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