF1 (sucrose non-fermenting 1)-related protein kinases 1 (SnRKs1) are the plant orthologs of the budding yeast SNF1 and mammalian AMPK (AMP-activated protein kinase). Sucrose 10-17 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 135-139 24904600-1 2014 The SNF1 (sucrose non-fermenting 1)-related protein kinases 1 (SnRKs1) are the plant orthologs of the budding yeast SNF1 and mammalian AMPK (AMP-activated protein kinase). Sucrose 10-17 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 141-169 24428821-1 2014 BACKGROUND AND PURPOSE: The objective of this study was to determine how the AMPK activating antidiabetic drug metformin affects the major activator of hepatic gluconeogenesis, PPARgamma coactivator 1alpha (PGC-1alpha) and liver functions regulated by PGC-1alpha. Metformin 111-120 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 77-81 24428821-5 2014 5-Aminoimidazole-4-carboxamide ribonucleotide (AICAR) (another AMPK activator) had the opposite effect. AICA ribonucleotide 0-45 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 63-67 24428821-5 2014 5-Aminoimidazole-4-carboxamide ribonucleotide (AICAR) (another AMPK activator) had the opposite effect. AICA ribonucleotide 47-52 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 63-67 24428821-6 2014 Metformin also increased PGC-1alpha in human primary hepatocytes; this effect of metformin was abolished by AMPK inhibitor compound C and sirtuin 1 siRNA. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 108-112 24428821-6 2014 Metformin also increased PGC-1alpha in human primary hepatocytes; this effect of metformin was abolished by AMPK inhibitor compound C and sirtuin 1 siRNA. Metformin 81-90 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 108-112 24856758-0 2014 Modified Si-Miao-San ameliorates pancreatic B cell dysfunction by inhibition of reactive oxygen species-associated inflammation through AMP-kinase activation. si-miao-san 9-20 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 136-146 24856758-0 2014 Modified Si-Miao-San ameliorates pancreatic B cell dysfunction by inhibition of reactive oxygen species-associated inflammation through AMP-kinase activation. Reactive Oxygen Species 80-103 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 136-146 24573187-4 2014 In addition, apelin-13 dose dependently stimulated the phosphorylation of AMP-activated protein kinase (AMPK) and endothelial nitric oxide synthase (eNOS) at Thr-172 and Ser-1179, respectively. Threonine 158-161 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 104-108 24573187-5 2014 The treatment with the AMPK (compound C) and protein kinase Akt/protein kinase B (Akt; LY294002) inhibitor significantly suppressed the apelin-13-induced AMPK, Akt and eNOS phosphorylation. 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one 87-95 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 154-158 24726357-6 2014 Importantly, RTG/AMPK activation reprograms energy metabolism to increase the supply of acetyl-CoA to lysine acetyltransferases and extend the chronological lifespan of rho(0) cells. Acetyl Coenzyme A 88-98 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 17-21 24365713-9 2014 Finally, we showed that, in human fibroblasts, RSV stimulated mitochondrial functions mainly in a SIRT1- and AMPK-independent manner and that its effects rather involved the estrogen receptor (ER) and estrogen-related receptor alpha (ERRalpha) signaling pathways. Resveratrol 47-50 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 109-113 24467442-1 2014 The insulin/IGF-1 (insulin-like growth factor 1)-activated protein kinase Akt (also known as protein kinase B) phosphorylates Ser487 in the "ST loop" (serine/threonine-rich loop) within the C-terminal domain of AMPK-alpha1 (AMP-activated protein kinase-alpha1), leading to inhibition of phosphorylation by upstream kinases at the activating site, Thr172. Serine 151-157 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 211-222 24467442-1 2014 The insulin/IGF-1 (insulin-like growth factor 1)-activated protein kinase Akt (also known as protein kinase B) phosphorylates Ser487 in the "ST loop" (serine/threonine-rich loop) within the C-terminal domain of AMPK-alpha1 (AMP-activated protein kinase-alpha1), leading to inhibition of phosphorylation by upstream kinases at the activating site, Thr172. Serine 151-157 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 224-259 24467442-1 2014 The insulin/IGF-1 (insulin-like growth factor 1)-activated protein kinase Akt (also known as protein kinase B) phosphorylates Ser487 in the "ST loop" (serine/threonine-rich loop) within the C-terminal domain of AMPK-alpha1 (AMP-activated protein kinase-alpha1), leading to inhibition of phosphorylation by upstream kinases at the activating site, Thr172. Threonine 158-167 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 211-222 24467442-1 2014 The insulin/IGF-1 (insulin-like growth factor 1)-activated protein kinase Akt (also known as protein kinase B) phosphorylates Ser487 in the "ST loop" (serine/threonine-rich loop) within the C-terminal domain of AMPK-alpha1 (AMP-activated protein kinase-alpha1), leading to inhibition of phosphorylation by upstream kinases at the activating site, Thr172. Threonine 158-167 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 224-259 24467442-3 2014 Stimulation of HEK (human embryonic kidney)-293 cells with IGF-1 caused reduced subsequent Thr172 phosphorylation and activation of AMPK-alpha1 in response to the activator A769662 and the Ca2+ ionophore A23187, effects we show to be dependent on Akt activation and Ser487 phosphorylation. Calcimycin 204-210 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 132-143 24563466-2 2014 Similar to phosphorylation, catalyzed by kinases such as AMPK, O-GlcNAcylation is a highly dynamic Ser/Thr-specific post-translational modification of nuclear, cytoplasmic, and mitochondrial proteins catalyzed exclusively by OGT. Serine 99-102 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 57-61 24563466-2 2014 Similar to phosphorylation, catalyzed by kinases such as AMPK, O-GlcNAcylation is a highly dynamic Ser/Thr-specific post-translational modification of nuclear, cytoplasmic, and mitochondrial proteins catalyzed exclusively by OGT. Threonine 103-106 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 57-61 24563466-7 2014 AMPK phosphorylates Thr-444 on OGT in vitro; phosphorylation of Thr-444 is tightly associated with AMPK activity and nuclear localization of OGT in myotubes, and phospho-mimetic T444E-OGT exhibits altered substrate selectivity. Threonine 20-23 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 24563466-7 2014 AMPK phosphorylates Thr-444 on OGT in vitro; phosphorylation of Thr-444 is tightly associated with AMPK activity and nuclear localization of OGT in myotubes, and phospho-mimetic T444E-OGT exhibits altered substrate selectivity. Threonine 64-67 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 24563466-7 2014 AMPK phosphorylates Thr-444 on OGT in vitro; phosphorylation of Thr-444 is tightly associated with AMPK activity and nuclear localization of OGT in myotubes, and phospho-mimetic T444E-OGT exhibits altered substrate selectivity. Threonine 64-67 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 99-103 24496445-0 2014 Purinergic control of AMPK activation by ATP released through connexin 43 hemichannels - pivotal roles in hemichannel-mediated cell injury. Adenosine Triphosphate 41-44 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 22-26 24496445-0 2014 Purinergic control of AMPK activation by ATP released through connexin 43 hemichannels - pivotal roles in hemichannel-mediated cell injury. hemichannel 74-85 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 22-26 24496445-3 2014 Hemichannel opening causes loss of ATP, we therefore speculated a potential role for AMPK in the biological actions of hemichannels. Adenosine Triphosphate 35-38 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 85-89 24496445-3 2014 Hemichannel opening causes loss of ATP, we therefore speculated a potential role for AMPK in the biological actions of hemichannels. hemichannels 119-131 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 85-89 24496445-4 2014 Activation of hemichannels by removal of extracellular Ca(2+) led to an efflux of ATP and a weak activation of AMPK. hemichannels 14-26 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 111-115 24496445-5 2014 Unexpectedly, dysfunction of hemichannels markedly potentiated AMPK activation, which was reproduced by promotion of extracellular ATP degradation or inhibition of P2 purinoceptors but counteracted by exogenous ATP. hemichannels 29-41 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 63-67 24496445-5 2014 Unexpectedly, dysfunction of hemichannels markedly potentiated AMPK activation, which was reproduced by promotion of extracellular ATP degradation or inhibition of P2 purinoceptors but counteracted by exogenous ATP. Adenosine Triphosphate 131-134 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 63-67 24496445-5 2014 Unexpectedly, dysfunction of hemichannels markedly potentiated AMPK activation, which was reproduced by promotion of extracellular ATP degradation or inhibition of P2 purinoceptors but counteracted by exogenous ATP. Adenosine Triphosphate 211-214 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 63-67 24496445-8 2014 In a pathological model of hemichannel opening triggered by Cd(2+), disclosure of hemichannels similarly enhanced AMPK activity, which protected cells from Cd(2+)-induced cell injury through suppression of mTOR. hemichannels 82-94 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 114-118 24423443-0 2014 AMPK-mediated downregulation of connexin43 and premature senescence of mesangial cells under high-glucose conditions. Glucose 98-105 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 24423443-8 2014 This study demonstrated that AMPK signaling pathways play an important role in the regulation of the Cx43 expression that accompanies GMC senescence under high-glucose conditions. Glucose 160-167 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 29-33 24531544-0 2014 Metformin interferes with bile acid homeostasis through AMPK-FXR crosstalk. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 56-60 24265487-0 2014 Antiangiogenic effects of N6-isopentenyladenosine, an endogenous isoprenoid end product, mediated by AMPK activation. Isopentenyladenosine 26-49 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 101-105 24265487-0 2014 Antiangiogenic effects of N6-isopentenyladenosine, an endogenous isoprenoid end product, mediated by AMPK activation. Terpenes 65-75 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 101-105 24265487-7 2014 iPAMP is the active form that inhibits angiogenesis through the direct activation of AMP-kinase (AMPK). Isopentenyl-AMP 0-5 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 85-95 24265487-7 2014 iPAMP is the active form that inhibits angiogenesis through the direct activation of AMP-kinase (AMPK). Isopentenyl-AMP 0-5 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 97-101 24531544-0 2014 Metformin interferes with bile acid homeostasis through AMPK-FXR crosstalk. Bile Acids and Salts 26-35 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 56-60 24531544-7 2014 Furthermore, treatment with AMPK activators, including the antidiabetic biguanide metformin, inhibited FXR agonist induction of FXR target genes in mouse liver and intestine. Biguanides 72-81 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 28-32 24531544-7 2014 Furthermore, treatment with AMPK activators, including the antidiabetic biguanide metformin, inhibited FXR agonist induction of FXR target genes in mouse liver and intestine. Metformin 82-91 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 28-32 24231522-2 2014 Omega-3 polyunsaturated fatty acid (omega-3 PUFA) is a potent activator of the Adenosine 5"-monophosphate-activated protein kinase-sirtuin1 (AMPK/SIRT1) pathway against macrophage inflammation. Fish Oils 0-34 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 141-145 24378334-4 2014 In this study, we investigated whether and how AMPK affected oxidative podocyte injury induced by Adriamycin (ADR; Wako Pure Chemical, Osaka, Japan). Doxorubicin 98-108 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 47-51 24668775-0 2014 Activation of autophagy and AMPK by gamma-tocotrienol suppresses the adipogenesis in human adipose derived stem cells. plastochromanol 8 36-53 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 28-32 24668775-3 2014 In searching a potential mechanism, we identified that gamma-T3 promoted two catabolic signaling pathways: (i) AMP kinase (AMPK), and (ii) enhanced autophagy, as assessed by autophagic flux and cytosolic autophagosome (LC3II) accumulation. gamma-t3 55-63 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 111-121 24668775-3 2014 In searching a potential mechanism, we identified that gamma-T3 promoted two catabolic signaling pathways: (i) AMP kinase (AMPK), and (ii) enhanced autophagy, as assessed by autophagic flux and cytosolic autophagosome (LC3II) accumulation. gamma-t3 55-63 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 123-127 24231522-2 2014 Omega-3 polyunsaturated fatty acid (omega-3 PUFA) is a potent activator of the Adenosine 5"-monophosphate-activated protein kinase-sirtuin1 (AMPK/SIRT1) pathway against macrophage inflammation. Fish Oils 36-48 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 141-145 24231522-2 2014 Omega-3 polyunsaturated fatty acid (omega-3 PUFA) is a potent activator of the Adenosine 5"-monophosphate-activated protein kinase-sirtuin1 (AMPK/SIRT1) pathway against macrophage inflammation. adenosine 5"-monophosphate 79-105 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 141-145 24702155-3 2014 Three separate AMPK activators (AICAR, Phenformin and A-769662) inhibited NKCC1 flux in a variety of nucleated cells. Phenformin 39-49 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 15-19 24295634-1 2014 AMP-activated protein kinase (AMPK) is a serine/threonine kinase that functions as a cellular and whole organism energy sensor to regulate ATP-consuming (anabolic) and ATP-generating (catabolic) pathways. Adenosine Triphosphate 139-142 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-28 24269733-2 2014 The loss of viability in retinoic acid-differentiated SH-SY5Y human neuroblastoma cells inducibly overexpressing wild-type ASYN was associated with the reduced activation of AMPK and its activator LKB1, as well as AMPK target Raptor. Tretinoin 25-38 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 174-178 24269733-2 2014 The loss of viability in retinoic acid-differentiated SH-SY5Y human neuroblastoma cells inducibly overexpressing wild-type ASYN was associated with the reduced activation of AMPK and its activator LKB1, as well as AMPK target Raptor. Tretinoin 25-38 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 214-218 24269733-4 2014 Restoration of AMPK activity by metformin or AICAR reduced the in vitro neurotoxicity of ASYN overexpression, acting independently of the prosurvival kinase Akt or the induction of autophagic response. Metformin 32-41 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 15-19 24269733-5 2014 The conditioned medium from ASYN-overexpressing cells, containing secreted ASYN, as well as dopamine-modified or nitrated recombinant ASYN oligomers, all inhibited AMPK activation in differentiated SH-SY5Y cells and reduced their viability, but not in the presence of metformin or AICAR. Dopamine 92-100 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 164-168 24795795-0 2014 Licochalcone Suppresses LXRalpha-Induced Hepatic Lipogenic Gene Expression through AMPK/Sirt1 Pathway Activation. licochalcone 0-12 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 83-87 24795795-6 2014 We found here that LCE increased AMPK phosphorylation and Sirt1 expression. licochalcone E 19-22 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 33-37 