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 4	Homo sapiens	195-199	
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 4	Homo sapiens	131-135	
27133040-12	2016	In addition, using GSH inhibitor, we proved ALA reduced the expressions of GRP78, ATF4 and IRE1alpha by generating GSH.	Thioctic Acid	44-47	activating transcription factor 4	Homo sapiens	82-86	
33235302-8	2020	ALA pre-treatment significantly reduced the expression of ER stress markers namely, GRP78, XBP1, sXBP1 and ATF4 in response to tunicamycin.	Thioctic Acid	0-3	activating transcription factor 4	Homo sapiens	107-111	
33573583-8	2021	On the other hand, only a higher dose of ALA was able to affect the ERUPR via moderation of PERK-ATF4 signaling in the oldest adults.	Thioctic Acid	41-44	activating transcription factor 4	Homo sapiens	97-101