PMID-sentid	Pub_year	Sent_text	comp_official_name	comp_offset	protein_name	organism	prot_offset
34011952-5	2021	Taken together, our data suggest that LMP with its deadly consequences represents a "default" death mechanism in cancer cells, when Caspase-8 is absent and apoptosis cannot be induced.	(2~{s},3~{r},4~{s})-2-[(2~{s},3~{r})-1,3-Bis(Oxidanyl)-1-Oxidanylidene-Butan-2-Yl]-4-[(3~{s},5~{s})-5-(Dimethylcarbamoyl)pyrrolidin-3-Yl]sulfanyl-3-Methyl-3,4-Dihydro-2~{h}-Pyrrole-5-Carboxylic Acid	38-41	caspase 8	Homo sapiens	132-141
3701067-6	1986	The amino acids required for binding of mAb Cap-4, Cap-5, Rh-4, and Rh-2 to hemoglobin are alanine at beta 5, threonine at beta 13, glutamine at beta 125, and leucine at alpha 68.	Alanine	91-98	caspase 8	Homo sapiens	44-49
3701067-6	1986	The amino acids required for binding of mAb Cap-4, Cap-5, Rh-4, and Rh-2 to hemoglobin are alanine at beta 5, threonine at beta 13, glutamine at beta 125, and leucine at alpha 68.	Threonine	110-119	caspase 8	Homo sapiens	44-49
3701067-6	1986	The amino acids required for binding of mAb Cap-4, Cap-5, Rh-4, and Rh-2 to hemoglobin are alanine at beta 5, threonine at beta 13, glutamine at beta 125, and leucine at alpha 68.	Glutamine	132-141	caspase 8	Homo sapiens	44-49
3701067-6	1986	The amino acids required for binding of mAb Cap-4, Cap-5, Rh-4, and Rh-2 to hemoglobin are alanine at beta 5, threonine at beta 13, glutamine at beta 125, and leucine at alpha 68.	Leucine	159-166	caspase 8	Homo sapiens	44-49
33845261-7	2021	Furthermore, the protein expression of P53, CASPASE 8 (Cleaved/Pro), CASPASE 9 (Cleaved/Pro) and CASPASE 3 (Cleaved/Pro) in granulosa cells of mice treated with spermidine were significantly upregulated, while BCL2 expression was significantly downregulated.	Spermidine	161-171	caspase 8	Homo sapiens	44-53
33845261-8	2021	In summary, our study demonstrates for the first time that spermidine at supraphysiological doses causes ovarian oxidative stress and induces granulosa cell apoptosis via the P53 and/or BCL2-CASPASEs pathway.	Spermidine	59-69	caspase 8	Homo sapiens	191-199
33581253-10	2021	Importantly, autophagy was downregulated by treatment with Autophinib, an activation of caspase-8 and cleaved caspase-3 increased.	Autophinib	59-69	caspase 8	Homo sapiens	88-97
33985619-3	2022	c-Src-mediated Caspase-8 phosphorylation essential for EMT in lung adenocarcinoma cell lines preferentially occurs in cells with the mesenchymal phenotype, resulting in chemoresistance to cisplatin plus paclitaxel inpatients with resectable lung adenocarcinoma and a significantly worse 5-year PFS.	Cisplatin	188-197	caspase 8	Homo sapiens	15-24
33985619-3	2022	c-Src-mediated Caspase-8 phosphorylation essential for EMT in lung adenocarcinoma cell lines preferentially occurs in cells with the mesenchymal phenotype, resulting in chemoresistance to cisplatin plus paclitaxel inpatients with resectable lung adenocarcinoma and a significantly worse 5-year PFS.	Paclitaxel	203-213	caspase 8	Homo sapiens	15-24
33985619-5	2022	Paclitaxel-triggered necroptosis in lung adenocarcinoma cells was dependent on the phosphorylation or deficiency of Caspase-8, during which FADD interacted with RIPK1 to activateRIPK1/RIPK3/MLKL signaling axis.	Paclitaxel	0-10	caspase 8	Homo sapiens	116-125
33985619-7	2022	Dasatinib mitigated c-Src-mediated phosphorylation of Caspase-8-induced EMT and enhanced necroptosis in mesenchymal-like lung adenocarcinoma cells treated with paclitaxel, while c-FLIP knockdown predominantly sensitized the mesenchymal-like lung adenocarcinoma cells to paclitaxel+dasatinib.	Dasatinib	0-9	caspase 8	Homo sapiens	54-63
33985619-7	2022	Dasatinib mitigated c-Src-mediated phosphorylation of Caspase-8-induced EMT and enhanced necroptosis in mesenchymal-like lung adenocarcinoma cells treated with paclitaxel, while c-FLIP knockdown predominantly sensitized the mesenchymal-like lung adenocarcinoma cells to paclitaxel+dasatinib.	Paclitaxel	160-170	caspase 8	Homo sapiens	54-63
33985619-7	2022	Dasatinib mitigated c-Src-mediated phosphorylation of Caspase-8-induced EMT and enhanced necroptosis in mesenchymal-like lung adenocarcinoma cells treated with paclitaxel, while c-FLIP knockdown predominantly sensitized the mesenchymal-like lung adenocarcinoma cells to paclitaxel+dasatinib.	Paclitaxel	270-280	caspase 8	Homo sapiens	54-63
33985619-7	2022	Dasatinib mitigated c-Src-mediated phosphorylation of Caspase-8-induced EMT and enhanced necroptosis in mesenchymal-like lung adenocarcinoma cells treated with paclitaxel, while c-FLIP knockdown predominantly sensitized the mesenchymal-like lung adenocarcinoma cells to paclitaxel+dasatinib.	Dasatinib	281-290	caspase 8	Homo sapiens	54-63
33578050-0	2021	Regulation of docosahexaenoic acid-induced apoptosis of confluent endothelial cells: Contributions of MAPKs and caspases.	Docosahexaenoic Acids	14-34	caspase 8	Homo sapiens	112-120
34002852-9	2021	In conclusion, our results reveal an important role of CD300a in the control of leukocyte infiltration, IL-1beta production and caspase-8 cleavage in neutrophils, contributing to the resolution of inflammation triggered by MSU injection.	Uric Acid	223-226	caspase 8	Homo sapiens	128-137
33985619-8	2022	c-Src-Caspase-8 interaction initiates EMT and chemoresistance viaCaspase-8 phosphorylation and lncCRLA expression, to which the dasatinib/paclitaxel liposome+siFLIP regimen was lethal.	Dasatinib	128-137	caspase 8	Homo sapiens	6-15
33985619-8	2022	c-Src-Caspase-8 interaction initiates EMT and chemoresistance viaCaspase-8 phosphorylation and lncCRLA expression, to which the dasatinib/paclitaxel liposome+siFLIP regimen was lethal.	Paclitaxel	138-148	caspase 8	Homo sapiens	6-15
33985619-8	2022	c-Src-Caspase-8 interaction initiates EMT and chemoresistance viaCaspase-8 phosphorylation and lncCRLA expression, to which the dasatinib/paclitaxel liposome+siFLIP regimen was lethal.	siflip	158-164	caspase 8	Homo sapiens	6-15
33578050-4	2021	Our results revealed that DHA induces apoptosis of confluent cells through both intrinsic and extrinsic pathways, which requires activation of p38 MAPK, and involves activation of JNK, caspase-9, caspase-8 and caspase-3 with the exception that cleavage of caspase-8 was incomplete and truncated BID was not detected at the maximum time (8 h) examined.	Docosahexaenoic Acids	26-29	caspase 8	Homo sapiens	196-205
33578050-4	2021	Our results revealed that DHA induces apoptosis of confluent cells through both intrinsic and extrinsic pathways, which requires activation of p38 MAPK, and involves activation of JNK, caspase-9, caspase-8 and caspase-3 with the exception that cleavage of caspase-8 was incomplete and truncated BID was not detected at the maximum time (8 h) examined.	Docosahexaenoic Acids	26-29	caspase 8	Homo sapiens	256-265
33578050-5	2021	Apoptosis induced by high levels of DHA in healthy endothelial cells is achieved through positive feedback loops linking these MAPKs to multiple caspases, as well as negative feedback from p38 MAPK to JNK.	Docosahexaenoic Acids	36-39	caspase 8	Homo sapiens	145-153
33578050-7	2021	This study has expanded the knowledge on the molecular mechanism of DHA-induced apoptosis in human endothelial cells and has also implied the differential roles of MAP kinases and caspases in apoptosis.	Docosahexaenoic Acids	68-71	caspase 8	Homo sapiens	180-188
33578238-4	2021	In the present study, we found that dehydrocrenatidine induced apoptosis in human oral cancer cells through both extrinsic and intrinsic pathways involving proteins such as caspase-3, caspase-8, caspase-9, poly (adenosine diphosphate-ribose) polymerase, and members of the Bcl-2 family.	dehydrocrenatidine	36-54	caspase 8	Homo sapiens	184-193
33876818-11	2021	Moreover, butyric acid alleviated CIH-induced cell proliferation, lipid formation and inflammatory status and promoted cell apoptosis through regulating related genes including p21, PPARgamma, C/EBPa, IL-1beta, IL-6, TLR4, caspase-8 and caspase-3.	Butyric Acid	10-22	caspase 8	Homo sapiens	223-232
33555513-0	2021	Tropical lichen, Dirinaria consimilis, induces ROS-mediated activation of MAPKs and triggers caspase cascade mediated apoptosis in brain and cervical cancer cells.	ros	47-50	caspase 8	Homo sapiens	93-100
33555513-12	2021	Performed in-depth anticancer study revealed the ROS-mediated regulation of MAP kinases and activation of caspase cascade in U87 and HeLa cells upon DCME treatment.	ros	49-52	caspase 8	Homo sapiens	106-113
33555513-12	2021	Performed in-depth anticancer study revealed the ROS-mediated regulation of MAP kinases and activation of caspase cascade in U87 and HeLa cells upon DCME treatment.	dcme	149-153	caspase 8	Homo sapiens	106-113
33930507-4	2021	Full-length BAP31 can be anti-apoptotic, but can also mediate activation of caspase-8, and itself be cleaved by caspase-8 into p20-BAP31, which promotes apoptosis by mobilizing ER calcium stores at MAMs.	Calcium	180-187	caspase 8	Homo sapiens	112-121
33922439-6	2021	Apoptosis induction was prevented by the caspase inhibitor QVD-Oph as well as by the antioxidant vitamin E.	quinoline-val-asp(OMe)-CH2-OPH	59-66	caspase 8	Homo sapiens	41-48
33875938-12	2021	Further analysis revealed that the mRNA and protein expression of caspase-3, caspase-8, and caspase-9 in the A. paniculata polysaccharide treatment groups increased significantly compared with that in the control groups, while the expression of CDK1 and cyclinB1 decreased significantly.	Polysaccharides	123-137	caspase 8	Homo sapiens	77-86
33953676-6	2021	The results showed that astragalin significantly inhibited the proliferation and diffusion of HCT116 cells by induced apoptosis (by modulation of Bax, Bcl-2, P53, caspase-3, caspase 6, caspase 7, caspase 8, caspase 9 protein express) and cell cycle arrest (by modulation of Cyclin D1, Cyclin E, P21, P27, CDK2, CDK4 protein express).	astragalin	24-34	caspase 8	Homo sapiens	196-205
33515314-0	2021	Progesterone induces apoptosis by activation of caspase-8 and calcitriol via activation of caspase-9 pathways in ovarian and endometrial cancer cells in vitro.	Progesterone	0-12	caspase 8	Homo sapiens	48-57
33953834-10	2021	Western blotting analysis showed that acetylshikonin treatment induced increase of cleaved PARP, gammaH2AX, FOXO3, Bax, Bim, Bad, p21, p27, and active forms of caspase-3, caspase-7, caspase-9, caspase-6, and caspase-8 protein levels, while those of inactive forms were decreased.	acetylshikonin	38-52	caspase 8	Homo sapiens	208-217
33515314-8	2021	Knockdown of FAS or FADD with specific siRNAs significantly blocked progesterone-induced caspase-8.	Progesterone	68-80	caspase 8	Homo sapiens	89-98
33515314-5	2021	Time-dependent treatment of ovarian cancer cells, ES-2, and TOV-21G with progesterone enhanced caspase -8 activity after 12 h, whereas OV-90, TOV-112D, HEC-1A, and HEC-59 cells showed increased activity after 24 h. Caspase 9 activity was increased in all cell lines after 24 h treatment with calcitriol.	Progesterone	73-85	caspase 8	Homo sapiens	95-105
33515314-11	2021	These findings indicate that progesterone induces apoptosis through activation of caspase-8 and calcitriol through caspase-9 activation in cancer cells.	Progesterone	29-41	caspase 8	Homo sapiens	82-91
33515314-6	2021	Pretreatment of cancer cells with a caspase-8 inhibitor (z-IETD-fmk) or caspase-9 inhibitor (Z-LEHD-fmk) significantly attenuated progesterone and calcitriol induced caspase-8 and caspase-9 expression, respectively.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	57-67	caspase 8	Homo sapiens	36-45
33515314-6	2021	Pretreatment of cancer cells with a caspase-8 inhibitor (z-IETD-fmk) or caspase-9 inhibitor (Z-LEHD-fmk) significantly attenuated progesterone and calcitriol induced caspase-8 and caspase-9 expression, respectively.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	57-67	caspase 8	Homo sapiens	166-175
33515314-6	2021	Pretreatment of cancer cells with a caspase-8 inhibitor (z-IETD-fmk) or caspase-9 inhibitor (Z-LEHD-fmk) significantly attenuated progesterone and calcitriol induced caspase-8 and caspase-9 expression, respectively.	benzyloxycarbonyl-leucyl-glutamyl-histidyl-aspartic acid fluoromethyl ketone	93-103	caspase 8	Homo sapiens	166-175
33515314-6	2021	Pretreatment of cancer cells with a caspase-8 inhibitor (z-IETD-fmk) or caspase-9 inhibitor (Z-LEHD-fmk) significantly attenuated progesterone and calcitriol induced caspase-8 and caspase-9 expression, respectively.	Progesterone	130-142	caspase 8	Homo sapiens	36-45
33515314-6	2021	Pretreatment of cancer cells with a caspase-8 inhibitor (z-IETD-fmk) or caspase-9 inhibitor (Z-LEHD-fmk) significantly attenuated progesterone and calcitriol induced caspase-8 and caspase-9 expression, respectively.	Progesterone	130-142	caspase 8	Homo sapiens	166-175
33515314-6	2021	Pretreatment of cancer cells with a caspase-8 inhibitor (z-IETD-fmk) or caspase-9 inhibitor (Z-LEHD-fmk) significantly attenuated progesterone and calcitriol induced caspase-8 and caspase-9 expression, respectively.	Calcitriol	147-157	caspase 8	Homo sapiens	36-45
33515314-6	2021	Pretreatment of cancer cells with a caspase-8 inhibitor (z-IETD-fmk) or caspase-9 inhibitor (Z-LEHD-fmk) significantly attenuated progesterone and calcitriol induced caspase-8 and caspase-9 expression, respectively.	Calcitriol	147-157	caspase 8	Homo sapiens	166-175
33515314-7	2021	The expression of FasL, Fas, FAD, and pro-caspase-8, which constitute the death-inducing signaling complex (DISC), was upregulated in progesterone treated cancer cells.	Progesterone	134-146	caspase 8	Homo sapiens	42-51
33796223-3	2021	E6 effects this oncogenic phenotype in part through inhibitory protein-protein interactions (PPIs) and accelerated degradation of proteins with tumor suppressor properties, such as p53 and caspase 8.	Polyurethane Y-290	0-2	caspase 8	Homo sapiens	189-198
33791383-6	2021	BP/LPPC induced cell apoptosis through activation of both the extrinsic (Fas-L and Caspase-8) and intrinsic (Bax and Caspase-9) apoptosis pathways and activated the caspase cascade to trigger HCC cell death.	butylidenephthalide	0-2	caspase 8	Homo sapiens	83-92
33791383-6	2021	BP/LPPC induced cell apoptosis through activation of both the extrinsic (Fas-L and Caspase-8) and intrinsic (Bax and Caspase-9) apoptosis pathways and activated the caspase cascade to trigger HCC cell death.	lppc	3-7	caspase 8	Homo sapiens	83-92
33691557-5	2022	GLY induced apoptosis in C33A cells via activation of capsase-9 (intrinsic pathway) and caspase-8 (extrinsic pathway) along with the modulation of pro- and antiapoptotic protein expression.	Glycyrrhizic Acid	0-3	caspase 8	Homo sapiens	88-97
33465425-7	2021	Western blotting assay indicated that brusatol pronouncedly suppressed the expression levels of mitochondrial apoptotic pathway-associated proteins Bcl-2 and Bcl-xl, accentuated the expression of Bax and Bak, and upregulated the protein expression of XIAP, cleaved caspase-3/pro caspase-3, cleaved caspase-8/pro caspase-8, and cleaved PARP/total PARP.	brusatol	38-46	caspase 8	Homo sapiens	298-307
33465425-7	2021	Western blotting assay indicated that brusatol pronouncedly suppressed the expression levels of mitochondrial apoptotic pathway-associated proteins Bcl-2 and Bcl-xl, accentuated the expression of Bax and Bak, and upregulated the protein expression of XIAP, cleaved caspase-3/pro caspase-3, cleaved caspase-8/pro caspase-8, and cleaved PARP/total PARP.	brusatol	38-46	caspase 8	Homo sapiens	312-321
33788717-4	2021	RESULTS: Treatment with erlotinib induced caspase 8 activation and up-regulation of TNF-related apoptosis-inducing ligand (TRAIL) expression only in 3D cultures.	Erlotinib Hydrochloride	24-33	caspase 8	Homo sapiens	42-51
33660894-5	2021	Baseline protein expression of cIAP1, caspase-8 and RIPK1 expression robustly correlated with response to Birinapant/chemotherapy combinations.	birinapant	106-116	caspase 8	Homo sapiens	38-47
33788717-5	2021	Knockdown of TRAIL attenuated both erlotinib-induced activation of caspase-8 and apoptosis in 3D cultures.	Erlotinib Hydrochloride	35-44	caspase 8	Homo sapiens	67-76
33841010-0	2021	20(S)-ginsenoside Rh2 induces caspase-dependent promyelocytic leukemia-retinoic acid receptor A degradation in NB4 cells via Akt/Bax/caspase9 and TNF-alpha/caspase8 signaling cascades.	Ginsenoside Rh2	0-21	caspase 8	Homo sapiens	30-37
33841010-11	2021	Z-VAD-FMK inhibited caspase activation and significantly reversed GRh2-induced apoptosis and PML-RARA degradation.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	0-9	caspase 8	Homo sapiens	20-27
33841010-14	2021	Conclusion: GRh2 induced caspase-dependent PML-RARA degradation and apoptosis in NB4 cells via the Akt/Bax/caspase9 and TNF-alpha/caspase8 pathways.	grh2	12-16	caspase 8	Homo sapiens	25-32
33841010-14	2021	Conclusion: GRh2 induced caspase-dependent PML-RARA degradation and apoptosis in NB4 cells via the Akt/Bax/caspase9 and TNF-alpha/caspase8 pathways.	grh2	12-16	caspase 8	Homo sapiens	130-138
33646592-0	2021	Synthesis and antitumor potential of new arylidene ursolic acid derivatives via caspase-8 activation.	arylidene ursolic acid	41-63	caspase 8	Homo sapiens	80-89
33646592-6	2021	A docking study revealed that the nitroxyethyl moiety of compound 5c may form hydrogen bonds with caspase-8 amino acid residues (SER256 and HIS255).	Hydrogen	78-86	caspase 8	Homo sapiens	98-107
33841010-0	2021	20(S)-ginsenoside Rh2 induces caspase-dependent promyelocytic leukemia-retinoic acid receptor A degradation in NB4 cells via Akt/Bax/caspase9 and TNF-alpha/caspase8 signaling cascades.	Ginsenoside Rh2	0-21	caspase 8	Homo sapiens	156-164
33841010-6	2021	Z-VAD-FMK, LY294002, and C 87, as inhibitors of caspase, and the phosphatidylinositol 3-kinase (PI3K) and tumor necrosis factor-alpha (TNF-alpha ) pathways were used to clarify the relationship between GRh2-induced apoptosis and PML-RARA degradation.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	0-9	caspase 8	Homo sapiens	48-55
33841010-8	2021	GRh2-induced apoptosis, cell cycle arrest, and caspase3, caspase8, and caspase9 activation in NB4 cells after a 12-hour treatment.	grh2	0-4	caspase 8	Homo sapiens	57-65
33596797-6	2022	RESULTS: DHA effectively inhibited the proliferation, invasion, and migration of SGC7901/DDP cells and induced cell apoptosis which was accompanied by caspase-8/9/3 activation.	artenimol	9-12	caspase 8	Homo sapiens	151-164
33669057-9	2021	One-day exposure to TEGDMA led to the activation of caspase-8, -9, -3, and -12 and an increased AIF production.	triethylene glycol dimethacrylate	20-26	caspase 8	Homo sapiens	52-78
33596797-9	2022	CONCLUSION: DHA exerts an anti-cancer effect on SGC7901/DDP cells and the mechanisms possibly include enhancement of autophagy via PI3K/AKT/mTOR inhibition, inducement of apoptosis through caspase-dependent and mitochondrial pathway, and enhancement of cisplatin sensitivity through P-gp inhibition.	artenimol	12-15	caspase 8	Homo sapiens	189-196
33557839-13	2021	When CHOP expression was knocked down and cells were treated with LiCl, the protein level of NOXA was partially increased, and Mcl-1 expression was increased, while the cleavage of caspase8, caspase9, caspase3 and PARP that was induced by the LiCl was reduced compared with the vehicle treated group.	Lithium Chloride	66-70	caspase 8	Homo sapiens	181-189
33599394-5	2021	Enabled by this examination of mapping strategies, we then integrated our chemoproteomics data with computational methods for predicting genetic variant pathogenicity, which revealed that codons of highly reactive cysteines are enriched for genetic variants that are predicted to be more deleterious and allowed us to identify and functionally characterize a new damaging residue in the cysteine protease caspase-8.	Cysteine	214-223	caspase 8	Homo sapiens	405-414
33545202-7	2022	Western blot results showed that ERK, P53, P21, Caspase 9, Caspase 8 and Caspase 3 were all activated; cytochrome C and Bax increased; and Bcl-2 decreased when OS was treated with ligustilide.	ligustilide	180-191	caspase 8	Homo sapiens	59-68
33350608-6	2021	Expression of necroptosis inhibitor caspase-8 was decreased and levels of necroptosis proteins RIP1, RIP3 and MLKL were increased in U87 and C6 cells after treatment with osthole, while levels of apoptosis-related proteins caspase-3, caspase-7 and caspase-9 were not increased.	osthol	171-178	caspase 8	Homo sapiens	36-45
33359023-5	2021	Whereas dioscin also effectively activated the marker genes and proteins (Fas, TNF-R1, and Caspase 8) related to the death receptor-mediated pathway which confirmed the involvement of both the pathways for dioscin-induced apoptosis.	dioscin	8-15	caspase 8	Homo sapiens	91-100
33549076-12	2021	UA arrested the cell cycle at the G0/G1 phase, and induced caspase-dependent apoptosis.	ursolic acid	0-2	caspase 8	Homo sapiens	59-66
33549076-17	2021	CONCLUSIONS: UA induced caspase-dependent apoptosis, and FAK/PI3K/AKT singling and EMT related anoikis in RKO cells.	ursolic acid	13-15	caspase 8	Homo sapiens	24-31
33498252-0	2021	Deoxynivalenol Induces Caspase-8-Mediated Apoptosis through the Mitochondrial Pathway in Hippocampal Nerve Cells of Piglet.	deoxynivalenol	0-14	caspase 8	Homo sapiens	23-32
33302164-9	2021	Low-dose NAC increased CCDN1 and decreased CASP3 and CASP8 mRNA levels (P < 0.05), whereas high-dose NAC decreased CDK4 and CCDN1 and increased CASP3 mRNA levels (P < 0.05).	Acetylcysteine	9-12	caspase 8	Homo sapiens	53-58
33525391-0	2021	Melatonin Alleviates Hypoxia-Induced Apoptosis of Granulosa Cells by Reducing ROS and Activating MTNR1B-PKA-Caspase8/9 Pathway.	Melatonin	0-9	caspase 8	Homo sapiens	108-118
33253717-7	2021	Moreover, reverse transcript quantitative polymerase chain reaction (RT-qPCR) demonstrated that acyclovir suppressed the expression of caspase 3, caspase 8 and caspase 9, while there was no significant impact on the expression of the apoptosis-inhibiting gene bcl-2 in CCV-infected cells.	Acyclovir	96-105	caspase 8	Homo sapiens	146-155
33508949-8	2021	Shikonin could enhance apoptosis and inhibit proliferation and invasion of QBC939 cells; such biological behaviors mainly occurred via upregulating the expression of caspase-3 and caspase-8 and downregulating the expression of MMP-9 and EGFR.	shikonin	0-8	caspase 8	Homo sapiens	180-189
33539018-4	2021	In mitochondria-controlled pathway, caspase-8 is activated with death domain-independent manner, whereas, Fas-dependent classical pathway involves ligand-independent oligomerization of Fas.Hydrophobic bile acids dose-dependently upregulate the inflammatory response by further stimulating production of inflammatory cytokines.	Bile Acids and Salts	201-211	caspase 8	Homo sapiens	36-45
33508949-7	2021	Moreover, Annexin V/PI assay and Transwell invasion assay results indicated that Shikonin induced apoptosis and invasion inhibitory probably due to upregulation of caspase-3 and caspase-8 expression and downregulation of MMP-9 and EGFR expression in a concentration-dependent fashion.	shikonin	81-89	caspase 8	Homo sapiens	178-187
32767960-12	2021	Subsequently, blocking of TNFA-TNFR1 signalling by small molecule inhibitor, R-7050, reduced the expression of cleaved caspase-8 and caspase-3 at the protein level.	R-7050	77-83	caspase 8	Homo sapiens	119-128
33248713-0	2021	Novel urea linked ciprofloxacin-chalcone hybrids having antiproliferative topoisomerases I/II inhibitory activities and caspases-mediated apoptosis.	Urea	6-10	caspase 8	Homo sapiens	120-128
33248713-0	2021	Novel urea linked ciprofloxacin-chalcone hybrids having antiproliferative topoisomerases I/II inhibitory activities and caspases-mediated apoptosis.	Ciprofloxacin	18-31	caspase 8	Homo sapiens	120-128
33248713-0	2021	Novel urea linked ciprofloxacin-chalcone hybrids having antiproliferative topoisomerases I/II inhibitory activities and caspases-mediated apoptosis.	Chalcone	32-40	caspase 8	Homo sapiens	120-128
32531842-4	2021	It is becoming increasingly clear that caspase-8 has many non-apoptotic roles, participating in multiple processes including regulation of necroptosis (mediated by receptor-interacting serine/threonine kinases, RIPK1-RIPK3), inflammatory cytokine expression, inflammasome activation, and cleavage of IL-1beta and gasdermin D, and protection against shock and microbial infection.	Serine	185-191	caspase 8	Homo sapiens	39-48
32532192-0	2021	Lignans and polyphenols of Phyllanthus amarus Schumach & Thonn induce apoptosis in HCT116 human colon cancer cells through caspases-dependent pathway.	Lignans	0-7	caspase 8	Homo sapiens	123-131
32532192-0	2021	Lignans and polyphenols of Phyllanthus amarus Schumach & Thonn induce apoptosis in HCT116 human colon cancer cells through caspases-dependent pathway.	Polyphenols	12-23	caspase 8	Homo sapiens	123-131
32532192-9	2021	CONCLUSION: P. amarus extract, phyllanthin and gallic acid exhibited apoptotic effect on HCT116 cells via caspases-dependent pathway.	phyllanthin	31-42	caspase 8	Homo sapiens	106-114
32532192-9	2021	CONCLUSION: P. amarus extract, phyllanthin and gallic acid exhibited apoptotic effect on HCT116 cells via caspases-dependent pathway.	Gallic Acid	47-58	caspase 8	Homo sapiens	106-114
33316542-8	2021	We also proved that the cytotoxic activity of DC-derived supernatant induced apoptosis in the target cells and not necroptosis, as it was completely abrogated with the pan caspase inhibitor (Z-VAD), while the necroptosis inhibitor (Nec-1) had no effect.	z-vad	191-196	caspase 8	Homo sapiens	172-179
33337352-8	2021	The activity of Caspase-8 and -9 decreased significantly after the addition of 14, 15-EET but increased after the addition of HMR-1098.	14,15-epoxy-5,8,11-eicosatrienoic acid	79-89	caspase 8	Homo sapiens	16-32
