PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 12747837-2 2003 Furthermore, metformin and rosiglitazone, frontline drugs used for the treatment of type II diabetes, activate AMPK. Metformin 13-22 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 111-115 33768205-2 2020 Therapeutic activation of AMPK by metformin could inhibit cyst enlargement by inhibition of both the mammalian target of rapamycin pathway and fluid secretion via the CFTR chloride channel. Metformin 34-43 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 26-30 33811249-3 2021 The antidiabetic drug metformin, a well-known activator of AMPK, has improved stroke outcomes in diabetic patients with normal renal function. Metformin 22-31 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 59-63 33811249-4 2021 We investigated whether chronic metformin pre-conditioning can rescue AMPK activity and prevent stroke damage in non-diabetic mice with CKD. Metformin 32-41 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 70-74 34772914-8 2021 Activation of AMPK using metformin reversed the EMT program and impaired the metastatic capacity of FATP5-depleted HCC cells. Metformin 25-34 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 14-18 34450310-5 2021 Here, the progression of lung fibroblast proliferation and the expression levels of AMPK and FOXM1 were observed by intratracheally instilled of bleomycin (BLM) and intraperitoneal injection of metformin in C57BL/6J mice. Metformin 194-203 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 84-88 34593558-4 2021 IM156 significantly increased cellular AMPK phosphorylation and was 60-fold more potent than metformin. Metformin 93-102 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 39-43 34450310-0 2021 Activated AMPK by metformin protects against fibroblast proliferation during pulmonary fibrosis by suppressing FOXM1. Metformin 18-27 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 10-14 34517004-0 2021 Metformin attenuates the epithelial-mesenchymal transition of lens epithelial cells through the AMPK/TGF-beta/Smad2/3 signalling pathway. Metformin 0-9 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 96-100 34450310-6 2021 Meanwhile, human fetal lung fibroblast1 (HFL1) cells were respectively treated with AMPK activator metformin or AMPK inhibitor Compound C, or FOXM1 depletion by transfected small interfering RNA (siRNA) to unveil roles of AMPK, FOXM1 and the link between them on platelet-derived growth factor (PDGF)-induced fibroblast proliferation. Metformin 99-108 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 84-88 34450310-7 2021 Our results demonstrated that AMPK activated by metformin could down-regulate FOXM1 and alleviate BLM-induced mouse PF model. Metformin 48-57 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 30-34 34548527-5 2021 Here, we show that metformin alters the acute inflammatory response through its activation of AMP-activated protein kinase (AMPK), but independently of HIF1-alpha and IL-10, in primary macrophages and two macrophage-like cell lines. Metformin 19-28 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 94-122 34396446-0 2021 Metformin inhibits cholesterol-induced adhesion molecule expression via activating the AMPK signaling pathway in vascular smooth muscle cells. Metformin 0-9 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 87-91 34396446-10 2021 Metformin decreased cholesterol-induced VSMC damage by activating the AMPK signaling pathway, and suppressing p38 MAPK and NF-kappaB signaling. Metformin 0-9 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 70-74 34588803-3 2021 Among these, in this review, we will examine above all the role of metformin, hypothesized to be able to activate the AMP-activated protein kinase (AMPK) pathway and potentially modulate some mechanisms implicated in the onset and the growth of the cysts. Metformin 67-76 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 118-146 34588803-3 2021 Among these, in this review, we will examine above all the role of metformin, hypothesized to be able to activate the AMP-activated protein kinase (AMPK) pathway and potentially modulate some mechanisms implicated in the onset and the growth of the cysts. Metformin 67-76 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 148-152 34548527-0 2021 Metformin selectively dampens the acute inflammatory response through an AMPK-dependent mechanism. Metformin 0-9 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 73-77 34548527-5 2021 Here, we show that metformin alters the acute inflammatory response through its activation of AMP-activated protein kinase (AMPK), but independently of HIF1-alpha and IL-10, in primary macrophages and two macrophage-like cell lines. Metformin 19-28 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 124-128 34577590-6 2021 Metformin, a first line antihyperglycemic medication, is a 5"-adenosine monophosphate (AMP)-activated protein kinase (AMPK) activator hypothesized to act as a geroprotective agent. Metformin 0-9 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 118-122 34296521-0 2021 Metformin alleviates oxidative stress-induced senescence of human lens epithelial cells via AMPK activation and autophagic flux restoration. Metformin 0-9 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 92-96 34296521-4 2021 In addition, we showed that metformin alleviated the oxidative stress-induced senescence of HLE-B3 cells via the activation of AMPK. Metformin 28-37 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 127-131 34296521-6 2021 Subsequently, we found that metformin restored autophagic flux that had been impaired by oxidative stress by activating AMPK. Metformin 28-37 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 120-124 34290400-2 2021 To date most of the anti-cancer properties of metformin have, in large part, been attributed either to the inhibition of mitochondrial NADH oxidase complex (Complex I in the electron transport chain) or the activation of AMP-activated kinase (AMPK). Metformin 46-55 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 221-241 34290400-2 2021 To date most of the anti-cancer properties of metformin have, in large part, been attributed either to the inhibition of mitochondrial NADH oxidase complex (Complex I in the electron transport chain) or the activation of AMP-activated kinase (AMPK). Metformin 46-55 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 243-247 34290400-3 2021 However, it is becoming increasingly clear that AMPK activation may be critical to alleviate metabolic and energetic stresses associated with tumor progression suggesting that it may, in fact, attenuate the toxicity of metformin instead of promoting it. Metformin 219-228 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 48-52 34290400-5 2021 We also found that metformin forces cells to rewire their metabolic grid in a manner that depends on AMPK, with AMPK-competent cells upregulating glycolysis and AMPK-deficient cell resorting to ketogenesis. Metformin 19-28 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 101-105 34290400-5 2021 We also found that metformin forces cells to rewire their metabolic grid in a manner that depends on AMPK, with AMPK-competent cells upregulating glycolysis and AMPK-deficient cell resorting to ketogenesis. Metformin 19-28 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 112-116 34577590-9 2021 Moreover, it has been recently demonstrated that metformin enhances synaptophysin, sirtuin-1, AMPK, and brain-derived neuronal factor (BDNF) immunoreactivity, which are essential markers of plasticity. Metformin 49-58 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 94-98 34434111-8 2021 These results suggest that metformin could inhibit silica-induced pulmonary fibrosis by activating autophagy through the AMPK-mTOR pathway. Metformin 27-36 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 121-125 34502359-0 2021 New Insight into the Effects of Metformin on Diabetic Retinopathy, Aging and Cancer: Nonapoptotic Cell Death, Immunosuppression, and Effects beyond the AMPK Pathway. Metformin 32-41 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 152-156 34502359-3 2021 At the molecular level, the most well-known mechanism of metformin-mediated cytoprotection is AMPK pathway activation, which modulates metabolism and protects cells from degradation or pathogenic changes, such as those related to aging and diabetic retinopathy (DR). Metformin 57-66 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 94-98 34502359-4 2021 Recently, it has been revealed that metformin acts via AMPK- and non-AMPK-mediated pathways to exert effects beyond those related to diabetes treatment that might prevent aging and ameliorate DR. Metformin 36-45 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 55-59 34502359-4 2021 Recently, it