PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 33000264-5 2020 In addition, triptolide was revealed to activate the calcium (Ca2+)/calmodulin-dependent protein kinase kinase beta (CaMKKbeta)/AMP-activated protein kinase (AMPK) signaling pathway by regulating the intracellular Ca2+ concentration levels, which increased the phosphorylation levels of AMPK and reduced the phosphorylation levels of AKT, ultimately leading to apoptosis. Calcium 53-60 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 158-162 34398293-0 2021 AMPK: a key regulator of energy stress and calcium-induced autophagy. Calcium 43-50 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 0-4 34398293-7 2021 Interestingly, cytoplasmic calcium is also found to be an activator of AMPK and autophagy through a calmodulin/CaMKKbeta pathway. Calcium 27-34 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 71-75 33790743-5 2021 Transient receptor stimulation induces autophagy and increases LC3-II levels, likely through calcium-dependent phosphorylation of AMPK, and activates microglia to an M1 or mixed M1/M2 state. Calcium 93-100 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 130-134 33344232-4 2020 Considering that TRPM8 is a non-selective Ca2+-permeable cation channel and plays a key role in calcium homoeostasis, we hypothesized that TRPM8 may control AMPK activity thus modulating cellular autophagy to regulate the proliferation and migration of breast cancer cells. Calcium 96-103 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 157-161 33000264-5 2020 In addition, triptolide was revealed to activate the calcium (Ca2+)/calmodulin-dependent protein kinase kinase beta (CaMKKbeta)/AMP-activated protein kinase (AMPK) signaling pathway by regulating the intracellular Ca2+ concentration levels, which increased the phosphorylation levels of AMPK and reduced the phosphorylation levels of AKT, ultimately leading to apoptosis. Calcium 53-60 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 287-291 32850483-2 2020 Human Cytomegalovirus (HCMV) infection has been found to actively manipulate the calcium-AMPK signaling axis to support infection. Calcium 81-88 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 89-93 32807122-11 2020 AMPK inactivation is accompanied by the activation of multiple oncogenic pathways associated with cell adhesion, calcium signaling and extracellular matrix organization. Calcium 113-120 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 0-4 32377301-0 2020 Melatonin Attenuates Calcium Deposition from Vascular Smooth Muscle Cells by Activating Mitochondrial Fusion and Mitophagy via an AMPK/OPA1 Signaling Pathway. Calcium 21-28 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 130-134 32650778-0 2020 Prion peptide-mediated calcium level alteration governs neuronal cell damage through AMPK-autophagy flux. Calcium 23-30 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 85-89 32650778-5 2020 This study is focused on the effect of the changes in intracellular calcium levels on AMPK/autophagy flux pathway and PrP (106-126)-induced neurotoxicity. Calcium 68-75 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 86-90 32650778-12 2020 Inhibition of calcium uptake prevented autophagic cell death and reduction in AMP-activated protein kinase (AMPK) activity induced by human prion peptide. Calcium 14-21 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 78-106 32650778-12 2020 Inhibition of calcium uptake prevented autophagic cell death and reduction in AMP-activated protein kinase (AMPK) activity induced by human prion peptide. Calcium 14-21 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 108-112 32650778-13 2020 CONCLUSION: Our data demonstrated that prion peptide-mediated calcium inflow plays a pivotal role in prion peptide-induced autophagic cell death, and reduction in AMPK activity in neurons. Calcium 62-69 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 163-167 30304690-5 2018 We highlight this with 3 demonstrated applications: (1) repositioned category of psychiatric drugs to inhibit the TGF-beta pathway; (2) antihypertensive calcium channel blockers predicted to activate AMPK and inhibit AKT pathways, and validated by clinical electronic medical records; and (3) 7 drugs predicted and validated to selectively target the AKT-FOXO and AMPK pathways and thus regulate worm lifespan. Calcium 153-160 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 200-204 26227473-10 2015 Additionally, the AMPK-activating function of the FDA-approved proteasome inhibitor bortezomib depends on an increase in intracellular calcium levels as calcium chelation abrogates its induced AMPK activation. Calcium 135-142 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 18-22 27226623-9 2016 We demonstrate that matrix deprivation leads to a spike in intracellular calcium as well as oxidant signaling, and both these intracellular messengers contribute to rapid AMPK activation upon detachment. Calcium 73-80 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 171-175 27226623-10 2016 We further show that endoplasmic reticulum calcium release-induced store-operated calcium entry contributes to intracellular calcium increase, leading to reactive oxygen species production, and AMPK activation. Calcium 43-50 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 194-198 27226623-10 2016 We further show that endoplasmic reticulum calcium release-induced store-operated calcium entry contributes to intracellular calcium increase, leading to reactive oxygen species production, and AMPK activation. Calcium 82-89 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 194-198 27226623-10 2016 We further show that endoplasmic reticulum calcium release-induced store-operated calcium entry contributes to intracellular calcium increase, leading to reactive oxygen species production, and AMPK activation. Calcium 82-89 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 194-198 26227473-10 2015 Additionally, the AMPK-activating function of the FDA-approved proteasome inhibitor bortezomib depends on an increase in intracellular calcium levels as calcium chelation abrogates its induced AMPK activation. Calcium 135-142 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 193-197 26227473-10 2015 Additionally, the AMPK-activating function of the FDA-approved proteasome inhibitor bortezomib depends on an increase in intracellular calcium levels as calcium chelation abrogates its induced AMPK activation. Calcium 153-160 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 18-22 26227473-10 2015 Additionally, the AMPK-activating function of the FDA-approved proteasome inhibitor bortezomib depends on an increase in intracellular calcium levels as calcium chelation abrogates its induced AMPK activation. Calcium 153-160 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 193-197 23583109-3 2013 We show that increased intracellular calcium [Ca2+](i) induced by NMDA receptor activation or membrane depolarization activates AMPK in a CAMKK2-dependent manner. Calcium 37-44 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 128-132