PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
33573583-7	2021	Remarkably, the lower dose of ALA modified ERUPR and supported the reduction of behavioral deficits in youngest adults through enhancement of GRP87/Bip, reduction of ATF6, downregulation of PERK-ATF4 pathway, and activation of the IRE1-XBP1 pathway.	Thioctic Acid	30-33	activating transcription factor 6	Homo sapiens	166-170	
27133040-11	2016	Simultaneously, ALA could inhibit activation of ER stress-associated sensors GRP78, IRE1alpha, ATF6, P-PERK, P-eIF2alpha, CHOP and ATF4 induced by HCY.	Thioctic Acid	16-19	activating transcription factor 6	Homo sapiens	95-99	
33235302-9	2020	In functional assays, ALA treatment abrogated significantly the tunicamycin-mediated transcriptional activation of ATF6 while it enhanced the insulin-stimulated glucose uptake and Glut4 translocation.	Thioctic Acid	22-25	activating transcription factor 6	Homo sapiens	115-119	
30606992-6	2019	In addition, ALA significantly attenuated glutamate-induced endoplasmic reticulum (ER) stress markers; namely, glucose-regulated protein 78 (GRP78), activating transcription factor 6 (ATF6), protein kinase regulated by RNA (PKR)-like ER-associated kinase (PERK), eukaryotic translation initiation factor 2 alpha (eIF2alpha), inositol-requiring enzyme 1 (IRE1), CCAAT/enhancer binding protein homologous protein (CHOP), and caspase-12.	Thioctic Acid	13-16	activating transcription factor 6	Homo sapiens	149-182	
30606992-6	2019	In addition, ALA significantly attenuated glutamate-induced endoplasmic reticulum (ER) stress markers; namely, glucose-regulated protein 78 (GRP78), activating transcription factor 6 (ATF6), protein kinase regulated by RNA (PKR)-like ER-associated kinase (PERK), eukaryotic translation initiation factor 2 alpha (eIF2alpha), inositol-requiring enzyme 1 (IRE1), CCAAT/enhancer binding protein homologous protein (CHOP), and caspase-12.	Thioctic Acid	13-16	activating transcription factor 6	Homo sapiens	184-188