has been revealed that metformin acts via AMPK- and non-AMPK-mediated pathways to exert effects beyond those related to diabetes treatment that might prevent aging and ameliorate DR. Metformin 36-45 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 69-73 34434111-0 2021 Metformin Attenuates Silica-Induced Pulmonary Fibrosis by Activating Autophagy via the AMPK-mTOR Signaling Pathway. Metformin 0-9 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 87-91 34163481-3 2021 The mechanisms by which metformin regulates the function of macrophages include AMPK, AMPK independent targets, NF-kappaB, ABCG5/8, Sirt1, FOXO1/FABP4 and HMGB1. Metformin 24-33 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 80-84 34434111-7 2021 Besides, metformin increased the expression levels of phosphorylated adenosine 5"-monophosphate (AMP)-activated protein kinase (p-AMPK), microtubule-associated protein (MAP) light chain 3B (LC3B) and Beclin1 proteins, and reduced levels of phosphorylated mammalian target of rapamycin (p-mTOR) and p62 proteins in vivo and in vitro. Metformin 9-18 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 130-134 34188521-12 2021 Conclusion: Two variants rs2727528 and rs1105842 in PRKAG2, encoding gamma2 subunit of AMP-activated protein kinase (AMPK), were found to be associated with metformin response in Chinese T2D patients. Metformin 157-166 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 117-121 34421608-0 2021 Metformin Potentiates the Effects of Anlotinib in NSCLC via AMPK/mTOR and ROS-Mediated Signaling Pathways. Metformin 0-9 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 60-64 34421608-4 2021 Interesting, metformin also exerts broad anticancer effects through the activation of AMP-activated protein kinase (AMPK) and inhibition of mammalian target of rapamycin (mTOR). Metformin 13-22 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 86-114 34421608-4 2021 Interesting, metformin also exerts broad anticancer effects through the activation of AMP-activated protein kinase (AMPK) and inhibition of mammalian target of rapamycin (mTOR). Metformin 13-22 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 116-120 34421608-7 2021 Moreover, anlotinib combined with metformin induced apoptosis and oxidative stress, which was associated with the activation of AMPK and inhibition of mTOR. Metformin 34-43 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 128-132 34115964-4 2021 By targeting electron transport chain complex 1 and independently of AMP-activated protein kinase (AMPK) or NF-kappaB, metformin blocked LPS-induced and ATP-dependent mitochondrial (mt) DNA synthesis and generation of oxidized mtDNA, an NLRP3 ligand. Metformin 119-128 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 99-103 34156429-6 2021 Aside from this, drugs that have been the subject of multiple clinical trials such as metformin, which targets AMPK signalling and somatostatins, which target cAMP signalling have shown great promise in reducing cyst formation and cellular proliferation. Metformin 86-95 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 111-115 34163481-3 2021 The mechanisms by which metformin regulates the function of macrophages include AMPK, AMPK independent targets, NF-kappaB, ABCG5/8, Sirt1, FOXO1/FABP4 and HMGB1. Metformin 24-33 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 86-90 34514769-9 2021 Metformin has been shown to act through both AMP-activated protein kinase (AMPK)-dependent mechanisms and AMPK-independent mechanisms. Metformin 0-9 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 45-73 34514769-9 2021 Metformin has been shown to act through both AMP-activated protein kinase (AMPK)-dependent mechanisms and AMPK-independent mechanisms. Metformin 0-9 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 75-79 34514769-9 2021 Metformin has been shown to act through both AMP-activated protein kinase (AMPK)-dependent mechanisms and AMPK-independent mechanisms. Metformin 0-9 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 106-110 35396800-5 2022 An ecto-enzyme (CD39) antagonist POM1 and AMP-activated protein kinase (AMPK) agonist metformin are both encapsulated into cancer cell-derived exosomes and used as nanocarriers for tumor targeting delivery. Metformin 86-95 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 42-70 35396800-5 2022 An ecto-enzyme (CD39) antagonist POM1 and AMP-activated protein kinase (AMPK) agonist metformin are both encapsulated into cancer cell-derived exosomes and used as nanocarriers for tumor targeting delivery. Metformin 86-95 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 72-76 35459945-3 2022 WHAT IS KNOWN ALREADY: AMPK is expressed in the ovarian follicle, and its activation by pharmacological medications, such as metformin, inhibits the production of steroids. Metformin 125-134 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 23-27 33838541-4 2021 The use of metformin for chemoprevention has been shown to reduce CRC and adenoma incidence through the upregulation of AMPK, which causes cell cycle arrest in the Gap 1-S (G1-S) phase and inhibits the mTOR pathway, even potentially reversing the epithelial-mesenchymal transition. Metformin 11-20 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 120-124 35431946-0 2022 Acute Administration of Metformin Protects Against Neuronal Apoptosis Induced by Cerebral Ischemia-Reperfusion Injury via Regulation of the AMPK/CREB/BDNF Pathway. Metformin 24-33 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 140-144 35431946-5 2022 Moreover, metformin up-regulated the brain-derived neurotrophic factor (BDNF) expression and increased phosphorylation levels of AMP-activated protein kinase (AMPK) and cAMP-response element binding protein (CREB) in the ischemia penumbra. Metformin 10-19 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 129-157 35431946-5 2022 Moreover, metformin up-regulated the brain-derived neurotrophic factor (BDNF) expression and increased phosphorylation levels of AMP-activated protein kinase (AMPK) and cAMP-response element binding protein (CREB) in the ischemia penumbra. Metformin 10-19 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 159-163 35431946-7 2022 Moreover, metformin could further promote BDNF expression and release in HUVECs under OGD/R conditions via the AMPK/CREB pathway. Metformin 10-19 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 111-115 35431946-9 2022 In summary, our results suggest that metformin upregulates the level of BDNF in the cerebral ischemic penumbra via the AMPK/CREB pathway, thereby playing a protective effect in cerebral I/R injury. Metformin 37-46 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 119-123 35134125-7 2022 Finally, systemic administration of metformin, an AMPK agonist and common diabetes treatment, profoundly increased spike-wave seizures. Metformin 36-45 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 50-54 35067907-7 2022 Recent studies have shown that metformin exerts its effects through the inhibition of mitochondrial respiratory chain complex 1 and the AMP-activated protein kinase (AMPK) activation, but it has been identified in the other studies that AMPK is not the sole hub in metformin mode of action or there are other unknown mechanisms which are involved and yet to be explored. Metformin 31-40 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 136-164 35067907-7 2022 Recent studies have shown that metformin exerts its effects through the inhibition of mitochondrial respiratory chain complex 1 and the AMP-activated protein kinase (AMPK) activation, but it has been identified in the other studies that AMPK is not the sole hub in metformin mode of action or there are other unknown mechanisms which are involved and yet to be explored. Metformin 31-40 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 166-170 35067907-7 2022 Recent studies have shown that metformin exerts its effects through the inhibition of mitochondrial respiratory chain complex 1 and the AMP-activated protein kinase (AMPK) activation, but it has been identified in the other studies that AMPK is not the sole hub in metformin mode of action or there are other unknown mechanisms which are involved and yet to be explored. Metformin 31-40 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 237-241 35067907-7 2022 Recent studies have shown that metformin exerts its effects through the inhibition of mitochondrial respiratory chain complex 1 and the AMP-activated protein kinase (AMPK) activation, but it has been identified in the other studies that AMPK is not the sole hub in metformin mode of action or there are other unknown mechanisms which are involved and yet to be explored. Metformin 265-274 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 237-241 35197629-0 2022 Low-dose metformin targets the lysosomal AMPK