24555415-4 2014 5-Aminoimidazole-4-carboxamide 1-beta-D-ribofuranoside (AICAR), an AMP-activated protein kinase (AMPK) activator, was used to determine the regulatory role of AMPK on HCC adhesion to the endothelium in regard to the resistin effects. acadesine 0-54 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 67-95 24555415-4 2014 5-Aminoimidazole-4-carboxamide 1-beta-D-ribofuranoside (AICAR), an AMP-activated protein kinase (AMPK) activator, was used to determine the regulatory role of AMPK on HCC adhesion to the endothelium in regard to the resistin effects. acadesine 0-54 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 97-101 24555415-4 2014 5-Aminoimidazole-4-carboxamide 1-beta-D-ribofuranoside (AICAR), an AMP-activated protein kinase (AMPK) activator, was used to determine the regulatory role of AMPK on HCC adhesion to the endothelium in regard to the resistin effects. acadesine 56-61 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 67-95 24419061-4 2014 However, one small molecule known as compound C (also called dorsomorphin) has been widely used in cell-based, biochemical, and in vivo assays as a selective AMPK inhibitor. dorsomorphin 61-73 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 158-162 24587072-3 2014 AMPK is a cellular energy sensor that regulates a plethora of signaling pathways, including cholesterol and isoprenoid synthesis via its downstream target hydroxy-methylglutaryl (HMG)-CoA reductase. Cholesterol 92-103 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 24587072-3 2014 AMPK is a cellular energy sensor that regulates a plethora of signaling pathways, including cholesterol and isoprenoid synthesis via its downstream target hydroxy-methylglutaryl (HMG)-CoA reductase. Terpenes 108-118 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 24555415-4 2014 5-Aminoimidazole-4-carboxamide 1-beta-D-ribofuranoside (AICAR), an AMP-activated protein kinase (AMPK) activator, was used to determine the regulatory role of AMPK on HCC adhesion to the endothelium in regard to the resistin effects. acadesine 56-61 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 97-101 24506865-6 2014 Thioredoxin1 (Trx1), an important reducing enzyme that cleaves disulfides in proteins, prevents AMPK oxidation, serving as an essential cofactor for AMPK activation. Disulfides 63-73 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 96-100 24506865-6 2014 Thioredoxin1 (Trx1), an important reducing enzyme that cleaves disulfides in proteins, prevents AMPK oxidation, serving as an essential cofactor for AMPK activation. Disulfides 63-73 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 149-153 24295634-1 2014 AMP-activated protein kinase (AMPK) is a serine/threonine kinase that functions as a cellular and whole organism energy sensor to regulate ATP-consuming (anabolic) and ATP-generating (catabolic) pathways. Adenosine Triphosphate 139-142 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-34 24295634-1 2014 AMP-activated protein kinase (AMPK) is a serine/threonine kinase that functions as a cellular and whole organism energy sensor to regulate ATP-consuming (anabolic) and ATP-generating (catabolic) pathways. Adenosine Triphosphate 168-171 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-28 24295634-1 2014 AMP-activated protein kinase (AMPK) is a serine/threonine kinase that functions as a cellular and whole organism energy sensor to regulate ATP-consuming (anabolic) and ATP-generating (catabolic) pathways. Adenosine Triphosphate 168-171 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-34 24297300-0 2014 AZD8055 induces cell death associated with autophagy and activation of AMPK in hepatocellular carcinoma. (5-(2,4-bis((3S)-3-methylmorpholin-4-yl)pyrido(2,3-d)pyrimidin-7-yl)-2-methoxyphenyl)methanol 0-7 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 71-75 23918588-8 2014 CONCLUSIONS: In patients with T2DM, treatment with resveratrol regulates energy expenditure through increased skeletal muscle SIRT1 and AMPK expression. Resveratrol 51-62 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 136-140 24297300-6 2014 Furthermore, AZD8055 caused the activation of AMPK and co-treatment with the AMPK inhibitor dorsomorphin also caused a partial but significant reduction of AZD8055-induced cell death. (5-(2,4-bis((3S)-3-methylmorpholin-4-yl)pyrido(2,3-d)pyrimidin-7-yl)-2-methoxyphenyl)methanol 156-163 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 77-81 24297300-7 2014 In conclusion, AZD8055-induced HCC cell death is associated with induction of autophagy and activation of AMPK. (5-(2,4-bis((3S)-3-methylmorpholin-4-yl)pyrido(2,3-d)pyrimidin-7-yl)-2-methoxyphenyl)methanol 15-22 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 106-110 24297300-6 2014 Furthermore, AZD8055 caused the activation of AMPK and co-treatment with the AMPK inhibitor dorsomorphin also caused a partial but significant reduction of AZD8055-induced cell death. (5-(2,4-bis((3S)-3-methylmorpholin-4-yl)pyrido(2,3-d)pyrimidin-7-yl)-2-methoxyphenyl)methanol 156-163 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 46-50 24297300-6 2014 Furthermore, AZD8055 caused the activation of AMPK and co-treatment with the AMPK inhibitor dorsomorphin also caused a partial but significant reduction of AZD8055-induced cell death. (5-(2,4-bis((3S)-3-methylmorpholin-4-yl)pyrido(2,3-d)pyrimidin-7-yl)-2-methoxyphenyl)methanol 13-20 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 46-50 24297300-6 2014 Furthermore, AZD8055 caused the activation of AMPK and co-treatment with the AMPK inhibitor dorsomorphin also caused a partial but significant reduction of AZD8055-induced cell death. dorsomorphin 92-104 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 46-50 24297300-6 2014 Furthermore, AZD8055 caused the activation of AMPK and co-treatment with the AMPK inhibitor dorsomorphin also caused a partial but significant reduction of AZD8055-induced cell death. dorsomorphin 92-104 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 77-81 24457597-0 2014 Metformin sensitizes anticancer effect of dasatinib in head and neck squamous cell carcinoma cells through AMPK-dependent ER stress. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 107-111 24416418-0 2014 Resveratrol induces vascular smooth muscle cell differentiation through stimulation of SirT1 and AMPK. Resveratrol 0-11 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 97-101 24416418-5 2014 Resveratrol induced VSMC differentiation through stimulation of SirT1 and AMPK. Resveratrol 0-11 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 74-78 24416418-7 2014 We found that low dose resveratrol stimulated differentiation through SirT1-mediated activation of AKT, whereas high dose resveratrol stimulated differentiation through AMPK-mediated inhibition of the mTORC1 pathway, allowing activation of AKT. Resveratrol 122-133 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 169-173 24457597-0 2014 Metformin sensitizes anticancer effect of dasatinib in head and neck squamous cell carcinoma cells through AMPK-dependent ER stress. Dasatinib 42-51 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 107-111 24457597-6 2014 AMPK activation induced by dasatinib might be due to ATP decrease through the up-regulation of pyruvate dehydrogenase kinase 4 (PDK4). Dasatinib 27-36 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 24457597-6 2014 AMPK activation induced by dasatinib might be due to ATP decrease through the up-regulation of pyruvate dehydrogenase kinase 4 (PDK4). Adenosine Triphosphate 53-56 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 24457597-7 2014 Furthermore, activation of AMPK by metformin sensitized dasatinib-induced in vitro and in vivo anti-cancer effect. Metformin 35-44 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 27-31 24457597-7 2014 Furthermore, activation of AMPK by metformin sensitized dasatinib-induced in vitro and in vivo anti-cancer effect. Dasatinib 56-65 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 27-31 24457597-9 2014 Our results disclose that AMPK-dependent ER stress plays a crucial role in the anti-cancer effect of dasatinib in HNSCC and further activation of AMPK by metformin might enhance dasatinib efficacy. Dasatinib 101-110 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 26-30 24457597-9 2014 Our results disclose that AMPK-dependent ER stress plays a crucial role in the anti-cancer effect of dasatinib in HNSCC and further activation of AMPK by metformin might enhance dasatinib efficacy. Metformin 154-163 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 26-30 24457597-9 2014 Our results disclose that AMPK-dependent ER stress plays a crucial role in the anti-cancer effect of dasatinib in HNSCC and further activation of AMPK by metformin might enhance dasatinib efficacy. Metformin 154-163 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 146-150 24457597-9 2014 Our results disclose that AMPK-dependent ER stress plays a crucial role in the anti-cancer effect of dasatinib in HNSCC and further activation of AMPK by metformin might enhance dasatinib efficacy. Dasatinib 178-187 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 26-30 24457597-9 2014 Our results disclose that AMPK-dependent ER stress plays a crucial role in the anti-cancer effect of dasatinib in HNSCC and further activation of AMPK by metformin might enhance dasatinib efficacy. Dasatinib 178-187 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 146-150 24897381-3 2014 Here, we show that dexamethasone stimulates an early activation of autophagy in L6 myotubes depending on protein kinase, AMPK, and glucocorticoid receptor activity. Dexamethasone 19-32 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 121-125 24897381-4 2014 Dexamethasone increases expression of several autophagy genes, including ATG5, LC3, BECN1, and SQSTM1 and triggers AMPK-dependent mitochondrial fragmentation associated with increased DNM1L protein levels. Dexamethasone 0-13 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 115-119 25041018-0 2014 Saponins from Rubus parvifolius L. induce apoptosis in human chronic myeloid leukemia cells through AMPK activation and STAT3 inhibition. Saponins 0-8 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 100-104 25087956-0 2014 Eugenol ameliorates hepatic steatosis and fibrosis by down-regulating SREBP1 gene expression via AMPK-mTOR-p70S6K signaling pathway. Eugenol 0-7 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 97-101 25329671-4 2014 Activation of LKB1/AMPK pathway and cancer stem cell destruction along with cell cycle arrest and apoptosis induction are the proposed mechanisms of anticancer potential of metformin. Metformin 173-182 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 19-23 24240701-0 2014 SIRT1 and AMPK mediate hypoxia-induced resistance of non-small cell lung cancers to cisplatin and doxorubicin. Cisplatin 84-93 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 10-14 24240701-0 2014 SIRT1 and AMPK mediate hypoxia-induced resistance of non-small cell lung cancers to cisplatin and doxorubicin. Doxorubicin 98-109 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 10-14 24240701-6 2014 Notably, hypoxic inactivation of this SIRT1-AMPK pathway led to cisplatin and doxorubicin resistance. Cisplatin 64-73 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 44-48 24240701-6 2014 Notably, hypoxic inactivation of this SIRT1-AMPK pathway led to cisplatin and doxorubicin resistance. Doxorubicin 78-89 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 44-48 24240701-9 2014 Furthermore, we demonstrated that a SIRT1 activator SRT1720 augmented the antitumor effects of cisplatin, and these effects could be blocked by administration of an AMPK inhibitor compound C. Taken together, our results offer preclinical proof-of-concept to target the SIRT1-AMPK pathway as a strategy to overcome hypoxia-induced chemoresistance in NSCLC. Cisplatin 95-104 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 165-169 24240701-9 2014 Furthermore, we demonstrated that a SIRT1 activator SRT1720 augmented the antitumor effects of cisplatin, and these effects could be blocked by administration of an AMPK inhibitor compound C. Taken together, our results offer preclinical proof-of-concept to target the SIRT1-AMPK pathway as a strategy to overcome hypoxia-induced chemoresistance in NSCLC. Cisplatin 95-104 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 275-279 25278128-0 2014 Inactivation of AMPK mediates high phosphate-induced extracellular matrix accumulation via NOX4/TGFss-1 signaling in human mesangial cells. Phosphates 35-44 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 16-20 25278128-7 2014 RESULTS: In iHMCs, a Pi transporter blocker (PFA) abrogated high Pi-induced AMPK inactivation, increase in NADPH oxidase-induced reactive oxygen species (ROS) levels, NOX4, p-SMAD3, alpha-SMA and C-IV expression. Foscarnet 45-48 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 76-80 25278128-8 2014 AMPK activation by AICAR, NOX4 silencing or NADPH oxidase blocker prevented high Pi-induced DHE levels, p-SMAD3, F/N, C-IV and alpha-SMA expression. dihydroethidium 92-95 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 25278128-9 2014 CONCLUSION: AMPK inactivation with NOX4-induced ROS formation and transforming growth factor ss-1 (TGFss-1) signaling activation mediates high Pi-induced ECM accumulation in iHMCs. Reactive Oxygen Species 48-51 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 12-16 27656338-7 2014 More recently, new work suggests that direct activation of AMPK may contribute to antihyperglycaemic/antihyperlipidemic actions of salicylates. Salicylates 131-142 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 59-63 24256410-0 2013 Discovery of 5-substituted pyrrolo[2,3-d]pyrimidine antifolates as dual-acting inhibitors of glycinamide ribonucleotide formyltransferase and 5-aminoimidazole-4-carboxamide ribonucleotide formyltransferase in de novo purine nucleotide biosynthesis: implications of inhibiting 5-aminoimidazole-4-carboxamide ribonucleotide formyltransferase to ampk activation and antitumor activity. 5-substituted pyrrolo[2,3-d]pyrimidine 13-51 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 343-347 24763872-0 2014 Cytoprotective effect of beta-lapachone by inducing heme oxygenase-1 expression and AMP-activated protein kinase activation in human endothelial cells. beta-lapachone 25-39 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 84-112 24763872-3 2014 beta-Lapachone (BL), a well-known substrate of NAD(P)H: quinone oxidoreductase (NQO1), stimulates AMPK activation via NQO1 activation. beta-lapachone 0-14 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 98-102 24763872-3 2014 beta-Lapachone (BL), a well-known substrate of NAD(P)H: quinone oxidoreductase (NQO1), stimulates AMPK activation via NQO1 activation. beta-lapachone 16-18 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 98-102 24763872-3 2014 beta-Lapachone (BL), a well-known substrate of NAD(P)H: quinone oxidoreductase (NQO1), stimulates AMPK activation via NQO1 activation. nad(p)h 47-54 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 98-102 24389195-3 2014 Once activated, AMPK stimulates hepatic fatty acid oxidation and ketogenesis, inhibits cholesterol synthesis, lipogenesis, and triglyceride synthesis, inhibits adipocyte lipolysis and lipogenesis, stimulates skeletal muscle fatty acid oxidation and muscle glucose uptake, and modulates insulin secretion by the pancreas. Fatty Acids 40-50 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 16-20 24389195-3 2014 Once activated, AMPK stimulates hepatic fatty acid oxidation and ketogenesis, inhibits cholesterol synthesis, lipogenesis, and triglyceride synthesis, inhibits adipocyte lipolysis and lipogenesis, stimulates skeletal muscle fatty acid oxidation and muscle glucose uptake, and modulates insulin secretion by the pancreas. Cholesterol 87-98 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 16-20 24389195-3 2014 Once activated, AMPK stimulates hepatic fatty acid oxidation and ketogenesis, inhibits cholesterol synthesis, lipogenesis, and triglyceride synthesis, inhibits adipocyte lipolysis and lipogenesis, stimulates skeletal muscle fatty acid oxidation and muscle glucose uptake, and modulates insulin secretion by the pancreas. Triglycerides 127-139 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 16-20 24389195-3 2014 Once activated, AMPK stimulates hepatic fatty acid oxidation and ketogenesis, inhibits cholesterol synthesis, lipogenesis, and triglyceride synthesis, inhibits adipocyte lipolysis and lipogenesis, stimulates skeletal muscle fatty acid oxidation and muscle glucose uptake, and modulates insulin secretion by the pancreas. Fatty Acids 224-234 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 16-20 24389195-3 2014 Once activated, AMPK stimulates hepatic fatty acid oxidation and ketogenesis, inhibits cholesterol synthesis, lipogenesis, and triglyceride synthesis, inhibits adipocyte lipolysis and lipogenesis, stimulates skeletal muscle fatty acid oxidation and muscle glucose uptake, and modulates insulin secretion by the pancreas. Glucose 256-263 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 16-20 24389195-11 2014 By inhibiting the formation of reactive oxygen species in the endothelium, AMPK can optimize the redox balance in the vasculature. Reactive Oxygen Species 31-54 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 75-79 24750786-3 2014 Metformin exerts anticancer effects by primarily blocking the pivotal LKB1/AMPK/mTOR/S6K1 pathway-dependent cell growth, induces selective lethal effects on GSC by impairing the GSC-initiating spherogenesis and inhibits the proliferation of CD133+ cells, while having a low or null effect on differentiated glioblastoma cells and normal human stem cells. