PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
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	
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	
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	
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	
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	
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	
31720741-10	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	
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	
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	
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	
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	
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