PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 23378049-0 2013 TAK1 activates AMPK-dependent cell death pathway in hydrogen peroxide-treated cardiomyocytes, inhibited by heat shock protein-70. Hydrogen Peroxide 52-69 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 15-19 32377712-0 2020 Ginsenoside Rb1 reduces H2O2-induced HUVEC dysfunction by stimulating the sirtuin-1/AMP-activated protein kinase pathway. Hydrogen Peroxide 24-28 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 84-112 32377712-6 2020 The present study examined the role of AMP-activated protein kinase (AMPK), an energy sensor of cellular metabolism, in the signaling pathway of SIRT1 during H2O2-stimulated HUVEC aging. Hydrogen Peroxide 158-162 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 39-67 32377712-6 2020 The present study examined the role of AMP-activated protein kinase (AMPK), an energy sensor of cellular metabolism, in the signaling pathway of SIRT1 during H2O2-stimulated HUVEC aging. Hydrogen Peroxide 158-162 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 69-73 32377712-9 2020 It was identified that the induction of phosphorylated AMPK by Rb1 markedly increased endothelial nitric oxide synthase expression and nitric oxide production, and suppressed PAI-1 expression, which were abrogated in HUVECs pretreated with compound C. Further experiments demonstrated that nicotinamide, a SIRT1 inhibitor, downregulated the phosphorylation of AMPK and reduced the protective effects of Rb1 against H2O2-induced endothelial aging. Hydrogen Peroxide 415-419 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 55-59 32377712-10 2020 Taken together, these results provide new insights into the possible molecular mechanisms by which Rb1 protects against H2O2-induced HUVEC senescence via the SIRT1/AMPK pathway. Hydrogen Peroxide 120-124 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 164-168 25682865-9 2015 After RNAi-mediated knockdown (KD) of Atg7 and AMPK, H2O2-treated cells displayed dense SA-beta-gal staining. Hydrogen Peroxide 53-57 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 47-51 23378049-8 2013 In conclusion, we here suggest that TAK1 activates AMPK-dependent cell death pathway in H2O2-treated cardiomyocytes, and HSP-70 inhibits the signaling pathway by reducing ROS content. Hydrogen Peroxide 88-92 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 51-55 34356388-6 2021 betaHB also alleviated the H2O2-induced inhibition of mTOR and AMPK, known targets of Trx1, in a Trx1-dependent manner, suggesting that betaHB potentiates Trx1 function. Hydrogen Peroxide 27-31 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 63-67 32590330-10 2020 Addition of extracellular H2O2 had only a nominal effect on phosphorylation of eNOS, kinase Akt or AMP-activated protein kinase (AMPK). Hydrogen Peroxide 26-30 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 99-127 32590330-10 2020 Addition of extracellular H2O2 had only a nominal effect on phosphorylation of eNOS, kinase Akt or AMP-activated protein kinase (AMPK). Hydrogen Peroxide 26-30 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 129-133 32590330-12 2020 We also found that the AMPK inhibitor Compound C completely blocked nuclear H2O2-promoted eNOS phosphorylation. Hydrogen Peroxide 76-80 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 23-27 32590330-14 2020 We conclude that H2O2 generated in the cell nucleus activates AMPK, leading to eNOS phosphorylation; in contrast, AMPK activation by cytosol- or caveolae-derived H2O2 does not promote eNOS phosphorylation via AMPK. Hydrogen Peroxide 17-21 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 62-66 32590330-14 2020 We conclude that H2O2 generated in the cell nucleus activates AMPK, leading to eNOS phosphorylation; in contrast, AMPK activation by cytosol- or caveolae-derived H2O2 does not promote eNOS phosphorylation via AMPK. Hydrogen Peroxide 162-166 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 114-118 32590330-14 2020 We conclude that H2O2 generated in the cell nucleus activates AMPK, leading to eNOS phosphorylation; in contrast, AMPK activation by cytosol- or caveolae-derived H2O2 does not promote eNOS phosphorylation via AMPK. Hydrogen Peroxide 162-166 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 114-118 32310822-13 2020 AMPK and beta-catenin