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 75-79 24750786-6 2014 In this regard, metformin acts via activation of the AMPK-FOXO3 axis, whereas ATO blocks the interleukin 6-induced promotion of STAT3 phosphorylation. Metformin 16-25 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 53-57 24522477-7 2014 L-arginine supplementation leads to redirection of AMP deamination on account of increased AMP dephosphorylation and subsequent adenosine production and may increase ATP regeneration via activation of AMP kinase (AMPK) pathway. Adenosine Triphosphate 166-169 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 201-211 24522477-7 2014 L-arginine supplementation leads to redirection of AMP deamination on account of increased AMP dephosphorylation and subsequent adenosine production and may increase ATP regeneration via activation of AMP kinase (AMPK) pathway. Adenosine Triphosphate 166-169 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 213-217 24522477-8 2014 The central role of AMPK in regulating cellular ATP regeneration, makes this enzyme as a central control point in energy homeostasis. Adenosine Triphosphate 48-51 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 20-24 24522477-7 2014 L-arginine supplementation leads to redirection of AMP deamination on account of increased AMP dephosphorylation and subsequent adenosine production and may increase ATP regeneration via activation of AMP kinase (AMPK) pathway. Arginine 0-10 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 201-211 24522477-7 2014 L-arginine supplementation leads to redirection of AMP deamination on account of increased AMP dephosphorylation and subsequent adenosine production and may increase ATP regeneration via activation of AMP kinase (AMPK) pathway. Arginine 0-10 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 213-217 24522477-7 2014 L-arginine supplementation leads to redirection of AMP deamination on account of increased AMP dephosphorylation and subsequent adenosine production and may increase ATP regeneration via activation of AMP kinase (AMPK) pathway. Adenosine Monophosphate 51-54 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 213-217 24187138-1 2013 AMP-activated protein kinase (AMPK) is a heterotrimeric enzyme that senses and governs changes in the cellular energy balance represented by concentrations of AMP, ADP, and ATP. Adenosine Monophosphate 0-3 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-34 24187138-1 2013 AMP-activated protein kinase (AMPK) is a heterotrimeric enzyme that senses and governs changes in the cellular energy balance represented by concentrations of AMP, ADP, and ATP. Adenosine Diphosphate 164-167 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-28 24187138-1 2013 AMP-activated protein kinase (AMPK) is a heterotrimeric enzyme that senses and governs changes in the cellular energy balance represented by concentrations of AMP, ADP, and ATP. Adenosine Diphosphate 164-167 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-34 24187138-1 2013 AMP-activated protein kinase (AMPK) is a heterotrimeric enzyme that senses and governs changes in the cellular energy balance represented by concentrations of AMP, ADP, and ATP. Adenosine Triphosphate 173-176 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-28 24187138-1 2013 AMP-activated protein kinase (AMPK) is a heterotrimeric enzyme that senses and governs changes in the cellular energy balance represented by concentrations of AMP, ADP, and ATP. Adenosine Triphosphate 173-176 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-34 24187138-6 2013 This chemical probe covalently attaches desthiobiotin to one or more conserved lysyl residues in the ATP-binding sites of protein kinases, including AMPK, while also labeling a wide range of ATP-utilizing proteins. desthiobiotin 40-53 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 149-153 24187138-6 2013 This chemical probe covalently attaches desthiobiotin to one or more conserved lysyl residues in the ATP-binding sites of protein kinases, including AMPK, while also labeling a wide range of ATP-utilizing proteins. Adenosine Triphosphate 101-104 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 149-153 24005536-0 2013 Capsaicin induces apoptosis in human osteosarcoma cells through AMPK-dependent and AMPK-independent signaling pathways. Capsaicin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 64-68 23657807-0 2013 Monacolin K affects lipid metabolism through SIRT1/AMPK pathway in HepG2 cells. Lovastatin 0-11 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 51-55 23657807-3 2013 In the present study, monacolin K increased protein expression of SIRT1 and phosphorylation level of AMP-activated protein kinase (AMPK) in HepG2 cells. Lovastatin 22-33 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 101-129 23657807-3 2013 In the present study, monacolin K increased protein expression of SIRT1 and phosphorylation level of AMP-activated protein kinase (AMPK) in HepG2 cells. Lovastatin 22-33 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 131-135 23657807-4 2013 Through activation of SIRT1/AMPK pathway, monacolin K increased phosphorylation of acetyl CoA carboxylase and caused nuclear translocation of forkhead box O1. Lovastatin 42-53 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 28-32 23657807-8 2013 All the demonstrated effects of monacolin K were counteracted by nicotinamide or compound C, the inhibitors of SIRT1 or AMPK. Lovastatin 32-43 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 120-124 23657807-8 2013 All the demonstrated effects of monacolin K were counteracted by nicotinamide or compound C, the inhibitors of SIRT1 or AMPK. Niacinamide 65-77 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 120-124 23657807-9 2013 In summary, monacolin K reduces the lipid content through SIRT1/AMPK pathway in HepG2 cells, which promotes catabolism and inhibits anabolism of lipid. Lovastatin 12-23 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 64-68 24005536-0 2013 Capsaicin induces apoptosis in human osteosarcoma cells through AMPK-dependent and AMPK-independent signaling pathways. Capsaicin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 83-87 24005536-3 2013 In the current study, we observed that capsaicin-induced growth inhibition and apoptosis in cultured osteosarcoma cells (U2OS and MG63), which were associated with a significant AMP-activated protein kinase (AMPK) activation. Capsaicin 39-48 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 178-206 24005536-3 2013 In the current study, we observed that capsaicin-induced growth inhibition and apoptosis in cultured osteosarcoma cells (U2OS and MG63), which were associated with a significant AMP-activated protein kinase (AMPK) activation. Capsaicin 39-48 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 208-212 24005536-4 2013 AMPK inhibition by compound C or RNA interference suppressed capsaicin-induced cytotoxicity, while AMPK activators (AICAR and A769662) promoted osteosarcoma cell death. Capsaicin 61-70 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 24403860-2 2013 Clinical trials using the United States Food and Drug Administration (FDA)-approved, AMPK-activating, antidiabetic drug metformin are promising in this regard, but the question of why metformin is protective for some women but not others still remains. Metformin 120-129 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 85-89 24403860-2 2013 Clinical trials using the United States Food and Drug Administration (FDA)-approved, AMPK-activating, antidiabetic drug metformin are promising in this regard, but the question of why metformin is protective for some women but not others still remains. Metformin 184-193 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 85-89 24403860-7 2013 Activation of AMPK by metformin triggered a growth inhibitory signal but also increased BCA2 protein levels, which correlated with AKT activation and could be curbed by an AMPK inhibitor, suggesting a potential feedback mechanism from pAMPKalpha1 to pAkt to BCA2. Metformin 22-31 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-18 24403860-7 2013 Activation of AMPK by metformin triggered a growth inhibitory signal but also increased BCA2 protein levels, which correlated with AKT activation and could be curbed by an AMPK inhibitor, suggesting a potential feedback mechanism from pAMPKalpha1 to pAkt to BCA2. Metformin 22-31 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 172-176 24334291-0 2013 Resistance to Dasatinib in primary chronic lymphocytic leukemia lymphocytes involves AMPK-mediated energetic re-programming. Dasatinib 14-23 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 85-89 24334291-10 2013 Differential metabolic reprogramming between subsets is supported by the contrasting effect on the survival of Dasatinib treated CLL lymphocytes with pharmacological inhibition of two master metabolic regulators (mTorc1 and AMPK) as well as induced autophagy. Dasatinib 111-120 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 224-228 24005536-5 2013 For the mechanism study, we found that AMPK activation was required for capsaicin-induced mTORC1 (mTOR complex 1) inhibition, B cell lymphoma 2 (Bcl-2) downregulation and Bax upregulation in MG63 cells. Capsaicin 72-81 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 39-43 24005536-6 2013 Capsaicin administration induced p53 activation, mitochondrial translocation and Bcl-2 killer association, such effects were dependent on AMPK activation. Capsaicin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 138-142 24005536-7 2013 Interestingly, we observed a significant pro-apoptotic c-Jun NH2-terminal kinases activation by capsaicin in MG63 cells, which appeared to be AMPK independent. Capsaicin 96-105 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 142-146 24005536-9 2013 Molecular studies revealed that capsaicin activated AMPK-dependent and AMPK-independent signalings to mediate cell apoptosis. Capsaicin 32-41 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 52-56 24005536-9 2013 Molecular studies revealed that capsaicin activated AMPK-dependent and AMPK-independent signalings to mediate cell apoptosis. Capsaicin 32-41 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 71-75 24002362-6 2013 AMP-activated protein kinase (AMPK) is suggested to be one of the various cellular targets of berberine, which regulates tumor progression and metastasis. Berberine 94-103 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-28 24002362-6 2013 AMP-activated protein kinase (AMPK) is suggested to be one of the various cellular targets of berberine, which regulates tumor progression and metastasis. Berberine 94-103 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-34 24002362-7 2013 However, the specific involvement of berberine-induced AMPK activation and its effects on the proliferation potential of Wilms" tumor cells remains unknown. Berberine 37-46 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 55-59 24002362-8 2013 The present study investigated the berberine-induced activation of AMPK and its effects on G401 Wilms" tumor cell proliferation. Berberine 35-44 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 67-71 23733596-10 2013 Treatment with LC (500 microM), Na2S (25 microM), and PIP3 (5 nM) increased the AMPK phosphorylation and PPARgamma expression in cells exposed to HG. Cysteine 15-17 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 80-84 23863464-3 2013 Here, we demonstrate that treatment of rabbit isolated, perfused collecting ducts with the AMPK activator 5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside (AICAR) inhibited V-ATPase-dependent H(+) secretion from intercalated cells after an acid load. acadesine 106-160 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 91-95 23863464-3 2013 Here, we demonstrate that treatment of rabbit isolated, perfused collecting ducts with the AMPK activator 5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside (AICAR) inhibited V-ATPase-dependent H(+) secretion from intercalated cells after an acid load. acadesine 162-167 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 91-95 23863464-4 2013 We have identified by mass spectrometry that Ser-384 is a major AMPK phosphorylation site in the V-ATPase A subunit, a result confirmed by comparing AMPK-dependent phosphate labeling of wild-type A-subunit (WT-A) with that of a Ser-384-to-Ala A subunit mutant (S384A-A) in vitro and in intact HEK-293 cells. Serine 45-48 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 64-68 23863464-4 2013 We have identified by mass spectrometry that Ser-384 is a major AMPK phosphorylation site in the V-ATPase A subunit, a result confirmed by comparing AMPK-dependent phosphate labeling of wild-type A-subunit (WT-A) with that of a Ser-384-to-Ala A subunit mutant (S384A-A) in vitro and in intact HEK-293 cells. Serine 45-48 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 149-153 23863464-4 2013 We have identified by mass spectrometry that Ser-384 is a major AMPK phosphorylation site in the V-ATPase A subunit, a result confirmed by comparing AMPK-dependent phosphate labeling of wild-type A-subunit (WT-A) with that of a Ser-384-to-Ala A subunit mutant (S384A-A) in vitro and in intact HEK-293 cells. Phosphates 164-173 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 64-68 23863464-4 2013 We have identified by mass spectrometry that Ser-384 is a major AMPK phosphorylation site in the V-ATPase A subunit, a result confirmed by comparing AMPK-dependent phosphate labeling of wild-type A-subunit (WT-A) with that of a Ser-384-to-Ala A subunit mutant (S384A-A) in vitro and in intact HEK-293 cells. Phosphates 164-173 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 149-153 23863464-8 2013 In summary, direct phosphorylation of the A subunit at Ser-384 by AMPK represents a novel regulatory mechanism of the V-ATPase in kidney intercalated cells. Serine 55-58 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 66-70 23568147-6 2013 While metformin induces early and transient activation of AMPK, inhibition of AMPKalpha1/2 does not abrogate anti-proliferative or pro-apoptotic effects of metformin. Metformin 6-15 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 