33337352-8	2021	The activity of Caspase-8 and -9 decreased significantly after the addition of 14, 15-EET but increased after the addition of HMR-1098.	histidylmethionylarginine	126-129	caspase 8	Homo sapiens	16-32
32329631-7	2021	The present study also indicated that Q used at IC90 triggers predominantly programed cell death of sensitive HL60 cells and their MDR counterparts by induction of apoptosis occurring with the involvement of caspase-3 and caspase-8 as well as by lysosome membrane permeabilization-dependent mechanisms.	Quercetin	38-39	caspase 8	Homo sapiens	222-231
33394232-11	2021	Furthermore, western blotting result confirmed the activation of intrinsic pathway of apoptosis upon acacetin treatment and activation of both extrinsic and intrinsic pathways of apoptosis upon apigenin treatment through the regulation of Bax, t-Bid, caspase 8, caspase 9, caspase 3, and PARP.	Apigenin	194-202	caspase 8	Homo sapiens	251-260
33394232-13	2021	Acacetin and apigenin-induced ROS is responsible for the induction of cell cycle arrest and activation of caspase-cascade pathways in U87 cells.	acacetin	0-8	caspase 8	Homo sapiens	106-113
33394232-13	2021	Acacetin and apigenin-induced ROS is responsible for the induction of cell cycle arrest and activation of caspase-cascade pathways in U87 cells.	Apigenin	13-21	caspase 8	Homo sapiens	106-113
33394232-13	2021	Acacetin and apigenin-induced ROS is responsible for the induction of cell cycle arrest and activation of caspase-cascade pathways in U87 cells.	ros	30-33	caspase 8	Homo sapiens	106-113
33290779-4	2021	Our results show that 6SA reduces tumor volume and size by inducing caspase-8-mediated apoptosis without reducing tumor infiltrated lymphocytes.	anacardic acid	22-25	caspase 8	Homo sapiens	68-77
33424864-4	2020	Here, we review current knowledge about the distinction channels or pore-forming proteins underlying potassium efflux for NLRP3 inflammasome activation with canonical/non-canonical signaling or following caspase-8 induced pyroptosis.	Potassium	101-110	caspase 8	Homo sapiens	204-213
33392195-7	2020	Using myeloma as a model system, we further revealed that either inhibition or genetic depletion of CASP-8 enhances the anti-myeloma activity of lenalidomide (Len) by impairing CRBN cleavage, leading to the attenuated IKZF1 and IKZF3 protein levels and the reduced viability of myeloma cell lines and primary myeloma cells from patients.	Lenalidomide	145-157	caspase 8	Homo sapiens	100-106
33392195-7	2020	Using myeloma as a model system, we further revealed that either inhibition or genetic depletion of CASP-8 enhances the anti-myeloma activity of lenalidomide (Len) by impairing CRBN cleavage, leading to the attenuated IKZF1 and IKZF3 protein levels and the reduced viability of myeloma cell lines and primary myeloma cells from patients.	Lenalidomide	159-162	caspase 8	Homo sapiens	100-106
33392195-8	2020	The present study discovered that the stability of the substrate receptor of an E3 ligase can be modulated by CASP-8 and suggested that administration of CASP-8 inhibitors enhances the overall effectiveness of Len-based combination therapy in myeloma.	Lenalidomide	210-213	caspase 8	Homo sapiens	110-116
33392195-8	2020	The present study discovered that the stability of the substrate receptor of an E3 ligase can be modulated by CASP-8 and suggested that administration of CASP-8 inhibitors enhances the overall effectiveness of Len-based combination therapy in myeloma.	Lenalidomide	210-213	caspase 8	Homo sapiens	154-160
33736280-7	2020	Consequently, the novel curcuminoid macromolecule showed significant feasibility in triggering the high expression of apoptotic caspases caspase 3, caspase 8, P53, and Bax (P < 0.01 to P < 0.001) after 48 h of chemotherapy.	Diarylheptanoids	24-35	caspase 8	Homo sapiens	148-157
33322363-8	2020	Haloperidol was observed to induce apoptosis and to increase caspase-8 activation.	Haloperidol	0-11	caspase 8	Homo sapiens	61-70
33488754-13	2020	CASP8, GSK3B, PRKCA, and VEGFR2 were identified as the correlative biotargets of DDI-CPI and PPI, and their binding sites were found to be indirubin, G-Rh2, and G-Rf.	ddi-cpi	81-88	caspase 8	Homo sapiens	0-5
33488754-14	2020	Conclusion: Taken together, our results revealed that YSQHP likely exerts its antitumor effects by binding to CASP8, GSK3B, PRKCA, and VEGFR2 and by regulating the apoptosis, p53, and PI3K/AKT pathways.	ysqhp	54-59	caspase 8	Homo sapiens	110-115
33680921-7	2020	Results: PTX sensitized SiHaCIS-R cells to the effects of CIS by inducing apoptosis, caspase activation, and PARP-1 cleavage.	Pentoxifylline	9-12	caspase 8	Homo sapiens	85-92
33171188-7	2020	The qRT PCR analysis showed that 4-DMOCP induces apoptosis in both cell lines via the down-regulation of Survivin and Bcl2, up-regulation of caspase-8 and -9, as well as a time-dependent increase in the Bax/Bcl2 transcripts.	4-dmocp	33-40	caspase 8	Homo sapiens	141-157
33108350-4	2020	Here, we show that knockdown of CASP8 renders HNSCCs susceptible to necroptosis by a second mitochondria-derived activator of caspase (SMAC) mimetic, Birinapant, in combination with pan-caspase inhibitors zVAD FMK or Emricasan and radiation.	birinapant	150-160	caspase 8	Homo sapiens	32-37
33205964-4	2020	[Au(L1)(PPh3)](TfO) (1a) was able to induce caspases 8 and 3 activation, loss of mitochondrial membrane potential, and reactive oxygen species (ROS)-dependent cell death on Caco-2 cells upon 24 h incubation.	[au(l1)(pph3)]	0-14	caspase 8	Homo sapiens	44-60
33205964-4	2020	[Au(L1)(PPh3)](TfO) (1a) was able to induce caspases 8 and 3 activation, loss of mitochondrial membrane potential, and reactive oxygen species (ROS)-dependent cell death on Caco-2 cells upon 24 h incubation.	tfo	15-18	caspase 8	Homo sapiens	44-60
33205964-6	2020	However, the silver(I) analogue, [Ag(TfO)(L1)(PPh3)] (2a), induced cell death independent of inhibition of thioredoxin reductase and 20S proteasome, triggered ROS-independent apoptosis mediated by caspase 8 and 3 activation, and loss of mitochondrial membrane potential, which points to a different mechanism of action for both derivatives, dependent on the metal center.	[ag(tfo)(l1)(pph3)]	33-52	caspase 8	Homo sapiens	197-212
33108350-4	2020	Here, we show that knockdown of CASP8 renders HNSCCs susceptible to necroptosis by a second mitochondria-derived activator of caspase (SMAC) mimetic, Birinapant, in combination with pan-caspase inhibitors zVAD FMK or Emricasan and radiation.	birinapant	150-160	caspase 8	Homo sapiens	126-133
33108350-4	2020	Here, we show that knockdown of CASP8 renders HNSCCs susceptible to necroptosis by a second mitochondria-derived activator of caspase (SMAC) mimetic, Birinapant, in combination with pan-caspase inhibitors zVAD FMK or Emricasan and radiation.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	205-213	caspase 8	Homo sapiens	32-37
33108350-4	2020	Here, we show that knockdown of CASP8 renders HNSCCs susceptible to necroptosis by a second mitochondria-derived activator of caspase (SMAC) mimetic, Birinapant, in combination with pan-caspase inhibitors zVAD FMK or Emricasan and radiation.	3-(2-(2-tert-butylphenylaminooxalyl)aminopropionylamino)-4-oxo-5-(2,3,5,6-tetrafluorophenoxy)pentanoic acid	217-226	caspase 8	Homo sapiens	32-37
33288584-7	2020	Intrinsic and extrinsic pathways were involved in flavopereirine-induced apoptosis, as demonstrated by an increase of cleaved caspase 8 and 9 by western blotting.	flavopereirine	50-64	caspase 8	Homo sapiens	126-135
32780285-9	2020	Eventually, the relative proteins expression levels of p53, cleaved caspase-9/3, cytochrome c, Fas-L, Fas, FADD and caspase-8 were substantially up-regulated in H2O2-triggered HepG2 cells, and Bax/Bcl-2 ratio and the relative protein expression levels of PARP were dramatically down-regulated.	Hydrogen Peroxide	161-165	caspase 8	Homo sapiens	116-125
33258341-5	2020	Mechanistically, PTL treatment resulted in downregulation of NF-kappaB activity and Bcl-2 expression, and upregulation of Caspase-8 activity.	parthenolide	17-20	caspase 8	Homo sapiens	122-131
33125149-0	2020	Auranofin inhibits the proliferation of lung cancer cells via necrosis and caspase-dependent apoptosis.	Auranofin	0-9	caspase 8	Homo sapiens	75-82
33125149-8	2020	Furthermore, various caspase inhibitors reduced apoptosis and MMP ( Psim) loss in auranofin-treated Calu-6 cells.	Auranofin	82-91	caspase 8	Homo sapiens	21-28
33125149-9	2020	In particular, the pan-caspase inhibitor, benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone (Z-VAD), decreased cleavage forms of caspase-3, -8, and -9 in these cells.	Caspase Inhibitor VI	42-90	caspase 8	Homo sapiens	23-30
33125149-9	2020	In particular, the pan-caspase inhibitor, benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone (Z-VAD), decreased cleavage forms of caspase-3, -8, and -9 in these cells.	z-vad	92-97	caspase 8	Homo sapiens	23-30
33125149-10	2020	In conclusion, auranofin inhibited the proliferation of lung cancer cells, especially Calu-6 cells, via cell cycle arrest and cell death due to necrosis or caspase-dependent apoptosis.	Auranofin	15-24	caspase 8	Homo sapiens	156-163
33191863-10	2020	VU0359595 also strengthened bortezomib-induced apoptosis via activating caspase-8, caspase-9, caspase-3; and down-regulating the expressions of anti-apoptosis proteins BCL-2.	VU0359595	0-9	caspase 8	Homo sapiens	72-81
33191863-10	2020	VU0359595 also strengthened bortezomib-induced apoptosis via activating caspase-8, caspase-9, caspase-3; and down-regulating the expressions of anti-apoptosis proteins BCL-2.	Bortezomib	28-38	caspase 8	Homo sapiens	72-81
32525021-7	2020	The caspase inhibitor Q-VD-OPH could rescue trophozoite-induced cell apoptosis.	quinoline-val-asp(OMe)-CH2-OPH	22-30	caspase 8	Homo sapiens	4-11
33125113-8	2020	Furthermore, PG upregulated the activities of caspase-3 and caspase-8 in Calu-6 cells.	pg	13-15	caspase 8	Homo sapiens	60-69
33125114-0	2020	Arsenic compounds activate the MAPK and caspase pathways to induce apoptosis in OEC-M1 gingival epidermal carcinoma.	Arsenic	0-7	caspase 8	Homo sapiens	40-47
33125114-10	2020	Furthermore, both arsenic compounds significantly activated the cleavage of caspase-8, -9, -3 and PARP, and the phosphorylation of JNK, ERK1/2 and p38 in OEC-M1 cells (P<0.05).	Arsenic	18-25	caspase 8	Homo sapiens	76-93
32726164-8	2020	The treatment of UA232 could lead to an increase of CHOP expression rather than an increase in Bax or caspase-8, indicating that the apoptosis induced by UA232 was correlated with the endoplasmic reticulum stress (ER stress) pathway.	ua232	17-22	caspase 8	Homo sapiens	102-111
33299414-13	2020	Western blot analyses showed that after 72 hours of BEL treatment, the level of caspase-8/3 in A549 cells increased, and the level of PARP1 decreased in a dose-dependent manner.	bellidifolin	52-55	caspase 8	Homo sapiens	80-91
33073770-7	2020	MHY2256-induced apoptosis was involved in the activation of caspase-8, -9, and -3 and was prevented by pretreatment with Z-VAD-FMK, a pan-caspase inhibitor.	mhy2256	0-7	caspase 8	Homo sapiens	60-81
33073770-7	2020	MHY2256-induced apoptosis was involved in the activation of caspase-8, -9, and -3 and was prevented by pretreatment with Z-VAD-FMK, a pan-caspase inhibitor.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	121-130	caspase 8	Homo sapiens	60-81
32629210-6	2020	Fluoride stimulation increased caspase-dependent apoptosis through miR-200c-3p upregulation, with repressing expression of its target gene Fas-associated phosphatase 1 (Fap-1), which functioned as Fas inhibitor.	Fluorides	0-8	caspase 8	Homo sapiens	31-38
33078103-11	2020	CONCLUSION: SA inhibits the proliferation of Y79 cells by arresting the cell cycle at the G2/M phase, and induces apoptosis via the caspase-related apoptosis pathway, indicating that SA may have promising potential as a chemotherapeutic drug.	sodium aescinate	183-185	caspase 8	Homo sapiens	132-139
33106070-9	2020	Furthermore, DHA suppressed protein expression of caspase-3 and caspase-8.	Docosahexaenoic Acids	13-16	caspase 8	Homo sapiens	64-73
33121290-8	2021	However, the level of TRIF protein and CASP8 decreased after both NOB and Poly I:C incubation.	Poly I	74-80	caspase 8	Homo sapiens	39-44
33126536-2	2020	After binding to this initiator caspase, vICA blocks caspase-8 proteolytic activity and ability to activate caspase-3 and/or caspase-7.	vica	41-45	caspase 8	Homo sapiens	53-62
33126536-10	2020	Caspase-8 suppression by vICA emerges as key to subverting innate immune elimination of a wide variety of infected cell types.	vica	25-29	caspase 8	Homo sapiens	0-9
33101585-6	2020	Compared with the H2O2-treated group, the expressions of cleaved caspase-3, cleaved caspase-9, cleaved polymerase (PARP), death receptor Fas, and cleaved caspase-8, as well as Bax/Bcl-2 ratio were decreased in RPE cells after the phillyrin intervention.	Hydrogen Peroxide	18-22	caspase 8	Homo sapiens	154-163
33194045-12	2020	Additionally, knockdown of caspase-8 reduced the doxorubicin, carboplatin, cisplatin, and etoposide sensitivity towards A549 cells.	Doxorubicin	49-60	caspase 8	Homo sapiens	27-36
33194045-12	2020	Additionally, knockdown of caspase-8 reduced the doxorubicin, carboplatin, cisplatin, and etoposide sensitivity towards A549 cells.	Carboplatin	62-73	caspase 8	Homo sapiens	27-36
33194045-12	2020	Additionally, knockdown of caspase-8 reduced the doxorubicin, carboplatin, cisplatin, and etoposide sensitivity towards A549 cells.	Cisplatin	75-84	caspase 8	Homo sapiens	27-36
33194045-12	2020	Additionally, knockdown of caspase-8 reduced the doxorubicin, carboplatin, cisplatin, and etoposide sensitivity towards A549 cells.	Etoposide	90-99	caspase 8	Homo sapiens	27-36
33081167-7	2020	Additionally, GSPE promotes osteoclast proliferation by increasing the phosphorylation of components of the Akt and mitogen-activated protein kinase signaling pathways and it also inhibits apoptosis by decreasing the activity of caspase-8, caspase-9, and caspase-3, as corroborated by a decrease in the Terminal deoxynucleotidyl transferase dUTP nick end labeling -positive cells.	gspe	14-18	caspase 8	Homo sapiens	229-238
33066043-5	2020	Cells treated with D089 exhibited high levels of the cleaved form of initiator caspase 8; but failed to show cleavage of executioner caspase 3, a classical apoptotic marker.	d089	19-23	caspase 8	Homo sapiens	79-88
33066043-7	2020	In contrast, cleaved caspase 1, an inflammatory caspase downstream of caspases 8/9, was increased by D089 treatment.	d089	101-105	caspase 8	Homo sapiens	70-82
33036527-8	2020	After c-myc silenced cells were treated with PM2.5 water soluble solution, The mRNA levels of c-myc, c-fos, and k-ras decreased by 84.1%, 45.4%, and 54.6% (P<0.05) , p53 increased by 192.9% (P<0.05) , and the expression of Caspase-3, Caspase-8, and Caspase-9 decreased by 24.4%, 36.1%, 60.9% (P<0.05) .	Water	51-56	caspase 8	Homo sapiens	234-243
33039058-7	2020	The results indicated that DpLE causes apoptosis and exerts intracellular ROS-independent anticancer effects on prostate cancer cells, associated with increased SOD-2, cleaved caspase-8, and cleaved-PARP expression and inhibited p-AKT signaling.	dple	27-31	caspase 8	Homo sapiens	176-185
32712543-12	2020	The FUC and DOX combination increased the levels and activity of caspases (CASP3, CASP8) and p53, while decreased the levels and activity of CYP3A4, GST, and PXR in resistant cancer cells.	fucoxanthin	4-7	caspase 8	Homo sapiens	65-73
32712543-12	2020	The FUC and DOX combination increased the levels and activity of caspases (CASP3, CASP8) and p53, while decreased the levels and activity of CYP3A4, GST, and PXR in resistant cancer cells.	fucoxanthin	4-7	caspase 8	Homo sapiens	82-87
32712543-12	2020	The FUC and DOX combination increased the levels and activity of caspases (CASP3, CASP8) and p53, while decreased the levels and activity of CYP3A4, GST, and PXR in resistant cancer cells.	Doxorubicin	12-15	caspase 8	Homo sapiens	65-73
32712543-12	2020	The FUC and DOX combination increased the levels and activity of caspases (CASP3, CASP8) and p53, while decreased the levels and activity of CYP3A4, GST, and PXR in resistant cancer cells.	Doxorubicin	12-15	caspase 8	Homo sapiens	82-87
32096279-2	2020	Caspases are a family of cysteine-dependent aspartate-directed proteases that play essential roles in regulating cell death and inflammation.	Cysteine	25-33	caspase 8	Homo sapiens	0-8
32567066-8	2020	Caspase 8 was activated in cells treated by CPF but accompaniment of PILO with CPF led to activation of caspase 9, 8 and 3 and ROS overproduction.	Pilocarpine	69-73	caspase 8	Homo sapiens	0-9
32567066-8	2020	Caspase 8 was activated in cells treated by CPF but accompaniment of PILO with CPF led to activation of caspase 9, 8 and 3 and ROS overproduction.	ros	127-130	caspase 8	Homo sapiens	0-9
31784978-10	2020	In support, data from q-RT PCR showed that SCFA treatments influenced the expression of the neurogenesis, proliferation, and apoptosis-related genes ATR, BCL2, BID, CASP8, CDK2, E2F1, FAS, NDN, and VEGFA.	Fatty Acids, Volatile	43-47	caspase 8	Homo sapiens	165-170
32894054-9	2020	RESULTS: Our results showed that maternal bupivacaine use caused a significant increment of cleaved caspase-3 and caspase-8 expression in fetal hippocampus compared with the sham group.	Bupivacaine	42-53	caspase 8	Homo sapiens	114-123
32894054-10	2020	In addition, maternally administered bupivacaine could significantly decrease hippocampal P.Akt/T.Akt ratio which was concurrent with an increment of cleaved caspase-3 and caspase-8 expression.	Bupivacaine	37-48	caspase 8	Homo sapiens	172-181
32894054-11	2020	CONCLUSION: Our data suggest that maternal bupivacaine use increases fetal hippocampal cell apoptosis markers such as caspase 8 and cleaved caspase 3, at least in part, via inhibiting the Akt activation.	Bupivacaine	43-54	caspase 8	Homo sapiens	118-127
32705266-7	2020	Flow cytometry revealed that LPB significantly induced apoptosis of NSCLC cells, along with changes in the expression of apoptosis-associated proteins, including an increase in Bax, caspase-3, and caspase-8 expression, and a decrease in Bcl-2 and Bcl-xl expression.	liriopesides B	29-32	caspase 8	Homo sapiens	197-206
32705246-0	2020	2-Hydroxypropyl-beta-cyclodextrin blocks autophagy flux and triggers caspase-8-mediated apoptotic cascades in HepG2 cells.	2-Hydroxypropyl-beta-cyclodextrin	0-33	caspase 8	Homo sapiens	69-78
32814042-6	2020	Finally, we show that the Trypanosoma Pcif1 is an m6Am methylase that contributes to the N6,N6,2"-O-trimethyladenosine (m62Am) in the hypermethylated cap4 structure of trypanosomatids.	N6,N6,2'-O-trimethyladenosine	89-118	caspase 8	Homo sapiens	150-154
30638055-3	2020	Valtrate induced cell cycle arrest at G2/M stage and apoptosis in MDA-MB-231 and MCF-7 cells, with reduced expression of p-Akt (Ser 473), cyclin B1 and caspase 8, and increased expression of p21, p-cdc2, cleaved-caspase 3, cleaved-caspase 7 and poly (ADP-ribose) polymerase (PARP).	valtrate	0-8	caspase 8	Homo sapiens	152-161
32814042-6	2020	Finally, we show that the Trypanosoma Pcif1 is an m6Am methylase that contributes to the N6,N6,2"-O-trimethyladenosine (m62Am) in the hypermethylated cap4 structure of trypanosomatids.	m62am	120-125	caspase 8	Homo sapiens	150-154
32792491-3	2020	In addition, we identify Gsta4 as a target of both dimethyl fumarate, an existing MS therapy, and clemastine fumarate, a candidate remyelinating agent in MS. Overexpression of Gsta4 reduces expression of Fas and activity of the mitochondria-associated Casp8-Bid-axis in adult oligodendrocyte precursor cells, leading to improved OL survival during differentiation.	Clemastine	98-117	caspase 8	Homo sapiens	252-257
32759757-5	2020	We found that EF-24 treatment induces several features of apoptosis, including an increase in the sub-G1 population, phosphatidylserine (PS) externalization, and significant activation of extrinsic proapoptotic signaling such as caspase-8 and -3 activation.	UNII-O5YT36MST0	14-19	caspase 8	Homo sapiens	229-245
32059077-3	2020	Apigenin induces apoptosis by the activation of extrinsic caspase-dependent pathway by upregulating the mRNA expressions of caspase-3, caspase-8, and TNF-alpha.	Apigenin	0-8	caspase 8	Homo sapiens	58-65
32190974-5	2020	Dose-dependent induction of Annexin V positive cells, activated caspase 8, activated caspase 9, activated caspase 3, and the cleavage of poly (ADP-ribose) polymerase were observed after the treatment with betulin, indicating betulin induces apoptosis in osteosarcoma cell lines.	betulin	205-212	caspase 8	Homo sapiens	64-73
32626921-6	2020	Inhibition of autophagy using autophagy inhibitors 3-methyladenine and chloroquine upregulated the expression of DR5 and enhanced TRAIL-induced apoptosis, as confirmed by the increase of pro-apoptotic proteins caspase-8 and caspase-3.	3-methyladenine	51-66	caspase 8	Homo sapiens	210-219
32626921-6	2020	Inhibition of autophagy using autophagy inhibitors 3-methyladenine and chloroquine upregulated the expression of DR5 and enhanced TRAIL-induced apoptosis, as confirmed by the increase of pro-apoptotic proteins caspase-8 and caspase-3.	Chloroquine	71-82	caspase 8	Homo sapiens	210-219
32626921-8	2020	Overall, sertraline enhanced TRAIL-mediated apoptosis via the downregulation of AMP-activated protein kinase phosphorylation, resulting in the inhibition of autophagic flux, upregulation of DR5 expression, and activation of the apoptotic caspase cascade.	Sertraline	9-19	caspase 8	Homo sapiens	238-245
32470830-4	2020	The induction of apoptosis by both isobutyrylshikonin and shikonin was accompanied by activation of caspase-8, -9, -3, and PARP, loss of mitochondrial trans-membrane potential, and release of cytochrome c from the mitochondria.	isobutyrylshikonin	35-53	caspase 8	Homo sapiens	100-117
32470830-4	2020	The induction of apoptosis by both isobutyrylshikonin and shikonin was accompanied by activation of caspase-8, -9, -3, and PARP, loss of mitochondrial trans-membrane potential, and release of cytochrome c from the mitochondria.	shikonin	45-53	caspase 8	Homo sapiens	100-117
32470830-9	2020	In addition, our data exhibit that both isobutyrylshikonin and shikonin induce caspase-dependent apoptosis via the mitochondrial pathway through accumulation of ROS in oral squamous carcinoma cells.	isobutyrylshikonin	40-58	caspase 8	Homo sapiens	79-86
32470830-9	2020	In addition, our data exhibit that both isobutyrylshikonin and shikonin induce caspase-dependent apoptosis via the mitochondrial pathway through accumulation of ROS in oral squamous carcinoma cells.	shikonin	50-58	caspase 8	Homo sapiens	79-86
32470830-9	2020	In addition, our data exhibit that both isobutyrylshikonin and shikonin induce caspase-dependent apoptosis via the mitochondrial pathway through accumulation of ROS in oral squamous carcinoma cells.	ros	161-164	caspase 8	Homo sapiens	79-86
32416217-8	2020	Moreover, DT-13 induced the death receptor pathway-dependent apoptosis of HL-60 and Kasumi-1 cells by up-regulating Fas, FasL, DR5 and TRAIL as well as promoted the cleavage of caspase 8, caspase 3 and PARP.	DT-13	10-15	caspase 8	Homo sapiens	177-186
32059077-3	2020	Apigenin induces apoptosis by the activation of extrinsic caspase-dependent pathway by upregulating the mRNA expressions of caspase-3, caspase-8, and TNF-alpha.	Apigenin	0-8	caspase 8	Homo sapiens	135-144
32717981-9	2020	Our study revealed that anticancer activity of 7-methyl-5-phenyl-pyrazolo[4,3-e]tetrazolo[4,5-b][1,2,4]triazine derivatives is related with initiation of apoptosis occur on the intrinsic pathway with mitochondrial membrane decrease and extrinsic with increase of activity of caspase-8.	7-methyl-5-phenyl-pyrazolo[4,3-e]tetrazolo[4,5-b][1,2,4]triazine	47-111	caspase 8	Homo sapiens	275-284
32461113-0	2020	Shikonin suppresses trophoblast cell growth via regulation of GLI1, and p62 mediated caspase 8activation.	shikonin	0-8	caspase 8	Homo sapiens	85-94
32461113-5	2020	Shikonin blocked autophagic flux and promoted p62 interaction with caspase 8, resulting in caspase 8 activation.	shikonin	0-8	caspase 8	Homo sapiens	67-76
32461113-5	2020	Shikonin blocked autophagic flux and promoted p62 interaction with caspase 8, resulting in caspase 8 activation.	shikonin	0-8	caspase 8	Homo sapiens	91-100
32461113-9	2020	In conclusion, shikonin suppressed trophoblast cell growth by silencing GLI1 and increasing p62 co-mediated activation of caspase 8, which suggested a potential novel therapeutic target for UEP.	shikonin	15-23	caspase 8	Homo sapiens	122-131
32714568-4	2020	We also identified roles for the extrinsic (TRAIL-R2/caspase-8) and intrinsic (BAX/BAK) apoptotic pathways in mediating the apoptotic effects of MLN4924 in CRC cells, as well as a role for BID, which modulates a cross-talk between these pathways.	pevonedistat	145-152	caspase 8	Homo sapiens	53-62
32714568-5	2020	Depletion of the anti-apoptotic protein FLIP, which we identify as a novel mediator of resistance to MLN4924, enhanced apoptosis in a p53-, TRAIL-R2/DR5-, and caspase-8-dependent manner.	pevonedistat	101-108	caspase 8	Homo sapiens	159-168
32351145-9	2020	The increase in initiator caspase-8 and -9 and executioner caspase-3/7 activities by DPA-induced apoptosis albeit prompting a decline in the levels of ATP.	dpa	85-88	caspase 8	Homo sapiens	26-42
32449282-5	2020	As results, the bioinformatic findings showed the core anti-NPC targets played by calycosin included tumor protein p53 (TP53), mitogen-activated protein kinase 14 (MAPK14), caspase 8 (CASP8), mitogen-activated protein kinase 3 (MAPK3), caspase 3 (CASP3), receptor interacting protein kinase 1 (RIPK1), proto-oncogene c (JUN), and estrogen receptor 1 (ESR1).	7,3'-dihydroxy-4'-methoxyisoflavone	82-91	caspase 8	Homo sapiens	173-182