pathway through PEN2. Metformin 9-18 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 41-45 35197629-2 2022 For clinical doses of metformin, AMP-activated protein kinase (AMPK) has a major role in its mechanism of action4,5; however, the direct molecular target of metformin remains unknown. Metformin 22-31 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 33-61 35197629-2 2022 For clinical doses of metformin, AMP-activated protein kinase (AMPK) has a major role in its mechanism of action4,5; however, the direct molecular target of metformin remains unknown. Metformin 22-31 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 63-67 35197629-2 2022 For clinical doses of metformin, AMP-activated protein kinase (AMPK) has a major role in its mechanism of action4,5; however, the direct molecular target of metformin remains unknown. Metformin 157-166 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 33-61 35197629-2 2022 For clinical doses of metformin, AMP-activated protein kinase (AMPK) has a major role in its mechanism of action4,5; however, the direct molecular target of metformin remains unknown. Metformin 157-166 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 63-67 35197629-3 2022 Here we show that clinically relevant concentrations of metformin inhibit the lysosomal proton pump v-ATPase, which is a central node for AMPK activation following glucose starvation6. Metformin 56-65 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 138-142 35197629-5 2022 Metformin-bound PEN2 forms a complex with ATP6AP1, a subunit of the v-ATPase8, which leads to the inhibition of v-ATPase and the activation of AMPK without effects on cellular AMP levels. Metformin 0-9 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 143-147 35197629-9 2022 Together, these findings reveal that metformin binds PEN2 and initiates a signalling route that intersects, through ATP6AP1, the lysosomal glucose-sensing pathway for AMPK activation. Metformin 37-46 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 167-171 35129424-7 2022 Metformin mainly affected the AMPK and FOXO signaling pathways, whereas vildagliptin affected insulin secretion and the HIF-1 signaling pathway. Metformin 0-9 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 30-34 34046440-6 2021 AMPK activators, like metformin, are associated with reduced calcification deposits in certain groups of patients, indicating that AMPK is a potential therapeutic target for VC. Metformin 22-31 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 0-4 33838154-6 2021 The inhibitory effect of metformin on NFE2L1 was investigated to occur through the N-terminal domain (NTD) of NFE2L1 protein, and its downregulation by metformin was in an AMP-activated protein kinase (AMPK)-independent manner. Metformin 25-34 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 172-200 33838154-6 2021 The inhibitory effect of metformin on NFE2L1 was investigated to occur through the N-terminal domain (NTD) of NFE2L1 protein, and its downregulation by metformin was in an AMP-activated protein kinase (AMPK)-independent manner. Metformin 25-34 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 202-206 33838154-6 2021 The inhibitory effect of metformin on NFE2L1 was investigated to occur through the N-terminal domain (NTD) of NFE2L1 protein, and its downregulation by metformin was in an AMP-activated protein kinase (AMPK)-independent manner. Metformin 152-161 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 172-200 33838154-6 2021 The inhibitory effect of metformin on NFE2L1 was investigated to occur through the N-terminal domain (NTD) of NFE2L1 protein, and its downregulation by metformin was in an AMP-activated protein kinase (AMPK)-independent manner. Metformin 152-161 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 202-206 33838154-7 2021 But the activation of AMPK signaling pathway by metformin in NFE2L1 knockdown HepG2 cells is reversed, indicating that NFE2L1 may be an important regulator of AMPK signal. Metformin 48-57 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 22-26 33838154-7 2021 But the activation of AMPK signaling pathway by metformin in NFE2L1 knockdown HepG2 cells is reversed, indicating that NFE2L1 may be an important regulator of AMPK signal. Metformin 48-57 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 159-163 33850550-0 2021 Metformin attenuates diabetic renal injury via the AMPK-autophagy axis. Metformin 0-9 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 51-55 33850550-10 2021 These findings suggested that metformin may reduce DN damage via regulation of the AMPK-mTOR-autophagy axis and indicated that metformin may be considered as a potential target in the treatment of DN. Metformin 30-39 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 83-87 33850550-10 2021 These findings suggested that metformin may reduce DN damage via regulation of the AMPK-mTOR-autophagy axis and indicated that metformin may be considered as a potential target in the treatment of DN. Metformin 127-136 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 83-87 34043989-10 2021 In suppressing LC progression, anti-tumor compounds including metformin, ginsenosides, casticin and duloxetine dually induce/inhibit AMPK signaling. Metformin 62-71 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 133-137 34046440-6 2021 AMPK activators, like metformin, are associated with reduced calcification deposits in certain groups of patients, indicating that AMPK is a potential therapeutic target for VC. Metformin 22-31 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 131-135 33946426-0 2021 Metformin Dysregulates the Unfolded Protein Response and the WNT/beta-Catenin Pathway in Endometrial Cancer Cells through an AMPK-Independent Mechanism. Metformin 0-9 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 125-129 33524789-6 2021 First, many studies showed that metformin could induce autophagy via a number of signaling pathways, including AMPK-related signaling pathways (e.g. AMPK/mTOR, AMPK/CEBPD, MiTF/TFE, AMPK/ULK1, and AMPK/miR-221), Redd1/mTOR, STAT, SIRT, Na+/H+ exchangers, MAPK/ERK, PK2/PKR/AKT/ GSK3beta, and TRIB3. Metformin 32-41 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 111-115 33524789-6 2021 First, many studies showed that metformin could induce autophagy via a number of signaling pathways, including AMPK-related signaling pathways (e.g. AMPK/mTOR, AMPK/CEBPD, MiTF/TFE, AMPK/ULK1, and AMPK/miR-221), Redd1/mTOR, STAT, SIRT, Na+/H+ exchangers, MAPK/ERK, PK2/PKR/AKT/ GSK3beta, and TRIB3. Metformin 32-41 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 149-153 33524789-6 2021 First, many studies showed that metformin could induce autophagy via a number of signaling pathways, including AMPK-related signaling pathways (e.g. AMPK/mTOR, AMPK/CEBPD, MiTF/TFE, AMPK/ULK1, and AMPK/miR-221), Redd1/mTOR, STAT, SIRT, Na+/H+ exchangers, MAPK/ERK, PK2/PKR/AKT/ GSK3beta, and TRIB3. Metformin 32-41 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 149-153 33524789-6 2021 First, many studies showed that metformin could induce autophagy via a number of signaling pathways, including AMPK-related signaling pathways (e.g. AMPK/mTOR, AMPK/CEBPD, MiTF/TFE, AMPK/ULK1, and AMPK/miR-221), Redd1/mTOR, STAT, SIRT, Na+/H+ exchangers, MAPK/ERK, PK2/PKR/AKT/ GSK3beta, and TRIB3. Metformin 32-41 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 149-153 33524789-6 2021 First, many studies showed that metformin could induce autophagy via a number of signaling pathways, including AMPK-related signaling pathways (e.g. AMPK/mTOR, AMPK/CEBPD, MiTF/TFE, AMPK/ULK1, and AMPK/miR-221), Redd1/mTOR, STAT, SIRT, Na+/H+ exchangers, MAPK/ERK, PK2/PKR/AKT/ GSK3beta, and TRIB3. Metformin 32-41 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 149-153 33524789-7 2021 Secondly, some signaling pathways were involved in the process of metformin inhibiting autophagy, such as AMPK-related signaling pathways (AMPK/NF-kappaB and other undetermined AMPK-related signaling pathways), Hedgehog, miR-570-3p, miR-142-3p, and MiR-3127-5p. Metformin 66-75 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 106-110 33524789-7 2021 Secondly, some signaling pathways were involved in the process of metformin inhibiting autophagy, such as AMPK-related signaling pathways (AMPK/NF-kappaB and other undetermined AMPK-related signaling pathways), Hedgehog, miR-570-3p, miR-142-3p, and MiR-3127-5p. Metformin 66-75 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 139-143 33524789-7 2021 Secondly, some signaling pathways were involved in the process of metformin inhibiting autophagy, such as AMPK-related signaling pathways (AMPK/NF-kappaB and other undetermined AMPK-related signaling pathways), Hedgehog, miR-570-3p, miR-142-3p, and MiR-3127-5p. Metformin 66-75 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 