affected beneficial function of ANRIL-miR-21 axis.Therefore, lncRNA ANRIL attenuated H2O2-induced cell injury in HELCs via up-regulating miR-21 via the activation of AMPK and beta-catenin. Hydrogen Peroxide 107-111 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 0-4 32310822-13 2020 AMPK and beta-catenin affected beneficial function of ANRIL-miR-21 axis.Therefore, lncRNA ANRIL attenuated H2O2-induced cell injury in HELCs via up-regulating miR-21 via the activation of AMPK and beta-catenin. Hydrogen Peroxide 107-111 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 188-192 23378049-1 2013 The aim of this current study is to investigate the potential role of AMP-activated protein kinase (AMPK) in hydrogen peroxide (H2O2)-induced cardiomyocyte death, and focused on the signaling mechanisms of AMPK activation by H2O2. Hydrogen Peroxide 109-126 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 70-98 23378049-1 2013 The aim of this current study is to investigate the potential role of AMP-activated protein kinase (AMPK) in hydrogen peroxide (H2O2)-induced cardiomyocyte death, and focused on the signaling mechanisms of AMPK activation by H2O2. Hydrogen Peroxide 109-126 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 100-104 23378049-1 2013 The aim of this current study is to investigate the potential role of AMP-activated protein kinase (AMPK) in hydrogen peroxide (H2O2)-induced cardiomyocyte death, and focused on the signaling mechanisms of AMPK activation by H2O2. Hydrogen Peroxide 109-126 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 206-210 23378049-1 2013 The aim of this current study is to investigate the potential role of AMP-activated protein kinase (AMPK) in hydrogen peroxide (H2O2)-induced cardiomyocyte death, and focused on the signaling mechanisms of AMPK activation by H2O2. Hydrogen Peroxide 128-132 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 70-98 23378049-1 2013 The aim of this current study is to investigate the potential role of AMP-activated protein kinase (AMPK) in hydrogen peroxide (H2O2)-induced cardiomyocyte death, and focused on the signaling mechanisms of AMPK activation by H2O2. Hydrogen Peroxide 128-132 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 100-104 23378049-1 2013 The aim of this current study is to investigate the potential role of AMP-activated protein kinase (AMPK) in hydrogen peroxide (H2O2)-induced cardiomyocyte death, and focused on the signaling mechanisms of AMPK activation by H2O2. Hydrogen Peroxide 128-132 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 206-210 23378049-1 2013 The aim of this current study is to investigate the potential role of AMP-activated protein kinase (AMPK) in hydrogen peroxide (H2O2)-induced cardiomyocyte death, and focused on the signaling mechanisms of AMPK activation by H2O2. Hydrogen Peroxide 225-229 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 70-98 23378049-1 2013 The aim of this current study is to investigate the potential role of AMP-activated protein kinase (AMPK) in hydrogen peroxide (H2O2)-induced cardiomyocyte death, and focused on the signaling mechanisms of AMPK activation by H2O2. Hydrogen Peroxide 225-229 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 206-210 23378049-2 2013 We observed a significant AMPK activation in H2O2-treated cardiomyocytes (both primary cells and H9c2 line). Hydrogen Peroxide 45-49 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 26-30 23378049-3 2013 Inhibition of AMPK by its inhibitor or RNAi-reduced H2O2-induced cardiomyocyte death. Hydrogen Peroxide 52-56 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 14-18 23378049-4 2013 We here proposed that transforming growth factor-beta-activating kinase 1 (TAK1) might be the upstream kinase for AMPK activation by H2O2. Hydrogen Peroxide 133-137 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 114-118 23378049-5 2013 H2O2-induced TAK1 activation, which recruited and activated AMPK. Hydrogen Peroxide 0-4 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 60-64 23378049-6 2013 TAK1 inhibitor significantly suppressed H2O2-induced AMPK activation and following cardiomyocyte death, while over-expression of TAK1-facilitated AMPK activation and aggregated cardiomyocyte death. Hydrogen Peroxide 40-44 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 53-57