32449282-5	2020	As results, the bioinformatic findings showed the core anti-NPC targets played by calycosin included tumor protein p53 (TP53), mitogen-activated protein kinase 14 (MAPK14), caspase 8 (CASP8), mitogen-activated protein kinase 3 (MAPK3), caspase 3 (CASP3), receptor interacting protein kinase 1 (RIPK1), proto-oncogene c (JUN), and estrogen receptor 1 (ESR1).	7,3'-dihydroxy-4'-methoxyisoflavone	82-91	caspase 8	Homo sapiens	184-189
32616191-8	2020	Taken together, our results revealed that ZLTE induced caspase-dependent apoptosis via ROS generation, suggesting that ZLTE is a promising herbal medicine for the treatment of NSCLC.	Reactive Oxygen Species	87-90	caspase 8	Homo sapiens	55-62
32439176-7	2020	Salidroside could activate intrinsic and extrinsic apoptotic pathways, by increasing activities of caspase-3, caspase-8 and caspase-9, up-regulating levels of Bax, Cytochrome c and decreasing level of Bcl-2 in HepG2 cells.	rhodioloside	0-11	caspase 8	Homo sapiens	110-119
32537005-7	2020	However, treatment with helenalin, a NF-kappaB inhibitor, decreased p65 phosphorylation, attenuated IL-17-induced podocyte apoptosis and suppressed the IL-17-activated Fas/FasL/caspase-8/caspase-3 apoptotic pathway.	helenalin	24-33	caspase 8	Homo sapiens	177-186
32351145-9	2020	The increase in initiator caspase-8 and -9 and executioner caspase-3/7 activities by DPA-induced apoptosis albeit prompting a decline in the levels of ATP.	Adenosine Triphosphate	151-154	caspase 8	Homo sapiens	26-42
32351145-11	2020	The cytotoxic effects of DPA in HEK293 cells may be mediated by induction of apoptosis via the caspase-dependent mechanism.	dpa	25-28	caspase 8	Homo sapiens	95-102
32247004-12	2020	Besides, Andro markedly down-regulated the 5-Fu-induced protein expression of caspase8/3, Bax and the phosphorylation of p38.	Fluorouracil	43-47	caspase 8	Homo sapiens	78-88
31898356-8	2020	The relative mRNA abundance of BAK, BAX, CASP3, CASP8, and TP53 and protein abundance of Bak, cleaved caspase-3, caspase-8, and P53 was activated by U73122 or inhibited by m-3M3FBS, while the relative mRNA and protein level of BCL6 showed the opposite trend.	1-(6-((3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione	149-155	caspase 8	Homo sapiens	48-53
31898356-8	2020	The relative mRNA abundance of BAK, BAX, CASP3, CASP8, and TP53 and protein abundance of Bak, cleaved caspase-3, caspase-8, and P53 was activated by U73122 or inhibited by m-3M3FBS, while the relative mRNA and protein level of BCL6 showed the opposite trend.	1-(6-((3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione	149-155	caspase 8	Homo sapiens	113-122
32545774-3	2020	We found that the human H4 glioma cell-killing effects of aspirin involved mitochondria-mediated apoptosis accompanied by endoplasmic reticulum (ER) stress, Noxa upregulation, Mcl-1 downregulation, Bax mitochondrial distribution and oligomerization, and caspase 3/caspase 8/caspase 9 activation.	Aspirin	58-65	caspase 8	Homo sapiens	264-273
32558229-5	2020	Moreover, the anticancer mechanism studies reveal that FUdR@affi-RA enhances the expression and activity of apoptosis-associated proteins in the Bcl-2/Bax-caspase 8,9-caspase 3 apoptotic pathway induced by FUdR.	Floxuridine	55-59	caspase 8	Homo sapiens	155-164
32418059-0	2020	Doxorubicin sensitizes cancer cells to Smac mimetic via synergistic activation of the CYLD/RIPK1/FADD/caspase-8-dependent apoptosis.	Doxorubicin	0-11	caspase 8	Homo sapiens	102-111
32444487-7	2020	Finally, we identify the molecular mechanism through which vICA acts, demonstrating the central contribution of caspase-8 signaling at a point of convergence of death receptor-induced apoptosis and perforin/granzyme-dependent cytotoxicity.	vica	59-63	caspase 8	Homo sapiens	112-121
31955141-6	2020	Cur-NLC significantly increased caspase-8 and caspase-3 activities, accompanied by increased apoptosis.	Cur1 compound	0-3	caspase 8	Homo sapiens	32-41
31955141-8	2020	Therefore, Cur-NLC induced activation of the extrinsic apoptosis pathway via modulating the DR5/caspase-8/-3 mediated apoptosis pathway in HepG2 cells, suggesting that Cur-NLC is a promising therapeutic agent or supplement for the treatment of hepatocellular carcinoma.	Cur1 compound	11-14	caspase 8	Homo sapiens	96-105
31955141-8	2020	Therefore, Cur-NLC induced activation of the extrinsic apoptosis pathway via modulating the DR5/caspase-8/-3 mediated apoptosis pathway in HepG2 cells, suggesting that Cur-NLC is a promising therapeutic agent or supplement for the treatment of hepatocellular carcinoma.	Cur1 compound	168-171	caspase 8	Homo sapiens	96-105
32418059-9	2020	Knockdown of caspase-8 or knockout of FADD significantly blocked apoptosis synergistically induced by Smac mimetic and doxorubicin, but had no effect on cell death caused by doxorubicin alone.	Doxorubicin	119-130	caspase 8	Homo sapiens	13-22
32418059-11	2020	These in vitro findings demonstrate that combination of Smac mimetic and doxorubicin synergistically triggers apoptosis through the TNF/CYLD/RIPK1/FADD/caspase-8 signaling pathway.	Doxorubicin	73-84	caspase 8	Homo sapiens	152-161
32539919-4	2020	A combination of UA and Oxa induced apoptosis in RKO cells and increased the activities of caspase-3, caspase-8, and caspase-9.	ursolic acid	17-19	caspase 8	Homo sapiens	102-111
32145587-7	2020	Interestingly, DSF/Cu induced caspase-3 activation was partly blocked by Z-VAD-FMK (zVAD), a pan-caspase inhibitor, indicating at caspase-dependent and -independent paths involved in DSF/Cu induced myeloma cell apoptosis machinery.	Disulfiram	15-18	caspase 8	Homo sapiens	30-37
32145587-7	2020	Interestingly, DSF/Cu induced caspase-3 activation was partly blocked by Z-VAD-FMK (zVAD), a pan-caspase inhibitor, indicating at caspase-dependent and -independent paths involved in DSF/Cu induced myeloma cell apoptosis machinery.	Disulfiram	15-18	caspase 8	Homo sapiens	97-104
32145587-7	2020	Interestingly, DSF/Cu induced caspase-3 activation was partly blocked by Z-VAD-FMK (zVAD), a pan-caspase inhibitor, indicating at caspase-dependent and -independent paths involved in DSF/Cu induced myeloma cell apoptosis machinery.	Copper	19-21	caspase 8	Homo sapiens	30-37
32145587-7	2020	Interestingly, DSF/Cu induced caspase-3 activation was partly blocked by Z-VAD-FMK (zVAD), a pan-caspase inhibitor, indicating at caspase-dependent and -independent paths involved in DSF/Cu induced myeloma cell apoptosis machinery.	Copper	19-21	caspase 8	Homo sapiens	97-104
32145587-7	2020	Interestingly, DSF/Cu induced caspase-3 activation was partly blocked by Z-VAD-FMK (zVAD), a pan-caspase inhibitor, indicating at caspase-dependent and -independent paths involved in DSF/Cu induced myeloma cell apoptosis machinery.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	73-82	caspase 8	Homo sapiens	30-37
32145587-7	2020	Interestingly, DSF/Cu induced caspase-3 activation was partly blocked by Z-VAD-FMK (zVAD), a pan-caspase inhibitor, indicating at caspase-dependent and -independent paths involved in DSF/Cu induced myeloma cell apoptosis machinery.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	73-82	caspase 8	Homo sapiens	97-104
32145587-7	2020	Interestingly, DSF/Cu induced caspase-3 activation was partly blocked by Z-VAD-FMK (zVAD), a pan-caspase inhibitor, indicating at caspase-dependent and -independent paths involved in DSF/Cu induced myeloma cell apoptosis machinery.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	84-88	caspase 8	Homo sapiens	30-37
32145587-7	2020	Interestingly, DSF/Cu induced caspase-3 activation was partly blocked by Z-VAD-FMK (zVAD), a pan-caspase inhibitor, indicating at caspase-dependent and -independent paths involved in DSF/Cu induced myeloma cell apoptosis machinery.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	84-88	caspase 8	Homo sapiens	97-104
32145587-7	2020	Interestingly, DSF/Cu induced caspase-3 activation was partly blocked by Z-VAD-FMK (zVAD), a pan-caspase inhibitor, indicating at caspase-dependent and -independent paths involved in DSF/Cu induced myeloma cell apoptosis machinery.	Disulfiram	183-186	caspase 8	Homo sapiens	30-37
32145587-7	2020	Interestingly, DSF/Cu induced caspase-3 activation was partly blocked by Z-VAD-FMK (zVAD), a pan-caspase inhibitor, indicating at caspase-dependent and -independent paths involved in DSF/Cu induced myeloma cell apoptosis machinery.	Copper	187-189	caspase 8	Homo sapiens	30-37
32539919-4	2020	A combination of UA and Oxa induced apoptosis in RKO cells and increased the activities of caspase-3, caspase-8, and caspase-9.	Oxaliplatin	24-27	caspase 8	Homo sapiens	102-111
32539919-5	2020	Z-VAD-FMK, a caspase inhibitor, significantly antagonized UA- and Oxa-activated caspase-3, caspase-8, and caspase-9 and induced apoptosis.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	0-9	caspase 8	Homo sapiens	13-20
32539919-5	2020	Z-VAD-FMK, a caspase inhibitor, significantly antagonized UA- and Oxa-activated caspase-3, caspase-8, and caspase-9 and induced apoptosis.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	0-9	caspase 8	Homo sapiens	91-100
32539919-5	2020	Z-VAD-FMK, a caspase inhibitor, significantly antagonized UA- and Oxa-activated caspase-3, caspase-8, and caspase-9 and induced apoptosis.	ursolic acid	58-60	caspase 8	Homo sapiens	13-20
31898278-2	2020	Here, we show that SCA2 patient cells exhibit higher levels of caspase-8- and caspase-9-mediated apoptotic activation than control cells, cellular phenotypes that we find to be exacerbated by reactive oxygen species (ROS) and inhibition of autophagy.	Oxygen	201-207	caspase 8	Homo sapiens	63-72
32455622-8	2020	BP/LPPC induced cell apoptosis by activating the extrinsic (Fas, Fas-L and Caspase-8) and intrinsic (Bax and Caspase-9) apoptosis pathways.	butylidenephthalide	0-2	caspase 8	Homo sapiens	75-84
32455622-8	2020	BP/LPPC induced cell apoptosis by activating the extrinsic (Fas, Fas-L and Caspase-8) and intrinsic (Bax and Caspase-9) apoptosis pathways.	lppc	3-7	caspase 8	Homo sapiens	75-84
32547191-11	2020	Western blot results showed that DIOS significantly suppressed the expression levels of Bcl-2, cdc2, cyclinB1, and promoted the expression levels of Bax, cleaved-caspase3, cleaved-caspase8, cleaved-PARP, Bak, P53, and P21.	diosmetin	33-37	caspase 8	Homo sapiens	180-188
32045101-7	2020	TRAN"s coadministration with MTX in the current study induced a significant tissue recovery via modulation of TRAIL/caspase-8 signaling and modulation of apoptosis-induced tissue proliferation confirmed by quantification of Ki67 expression.	tranilast	0-4	caspase 8	Homo sapiens	116-125
32045101-7	2020	TRAN"s coadministration with MTX in the current study induced a significant tissue recovery via modulation of TRAIL/caspase-8 signaling and modulation of apoptosis-induced tissue proliferation confirmed by quantification of Ki67 expression.	Methotrexate	29-32	caspase 8	Homo sapiens	116-125
32365525-5	2020	Caspase 8 was determined to interact with rutaecarpine through five amino acid residues, specifically Thr337, Lys353, Val354, Phe355, and Phe356, and two hydrogen bonds (ligand: H35-A: LYS353:O and A:PHE355: N-ligand: N5).	rutecarpine	42-54	caspase 8	Homo sapiens	0-9
32365525-5	2020	Caspase 8 was determined to interact with rutaecarpine through five amino acid residues, specifically Thr337, Lys353, Val354, Phe355, and Phe356, and two hydrogen bonds (ligand: H35-A: LYS353:O and A:PHE355: N-ligand: N5).	Hydrogen	154-162	caspase 8	Homo sapiens	0-9
32365525-7	2020	The obtained results propose that rutaecarpine could be a lead compound that bears remarkable anti-Alzheimer"s potential against caspase 8.	rutecarpine	34-46	caspase 8	Homo sapiens	129-138
32368052-12	2020	We concluded that one of the important mechanisms of BA-C60(OH)n-GBP-TPGS-NPs inhibiting MHCC97H cells is achieved by up-regulating the expression of Caspase-3, Caspase-8 and Caspase-9.	betulinic acid	53-55	caspase 8	Homo sapiens	161-170
32316340-5	2020	Cell death was mediated by the processing and activation of initiator and effector caspases and the cleavage of poly(ADP-ribose) polymerase, and it was blocked by a broad-spectrum caspase inhibitor and (in the case of sesquiterpene lactone 2) by the selective caspase-3/7, -8, and -9 inhibitors.	sesquiterpene lactone	218-239	caspase 8	Homo sapiens	83-91
32316340-5	2020	Cell death was mediated by the processing and activation of initiator and effector caspases and the cleavage of poly(ADP-ribose) polymerase, and it was blocked by a broad-spectrum caspase inhibitor and (in the case of sesquiterpene lactone 2) by the selective caspase-3/7, -8, and -9 inhibitors.	sesquiterpene lactone	218-239	caspase 8	Homo sapiens	83-90
32053770-6	2020	We further demonstrate that the C-terminal of caspase-8 is mainly responsible for the interaction with V-ATPase and can suffice to inhibit survival of cancer cells.	Carbon	32-33	caspase 8	Homo sapiens	46-55
32624694-4	2020	Furthermore, we showed that cladribine induced apoptosis by decreasing the expression of c-FLIPL and increasing the expression of DR4 and the cleaved form of caspase8.	Cladribine	28-38	caspase 8	Homo sapiens	158-166
32581545-13	2020	Cytotoxicity of bufalin to caspase-8 knockdown cell lines made control cell lines more sensitive to bufalin in their mixture.	bufalin	16-23	caspase 8	Homo sapiens	27-36
32581545-13	2020	Cytotoxicity of bufalin to caspase-8 knockdown cell lines made control cell lines more sensitive to bufalin in their mixture.	bufalin	100-107	caspase 8	Homo sapiens	27-36
31927382-7	2020	Slightly negative trends of promoter methylations in Rb1 and CASP8, while a strong positive trend of MeCP2 promoter methylation, were found along with increasing Pb and Cd levels.	Lead	162-164	caspase 8	Homo sapiens	61-66
31927382-7	2020	Slightly negative trends of promoter methylations in Rb1 and CASP8, while a strong positive trend of MeCP2 promoter methylation, were found along with increasing Pb and Cd levels.	Cadmium	169-171	caspase 8	Homo sapiens	61-66
32274578-7	2020	Additionally, the real-time quantitative PCR analysis revealed that Cu-TSC triggers apoptosis in both cell lines via the upregulation of caspases-8, -9, and the changing of Bax/Bcl2 ratio.	Copper	68-70	caspase 8	Homo sapiens	137-151
31996318-8	2020	ART-induced apoptosis corresponded to activation of caspase-8/9/3; decreased expression of Bcl-xL, Bcl-2, myeloid cell leukemia-1, survivin, X-linked inhibitor of apoptosis protein and cellular inhibitor of apoptosis 1/2; and increased expression of Bak.	artesunate	0-3	caspase 8	Homo sapiens	52-65
31278615-6	2020	Our study presents two preliminary findings: (a) in HaVSMCs, FOLFIRI treatment significantly induces oxidative damage to both DNA and protein, leading to a dramatic increase in caspase-dependent apoptotic death through P53-mediated Caspase3-dependent mitochondrial apoptosis, and results in TNF-alpha/Caspase8-mediated necrotic death, and (b) flavonoids not only regulate the expression of genes encoding antioxidant enzymes and increase DNA damage but also limit programmed and necrotic cell death processes in HaVSMCs.	FOLFIRI regimen	61-68	caspase 8	Homo sapiens	301-309
32017928-4	2020	In this study, we showed that sodium selenite switched protective autophagy to apoptosis in p53-wild type NB4 cells without obvious caspase-8/apoptosis-inducing factor (AIF) axis activation, while induced autophagy-dependent caspase-8/AIF axis activation in p53-mutant Jurkat cells.	Sodium Selenite	30-45	caspase 8	Homo sapiens	132-141
31812766-5	2020	Moreover, formaldehyde significantly potentiated the induction of death receptor-5, caspase 8/10, cleaved caspase 3/7/9, pro-apoptotic proteins (Bim, Bad and Bax), depolarization of MMP (mitochondrial membrane potential) and AIF (apoptosis-inducing factor) induced by acrolein, and synergistically decreased expressions of pro-survival proteins (Bcl-2 and Bcl-XL) and poly ADP-ribose polymerase.	Formaldehyde	10-22	caspase 8	Homo sapiens	84-96
32109484-4	2020	AJ-374 promoted the arrest of the cells in the subG0/G1 phase of the cell cycle in the first 24 h. Treatment of HL-60 cells with AJ-374 caused an increase in annexin-V positive cells, activation of caspase-8, -9 and -3, dissipation of the mitochondrial membrane potential and enhancement of FAS protein level.	aj-374	0-6	caspase 8	Homo sapiens	198-218
32109484-4	2020	AJ-374 promoted the arrest of the cells in the subG0/G1 phase of the cell cycle in the first 24 h. Treatment of HL-60 cells with AJ-374 caused an increase in annexin-V positive cells, activation of caspase-8, -9 and -3, dissipation of the mitochondrial membrane potential and enhancement of FAS protein level.	aj-374	129-135	caspase 8	Homo sapiens	198-218
32109484-5	2020	Apoptosis induction triggered by this quinolinone was blocked by the pre-treatment of the cells with caspase-8, -9 and -3 inhibitors.	Quinolones	38-49	caspase 8	Homo sapiens	101-121
32017928-7	2020	Furthermore, sodium selenite induced the release of AIF from mitochondria to cytosol with the facilitation of caspase-8 in Jurkat cells, while not in NB4 cells.	Sodium Selenite	13-28	caspase 8	Homo sapiens	110-119
32244330-5	2020	Following infection with SRV-8, the autophagic proteins LC3 and p62/SQSTM1 interacted with procaspase-8, which might be responsible for the activation of the caspase-8/-3 cascade and apoptosis in SRV-8-infected Jurkat cells.	srv-8	25-30	caspase 8	Homo sapiens	158-170
32155920-4	2020	OMEO induced protective autophagy, associated with downregulation of the mTOR/p70S6K pathway, and activated caspase-8 and caspase-9-dependent apoptosis.	omeo	0-4	caspase 8	Homo sapiens	108-117
31816367-7	2020	The mechanism of apoptosis was associated with the death receptor pathway by the activation of caspases -8, -9, and -3, and correlated to its fatty acids action.	Fatty Acids	142-153	caspase 8	Homo sapiens	95-118
32188144-4	2020	Mechanistic investigations found that the downregulation of cellular IAP 1 (cIAP1)/X-chromosome-linked IAP (XIAP) and upregulation of heme oxygenase-1 (HO-1) were critical for DMC-induced caspase-8/-9/-3 activation and apoptotic cell death.	demethoxycurcumin	176-179	caspase 8	Homo sapiens	188-197
32188144-5	2020	Moreover, p38 mitogen-activated protein kinase (MAPK) and c-Jun N-terminal kinase (JNK)1/2 were activated by DMC treatment in OSCC cells, and only the inhibition of p38 MAPK significantly abolished DMC-induced HO-1 expression and caspase-8/-9/-3 activation.	demethoxycurcumin	109-112	caspase 8	Homo sapiens	230-239
31809793-8	2020	ERK inhibitor PD98059 significantly alleviated BDMC induced decrease in  psim, alteration in BCl-2, caspase-8 activation and PS externalization.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	14-21	caspase 8	Homo sapiens	100-109
31812624-9	2020	21-BD also activated caspases-8, -9 and -3, and induced the cleavage of poly (ADP-ribose) polymerase-1 (PARP-1).	Digoxin	0-5	caspase 8	Homo sapiens	21-42
31838086-6	2020	Efficacy of the combined treatment relied on cisplatin-induced downregulation of c-FLIP, the main regulator of the extrinsic apoptotic pathway, leading to an enhanced caspase-8-mediated pathway.	Cisplatin	45-54	caspase 8	Homo sapiens	167-176
31809793-8	2020	ERK inhibitor PD98059 significantly alleviated BDMC induced decrease in  psim, alteration in BCl-2, caspase-8 activation and PS externalization.	bisdemethoxycurcumin	47-51	caspase 8	Homo sapiens	100-109
32098126-5	2020	Furthermore, cells treated with K313 showed a significant decrease in mitochondrial membrane potential (MMP), which may have been caused by the caspase-8-mediated cleavage of Bid, as detected by Western blot analysis.	palladium chloride	32-36	caspase 8	Homo sapiens	144-153
32120831-7	2020	Moreover, diminished expression of anti-apoptotic proteins, including Bcl-2, Caspase3, Caspase7, and Caspase8 in METH-exposed SH-SY5y cells, was significantly recovered by treatment with lupenone.	Methamphetamine	113-117	caspase 8	Homo sapiens	101-109
32120831-7	2020	Moreover, diminished expression of anti-apoptotic proteins, including Bcl-2, Caspase3, Caspase7, and Caspase8 in METH-exposed SH-SY5y cells, was significantly recovered by treatment with lupenone.	lupenone	187-195	caspase 8	Homo sapiens	101-109
32060646-9	2020	The viral UL39-encoded viral protein ICP6, the large subunit of the virus-encoded ribonucleotide reductase, functions as a suppressor of both caspase-8 and RHIM-dependent RIPK3 activities in the natural human host.	Ribonucleotides	82-96	caspase 8	Homo sapiens	142-151
32093309-8	2020	In addition, upon enzyme upregulation, both the production of reactive oxygen species and activation of caspase-3 and caspase-8 were reduced.	Reactive Oxygen Species	62-85	caspase 8	Homo sapiens	118-127
32014914-0	2020	Luteolin-regulated MicroRNA-301-3p Targets Caspase-8 and Modulates TRAIL Sensitivity in PANC-1 Cells.	Luteolin	0-8	caspase 8	Homo sapiens	43-52
32032391-8	2020	Less active caspase-8 and caspase-9, and consequently less active caspase-3, was observed in infected compared to uninfected staurosporine-exposed cells.	Staurosporine	125-138	caspase 8	Homo sapiens	12-21
31714653-9	2020	Most important, major extrinsic and intrinsic apoptosis signaling factors, including active caspase-8 and caspase-9 were both enhanced by magnolol.	magnolol	138-146	caspase 8	Homo sapiens	92-101
32099733-5	2020	The activities of caspase-3, caspase-8, and caspase-9 increased with increasing concentration of the nanoparticles indicating that activities of caspase can be activated by iron nanoparticles.	Iron	173-177	caspase 8	Homo sapiens	29-38
32099733-5	2020	The activities of caspase-3, caspase-8, and caspase-9 increased with increasing concentration of the nanoparticles indicating that activities of caspase can be activated by iron nanoparticles.	Iron	173-177	caspase 8	Homo sapiens	18-25
31987044-7	2020	RESULTS: In both cell lines, Tg-induced cell death depended on death receptor 5 and caspase-8.	Thapsigargin	29-31	caspase 8	Homo sapiens	84-93
31910706-5	2020	Caspases (cysteine aspartic proteases and cysteine aspartases) are cysteine dependent aspartate-specific proteases.	Cysteine	10-18	caspase 8	Homo sapiens	0-8
31910706-5	2020	Caspases (cysteine aspartic proteases and cysteine aspartases) are cysteine dependent aspartate-specific proteases.	Cysteine	42-50	caspase 8	Homo sapiens	0-8
31910706-5	2020	Caspases (cysteine aspartic proteases and cysteine aspartases) are cysteine dependent aspartate-specific proteases.	Cysteine	42-50	caspase 8	Homo sapiens	0-8
31910706-5	2020	Caspases (cysteine aspartic proteases and cysteine aspartases) are cysteine dependent aspartate-specific proteases.	Aspartic Acid	86-95	caspase 8	Homo sapiens	0-8
31734898-10	2020	In conclusion, Acacetin induces mitochondrial ROS-mediated cell death in a caspase-independent manner in SW480 and HCT-116 colon carcinoma cells by inducing apoptosis inducing factor (AIF), which may potentiate its anticancer and chemotherapeutic prospects against colorectal carcinoma.	acacetin	15-23	caspase 8	Homo sapiens	75-82
31706006-8	2020	Further studies showed that crizotinib significantly increased cleaved-caspase-8, a signaling protein of extrinsic apoptosis pathway, in a concentration and time-dependent manner.	crizotinib	28-38	caspase 8	Homo sapiens	71-80
31706006-11	2020	We also reveal crizotinib induce apoptosis through the extrinsic apoptosis pathway due to detected up-regulated cleaved-caspase-8.	crizotinib	15-25	caspase 8	Homo sapiens	120-129
31614198-8	2020	Furthermore, we found that DHA and EPA treatment can either prevent caspase-3 activation on 17-kDa form cleavage or Bid cleaved (15-kDa form) for activation by caspase-8, apparently.	Docosahexaenoic Acids	27-30	caspase 8	Homo sapiens	160-169
31614198-8	2020	Furthermore, we found that DHA and EPA treatment can either prevent caspase-3 activation on 17-kDa form cleavage or Bid cleaved (15-kDa form) for activation by caspase-8, apparently.	Eicosapentaenoic Acid	35-38	caspase 8	Homo sapiens	160-169
31947862-7	2020	Additionally, ferrugone-induced apoptosis was found to be caspase-8-dependent, while DMI-induced apoptosis was caspase-9-dependent.	Ferrugone	14-23	caspase 8	Homo sapiens	58-67
31952288-5	2020	Indomethacin-induced glioma cell apoptosis was accompanied by a series of biochemical changes, including reactive oxygen species generation, endoplasmic reticulum (ER) stress, apoptosis signal-regulating kinase-1 (Ask1) activation, p38 hyperphosphorylation, protein phosphatase 2A (PP2A) activation, Akt dephosphorylation, Mcl-1 and FLICE-inhibiting protein (FLIP) downregulation, Bax mitochondrial distribution, and caspases 3/caspase 8/caspase 9 activation.	Indomethacin	0-12	caspase 8	Homo sapiens	428-437
31734250-7	2020	Furthermore, caspase-8 was found being activated 4 h after MC-LR treatment, earlier than observed activation of caspase-9 (8 h after MC-LR treatment).	nangibotide	59-64	caspase 8	Homo sapiens	13-22
32187278-8	2020	CASPASE-8 and TNFRSF10B expression levels could predict the response of both the cell lines to rhTRAIL alone or the response to a combination of rhTRAIL and cisplatin.	Cisplatin	157-166	caspase 8	Homo sapiens	0-9
31634424-12	2020	zVAD suppressed the fisetin-induced expression of caspase-8, RIPK1, RIPK3, and MLKL as opposed to fisetin treatment.	fisetin	20-27	caspase 8	Homo sapiens	50-59
32407273-0	2020	The Influence of Salinomycin on the Expression Profile of mRNAs Encoding Selected Caspases and MiRNAs Regulating their Expression in Endometrial Cancer Cell Line.	salinomycin	17-28	caspase 8	Homo sapiens	82-90
32407273-3	2020	AIM: The aim of this study was to assess the variances in the expression pattern of caspase-dependent signaling pathways in the endometrial cancer cell line when treated with salinomycin.	salinomycin	175-186	caspase 8	Homo sapiens	84-91
31869409-9	2020	Treatment with H2O2 increased apoptosis and the activity of the pro-apoptotic factors caspase-8 and caspase-3, both of which were attenuated by TUDCA.	Water	15-19	caspase 8	Homo sapiens	86-95