139-143 33946426-2 2021 Metformin has been reported to affect cancer cells" metabolism and proliferation mainly through the activation of AMP-activated protein kinase (AMPK). Metformin 0-9 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 114-142 33946426-2 2021 Metformin has been reported to affect cancer cells" metabolism and proliferation mainly through the activation of AMP-activated protein kinase (AMPK). Metformin 0-9 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 144-148 33439105-8 2021 Metformin increased the phosphorylation of AMPK and decreased the phosphorylation of mammalian target of rapamycin and extracellular signal-regulated kinase and the expression of cystic fibrosis transmembrane conductance regulator, aquaporin I, transforming growth factor-beta and type 1 collagen in the liver. Metformin 0-9 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 43-47 33681180-0 2020 Metformin Resensitizes Sorafenib-Resistant HCC Cells Through AMPK-Dependent Autophagy Activation. Metformin 0-9 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 61-65 33915902-9 2021 In addition, metformin treatment increased the expression of monophosphate (AMP)-activated protein kinase (AMPK) and p53 in both HCT116 xenografts and colorectal cancer cell lines and decreased the expression of the urea cycle enzymes, including carbamoyl phosphate synthase 1 (CPS1), arginase 1 (ARG1), ornithine trans-carbamylase (OTC), and ODC. Metformin 13-22 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 107-111 33915902-11 2021 These results demonstrate that metformin inhibited CRC cell proliferation via activating AMPK/p53 and that there was an association between metformin, urea cycle inhibition and a reduction in putrescine generation. Metformin 31-40 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 89-93 33681180-6 2020 In response to metformin, the AMPK/cAMP-response element binding protein (CREB) pathway contributes to CEBPD activation, which promotes autophagic cell death. Metformin 15-24 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 30-34 33681180-7 2020 Moreover, treatment with metformin can increase sorafenib sensitivity through AMPK activation in EGFR-overexpressed liver cancer cells. Metformin 25-34 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 78-82 32798506-6 2020 Then, current therapeutic strategies (e.g., metformin, adiponectin) used to ameliorate I/R injury by modulating AMPK activity are reviewed in detail. Metformin 44-53 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 112-116 33161784-0 2021 Metformin as a potential therapeutic for neurological disease: mobilizing AMPK to repair the nervous system. Metformin 0-9 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 74-78 33161784-2 2021 The mechanism of action of metformin involves activation of AMP-activated protein kinase (AMPK) to enhance mitochondrial function (for example, biogenesis, refurbishment and dynamics) and autophagy. Metformin 27-36 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 60-88 33161784-2 2021 The mechanism of action of metformin involves activation of AMP-activated protein kinase (AMPK) to enhance mitochondrial function (for example, biogenesis, refurbishment and dynamics) and autophagy. Metformin 27-36 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 90-94 33161784-6 2021 Expert opinion: Metformin, through activation of AMPK and autophagy, can enhance neuronal bioenergetics, promote nerve repair and reduce toxic protein aggregates in neurological diseases. Metformin 16-25 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 49-53 33161784-8 2021 Future studies in animal models of neurological disease should strive to further dissect in a mechanistic manner the pathways downstream from metformin-dependent AMPK activation, and to further investigate mTOR dependent and independent signaling pathways driving neuroprotection. Metformin 142-151 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 162-166 32386485-4 2021 Clinical data suggest the direct effects of this drug on cardiac metabolism and studies in animal models showed that metformin activates the classical pathway of AMP-activated protein kinase (AMPK), generating cardioprotective effects during cardiac remodeling, hypertrophy and fibrosis. Metformin 117-126 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 162-190 32386485-4 2021 Clinical data suggest the direct effects of this drug on cardiac metabolism and studies in animal models showed that metformin activates the classical pathway of AMP-activated protein kinase (AMPK), generating cardioprotective effects during cardiac remodeling, hypertrophy and fibrosis. Metformin 117-126 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 192-196 32940892-8 2021 The AMPK activator AICAR alone lowered TF expression in THP-1, while the AMPK inhibitor compound C abrogated the metformin-dependent reduction in TF expression. Metformin 113-122 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 4-8 32748028-0 2020 Evaluating the impact of AMPK activation, a target of metformin, on risk of cardiovascular diseases and cancer in the UK Biobank: a Mendelian randomisation study. Metformin 54-63 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 25-29 32748028-2 2020 This study evaluated the effect of AMP-activated protein kinase (AMPK), the target of metformin, on risk of cardiovascular disease and cancer. Metformin 86-95 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 35-63 32748028-2 2020 This study evaluated the effect of AMP-activated protein kinase (AMPK), the target of metformin, on risk of cardiovascular disease and cancer. Metformin 86-95 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 65-69 32748028-3 2020 METHODS: This is a Mendelian randomisation design, using AMPK, the pharmacological target of metformin, to infer the AMPK pathway-dependent effects of metformin on risk of cardiovascular disease and cancer in participants of white British ancestry in the UK Biobank. Metformin 93-102 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 57-61 32748028-3 2020 METHODS: This is a Mendelian randomisation design, using AMPK, the pharmacological target of metformin, to infer the AMPK pathway-dependent effects of metformin on risk of cardiovascular disease and cancer in participants of white British ancestry in the UK Biobank. Metformin 93-102 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 117-121 32748028-3 2020 METHODS: This is a Mendelian randomisation design, using AMPK, the pharmacological target of metformin, to infer the AMPK pathway-dependent effects of metformin on risk of cardiovascular disease and cancer in participants of white British ancestry in the UK Biobank. Metformin 151-160 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 57-61 32748028-3 2020 METHODS: This is a Mendelian randomisation design, using AMPK, the pharmacological target of metformin, to infer the AMPK pathway-dependent effects of metformin on risk of cardiovascular disease and cancer in participants of white British ancestry in the UK Biobank. Metformin 151-160 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 117-121 32748028-7 2020 CONCLUSIONS/INTERPRETATION: This study provides some genetic evidence that AMPK activation by metformin may protect against cardiovascular disease and cancer, which needs to be confirmed by randomised controlled trials. Metformin 94-103 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 75-79 32312181-7 2020 Addition of metformin increased transport, in the context of a transient effect on AMPK phosphorylation. Metformin 12-21 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 83-87 32738111-3 2020 Metformin can activate 5"-AMP-activated protein kinase (AMPK) to improve metabolic flexibility and maintain energy homeostasis. Metformin 0-9 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 56-60 32738111-4 2020 Thus, the aim of the present study was to investigate whether metformin can improve boar sperm quality through AMPK mediation of energy metabolism. Metformin 62-71 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 111-115 32738111-7 2020 We found that metformin treatment significantly increased sperm motility parameters, mitochondrial membrane potential, and ATP content during storage at 17 C. Moreover, results showed that AMPK was localized at the acrosomal region, connecting piece, and midpiece of sperm and p-AMPK was distributed at the post-acrosomal region, connecting piece, and midpiece. Metformin 14-23 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 190-194 32738111-7 2020 We found that metformin treatment significantly increased sperm motility parameters, mitochondrial membrane potential, and ATP content during storage at 17 C. Moreover, results showed that AMPK was localized at the acrosomal region, connecting piece, and