58-62 23800577-9 2013 The skeletal muscle cells that were cultured in serum collected after CR showed an increase in AMPK and SIRT1 activity as well as mitochondrial biogenesis. Chromium 70-72 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 95-99 23800577-10 2013 GENERAL SIGNIFICANCE: CR is beneficial for obesity-related metabolic alterations and induces cellular adaptations against aging, possibly through AMPK and SIRT1 activation via circulating factors. Chromium 22-24 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 146-150 23688633-8 2013 Moreover, knock-down of AMPK by small interfering RNA (siRNA) blocked gAcrp-induced expression of genes related to autophagy, which in turn prevented protection from ethanol-induced apoptosis, suggesting that AMPK plays an important role in the induction of autophagy and protection of liver cells by gAcrp. Ethanol 166-173 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 24-28 23688633-8 2013 Moreover, knock-down of AMPK by small interfering RNA (siRNA) blocked gAcrp-induced expression of genes related to autophagy, which in turn prevented protection from ethanol-induced apoptosis, suggesting that AMPK plays an important role in the induction of autophagy and protection of liver cells by gAcrp. Ethanol 166-173 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 209-213 23688633-8 2013 Moreover, knock-down of AMPK by small interfering RNA (siRNA) blocked gAcrp-induced expression of genes related to autophagy, which in turn prevented protection from ethanol-induced apoptosis, suggesting that AMPK plays an important role in the induction of autophagy and protection of liver cells by gAcrp. gacrp 70-75 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 24-28 23688633-8 2013 Moreover, knock-down of AMPK by small interfering RNA (siRNA) blocked gAcrp-induced expression of genes related to autophagy, which in turn prevented protection from ethanol-induced apoptosis, suggesting that AMPK plays an important role in the induction of autophagy and protection of liver cells by gAcrp. gacrp 70-75 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 209-213 23688633-11 2013 Further, the AMPK-FoxO3A axis plays a cardinal role in gAcrp-induced autophagy and subsequent inhibition of ethanol-induced apoptosis. Ethanol 108-115 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 13-17 23733596-0 2013 L-cysteine and hydrogen sulfide increase PIP3 and AMPK/PPARgamma expression and decrease ROS and vascular inflammation markers in high glucose treated human U937 monocytes. Cysteine 0-10 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 50-54 23733596-0 2013 L-cysteine and hydrogen sulfide increase PIP3 and AMPK/PPARgamma expression and decrease ROS and vascular inflammation markers in high glucose treated human U937 monocytes. Hydrogen Sulfide 15-31 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 50-54 23733596-10 2013 Treatment with LC (500 microM), Na2S (25 microM), and PIP3 (5 nM) increased the AMPK phosphorylation and PPARgamma expression in cells exposed to HG. sodium sulfide 32-36 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 80-84 23733596-10 2013 Treatment with LC (500 microM), Na2S (25 microM), and PIP3 (5 nM) increased the AMPK phosphorylation and PPARgamma expression in cells exposed to HG. PIP3 54-58 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 80-84 23794020-3 2013 These results have drawn attention to the mechanisms underlying metformin"s anti-cancer effects, which may include triggering of the AMP-activated protein kinase (AMPK) pathway, resulting in vulnerability to an energy crisis (leading to cell death under conditions of nutrient deprivation) and a reduction in circulating insulin/IGF-1 levels. Metformin 64-73 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 133-161 23794020-3 2013 These results have drawn attention to the mechanisms underlying metformin"s anti-cancer effects, which may include triggering of the AMP-activated protein kinase (AMPK) pathway, resulting in vulnerability to an energy crisis (leading to cell death under conditions of nutrient deprivation) and a reduction in circulating insulin/IGF-1 levels. Metformin 64-73 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 163-167 23979843-5 2013 Strikingly, stimulating the key energy-sensor AMP-activated protein kinase (AMPK) increased the phosphorylation at the anti-fission site Serine 637 and largely prevented the alterations in ER and mitochondrial morphology. Serine 137-143 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 46-74 23979843-5 2013 Strikingly, stimulating the key energy-sensor AMP-activated protein kinase (AMPK) increased the phosphorylation at the anti-fission site Serine 637 and largely prevented the alterations in ER and mitochondrial morphology. Serine 137-143 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 76-80 23707377-9 2013 Alpha-lipoic acid might exert its appetite-decreasing effect by the AMPK signaling pathway. Thioctic Acid 0-17 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 68-72 23891087-0 2013 Contributions of AMPK and p53 dependent signaling to radiation response in the presence of metformin. Metformin 91-100 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 17-21 25337554-10 2013 CONCLUSIONS: We suggested that quercetin-induced apoptosis involved Sestrin 2/AMPK/mTOR pathway, which was regulated by increased intracellular ROS by quercetin. Quercetin 31-40 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 78-82 25337554-10 2013 CONCLUSIONS: We suggested that quercetin-induced apoptosis involved Sestrin 2/AMPK/mTOR pathway, which was regulated by increased intracellular ROS by quercetin. Reactive Oxygen Species 144-147 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 78-82 25337554-10 2013 CONCLUSIONS: We suggested that quercetin-induced apoptosis involved Sestrin 2/AMPK/mTOR pathway, which was regulated by increased intracellular ROS by quercetin. Quercetin 151-160 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 78-82 23891087-10 2013 CONCLUSIONS: The anti-proliferative activity of metformin may confer benefit in combination with radiotherapy, and this benefit is intensified upon loss of AMPK or p53 signaling. Metformin 48-57 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 156-160 25337554-0 2013 Quercetin Regulates Sestrin 2-AMPK-mTOR Signaling Pathway and Induces Apoptosis via Increased Intracellular ROS in HCT116 Colon Cancer Cells. Quercetin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-34 25337554-2 2013 In this study, we investigated the regulatory mechanism of quercetin-induced apoptosis through regulation of Sestrin 2 and AMPK signaling pathway. Quercetin 59-68 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 123-127 23891087-2 2013 Metformin activates AMPK that in turn can launch a p53-dependent metabolic checkpoint. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 20-24 23891087-4 2013 Since radiation-induced signaling also involves AMPK and p53, we investigated their importance in mediating responses to metformin and radiation. Metformin 121-130 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 48-52 23891087-8 2013 Loss of AMPK sensitized cells to the anti-proliferative effects of metformin, while loss of p53 promoted both the growth inhibitory and toxic effects of metformin. Metformin 67-76 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 8-12 24180199-6 2013 Metformin may exert its anti-cancer activity by a direct effect (insulin) and an indirect effect (AMPK and mTOR). Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 98-102 23707609-9 2013 The inactivation of AMPK by siRNA, DN-AMPK or the pharmacological AMPK inhibitor compound C, revealed that metformin reduced HO-1 expression in an AMPK-independent manner. Metformin 107-116 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 38-42 23707609-9 2013 The inactivation of AMPK by siRNA, DN-AMPK or the pharmacological AMPK inhibitor compound C, revealed that metformin reduced HO-1 expression in an AMPK-independent manner. Metformin 107-116 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 38-42 23707609-0 2013 Metformin inhibits heme oxygenase-1 expression in cancer cells through inactivation of Raf-ERK-Nrf2 signaling and AMPK-independent pathways. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 114-118 23707609-9 2013 The inactivation of AMPK by siRNA, DN-AMPK or the pharmacological AMPK inhibitor compound C, revealed that metformin reduced HO-1 expression in an AMPK-independent manner. Metformin 107-116 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 38-42 23707609-9 2013 The inactivation of AMPK by siRNA, DN-AMPK or the pharmacological AMPK inhibitor compound C, revealed that metformin reduced HO-1 expression in an AMPK-independent manner. Metformin 107-116 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 20-24 24082825-2 2013 LKB1 functions as a key upstream activator of the AMP-activated protein kinase (AMPK), a central metabolic switch found in all eukaryotes that govern glucose and lipid metabolism and autophagy in response to alterations in nutrients and intracellular energy levels. Glucose 150-157 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 50-78 24009772-0 2013 Metformin induces apoptosis through AMPK-dependent inhibition of UPR signaling in ALL lymphoblasts. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 36-40 24009772-3 2013 Metformin activated AMPK, down-regulated the unfolded protein response (UPR) demonstrated by significant decrease in the main UPR regulator GRP78, and led to UPR-mediated cell death via up-regulation of the ER stress/UPR cell death mediators IRE1alpha and CHOP. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 20-24 24009772-4 2013 Using shRNA, we demonstrate that metformin-induced apoptosis is AMPK-dependent since AMPK knock-down rescued ALL cells, which correlated with down-regulation of IRE1alpha and CHOP and restoration of the UPR/GRP78 function. Metformin 33-42 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 64-68 24009772-4 2013 Using shRNA, we demonstrate that metformin-induced apoptosis is AMPK-dependent since AMPK knock-down rescued ALL cells, which correlated with down-regulation of IRE1alpha and CHOP and restoration of the UPR/GRP78 function. Metformin 33-42 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 85-89 24009772-7 2013 Similar synergism was seen with agents targeting Akt in combination with metformin, supporting our original postulate that AMPK and Akt exert opposite regulatory roles on UPR activity in ALL. Metformin 73-82 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 123-127 24082825-2 2013 LKB1 functions as a key upstream activator of the AMP-activated protein kinase (AMPK), a central metabolic switch found in all eukaryotes that govern glucose and lipid metabolism and autophagy in response to alterations in nutrients and intracellular energy levels. Glucose 150-157 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 80-84 23770982-0 2013 Danthron activates AMP-activated protein kinase and regulates lipid and glucose metabolism in vitro. danthron 0-8 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 19-47 23770982-7 2013 RESULTS: Danthron (0.1, 1, and 10 mumol/L) dose-dependently promoted the phosphorylation of AMPK and acetyl-CoA carboxylase (ACC) in both HepG2 and C2C12 cells. danthron 9-17 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 92-96 23770982-1 2013 AIM: To discover the active compound on AMP-activated protein kinase (AMPK) activation and investigate the effects of the active compound 1,8-dihydroxyanthraquinone (danthron) from the traditional Chinese medicine rhubarb on AMPK-mediated lipid and glucose metabolism in vitro. danthron 138-164 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 225-229 23770982-10 2013 The actions of danthron on lipid and glucose metabolism were abolished or reversed by co-treatment with the AMPK inhibitor compound C. CONCLUSION: Danthron effectively reduces intracellular lipid contents and enhanced glucose consumption in vitro via activation of AMPK signaling pathway. danthron 15-23 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 108-112 23770982-1 2013 AIM: To discover the active compound on AMP-activated protein kinase (AMPK) activation and investigate the effects of the active compound 1,8-dihydroxyanthraquinone (danthron) from the traditional Chinese medicine rhubarb on AMPK-mediated lipid and glucose metabolism in vitro. danthron 166-174 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 225-229 23770982-10 2013 The actions of danthron on lipid and glucose metabolism were abolished or reversed by co-treatment with the AMPK inhibitor compound C. CONCLUSION: Danthron effectively reduces intracellular lipid contents and enhanced glucose consumption in vitro via activation of AMPK signaling pathway. danthron 15-23 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 265-269 23770982-10 2013 The actions of danthron on lipid and glucose metabolism were abolished or reversed by co-treatment with the AMPK inhibitor compound C. CONCLUSION: Danthron effectively reduces intracellular lipid contents and enhanced glucose consumption in vitro via activation of AMPK signaling pathway. danthron 147-155 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 108-112 23557706-4 2013 High glucose (HG) induces apoptosis of podocytes, inhibits AMP-activated protein kinase (AMPK) activation, inactivates tuberin, and activates mTOR. Glucose 5-12 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 59-87 23770982-10 2013 The actions of danthron on lipid and glucose metabolism were abolished or reversed by co-treatment with the AMPK inhibitor compound C. CONCLUSION: Danthron effectively reduces intracellular lipid contents and enhanced glucose consumption in vitro via activation of AMPK signaling pathway. danthron 147-155 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 265-269 23747347-2 2013 AMPK is an alphabetagamma heterotrimer controlled by allosteric regulation by AMP, ADP and ATP, auto-inhibitory features and phosphorylation, with the threonine-172 phosphorylation on the catalytic alpha-subunit by LKB1, CaMKKbeta or Tak1 being essential for its fully activation. Adenosine Diphosphate 83-86 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 23747347-2 2013 AMPK is an alphabetagamma heterotrimer controlled by allosteric regulation by AMP, ADP and ATP, auto-inhibitory features and phosphorylation, with the threonine-172 phosphorylation on the catalytic alpha-subunit by LKB1, CaMKKbeta or Tak1 being essential for its fully activation. Adenosine Triphosphate 91-94 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 23747347-2 2013 AMPK is an alphabetagamma heterotrimer controlled by allosteric regulation by AMP, ADP and ATP, auto-inhibitory features and phosphorylation, with the threonine-172 phosphorylation on the catalytic alpha-subunit by LKB1, CaMKKbeta or Tak1 being essential for its fully activation. Threonine 151-160 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 23747347-4 2013 Pharmacological activation of AMPK by metformin or other compounds holds a considerable potential to reverse the metabolic abnormalities associated with type 2 diabetes. Metformin 38-47 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-34 23878245-0 2013 Reactive nitrogen species regulate autophagy through ATM-AMPK-TSC2-mediated suppression of mTORC1. Reactive Nitrogen Species 0-25 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 57-61 23878245-2 2013 We found that nitrosative stress induced by steady-state nitric oxide (NO) caused rapid activation of an ATM damage-response pathway leading to downstream signaling by this stress kinase to LKB1 and AMPK kinases, and activation of the TSC tumor suppressor. Nitric Oxide 57-69 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 199-203 23557706-4 2013 High glucose (HG) induces apoptosis of podocytes, inhibits AMP-activated protein kinase (AMPK) activation, inactivates tuberin, and activates mTOR. Glucose 5-12 