32405344-8	2020	Crocin can induce apoptosis through activation of caspase 8, up-regulation of p53 expression, Bax/Bcl-2 ratio, and down-regulation expression of Bcl-2, survivin, and cyclin D1.	crocin	0-6	caspase 8	Homo sapiens	50-59
31689624-10	2020	[PtCl2(TdTn)] and [PdCl2(TdTn)] caused caspase-3 activation in U-937 cells, simultaneously with caspase-9 activation due to complexes; however, in HT-29 caspase-3 activation occurred simultaneously with caspase-8 activation induced by the ligand TdTn.	ptcl2	1-6	caspase 8	Homo sapiens	203-212
31689624-10	2020	[PtCl2(TdTn)] and [PdCl2(TdTn)] caused caspase-3 activation in U-937 cells, simultaneously with caspase-9 activation due to complexes; however, in HT-29 caspase-3 activation occurred simultaneously with caspase-8 activation induced by the ligand TdTn.	palladium chloride	19-24	caspase 8	Homo sapiens	203-212
32922486-12	2020	We concluded that nanoparticles-loaded Hydroxyurea and it in combination with radiation and hyperthermia induces mitochondrial-dependent apoptosis by down-regulation of caspase-8 and up-regulation of caspase-9 expressions and have higher toxicity effect on MCF-7 cells in comparison with pure Hydroxyurea.	Hydroxyurea	39-50	caspase 8	Homo sapiens	169-178
31869409-9	2020	Treatment with H2O2 increased apoptosis and the activity of the pro-apoptotic factors caspase-8 and caspase-3, both of which were attenuated by TUDCA.	ursodoxicoltaurine	144-149	caspase 8	Homo sapiens	86-95
31587185-1	2019	The objective of this research was to assess the association of genetic polymorphisms related to intrinsic apoptosis pathway CASP8 rs3834129 and CASP3 rs4647601 with the risk, clinical and pathological aspects, and survival of oropharynx squamous cell carcinoma (OPSCC) patients that received cisplatin and radiotherapy.	Cisplatin	293-302	caspase 8	Homo sapiens	125-130
31819254-5	2020	This triggers Lyn/Syk-dependent calcium entry and the production of reactive oxygen species, leading to activation of caspase-8.	Calcium	32-39	caspase 8	Homo sapiens	118-127
31819254-5	2020	This triggers Lyn/Syk-dependent calcium entry and the production of reactive oxygen species, leading to activation of caspase-8.	Oxygen	77-83	caspase 8	Homo sapiens	118-127
31926620-0	2020	Triggering apoptosis by oroxylin A through caspase-8 activation and p62/SQSTM1 proteolysis.	5,7-dihydroxy-6-methoxy-2-phenylchromen-4-one	24-34	caspase 8	Homo sapiens	43-52
31926620-3	2020	Here we report that the apoptosis induced by oroxylin A was dependent on p62-mediated activation of caspase-8 in hepatocellular carcinoma cells.	5,7-dihydroxy-6-methoxy-2-phenylchromen-4-one	45-55	caspase 8	Homo sapiens	100-109
31926620-4	2020	Furthermore, oroxylin A also caused p62/SQSTM1 proteolysis at Asp329 by activating caspase-8.	5,7-dihydroxy-6-methoxy-2-phenylchromen-4-one	13-23	caspase 8	Homo sapiens	83-92
31926620-8	2020	In conclusion, our findings indicated that oroxylin A triggered apoptosis through caspase-8 activation and p62/SQSTM1 proteolysis.	5,7-dihydroxy-6-methoxy-2-phenylchromen-4-one	43-53	caspase 8	Homo sapiens	82-91
31839995-5	2019	At the protein level, DDAs alter DR5 disulfide bonding to increase steady-state DR5 levels and oligomerization, leading to downstream caspase 8 and 3 activation.	Disulfides	37-46	caspase 8	Homo sapiens	134-143
31816985-4	2019	The compound TMS-TMF-4f enhanced the activation of caspase-3, caspase-8, and caspase-9 and regulated Bcl-2 family proteins, which led to mitochondrial membrane potential (MMP) loss and resulted in the release of cytochrome c and Smac/DIABLO into the cytosol.	thiomarinol F	13-23	caspase 8	Homo sapiens	62-71
31638181-7	2019	Western blotting demonstrated that treatment with bruceine D significantly suppressed the expression of the anti-apoptotic proteins Bcl-2, Bcl-xL and X-linked inhibitor of apoptosis, enhanced the expression levels of apoptotic proteins Bax and Bak, and inhibited the expression of pro-caspase-3 and pro-caspase-8.	bruceine D	50-60	caspase 8	Homo sapiens	303-312
31306050-4	2020	In particular, AMP induced caspase-8 dependent apoptosis via upregulation of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and death receptor (DR5).	ampelopsin	15-18	caspase 8	Homo sapiens	27-36
31491480-7	2019	Copper also down-regulated Bcl2 and up-regulated Bax, Casp8 and Casp3 linking the effects of copper to increased apoptosis.	Copper	0-6	caspase 8	Homo sapiens	54-59
31541852-5	2019	Presence of GMG-ITC prior to development of oxidative stress condition, downregulated the expression of cyt-c, p53, Apaf-1, Bax, CASP3, CASP8 and CASP9 genes with concurrent upregulation of Bcl-2 gene in mitochondrial apoptotic signalling pathway.	Isothiocyanates	12-19	caspase 8	Homo sapiens	136-141
31542488-10	2019	Furthermore, ROS production was found to be a consequence of caspase activation via caspases inhibition.	Reactive Oxygen Species	13-16	caspase 8	Homo sapiens	61-68
31542488-10	2019	Furthermore, ROS production was found to be a consequence of caspase activation via caspases inhibition.	Reactive Oxygen Species	13-16	caspase 8	Homo sapiens	84-92
31827702-5	2019	Wild-type A3, FADD-deficient I2.1, and caspase-8-deficient I9.2 Jurkat clones exhibited similar susceptibilities to the cytotoxicity of quercetin, excluding an involvement of extrinsic pathway in triggering the apoptosis.	Quercetin	136-145	caspase 8	Homo sapiens	39-48
31717557-7	2019	Cleavage of caspase-8, -9, and -3 was found in AGS and DLD-1 cells treated with all three seco-acids, indicating the induction of apoptosis via extrinsic and intrinsic pathways.	seco-milbemycin A	90-100	caspase 8	Homo sapiens	12-33
31541852-6	2019	Protein Multiplex revealed significant decreased in cyt-c, p53, Apaf-1, Bax, CASP8 and CASP9 due to GMG-ITC pre-treatment in oxidative stress condition.	Isothiocyanates	100-107	caspase 8	Homo sapiens	77-82
31839747-7	2019	LPS+PA treatment group significantly decreases the relative expression level of IRS-1, PI3K, AKT, phosphorylation of AKT, TLR-4, MyD88, phosphorylation of IKKalpha, NF-kappaB, Bcl-2 and increases the relative expression level of Bax, cleaved caspase 3 and cleaved caspase 8, compared with the cells treated with NAFLD model.	Palmitic Acid	4-6	caspase 8	Homo sapiens	264-273
31343754-0	2019	Anticancer activity of newly synthesized 1,1-disubstituted cyclohexane-1-carboxamides: in vitro caspases mediated apoptosis activators in human cancer cell lines and their molecular modeling.	1,1-disubstituted cyclohexane-1-carboxamides	41-85	caspase 8	Homo sapiens	96-104
31407254-0	2019	FF-10501 induces caspase-8-mediated apoptotic and endoplasmic reticulum stress-mediated necrotic cell death in hematological malignant cells.	4-carbamoylimidazolium 5-olate	0-8	caspase 8	Homo sapiens	17-26
31407254-8	2019	FF-10501-induced apoptosis was mediated by caspase-8 activation followed by activation of the mitochondrial pathway in MOLM-13 and MOLT-3 cells.	4-carbamoylimidazolium 5-olate	0-8	caspase 8	Homo sapiens	43-52
31392779-5	2019	Caspase activation is dependent on ROS as shown by the ability of CGs to generate ROS and the ROS-N-acetylcysteine (NAC) relationship, which inhibits apoptosis during cotreatment by preventing the formation of caspase-8 and -3.	Acetylcysteine	98-114	caspase 8	Homo sapiens	210-226
31392779-5	2019	Caspase activation is dependent on ROS as shown by the ability of CGs to generate ROS and the ROS-N-acetylcysteine (NAC) relationship, which inhibits apoptosis during cotreatment by preventing the formation of caspase-8 and -3.	nac	116-119	caspase 8	Homo sapiens	210-226
31702036-7	2019	Silencing of ST3Gal3 by small interfering RNA reversed these effects and increased the protein levels of caspase-8/3, which may contribute to paclitaxel-induced apoptosis.	Paclitaxel	142-152	caspase 8	Homo sapiens	105-116
31695422-4	2019	Results: Methyloleanolate increased the fraction of Annexin V/PI apoptotic cells and activated caspase-8, caspase-3, and death receptor 5 (DR5) more than oleanolate in A549 and H1299 cells pretreated with pancaspase inhibitor z-VAD-fmk and DR5 depletion.	Methyloleanolate	9-25	caspase 8	Homo sapiens	95-104
31695422-4	2019	Results: Methyloleanolate increased the fraction of Annexin V/PI apoptotic cells and activated caspase-8, caspase-3, and death receptor 5 (DR5) more than oleanolate in A549 and H1299 cells pretreated with pancaspase inhibitor z-VAD-fmk and DR5 depletion.	28-O-glucopyranosyl-3-O-(O-rhamnopyranosyl-1-3-O-(O-glucopyranosyl)glucopyranosyl)oleanolate	15-25	caspase 8	Homo sapiens	95-104
31324954-11	2019	Accumulation of cleaved caspase-8 in MDA-MB-231 cells on bisphosphonate-treated bone indicated increased apoptosis in the cells.	Diphosphonates	57-71	caspase 8	Homo sapiens	24-33
31390533-6	2019	Phthalates caused an increase of caspases activity.	phthalic acid	0-10	caspase 8	Homo sapiens	33-41
31588915-6	2019	In addition, Isorhamnetin-induced apoptosis was associated with increased expression of Fas/Fas ligand, reduced ratio of Bcl-2/Bax expression, truncation of Bid, cytosolic release of cytochrome c, and activation of caspase-8, -9 and -3.	3-methylquercetin	13-25	caspase 8	Homo sapiens	215-235
31392779-5	2019	Caspase activation is dependent on ROS as shown by the ability of CGs to generate ROS and the ROS-N-acetylcysteine (NAC) relationship, which inhibits apoptosis during cotreatment by preventing the formation of caspase-8 and -3.	Reactive Oxygen Species	35-38	caspase 8	Homo sapiens	210-226
31392779-5	2019	Caspase activation is dependent on ROS as shown by the ability of CGs to generate ROS and the ROS-N-acetylcysteine (NAC) relationship, which inhibits apoptosis during cotreatment by preventing the formation of caspase-8 and -3.	Cardiac Glycosides	66-69	caspase 8	Homo sapiens	210-226
31702036-0	2019	ST3Gal3 confers paclitaxel-mediated chemoresistance in ovarian cancer cells by attenuating caspase-8/3 signaling.	Paclitaxel	16-26	caspase 8	Homo sapiens	91-102
31702036-3	2019	The present study demonstrated that paclitaxel-induced chemoresistance in ovarian cancer cells upregulated the expression of ST3Gal3 and reduced the activity of caspase-8/3.	Paclitaxel	36-46	caspase 8	Homo sapiens	161-172
31436296-5	2019	Western blot analysis and reverse transcription-quantitative polymerase chain reaction revealed that Fe3O4-TMZ-ICG MNPs with NIR laser irradiation lead to significantly enhanced anticancer effects on U-87 MG glioblastoma cells through the modulation of intrinsic and extrinsic apoptosis genes, including Bcl-2-associated X protein, Bcl-2, cytochrome c, caspase-3, Fas associated via death domain and caspase-8.	fe3o4-tmz	101-110	caspase 8	Homo sapiens	400-409
31695421-12	2019	Moreover, apiosporamide induced apoptosis, activated caspase-3, caspase-8 and caspase-9, and regulated expression of Bax and Bcl-2 in MG63 cells.	apiosporamide	10-23	caspase 8	Homo sapiens	64-73
31637186-11	2019	Additionally, GFX could activate the caspase-8, caspase-9, and caspase-3, induce MTP disruption, downregulate B-cell leukemia-2 (Bcl-2) and B-cell leukemia-XL (Bcl-XL), and upregulate Bcl-2 assaciated X protein (Bax), Bcl-2-associated death promoter (Bad), Bcl-2 interacting domain (Bid) and cytoplasmic cytochrome C in SFs, suggesting that caspase-dependent extrinsic and intrinsic pathways were related to GFX-contributed apoptosis of SFs.	gfx	14-17	caspase 8	Homo sapiens	37-46
31608167-11	2019	In addition, gene expression analysis revealed that MnIII complex exerts its antiproliferative effect via up-and down-regulation of p21 and cyclin D1, respectively, along with increased expression of Bax/Bcl-2 ratio, TNF-alpha, initiator caspase-8 and -10 and effector caspase-3 in MCF-7 and MDA-MB-231 cells.	Manganese	52-57	caspase 8	Homo sapiens	238-255
31623058-3	2019	PAB-induced apoptosis is through inducing death receptor 5 (DR5) together with the increase in the expression of cleaved caspase-8.	pseudolaric acid B	0-3	caspase 8	Homo sapiens	121-130
31597910-9	2019	Imidazole treatment of DLD-1 cells markedly promoted activation of caspase-3, caspase-8, and caspase-9.	imidazole	0-9	caspase 8	Homo sapiens	78-87
31597910-14	2019	CONCLUSIONS The present study demonstrated that imidazole inhibited colon cancer cell viability through activation of apoptosis and cell cycle arrest by increasing the generation of ROS, caspase activation, and apoptotic protein expression.	imidazole	48-57	caspase 8	Homo sapiens	187-194
31411503-11	2019	Deletion of the caspase-8 gene results not only in ileocolitis but also in gut barrier dysfunction, liver steatosis, and malassimilation, which can be partially attenuated by oral inulin or sodium butyrate.	Butyric Acid	190-205	caspase 8	Homo sapiens	16-25
31569691-7	2019	We further found that garciniaxanthone I (GXI) could induce HepG2 apoptosis and enhance the expression of cleaved caspase-8, caspase-9, and caspase-3.	garciniaxanthone i	22-40	caspase 8	Homo sapiens	114-123
31281953-15	2019	Furthermore, celastrol upregulated death receptor 5 (DR5) at the mRNA and protein levels, and siRNA-mediated DR5 knockdown reduced the killing effect of the combination drug treatment on glioma cells and reduced the activation of caspase-3, caspase-8 and PARP.	celastrol	13-22	caspase 8	Homo sapiens	241-250
30826899-0	2019	Nuphar alkaloids induce very rapid apoptosis through a novel caspase-dependent but BAX/BAK-independent pathway.	nuphar alkaloids	0-16	caspase 8	Homo sapiens	61-68
31569380-9	2019	Results showed the viability of preadipocytes was significantly decreased by treatment with 30 microM curcumin, a concentration that caused apoptosis in preadipocytes, as assessed by the TUNEL assay, and caused activation of caspases 8, 9, and 3.	Curcumin	102-110	caspase 8	Homo sapiens	225-245
31534206-4	2019	Analyses of apoptotic signaling events revealed that pinoresinol enhanced the formation of TRAIL-mediated death-inducing signaling complex (DISC) and complete processing of procaspase-8 within the DISC in glioblastoma cells, in which caspase-8 was inactivated.	pinoresinol	53-64	caspase 8	Homo sapiens	176-185
31673231-6	2019	Combined treatment of TRAIL with bortezomib resulted in strong synergistic response with enhanced activation of caspases-8, -9 and -3, and increased Annexin V-binding cell fractions in TRAIL-resistant SNU-216 cells.	bortezomib	33-43	caspase 8	Homo sapiens	112-133
31637258-1	2019	TNFalpha/CHX-induced apoptosis is dependent on caspase-8 activation and regulated by Bcl-2.	N-(2-amino-3-(4-isothiocyanatophenyl)propyl)cyclohexane-1,2-diamine-N,N',N',N'',N''-pentaacetic acid	9-12	caspase 8	Homo sapiens	47-56
31534206-7	2019	Taken together, our results indicate that pinoresinol facilitates DISC-mediated caspase-8 activation by targeting cFLIPL in an early event in apoptotic signaling, which provides a potential therapeutic module for TRAIL-based chemotherapy.	pinoresinol	42-53	caspase 8	Homo sapiens	80-89
31551765-7	2019	Pretreatment with caspase inhibitors diminishes the activities of caspase 8, 9, and 3 and maintains the percentage of viable glioblastoma cells, indicating that alpha-H induced cell apoptosis through both the extrinsic and the intrinsic pathways.	MK 316	161-168	caspase 8	Homo sapiens	66-75
31571909-9	2019	Chitin oligosaccharide plus cisplatin up-regulated the expression level of caspase8 and caspase3, while had minor influence on the expression level of BAK.	Cisplatin	28-37	caspase 8	Homo sapiens	75-83
31571909-11	2019	Conclusion: The study demonstrated that chitin oligosaccharide plus cisplatin had positive synergistic effects, and it is possible to improve the prognosis of lung adenocarcinoma patients by up-regulating the expression level of caspase8, caspase3 and down-regulating the expression level of Ki67.	Cisplatin	68-77	caspase 8	Homo sapiens	229-237
31369761-9	2019	KEY FINDINGS: Doxorubicin caused to depolarize MMP, resulting in enhancing apoptosis by activation of caspase-8 via MAPKs/NF-kB pathway via elevation of TOS and decreasing TAS.	Doxorubicin	14-25	caspase 8	Homo sapiens	102-111
31369761-9	2019	KEY FINDINGS: Doxorubicin caused to depolarize MMP, resulting in enhancing apoptosis by activation of caspase-8 via MAPKs/NF-kB pathway via elevation of TOS and decreasing TAS.	Tantalum	172-175	caspase 8	Homo sapiens	102-111
31545303-0	2019	Inhibition of Proliferation of SGC7901 and BGC823 Human Gastric Cancer Cells by Ursolic Acid Occurs Through a Caspase-Dependent Apoptotic Pathway.	ursolic acid	80-92	caspase 8	Homo sapiens	110-117
31545303-11	2019	Ursolic acid treatment significantly induced apoptosis in SGC7901 and BGC823 cells when compared with GES-1 cells (P<0.05), and significantly increased the activation of caspase-3, caspase-8, caspase-9, poly ADPribose polymerase (PARP), and the production of reactive oxygen species (ROS).	ursolic acid	0-12	caspase 8	Homo sapiens	181-190
31545303-13	2019	<strong>CONCLUSIONS</strong> Ursolic acid inhibited the proliferation of SGC7901 and BGC823 human gastric cancer cells <i>in vitro</i> through a caspase-dependent apoptotic pathway.	ursolic acid	29-41	caspase 8	Homo sapiens	145-152
31572184-4	2019	Apigenin significantly and dose-dependently inhibited cell proliferation and promoted apoptosis while stimulating the cleaved PARP (poly ADP-ribose polymerase) (C-PARP) and caspase-8 expression.	Apigenin	0-8	caspase 8	Homo sapiens	173-182
31074052-4	2019	In the present study, we examined the effect of curcumin on the gene expression of caspase-8, caspase-10, and anti-apoptotic protein c-FLIP, in HAM/TSP patients.	Curcumin	48-56	caspase 8	Homo sapiens	83-92
31470629-9	2019	FUS also decreased Akt phosphorylation and resulted in increased Fas ligand production and caspase-8/3-dependent apoptosis.	fusarubin	0-3	caspase 8	Homo sapiens	91-102
30712124-9	2019	The interaction between H2O2 at 50 muM and LLLT at 4 J showed partially reversion of the higher levels of DNA oxidation, CASP 3, CASP 8, IL-1B, IL-6, and INFy induced by H2O2 exposure.	Hydrogen Peroxide	170-174	caspase 8	Homo sapiens	129-135
31661481-4	2019	Caspase-8 (also called SAP4, FLICE, MACH, MCH5) is one of two members of the death effector domain (DED)-containing caspases.	mach	36-40	caspase 8	Homo sapiens	0-9
31470686-5	2019	Our studies show the complexity of the potential mechanism of cytotoxic action of PAMAM-drug-trastuzumab conjugates that should be sought as a resultant of oxidative stress, mitochondrial activation of the caspase cascade and the HER-2 receptor blockade.	pamam	82-87	caspase 8	Homo sapiens	206-213
30712124-9	2019	The interaction between H2O2 at 50 muM and LLLT at 4 J showed partially reversion of the higher levels of DNA oxidation, CASP 3, CASP 8, IL-1B, IL-6, and INFy induced by H2O2 exposure.	Hydrogen Peroxide	24-28	caspase 8	Homo sapiens	129-135
31496721-8	2019	Additionally, kurarinone promoted Fas and TRAIL receptor-1 and -2 expression via the caspase-8/Bid pathway, suggesting that kurarinone triggered apoptosis via the mitochondria-mediated and receptor-mediated apoptotic pathways.	kurarinone	14-24	caspase 8	Homo sapiens	85-94
31475104-11	2019	Phospho T273 Caspase 8 similarly corresponded to decreased risk of distant failure (p = 0.021), and increased CSS (p &lt; 0.001) and OS (p &lt; 0.001) and remained a significant predictor for OS on multivariate analysis.	thiocysteine	110-113	caspase 8	Homo sapiens	13-22
31475104-13	2019	Finally, a combined PLK3 and pT273 Caspase 8 score predicted for decreased distant relapse (p = 0.005), and both improved CSS (p &lt; 0.001) and OS (p &lt; 0.001); this combined score independently predicted distant failure (p = 0.041) and CSS (p = 0.003) on multivariate analyses.	thiocysteine	122-125	caspase 8	Homo sapiens	35-44
31475104-13	2019	Finally, a combined PLK3 and pT273 Caspase 8 score predicted for decreased distant relapse (p = 0.005), and both improved CSS (p &lt; 0.001) and OS (p &lt; 0.001); this combined score independently predicted distant failure (p = 0.041) and CSS (p = 0.003) on multivariate analyses.	thiocysteine	240-243	caspase 8	Homo sapiens	35-44
31387245-5	2019	LCA activated caspase-8 and -9, which are involved in the initiation of extrinsic and intrinsic apoptosis pathways, respectively, and also increased caspase-3 activity, a typical effect caspase, subsequently leading to poly (ADP-ribose) polymerase cleavage.	licochalcone A	0-3	caspase 8	Homo sapiens	14-30
31387245-5	2019	LCA activated caspase-8 and -9, which are involved in the initiation of extrinsic and intrinsic apoptosis pathways, respectively, and also increased caspase-3 activity, a typical effect caspase, subsequently leading to poly (ADP-ribose) polymerase cleavage.	licochalcone A	0-3	caspase 8	Homo sapiens	14-21
31534470-9	2019	DHA treatment significantly upregulated the apoptotic genes CASP3, CASP8, CASP9, and TNF.	artenimol	0-3	caspase 8	Homo sapiens	67-72
31438633-4	2019	Furthermore, genistein induced the activation of caspases (caspase-3, -8 and -9), and cleavage of poly (ADP-ribose) polymerase cleavage.	Genistein	13-22	caspase 8	Homo sapiens	49-57
31438633-5	2019	However, genistein-induced apoptosis was significantly inhibited by a pan-caspase inhibitor, indicating that the induction of apoptosis by genestein was caspase-dependent.	Genistein	9-18	caspase 8	Homo sapiens	74-81
31438633-5	2019	However, genistein-induced apoptosis was significantly inhibited by a pan-caspase inhibitor, indicating that the induction of apoptosis by genestein was caspase-dependent.	Genistein	9-18	caspase 8	Homo sapiens	153-160
31406162-5	2019	Danazol induced the arrest of MDR cancer cells at the G2/M phase and caspase-8-related early apoptosis.	Danazol	0-7	caspase 8	Homo sapiens	69-78
31391500-0	2019	Ruthenium(II) complexes with 6-methyl-2-thiouracil selectively reduce cell proliferation, cause DNA double-strand break and trigger caspase-mediated apoptosis through JNK/p38 pathways in human acute promyelocytic leukemia cells.	Ruthenium(II)	0-13	caspase 8	Homo sapiens	132-139
31391500-0	2019	Ruthenium(II) complexes with 6-methyl-2-thiouracil selectively reduce cell proliferation, cause DNA double-strand break and trigger caspase-mediated apoptosis through JNK/p38 pathways in human acute promyelocytic leukemia cells.	6-methyl-2-thiouracil	29-50	caspase 8	Homo sapiens	132-139
31391500-5	2019	Cotreatment with Z-VAD(OMe)-FMK, a pan-caspase inhibitor, reduced Ru(II) complexes-induced apoptosis.	z-vad	17-22	caspase 8	Homo sapiens	39-46
31391500-5	2019	Cotreatment with Z-VAD(OMe)-FMK, a pan-caspase inhibitor, reduced Ru(II) complexes-induced apoptosis.	ome)-fmk	23-31	caspase 8	Homo sapiens	39-46
31391500-5	2019	Cotreatment with Z-VAD(OMe)-FMK, a pan-caspase inhibitor, reduced Ru(II) complexes-induced apoptosis.	ru(ii)	66-72	caspase 8	Homo sapiens	39-46
31391500-6	2019	In addition, both metal complexes induced phosphorylation of histone H2AX (S139), JNK2 (T183/Y185) and p38alpha (T180/Y182), and cotreatment with JNK/SAPK and p38 MAPK inhibitors reduced complexes-induced apoptosis, indicating DNA double-strand break and activation of caspase-mediated apoptosis through JNK/p38 pathways.	Metals	18-23	caspase 8	Homo sapiens	269-276
31496721-8	2019	Additionally, kurarinone promoted Fas and TRAIL receptor-1 and -2 expression via the caspase-8/Bid pathway, suggesting that kurarinone triggered apoptosis via the mitochondria-mediated and receptor-mediated apoptotic pathways.	kurarinone	124-134	caspase 8	Homo sapiens	85-94
31091501-11	2019	Furthermore, the expressions of caspase-3, caspase-8 caspase-9 and Bax were positively correlated with ROS level, but negatively correlated with T-AOC in testis.	Reactive Oxygen Species	103-106	caspase 8	Homo sapiens	43-52
30556589-3	2019	In this study, CA-induced apoptotic cell death resulted in the activation of the caspase-8-mediated caspase cascade, as evidenced by the cleavage of the substrate protein Bid and the caspase-8 inhibitor Z-VAD-FMK.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	203-212	caspase 8	Homo sapiens	81-90
30937691-1	2019	The blots of control and docetaxel for caspase-9, caspase-3, caspase-8, Bcl-XL, and tubulin in the Figure 4f were reused from Figure 4 of our previous paper published in Journal of Urology in 2010 ( https://doi.org/10.1016/j.juro.2010.07.035 ).	Docetaxel	25-34	caspase 8	Homo sapiens	61-70
30556589-3	2019	In this study, CA-induced apoptotic cell death resulted in the activation of the caspase-8-mediated caspase cascade, as evidenced by the cleavage of the substrate protein Bid and the caspase-8 inhibitor Z-VAD-FMK.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	203-212	caspase 8	Homo sapiens	183-192
31115653-9	2019	MCMV m157-responsive Ly49H+ NK cells support increased expansion of both Ly49H- NK cells and CD8 T cells in Casp8-/-Ripk3-/- mice.	ly49h	21-26	caspase 8	Homo sapiens	108-113
31351078-5	2019	Mechanistically, the metabolic imbalance in VHL-deficient B cells, arising from over-stabilization of hypoxia-inducible factor-1alpha (HIF-1alpha), triggers reductive glutamine metabolism leading to increased Fas palmitoylation and caspase-8-mediated apoptosis.	Glutamine	167-176	caspase 8	Homo sapiens	232-241
31839714-7	2019	Results: Both simvastatin and fluvastatin produced a dose- and time-dependent inhibition of cell viability and colony formation while a promotion of cell apoptosis as evident with increases in caspase-3 activity, cleaved-caspase-3, cleaved-caspase-8 and cleaved-PARP levels in PC3 cells.	Simvastatin	14-25	caspase 8	Homo sapiens	240-249
31839714-7	2019	Results: Both simvastatin and fluvastatin produced a dose- and time-dependent inhibition of cell viability and colony formation while a promotion of cell apoptosis as evident with increases in caspase-3 activity, cleaved-caspase-3, cleaved-caspase-8 and cleaved-PARP levels in PC3 cells.	fluvastatin	30-41	caspase 8	Homo sapiens	240-249