midpiece of sperm and p-AMPK was distributed at the post-acrosomal region, connecting piece, and midpiece. Metformin 14-23 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 280-284 32738111-8 2020 When sperm were incubated with metformin for 4 h at 37 C, sperm motility parameters, mitochondrial membrane potential, ATP content, p-AMPK, glucose uptake, and lactate efflux all significantly increased, whereas the addition of Compound C treatment, an inhibitor of AMPK, counteracted these positive effects. Metformin 31-40 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 135-139 33126710-4 2020 Although metformin has been demonstrated to benefit several diseases possibly via AMP-activated protein kinase (AMPK) activation, it remains unknown how AMPK affects retinopathy in NaIO3 model. Metformin 9-18 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 82-110 33126710-4 2020 Although metformin has been demonstrated to benefit several diseases possibly via AMP-activated protein kinase (AMPK) activation, it remains unknown how AMPK affects retinopathy in NaIO3 model. Metformin 9-18 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 112-116 32347398-1 2020 Metformin, a potent AMPK activator is the most commonly used drug for diabetes. Metformin 0-9 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 20-24 32738111-8 2020 When sperm were incubated with metformin for 4 h at 37 C, sperm motility parameters, mitochondrial membrane potential, ATP content, p-AMPK, glucose uptake, and lactate efflux all significantly increased, whereas the addition of Compound C treatment, an inhibitor of AMPK, counteracted these positive effects. Metformin 31-40 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 267-271 32738111-9 2020 Together, our results suggest that metformin promotes AMPK activation, which contributes to the maintenance of energy hemostasis and mitochondrial activity, thereby maintaining boar sperm functionality and improving the efficacy of semen preservation. Metformin 35-44 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 54-58 32940892-8 2021 The AMPK activator AICAR alone lowered TF expression in THP-1, while the AMPK inhibitor compound C abrogated the metformin-dependent reduction in TF expression. Metformin 113-122 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 73-77 32453427-2 2020 Recent studies have demonstrated that metformin, which is an AMPK activator, modifies alternative precursor mRNA (pre-mRNA) splicing. Metformin 38-47 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 61-65 32863218-0 2020 Metformin alleviates lead-induced mitochondrial fragmentation via AMPK/Nrf2 activation in SH-SY5Y cells. Metformin 0-9 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 66-70 32863218-5 2020 By applying metformin, an AMP-activated protein kinase (AMPK) activator, these impairments could be alleviated via activation of AMPK, validated by experiments of pharmacological inhibition of AMPK. Metformin 12-21 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 26-54 32863218-5 2020 By applying metformin, an AMP-activated protein kinase (AMPK) activator, these impairments could be alleviated via activation of AMPK, validated by experiments of pharmacological inhibition of AMPK. Metformin 12-21 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 56-60 32863218-5 2020 By applying metformin, an AMP-activated protein kinase (AMPK) activator, these impairments could be alleviated via activation of AMPK, validated by experiments of pharmacological inhibition of AMPK. Metformin 12-21 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 129-133 32863218-5 2020 By applying metformin, an AMP-activated protein kinase (AMPK) activator, these impairments could be alleviated via activation of AMPK, validated by experiments of pharmacological inhibition of AMPK. Metformin 12-21 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 129-133 32863218-9 2020 To conclude, metformin could ameliorate Pb-induced mitochondrial fragmentation via antioxidative effects originated from AMPK/Nrf2 pathway activation, promoting energy supply and cell survival. Metformin 13-22 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 121-125 32703218-10 2020 On the contrary, the activation of AMPK by metformin (Met) or 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR) could overcome the KRAS-induced resistance to the anti-EGFR antibody in vivo and in vitro. Metformin 43-52 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 35-39 32703218-10 2020 On the contrary, the activation of AMPK by metformin (Met) or 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR) could overcome the KRAS-induced resistance to the anti-EGFR antibody in vivo and in vitro. Metformin 54-57 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 35-39 32364526-4 2020 Metformin may interfere with these pathways by orchestrating AMPK signaling and AMPK-independent pathways to protect the kidneys from injury. Metformin 0-9 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 61-65 32364526-4 2020 Metformin may interfere with these pathways by orchestrating AMPK signaling and AMPK-independent pathways to protect the kidneys from injury. Metformin 0-9 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 80-84 32246808-5 2020 Pharmacologic activation of AMPK with 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR) or metformin during sepsis improved the survival, while AMPK inhibition with Compound C increased mortality, impaired mitochondrial respiration, decreased OCR, and disrupted TEC metabolic fitness. Metformin 95-104 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 28-32 31439934-3 2019 In addition, the discovery that metformin inhibits the mitochondrial respiratory chain complex 1 has placed energy metabolism and activation of AMP-activated protein kinase (AMPK) at the centre of its proposed mechanism of action. Metformin 32-41 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 144-172 32221038-5 2020 In addition, AMP-activated protein kinase (AMPK) activation decreased microRNA-107 expression, thus enhancing Eomesodermin expression, which suppressed the transcription of PDCD1 in metformin-treated CD8+ T cells. Metformin 182-191 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 13-41 32221038-5 2020 In addition, AMP-activated protein kinase (AMPK) activation decreased microRNA-107 expression, thus enhancing Eomesodermin expression, which suppressed the transcription of PDCD1 in metformin-treated CD8+ T cells. Metformin 182-191 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 43-47 31654752-2 2020 Metformin is an AMPK inducer that has been used in cancer therapeutic trials. Metformin 0-9 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 16-20 32281270-3 2020 Metformin (MET), a first-line diabetes medication that also has anti-tumour activities, induces AMP-activated protein kinase (AMPK), directly phosphorylates YAP and inhibits YAP transcriptional activity. Metformin 0-9 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 96-124 32281270-3 2020 Metformin (MET), a first-line diabetes medication that also has anti-tumour activities, induces AMP-activated protein kinase (AMPK), directly phosphorylates YAP and inhibits YAP transcriptional activity. Metformin 0-9 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 126-130 31833226-2 2019 Metformin may exacerbate the energy disturbances observed during exercise leading to enhanced AMPK activation, and these disturbances may provoke early muscular fatigue. Metformin 0-9 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 94-98 31833226-3 2019 We studied acute (1 day) and short-term (4 days) effects of metformin treatment on AMPK and its downstream signaling network, in healthy human skeletal muscle and adipose tissue at rest and during exercise, by applying a randomized blinded crossover study design in 10 lean men. Metformin 60-69 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 83-87 31439934-3 2019 In addition, the discovery that metformin inhibits the mitochondrial respiratory chain complex 1 has placed energy metabolism and activation of AMP-activated protein kinase (AMPK) at the centre of its proposed mechanism of action. Metformin 32-41 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 174-178 31082618-0 2019 Metformin inhibits beta-catenin phosphorylation on Ser-552 through an AMPK/PI3K/Akt pathway in colorectal cancer cells. Metformin 0-9 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 70-74 30989716-12 2019 We also discuss the activation of AMP activated protein kinase (AMPK) by the most widely used drug for type 2 diabetes, metformin, which exerts a dual negative regulatory effect on mTOR and BMP signaling, suggesting that metformin is a promising drug treatment for HO. Metformin 120-129 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 34-62 