PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
21970967-5	2011	Annexin V and propidium iodide labeling revealed cells transiently expressing GRP78 prior to injury were protected against high-concentrations of tunicamycin and glutamate within 72 h. Our findings support the hypothesis that GRP78 inhibits cell death associated with ER stress.	Glutamic Acid	162-171	heat shock protein family A (Hsp70) member 5	Rattus norvegicus	78-83	
21970967-5	2011	Annexin V and propidium iodide labeling revealed cells transiently expressing GRP78 prior to injury were protected against high-concentrations of tunicamycin and glutamate within 72 h. Our findings support the hypothesis that GRP78 inhibits cell death associated with ER stress.	Glutamic Acid	162-171	heat shock protein family A (Hsp70) member 5	Rattus norvegicus	226-231	
26163046-6	2015	Moreover, NS11021 significantly attenuated the glutamate-induced endoplasmic reticulum (ER) calcium release and activation of ER stress markers, including glucose-regulated protein 78 (GRP78), C/EBP homologous protein (CHOP) and caspase-12.	Glutamic Acid	47-56	heat shock protein family A (Hsp70) member 5	Rattus norvegicus	155-183	
21970967-3	2011	Using the rat C6 glioma cell line and flow cytometry, we assessed GRP78 expression following tunicamycin- and glutamate-induced ER stress.	Glutamic Acid	110-119	heat shock protein family A (Hsp70) member 5	Rattus norvegicus	66-71	
17303341-3	2007	It was therefore hypothesized that cocaine upregulates the expression of the ER stress proteins, immunoglobulin heavy chain binding protein (BiP), Ire1alpha and perk via glutamate and dopamine receptor activation.	Glutamic Acid	170-179	heat shock protein family A (Hsp70) member 5	Rattus norvegicus	141-144	
10072306-2	1999	We report that levels of GRP78 are increased in cultured rat hippocampal neurons exposed to glutamate and oxidative insults (Fe2+ and amyloid beta-peptide) and that treatment of cultures with a GRP78 antisense oligodeoxynucleotide increases neuronal death following exposure to each insult.	Glutamic Acid	92-101	heat shock protein family A (Hsp70) member 5	Rattus norvegicus	25-30	
10072306-2	1999	We report that levels of GRP78 are increased in cultured rat hippocampal neurons exposed to glutamate and oxidative insults (Fe2+ and amyloid beta-peptide) and that treatment of cultures with a GRP78 antisense oligodeoxynucleotide increases neuronal death following exposure to each insult.	Glutamic Acid	92-101	heat shock protein family A (Hsp70) member 5	Rattus norvegicus	194-199	
10072306-5	1999	GRP78 expression may function to suppress oxidative stress and stabilize calcium homeostasis because treatment with GRP78 antisense resulted in increased levels of reactive oxygen species and intracellular calcium following exposure to glutamate and oxidative insults in hippocampal neurons.	Glutamic Acid	236-245	heat shock protein family A (Hsp70) member 5	Rattus norvegicus	0-5	
10072306-5	1999	GRP78 expression may function to suppress oxidative stress and stabilize calcium homeostasis because treatment with GRP78 antisense resulted in increased levels of reactive oxygen species and intracellular calcium following exposure to glutamate and oxidative insults in hippocampal neurons.	Glutamic Acid	236-245	heat shock protein family A (Hsp70) member 5	Rattus norvegicus	116-121	
26584276-6	2015	RESULTS: Administration of glutamate in PC12 cells in doses as low as 10 muM causes an up-regulation of GRP78, GRP94 and HSC70 protein levels, while their mRNA levels show the opposite kinetics.	Glutamic Acid	27-36	heat shock protein family A (Hsp70) member 5	Rattus norvegicus	104-109