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 89-93 23680031-0 2013 Autophagic cell death induced by resveratrol depends on the Ca(2+)/AMPK/mTOR pathway in A549 cells. Resveratrol 33-44 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 67-71 23963659-6 2013 In MCF-7 and SKBR3 cells, AMPK enhanced glucose uptake by up-regulating the expression of GLUT-1 glucose transporter, as also demonstrated by AMPKalpha1 RNA interference, and stimulated aerobic glycolysis thus increasing lactate production. Glucose 40-47 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 26-30 23963659-6 2013 In MCF-7 and SKBR3 cells, AMPK enhanced glucose uptake by up-regulating the expression of GLUT-1 glucose transporter, as also demonstrated by AMPKalpha1 RNA interference, and stimulated aerobic glycolysis thus increasing lactate production. Lactic Acid 221-228 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 26-30 23963659-8 2013 Persistent activation of AMPK by sorafenib finally led to the impairment of glucose metabolism both in MCF-7 and SKBR3 cells as well as in the highly glycolytic MDA-MB-231 cells, resulting in cell death. Sorafenib 33-42 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 25-29 23963659-9 2013 This previously unrecognized long-term effect of sorafenib was mediated by AMPK-dependent inhibition of the mTORC1 pathway. Sorafenib 49-58 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 75-79 23963659-11 2013 The key role of AMPK-dependent inhibition of mTORC1 in sorafenib mechanisms of action was confirmed by AMPKalpha1 silencing, which restored mTORC1 activity conferring a significant protection from cell death. Sorafenib 55-64 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 16-20 23963659-11 2013 The key role of AMPK-dependent inhibition of mTORC1 in sorafenib mechanisms of action was confirmed by AMPKalpha1 silencing, which restored mTORC1 activity conferring a significant protection from cell death. Sorafenib 55-64 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 103-113 23584792-3 2013 We have previously demonstrated that the CREB co-activator CRTC2 binds directly to PII and stimulates its activity via mechanisms involving LKB1-AMPK in response to prostaglandin E(2) (PGE(2)). Dinoprostone 165-183 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 145-149 23584792-3 2013 We have previously demonstrated that the CREB co-activator CRTC2 binds directly to PII and stimulates its activity via mechanisms involving LKB1-AMPK in response to prostaglandin E(2) (PGE(2)). Prostaglandins E 185-188 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 145-149 23551302-0 2013 AMPK involvement in endoplasmic reticulum stress and autophagy modulation after fatty liver graft preservation: a role for melatonin and trimetazidine cocktail. Melatonin 123-132 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 23551302-0 2013 AMPK involvement in endoplasmic reticulum stress and autophagy modulation after fatty liver graft preservation: a role for melatonin and trimetazidine cocktail. Trimetazidine 137-150 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 23551302-5 2013 Here, we evaluated the combined effect of melatonin and trimetazidine as additives to IGL-1 solution in the modulation of ER stress and autophagy in steatotic liver grafts through activation of AMPK. Melatonin 42-51 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 194-198 23551302-5 2013 Here, we evaluated the combined effect of melatonin and trimetazidine as additives to IGL-1 solution in the modulation of ER stress and autophagy in steatotic liver grafts through activation of AMPK. Trimetazidine 56-69 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 194-198 23551302-14 2013 The addition of melatonin and TMZ to IGL-1 solution improved steatotic liver graft preservation through AMPK activation, which reduces ER stress and increases autophagy. Melatonin 16-25 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 104-108 23551302-14 2013 The addition of melatonin and TMZ to IGL-1 solution improved steatotic liver graft preservation through AMPK activation, which reduces ER stress and increases autophagy. Temozolomide 30-33 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 104-108 23887727-8 2013 AMPK can also modulate the circadian rhythms through nicotinamide adenine dinucleotide-dependent regulation of silent information regulator 1. NAD 53-86 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 23680031-10 2013 Intracellular free calcium accumulated immediately following resveratrol addition, which led to the activation of phospho-AMPK and phospho-Raptor, and a reduction in the amount of phospho-p70S6K. Calcium 19-26 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 122-126 23680031-10 2013 Intracellular free calcium accumulated immediately following resveratrol addition, which led to the activation of phospho-AMPK and phospho-Raptor, and a reduction in the amount of phospho-p70S6K. Resveratrol 61-72 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 122-126 23680031-12 2013 In conclusion, we demonstrate that resveratrol-induced A549 cell death was mediated by the process of autophagic cell death via Ca(2+)/AMPK-mTOR signaling pathway. Resveratrol 35-46 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 135-139 23673223-0 2013 Synthesis and biological evaluation of arctigenin ester and ether derivatives as activators of AMPK. arctigenin ester 39-55 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 95-99 23777448-0 2013 Demethoxycurcumin inhibits energy metabolic and oncogenic signaling pathways through AMPK activation in triple-negative breast cancer cells. demethoxycurcumin 0-17 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 85-89 23777448-6 2013 The study showed that DMC activated AMPK in TNBC cells. demethoxycurcumin 22-25 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 36-40 23777448-8 2013 DMC also targeted multiple AMPK downstream pathways. demethoxycurcumin 0-3 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 27-31 23777448-12 2013 These results suggest that DMC is a potent AMPK activator that acts through a broad spectrum of anti-TNBC activities. demethoxycurcumin 27-30 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 43-47 23819460-5 2013 METHODS: Effect of the activation of AMPK on FOXM1 expression was examined by hypoxia and glucose deprivation, as well as pharmacological AMPK activators such as A23187, AICAR and metformin. AICA ribonucleotide 170-175 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 37-41 23819460-5 2013 METHODS: Effect of the activation of AMPK on FOXM1 expression was examined by hypoxia and glucose deprivation, as well as pharmacological AMPK activators such as A23187, AICAR and metformin. Metformin 180-189 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 37-41 23819460-7 2013 RESULTS: Consistent with our previous findings, the activation of AMPK by either AMPK activators such as AICAR, A23187, metformin, glucose deprivation or hypoxia significantly inhibited the cervical cancer cell growth. AICA ribonucleotide 105-110 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 66-70 23819460-7 2013 RESULTS: Consistent with our previous findings, the activation of AMPK by either AMPK activators such as AICAR, A23187, metformin, glucose deprivation or hypoxia significantly inhibited the cervical cancer cell growth. AICA ribonucleotide 105-110 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 81-85 23819460-7 2013 RESULTS: Consistent with our previous findings, the activation of AMPK by either AMPK activators such as AICAR, A23187, metformin, glucose deprivation or hypoxia significantly inhibited the cervical cancer cell growth. Calcimycin 112-118 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 66-70 23819460-7 2013 RESULTS: Consistent with our previous findings, the activation of AMPK by either AMPK activators such as AICAR, A23187, metformin, glucose deprivation or hypoxia significantly inhibited the cervical cancer cell growth. Calcimycin 112-118 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 81-85 23819460-7 2013 RESULTS: Consistent with our previous findings, the activation of AMPK by either AMPK activators such as AICAR, A23187, metformin, glucose deprivation or hypoxia significantly inhibited the cervical cancer cell growth. Metformin 120-129 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 66-70 23819460-7 2013 RESULTS: Consistent with our previous findings, the activation of AMPK by either AMPK activators such as AICAR, A23187, metformin, glucose deprivation or hypoxia significantly inhibited the cervical cancer cell growth. Metformin 120-129 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 81-85 23673223-3 2013 Further structure-activity relationship analysis shows that arctigenin ester derivatives 3a, 3h and 9-deoxy-arctigenin phenethyl ether derivatives 6a, 6c, 6d activate AMPK more potently than arctigenin. arctigenin ester 60-76 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 167-171 23673223-3 2013 Further structure-activity relationship analysis shows that arctigenin ester derivatives 3a, 3h and 9-deoxy-arctigenin phenethyl ether derivatives 6a, 6c, 6d activate AMPK more potently than arctigenin. Tritium 93-95 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 167-171 23673223-3 2013 Further structure-activity relationship analysis shows that arctigenin ester derivatives 3a, 3h and 9-deoxy-arctigenin phenethyl ether derivatives 6a, 6c, 6d activate AMPK more potently than arctigenin. 9-deoxy-arctigenin phenethyl ether 100-134 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 167-171 23673223-4 2013 Moreover, the 2-(3,4-dimethoxyphenyl)ethyl ether moiety of 6c has been demonstrated as a potential functional group to improve the effect of AMPK phosphorylation. 2-(3,4-dimethoxyphenyl)ethyl ether 14-48 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 141-145 23673223-0 2013 Synthesis and biological evaluation of arctigenin ester and ether derivatives as activators of AMPK. Ether 60-65 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 95-99 23673223-2 2013 Initial biological evaluation indicates that some alkyl ester and phenethyl ether arctigenin derivatives display potential activities in AMPK phosphorylation improvement. alkyl ester 50-61 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 137-141 23673223-2 2013 Initial biological evaluation indicates that some alkyl ester and phenethyl ether arctigenin derivatives display potential activities in AMPK phosphorylation improvement. phenethyl ether arctigenin 66-92 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 137-141 23559539-0 2013 AMPK synergizes with the combined treatment of 1"-acetoxychavicol acetate and sodium butyrate to upregulate phase II detoxifying enzyme activities. 1'-acetoxychavicol acetate 47-73 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 23559539-0 2013 AMPK synergizes with the combined treatment of 1"-acetoxychavicol acetate and sodium butyrate to upregulate phase II detoxifying enzyme activities. Butyric Acid 78-93 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 23603572-9 2013 In addition, fenofibrate up-regulated SIRT1 expression through AMPK in TNF-alpha-stimulated adipocytes. Fenofibrate 13-24 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 63-67 23559539-8 2013 Inhibition of AMPK activity decreased phase II enzyme activities that were upregulated by treatment with ACA plus sodium butyrate or other phytochemicals, including kaempferol, quercetin, and epigallocatechin-3-gallate. Acetates 105-108 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-18 23559539-8 2013 Inhibition of AMPK activity decreased phase II enzyme activities that were upregulated by treatment with ACA plus sodium butyrate or other phytochemicals, including kaempferol, quercetin, and epigallocatechin-3-gallate. Butyric Acid 114-129 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-18 23559539-8 2013 Inhibition of AMPK activity decreased phase II enzyme activities that were upregulated by treatment with ACA plus sodium butyrate or other phytochemicals, including kaempferol, quercetin, and epigallocatechin-3-gallate. kaempferol 165-175 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-18 23559539-8 2013 Inhibition of AMPK activity decreased phase II enzyme activities that were upregulated by treatment with ACA plus sodium butyrate or other phytochemicals, including kaempferol, quercetin, and epigallocatechin-3-gallate. Quercetin 177-186 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-18 23559539-8 2013 Inhibition of AMPK activity decreased phase II enzyme activities that were upregulated by treatment with ACA plus sodium butyrate or other phytochemicals, including kaempferol, quercetin, and epigallocatechin-3-gallate. epigallocatechin gallate 192-218 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-18 23559539-9 2013 Combined treatment with ACA and sodium butyrate increased phosphorylated AMPK levels. Acetates 24-27 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 73-77 23559539-9 2013 Combined treatment with ACA and sodium butyrate increased phosphorylated AMPK levels. Butyric Acid 32-47 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 73-77 23559539-11 2013 The combined ACA and sodium butyrate treatment synergistically upregulated phase II enzyme activities through AMPK activation and p53 acetylation. Butyric Acid 21-36 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 110-114 23825542-0 2013 Salsalate and Adiponectin Improve Palmitate-Induced Insulin Resistance via Inhibition of Selenoprotein P through the AMPK-FOXO1alpha Pathway. Palmitates 34-43 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 117-121 23825542-6 2013 Palmitate-induced SeP expression was inhibited by both salsalate and salicylate, which was mediated by AMPK activation, and was blocked by AMPK siRNA or an inhibitor of AMPK. Palmitates 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 103-107 23825542-6 2013 Palmitate-induced SeP expression was inhibited by both salsalate and salicylate, which was mediated by AMPK activation, and was blocked by AMPK siRNA or an inhibitor of AMPK. Palmitates 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 139-143 23825542-6 2013 Palmitate-induced SeP expression was inhibited by both salsalate and salicylate, which was mediated by AMPK activation, and was blocked by AMPK siRNA or an inhibitor of AMPK. Palmitates 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 139-143 23612997-9 2013 Despite exercise being performed at the same relative intensity (65% of Vo2peak), the acute exercise response on AMPK Thr(172), ACC2 Ser(221), AMPKalpha2beta2gamma1, and AMPKalpha2beta2gamma3 activities, GS activity, and adenine nucleotides as well as hexokinase II mRNA levels were all reduced after exercise training. Threonine 118-121 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 113-117 23612997-9 2013 Despite exercise being performed at the same relative intensity (65% of Vo2peak), the acute exercise response on AMPK Thr(172), ACC2 Ser(221), AMPKalpha2beta2gamma1, and AMPKalpha2beta2gamma3 activities, GS activity, and adenine nucleotides as well as hexokinase II mRNA levels were all reduced after exercise training. Adenine Nucleotides 221-240 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 113-117 23612997-10 2013 Increased exercise-induced muscle AMPK activation and ACC2 Ser(221) phosphorylation in LBW subjects may indicate a more sensitive AMPK system in this population. Serine 59-62 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 130-134 23592276-4 2013 In this study we identify a novel ability of LMP1 to inhibit the LKB1-AMPK pathway through phosphorylation of LKB1 at serine 428 with subsequent suppression of the phosphorylation of AMPK and its substrates, ACC and Raptor. Serine 118-124 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 70-74 23709749-0 2013 Globular adiponectin induces LKB1/AMPK-dependent glucose uptake via actin cytoskeleton remodeling. Glucose 49-56 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 