30989716-12 2019 We also discuss the activation of AMP activated protein kinase (AMPK) by the most widely used drug for type 2 diabetes, metformin, which exerts a dual negative regulatory effect on mTOR and BMP signaling, suggesting that metformin is a promising drug treatment for HO. Metformin 120-129 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 64-68 30989716-12 2019 We also discuss the activation of AMP activated protein kinase (AMPK) by the most widely used drug for type 2 diabetes, metformin, which exerts a dual negative regulatory effect on mTOR and BMP signaling, suggesting that metformin is a promising drug treatment for HO. Metformin 221-230 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 34-62 30989716-12 2019 We also discuss the activation of AMP activated protein kinase (AMPK) by the most widely used drug for type 2 diabetes, metformin, which exerts a dual negative regulatory effect on mTOR and BMP signaling, suggesting that metformin is a promising drug treatment for HO. Metformin 221-230 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 64-68 30445633-9 2019 Treatment of metformin led to activation of AMP-activated protein kinase (AMPK) and attenuated signaling of the downstream molecules such as p-mTOR, p-p70S6K and cyclin D1 expression both in vivo and in vitro. Metformin 13-22 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 74-78 30445633-10 2019 Taken together, our study demonstrated that metformin suppressed the carcinogenesis of ESCC through inhibiting AMPK/mammalian target of the rapamycin (mTOR) signaling pathway, resulting in its chemopreventive effects on the carcinogenesis of ESCC. Metformin 44-53 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 111-115 31082618-4 2019 Here we report that a non-canonical Ser552 phosphorylation in beta-catenin, which promotes its nuclear accumulation and transcriptional activity, is blocked by metformin via AMPK-mediated PI3K/Akt signaling inhibition. Metformin 160-169 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 174-178 30666163-12 2019 Conclusion: This study provided evidence that metformin killed NSCLC cells through AMPK/PKA/GSK-3beta axis-mediated c-FLIPL degradation. Metformin 46-55 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 83-87 31186373-3 2019 Activation of AMPK with the type 2 diabetes drug metformin (GlucoPhage) also increased mTORC2 signaling in liver in vivo and in primary hepatocytes in an AMPK-dependent manner. Metformin 49-58 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 14-18 31186373-3 2019 Activation of AMPK with the type 2 diabetes drug metformin (GlucoPhage) also increased mTORC2 signaling in liver in vivo and in primary hepatocytes in an AMPK-dependent manner. Metformin 49-58 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 154-158 31186373-3 2019 Activation of AMPK with the type 2 diabetes drug metformin (GlucoPhage) also increased mTORC2 signaling in liver in vivo and in primary hepatocytes in an AMPK-dependent manner. Metformin 60-70 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 14-18 31186373-3 2019 Activation of AMPK with the type 2 diabetes drug metformin (GlucoPhage) also increased mTORC2 signaling in liver in vivo and in primary hepatocytes in an AMPK-dependent manner. Metformin 60-70 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 154-158 30903363-4 2019 The major molecular targets of metformin include complex I of the mitochondrial electron transport chain, adenosine monophosphate (AMP)-activated protein kinase (AMPK), and mechanistic target of rapamycin complex 1 (mTORC1), but AMPK-independent effects of metformin have also been described. Metformin 31-40 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 162-166 30903363-4 2019 The major molecular targets of metformin include complex I of the mitochondrial electron transport chain, adenosine monophosphate (AMP)-activated protein kinase (AMPK), and mechanistic target of rapamycin complex 1 (mTORC1), but AMPK-independent effects of metformin have also been described. Metformin 31-40 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 229-233 31042624-4 2019 This study shows that metformin suppressed CD133 expression mainly by affecting the CD133 P1 promoter via adenosine monophosphate (AMP)-activated protein kinase (AMPK) signaling but not the mammalian target of rapamycin (mTOR). Metformin 22-31 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 162-166 31042624-5 2019 AMPK inhibition rescued the reduction of CD133 by metformin. Metformin 50-59 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 0-4 31042624-9 2019 Our results indicated that metformin-AMPK-CEBPbeta signaling plays a crucial role in regulating the gene expression of CD133. Metformin 27-36 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 37-41 30718758-11 2019 Pharmacological inhibition of AMP-activated protein kinase (AMPK) demonstrated that metformin enhances the radiosensitizing effect of cisplatin through an AMPK-dependent pathway only in H460 but not in A549 cells. Metformin 84-93 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 30-58 30718758-11 2019 Pharmacological inhibition of AMP-activated protein kinase (AMPK) demonstrated that metformin enhances the radiosensitizing effect of cisplatin through an AMPK-dependent pathway only in H460 but not in A549 cells. Metformin 84-93 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 60-64 30718758-11 2019 Pharmacological inhibition of AMP-activated protein kinase (AMPK) demonstrated that metformin enhances the radiosensitizing effect of cisplatin through an AMPK-dependent pathway only in H460 but not in A549 cells. Metformin 84-93 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 155-159 30666163-0 2019 Metformin induces apoptotic cytotoxicity depending on AMPK/PKA/GSK-3beta-mediated c-FLIPL degradation in non-small cell lung cancer. Metformin 0-9 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 54-58 30666163-10 2019 Furthermore, metformin significantly activated Adenosine 5"-monophosphate (AMP)-activated protein kinase (AMPK) and its downstream glycogen synthase kinase 3beta (GSK-3beta), block the expression of AMPK, and GSK-3beta with siRNA partially reversed metformin-induced cytotoxicity and restored the expression of c-FLIPL in lung cancer cells. Metformin 13-22 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 106-110 30666163-10 2019 Furthermore, metformin significantly activated Adenosine 5"-monophosphate (AMP)-activated protein kinase (AMPK) and its downstream glycogen synthase kinase 3beta (GSK-3beta), block the expression of AMPK, and GSK-3beta with siRNA partially reversed metformin-induced cytotoxicity and restored the expression of c-FLIPL in lung cancer cells. Metformin 13-22 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 199-203 30666163-10 2019 Furthermore, metformin significantly activated Adenosine 5"-monophosphate (AMP)-activated protein kinase (AMPK) and its downstream glycogen synthase kinase 3beta (GSK-3beta), block the expression of AMPK, and GSK-3beta with siRNA partially reversed metformin-induced cytotoxicity and restored the expression of c-FLIPL in lung cancer cells. Metformin 249-258 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 106-110 30666163-10 2019 Furthermore, metformin significantly activated Adenosine 5"-monophosphate (AMP)-activated protein kinase (AMPK) and its downstream glycogen synthase kinase 3beta (GSK-3beta), block the expression of AMPK, and GSK-3beta with siRNA partially reversed metformin-induced cytotoxicity and restored the expression of c-FLIPL in lung cancer cells. Metformin 249-258 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 199-203 30666163-11 2019 Metformin also suppressed the activity of AMPK downstream protein kinase A (PKA), PKA activators, both 8-Br-cAMP and forskolin, greatly increased c-FLIPL expression in NSCLC cells. Metformin 0-9 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 42-46 30745848-0 2019 Activation of AMPK by metformin promotes renal cancer cell proliferation under glucose deprivation through its interaction with PKM2. Metformin 22-31 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 14-18 30745848-3 2019 In this study, we found that metformin treatment in RCC cells lead to activation of AMPK, which suppressed the cell proliferation under normal condition, but enhanced cell proliferation under glucose deprivation (GD) condition. Metformin 29-38 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 84-88 30536344-12 2018 Additionally, we also found that AMPK plays an essential role in the inhibition of GSK3beta by metformin. Metformin 95-104 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 33-37 30129983-5 2018 Preincubation at high glucose concentration followed by moderate-glucose incubation activated the AMPK pathway, but the activation was abolished