PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 23660334-3 2013 Sanguinarine also promoted the activation of caspase-8 and truncation of Bid (tBid). sanguinarine 0-12 BH3 interacting domain death agonist Homo sapiens 73-76 27363951-3 2016 Sanguinarine treatment increased DR5/TRAILR2 (death receptor 5/TRAIL receptor 2) expression and enhanced the activation of caspase-8 and cleavage of its substrate, Bid. sanguinarine 0-12 BH3 interacting domain death agonist Homo sapiens 164-167 18667818-8 2008 Sanguinarine also promoted the activation of caspase-8 and truncation of Bid (tBid). sanguinarine 0-12 BH3 interacting domain death agonist Homo sapiens 73-76 20032392-5 2009 Combined treatment with sanguinarine and TRAIL effectively induced Bid cleavage and loss of mitochondrial membrane potential, leading to the activation of caspases, and cleavage of poly(ADP-ribose) polymerase and beta-catenin. sanguinarine 24-36 BH3 interacting domain death agonist Homo sapiens 67-70 23717422-4 2013 Sanguinarine-induced apoptosis was correlated with the up-regulation of Bax, the down-regulation of Bid and XIAP, the activation of caspases (-3, -8, and -9), and the generation of increased reactive oxygen species (ROS). sanguinarine 0-12 BH3 interacting domain death agonist Homo sapiens 100-103 17005319-6 2007 Further, sanguinarine-treatment to AsPC-1 and BxPC-3 cells resulted in a dose dependent (i) increase in pro-apoptotic Bax, Bid and Bak proteins; (ii) decrease in anti-apoptotic Bcl-2 and Bcl-X(L) proteins; and (iii) decrease in p53 with an increase in its phosphorylation. sanguinarine 9-21 BH3 interacting domain death agonist Homo sapiens 123-126 17440103-3 2007 Our data show that sanguinarine treatment of PEL cells results in up-regulation of death receptor 5 (DR5) expression via generation of reactive oxygen species (ROS) and causes activation of caspase-8 and truncation of Bid (tBid). sanguinarine 19-31 BH3 interacting domain death agonist Homo sapiens 218-221 12912970-9 2003 Sanguinarine also resulted in significant increases in the proapoptotic members of Bcl-2 family proteins, i.e., Bak and Bid. sanguinarine 0-12 BH3 interacting domain death agonist Homo sapiens 120-123 16505117-5 2006 These responses on UVB and/or sanguinarine treatments were associated with (a) decrease in Bcl-2 and Bcl-X(L) and (b) increase in Bax, Bid, and Bak protein levels. sanguinarine 30-42 BH3 interacting domain death agonist Homo sapiens 135-138