34-38 23825542-6 2013 Palmitate-induced SeP expression was inhibited by both salsalate and salicylate, which was mediated by AMPK activation, and was blocked by AMPK siRNA or an inhibitor of AMPK. salicylsalicylic acid 55-64 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 103-107 23825542-6 2013 Palmitate-induced SeP expression was inhibited by both salsalate and salicylate, which was mediated by AMPK activation, and was blocked by AMPK siRNA or an inhibitor of AMPK. Salicylates 69-79 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 103-107 23825542-7 2013 Chromatin immunoprecipitation (ChIP) and electrophoretic mobility shift (EMSA) assay showed that salsalate suppressed SeP expression by AMPK-mediated phosphorylation of FOXO1alpha. salicylsalicylic acid 97-106 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 136-140 23825542-8 2013 Moreover, fAd also reduced palmitate-induced SeP expression through the activation of AMPK, which results in improved IR. Palmitates 27-36 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 86-90 23825542-10 2013 Taken together, we found that salsalate and adiponectin ameliorated palmitate-induced IR in hepatocytes via SeP inhibition through the AMPK-FOXO1alpha pathway. salicylsalicylic acid 30-39 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 135-139 23825542-10 2013 Taken together, we found that salsalate and adiponectin ameliorated palmitate-induced IR in hepatocytes via SeP inhibition through the AMPK-FOXO1alpha pathway. Palmitates 68-77 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 135-139 23625915-5 2013 Activation of AMPK using 5-aminoimidazole-4-carboxamide-1-beta-d-ribofuranoside (AICAR) resulted in STIM1 phosphorylation on serine residues and prevented protease-activated receptor-1 (PAR-1)-induced Ca(2+) entry. acadesine 81-86 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-18 23625915-5 2013 Activation of AMPK using 5-aminoimidazole-4-carboxamide-1-beta-d-ribofuranoside (AICAR) resulted in STIM1 phosphorylation on serine residues and prevented protease-activated receptor-1 (PAR-1)-induced Ca(2+) entry. acadesine 25-79 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-18 23625915-5 2013 Activation of AMPK using 5-aminoimidazole-4-carboxamide-1-beta-d-ribofuranoside (AICAR) resulted in STIM1 phosphorylation on serine residues and prevented protease-activated receptor-1 (PAR-1)-induced Ca(2+) entry. Serine 125-131 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 14-18 23665322-6 2013 Further, we provided evidence to support that AMPK (AMP-activated protein kinase) activation mediated gambogic acid-induced LRIG1 upregulation, U87 cell apoptosis and growth inhibition, while AMPK inhibition by shRNA or compound C reduced gambogic acid-induced EGFR/Akt inhibition and cytotoxicity in U87 cells. gambogic acid 102-115 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 46-50 23665322-6 2013 Further, we provided evidence to support that AMPK (AMP-activated protein kinase) activation mediated gambogic acid-induced LRIG1 upregulation, U87 cell apoptosis and growth inhibition, while AMPK inhibition by shRNA or compound C reduced gambogic acid-induced EGFR/Akt inhibition and cytotoxicity in U87 cells. gambogic acid 239-252 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 46-50 23764845-0 2013 Cannabinoids inhibit energetic metabolism and induce AMPK-dependent autophagy in pancreatic cancer cells. Cannabinoids 0-12 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 53-57 23764845-3 2013 Panc1 cells treated with cannabinoids show elevated AMPK activation induced by a ROS-dependent increase of AMP/ATP ratio. Cannabinoids 25-37 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 52-56 23665322-6 2013 Further, we provided evidence to support that AMPK (AMP-activated protein kinase) activation mediated gambogic acid-induced LRIG1 upregulation, U87 cell apoptosis and growth inhibition, while AMPK inhibition by shRNA or compound C reduced gambogic acid-induced EGFR/Akt inhibition and cytotoxicity in U87 cells. gambogic acid 102-115 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 52-80 23764845-3 2013 Panc1 cells treated with cannabinoids show elevated AMPK activation induced by a ROS-dependent increase of AMP/ATP ratio. ros 81-84 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 52-56 23665322-0 2013 Gambogic acid induces EGFR degradation and Akt/mTORC1 inhibition through AMPK dependent-LRIG1 upregulation in cultured U87 glioma cells. gambogic acid 0-13 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 73-77 23665322-6 2013 Further, we provided evidence to support that AMPK (AMP-activated protein kinase) activation mediated gambogic acid-induced LRIG1 upregulation, U87 cell apoptosis and growth inhibition, while AMPK inhibition by shRNA or compound C reduced gambogic acid-induced EGFR/Akt inhibition and cytotoxicity in U87 cells. gambogic acid 102-115 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 192-196 23764845-3 2013 Panc1 cells treated with cannabinoids show elevated AMPK activation induced by a ROS-dependent increase of AMP/ATP ratio. Adenosine Triphosphate 111-114 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 52-56 23764845-4 2013 ROS promote nuclear translocation of GAPDH, which is further amplified by AMPK, thereby attenuating glycolysis. ros 0-3 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 74-78 23665322-6 2013 Further, we provided evidence to support that AMPK (AMP-activated protein kinase) activation mediated gambogic acid-induced LRIG1 upregulation, U87 cell apoptosis and growth inhibition, while AMPK inhibition by shRNA or compound C reduced gambogic acid-induced EGFR/Akt inhibition and cytotoxicity in U87 cells. gambogic acid 239-252 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 52-80 23718875-10 2013 Long-term exposure of ARG with or without CMP-C or L-NAME suppressed NO2-/NO3-, glucose uptake, GLUT-1, AMPK expression and activity below control, and increased overall cellular glucose, O2 - and ONOO-. Arginine 22-25 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 104-108 23718875-0 2013 AMP-activated protein kinase regulates L-arginine mediated cellular responses. Arginine 39-49 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-28 23358928-0 2013 Resveratrol protects HUVECs from oxidized-LDL induced oxidative damage by autophagy upregulation via the AMPK/SIRT1 pathway. Resveratrol 0-11 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 105-109 23358928-10 2013 This effect accompanied by upregulation of autophagy and increased protein expression of Sirt1 and AMPK phosphorylation on threonine 172 (p-AMPK). Threonine 123-132 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 99-103 23358928-10 2013 This effect accompanied by upregulation of autophagy and increased protein expression of Sirt1 and AMPK phosphorylation on threonine 172 (p-AMPK). Threonine 123-132 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 140-144 23718875-10 2013 Long-term exposure of ARG with or without CMP-C or L-NAME suppressed NO2-/NO3-, glucose uptake, GLUT-1, AMPK expression and activity below control, and increased overall cellular glucose, O2 - and ONOO-. NG-Nitroarginine Methyl Ester 51-57 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 104-108 23718875-12 2013 Continuous co-incubation with CDB and ARG increased NO2-/NO3-, glucose uptake, GLUT-1, AMPK expression and activity, and maintained overall cellular glucose, O2 - and ONOO- to control conditions. cdb 30-33 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 87-91 23718875-12 2013 Continuous co-incubation with CDB and ARG increased NO2-/NO3-, glucose uptake, GLUT-1, AMPK expression and activity, and maintained overall cellular glucose, O2 - and ONOO- to control conditions. Arginine 38-41 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 87-91 23718875-13 2013 CONCLUSION: The present study provides the fundamental evidence for AMPK as the primary modulator of ARG cellular responses and for regulating the mode of glucose accumulation during short-term and continuous ARG treatments. Arginine 101-104 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 68-72 23632475-0 2013 Metformin inhibits growth and enhances radiation response of non-small cell lung cancer (NSCLC) through ATM and AMPK. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 112-116 23718875-13 2013 CONCLUSION: The present study provides the fundamental evidence for AMPK as the primary modulator of ARG cellular responses and for regulating the mode of glucose accumulation during short-term and continuous ARG treatments. Glucose 155-162 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 68-72 23632475-4 2013 Metformin (i) activated the ataxia telengiectasia-mutated (ATM)-AMPK-p53/p21(cip1) and inhibited the Akt-mammalian target of rapamycin (mTOR)-eIF4E-binding protein 1 (4EBP1) pathways, (ii) induced G1 cycle arrest and (iii) enhanced apoptosis. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 64-68 23718875-13 2013 CONCLUSION: The present study provides the fundamental evidence for AMPK as the primary modulator of ARG cellular responses and for regulating the mode of glucose accumulation during short-term and continuous ARG treatments. Arginine 209-212 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 68-72 23632475-10 2013 Metformin and IR mediate their action through an ATM-AMPK-dependent pathway. Metformin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 53-57 23500383-0 2013 Licochalcone A regulates hepatic lipid metabolism through activation of AMP-activated protein kinase. licochalcone A 0-14 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 72-100 23603990-0 2013 Serine79-phosphorylated acetyl-CoA carboxylase, a downstream target of AMPK, localizes to the mitotic spindle poles and the cytokinesis furrow. serine79 0-8 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 71-75 23615262-0 2013 Caffeine attenuates lipid accumulation via activation of AMP-activated protein kinase signaling pathway in HepG2 cells. Caffeine 0-8 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 57-85 23615262-5 2013 Next, the effect of caffeine on AMP-activated protein kinase (AMPK) signaling pathway was examined. Caffeine 20-28 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 32-60 23615262-5 2013 Next, the effect of caffeine on AMP-activated protein kinase (AMPK) signaling pathway was examined. Caffeine 20-28 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 62-66 23615262-6 2013 Phosphorylation of AMPK and acetyl-CoA carboxylase were evidently increased when the cells were treated with caffeine as indicated for 24 h. These effects were all reversed in the presence of compound C, an AMPK inhibitor. Caffeine 109-117 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 19-23 23615262-6 2013 Phosphorylation of AMPK and acetyl-CoA carboxylase were evidently increased when the cells were treated with caffeine as indicated for 24 h. These effects were all reversed in the presence of compound C, an AMPK inhibitor. Caffeine 109-117 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 207-211 23615262-7 2013 In summary, these data indicate that caffeine effectively depleted TG and cholesterol levels by inhibition of lipogenesis and stimulation of lipolysis through modulating AMPK-SREBP signaling pathways. Caffeine 37-45 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 170-174 23310952-0 2013 AMPKalpha1: a glucose sensor that controls CD8 T-cell memory. Glucose 14-21 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-10 23310952-4 2013 We show that AMPKalpha1 activates rapidly in response to the metabolic stress caused by glucose deprivation of CD8 cytotoxic T lymphocytes (CTLs). Glucose 88-95 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 13-23 23548904-0 2013 Phenformin activates the unfolded protein response in an AMP-activated protein kinase (AMPK)-dependent manner. Phenformin 0-10 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 57-85 23548904-0 2013 Phenformin activates the unfolded protein response in an AMP-activated protein kinase (AMPK)-dependent manner. Phenformin 0-10 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 87-91 23548904-2 2013 RESULTS: Phenformin treatment activates the IRE1alpha and PERK pathways in an AMPK-dependent manner. Phenformin 9-19 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 78-82 23548904-3 2013 CONCLUSION: AMPK is required for phenformin-mediated IRE1alpha and PERK activation. Phenformin 33-43 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 12-16 23508546-3 2013 We develop a novel multi-scale mathematical model where cell migration and proliferation are controlled through a core intracellular control system (miR-451-AMPK complex) in response to glucose availability and physical constraints in the microenvironment. Glucose 186-193 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 157-161 23500383-7 2013 LA significantly inhibited the mitochondrial respiration and ATP levels, suggesting that LA activated AMPK indirectly. Adenosine Triphosphate 61-64 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 102-106 23500383-10 2013 In conclusion, the current study suggests that LA suppressed hepatic triglyceride accumulation through modulation of AMPK-SREBP signaling pathway and thus LA may be a potential therapeutic agent for treating fatty liver disease. Triglycerides 69-81 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 117-121 23364526-8 2013 We conclude that the exercise-induced increase in p53 phosphorylation is enhanced in conditions of reduced CHO availability, which may be related to upstream signaling through AMPK. CAV protocol 107-110 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 176-180 23238993-5 2013 Furthermore, CP-31398 and RITA regulate the axis SESN1-2/AMPK/mTOR by inducing AMPK phosphorylation on Thr172, which has a crucial role in the autophagic response. CP 31398 13-21 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 57-61 23238993-5 2013 Furthermore, CP-31398 and RITA regulate the axis SESN1-2/AMPK/mTOR by inducing AMPK phosphorylation on Thr172, which has a crucial role in the autophagic response. CP 31398 13-21 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 79-83 23349077-1 2013 SCOPE: Increasing evidence indicates that polyphenols may protect against metabolic disease through activating AMP-activated protein kinase (AMPK). Polyphenols 42-53 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 141-145 22976217-11 2013 Phosphorylation of AMPK (Thr(172)) decreased during both treatments (both p = 0.001). Threonine 25-28 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 19-23 23288553-1 2013 The extremely high energy demand elicited by sprint exercise is satisfied by an increase in O2 consumption combined with a high glycolytic rate, leading to a marked lactate accumulation, increased AMP-to-ATP ratio, and reduced NAD(+)/NADH.H(+) and muscle pH, which are accompanied by marked Thr(172) AMP-activated protein kinase (AMPK)-alpha phosphorylation during the recovery period by a mechanism not fully understood. Oxygen 92-94 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 330-334 23288553-7 2013 Ser(485)-AMPKalpha1/Ser(491)-AMPKalpha2 phosphorylation, a known inhibitory mechanism of Thr(172)-AMPKalpha phosphorylation, was increased only with antioxidant ingestion. Serine 0-3 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 9-19 23288553-7 2013 Ser(485)-AMPKalpha1/Ser(491)-AMPKalpha2 phosphorylation, a known inhibitory mechanism of Thr(172)-AMPKalpha phosphorylation, was increased only with antioxidant ingestion. Serine 20-23 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 9-19 23288553-7 2013 Ser(485)-AMPKalpha1/Ser(491)-AMPKalpha2 phosphorylation, a known inhibitory mechanism of Thr(172)-AMPKalpha phosphorylation, was increased only with antioxidant ingestion. Threonine 89-92 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 9-19 23277190-8 2013 In cardiomyocytes exposed to 1nM CT-1 there was also reduced phosphorylation of Akt and AS160 in response to insulin, and of AMPK in response to oligomycin. Oligomycins 145-155 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 125-129 23277190-11 2013 Most importantly, basal and oligomycin-stimulated phosphorylation of AMPK was markedly increased in cardiomyocytes exposed to 10nM CT-1. Oligomycins 28-38 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 69-73 23277190-12 2013 The enhancement of basal and stimulated-glucose transport was abolished in cardiomyocytes treated with the calmodulin-dependent kinase II (CaMKII) inhibitor KN93, and so was AMPK phosphorylation. Glucose 40-47 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 174-178 23349077-8 2013 CONCLUSION: These results indicate that CDCQ prevented lipid accumulation by blocking the expression of SREBP-1c and FAS through LKB1/SIRT1 and AMPK activation in HepG2 cells, suggesting that CDCQ plays a potential role in the prevention of lipogenesis by AMPK activation. 