with berberine or metformin treatment. Metformin 163-172 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 98-102 30129983-6 2018 In contrast, alteration from normal glucose to moderate glucose concentration in the medium suppressed AMPK activity, which was activated by berberine or metformin. Metformin 154-163 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 103-107 30129983-8 2018 In conclusion, AMPK activated by glucose reduction is inhibited by berberine or metformin. Metformin 80-89 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 15-19 30129983-10 2018 The potent glucose-lowering effects with minimal hypoglycemia of berberine and metformin may be partially due to their bidirectional regulation of the AMPK signaling pathway. Metformin 79-88 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 151-155 28847510-7 2017 To evaluate the biological relevance of AMPK action on ALK2 activity, we induced FOP fibroblasts into iPS cells and found that their osteogenic differentiation in vitro was inhibited by metformin. Metformin 186-195 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 40-44 29922884-0 2018 Comment on "Targeting AMPK, mTOR and beta-Catenin by Combined Metformin and Aspirin Therapy in HCC: An Appraisal in Egyptian HCC Patients". Metformin 62-71 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 22-26 29094287-0 2018 Targeting AMPK, mTOR and beta-Catenin by Combined Metformin and Aspirin Therapy in HCC: An Appraisal in Egyptian HCC Patients. Metformin 50-59 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 10-14 29094287-3 2018 OBJECTIVE: The current work aimed to investigate the possibility of targeting AMP-activated protein kinase (AMPK), mammalian target of rapamycin (mTOR), and beta-catenin proteins through combined metformin/aspirin treatment in the HepG2 cell line, and to explore such molecular targets in Egyptian HCC patients. Metformin 196-205 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 78-106 29094287-3 2018 OBJECTIVE: The current work aimed to investigate the possibility of targeting AMP-activated protein kinase (AMPK), mammalian target of rapamycin (mTOR), and beta-catenin proteins through combined metformin/aspirin treatment in the HepG2 cell line, and to explore such molecular targets in Egyptian HCC patients. Metformin 196-205 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 108-112 29094287-10 2018 CONCLUSIONS: Targeting AMPK, mTOR and beta-catenin by combined metformin/aspirin treatment could be a promising therapeutic strategy for Egyptian HCC patients, and possibly other HCC patients. Metformin 63-72 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 23-27 29779024-1 2018 BACKGROUND: Metformin inhibits cyclic AMP generation and activates AMP-activated protein kinase (AMPK), which inhibits the cystic fibrosis transmembrane conductance regulator and Mammalian Target of Rapamycin pathways. Metformin 12-21 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 67-95 29779024-1 2018 BACKGROUND: Metformin inhibits cyclic AMP generation and activates AMP-activated protein kinase (AMPK), which inhibits the cystic fibrosis transmembrane conductance regulator and Mammalian Target of Rapamycin pathways. Metformin 12-21 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 97-101 29779024-10 2018 Furthermore, results may support or refute the hypothesis that metformin effects on disease progression are mediated through the activation of the AMPK pathway. Metformin 63-72 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 147-151 28847510-4 2017 The activity of the mutated ALK2 was suppressed by pharmacological AMPK activators such as metformin and aspirin, while their actions were blocked by the dominant negative mutant of AMPK and mimicked by the constitutively active mutant of AMPK. Metformin 91-100 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 67-71 28847510-8 2017 Our studies provide novel insight into potential approaches to treatment of FOP, since several AMPK activators (e.g. metformin, berberine, and aspirin) are already in clinical use for the treatment of diabetes and metabolic syndromes. Metformin 117-126 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 95-99 29085506-6 2017 Metformin significantly decreased E2-stimulated cell proliferation; an effect that was rescued in the presence of compound C. Metformin treatment markedly increased the phosphorylation of AMPK while decreasing p70S6K phosphorylation, indicating that metformin exerts its effects through stimulation of AMPK and subsequent inhibition of the mammalian target of rapamycin (mTOR) signaling pathway. Metformin 0-9 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 188-192 29085506-6 2017 Metformin significantly decreased E2-stimulated cell proliferation; an effect that was rescued in the presence of compound C. Metformin treatment markedly increased the phosphorylation of AMPK while decreasing p70S6K phosphorylation, indicating that metformin exerts its effects through stimulation of AMPK and subsequent inhibition of the mammalian target of rapamycin (mTOR) signaling pathway. Metformin 0-9 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 302-306 29085506-6 2017 Metformin significantly decreased E2-stimulated cell proliferation; an effect that was rescued in the presence of compound C. Metformin treatment markedly increased the phosphorylation of AMPK while decreasing p70S6K phosphorylation, indicating that metformin exerts its effects through stimulation of AMPK and subsequent inhibition of the mammalian target of rapamycin (mTOR) signaling pathway. Metformin 126-135 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 188-192 29085506-6 2017 Metformin significantly decreased E2-stimulated cell proliferation; an effect that was rescued in the presence of compound C. Metformin treatment markedly increased the phosphorylation of AMPK while decreasing p70S6K phosphorylation, indicating that metformin exerts its effects through stimulation of AMPK and subsequent inhibition of the mammalian target of rapamycin (mTOR) signaling pathway. Metformin 126-135 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 302-306 29085506-8 2017 Reverse transcription-quantitative polymerase chain reaction analysis demonstrated that c-fos and c-myc expression were attenuated by metformin, an effect that was rescued in the presence of compound C. Therefore, metformin regulates the expression of ERs, and inhibits estrogen-mediated proliferation of human EC cells through the activation of AMPK and subsequent inhibition of the mTOR signaling pathway. Metformin 134-143 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 346-350 29085506-8 2017 Reverse transcription-quantitative polymerase chain reaction analysis demonstrated that c-fos and c-myc expression were attenuated by metformin, an effect that was rescued in the presence of compound C. Therefore, metformin regulates the expression of ERs, and inhibits estrogen-mediated proliferation of human EC cells through the activation of AMPK and subsequent inhibition of the mTOR signaling pathway. Metformin 214-223 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 346-350 25913633-5 2016 In contrast, metformin has a positive effect on osteoblast differentiation due to increased activity of Runx2 via the AMPK/USF-1/SHP regulatory cascade resulting in a neutral or potentially protective effect on bone. Metformin 13-22 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 118-122 27467571-2 2016 Animal and retrospective human studies indicate that Metformin treatment is neuroprotective in Parkinson"s Disease (PD), although the neuroprotective mechanism is unknown, numerous studies suggest the beneficial effects on glucose homeostasis may be through AMPK activation. Metformin 53-62 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 258-262 27128966-0 2017 Metformin induces degradation of cyclin D1 via AMPK/GSK3beta axis in ovarian cancer. Metformin 0-9 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 47-51 27128966-3 2017 Here, we first describe that the anti-cancer effect of metformin is mediated by cyclin D1 deregulation via AMPK/GSK3beta axis in ovarian cancer cells. Metformin 55-64 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 107-111 27128966-8 2017 The activation of GSK3beta correlated with the inhibitory phosphorylation by Akt as well as p70S6K through AMPK activation in response to metformin. Metformin 138-147 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 107-111 27128966-9 2017 These findings suggested that the anticancer effects of metformin was induced due to cyclin D1 degradation via AMPK/GSK3beta signaling axis that involved the ubiquitin/proteasome pathway specifically in ovarian cancer cells. Metformin 56-65 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 111-115 27163626-5 2016 Known cellular mechanisms