PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 11790791-11 2002 It is concluded that the cleaving of PARP in Fas-mediated apoptosis allowed expression of an energy-dependent cell death program that included the translocation of full-length Bid to the mitochondria with induction of the MPT. ammonium ferrous sulfate 45-48 BH3 interacting domain death agonist Homo sapiens 176-179 27622714-7 2016 In contrast, in functional p53-impaired cells, this phytochemical exploits p53-paralogue p73, which up-regulates FAS to cleave BID through FAS-FADD-caspase-8-pathway. ammonium ferrous sulfate 113-116 BH3 interacting domain death agonist Homo sapiens 127-130 10801880-2 2000 In Fas-induced apoptosis, Bid is activated through cleavage by caspase 8 into a 15.5-kDa C-terminal fragment (t(c)Bid) and a 6.5 kDa N-terminal fragment (t(n)Bid). ammonium ferrous sulfate 3-6 BH3 interacting domain death agonist Homo sapiens 26-29 10801880-2 2000 In Fas-induced apoptosis, Bid is activated through cleavage by caspase 8 into a 15.5-kDa C-terminal fragment (t(c)Bid) and a 6.5 kDa N-terminal fragment (t(n)Bid). ammonium ferrous sulfate 3-6 BH3 interacting domain death agonist Homo sapiens 114-117 10801880-2 2000 In Fas-induced apoptosis, Bid is activated through cleavage by caspase 8 into a 15.5-kDa C-terminal fragment (t(c)Bid) and a 6.5 kDa N-terminal fragment (t(n)Bid). ammonium ferrous sulfate 3-6 BH3 interacting domain death agonist Homo sapiens 114-117 26758067-9 2016 Our results indicate that BID-independent pathways are responsible for FAS-dependent human islet cell death. ammonium ferrous sulfate 71-74 BH3 interacting domain death agonist Homo sapiens 26-29 23285096-6 2012 However, GTP-induced FAS upregulation through activation of c-jun-N-terminal kinase resulted in FADD phosphorylation, caspase-8 activation and truncation of BID, leading to apoptosis in both LNCaPshV and LNCaPshp53 cells. ammonium ferrous sulfate 21-24 BH3 interacting domain death agonist Homo sapiens 157-160 21768356-0 2011 Fas-mediated neutrophil apoptosis is accelerated by Bid, Bak, and Bax and inhibited by Bcl-2 and Mcl-1. ammonium ferrous sulfate 0-3 BH3 interacting domain death agonist Homo sapiens 52-55 21382479-0 2011 Caveolin-1 mediates Fas-BID signaling in hyperoxia-induced apoptosis. ammonium ferrous sulfate 20-23 BH3 interacting domain death agonist Homo sapiens 24-27 21478427-3 2011 Whereas FAS-induced apoptosis was followed by caspase-8 activation and required Bid to initiate the mitochondrial amplification loop, TNF-alpha-induced apoptosis involved class IA PI3Ks, which were activated by MAPK p38. ammonium ferrous sulfate 8-11 BH3 interacting domain death agonist Homo sapiens 80-83 20187936-0 2010 Akt activity protects rheumatoid synovial fibroblasts from Fas-induced apoptosis by inhibition of Bid cleavage. ammonium ferrous sulfate 59-62 BH3 interacting domain death agonist Homo sapiens 98-101 19640637-7 2010 Knocking down Bid by RNAi and Fas antisense oligodeoxynucleotides resulted in a decreased release and cleavage. ammonium ferrous sulfate 30-33 BH3 interacting domain death agonist Homo sapiens 14-17 20187936-10 2010 RESULTS: PI3 kinase inhibition sensitizes RA FLS to Fas-induced apoptosis by increasing cleavage of Bid protein. ammonium ferrous sulfate 52-55 BH3 interacting domain death agonist Homo sapiens 100-103 20187936-11 2010 Bid suppression completely abrogated Fas-induced apoptosis and Bid overexpression highly increased apoptotic rate of RA FLS in association with cleavage of caspase-9. ammonium ferrous sulfate 37-40 BH3 interacting domain death agonist Homo sapiens 0-3 15863130-0 2005 Sensitivity to Fas-mediated apoptosis in high-risk HPV-positive human cervical cancer cells: relationship with Fas, caspase-8, and Bid. ammonium ferrous sulfate 15-18 BH3 interacting domain death agonist Homo sapiens 131-134 19626005-3 2009 In type I cells, such as