31528215-6	2019	In addition, we observed that the pretreatment of cancer cells with quercetin improves extrinsic and intrinsic apoptosis by activating caspase-8 and caspase-9, respectively.	Quercetin	68-77	caspase 8	Homo sapiens	135-144
31250646-9	2019	Astrakurkurol persuaded the expression of death receptor associated proteins (Fas), which triggered caspase-8 activation following tBid cleavage.	Astrakurkurol	0-13	caspase 8	Homo sapiens	100-109
31295870-9	2019	Decursinol angelate (18) increased the expression of cleaved caspase-8 and -7.	decursin	0-19	caspase 8	Homo sapiens	61-77
31315220-6	2019	Mechanistically, HDACs inhibition by oleacein was associated with down-regulation of Sp1, the major transactivator of HDACs promoter, via Caspase 8 activation.	oleacein	37-45	caspase 8	Homo sapiens	138-147
31311168-7	2019	DW-CUR 20 inhibited the release of lactate dehydrogenase and decreased apoptosis-related proteins such as Poly (ADP-ribose) polymerase, cleaved caspase-7 and cleaved caspase-8 on t-BHP-treated HepG2 cells.	dw-cur 20	0-9	caspase 8	Homo sapiens	166-175
31311168-7	2019	DW-CUR 20 inhibited the release of lactate dehydrogenase and decreased apoptosis-related proteins such as Poly (ADP-ribose) polymerase, cleaved caspase-7 and cleaved caspase-8 on t-BHP-treated HepG2 cells.	tert-Butylhydroperoxide	179-184	caspase 8	Homo sapiens	166-175
31250646-9	2019	Astrakurkurol persuaded the expression of death receptor associated proteins (Fas), which triggered caspase-8 activation following tBid cleavage.	tBID	131-135	caspase 8	Homo sapiens	100-109
31250646-11	2019	Astrakurkurol cytotoxicity was based on caspase-8-mediated intrinsic apoptotic pathway and was associated with inhibition at Akt and NF-kappaB pathway.	Astrakurkurol	0-13	caspase 8	Homo sapiens	40-49
31277238-8	2019	The results indicated that the expression levels of cleaved caspase-8, -3, -9, and Bax were increased in A2780 cells treated with betulinic acid, whereas those of Bcl-2 were decreased.	betulinic acid	130-144	caspase 8	Homo sapiens	60-77
30983163-9	2019	Co-administration of a JNK inhibitor (JNK-IN-8) or p38 inhibitor (SB203580) abolishes the activation of caspase-9, caspase-8, and caspase-3 protein expression during licochalcone A treatment.	SB 203580	66-74	caspase 8	Homo sapiens	115-124
30983163-7	2019	Results indicated that licochalcone A reduces cell viability and induces apoptosis, as evidenced by the upregulation of caspase-8 and caspase-9, caspase-3 activation, and cleaved-poly ADP-ribose polymerase expression.	licochalcone	23-35	caspase 8	Homo sapiens	120-129
31063955-8	2019	HCPT and TPL combination treatment also significantly increased the apoptosis rate and apoptosis-related protein levels (Caspase8 and Bcl-xl).	hydroxycamptothecinum	0-4	caspase 8	Homo sapiens	121-129
31063955-8	2019	HCPT and TPL combination treatment also significantly increased the apoptosis rate and apoptosis-related protein levels (Caspase8 and Bcl-xl).	triptolide	9-12	caspase 8	Homo sapiens	121-129
30983163-9	2019	Co-administration of a JNK inhibitor (JNK-IN-8) or p38 inhibitor (SB203580) abolishes the activation of caspase-9, caspase-8, and caspase-3 protein expression during licochalcone A treatment.	licochalcone	166-178	caspase 8	Homo sapiens	115-124
31646804-0	2019	Inhibition of cancer cell growth by Tangeretin flavone in drug-resistant MDA-MB-231 human breast carcinoma cells is facilitated via targeting cell apoptosis, cell cycle phase distribution, cell invasion and activation of numerous Caspases.	tangeretin flavone	36-54	caspase 8	Homo sapiens	230-238
31280209-4	2019	RESULTS: Necroptosis occured by up-regulating TNF-alpha, RIP1/RIP3 activities, and down-regulating caspase-3/caspase-8 activities after citronellol treatment in NCI-H1299 cells.	citronellol	136-147	caspase 8	Homo sapiens	109-118
31680075-11	2019	Significant alterations in expression level of apoptosis-related proteins in methadone hydrochloride treated CCRF-CEM cells were found involving upregulation of caspase-8 expression and downregulation of survivin expression.	Methadone	77-100	caspase 8	Homo sapiens	161-170
31353737-3	2019	After 4 weeks" treatment, the extract (standardized to epicatechin and scopoletin), arrested Jurkat cell-cycle at the G0/G1 phase and activated the caspase-3 and caspase-8 (death-receptor extrinsic pathways).	Catechin	55-66	caspase 8	Homo sapiens	162-171
31353737-3	2019	After 4 weeks" treatment, the extract (standardized to epicatechin and scopoletin), arrested Jurkat cell-cycle at the G0/G1 phase and activated the caspase-3 and caspase-8 (death-receptor extrinsic pathways).	Scopoletin	71-81	caspase 8	Homo sapiens	162-171
31680075-12	2019	Methadone hydrochloride induced apoptosis in HL-60 cells involved upregulation of Bid and caspase-8 expression and downregulation of Bcl-2, p21 and survivin expression.	Methadone	0-23	caspase 8	Homo sapiens	90-99
31275848-7	2019	Curcumin induces apoptosis in B-Pre-ALL cell lines via activation of caspase-8 and truncation of BID.	Curcumin	0-8	caspase 8	Homo sapiens	69-78
31602860-7	2019	Moreover,curcumin could inhibit the migration and invasion of MKN45 cells,downregulate the expression of N-cadherin,snail1,Wnt3 a,p-beta-catenin,p-LRP6 and Bcl-2,and upregulate the expression of E-cadherin and Bax,it could increase the activity of caspase-3,caspase-8,caspase-9 and induce apoptosis as well.	Curcumin	9-17	caspase 8	Homo sapiens	258-267
31238539-8	2019	After regorafenib treatment, downregulation of related genes in invasion (vascular endothelial growth factor (VEGF) and matrix metallopeptidase 9 (MMP-9)), proliferation (CyclinD1) and anti-apoptosis (X-linked inhibitor of apoptosis protein (XIAP), myeloid cell leukemia-1 (MCL-1), and cellular FLICE (FADD-like IL-1beta-converting enzyme)-inhibitory protein (C-FLIP)) were found.	regorafenib	6-17	caspase 8	Homo sapiens	295-300
31312348-8	2019	Baicalein decreased the ratio of Bcl-2/Bax but increased the expression of Caspase-3 and Caspase-8.	baicalein	0-9	caspase 8	Homo sapiens	89-98
31236120-3	2019	Apoptosis of HBE-Dp71AS cells induced by H2O2 was increased via enhancing caspase 3, caspase 8 and caspase 9.	Hydrogen Peroxide	41-45	caspase 8	Homo sapiens	85-94
30925454-6	2019	Moreover, Western blot analysis also showed that the apoptosis-inducing effects of lobaplatin was associated with the reduction of Bcl-2 expression while upregulation of cleaved-caspase-3, cleaved-caspase-8, cleaved-caspase-9 and Bax.	lobaplatin	83-93	caspase 8	Homo sapiens	197-206
30879166-0	2019	Activator protein-1 and caspase 8 mediate p38alpha MAPK-dependent cardiomyocyte apoptosis induced by palmitic acid.	Palmitic Acid	101-114	caspase 8	Homo sapiens	24-33
30879166-5	2019	Human adult ventricular cardiomyocyte line (AC16 cells) exposed to high physiological levels of PA for 16 h showed enhanced transcription and phosphorylation of c-fos and c-jun subunits of AP-1 and transcription of caspase 8.	Palmitic Acid	96-98	caspase 8	Homo sapiens	215-224
30879166-8	2019	Inhibition of caspase 8 for 24 h reduced apoptosis in PA-treated cardiomyocytes.	Palmitic Acid	54-56	caspase 8	Homo sapiens	14-23
30941888-6	2019	Furthermore, p62 functional domain UBA and LIR mutants regulated autophagic flux and attenuated Caspase 8 activation, which indicates that autophagic degradation is involved in p62-mediated activation of Caspase 8 in ovarian cancer cells.	UBP 310	35-38	caspase 8	Homo sapiens	96-105
30991286-10	2019	On the contrary, rhein, kaempferol, aloe-emodin and quercetin inhibited the proliferation of LX2 cells and up-regulated the protein levels of Bax and cleaved caspase-8.	kaempferol	24-34	caspase 8	Homo sapiens	158-167
30991286-10	2019	On the contrary, rhein, kaempferol, aloe-emodin and quercetin inhibited the proliferation of LX2 cells and up-regulated the protein levels of Bax and cleaved caspase-8.	Quercetin	52-61	caspase 8	Homo sapiens	158-167
30953339-8	2019	Moreover, the caspase-8, a part of the extrinsic apoptotic pathway, was activated by reversine treatments.	2-(4-morpholinoanilino)-6-cyclohexylaminopurine	85-94	caspase 8	Homo sapiens	14-23
30941888-6	2019	Furthermore, p62 functional domain UBA and LIR mutants regulated autophagic flux and attenuated Caspase 8 activation, which indicates that autophagic degradation is involved in p62-mediated activation of Caspase 8 in ovarian cancer cells.	UBP 310	35-38	caspase 8	Homo sapiens	204-213
30941888-7	2019	Collectively, our study demonstrates that p62 promotes Caspase 8 activation through autophagy flux blockage with cisplatin treatment.	Cisplatin	113-122	caspase 8	Homo sapiens	55-64
30648790-6	2019	On screening a library of 86 fluorescent natural products, we found for the first time that gossypol showed potent inhibition of caspase-8 in vitro and in situ.	Gossypol	92-100	caspase 8	Homo sapiens	129-138
30900802-12	2019	Induction of extrinsic Fas-mediated apoptosis is verified by Western blotting for cleaved caspase 8, the initiator caspase of extrinsic apoptosis.	ammonium ferrous sulfate	23-26	caspase 8	Homo sapiens	90-99
30942074-4	2019	In the real-time fluorescence imaging of apoptotic HeLa cells induced by staurosporine using GNP-Se-Casp, the fluorescence signals corresponding to casp-8 and casp-9 sequentially turn on, followed by the appearance of the fluorescence of casp-3, which visualizes the upstream and downstream relationships of casp-3, -8, and -9.	Staurosporine	73-86	caspase 8	Homo sapiens	148-154
31040202-9	2019	These results indicate that Tet induces apoptosis of colon cancer cells through the mitochondrial pathway and caspase family pathway.	tetrandrine	28-31	caspase 8	Homo sapiens	110-117
30975734-5	2019	Furthermore, results of western blotting showed that the involvement of mitochondrial apoptotic pathway in the L-securinine-induced apoptosis of DU145 cell, as evidenced by an increase in the protein expression of Bax, cleaved caspase-9, cleaved caspase-3, cytosolic cytochrome c, and cleaved PARP, together with a unchanged cleaved caspase-8 and decreased Bcl-2 protein expression.	securinine	111-123	caspase 8	Homo sapiens	333-342
30724400-10	2019	CONCLUSIONS: N-myc and caspase-8 expressions are involved in TRAIL susceptibility in IMR-32 cells, and the combination of treatment with cisplatin and TRAIL may serve as a promising strategy for the development of therapeutics against neuroblastoma that is controlled by N-myc and caspase-8 expression.	Cisplatin	137-146	caspase 8	Homo sapiens	23-32
30724400-10	2019	CONCLUSIONS: N-myc and caspase-8 expressions are involved in TRAIL susceptibility in IMR-32 cells, and the combination of treatment with cisplatin and TRAIL may serve as a promising strategy for the development of therapeutics against neuroblastoma that is controlled by N-myc and caspase-8 expression.	Cisplatin	137-146	caspase 8	Homo sapiens	281-290
30868675-9	2019	Further study showed that CAF-CM enhanced cisplatin resistance by inhibiting cisplatin-induced apoptosis, determined by repression of caspase-3 and caspase-8, through activation of the ANXA3/JNK pathway.	Cisplatin	77-86	caspase 8	Homo sapiens	148-157
31391686-4	2019	Protein structure of caspase-3 (3DEI) and caspase-8 (3KJQ) was obtained from the protein data bank and docked with selected triterpenoids using AutoDock Tools and AutoDock Vina.	triterpenoids	124-137	caspase 8	Homo sapiens	42-51
30889542-4	2019	Andrographolide treatment effectively reduced NF-kappabeta nuclear localization by modulating protein kinase A- protein phosphatase 2 A- Ikappabeta kinase (PKA/PP2 A/IKK) axis that in turn maintains initiator caspase8 activity.	andrographolide	0-15	caspase 8	Homo sapiens	209-217
31391686-6	2019	RESULTS: The high docking score of -10.0, -9.9, -9.8, and -9.5 were shown by friedelin, tingenone, albiziasaponin A, and albiziasaponin C, respectively, for caspase-3, and -11.0, -9.6, -9.6, and -9.4 by beta-boswellic acid, bryonolic acid, canophyllic acid, and CDDO, respectively, for caspase-8.	friedelin	77-86	caspase 8	Homo sapiens	286-295
30945115-5	2019	Also, tetrandrine treatment revealed an elevated levels of reactive oxygen species and increased activities of caspase-8, -9 and -3 confirming the apoptosis of cells through both extrinsic death receptor and intrinsic caspase activation.	tetrandrine	6-17	caspase 8	Homo sapiens	111-131
31391686-6	2019	RESULTS: The high docking score of -10.0, -9.9, -9.8, and -9.5 were shown by friedelin, tingenone, albiziasaponin A, and albiziasaponin C, respectively, for caspase-3, and -11.0, -9.6, -9.6, and -9.4 by beta-boswellic acid, bryonolic acid, canophyllic acid, and CDDO, respectively, for caspase-8.	tingenone	88-97	caspase 8	Homo sapiens	286-295
31391686-6	2019	RESULTS: The high docking score of -10.0, -9.9, -9.8, and -9.5 were shown by friedelin, tingenone, albiziasaponin A, and albiziasaponin C, respectively, for caspase-3, and -11.0, -9.6, -9.6, and -9.4 by beta-boswellic acid, bryonolic acid, canophyllic acid, and CDDO, respectively, for caspase-8.	albiziasaponin	99-113	caspase 8	Homo sapiens	286-295
31391686-6	2019	RESULTS: The high docking score of -10.0, -9.9, -9.8, and -9.5 were shown by friedelin, tingenone, albiziasaponin A, and albiziasaponin C, respectively, for caspase-3, and -11.0, -9.6, -9.6, and -9.4 by beta-boswellic acid, bryonolic acid, canophyllic acid, and CDDO, respectively, for caspase-8.	albiziasaponin	121-135	caspase 8	Homo sapiens	286-295
31391686-6	2019	RESULTS: The high docking score of -10.0, -9.9, -9.8, and -9.5 were shown by friedelin, tingenone, albiziasaponin A, and albiziasaponin C, respectively, for caspase-3, and -11.0, -9.6, -9.6, and -9.4 by beta-boswellic acid, bryonolic acid, canophyllic acid, and CDDO, respectively, for caspase-8.	boswellic acid	203-222	caspase 8	Homo sapiens	286-295
31391686-6	2019	RESULTS: The high docking score of -10.0, -9.9, -9.8, and -9.5 were shown by friedelin, tingenone, albiziasaponin A, and albiziasaponin C, respectively, for caspase-3, and -11.0, -9.6, -9.6, and -9.4 by beta-boswellic acid, bryonolic acid, canophyllic acid, and CDDO, respectively, for caspase-8.	bryonolic acid	224-238	caspase 8	Homo sapiens	286-295
31391686-6	2019	RESULTS: The high docking score of -10.0, -9.9, -9.8, and -9.5 were shown by friedelin, tingenone, albiziasaponin A, and albiziasaponin C, respectively, for caspase-3, and -11.0, -9.6, -9.6, and -9.4 by beta-boswellic acid, bryonolic acid, canophyllic acid, and CDDO, respectively, for caspase-8.	canophyllic acid	240-256	caspase 8	Homo sapiens	286-295
31391686-6	2019	RESULTS: The high docking score of -10.0, -9.9, -9.8, and -9.5 were shown by friedelin, tingenone, albiziasaponin A, and albiziasaponin C, respectively, for caspase-3, and -11.0, -9.6, -9.6, and -9.4 by beta-boswellic acid, bryonolic acid, canophyllic acid, and CDDO, respectively, for caspase-8.	2-cyano-3,12-dioxoolean-1,9-dien-28-oic acid	262-266	caspase 8	Homo sapiens	286-295
30944654-8	2019	Subsequent mechanistic analysis demonstrated that TNFAIP8 silencing promoted caspase-8/-3 activation and p38 phosphorylation in HeLa cells treated with cisplatin, whereas apoptosis regulator B-cell lymphoma-2 expression was inhibited with TNFAIP8-silenced HeLa cells following treatment with cisplatin.	Cisplatin	152-161	caspase 8	Homo sapiens	77-86
30362578-0	2019	Apoptosis in HepaRG and HL-7702 cells inducted by polyphyllin II through caspases activation and cell-cycle arrest.	polyphyllin II	50-64	caspase 8	Homo sapiens	73-81
30362578-3	2019	However, our results in this study proved that the polyphyllin II has hepatotoxicity in vitro through caspases activation and cell-cycle arrest.	polyphyllin II	51-65	caspase 8	Homo sapiens	102-110
30903942-13	2019	In addition, liposomal Avicequinone-B showed significant cytotoxic effect on HSC-1 cells, through reduction of mitochondrial membrane potential, increased cytosolic cytochrome-c level, increased cleaved caspase 8 level, and induction of apoptosis.	Naphtho[2,3-b]furan-4,9-dione	23-37	caspase 8	Homo sapiens	203-212
31149366-7	2019	Furthermore, TFAC was the only extract that significantly upregulated the expression of caspase 3, caspase 8 and P53.	tfac	13-17	caspase 8	Homo sapiens	99-108
31032087-3	2019	In an effort to overcome TRAIL-refractory cancer, we investigated the effect of artonin E in regulating death receptor 5 (DR5) and cellular FLICE (FADD-like IL-1beta-converting enzyme)-inhibitory protein (cFLIP), two major mediators regulate TRAIL-induced apoptosis, in LoVo cells as a model of TRAIL refractory CRC.	artonin E	80-89	caspase 8	Homo sapiens	140-145
30902881-6	2019	Importantly, the loss of cIAP1 enhanced TNF-alpha/cycloheximide-induced apoptosis in higher activation statuses of Caspase-8, Caspase-3 without the induction of Complex II.	Cycloheximide	50-63	caspase 8	Homo sapiens	115-124
30229430-8	2019	We propose that 5-DMN cooperates with PTX to induce apoptosis via the caspase pathway (by modulating caspase-3, caspase-8, and caspase-9 activities).	5-demethylnobiletin	16-21	caspase 8	Homo sapiens	112-121
30229430-8	2019	We propose that 5-DMN cooperates with PTX to induce apoptosis via the caspase pathway (by modulating caspase-3, caspase-8, and caspase-9 activities).	Paclitaxel	38-41	caspase 8	Homo sapiens	112-121
30911132-5	2019	CFZ reduced cell viability via cell cycle arrest at G2/M and apoptosis, which involved caspase activation (caspases-8, 9, 4, and 3), endoplasmic reticulum stress, reactive oxygen species production, mitochondrial membrane potential loss, and autophagy in a dose- and time-dependent manner.	carfilzomib	0-3	caspase 8	Homo sapiens	107-130
30838722-7	2019	In contrast, EA provoked a significant activation of these caspases in all studied leukaemia cells.	Ellagic Acid	13-15	caspase 8	Homo sapiens	59-67
30689998-10	2019	Overall, our findings suggest that galbanic acid enhances TRAIL induced apoptosis via inhibition of MDR1 and activation of caspases and DR5 in H460/R cells as a potent TRAIL sensitizer.	galbanic acid	35-48	caspase 8	Homo sapiens	123-131
30835110-6	2019	The inhibition of Caspase 8 and Caspase 9 proteins abolished the licochalcone B induced apoptosis.	licochalcone B	65-79	caspase 8	Homo sapiens	18-27
30309851-6	2019	Activation of caspase-8 and cleavage of B-cell receptor-associated protein 31 stimulate a pro-apoptotic crosstalk including release of calcium from the endoplasmic reticulum and an increase in the levels of reactive oxygen species resulting in amplification of mitochondrial apoptosis.	Calcium	135-142	caspase 8	Homo sapiens	14-23
30845975-10	2019	The regimen sharply increased extrinsic apoptotic pathway activation, and cells expressing dominant-negative FADD or caspase-8 displayed markedly reduced birinapant/bortezomib sensitivity.	birinapant	154-164	caspase 8	Homo sapiens	117-126
30845975-10	2019	The regimen sharply increased extrinsic apoptotic pathway activation, and cells expressing dominant-negative FADD or caspase-8 displayed markedly reduced birinapant/bortezomib sensitivity.	Bortezomib	165-175	caspase 8	Homo sapiens	117-126
30668194-7	2019	Clozapine inhibited caspase-8 and caspase-3 activation and prevented loss of mitochondrial membrane potential.	Clozapine	0-9	caspase 8	Homo sapiens	20-29
30668194-11	2019	When apoptosis signalling pathways were studied, clozapine-mediated inhibition of apoptosis was dependent on caspase-3 and caspase-8.	Clozapine	49-58	caspase 8	Homo sapiens	123-132
30689998-0	2019	Galbanic acid potentiates TRAIL induced apoptosis in resistant non-small cell lung cancer cells via inhibition of MDR1 and activation of caspases and DR5.	galbanic acid	0-13	caspase 8	Homo sapiens	137-145
30309851-6	2019	Activation of caspase-8 and cleavage of B-cell receptor-associated protein 31 stimulate a pro-apoptotic crosstalk including release of calcium from the endoplasmic reticulum and an increase in the levels of reactive oxygen species resulting in amplification of mitochondrial apoptosis.	Reactive Oxygen Species	207-230	caspase 8	Homo sapiens	14-23
30408535-15	2019	Treatment with saponin rich fraction of A. lebbeck increased levels of Caspases-3 (optical density of 0.24 at 450 nm) and Caspase-8 (optical density of 0.31 at 450 nm) as compared to staurosporine (optical density of 2.47 and 2.65 for caspases-3 and -8 respectively at 450 nm).	Saponins	15-22	caspase 8	Homo sapiens	122-131
30569123-8	2019	Specific inhibition of AKT by MK2206 reduced the expression of p-PEA-15 at the Ser116 residue, resulting in sequential downregulation of p-ERK1/2, cyclin D1 and caspase-8 activation.	MK 2206	30-36	caspase 8	Homo sapiens	161-170
30562828-6	2019	Furthermore, damulin B activated the following: both intrinsic and extrinsic apoptosis pathways along with early G1 phase arrest via the upregulation of the Bax, Bid, tBid, cleaved caspase-8, and p53 expression levels; downregulation of the procaspase-8/-9, CDK4, CDK6, and cyclin D1 expression levels; and more release of cytochrome c in the cytoplasm.	damulin B	13-22	caspase 8	Homo sapiens	181-190
30867764-9	2019	In addition, it was observed that celastrol/cisplatin upregulated the expression of Bcl-associated X protein, cytochrome c, caspase-3 and C/EBP homologous protein, and downregulated the expression of Bcl-2, poly(ADP-ribose) polymerase, 78 kDa glucose-regulated protein and caspase-9, whereas the expression of caspase-8 remained unchanged.	celastrol	34-43	caspase 8	Homo sapiens	310-319
30867764-9	2019	In addition, it was observed that celastrol/cisplatin upregulated the expression of Bcl-associated X protein, cytochrome c, caspase-3 and C/EBP homologous protein, and downregulated the expression of Bcl-2, poly(ADP-ribose) polymerase, 78 kDa glucose-regulated protein and caspase-9, whereas the expression of caspase-8 remained unchanged.	Cisplatin	44-53	caspase 8	Homo sapiens	310-319
30668359-10	2019	The present study demonstrated that celastrol triggered apoptotic cell death by inducing cell cycle arrest at the G2/M phase via the intrinsic and extrinsic pathways (increased cleaved caspase-3, caspase-8, caspase-9, and PARP).	celastrol	36-45	caspase 8	Homo sapiens	196-205
30569134-6	2019	Furthermore, the study showed that corilagin induced the apoptosis of gastric cancer cells mainly via activating caspase-8, -9, -3 and poly ADP-ribose polymerase proteins.	corilagin	35-44	caspase 8	Homo sapiens	113-130
30863083-12	2019	Biochemical analysis revealed that HIFU+bufalin treatment elevated PARP expression and increased caspase-8 activation in MiaPaCa2 and Panc-1 cells.	bufalin	40-47	caspase 8	Homo sapiens	97-106
30389373-9	2019	Our data indicate that PIM1 inhibition and ABT-737 synergistically induce apoptosis in an MCL1-independent but CASP8-dependent manner in GB.	ABT-737	43-50	caspase 8	Homo sapiens	111-116
30754643-7	2019	Fluoxetine also significantly induced apoptosis, unregulated extrinsic (activation of first apoptosis signal protein and ligand (Fas/FasL), and caspase-8) and intrinsic (loss of mitochondrial membrane potential (DeltaPsim) pathways and increased Bcl-2 homologous antagonist killer (BAK) apoptosis signaling.	Fluoxetine	0-10	caspase 8	Homo sapiens	144-153
30429411-7	2019	At last, Western blot and real-time PCR were performed to explore the expression of caspases-8, -9, and -3 after the treatment of ghrelin.	Ghrelin	130-137	caspase 8	Homo sapiens	84-106
30429411-10	2019	Western blot showed that expression of cleaved-caspases-8, -9, and -3 were increased in ghrelin stimulation group compared with the control group, while expression of pro-caspases-8, -9, and -3 had no significant difference.	Ghrelin	88-95	caspase 8	Homo sapiens	47-69
30429411-11	2019	In mRNA levels, ghrelin can decrease pro-caspases-8, -9, and -3 mRNA expression, which confirmed the results of protein levels.	Ghrelin	16-23	caspase 8	Homo sapiens	41-63
32186020-12	2019	YGJDSJ-induced apoptosis was completely abrogated by a pan caspase inhibitor, Z-VAD-FMK.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	78-87	caspase 8	Homo sapiens	59-66
30668391-10	2019	Blockade of caspases with Z-VAD-FMK converted apoptosis-related proteins.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	26-35	caspase 8	Homo sapiens	12-20
30586302-5	2019	The resulting IL-1Ra/caspase-8(9) adducts are stabilized by hydrophobic and by few key hydrogen bonding interactions, formed by residues fully conserved across distinct caspases (-3, -6, -7, -8, and -9), and closely resemble the binding mode of the caspases inhibitors XIAP (X-linked inhibitor of apoptosis) and c-FLIP (cellular FLICE-like inhibitory protein).	Hydrogen	87-95	caspase 8	Homo sapiens	21-30
30686270-8	2019	Staurosporine stimulation and its effects on the expression of Bcl2, BAX, Bad, caspase-8, and caspase-9 were investigated with immunoblot.	Staurosporine	0-13	caspase 8	Homo sapiens	79-88
30666163-2	2019	The aim of the present study was to investigate the role of cellular FADD-like IL-1beta-converting enzyme (FLICE)-inhibitory protein large (c-FLIPL) in metformin-induced anticancer activity in non-small cell lung cancer (NSCLC) in vitro.	Metformin	152-161	caspase 8	Homo sapiens	69-105
30805008-6	2019	Interestingly, cisplatin upregulated critical components of the extrinsic apoptotic pathway-initiator caspase 8, effector caspase 3, and the cell death receptors.	Cisplatin	15-24	caspase 8	Homo sapiens	102-111
30805008-8	2019	Finally, we have demonstrated the central role of caspase 8 in this process, since its downregulation abrogated the sensitizing effect of cisplatin.	Cisplatin	138-147	caspase 8	Homo sapiens	50-59
30576621-0	2019	6"-Benzyloxy-4-bromo-2"-hydroxychalcone is cytotoxic against human leukaemia cells and induces caspase-8- and reactive oxygen species-dependent apoptosis.	6"-benzyloxy-4-bromo-2"-hydroxychalcone	0-39	caspase 8	Homo sapiens	95-104