of metformin, such as increased lactate secretion, reduced oxygen consumption and activated AMPK-signaling, could be confirmed. Metformin 29-38 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 118-122 32309575-3 2015 Indirect AMPK activators, such as resveratrol, metformin and exercise, are currently in clinical trials for studying their impact on human aging-related characteristics, tissue homeostasis and metabolic dysfunctions. Metformin 47-56 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 9-13 25940306-2 2015 Salicylate activates the AMP-activated protein kinase (AMPK) by binding at the A-769662 drug binding site on the AMPK beta1-subunit, a mechanism that is distinct from metformin which disrupts the adenylate charge of the cell. Metformin 167-176 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 55-59 25981932-8 2015 However, subsequent AMPK activation and mTOR pathway inhibition were prominent only in metformin-insensitive non-metastatic cells. Metformin 87-96 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 20-24 25981932-11 2015 In conclusion, metformin exhibited an anti-tumour effect in metastatic CMGT cells through AMPK-independent cell cycle arrest. Metformin 15-24 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 90-94 25940306-6 2015 Salicylate concentrations of 1 mM increased the phosphorylation of ACC and suppressed de novo lipogenesis and these effects were enhanced with the addition of clinical concentrations of metformin (100 muM) and eliminated in mouse embryonic fibroblasts (MEFs) deficient in AMPK beta1. Metformin 186-195 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 272-276 18855699-5 2008 In fact, it has been recently reported that drugs used in the treatment of diabetes, such as metformin and thiazolidinediones (TZDs), exert their beneficial effects through the activation of AMPK. Metformin 93-102 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 191-195 24714080-8 2014 Taken together, our results indicate that metformin sensitizes human bladder cancer cells to TRAIL-induced apoptosis through downregulation of c-FLIP, which is mediated by the mTOR/S6K1 pathway, but independent of AMPK; furthermore, these findings provide a rationale for the combined application of metformin with TRAIL in the treatment of bladder cancer. Metformin 42-51 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 214-218 24059314-7 2014 Some drug agonists of AMPK are known to mimic these effects such as metformin or resveratrol, a polyphenol extracted from plants and present in red wine, a component of the French paradox related diet. Metformin 68-77 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 22-26 19237574-8 2009 Finally, inhibition of AMP-activated protein kinase (AMPK) by the pharmacological inhibitor Compound C largely suppresses metformin"s effect on Abeta generation and BACE1 transcription, suggesting an AMPK-dependent mechanism. Metformin 122-131 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 23-51 19237574-8 2009 Finally, inhibition of AMP-activated protein kinase (AMPK) by the pharmacological inhibitor Compound C largely suppresses metformin"s effect on Abeta generation and BACE1 transcription, suggesting an AMPK-dependent mechanism. Metformin 122-131 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 53-57 19237574-8 2009 Finally, inhibition of AMP-activated protein kinase (AMPK) by the pharmacological inhibitor Compound C largely suppresses metformin"s effect on Abeta generation and BACE1 transcription, suggesting an AMPK-dependent mechanism. Metformin 122-131 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 200-204 25742316-0 2015 Metformin and salicylate synergistically activate liver AMPK, inhibit lipogenesis and improve insulin sensitivity. Metformin 0-9 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 56-60 25742316-2 2015 Metformin and salicylate both increase AMP-activated protein kinase (AMPK) activity but by distinct mechanisms, with metformin altering cellular adenylate charge (increasing AMP) and salicylate interacting directly at the AMPK beta1 drug-binding site. Metformin 0-9 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 39-67 25742316-2 2015 Metformin and salicylate both increase AMP-activated protein kinase (AMPK) activity but by distinct mechanisms, with metformin altering cellular adenylate charge (increasing AMP) and salicylate interacting directly at the AMPK beta1 drug-binding site. Metformin 0-9 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 69-73 25742316-2 2015 Metformin and salicylate both increase AMP-activated protein kinase (AMPK) activity but by distinct mechanisms, with metformin altering cellular adenylate charge (increasing AMP) and salicylate interacting directly at the AMPK beta1 drug-binding site. Metformin 0-9 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 222-226 25742316-2 2015 Metformin and salicylate both increase AMP-activated protein kinase (AMPK) activity but by distinct mechanisms, with metformin altering cellular adenylate charge (increasing AMP) and salicylate interacting directly at the AMPK beta1 drug-binding site. Metformin 117-126 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 222-226 25742316-4 2015 We find doses of metformin and salicylate used clinically synergistically activate AMPK in vitro and in vivo, resulting in reduced liver lipogenesis, lower liver lipid levels and improved insulin sensitivity in mice. Metformin 17-26 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 83-87 24748590-8 2014 However, when combined with classical AMPK activators, such as metformin, phenformin, oligomycin, or hypoxia, which impact AMPK heterotrimers more broadly via elevation of cellular AMP levels, A-769662 induced more profound AMPK phosphorylation and subsequent glucose uptake stimulation. Metformin 63-72 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 38-42 24748590-8 2014 However, when combined with classical AMPK activators, such as metformin, phenformin, oligomycin, or hypoxia, which impact AMPK heterotrimers more broadly via elevation of cellular AMP levels, A-769662 induced more profound AMPK phosphorylation and subsequent glucose uptake stimulation. Metformin 63-72 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 123-127 24748590-8 2014 However, when combined with classical AMPK activators, such as metformin, phenformin, oligomycin, or hypoxia, which impact AMPK heterotrimers more broadly via elevation of cellular AMP levels, A-769662 induced more profound AMPK phosphorylation and subsequent glucose uptake stimulation. Metformin 63-72 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 123-127 24520038-0 2014 Repurposing of metformin and aspirin by targeting AMPK-mTOR and inflammation for pancreatic cancer prevention and treatment. Metformin 15-24 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 50-54 24520038-6 2014 For metformin, the most important mechanism may involve the inhibition of mTOR signaling via AMP-activated protein kinase (AMPK)-dependent and -independent pathways. Metformin 4-13 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 93-121 24520038-6 2014 For metformin, the most important mechanism may involve the inhibition of mTOR signaling via AMP-activated protein kinase (AMPK)-dependent and -independent pathways. Metformin 4-13 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 123-127 22421144-10 2012 In other studies, metformin decreased the phosphorylation of 4E-BP1 at Ser65, Thr37/46 and Thr70 sites, but drastically increased the phosphorylation of EF2 at Thr56 and AMPK at Thr172, which results in global translational inhibition. Metformin 18-27 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 170-174 19237574-4 2009 We demonstrate that metformin, at doses that lead to activation of the AMP-activated protein kinase (AMPK), significantly increases the generation of both intracellular and extracellular Abeta species. Metformin 20-29 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 71-99 19237574-4 2009 We demonstrate that metformin, at doses that lead to activation of the AMP-activated protein kinase (AMPK), significantly increases the generation of both intracellular and extracellular Abeta species. Metformin 20-29 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 101-105 16505254-1 2006 AMP-activated protein kinase (AMPK) is a key molecular regulator of cellular metabolism, and its activity is induced by both metformin and thiazolidinedione antidiabetic medications. Metformin 125-134 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 0-28 16505254-1 2006 AMP-activated protein kinase (AMPK) is a key molecular regulator of cellular metabolism, and its activity is induced by both metformin and thiazolidinedione antidiabetic medications. Metformin 125-134 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 30-34