3-caffeoyl-4-dihydrocaffeoylquinic acid 40-44 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 144-148 23349077-8 2013 CONCLUSION: These results indicate that CDCQ prevented lipid accumulation by blocking the expression of SREBP-1c and FAS through LKB1/SIRT1 and AMPK activation in HepG2 cells, suggesting that CDCQ plays a potential role in the prevention of lipogenesis by AMPK activation. 3-caffeoyl-4-dihydrocaffeoylquinic acid 40-44 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 256-260 23147595-6 2013 Depleting cellular geranylgeranyl diphosphate activates AMPK and inactivates TOR, leading to autophagic responses. geranylgeranyl pyrophosphate 19-45 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 56-60 23525626-0 2013 beta-Lapachone, a substrate of NAD(P)H:quinone oxidoreductase, induces anti-inflammatory heme oxygenase-1 via AMP-activated protein kinase activation in RAW264.7 macrophages. beta-lapachone 0-14 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 110-138 23525626-3 2013 beta-Lapachone (BL), a well-known substrate of NAD(P)H:quinone oxidoreductase (NQO1), has been demonstrated to stimulate AMPK activation via NQO1 activation, and to exert anti-inflammatory effects in macrophages. beta-lapachone 0-14 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 121-125 23525626-3 2013 beta-Lapachone (BL), a well-known substrate of NAD(P)H:quinone oxidoreductase (NQO1), has been demonstrated to stimulate AMPK activation via NQO1 activation, and to exert anti-inflammatory effects in macrophages. beta-lapachone 16-18 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 121-125 23525626-6 2013 5-Aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside, an AMPK activator, also induced HO-1 expression. acadesine 0-54 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 59-63 23349077-7 2013 Moreover, the use of both a specific inhibitor and liver kinase B1 (LKB1)-siRNA transfected HepG2 cells showed that CDCQ activated AMPK via silent information regulator T1 (SIRT1) or LKB1 in HepG2 cells. 3-caffeoyl-4-dihydrocaffeoylquinic acid 116-120 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 131-135 23291169-4 2013 In this study, we found that an activated AMP-activated protein kinase (AMPK) phosphorylates CtBP1 on Ser-158 upon metabolic stresses. Serine 102-105 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 42-70 22789749-2 2013 AMPK is an intracellular energy sensor that switches off ATP-consuming pathways and switches on ATP-producing pathways such as glucose uptake and fatty acid oxidation. Adenosine Triphosphate 57-60 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 22789749-2 2013 AMPK is an intracellular energy sensor that switches off ATP-consuming pathways and switches on ATP-producing pathways such as glucose uptake and fatty acid oxidation. Adenosine Triphosphate 96-99 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 22789749-2 2013 AMPK is an intracellular energy sensor that switches off ATP-consuming pathways and switches on ATP-producing pathways such as glucose uptake and fatty acid oxidation. Glucose 127-134 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 22789749-2 2013 AMPK is an intracellular energy sensor that switches off ATP-consuming pathways and switches on ATP-producing pathways such as glucose uptake and fatty acid oxidation. Fatty Acids 146-156 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 22789749-9 2013 These mechanisms include (1) ghrelin stimulation of AMPK in NPY/AgRP in the arcuate nucleus (2) ghrelin stimulation of AMPK in the ventromedial hypothalamic nucleus, (3) a novel ghrelin-stimulated AMPK-dependent presynaptic mechanism that sustains AgRP neuron firing via a local synaptic memory system, (4) adiponectin stimulation of hypothalamic AMPK and (5) hypothalamic AMPK control of energy expenditure by thyroid hormone or leptin. Ghrelin 29-36 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 52-56 22789749-9 2013 These mechanisms include (1) ghrelin stimulation of AMPK in NPY/AgRP in the arcuate nucleus (2) ghrelin stimulation of AMPK in the ventromedial hypothalamic nucleus, (3) a novel ghrelin-stimulated AMPK-dependent presynaptic mechanism that sustains AgRP neuron firing via a local synaptic memory system, (4) adiponectin stimulation of hypothalamic AMPK and (5) hypothalamic AMPK control of energy expenditure by thyroid hormone or leptin. Ghrelin 96-103 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 119-123 22789749-9 2013 These mechanisms include (1) ghrelin stimulation of AMPK in NPY/AgRP in the arcuate nucleus (2) ghrelin stimulation of AMPK in the ventromedial hypothalamic nucleus, (3) a novel ghrelin-stimulated AMPK-dependent presynaptic mechanism that sustains AgRP neuron firing via a local synaptic memory system, (4) adiponectin stimulation of hypothalamic AMPK and (5) hypothalamic AMPK control of energy expenditure by thyroid hormone or leptin. Ghrelin 96-103 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 119-123 22789749-9 2013 These mechanisms include (1) ghrelin stimulation of AMPK in NPY/AgRP in the arcuate nucleus (2) ghrelin stimulation of AMPK in the ventromedial hypothalamic nucleus, (3) a novel ghrelin-stimulated AMPK-dependent presynaptic mechanism that sustains AgRP neuron firing via a local synaptic memory system, (4) adiponectin stimulation of hypothalamic AMPK and (5) hypothalamic AMPK control of energy expenditure by thyroid hormone or leptin. Ghrelin 96-103 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 119-123 22789749-9 2013 These mechanisms include (1) ghrelin stimulation of AMPK in NPY/AgRP in the arcuate nucleus (2) ghrelin stimulation of AMPK in the ventromedial hypothalamic nucleus, (3) a novel ghrelin-stimulated AMPK-dependent presynaptic mechanism that sustains AgRP neuron firing via a local synaptic memory system, (4) adiponectin stimulation of hypothalamic AMPK and (5) hypothalamic AMPK control of energy expenditure by thyroid hormone or leptin. Ghrelin 96-103 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 119-123 22789749-9 2013 These mechanisms include (1) ghrelin stimulation of AMPK in NPY/AgRP in the arcuate nucleus (2) ghrelin stimulation of AMPK in the ventromedial hypothalamic nucleus, (3) a novel ghrelin-stimulated AMPK-dependent presynaptic mechanism that sustains AgRP neuron firing via a local synaptic memory system, (4) adiponectin stimulation of hypothalamic AMPK and (5) hypothalamic AMPK control of energy expenditure by thyroid hormone or leptin. Ghrelin 96-103 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 119-123 22789749-9 2013 These mechanisms include (1) ghrelin stimulation of AMPK in NPY/AgRP in the arcuate nucleus (2) ghrelin stimulation of AMPK in the ventromedial hypothalamic nucleus, (3) a novel ghrelin-stimulated AMPK-dependent presynaptic mechanism that sustains AgRP neuron firing via a local synaptic memory system, (4) adiponectin stimulation of hypothalamic AMPK and (5) hypothalamic AMPK control of energy expenditure by thyroid hormone or leptin. Ghrelin 96-103 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 119-123 22789749-9 2013 These mechanisms include (1) ghrelin stimulation of AMPK in NPY/AgRP in the arcuate nucleus (2) ghrelin stimulation of AMPK in the ventromedial hypothalamic nucleus, (3) a novel ghrelin-stimulated AMPK-dependent presynaptic mechanism that sustains AgRP neuron firing via a local synaptic memory system, (4) adiponectin stimulation of hypothalamic AMPK and (5) hypothalamic AMPK control of energy expenditure by thyroid hormone or leptin. Ghrelin 96-103 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 119-123 22789749-9 2013 These mechanisms include (1) ghrelin stimulation of AMPK in NPY/AgRP in the arcuate nucleus (2) ghrelin stimulation of AMPK in the ventromedial hypothalamic nucleus, (3) a novel ghrelin-stimulated AMPK-dependent presynaptic mechanism that sustains AgRP neuron firing via a local synaptic memory system, (4) adiponectin stimulation of hypothalamic AMPK and (5) hypothalamic AMPK control of energy expenditure by thyroid hormone or leptin. Ghrelin 96-103 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 119-123 23291169-4 2013 In this study, we found that an activated AMP-activated protein kinase (AMPK) phosphorylates CtBP1 on Ser-158 upon metabolic stresses. Serine 102-105 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 72-76 23201261-5 2013 Taken together, data from this study reveal a novel mechanism in controlling MNNG-mediated autophagy via AMPK activation downstream of PARP-1 activation and ATP depletion. Adenosine Triphosphate 157-160 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 105-109 22704782-5 2013 CLA isomers showed synergistic effects with the AMPK activator, 5-aminoimidazole-4-carboxamide-1-beta-d-ribonucleoside (AICAR). Linoleic Acids, Conjugated 0-3 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 48-52 22704782-5 2013 CLA isomers showed synergistic effects with the AMPK activator, 5-aminoimidazole-4-carboxamide-1-beta-d-ribonucleoside (AICAR). 5-aminoimidazole-4-carboxamide-1-beta-d-ribonucleoside 64-118 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 48-52 22704782-5 2013 CLA isomers showed synergistic effects with the AMPK activator, 5-aminoimidazole-4-carboxamide-1-beta-d-ribonucleoside (AICAR). acadesine 120-125 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 48-52 22704782-6 2013 Blocking PI3-kinase and AMPK prevented the stimulatory effects of t10,c12-CLA on AS160 phosphorylation and glucose uptake, indicating that this isomer acts via a PI3-kinase and AMPK-dependent mechanism, whereas the mechanism of c9,t11-CLA remains unclear. Glucose 107-114 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 24-28 21676631-8 2013 Further study revealed metformin induced the activation of AMP-activated protein kinase (AMPK), and inhibited mammalian target of rapamycin (mTOR), which is a central regulator of protein synthesis and cell growth, and negatively regulated by AMPK. Metformin 23-32 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 59-87 21676631-8 2013 Further study revealed metformin induced the activation of AMP-activated protein kinase (AMPK), and inhibited mammalian target of rapamycin (mTOR), which is a central regulator of protein synthesis and cell growth, and negatively regulated by AMPK. Metformin 23-32 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 89-93 21676631-8 2013 Further study revealed metformin induced the activation of AMP-activated protein kinase (AMPK), and inhibited mammalian target of rapamycin (mTOR), which is a central regulator of protein synthesis and cell growth, and negatively regulated by AMPK. Metformin 23-32 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 243-247 23192487-6 2013 In contrast with the diabetic non-treated hearts, the diabetic hearts treated with metformin showed more organized and elongated mitochondria and demonstrated a significant increase in phosphorylated AMPK and in PGC-1alpha expression. Metformin 83-92 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 200-204 23122079-0 2013 Phillyrin attenuates high glucose-induced lipid accumulation in human HepG2 hepatocytes through the activation of LKB1/AMP-activated protein kinase-dependent signalling. phillyrin 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 119-147 23332761-4 2013 AMPK inhibits the nonautophagy Vps34 complex by phosphorylating T163/S165 in Vps34 and therefore suppresses overall PI(3)P production and protects cells from starvation. 1,2-dipalmitoyl-sn-glycero-3-phospho-(1'D-myo-inositol-3'-phosphate) 116-122 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 23122079-5 2013 Moreover, use of the pharmacological AMP-activated protein kinase (AMPK) inhibitor compound C revealed that AMPK is essential for suppressing SREBP-1c expression in phillyrin-treated cells. phillyrin 165-174 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 37-65 23122079-5 2013 Moreover, use of the pharmacological AMP-activated protein kinase (AMPK) inhibitor compound C revealed that AMPK is essential for suppressing SREBP-1c expression in phillyrin-treated cells. phillyrin 165-174 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 67-71 23122079-5 2013 Moreover, use of the pharmacological AMP-activated protein kinase (AMPK) inhibitor compound C revealed that AMPK is essential for suppressing SREBP-1c expression in phillyrin-treated cells. phillyrin 165-174 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 108-112 23122079-6 2013 Finally, we found that liver kinase B1 (LKB1) phosphorylation is required for the phillyrin-enhanced activation of AMPK in HepG2 hepatocytes. phillyrin 82-91 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 115-119 23143974-11 2013 Moreover, we found that the central metabolic checkpoint LKB1/AMPK-a cellular sensor of ATP levels that supports cell viability in response to energy stress-is activated by anti-VEGF therapy in experimental tumors and it has a key role in induction of sustained tumor regression. Adenosine Triphosphate 88-91 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 62-66 23116132-4 2013 It is commonly accepted that glucose inhibits autophagy, since its deprivation from cells cultured in full medium induces autophagy by a mechanism involving AMPK (AMP-activated protein kinase), mTOR and Ulk1. Glucose 29-36 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 163-191 23116132-8 2013 Moreover, we also show that, surprisingly, the induction of autophagy by glucose is independent of AMPK and mTOR and mainly relies on p38 MAPK (mitogen-activated protein kinase). Glucose 73-80 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 99-103 23344047-9 2013 Bufalin treatment dose-dependently promoted AMPK phosphorylation while AMPK inhibition by compound C significantly attenuated bufalin-induced autophagy. bufalin 0-7 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 44-48 23344047-9 2013 Bufalin treatment dose-dependently promoted AMPK phosphorylation while AMPK inhibition by compound C significantly attenuated bufalin-induced autophagy. bufalin 127-134 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 71-75 23344047-10 2013 Taken together, we report for the first time that bufalin induces HepG2 cells PCD, especially for autophagy, and the mechanism of action is, at least in part, AMPK-mTOR dependent. bufalin 50-57 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 159-163 23991948-2 2013 Besides the discovery of somatic mutations in the LKB1 gene in certain type of cancers, a critical emerging point was that the LKB1/AMPK axis remains generally functional and could be stimulated by pharmacological molecules such as metformin in cancer cells. Metformin 232-241 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 132-136 23302650-0 2013 An ent-kaurane diterpenoid from Croton tonkinensis induces apoptosis by regulating AMP-activated protein kinase in SK-HEP1 human hepatocellular carcinoma cells. Diterpenes, Kaurane 7-14 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 83-111 23302650-0 2013 An ent-kaurane diterpenoid from Croton tonkinensis induces