30666163-2	2019	The aim of the present study was to investigate the role of cellular FADD-like IL-1beta-converting enzyme (FLICE)-inhibitory protein large (c-FLIPL) in metformin-induced anticancer activity in non-small cell lung cancer (NSCLC) in vitro.	Metformin	152-161	caspase 8	Homo sapiens	107-112
30389635-6	2019	Celastrol induced apoptosis primarily via up-regulation of caspase-3, caspase-8, and Bax, and down-regulation of Bcl-2.	celastrol	0-9	caspase 8	Homo sapiens	70-79
30615617-9	2019	The results of Western blotting indicated the expressions of Bcl-2, procaspase-3, procaspase-8, procaspase-9, and PARP decreased in HepG2 cells treated with peiminine, while the expressions of Bax, caspase-3, caspase-8, caspase-9, and cleaved PARP1 increased.	peiminine	157-166	caspase 8	Homo sapiens	85-94
31168030-0	2019	The anti-cancer drug gefitinib accelerates Fas-mediated apoptosis by enhancing caspase-8 activation in cancer cells.	Gefitinib	21-30	caspase 8	Homo sapiens	79-88
30655700-15	2019	Additionally, HCEE activated the caspase cascade by increasing the activities of caspase-9, caspase-8, and caspase-3.	hcee	14-18	caspase 8	Homo sapiens	92-101
31488032-4	2019	Dehydrocostus lactone stimulated the activation of caspase-3, -8, and -9, while caspase inhibitors significantly reversed the dehydrocostus lactone-induced cell death in 12Z cells.	dehydrocostus lactone	0-21	caspase 8	Homo sapiens	51-58
30258223-3	2019	Herein, we performed an in vitro biology test and found that 4,4"-SAD stimulated the apoptosis of tumor cells in the human hepatocellular carcinoma cell lines PLC/PRF/5 and HuH-7 by activating caspase-3, caspase-8, caspase-9, PARP, p53, and cyclin B1, as well as by regulating the Bax/Bcl-2 ratio.	4,4"-sad	61-69	caspase 8	Homo sapiens	204-213
31362681-9	2019	Also, Bax, caspase-3 and caspase-8 expression was significantly improved in K-562 cells upon quercetin exposure.	Quercetin	93-102	caspase 8	Homo sapiens	25-34
30137403-8	2019	In HepG2 hepatocytes, acylated and desacyl ghrelin treatment reduced TNF-alpha-induced apoptosis, evidenced by lower caspase-8 and caspase-3 cleavage, as well as TUNEL-positive cells and pyroptosis, revealed by decreased caspase-1 activation and lower high-mobility group box 1 expression.	ghrelin, des-n-octanoyl	35-50	caspase 8	Homo sapiens	117-126
31378763-0	2019	Stephanthraniline A suppresses proliferation of HCT116 human colon cancer cells through induction of caspase-dependent apoptosis, dysregulation of mitochondrial function, cell cycle arrest and regulation of Akt/p38 signaling pathways.	stephanthraniline A	0-19	caspase 8	Homo sapiens	101-108
31378763-6	2019	Activated caspase-3, caspase-8 and caspase-9, along with a decreased Bcl-2/Bcl-x ratio and loss of mitochondrial membrane potential (Deltapsim), were observed in response to STA treatment.	stephanthraniline A	174-177	caspase 8	Homo sapiens	21-30
31168030-0	2019	The anti-cancer drug gefitinib accelerates Fas-mediated apoptosis by enhancing caspase-8 activation in cancer cells.	ammonium ferrous sulfate	43-46	caspase 8	Homo sapiens	79-88
31168030-4	2019	In the presence of nontoxic concentrations of gefitinib, Fas-induced activation of caspase-8 and subsequent apoptosis was dramatically promoted, suggesting that gefitinib increases the sensitivity to Fas-mediated apoptosis.	Gefitinib	46-55	caspase 8	Homo sapiens	83-92
31168030-4	2019	In the presence of nontoxic concentrations of gefitinib, Fas-induced activation of caspase-8 and subsequent apoptosis was dramatically promoted, suggesting that gefitinib increases the sensitivity to Fas-mediated apoptosis.	ammonium ferrous sulfate	57-60	caspase 8	Homo sapiens	83-92
31168030-4	2019	In the presence of nontoxic concentrations of gefitinib, Fas-induced activation of caspase-8 and subsequent apoptosis was dramatically promoted, suggesting that gefitinib increases the sensitivity to Fas-mediated apoptosis.	Gefitinib	161-170	caspase 8	Homo sapiens	83-92
31168030-4	2019	In the presence of nontoxic concentrations of gefitinib, Fas-induced activation of caspase-8 and subsequent apoptosis was dramatically promoted, suggesting that gefitinib increases the sensitivity to Fas-mediated apoptosis.	ammonium ferrous sulfate	200-203	caspase 8	Homo sapiens	83-92
30663403-4	2019	In the present study we identified that the expression levels of Bcl-2, Bax, caspase 8, 9 and cyclinD1 using Q-PCR method in SKOV3 cell lines treated with Isochamanetin.	Isochamanetin	155-168	caspase 8	Homo sapiens	77-86
30663403-6	2019	Further the expression levels of Bcl-2, caspase8,9, Cytochrome C and CyclinD1 were significantly down regulated in SKOV3 cancer cells treated with isochamanetin, a specific binding molecule to CyclinD1.	Isochamanetin	147-160	caspase 8	Homo sapiens	40-48
30542729-8	2019	In addition, western blot analysis revealed that treatment of the K562 cells with lidamycin at low concentrations upregulated the expression of caspase-8 and caspase-3.	C 1027	82-91	caspase 8	Homo sapiens	144-153
30365122-5	2019	The addition of 4-(2-aminoethyl) benzenesulfonyl fluoride hydrochloride, a scavenger of reactive oxygen species (ROS), inhibited the degradation of HSP90 client proteins and HSP90 cleavage that was induced by co-treatment as well as the cleavage of caspase-3, caspase-8, and caspase-9 and cell death.	Reactive Oxygen Species	88-111	caspase 8	Homo sapiens	260-269
30542729-13	2019	The results of the present study suggest that a low-concentration lidamycin exerts effects on apoptosis and erythroid differentiation induction by increasing the expression of caspases and GATA-1 protein.	C 1027	66-75	caspase 8	Homo sapiens	176-184
30365122-5	2019	The addition of 4-(2-aminoethyl) benzenesulfonyl fluoride hydrochloride, a scavenger of reactive oxygen species (ROS), inhibited the degradation of HSP90 client proteins and HSP90 cleavage that was induced by co-treatment as well as the cleavage of caspase-3, caspase-8, and caspase-9 and cell death.	Reactive Oxygen Species	113-116	caspase 8	Homo sapiens	260-269
30365122-5	2019	The addition of 4-(2-aminoethyl) benzenesulfonyl fluoride hydrochloride, a scavenger of reactive oxygen species (ROS), inhibited the degradation of HSP90 client proteins and HSP90 cleavage that was induced by co-treatment as well as the cleavage of caspase-3, caspase-8, and caspase-9 and cell death.	4-(2-aminoethyl)benzenesulfonylfluoride	16-71	caspase 8	Homo sapiens	260-269
31818225-9	2019	Among these 5 sequences, only phosphorothioate oligonucleotide 4 inhibited the proliferation of H1650 cells, and this effect was due to the induction of cancer cell apoptosis by activating the caspase-8 apoptotic pathway.	4-nitrophenyl phosphorothioate	30-46	caspase 8	Homo sapiens	193-202
30300966-0	2018	Cucurbit[8]uril Reactivation of an Inactivated Caspase-8 Mutant Reveals Differentiated Enzymatic Substrate Processing.	uril	11-15	caspase 8	Homo sapiens	47-56
30551620-0	2018	23-Hydroxyursolic Acid Isolated from the Stem Bark of Cussonia bancoensis Induces Apoptosis through Fas/Caspase-8-Dependent Pathway in HL-60 Human Promyelocytic Leukemia Cells.	23-hydroxyursolic acid	0-22	caspase 8	Homo sapiens	104-113
30551620-7	2018	Pretreatment with a broad caspase inhibitor (z-VAD-fmk), a caspase-3 inhibitor (z-DEVD-fmk), and a caspase-8 inhibitor (z-IETD-fmk) significantly attenuated 23-HUA-induced DNA fragmentation.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	120-130	caspase 8	Homo sapiens	99-108
30671458-6	2018	Additionally, suppression of the death receptor signaling pathways with a caspase-8 inhibitor, Z-IETD-FMK, revealed an increase in the death rate and apoptotic rate of HepG2 cells.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	95-105	caspase 8	Homo sapiens	74-83
30339814-0	2018	Isoliquiritigenin-mediated p62/SQSTM1 induction regulates apoptotic potential through attenuation of caspase-8 activation in colorectal cancer cells.	isoliquiritigenin	0-17	caspase 8	Homo sapiens	101-110
30339814-6	2018	In a p62/SQSTM1 siRNA transfection study, ISL-induced p62/SQSTM1 expression attenuated ISL-mediated apoptosis by reducing caspase-8 activation.	isoliquiritigenin	42-45	caspase 8	Homo sapiens	122-131
30339814-9	2018	Our results demonstrate that ISL-induced p62/SQSTM1 upregulation affects ISL-mediated apoptotic potential through attenuation of caspase-8 activation in CRC cells.	isoliquiritigenin	29-32	caspase 8	Homo sapiens	129-138
30300966-1	2018	Caspase-8 constructs featuring an N-terminal FGG sequence allow for selective twofold recognition by cucurbit[8]uril, which leads to an increase of the enzymatic activity in a cucurbit[8]uril dose-dependent manner.	uril	112-116	caspase 8	Homo sapiens	0-9
30300966-1	2018	Caspase-8 constructs featuring an N-terminal FGG sequence allow for selective twofold recognition by cucurbit[8]uril, which leads to an increase of the enzymatic activity in a cucurbit[8]uril dose-dependent manner.	uril	187-191	caspase 8	Homo sapiens	0-9
30300966-2	2018	This supramolecular switching has enabled for the first time the study of the same caspase-8 in its two extreme states; as full monomer and as cucurbit[8]uril induced dimer.	uril	154-158	caspase 8	Homo sapiens	83-92
30300966-3	2018	A mutated, fully monomeric caspase-8 (D384A), which is enzymatically inactive towards its natural substrate caspase-3, could be fully reactivated upon addition of cucurbit[8]uril.	uril	174-178	caspase 8	Homo sapiens	27-36
30514811-3	2018	Here, we report that p62 was proteolytically trimmed by the protease caspase-8 into a stable protein, which we called p62TRM We found that p62TRM, but not full-length p62, was involved in nutrient sensing and homeostasis through the mechanistic target of rapamycin complex 1 (mTORC1).	Sirolimus	255-264	caspase 8	Homo sapiens	69-78
29742927-5	2018	Furthermore, the pro-apoptotic signalling pathway induced by tetracaine was explored through detecting the activation of various caspases, the changes of mitochondrial transmembrane potential (MTP), the expression level of Bcl-2 family proteins and the amount of mitochondria-released apoptosis regulating proteins in cytoplasm.	Tetracaine	61-71	caspase 8	Homo sapiens	129-137
29742927-8	2018	Tetracaine not only resulted in caspase-3, caspase-8 and caspase-9 activation and disruption of MTP but also downregulated Bcl-2 and Bcl-xL and upregulated Bad and Bax, along with the upregulation of cytoplasmic cytochrome c (<protein-id="54205">Cyt.	Tetracaine	0-10	caspase 8	Homo sapiens	43-52
30262279-8	2018	On the contrary, DMMTAV exposure resulted in markedly elevated activity of caspase-8 as well as caspase-9.	dmmtav	17-23	caspase 8	Homo sapiens	75-84
30001631-9	2018	The positive staining using gamma-H2AX and AO/EB dye, showed increased cleaved caspase-3, caspase-8, caspase-9, increased ROS production, MMP and enhanced mRNA expression of apoptotic genes, suggesting that anticancer effects are also exerted through its apoptosis-inducing properties.	gamma-h2ax	28-38	caspase 8	Homo sapiens	90-99
30320340-0	2018	Effects of polymorphic DNA genes involved in BER and caspase pathways on the clinical outcome of myeloproliferative neoplasms under treatment with hydroxyurea.	Hydroxyurea	147-158	caspase 8	Homo sapiens	53-60
30320341-7	2018	Poly(I:C)-HMW induced the expression of active caspase-8 and -9, and the Poly(I:C)-HMW-induced increase in the cell cycle sub-G1 population, which is one of the hallmarks of apoptosis, was decreased by treatment with a caspase-8 inhibitor and caspase-9 inhibitor.	Poly I-C	0-9	caspase 8	Homo sapiens	47-63
30272304-6	2018	At later stages, expression of caspase-8 was increased due to the apoptotic signals originating from CBCDA-induced DNA damage, as well as caspase-9 and poly ADP ribose polymerase (PARP) expression upregulation.	cbcda	101-106	caspase 8	Homo sapiens	31-40
30320341-7	2018	Poly(I:C)-HMW induced the expression of active caspase-8 and -9, and the Poly(I:C)-HMW-induced increase in the cell cycle sub-G1 population, which is one of the hallmarks of apoptosis, was decreased by treatment with a caspase-8 inhibitor and caspase-9 inhibitor.	Poly I-C	0-9	caspase 8	Homo sapiens	47-56
30320341-8	2018	When cells were treated with Poly(I:C)-HMW and IR, the sub-G1 population, and the active caspase-8 and caspase-9 expression were all increased compared with cells treated with Poly(I:C)-HMW or IR alone.	Poly I-C	29-38	caspase 8	Homo sapiens	89-98
30320341-10	2018	Notably, treatment with an inhibitor for caspase-8, not caspase-9, partially reversed the net increase in the sub-G1 population induced by cotreatment with Poly(I:C)-HMW and IR.	Poly I-C	156-164	caspase 8	Homo sapiens	41-50
30320341-11	2018	Collectively, these results suggested that Poly(I:C)-HMW induces apoptosis through caspase-8 and caspase-9 activation; however, the apoptotic pathway mediated by casapse-8, and not casapse-9, is involved in the enhancement of apoptosis caused by cotreatment with Poly(I:C)-HMW and IR.	Poly I-C	43-52	caspase 8	Homo sapiens	83-92
30626478-8	2018	Compared with the group without celastrol treatment, the mRNA and protein level of Bcl2 in A549 cells treated with (1, 3) mumol/L celastrol decreased significantly, while the expression levels of BAX, caspase-3, caspase-8, caspase-9, c-caspase-3, c-caspase-8, c-caspase-9 increased significantly.	celastrol	130-139	caspase 8	Homo sapiens	212-221
30195041-7	2018	Alpha-mangostin significantly sensitized anoikis in HepG2 through the inhibition of cell survival by induced caspase-9, caspase-8 and caspase-3 activities, increased pro-apoptotic protein (Bax, Bim, t-Bid) levels, and decreased anti-apoptotic protein (c-FLIP, Mcl-1) levels.	mangostin	0-15	caspase 8	Homo sapiens	120-129
30626478-8	2018	Compared with the group without celastrol treatment, the mRNA and protein level of Bcl2 in A549 cells treated with (1, 3) mumol/L celastrol decreased significantly, while the expression levels of BAX, caspase-3, caspase-8, caspase-9, c-caspase-3, c-caspase-8, c-caspase-9 increased significantly.	celastrol	130-139	caspase 8	Homo sapiens	249-258
30626478-5	2018	The effects of celastrol on the expression of BAX, B-cell lymphoma 2 (Bcl2), caspase-3, caspase-8, caspase-9 mRNA in A549 cells were detected by real-time quantitative PCR.	celastrol	15-24	caspase 8	Homo sapiens	88-97
30400347-6	2018	Treating hPSCs seeded on a TCP surface with a caspase-8 inhibitor significantly suppressed cellular apoptotic pathway and improved cell proliferation and metabolism.	tcp	27-30	caspase 8	Homo sapiens	46-55
30381458-3	2018	Here, using Yersinia pseudotuberculosis in corroboration with costimulation of lipopolysaccharide and (5Z)-7-Oxozeaenol, a small-molecule inhibitor of TAK1, we show that caspase-8 activation during TAK1 inhibition results in cleavage of both gasdermin D (GSDMD) and gasdermin E (GSDME) in murine macrophages, resulting in pyroptosis.	5-7-oxo-zeaenol	102-119	caspase 8	Homo sapiens	170-179
30381458-3	2018	Here, using Yersinia pseudotuberculosis in corroboration with costimulation of lipopolysaccharide and (5Z)-7-Oxozeaenol, a small-molecule inhibitor of TAK1, we show that caspase-8 activation during TAK1 inhibition results in cleavage of both gasdermin D (GSDMD) and gasdermin E (GSDME) in murine macrophages, resulting in pyroptosis.	gsdmd	255-260	caspase 8	Homo sapiens	170-179
30515160-3	2018	For IL-1beta production, betaine affects canonical and non-canonical inflammasome-mediated processing of IL-1beta through signaling pathways, such as NF-kappaB, NLRP3 and caspase-8/11.	Betaine	25-32	caspase 8	Homo sapiens	171-180
30585261-7	2018	The cGMP analog 8-Br-cGMP blocked H2O2-induced apoptotic cell death; reduction of caspase-3 enzyme, cytochrome c release, and caspase-8 and -9.	Cyclic GMP	4-8	caspase 8	Homo sapiens	126-142
30585261-7	2018	The cGMP analog 8-Br-cGMP blocked H2O2-induced apoptotic cell death; reduction of caspase-3 enzyme, cytochrome c release, and caspase-8 and -9.	8-bromoguanosino-3',5'-cyclic monophosphorothioate	16-25	caspase 8	Homo sapiens	126-142
30585261-7	2018	The cGMP analog 8-Br-cGMP blocked H2O2-induced apoptotic cell death; reduction of caspase-3 enzyme, cytochrome c release, and caspase-8 and -9.	Hydrogen Peroxide	34-38	caspase 8	Homo sapiens	126-142
30385739-9	2018	Our study therefore demonstrates that a high caspase-8/Bid signature is associated with synergistic TRAIL/TL32711-induced apoptosis in GBM cells and outlines Bcl-2 antagonism as a highly potent intervention to sensitize highly TRAIL-resistant GBM cells to TRAIL/TL32711 combination treatment.	birinapant	106-113	caspase 8	Homo sapiens	45-54
30035337-0	2018	Phenalenone-photodynamic therapy induces apoptosis on human tumor cells mediated by caspase-8 and p38-MAPK activation.	phenalen-1-one	0-11	caspase 8	Homo sapiens	84-93
30035337-9	2018	Using pharmacologic inhibitors, we also find that PN-PDT activates caspase-8/tBid and p38-MAPK, triggering the activation of the apoptotic pathways.	tBID	77-81	caspase 8	Homo sapiens	67-76
30519344-6	2018	In vivo, ZD55-IL-24 and DTX synergistically inhibited the growth and activated the apoptosis of DU145 xenografts, accompanied by significantly decreased PARP-1 levels and increased caspase-3 and caspase-8 levels as well as decreased CD31 expression.	Docetaxel	24-27	caspase 8	Homo sapiens	195-204
30349042-5	2018	By decreasing FLIP expression at the post-transcriptional level in PC3 and DU145 cells (but not VCaP), the Class-I histone deacetylase (HDAC) inhibitor Entinostat promoted IAP antagonist-induced cell death in these models in a manner dependent on RIPK1, FADD and Caspase-8.	entinostat	152-162	caspase 8	Homo sapiens	263-272
30515223-11	2018	In addition, pretreatment of PDLSCs with AZM (10 mug/ml, 20 mug/ml) prevented TNF-alpha-induced apoptosis by decreasing caspase-8 and caspase-3 expression.	Azithromycin	41-44	caspase 8	Homo sapiens	120-129
30119201-8	2018	Significantly increased apoptosis and increases in apoptosis-related proteins (caspase 8 and Bcl-xL) were observed in cells treated with GEM plus TPL.	gemcitabine	137-140	caspase 8	Homo sapiens	79-88
30119201-8	2018	Significantly increased apoptosis and increases in apoptosis-related proteins (caspase 8 and Bcl-xL) were observed in cells treated with GEM plus TPL.	triptolide	146-149	caspase 8	Homo sapiens	79-88
30125548-4	2018	The induction of apoptosis as evidenced by the increase of sub-G1 cells, DNA fragmentation, annexin V-positive cells and the activation of caspase-8, -9 and -3 was observed in HL-60 cells co-treated with As(III) and delphinidin.	as(iii)	204-211	caspase 8	Homo sapiens	139-159
30125548-4	2018	The induction of apoptosis as evidenced by the increase of sub-G1 cells, DNA fragmentation, annexin V-positive cells and the activation of caspase-8, -9 and -3 was observed in HL-60 cells co-treated with As(III) and delphinidin.	delphinidin	216-227	caspase 8	Homo sapiens	139-159
29990575-6	2018	The inhibition of Caspase-8 and Caspase-9 proteins in these pathways abolished the dioscin induced apoptosis significantly; while dioscin inhibited the PI3K/Akt/mTOR pathway.	dioscin	83-90	caspase 8	Homo sapiens	18-27
30189374-5	2018	In particular, the expression levels of mitochondrial apoptosis-related proteins, such as AKT1, BAX, HSPD1, TNF, CASP8 and DAP, were increased after SiO2 exposure.	Silicon Dioxide	149-153	caspase 8	Homo sapiens	113-118
30066934-12	2018	The knockdown of cFLIP reversed the acquired sorafenib resistance by activating caspase-8 and inhibiting activated ERS in the sorafenib-resistant HCC cells.	Sorafenib	45-54	caspase 8	Homo sapiens	80-89
30115673-5	2018	The mechanism of bortezomib-mediated downregulation of Sp transcription factors in MM was due to the induction of caspase-8 and upstream factors, including Fas-associated death domain.	Bortezomib	17-27	caspase 8	Homo sapiens	114-123
30115673-6	2018	These results demonstrate that an important underlying mechanism of action of bortezomib was due to the activation of caspase-8-dependent downregulation of Sp1, Sp3, Sp4, and pro-oncogenic Sp-regulated genes.	Bortezomib	78-88	caspase 8	Homo sapiens	118-127
30211553-7	2018	Therefore, these findings provide novel insight that ROS and p53 signalings mediate p38 phosphorylation and caspase activation in Kaempferol stimulated apoptosis in CRCs.	Reactive Oxygen Species	53-56	caspase 8	Homo sapiens	108-115
29876988-5	2018	Consistently, Tan I cleaved poly (adenosine diphosphate-ribose) polymerase (PARP) and caspase-8, caspase-3, attenuated the expression of Bid and activated tBid as a caspase-8 substrate and activated phosphorylation of p38 MAPK in HCT116and HT29 cells.	tBID	155-159	caspase 8	Homo sapiens	86-95
29876988-5	2018	Consistently, Tan I cleaved poly (adenosine diphosphate-ribose) polymerase (PARP) and caspase-8, caspase-3, attenuated the expression of Bid and activated tBid as a caspase-8 substrate and activated phosphorylation of p38 MAPK in HCT116and HT29 cells.	tBID	155-159	caspase 8	Homo sapiens	165-174
30009775-1	2018	Recently, we have reported that Demethoxycurcumin induced Reactive oxygen species via inhibition of Mitochondrial Superoxide Dismutase is an initial event to trigger apoptosis through caspase-8 and 9 activation and to inhibit Akt/NF-kappaB survival signaling in human glioma U87 MG cells (Kumar et al., 2018).	demethoxycurcumin	32-49	caspase 8	Homo sapiens	184-193
30009775-1	2018	Recently, we have reported that Demethoxycurcumin induced Reactive oxygen species via inhibition of Mitochondrial Superoxide Dismutase is an initial event to trigger apoptosis through caspase-8 and 9 activation and to inhibit Akt/NF-kappaB survival signaling in human glioma U87 MG cells (Kumar et al., 2018).	Reactive Oxygen Species	58-81	caspase 8	Homo sapiens	184-193
30211553-0	2018	Reactive Oxygen Species and p53 Mediated Activation of p38 and Caspases is Critically Involved in Kaempferol Induced Apoptosis in Colorectal Cancer Cells.	Reactive Oxygen Species	0-23	caspase 8	Homo sapiens	63-71
30211553-0	2018	Reactive Oxygen Species and p53 Mediated Activation of p38 and Caspases is Critically Involved in Kaempferol Induced Apoptosis in Colorectal Cancer Cells.	kaempferol	98-108	caspase 8	Homo sapiens	63-71
30211553-7	2018	Therefore, these findings provide novel insight that ROS and p53 signalings mediate p38 phosphorylation and caspase activation in Kaempferol stimulated apoptosis in CRCs.	kaempferol	130-140	caspase 8	Homo sapiens	108-115
30211553-4	2018	Also, Kaempferol increased the PARP cleavages and activation of caspase-8, -9, and -3, phospho-p38 MAPK, p53, and p21 in HCT116 and HCT15 cells.	kaempferol	6-16	caspase 8	Homo sapiens	64-85
29792952-7	2018	The IC50 dose of SA in PC-3 and LNCaP cells was found to be 1000 muM for 72 h. SA treatment increased the expression of BAX, CASP3, CASP8, CYCS, FAS, TIMP-1 and CDH1 however significantly decreased the expression of MMP-9 in PC-3 cells.	sinapinic acid	79-81	caspase 8	Homo sapiens	132-137
30238673-4	2018	The current study reveals that low-dose BPA treatment induced cytotoxicity, NO, and caspase-8 levels in SH-SY5Y cells.	bisphenol A	40-43	caspase 8	Homo sapiens	84-93
30107166-9	2018	Luteolin led a significantly increase in apoptosis accompanied by activation of caspase 8, -9 and -3 and cleavage of poly (ADP-ribose) polymerase (PARP), which was completely blocked by Z-VAD-FMK, a pan caspase inhibitor.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	186-195	caspase 8	Homo sapiens	80-100
30206207-6	2018	The cytotoxic activity of ABT-737 in CERS6 knockdown cells was significantly reduced by the addition of a caspase-8 inhibitor Z-IETD, suggesting that CERS6 alters the cytotoxicity via extrinsic pathway of apoptosis.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	26-29	caspase 8	Homo sapiens	106-115
30206207-6	2018	The cytotoxic activity of ABT-737 in CERS6 knockdown cells was significantly reduced by the addition of a caspase-8 inhibitor Z-IETD, suggesting that CERS6 alters the cytotoxicity via extrinsic pathway of apoptosis.	z-ietd	126-132	caspase 8	Homo sapiens	106-115
30125721-6	2018	The mechanism studies indicated the mitochondrial localization of BODIPY3-PEG3 was able to generate ROS in mitochondria, which further result in mitochondrial dysfunction and photoinduced apoptosis via caspase-8 and caspase-3 pathway.	ros	100-103	caspase 8	Homo sapiens	202-211
29957841-5	2018	Compared to beta-elemene or TRAIL alone, treatment with beta-elemene and TRAIL obviously promoted DR5 clustering as well as translocation of Caspase-8, DR5 and FADD into lipid rafts.	beta-elemene	56-68	caspase 8	Homo sapiens	141-150
30127928-4	2018	It was revealed that resibufogenin effectively inhibited cell proliferation, and induced apoptosis and caspase-3 and caspase-8 activity in MGC-803 cells.	bufogenin	21-34	caspase 8	Homo sapiens	117-126
29956787-8	2018	All the tested caspase inhibitors (Z-VAD for pan-caspases, Z-DEVD for caspase-3, Z-IETD for caspase-8 and Z-LEHD for caspase-9) decreased the percentages of sub-G1 and Annexin V-FITC-stained cells in the H2O2-treated Calu-6 and A549 cells.	z-ietd	81-87	caspase 8	Homo sapiens	92-101
29574877-7	2018	Western blot assays suggested that apoptosis was induced by fisetin administration, promoting Caspase-8, and Cytochrome-C expressions possibly by inhibiting aberrant activation of IGF1R and AKT proteins.	fisetin	60-67	caspase 8	Homo sapiens	94-103
30204479-7	2018	ROS production caused DNA damage and apoptosis was marked by cell cycle arrest, up-regulation of Bax and FasL protein as well as cleavage of caspase-9, caspase-8 and caspase-3 protein.	Reactive Oxygen Species	0-3	caspase 8	Homo sapiens	152-161
30087276-0	2018	Design, Synthesis, and Antiproliferative Evaluation of Novel Coumarin/2-Cyanoacryloyl Hybrids as Apoptosis Inducing Agents by Activation of Caspase-Dependent Pathway.	coumarin	61-69	caspase 8	Homo sapiens	140-147
