PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
33857568-4	2021	Increased DDIT3 in these Dox-treated cardiomyocytes at 24h suggested that increased MitoBax may have promoted ER stress related changes in DDIT3.	Doxorubicin	25-28	DNA damage inducible transcript 3	Homo sapiens	10-15	
33857568-4	2021	Increased DDIT3 in these Dox-treated cardiomyocytes at 24h suggested that increased MitoBax may have promoted ER stress related changes in DDIT3.	Doxorubicin	25-28	DNA damage inducible transcript 3	Homo sapiens	139-144	
33857568-6	2021	In contrast, breast cancer MCF7 cells showed an ER stress response to Dox with increased DDIT3 as early as 3h which may have triggered a positive feedback activation of ATF6 at 12 and 24h and promoted Calnexin.	Doxorubicin	70-73	DNA damage inducible transcript 3	Homo sapiens	89-94	
33857568-8	2021	DDIT3 response in tumors was evoked by Dox, however this response was inversely correlated with increased Bip and Bax expression in hearts from tumor bearing animals.	Doxorubicin	39-42	DNA damage inducible transcript 3	Homo sapiens	0-5	
33857568-9	2021	It is suggested that in Dox-induced cardiotoxicity both mitochondrial and ER stresses play an integral role through a mutual interaction where an inhibition of DDIT3 or Calnexin may also be crucial to achieve Dox resistance in cardiomyocytes.	Doxorubicin	24-27	DNA damage inducible transcript 3	Homo sapiens	160-165	
33857568-9	2021	It is suggested that in Dox-induced cardiotoxicity both mitochondrial and ER stresses play an integral role through a mutual interaction where an inhibition of DDIT3 or Calnexin may also be crucial to achieve Dox resistance in cardiomyocytes.	Doxorubicin	209-212	DNA damage inducible transcript 3	Homo sapiens	160-165