apoptosis by regulating AMP-activated protein kinase in SK-HEP1 human hepatocellular carcinoma cells. Diterpenes 15-26 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 83-111 23302650-6 2013 In this study, we determined whether the ent-kaurane diterpenoid ent-18-acetoxy-7beta-hydroxy kaur-15-oxo-16-ene (CrT1) isolated from this plant plays a role as a chemotherapeutic drug targeting AMPK. Diterpenes, Kaurane 41-52 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 195-199 23302650-6 2013 In this study, we determined whether the ent-kaurane diterpenoid ent-18-acetoxy-7beta-hydroxy kaur-15-oxo-16-ene (CrT1) isolated from this plant plays a role as a chemotherapeutic drug targeting AMPK. Diterpenes 53-64 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 195-199 23302650-6 2013 In this study, we determined whether the ent-kaurane diterpenoid ent-18-acetoxy-7beta-hydroxy kaur-15-oxo-16-ene (CrT1) isolated from this plant plays a role as a chemotherapeutic drug targeting AMPK. ent-18-acetoxy-7beta-hydroxy kaur-15-oxo-16-ene 65-112 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 195-199 23302650-12 2013 We showed that CrT1-activated AMPK activation was followed by modulating the mammalian target of rapamycin/p70S6K pathway and was inactivated by treating cells with compound C. Treatment with CrT1 and aminoimidazole carboxamide ribonucleotide (AICAR) synergistically activated AMPK. AICA ribonucleotide 201-242 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-34 23302650-12 2013 We showed that CrT1-activated AMPK activation was followed by modulating the mammalian target of rapamycin/p70S6K pathway and was inactivated by treating cells with compound C. Treatment with CrT1 and aminoimidazole carboxamide ribonucleotide (AICAR) synergistically activated AMPK. AICA ribonucleotide 244-249 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 30-34 23041548-2 2012 Prior studies suggest that the primary action of metformin is inhibition of oxidative phosphorylation, resulting in reduced mitochondrial ATP production and activation of AMPK. Metformin 49-58 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 171-175 24048094-0 2013 Curcumin induces autophagy via activating the AMPK signaling pathway in lung adenocarcinoma cells. Curcumin 0-8 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 46-50 24048094-6 2013 Curcumin markedly increased the phosphorylation of AMP-activated protein kinase (AMPK) and acetylCoA carboxylase in A549 cells. Curcumin 0-8 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 81-85 24048094-7 2013 At last, pharmacological blockade of the AMPK signaling pathway by compound C and genetic disruption of the AMPK signaling pathway with siRNA-mediated AMPKalpha1 knockdown impaired the autophagy-inducing effect of curcumin. Curcumin 214-222 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 41-45 24048094-7 2013 At last, pharmacological blockade of the AMPK signaling pathway by compound C and genetic disruption of the AMPK signaling pathway with siRNA-mediated AMPKalpha1 knockdown impaired the autophagy-inducing effect of curcumin. Curcumin 214-222 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 108-112 24048094-7 2013 At last, pharmacological blockade of the AMPK signaling pathway by compound C and genetic disruption of the AMPK signaling pathway with siRNA-mediated AMPKalpha1 knockdown impaired the autophagy-inducing effect of curcumin. Curcumin 214-222 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 151-161 24048094-8 2013 Collectively, our data suggests that curcumin induces autophagy via activating the AMPK signaling pathway and the autophagy is important for the inhibiting effect of curcumin in lung adenocarcinoma cells. Curcumin 37-45 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 83-87 24385682-0 2013 Berberine protects against palmitate-induced endothelial dysfunction: involvements of upregulation of AMPK and eNOS and downregulation of NOX4. Berberine 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 102-106 22960274-0 2013 ATM and LKB1 dependent activation of AMPK sensitizes cancer cells to etoposide-induced apoptosis. Etoposide 69-78 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 37-41 22960274-1 2013 The present study aims to determine the effect of AMPK on etoposide-induced apoptosis of cancer cells. Etoposide 58-67 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 50-54 22960274-2 2013 Our results revealed that etoposide induced AMPK activation in prostate C4-2 cancer cells, an event that was attenuated by ATM siRNA. Etoposide 26-35 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 44-48 22960274-5 2013 Finally, etoposide displayed a potent pro-apoptotic effect in cancer cells with functional LKB1 and AMPK. Etoposide 9-18 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 100-104 23323614-5 2013 AMPK is insulin mimetic in many of its actions like glucose uptake and inhibition of lipolysis, and these properties of AMPK are made used in conditions like insulin resistance and diabetes. Glucose 52-59 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 0-4 23323614-6 2013 Nevertheless, if AMPK is activated by GC in the absence of diabetes or decreased insulin signaling, accumulation of substrates in the form of glycogen and triglycerides could precipitate cardiac abnormalities. Glycogen 142-150 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 17-21 23323614-6 2013 Nevertheless, if AMPK is activated by GC in the absence of diabetes or decreased insulin signaling, accumulation of substrates in the form of glycogen and triglycerides could precipitate cardiac abnormalities. Triglycerides 155-168 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 17-21 23573117-7 2013 QHD supplementation reversed the FFA-induced decrease in the phosphorylation levels of AMPK and ACC and decreased the hepatic nuclear protein expression of SREBP-1 and ChREBP. Fatty Acids, Nonesterified 33-36 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 87-91 24385682-0 2013 Berberine protects against palmitate-induced endothelial dysfunction: involvements of upregulation of AMPK and eNOS and downregulation of NOX4. Palmitates 27-36 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 102-106 24385682-10 2013 Moreover, berberine upregulated the protein expression of AMPK and p-AMPK in palmitate-treated HUVECs, but had no effect on the levels of Akt. Berberine 10-19 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 58-62 24385682-10 2013 Moreover, berberine upregulated the protein expression of AMPK and p-AMPK in palmitate-treated HUVECs, but had no effect on the levels of Akt. Berberine 10-19 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 69-73 24385682-10 2013 Moreover, berberine upregulated the protein expression of AMPK and p-AMPK in palmitate-treated HUVECs, but had no effect on the levels of Akt. Palmitates 77-86 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 58-62 24385682-10 2013 Moreover, berberine upregulated the protein expression of AMPK and p-AMPK in palmitate-treated HUVECs, but had no effect on the levels of Akt. Palmitates 77-86 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 69-73 24385682-12 2013 This regulatory effect of berberine may be related to the activation of AMPK. Berberine 26-35 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 72-76 23525940-1 2012 The gerosuppressant metformin operates as an efficient inhibitor of the mTOR/S6K1 gerogenic pathway due to its ability to ultimately activate the energy-sensor AMPK. Metformin 20-29 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 160-164 23525940-2 2012 If an aging-related decline in the AMPK sensitivity to cellular stress is a crucial event for mTOR-driven aging and aging-related diseases, including cancer, unraveling new proximal causes through which AMPK activation endows its gerosuppressive effects may offer not only a better understanding of metformin function but also the likely possibility of repositioning our existing gerosuppressant drugs. Metformin 299-308 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 35-39 23525940-2 2012 If an aging-related decline in the AMPK sensitivity to cellular stress is a crucial event for mTOR-driven aging and aging-related diseases, including cancer, unraveling new proximal causes through which AMPK activation endows its gerosuppressive effects may offer not only a better understanding of metformin function but also the likely possibility of repositioning our existing gerosuppressant drugs. Metformin 299-308 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 203-207 23103546-0 2012 Nanosecond pulsed electric fields activate AMP-activated protein kinase: implications for calcium-mediated activation of cellular signaling. Calcium 90-97 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 43-71 22968630-7 2012 These results suggest that NYGGF4 plays a role in IR and its effects on IR could be reversed by metformin through activating IRS-1/PI3K/Akt and AMPK-PGC1-alpha pathways. Metformin 96-105 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 144-148 23063129-7 2012 Intriguingly, activation of the Smo-Ampk axis in vivo drives robust insulin-independent glucose uptake in muscle and brown adipose tissue. Glucose 88-95 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 36-40 22846543-0 2012 Wogonin induces apoptosis by activating the AMPK and p53 signaling pathways in human glioblastoma cells. wogonin 0-7 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 44-48 23102217-5 2012 Indeed, AMPK is activated by the drugs metformin and salicylate, the latter being the major breakdown product of aspirin. Metformin 39-48 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 8-12 23102217-5 2012 Indeed, AMPK is activated by the drugs metformin and salicylate, the latter being the major breakdown product of aspirin. Salicylates 53-63 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 8-12 23102217-5 2012 Indeed, AMPK is activated by the drugs metformin and salicylate, the latter being the major breakdown product of aspirin. Aspirin 113-120 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 8-12 22674626-1 2012 BACKGROUND AND OBJECTIVES: AMP-activated protein kinase (AMPK) is a main regulator of energy metabolism through the inhibition of biosynthetic pathways and enhancement of ATP-generating pathways. Adenosine Triphosphate 171-174 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 27-55 22674626-1 2012 BACKGROUND AND OBJECTIVES: AMP-activated protein kinase (AMPK) is a main regulator of energy metabolism through the inhibition of biosynthetic pathways and enhancement of ATP-generating pathways. Adenosine Triphosphate 171-174 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 57-61 23285817-8 2012 Furthermore, 1,5-AF increased the levels of reactive oxygen species, an important upstream signal for AMPK activation in 3T3-L1 adipocytes. 1,5-anhydrofructose 13-19 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 102-106 23285817-8 2012 Furthermore, 1,5-AF increased the levels of reactive oxygen species, an important upstream signal for AMPK activation in 3T3-L1 adipocytes. Reactive Oxygen Species 44-67 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 102-106 23676995-3 2012 These findings suggest that physiological activation of AMPK is critical for tumor growth/migration, possibly through maintenance of ATP levels. Adenosine Triphosphate 133-136 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 56-60 23676995-4 2012 Our recent study provides the first evidence that the maintenance of cellular NADPH homeostasis is the predominant mechanism by which AMPK promotes tumor cell survival and solid tumor formation. NADP 78-83 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 134-138 23676995-5 2012 We showed that AMPK activation is required to maintain intracellular NADPH levels through the activation of fatty acid oxidation (FAO) or the inhibition of fatty acid synthesis (FAS) during glucose deprivation or matrix detachment respectively. NADP 69-74 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 15-19 23676995-5 2012 We showed that AMPK activation is required to maintain intracellular NADPH levels through the activation of fatty acid oxidation (FAO) or the inhibition of fatty acid synthesis (FAS) during glucose deprivation or matrix detachment respectively. Fatty Acids 108-118 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 15-19 23676995-5 2012 We showed that AMPK activation is required to maintain intracellular NADPH levels through the activation of fatty acid oxidation (FAO) or the inhibition of fatty acid synthesis (FAS) during glucose deprivation or matrix detachment respectively. fao 130-133 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 15-19 23676995-5 2012 We showed that AMPK activation is required to maintain intracellular NADPH levels through the activation of fatty acid oxidation (FAO) or the inhibition of fatty acid synthesis (FAS) during glucose deprivation or matrix detachment respectively. Fatty Acids 156-166 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 15-19 23676995-5 2012 We showed that AMPK activation is required to maintain intracellular NADPH levels through the activation of fatty acid oxidation (FAO) or the inhibition of fatty acid synthesis (FAS) during glucose deprivation or matrix detachment respectively. fas 178-181 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 15-19 23676995-6 2012 Through these processes AMPK activation inhibits the rise in reactive oxygen species (ROS) levels and promotes metabolic adaptation in response to metabolic stress. Reactive Oxygen Species 61-84 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 24-28 23676995-6 2012 Through these processes AMPK activation inhibits the rise in reactive oxygen species (ROS) levels and promotes metabolic adaptation in response to metabolic stress. Reactive Oxygen Species 86-89 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 24-28 22943849-0 2012 Berberine inhibits human colon cancer cell migration via AMP-activated protein kinase-mediated downregulation of integrin beta1 signaling. Berberine 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 57-85 22943849-5 2012 Among the various cellular targets of berberine is AMP-activated protein kinase (AMPK), which regulates tumor progression and metastasis. Berberine 38-47 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 51-79 22943849-5 2012 Among the various cellular targets of berberine is AMP-activated protein kinase (AMPK), which regulates tumor progression and metastasis. Berberine 38-47 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 81-85 22943849-6 2012 However, the specific role of berberine-induced AMPK activation and its effects on the metastatic potential of colon cancer remain largely unknown. Berberine 30-39 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 48-52 22943849-7 2012 The present study investigated berberine-induced activation of AMPK and its effects on colon cancer cell migration. Berberine 31-40 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 63-67 22943849-9 2012 We found that berberine activated AMPK in human colon cancer cell lines. Berberine 14-23 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 34-38 22943849-10 2012 Notably, berberine-induced activation of AMPK reduced the integrin beta1 protein levels and decreased the phosphorylation of integrin beta1 signaling targets. Berberine 9-18 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 41-45 22943849-11 2012 Knockdown of AMPKalpha1 subunits using small interfering RNA significantly attenuated berberine-induced downregulation of integrin beta1 and inhibition of tumor cell migration. Berberine 86-95 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 13-23 22943849-12 2012 Collectively, our results suggest that berberine-induced AMPK activation inhibits the metastatic potential of colon cancer cells by decreasing integrin beta1 protein levels and downstream signaling. Berberine 39-48 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 57-61