30087276-0	2018	Design, Synthesis, and Antiproliferative Evaluation of Novel Coumarin/2-Cyanoacryloyl Hybrids as Apoptosis Inducing Agents by Activation of Caspase-Dependent Pathway.	2-cyanoacryloyl	70-85	caspase 8	Homo sapiens	140-147
29845207-5	2018	The upregulation of these miRNAs specifically and markedly downregulated the expression of Casp-8, as well as significantly enhanced the Z-VAD/TNF-alpha-induced necroptosis of HCC cells.	z-vad	137-142	caspase 8	Homo sapiens	91-97
30190788-0	2018	Terpenes from essential oils and hydrolate of Teucrium alopecurus triggered apoptotic events dependent on caspases activation and PARP cleavage in human colon cancer cells through decreased protein expressions.	Terpenes	0-8	caspase 8	Homo sapiens	106-114
30190788-0	2018	Terpenes from essential oils and hydrolate of Teucrium alopecurus triggered apoptotic events dependent on caspases activation and PARP cleavage in human colon cancer cells through decreased protein expressions.	Oils, Volatile	14-28	caspase 8	Homo sapiens	106-114
30154785-7	2018	Human neutrophils pretreated with zVAD-fmk (pan-caspase inhibitor) and zIETD-fmk (caspase-8 inhibitor) increased reactive oxygen species (ROS) level in response to Leishmania infection, which is associated with necroptotic cell death.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	71-80	caspase 8	Homo sapiens	82-91
30154785-7	2018	Human neutrophils pretreated with zVAD-fmk (pan-caspase inhibitor) and zIETD-fmk (caspase-8 inhibitor) increased reactive oxygen species (ROS) level in response to Leishmania infection, which is associated with necroptotic cell death.	Reactive Oxygen Species	113-136	caspase 8	Homo sapiens	82-91
30154785-7	2018	Human neutrophils pretreated with zVAD-fmk (pan-caspase inhibitor) and zIETD-fmk (caspase-8 inhibitor) increased reactive oxygen species (ROS) level in response to Leishmania infection, which is associated with necroptotic cell death.	Reactive Oxygen Species	138-141	caspase 8	Homo sapiens	82-91
30017071-2	2018	Bid and its caspase-8 cleavage product, tBid, promote the permeabilization of the mitochondrial outer membrane and sequester antiapoptotic Bcl-2 proteins to counter their cytoprotective activity.	tBID	40-44	caspase 8	Homo sapiens	12-21
30111412-4	2018	Furtherly, LY2409881 inhibited the expression of c-FLIP, induced the activation of DR4 and caspase 8.	LY2409881	11-20	caspase 8	Homo sapiens	91-100
30008897-0	2018	Metformin-induced apoptosis facilitates degradation of the cellular caspase 8 (FLICE)-like inhibitory protein through a caspase-dependent pathway in human renal cell carcinoma A498 cells.	Metformin	0-9	caspase 8	Homo sapiens	68-77
30008897-0	2018	Metformin-induced apoptosis facilitates degradation of the cellular caspase 8 (FLICE)-like inhibitory protein through a caspase-dependent pathway in human renal cell carcinoma A498 cells.	Metformin	0-9	caspase 8	Homo sapiens	79-84
30008897-0	2018	Metformin-induced apoptosis facilitates degradation of the cellular caspase 8 (FLICE)-like inhibitory protein through a caspase-dependent pathway in human renal cell carcinoma A498 cells.	Metformin	0-9	caspase 8	Homo sapiens	68-75
30008897-7	2018	It was revealed that degradation of cellular caspase 8 (FLICE)-like inhibitory protein (c-FLIP) and activation of procaspase-8 were associated with metformin-mediated apoptosis.	Metformin	148-157	caspase 8	Homo sapiens	45-54
30008897-7	2018	It was revealed that degradation of cellular caspase 8 (FLICE)-like inhibitory protein (c-FLIP) and activation of procaspase-8 were associated with metformin-mediated apoptosis.	Metformin	148-157	caspase 8	Homo sapiens	56-61
30008897-9	2018	Treatment with benzyloxycarbonyl-Val-Ala-Asp-fluoromethyl ketone (z-VAD-fmk, a pan-caspase inhibitor) almost completely blocked metformin-induced apoptosis and degradation of c-FLIPL protein.	Caspase Inhibitor VI	15-64	caspase 8	Homo sapiens	83-90
30008897-9	2018	Treatment with benzyloxycarbonyl-Val-Ala-Asp-fluoromethyl ketone (z-VAD-fmk, a pan-caspase inhibitor) almost completely blocked metformin-induced apoptosis and degradation of c-FLIPL protein.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	66-75	caspase 8	Homo sapiens	83-90
30008897-9	2018	Treatment with benzyloxycarbonyl-Val-Ala-Asp-fluoromethyl ketone (z-VAD-fmk, a pan-caspase inhibitor) almost completely blocked metformin-induced apoptosis and degradation of c-FLIPL protein.	Metformin	128-137	caspase 8	Homo sapiens	83-90
30008897-11	2018	Taken together, the results of the present study demonstrated that metformin-induced apoptosis involved degradation of the c-FLIPL protein and activation of caspase-8 in human renal cell carcinoma A498 cells and suggested that metformin could be potentially used for the treatment of renal cancer.	Metformin	67-76	caspase 8	Homo sapiens	157-166
30061622-10	2018	Therefore, we demonstrated that a novel Fas-binding OMP and LPS of L. interrogans induce macrophage apoptosis through the Fas/FasL-caspase-8/-3 pathway.	ammonium ferrous sulfate	40-43	caspase 8	Homo sapiens	131-140
30100745-14	2018	The levels of cleaved caspase-3, caspase-8, caspase-9, and caspase-10 were also markedly increased by euphornin treatment.	euphornin	102-111	caspase 8	Homo sapiens	33-42
29606028-7	2018	Our results showed that nifuroxazide treatment, attenuated diabetes-induced damage in renal structure, ameliorated oxidative stress, triggered antioxidant defense, reduced NFkappaB nuclear translocation and cleaved caspase-3 expression and down regulated the activity of apoptotic enzymes (caspase-3/caspase-8/caspase-9) in diabetic kidney.	nifuroxazide	24-36	caspase 8	Homo sapiens	300-309
30022842-12	2018	Furthermore, Western blot demonstrated that TBMS1 downregulated apoptosis-associated proteins such as PARP, p-ERK1/2, Bcl-2, caspase-3, caspase-7 and caspase-8 and upregulated cleaved PARP, cleaved caspase-3 and cleaved caspase-9.	tubeimoside I	44-49	caspase 8	Homo sapiens	150-159
30044423-6	2018	In addition, (-)-asarinin (1) increased the activation of caspase-3, caspase-8, and caspase-9 in ovarian cancer cells.	sesamin	13-25	caspase 8	Homo sapiens	69-78
29514461-7	2018	Apoptosis was measured by activity of several cysteine-dependent aspartate-specific protease (abbreviated as caspase) enzymes that initiate (caspases 8 and 9) or execute (caspases 3/7) apoptosis.	Cysteine	46-54	caspase 8	Homo sapiens	141-157
29250709-6	2018	We showed that folic acid increased cell viability and decreased apoptosis in a dose-dependent manner, and that this effect was mediated by decreased caspase-3/7 activity, upregulated BCL2/BAX ratio, and downregulated TP53, CASP3, and CASP8 expressions.	Folic Acid	15-25	caspase 8	Homo sapiens	235-240
29874795-4	2018	The study demonstrated that luteoloside could inhibit proliferation remarkably; promote apoptosis and cytochrome C release; decrease the mitochondrial membrane potential and reactive oxygen species level; upregulate the expression of Fas, Bax, p53, phospho-p38, phospho-JNK, and cleaved PARP; downregulate the expression of Bcl-2 and phospho-mTOR; activate caspase-3 and caspase-8; change the nuclear morphology, and fragmentate DNA in Hela cells.	luteolin-7-glucoside	28-39	caspase 8	Homo sapiens	371-380
29936715-0	2018	Calotroposid A: a Glycosides Terpenoids from Calotropis gigantea Induces Apoptosis of Colon Cancer WiDr Cellsthrough Cell Cycle Arrest G2/M and Caspase 8 Expression Objective: This study aims to isolate the active anticancer compound from ethyl acetate fraction extracted fromthe roots of Calotropis gigantea and to determine the operating mechanism of the isolates towards WiDr colon cancercells.	calotroposid a	0-14	caspase 8	Homo sapiens	144-153
29936715-0	2018	Calotroposid A: a Glycosides Terpenoids from Calotropis gigantea Induces Apoptosis of Colon Cancer WiDr Cellsthrough Cell Cycle Arrest G2/M and Caspase 8 Expression Objective: This study aims to isolate the active anticancer compound from ethyl acetate fraction extracted fromthe roots of Calotropis gigantea and to determine the operating mechanism of the isolates towards WiDr colon cancercells.	Terpenes	29-39	caspase 8	Homo sapiens	144-153
29936715-8	2018	Conclusion:Calotroposide A induces anticancer activity against WiDr colon cancer cells by means of apoptosis induction mechanismthrough extrinsic pathway with increased expression of caspase-8.	calotroposide A	11-26	caspase 8	Homo sapiens	183-192
29946223-10	2018	IFNgamma/AZD5582-induced cell death in NSCLC cells was independent of TNFalpha autocrine but relied on apoptosis mediated by JAK kinase, caspase 8 and RIPK1 pathways.	N,N'-(2,2'-(hexa-2,4-diyne-1,6-diylbis(oxy))bis(2,3-dihydro-1H-indene-2,1-diyl))bis(1-(2-cyclohexyl-2-(2-(methylamino)propanamido)acetyl)pyrrolidine-2-carboxamide)	9-16	caspase 8	Homo sapiens	137-146
29643240-6	2018	Ixazomib, a proteasome inhibitor in clinical use, blocks this pathway, increasing the abundance of Casp8p41 and causing more cells to die in a Casp8p41-dependent manner.IMPORTANCE The Casp8p41 pathway of cell death is unique to HIV-infected cells yet is blocked by Bcl2.	ixazomib	0-8	caspase 8	Homo sapiens	99-105
29950991-7	2018	The activity of caspase-8, caspase-9 and the expression of p53 were significantly increased after treatment with HJB.	3-[7,7-bis(oxidanyl)-8-oxa-7-boranuidabicyclo[4.3.0]nona-1(6),2,4-trien-5-yl]propanoic acid	113-116	caspase 8	Homo sapiens	16-25
29476302-13	2018	Caspase-8 activation in C6 cells increased to a maximum (12.5%) after 6 h by using combined cis-platin/epsilon-viniferin treatment (13.25/95 muM).	Viniferin	111-120	caspase 8	Homo sapiens	0-9
29754265-7	2018	CS caused cytotoxicity in HCT116 cells through several apoptotic events including activation of the Fas death receptor, FADD, caspase 8, caspase 3, caspase 9, and cleaved PARP, which occurred alongside cell cycle arrest from the up-regulation of p53 and p21.	Cesium	0-2	caspase 8	Homo sapiens	126-135
29526802-5	2018	In this context, apoptosis triggered by olaparib is associated with a dose-dependent up-regulation of death receptors expression and caspase 8 activation.	olaparib	40-48	caspase 8	Homo sapiens	133-142
28537448-4	2018	This study shows that hesperetin induces apoptosis in H522 cells via a pathway independentof p53 and Bax but triggers the death-receptor Fas-initiated FADD/ caspase-8-dependent apoptotic pathway.	hesperetin	22-32	caspase 8	Homo sapiens	157-166
29928342-6	2018	The results from western blotting revealed that quercetin increased Fas, Fas-Ligand, fas-associated protein with death domain and caspase-8, all of which associated with cell surface death receptor.	Quercetin	48-57	caspase 8	Homo sapiens	130-139
29693193-7	2018	Moreover, following treatment with corilagin, we noted upregulation of Fas and FasL and activation of caspase-8 which represented activation of the death receptor pathway, and we also observed downregulation of Bcl-2 and survivin which was also attributed to the antitumor effect of corilagin.	corilagin	35-44	caspase 8	Homo sapiens	102-111
29788929-8	2018	Mitochondrial membrane potential and apoptosis-related markers, such as an increased Bax/Bcl-2 ratio, and cleaved forms of caspase-8 and caspase-3, arise following resveratrol addition.	Resveratrol	164-175	caspase 8	Homo sapiens	123-132
29950209-6	2018	CONCLUSION: Artesunate can inhibit the proliferation of THP-1 cells, which may relate with the down-regulation of STAT3 expression and the activation of Capase3 and Caspase8.	Artesunate	12-22	caspase 8	Homo sapiens	165-173
29928578-8	2018	Increased caspase-8 activity as a consequence of reduction in fatty acid synthesis was also found to cause disruption of DeltaPsim.	Fatty Acids	62-72	caspase 8	Homo sapiens	10-19
29772677-0	2018	Lambertianic Acid Sensitizes Non-Small Cell Lung Cancers to TRAIL-Induced Apoptosis via Inhibition of XIAP/NF-kappaB and Activation of Caspases and Death Receptor 4.	lambertianic acid	0-17	caspase 8	Homo sapiens	135-143
29780394-7	2018	Results showed that uric acid serum concentration was significantly increased in PPMS; in these and in AMS patients, mRNA for NLRP3, ASC, and IL-18 was upregulated as well, but caspase-8 mRNA was upregulated only in PPMS.	Uric Acid	20-29	caspase 8	Homo sapiens	177-186
29734760-7	2018	Kaempferol stimulated extrinsic apoptosis via death receptors/FADD/Caspase-8 pathway.	kaempferol	0-10	caspase 8	Homo sapiens	67-76
29218444-5	2018	We observed that actinomycin D-induced apoptosis in U-937 cells, evaluated by Annexin V-CY3, DNA fragmentation and caspase-3, caspase-8, caspase-9 activation assays, was inhibited in the presence of L. infantum promastigotes and that, in these conditions, Bcl-2 protein expression resulted significantly upregulated.	Dactinomycin	17-30	caspase 8	Homo sapiens	126-135
29490557-13	2018	The expression of PARP and casp-8 were increased in BLE-treated nasal polyp tissue compared with PBS-treated tissue.	Lead	97-100	caspase 8	Homo sapiens	27-33
29568883-6	2018	It was demonstrated that everolimus induced apoptosis through decreasing B cell lymphoma (Bcl)-2 and Bcl-w and increasing caspase-3 and caspase-8 expression levels in breast cancer cells.	Everolimus	25-35	caspase 8	Homo sapiens	136-145
29921390-9	2018	The percentage of cell apoptosis increased, and the Western blot showed that the expression of caspase-3, caspase-8, and c-myc, respectively, in the semi-combination group, the 5-Fluorouracil group, and the combination group increased successively and that the successive increasing of c-myc was the most significant.	Fluorouracil	177-191	caspase 8	Homo sapiens	106-115
29695684-9	2018	Moreover, 5-fluorouracil plus circularly permuted tumor necrosis factor-related apoptosis-inducing ligand increased apoptosis-related protein levels such as cleaved caspase-3, caspase-8, and poly-ADP-ribose polymerase and downregulated that of the survival protein B-cell lymphoma-extra-large.	Fluorouracil	10-24	caspase 8	Homo sapiens	176-185
29764340-5	2018	Silymarin increased cleaved caspase-8 and truncated Bid, leading to accumulation of cytochrome c.	Silymarin	0-9	caspase 8	Homo sapiens	28-37
29764340-8	2018	Taken together, these results provide in vitro and in vivo evidence supporting the anti-cancer effect of silymarin and death receptor 5, and caspase-8 may be essential players in silymarin-mediated apoptosis in oral cancer.	Silymarin	179-188	caspase 8	Homo sapiens	141-150
29693341-0	2018	Clausenidin Induces Caspase 8-Dependent Apoptosis and Suppresses Production of VEGF in Liver Cancer Cells Clausena excavata Burm f. is used by traditional healers to treat cancer patients in South East Asia.	Clausenidin	0-11	caspase 8	Homo sapiens	20-29
29747757-9	2018	Ardisiacrispin B induced apoptosis in CCRF-CEM cells via activation of inititator caspases 8 and 9 and effector caspase 3/7, alteration of MMP and increase in ROS production.	ardisiacrispin B	0-16	caspase 8	Homo sapiens	82-121
29693341-1	2018	The use of theplant and its compounds is based on Asian folklore with little or no scientific evidence supporting the therapeutic efficacyThe current study aimed to determine the effect of pure clausenidin isolated from C. excavata on caspase-8-induced celldeath as well as angiogenesis in the HepG2 hepatocellular carcinoma cell line.	Clausenidin	194-205	caspase 8	Homo sapiens	235-244
29693341-5	2018	Clausenidin significantly (p&lt;0.05) increased theactivity of caspase-8 and expression of protein components of the death inducing signaling complex (DISC) in HepG2cells.	Clausenidin	0-11	caspase 8	Homo sapiens	63-72
29589006-6	2018	In vitro, treatment with DHQ protected HepG2 cells against TNF-alpha/ActD-induced apoptosis by inhibiting the activation of caspase-3, caspase-7, and caspase-8.	taxifolin	25-28	caspase 8	Homo sapiens	150-159
29719396-6	2018	Results: The inhibitory and apoptotic rates of Fe3O4@Au-C225 composite-targeted MNPs-mediated combined hyperthermia (MFH+NIR) group were significantly higher than other groups in vitro and the marked upregulation of caspase-3, caspase-8, and caspase-9 expression indicated excellent antitumor effect by inducing intrinsic apoptosis.	ferryl iron	47-52	caspase 8	Homo sapiens	227-236
29510157-5	2018	DMC-induced anti-proliferation was mediated by Akt/NF-kappaB signalling inhibition and apoptosis through caspase-8 and 9 activation.	demethoxycurcumin	0-3	caspase 8	Homo sapiens	105-114
29435611-10	2018	RESULTS: 17-oxo-DHA (50 microM, 72 h) significantly reduced proliferation, increased cell apoptosis, Fas and FasL expression as well as active caspase-8 and -3/7.	(4Z,7Z,10Z,13Z,15E,19Z)-17-Oxodocosahexaenoic acid	9-19	caspase 8	Homo sapiens	143-159
29682185-6	2018	Pimozide induced PTCL cell death is caspase 8 dependent, increases the expression of the TRAIL receptor, DR4, on the surface of pre-apoptotic PTCL cells, and enhances TRAIL induced apoptosis in a TRAIL dependent manner.	Pimozide	0-8	caspase 8	Homo sapiens	36-45
29642488-6	2018	These caspases and PARP activations were suppressed by N-acetylcysteine (NAC) pretreatment.	Acetylcysteine	55-71	caspase 8	Homo sapiens	6-14
29642488-6	2018	These caspases and PARP activations were suppressed by N-acetylcysteine (NAC) pretreatment.	Acetylcysteine	73-76	caspase 8	Homo sapiens	6-14
29233910-6	2018	Cells isogenic or ectopic for BRAFV600E displayed resistance to CDK1 inhibitors, as did cells with ectopic expression of constitutively active MEK CDK1 inhibitors induced a CASP8-dependent apoptosis shown by caspase-8 restoration in deficient NB7 cells that enhanced dinaciclib-induced CASP3 cleavage.	dinaciclib	267-277	caspase 8	Homo sapiens	173-178
29475156-4	2018	6p also significantly induces both EC9706 and EC109 cell cycle arrest at G0/G1 phase and cell apoptosis, as well as intracellular ROS accumulation, which could be markedly reversed caspase or ROS inhibitor: NAC.	ros	130-133	caspase 8	Homo sapiens	181-188
29744288-4	2018	The results showed that, in the presence of dasatinib, proliferation of GC cells decreased and apoptosis increased, and that Fas-associated death domain protein and caspase-8 are essential to dasatinib-induced cell apoptosis in GC.	Dasatinib	192-201	caspase 8	Homo sapiens	165-174
29158005-9	2018	In the 1,25(OH)2D3 + HDAC2 overexpression group, the expressions of p53, Bax, DR5 and caspase 8 were significantly lower but the expression of Bcl-2 was significantly higher than those of the 1,25(OH)2D3 treatment group (P &lt; 0.05).	25(oh)	9-15	caspase 8	Homo sapiens	86-95
29158005-9	2018	In the 1,25(OH)2D3 + HDAC2 overexpression group, the expressions of p53, Bax, DR5 and caspase 8 were significantly lower but the expression of Bcl-2 was significantly higher than those of the 1,25(OH)2D3 treatment group (P &lt; 0.05).	Calcitriol	7-18	caspase 8	Homo sapiens	86-95
29554103-8	2018	RESULTS: Culture of HUVECs in low-glucose medium for 24 or 48 h resulted in reduction of cell viability accompanied by activation of caspase-3/7 and caspase-8.	Glucose	34-41	caspase 8	Homo sapiens	149-158
29554103-13	2018	CONCLUSIONS/INTERPRETATION: These observations showed that exposure to low glucose induces ER stress, caspase activation, endothelial cell dysfunction and cell death.	Glucose	75-82	caspase 8	Homo sapiens	102-109
29534504-8	2018	Finally, formononetin-inhibited c-Jun N-terminal kinase (JNK) phosphorylation, cleavage of caspase-8 and caspase-3, and the ratio of Bax to Bcl-2 increased with cisplatin.	formononetin	9-21	caspase 8	Homo sapiens	91-100
29102767-9	2018	Western blotting analysis showed that curcuzedoalide inhibited AGS human gastric cancer cell viability by activating caspase-8, caspase-9, caspase-3, and PARP, which contributed to apoptotic cell death in AGS human gastric cancer cells.	curcuzedoalide	38-52	caspase 8	Homo sapiens	117-126
29102767-10	2018	CONCLUSION: These data indicate that curcuzedoalide contributed to the cytotoxicity of C. zedoaria by activating the cleavage of caspases and PARP, which are representative markers for apoptosis.	curcuzedoalide	37-51	caspase 8	Homo sapiens	129-137
28283885-8	2018	Atorvastatin induced the expression of caspase-3 and caspase-8 and downregulated the expression of Bcl-2, TRAF3IP2, and IL-17RA especially at 10 muM concentration.	Atorvastatin	0-12	caspase 8	Homo sapiens	53-62
29223591-5	2018	Western blot and immunofluorescence staining were conducted to analyze the effects of MH and Ac-DEVD-CHO on the expressions of caspase-3, caspase-8, and PARP.	mh	86-88	caspase 8	Homo sapiens	138-147
29467593-0	2018	Depletion of membrane cholesterol compromised caspase-8 imparts in autophagy induction and inhibition of cell migration in cancer cells.	Cholesterol	22-33	caspase 8	Homo sapiens	46-55
29467593-8	2018	Caspase activation was assessed by MTT and PI after treatments with Z-VAD [OME]-FMK, mitomycin c and cycloheximide.	monooxyethylene trimethylolpropane tristearate	35-38	caspase 8	Homo sapiens	0-7
29467593-8	2018	Caspase activation was assessed by MTT and PI after treatments with Z-VAD [OME]-FMK, mitomycin c and cycloheximide.	z-Val-Ala-Asp(Ome)-fluoromethylketone	68-83	caspase 8	Homo sapiens	0-7
29467593-8	2018	Caspase activation was assessed by MTT and PI after treatments with Z-VAD [OME]-FMK, mitomycin c and cycloheximide.	Mitomycin	85-96	caspase 8	Homo sapiens	0-7
29467593-8	2018	Caspase activation was assessed by MTT and PI after treatments with Z-VAD [OME]-FMK, mitomycin c and cycloheximide.	Cycloheximide	101-114	caspase 8	Homo sapiens	0-7
29467593-12	2018	Results: We found caspase independent cell death in cholesterol depleted MDA-MB 231 cells which was reduced by (3-MA) an autophagy inhibitor.	Cholesterol	52-63	caspase 8	Homo sapiens	18-25
29467593-14	2018	Subsequent activation of caspase-8 after co-incubation of mitomycin c and cycloheximide separately, restored the cell viability in cholesterol depleted MDA-MB 231 cells.	Mitomycin	58-69	caspase 8	Homo sapiens	25-34
29467593-14	2018	Subsequent activation of caspase-8 after co-incubation of mitomycin c and cycloheximide separately, restored the cell viability in cholesterol depleted MDA-MB 231 cells.	Cycloheximide	74-87	caspase 8	Homo sapiens	25-34
29467593-14	2018	Subsequent activation of caspase-8 after co-incubation of mitomycin c and cycloheximide separately, restored the cell viability in cholesterol depleted MDA-MB 231 cells.	Cholesterol	131-142	caspase 8	Homo sapiens	25-34
29467593-15	2018	Down regulation of caspase-8 mRNA in cholesterol depleted cancer cells ensures that caspase-8 indirectly promotes the induction of autophagy.	Cholesterol	37-48	caspase 8	Homo sapiens	19-28
29467593-15	2018	Down regulation of caspase-8 mRNA in cholesterol depleted cancer cells ensures that caspase-8 indirectly promotes the induction of autophagy.	Cholesterol	37-48	caspase 8	Homo sapiens	84-93
29467593-17	2018	Conclusion: Together our experimental data suggests that membrane cholesterol is the crucial for the recruitment and activation of caspase-8 as well as its non-apoptotic functions in cancer cells.	Cholesterol	66-77	caspase 8	Homo sapiens	131-140
29467593-18	2018	Enriched cholesterol in lipid raft of cancer cells may be regulating the cross talk between caspase-8 and autophagy machineries to promote their survival and migration.	Cholesterol	9-20	caspase 8	Homo sapiens	92-101
29099485-3	2018	During FADDosome-induced apoptosis, cFLIPL is ubiquitinated by TRAF2, leading to its degradation and subsequent FADD-dependent caspase-8 activation.	faddosome	7-16	caspase 8	Homo sapiens	127-136
29223591-5	2018	Western blot and immunofluorescence staining were conducted to analyze the effects of MH and Ac-DEVD-CHO on the expressions of caspase-3, caspase-8, and PARP.	acetyl-aspartyl-glutamyl-valyl-aspartal	93-104	caspase 8	Homo sapiens	138-147
29223591-8	2018	We found that MH (32  C) and Ac-DEVD-CHO (5.96 muMol/L) had equal effects on blocking the activation of caspase-3 and the OGD-induced cleavage of PARP, but neither had any effect on the activation of caspase-8, which goes on to activate caspase-3 in the apoptotic pathway.	mh	14-16	caspase 8	Homo sapiens	200-209
29223591-8	2018	We found that MH (32  C) and Ac-DEVD-CHO (5.96 muMol/L) had equal effects on blocking the activation of caspase-3 and the OGD-induced cleavage of PARP, but neither had any effect on the activation of caspase-8, which goes on to activate caspase-3 in the apoptotic pathway.	acetyl-aspartyl-glutamyl-valyl-aspartal	29-40	caspase 8	Homo sapiens	200-209
29316635-6	2018	Furthermore, we confirmed the antioxidant activity of EGCG and also showed a preventive effect against radical-evoked apoptosis by downregulation of caspase-8 and -3 in HaCaT cells.	epigallocatechin gallate	54-58	caspase 8	Homo sapiens	149-165
29434892-6	2018	Additionally, treatment with harmaline significantly increased the expression of caspase-8 and caspase-8/3 activity.	Harmaline	29-38	caspase 8	Homo sapiens	81-90
29434892-6	2018	Additionally, treatment with harmaline significantly increased the expression of caspase-8 and caspase-8/3 activity.	Harmaline	29-38	caspase 8	Homo sapiens	95-104
29291406-8	2018	Furthermore, bortezomib-induced cell death in BaxDelta2-positive cells was predominantly dependent on the caspase 8/3 pathway, consistent with our previous studies.	Bortezomib	13-23	caspase 8	Homo sapiens	106-115
29301308-7	2018	Thus, a pretreatment system with a particular inhibitor of Z-IETD-FMK (caspase-8 inhibitor) and Z-LEHD-FMK (caspase-9 inhibitor) significantly attenuated the cleavage of caspase-3 and prevented apoptosis.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	59-69	caspase 8	Homo sapiens	71-80
29174417-7	2018	Isoasarone (2) markedly elevated caspase -8 and -3/7 activities and caused a decline in nuclear NF-kappaB translocation, suggesting extrinsic, death receptor-linked apoptosis pathway.	asarone	0-10	caspase 8	Homo sapiens	33-50