lymphocytes, activation of "effector caspases" by FAS-induced activation of caspase-8 suffices for cell killing, whereas in type II cells, including hepatocytes and pancreatic beta-cells, caspase cascade amplification through caspase-8-mediated activation of the pro-apoptotic BCL-2 family member BID (BH3 interacting domain death agonist) is essential. ammonium ferrous sulfate 75-78 BH3 interacting domain death agonist Homo sapiens 322-325 19626005-3 2009 In type I cells, such as lymphocytes, activation of "effector caspases" by FAS-induced activation of caspase-8 suffices for cell killing, whereas in type II cells, including hepatocytes and pancreatic beta-cells, caspase cascade amplification through caspase-8-mediated activation of the pro-apoptotic BCL-2 family member BID (BH3 interacting domain death agonist) is essential. ammonium ferrous sulfate 75-78 BH3 interacting domain death agonist Homo sapiens 327-363 19135479-6 2009 FasL linking to Fas on DCs triggers the activation of caspase-8, which eventually leads to mitochondria-mediated apoptosis via truncation of BID. ammonium ferrous sulfate 0-3 BH3 interacting domain death agonist Homo sapiens 141-144 18665234-5 2008 Stable knockdown of bid lead to a pronounced resistance to Fas/CD95- and TRAIL-induced caspase activation and apoptosis, and significantly increased clonogenic survival. ammonium ferrous sulfate 59-62 BH3 interacting domain death agonist Homo sapiens 20-23 19239902-6 2009 In certain cells such as hepatocytes, albeit not lymphocytes, FAS-induced apoptosis requires amplification through proteolytic activation of the proapoptotic BCL-2 family member BID. ammonium ferrous sulfate 62-65 BH3 interacting domain death agonist Homo sapiens 178-181 17640998-9 2007 In conclusion, our data suggest that both p38 MAPK and iNOS are involved in IFN-gamma/IL-1beta-induced sensitization of the thyroid cells to Fas-mediated apoptosis via the activation of caspases 3, 7, and 10 and that this pathway may be further activated by BID. ammonium ferrous sulfate 141-144 BH3 interacting domain death agonist Homo sapiens 258-261 16461788-3 2005 CD40-ligation induces CLL cells to express the proapoptotic molecule Bid and death receptors CD95 (Fas) and DR5, rendering CLL B cells first resistant and then sensitive to Fas-mediated apoptosis. ammonium ferrous sulfate 99-102 BH3 interacting domain death agonist Homo sapiens 69-72 15863130-9 2005 Analysis of the Fas apoptotic pathway showed that anti-Fas treatment induced caspase-8 activation and concomitantly Bid cleavage, caspase-9 and caspase-3 activation, PARP cleavage and apoptosis in HeLa and CaSki. ammonium ferrous sulfate 55-58 BH3 interacting domain death agonist Homo sapiens 116-119 15863130-12 2005 CONCLUSION: Sensitivity to anti-Fas depends on Fas, caspase-8, and Bid protein levels in cervical cancer cells. ammonium ferrous sulfate 32-35 BH3 interacting domain death agonist Homo sapiens 67-70 12529377-3 2003 In human KB epithelial cells expressing the caspase-resistant mutant crBAP31, Fas stimulation resulted in cleavage of BID and insertion of BAX into mitochondrial membrane, but subsequent oligomerization of BAX and BAK, egress of cytochrome c to the cytosol, and apoptosis were impaired. ammonium ferrous sulfate 78-81 BH3 interacting domain death agonist Homo sapiens 118-121 14623946-9 2004 RESULTS: Fas ligation induced Bid cleavage, loss of DeltaPsim, cytochrome c release to the cytosol and activation of caspase-9 and -3 in RA synovial fibroblasts. ammonium ferrous sulfate 9-12 BH3 interacting domain death agonist Homo sapiens 30-33 12938225-2 2003 Using the B lymphoma line A20.2J, BCR signaling immediately inhibited Fas-induced apoptosis upstream of caspase-8 activation, as determined by Ile-Glu-Thr-Asp-(IETD)ase activity and cleavage of the caspase-8 substrate Bid. ammonium ferrous sulfate 70-73 BH3 interacting domain death agonist Homo sapiens 218-221