29847820-6	2018	RESULTS: We observed significant upregulation of apoptosis in monocytes exposed to CRS type 1 plasma compared to AHF, with increased levels of caspase-3 (p &lt; 0.01), caspase-9 (p &lt; 0.01), and caspase-8 (p &lt; 0.03) showing activation of both intrinsic and extrinsic pathways.	Chromium	83-86	caspase 8	Homo sapiens	197-206
29162448-10	2018	These findings suggest that intracellular cholesterol level affects TMZ treatment of GBM mediated via a DR5-caspase-8 mechanism.	Cholesterol	42-53	caspase 8	Homo sapiens	108-117
29162448-10	2018	These findings suggest that intracellular cholesterol level affects TMZ treatment of GBM mediated via a DR5-caspase-8 mechanism.	Temozolomide	68-71	caspase 8	Homo sapiens	108-117
29923797-3	2018	In parallel, niraparib activated a CD95-FADD-caspase 8 pathway, and collectively these signals caused tumor cell death that was suppressed by knock down of Beclin1, ATG5, CD95, FADD or AIF; or by expression of c-FLIP-s, BCL-XL or dominant negative caspase 9.	niraparib	13-22	caspase 8	Homo sapiens	45-54
29923797-5	2018	HDAC inhibitors enhanced niraparib lethality by increasing activation of the ATM-AMPK-ULK1-autophagy and CD95-FADD-caspase 8 pathways.	niraparib	25-34	caspase 8	Homo sapiens	115-124
29162448-0	2018	Intracellular cholesterol level regulates sensitivity of glioblastoma cells against temozolomide-induced cell death by modulation of caspase-8 activation via death receptor 5-accumulation and activation in the plasma membrane lipid raft.	Cholesterol	14-25	caspase 8	Homo sapiens	133-142
29162448-0	2018	Intracellular cholesterol level regulates sensitivity of glioblastoma cells against temozolomide-induced cell death by modulation of caspase-8 activation via death receptor 5-accumulation and activation in the plasma membrane lipid raft.	Temozolomide	84-96	caspase 8	Homo sapiens	133-142
29162448-7	2018	TMZ without or with MbetaCD and/or Chol caused accumulation of DR5 into the plasma membrane lipid raft and formed a complex with caspase-8, an extrinsic caspase cascade inducer, reflected in the induction of cell death.	Temozolomide	0-3	caspase 8	Homo sapiens	129-138
29162448-7	2018	TMZ without or with MbetaCD and/or Chol caused accumulation of DR5 into the plasma membrane lipid raft and formed a complex with caspase-8, an extrinsic caspase cascade inducer, reflected in the induction of cell death.	methyl-beta-cyclodextrin	20-27	caspase 8	Homo sapiens	129-138
29162448-7	2018	TMZ without or with MbetaCD and/or Chol caused accumulation of DR5 into the plasma membrane lipid raft and formed a complex with caspase-8, an extrinsic caspase cascade inducer, reflected in the induction of cell death.	Cholesterol	35-39	caspase 8	Homo sapiens	129-138
29162448-8	2018	In addition, treatment with caspase-8 inhibitor or knockdown of DR5 dramatically suppressed U251-Con cell death induced by combination treatment with TMZ, MbetaCD, and Chol.	Temozolomide	150-153	caspase 8	Homo sapiens	28-37
29162448-8	2018	In addition, treatment with caspase-8 inhibitor or knockdown of DR5 dramatically suppressed U251-Con cell death induced by combination treatment with TMZ, MbetaCD, and Chol.	methyl-beta-cyclodextrin	155-162	caspase 8	Homo sapiens	28-37
29162448-8	2018	In addition, treatment with caspase-8 inhibitor or knockdown of DR5 dramatically suppressed U251-Con cell death induced by combination treatment with TMZ, MbetaCD, and Chol.	Cholesterol	168-172	caspase 8	Homo sapiens	28-37
30562734-10	2018	RESULTS: DVDMS-SDT-treated H446 cells increased the rate of cellular apoptosis and the levels of reactive oxygen species (ROS), cleaved caspase-3, cleaved caspase-8, cleaved caspase-9, and caspase-10, and decreased the levels of MMP, RIP3, B-cell lymphoma 2, vascular endothelial growth factor, and tumor necrosis factor-alpha.	3,4-Dihydroxy-9,10-secoandrosta-1,3,5(10)-triene-9,17-dione	15-18	caspase 8	Homo sapiens	155-164
30001535-7	2018	The expression of p65 protein decreased, the expression of caspases 8 and 9 increased, and the expression of c-Jun N-terminal kinase (JNK) and p38 protein was altered in infected cells after parthenolide treatment, resulting in lower cell survival.	parthenolide	191-203	caspase 8	Homo sapiens	59-75
29115423-7	2018	After exposure to a combination of GNPs (6.25 microg/ml) and carvedilol (3 microM), death as promoted by apoptosis was detected using flow cytometry, for expression of pro-apoptotic proteins FADD, caspase-3, caspase-8 and sub-regulation of anti-apoptotic MAPK/ERK, Akt, mTOR, EGFR and MDR1 resistance.	Carvedilol	61-71	caspase 8	Homo sapiens	208-217
28081667-0	2018	Contributions of caspase-8 and -9 to liver injury from CYP2E1-produced metabolites of halogenated hydrocarbons.	Hydrocarbons	98-110	caspase 8	Homo sapiens	17-33
29128513-10	2018	DHA activated caspase 3, caspase 8, and caspase 9 and cleaved poly (ADP-ribose) polymerase (PARP).	artenimol	0-3	caspase 8	Homo sapiens	25-34
29128513-11	2018	DHA-induced apoptotic cell death, activation of caspases and cleavage of PARP were dramatically inhibited by pan caspase inhibitor Z-VAD-FMK.	artenimol	0-3	caspase 8	Homo sapiens	48-56
29128513-11	2018	DHA-induced apoptotic cell death, activation of caspases and cleavage of PARP were dramatically inhibited by pan caspase inhibitor Z-VAD-FMK.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	131-140	caspase 8	Homo sapiens	48-56
28081667-10	2018	In co-culture, halothane increased caspase-8 activity and decreased MMP and cellular viability.	Halothane	15-24	caspase 8	Homo sapiens	35-44
29286349-6	2017	The SH1-SH3 extracts protected SH-SY5Y cells from 6-hydroxydopamine (6-OHDA)-induced apoptosis as illustrated by cell cycle distribution, cytochrome c release, activation of caspase-8, -9, and -3, and DNA fragmentation analyses.	Oxidopamine	50-67	caspase 8	Homo sapiens	174-195
29278364-8	2017	In terms of results, SK-N-MC cells treated with a combination of, but not individually with, IFN-gamma and TNF-alpha induced apoptosis characterized by hypodiploidy, DNA fragmentation, PARP cleavage, and increased caspase-8 activity.	sk-n-mc	21-28	caspase 8	Homo sapiens	214-223
29435156-8	2018	Wild-type Jurkat clone A3, FADD-deficient Jurkat clone I2.1, and caspase-8-deficient Jurkat clone I9.2 exhibited similar susceptibilities to the cytotoxicity of cis-3M-RES, excluding contribution of the extrinsic death receptor-dependent pathway to the apoptosis.	cis-3m-res	161-171	caspase 8	Homo sapiens	65-74
29242562-0	2017	ROS-induced cleavage of NHLRC2 by caspase-8 leads to apoptotic cell death in the HCT116 human colon cancer cell line.	Reactive Oxygen Species	0-3	caspase 8	Homo sapiens	34-43
29242562-3	2017	Here we show that the NHL-repeat-containing protein 2 (NHLRC2) thioredoxin-like domain protein is cleaved by caspase-8 in ROS-induced apoptosis in the HCT116 human colon cancer cell line.	Reactive Oxygen Species	122-125	caspase 8	Homo sapiens	109-118
29242562-7	2017	Furthermore, siRNA-mediated knockdown of caspase-8 blocked the ROS-induced decrease in NHLRC2 protein levels.	Reactive Oxygen Species	63-66	caspase 8	Homo sapiens	41-50
29242562-9	2017	These results suggest that excess ROS production causes a caspase-8-mediated decrease in NHLRC2 protein levels, leading to apoptotic cell death in colon cancer cells, and indicate an important role of NHLRC2 in the regulation of ROS-induced apoptosis.	Reactive Oxygen Species	34-37	caspase 8	Homo sapiens	58-67
29242562-9	2017	These results suggest that excess ROS production causes a caspase-8-mediated decrease in NHLRC2 protein levels, leading to apoptotic cell death in colon cancer cells, and indicate an important role of NHLRC2 in the regulation of ROS-induced apoptosis.	Reactive Oxygen Species	229-232	caspase 8	Homo sapiens	58-67
29535810-2	2018	Combined treatment with silibinin and TRAIL (silibinin/TRAIL) induced apoptosis accompanied by the activation of caspase-3, caspase-8, caspase-9, and Bax, and cytosolic accumulation of cytochrome c.	Silybin	24-33	caspase 8	Homo sapiens	124-133
29416631-0	2018	In vitro and in vivo anti-leukemic effects of cladoloside C2 are mediated by activation of Fas/ceramide synthase 6/p38 kinase/c-Jun NH2-terminal kinase/caspase-8.	cladoloside	46-57	caspase 8	Homo sapiens	152-161
29416631-6	2018	Cladoloside C2 dose- and time-dependently induced apoptosis in the analyzed cells, and led to the activation of Fas/ceramide synthase 6 (CerS6)/p38 kinase/JNK/caspase-8.	cladoloside	0-11	caspase 8	Homo sapiens	159-168
29416631-10	2018	Our results suggest that cladoloside C2 has in vitro and in vivo anti-leukemic effects due to the activation of Fas/CerS6/p38 kinase/JNK/caspase-8 in lipid rafts.	cladoloside c2	25-39	caspase 8	Homo sapiens	137-146
29535810-2	2018	Combined treatment with silibinin and TRAIL (silibinin/TRAIL) induced apoptosis accompanied by the activation of caspase-3, caspase-8, caspase-9, and Bax, and cytosolic accumulation of cytochrome c.	Silybin	45-54	caspase 8	Homo sapiens	124-133
28278082-0	2017	Caspase 8 polymorphisms contribute to the prognosis of advanced lung adenocarcinoma patients after platinum-based chemotherapy.	Platinum	99-107	caspase 8	Homo sapiens	0-9
28278082-3	2017	To explore the relationship between tagSNPs or haplotypes of CASP8 and the efficacy of platinum-based chemotherapy in advanced lung adenocarcinoma patients of China, we recruited 555 advanced adenocarcinoma patients.	Platinum	87-95	caspase 8	Homo sapiens	61-66
28951205-8	2017	Overexpression of YAP1-5SA significantly inhibited tunicamycin-induced caspase-8 processing without affecting phosphorylation of p-38 and Akt.	Tunicamycin	51-62	caspase 8	Homo sapiens	71-80
29200826-8	2017	Conclusion: Results of this study indicate that the apoptotic pathway caused by DEN and DEN-HPbetaCD complex are mediated by the regulation of caspases and Bcl-2 families in human colon HT-29 cancer cells.	dentatin	80-83	caspase 8	Homo sapiens	143-151
29200826-8	2017	Conclusion: Results of this study indicate that the apoptotic pathway caused by DEN and DEN-HPbetaCD complex are mediated by the regulation of caspases and Bcl-2 families in human colon HT-29 cancer cells.	den-hpbetacd	88-100	caspase 8	Homo sapiens	143-151
28972304-5	2017	The proteasome inhibitor bortezomib markedly enriched the p43/41 products of caspase-8 activated by TRAIL, indicating proteasomal degradation of caspase-8.	Bortezomib	25-35	caspase 8	Homo sapiens	77-86
28972304-5	2017	The proteasome inhibitor bortezomib markedly enriched the p43/41 products of caspase-8 activated by TRAIL, indicating proteasomal degradation of caspase-8.	Bortezomib	25-35	caspase 8	Homo sapiens	145-154
28888620-7	2017	In a cell-free reconstitution system, caspase-8-mediated Bid cleavage and recombinant tBid induced mitochondrial cytochrome c release and ROS generation, which were blocked by Bcl-xL and antioxidant enzymes.	Reactive Oxygen Species	138-141	caspase 8	Homo sapiens	38-47
29061820-5	2017	RESULTS: 4-OOH-IF and 4-OOH-CP distinctly reduced cell viability and triggered apoptosis and necrosis, causing changes in intracellular esterase activity, plasma membrane structure and integrity, caspase activation, and mitochondrial membrane potential.	4-ooh	9-14	caspase 8	Homo sapiens	196-203
29061820-5	2017	RESULTS: 4-OOH-IF and 4-OOH-CP distinctly reduced cell viability and triggered apoptosis and necrosis, causing changes in intracellular esterase activity, plasma membrane structure and integrity, caspase activation, and mitochondrial membrane potential.	4-ooh-cp	22-30	caspase 8	Homo sapiens	196-203
29061821-4	2017	RESULTS: The leukemia cell responses to the action of the anthracyclines were manifested in their different viability, count and volume, degree of apoptosis and necrosis, activity of caspases -8, -9, and -3/7, mitochondrial membrane potential, and in the cell-cycle distribution.	Anthracyclines	58-72	caspase 8	Homo sapiens	183-206
28865364-8	2017	Lobaplatin significantly inhibited the growth of KYSE-410 and EC-109 cells in a dose- and time-dependent manner and induced cell apoptosis by increasing expressions of cleaved-caspase-3, cleaved-caspase-8, cleaved-caspase-9 and Bax, decreasing expression of Bcl-2.	lobaplatin	0-10	caspase 8	Homo sapiens	195-204
28888620-0	2017	The caspase-8/Bid/cytochrome c axis links signals from death receptors to mitochondrial reactive oxygen species production.	Reactive Oxygen Species	88-111	caspase 8	Homo sapiens	4-13
28888620-4	2017	ROS generation was accompanied by caspase-8 activation, Bid cleavage, and cytochrome c release; it was blocked in FADD- and caspase-8-deficient cells, as well as by caspase-8 knockdown and inhibitor.	Reactive Oxygen Species	0-3	caspase 8	Homo sapiens	34-43
28888620-9	2017	These data provide evidence that the FADD/caspase-8/Bid/cytochrome c axis is a crucial linker between death receptors and mitochondria, where they play a role in ROS generation and apoptosis.	Reactive Oxygen Species	162-165	caspase 8	Homo sapiens	42-51
28888620-4	2017	ROS generation was accompanied by caspase-8 activation, Bid cleavage, and cytochrome c release; it was blocked in FADD- and caspase-8-deficient cells, as well as by caspase-8 knockdown and inhibitor.	Reactive Oxygen Species	0-3	caspase 8	Homo sapiens	124-133
29102932-4	2017	Materials and Methods/Results: We used flow cytometric assay to show fisetin induced apoptotic cell death through increased reactive oxygen species and Ca2+, but reduced the mitochondrial membrane potential and increased caspase-8, -9 and -3 activities in HSC3 cells.	fisetin	69-76	caspase 8	Homo sapiens	221-241
28888620-4	2017	ROS generation was accompanied by caspase-8 activation, Bid cleavage, and cytochrome c release; it was blocked in FADD- and caspase-8-deficient cells, as well as by caspase-8 knockdown and inhibitor.	Reactive Oxygen Species	0-3	caspase 8	Homo sapiens	124-133
28610909-8	2017	We show here that CD40-induced apoptosis was dependent on caspase-8 activation because caspase-8 specific inhibitor, Z-IETD-FMK completely prevented apoptosis.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	117-127	caspase 8	Homo sapiens	58-67
28610909-8	2017	We show here that CD40-induced apoptosis was dependent on caspase-8 activation because caspase-8 specific inhibitor, Z-IETD-FMK completely prevented apoptosis.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	117-127	caspase 8	Homo sapiens	87-96
29245990-1	2017	Saikosaponin a (SSa), a bioactive phytochemical from Bupleurum, triggers sequential caspase-2 and caspase-8 activation, and thereby induces caspase-mediated apoptosis in human colon carcinoma (HCC) cells.	saikosaponin D	0-14	caspase 8	Homo sapiens	98-107
28849057-12	2017	Following the downregulation of TIPE2 the aforementioned effect of Poly I:C treatment was reversed and may be associated with the reduced activity of caspase-8 that was observed in the TIPE2 silenced group.	Poly I-C	67-75	caspase 8	Homo sapiens	150-159
29072704-4	2017	In the present study, we investigated the impact of Caspase-8 in human and murine alcohol-induced apoptosis and in ALD.	Alcohols	82-89	caspase 8	Homo sapiens	52-61
29296860-7	2017	The TAK1 inhibitor LLZ1640-2 abrogated the TRAIL-induced c-FLIP upregulation and NF-kappaB activation, and triggered TRAIL-induced caspase-8 activation and cell death in OCs.	LL Z1640-2	19-28	caspase 8	Homo sapiens	131-140
29072704-6	2017	Caspase-8 activation was detected in liver biopsies from ALD patients, as well as in livers of wild-type (WT) mice after chronic ethanol feeding for 8 weeks using the Lieber-DeCarli model.	Ethanol	129-136	caspase 8	Homo sapiens	0-9
29058293-10	2017	After 24-h exposure to CE-SS, the expression of cleaved-caspase-9, cleaved-caspase-8 and cleaved-caspase-3 protein was activated, the expression of p53 protein increased while the ratio of Bax/Bcl-2 also increased.	ce-ss	23-28	caspase 8	Homo sapiens	75-84
29036189-0	2017	Inhibition of CUG-binding protein 1 and activation of caspases are critically involved in piperazine derivative BK10007S induced apoptosis in hepatocellular carcinoma cells.	Piperazine	90-100	caspase 8	Homo sapiens	54-62
29036189-8	2017	Overall, these findings provide scientific evidences that BK10007S induces apoptosis via inhibition of CUGBP1 and activation of caspases in hepatocellular carcinomas as a potent anticancer candidate.	BK10007S	58-66	caspase 8	Homo sapiens	128-136
28985224-4	2017	For two CASP8 variants, p.K148R and p.I298V, the association remained significant in a combined sample of 10,820 cases and 8,881 controls.	k148r	26-31	caspase 8	Homo sapiens	8-13
28985224-4	2017	For two CASP8 variants, p.K148R and p.I298V, the association remained significant in a combined sample of 10,820 cases and 8,881 controls.	Phosphorus	24-25	caspase 8	Homo sapiens	8-13
28973192-8	2017	Addition of CQ to low-dose CAB blocked normal autophagic cycles and induced apoptosis, evidenced by the further accumulation of p62/caspase-8/LC3-II.	Chloroquine	12-14	caspase 8	Homo sapiens	132-141
32719725-5	2017	Further study showed that TFS decreased mitochondrial membrane potential, activated Caspase-3/7, Caspase-8 and Caspase-9 activities, and that the p53 inhibitor PFT-alpha reversed the TFS-induced cell growth inhibition and apoptosis.	pifithrin	160-169	caspase 8	Homo sapiens	97-106
28710022-3	2017	The cholesterol oxidation products also induced a decrease in the levels of Bid and Bcl-2, increase in the levels of p53 and Bax, loss of the mitochondrial transmembrane potential, release of cytochrome c, activation of caspases (-8, -9 and -3), production of reactive oxygen species, depletion of GSH and cell death in both cell lines.	Cholesterol	4-15	caspase 8	Homo sapiens	220-243
29845064-10	2017	Besides, caspase colorimetric assays revealed a significant rise in cellular levels of the initiators (caspase-8 and -9) and effector (caspase-3) in the cells treated by artesunate.	Artesunate	170-180	caspase 8	Homo sapiens	103-119
28551013-5	2017	Pretreatment of HASMCs with nomilin stimulated extrinsic caspase-8, intrinsic caspase-9, and apoptotic caspase-3 and resulted in significant inhibition of TNF-alpha-induced proliferation.	hasmcs	16-22	caspase 8	Homo sapiens	57-66
28551013-5	2017	Pretreatment of HASMCs with nomilin stimulated extrinsic caspase-8, intrinsic caspase-9, and apoptotic caspase-3 and resulted in significant inhibition of TNF-alpha-induced proliferation.	nomilin	28-35	caspase 8	Homo sapiens	57-66
28793767-3	2017	In our study, 20(S)-Rh2 induced the expression of orphan nuclear receptor Nur77 and death receptor proteins Fas, FasL, DR5, and TRAIL, as well as the cleavage of caspase 8 and caspase 3 in HL-60 cells.	rh2	20-23	caspase 8	Homo sapiens	162-171
28716455-10	2017	Pyridoxine significantly increased the expression of Bax and caspase-8.	Pyridoxine	0-10	caspase 8	Homo sapiens	61-70
28870913-5	2017	In addition, regorafenib significantly induced accumulation of sub-G1 phase cells, loss of mitochondrial membrane potential, and expression of active caspase-3 and caspase-8.	regorafenib	13-24	caspase 8	Homo sapiens	164-173
27862857-9	2017	Results suggest that casticin induced cell apoptosis via the activation of the caspase- and/or mitochondria-dependent signaling cascade, the accumulation of ROS and altered associated gene expressions in colo 205 human colon cancer cells.	casticin	21-29	caspase 8	Homo sapiens	79-86
28856117-8	2017	MH induced apoptosis of MDA-MB-231 cells through activation of caspases 8, 9, 6, and 3/7 and this correlated with a loss of Bcl-2 and increased Bax protein expression in MH-treated cells.	mh	0-2	caspase 8	Homo sapiens	63-86
28856117-8	2017	MH induced apoptosis of MDA-MB-231 cells through activation of caspases 8, 9, 6, and 3/7 and this correlated with a loss of Bcl-2 and increased Bax protein expression in MH-treated cells.	mh	170-172	caspase 8	Homo sapiens	63-86
28927092-7	2017	The rate of apoptosis, caspase-3/caspase-8 activity and the expression of Bax were significantly increased, whereas Bcl-2 expression was significantly reduced following treatment with curcumin and/or FP, compared with the untreated control group.	Curcumin	184-192	caspase 8	Homo sapiens	33-42
28927092-9	2017	Therefore, curcumin may enhance the anticancer effects of FP chemotherapy in MGC-803 cells through the promotion of apoptosis via the caspase-3/caspase-8, Bcl-2 and Bax signaling pathways.	Curcumin	11-19	caspase 8	Homo sapiens	144-153
28662964-11	2017	Peptide 15 c(Pro1-Pro2-R-gamma4-hhPhe3-Phe4-Leu5-Ile6-Ile7-Leu8-Val9) blocked the expression of caspase-3, inhibited the expression of caspases-8 and -9 in 24h culture of Jurkat cells, and caused DNA fragmentation in these cells, as an indicator of apoptosis.	-gamma4-hhphe3	24-38	caspase 8	Homo sapiens	135-152
28586029-11	2017	Moreover, fangchinoline-treated MG63 cells showed downregulated expression of cyclin D1 and matrix metalloproteinase 2 and 9, which act downstream of PI3K, and upregulated expression of caspase-3 and caspase-8.	fangchinoline	10-23	caspase 8	Homo sapiens	200-209
28696167-4	2017	alpha-Mangostin treatment also reversed the rotenone-induced overproduction of reactive oxygen species, activation of caspases (-8 and -3) and mitochondrial dysfunction, reflected by decrease in mitochondrial membrane potential and cellular ATP levels.	mangostin	0-15	caspase 8	Homo sapiens	118-137
28696167-4	2017	alpha-Mangostin treatment also reversed the rotenone-induced overproduction of reactive oxygen species, activation of caspases (-8 and -3) and mitochondrial dysfunction, reflected by decrease in mitochondrial membrane potential and cellular ATP levels.	Rotenone	44-52	caspase 8	Homo sapiens	118-137
28337703-4	2017	Combination of UMI-77 and TRAIL in glioma cells led to the activation of caspase-8 and Bid, cleavage of caspase-3 and poly-ADP ribose polymerase (PARP), accumulation of tBid in the mitochondria and release of cytochrome c into the cytosol.	UMI-77	15-21	caspase 8	Homo sapiens	73-82
28627461-14	2017	8-MOP reduced the phosphorylation of AKT308, decreased the expression of Bcl-2, increased the Bax protein level, and activated caspases -8, -9, and -3 in both cell lines.	Methoxsalen	0-5	caspase 8	Homo sapiens	127-150
28627658-0	2017	Shikonin promotes adriamycin-induced apoptosis by upregulating caspase-3 and caspase-8 in osteosarcoma.	shikonin	0-8	caspase 8	Homo sapiens	77-86
28627658-0	2017	Shikonin promotes adriamycin-induced apoptosis by upregulating caspase-3 and caspase-8 in osteosarcoma.	Doxorubicin	18-28	caspase 8	Homo sapiens	77-86
28414160-3	2017	PQ increased cleavage of caspase-8 and Bid, indicating caspase-8 activation and truncated Bid, the two key mediators of extrinsic apoptosis.	Paraquat	0-2	caspase 8	Homo sapiens	25-34
28414160-3	2017	PQ increased cleavage of caspase-8 and Bid, indicating caspase-8 activation and truncated Bid, the two key mediators of extrinsic apoptosis.	Paraquat	0-2	caspase 8	Homo sapiens	55-64
27541197-9	2017	This study further highlights the importance of polymorphisms within COL5A1 and CASP8 in the aetiology of ATP.	Adenosine Triphosphate	106-109	caspase 8	Homo sapiens	80-85
28414160-4	2017	Additionally, PQ treatment caused an increase in DR5 (death receptor-5) and caspase-8 interaction, indicating formation of DISC (death-inducing signaling complex).	Paraquat	14-16	caspase 8	Homo sapiens	76-85
28758971-5	2017	Tricetin induced morphological features of apoptosis such as chromatin condensation and phosphatidylserine (PS) externalization, and significantly activated proapoptotic signaling including caspase-8, -9, and -3 activation and poly(ADP-ribose) polymerase (PARP) cleavage in HL-60 AML cells.	tricetin	0-8	caspase 8	Homo sapiens	190-211
28758971-6	2017	Of note, tricetin-induced cell growth inhibition was dramatically reversed by a pan caspase and caspase-8- and -9-specific inhibitors, suggesting that this compound mainly acts through a caspase-dependent pathway.	tricetin	9-17	caspase 8	Homo sapiens	84-91
28758971-6	2017	Of note, tricetin-induced cell growth inhibition was dramatically reversed by a pan caspase and caspase-8- and -9-specific inhibitors, suggesting that this compound mainly acts through a caspase-dependent pathway.	tricetin	9-17	caspase 8	Homo sapiens	96-113
28758971-6	2017	Of note, tricetin-induced cell growth inhibition was dramatically reversed by a pan caspase and caspase-8- and -9-specific inhibitors, suggesting that this compound mainly acts through a caspase-dependent pathway.	tricetin	9-17	caspase 8	Homo sapiens	96-103
28534969-6	2017	Co-treatment with purvalanol A and taxol weakened the expression of Bcl-2 and activated the extrinsic cell death pathway through the activation of caspase-3 and caspase-8.	6-((3-chloro)anilino)-2-(isopropyl-2-hydroxyethylamino)-9-isopropylpurine	18-30	caspase 8	Homo sapiens	161-170
28696369-5	2017	DHAP inhibited cell proliferation and induced apoptosis, as characterized by the cleavage of PARP and the activation of caspase-3, caspase-8, and caspase-9.	Dihydroxyacetone Phosphate	0-4	caspase 8	Homo sapiens	131-140
28559202-12	2017	Additionally, the induction of extrinsic apoptosis on PECs by RA was associated with increasing expressions levels of Fas, Fas-associated protein with death domain (FADD), tumor necrosis factor-alpha (TNF-alpha), and caspase 8 protein.	rosmarinic acid	62-64	caspase 8	Homo sapiens	217-226
28534969-6	2017	Co-treatment with purvalanol A and taxol weakened the expression of Bcl-2 and activated the extrinsic cell death pathway through the activation of caspase-3 and caspase-8.	Paclitaxel	35-40	caspase 8	Homo sapiens	161-170
28638867-7	2017	Chrysanthemin also enhanced the activity of all three caspases viz., caspase-3, 8 and 9 in a dose-dependent fashion.	asterin	0-13	caspase 8	Homo sapiens	54-62
28586001-6	2017	DHA increased the levels of cleaved caspase-8, -9 and -3.	Docosahexaenoic Acids	0-3	caspase 8	Homo sapiens	36-56
29039326-6	2017	The two flavonoids activated caspase-8, which cleaved Bid into tBid; simultaneously, Bax transferred from cytosol into mitochondria to decrease MMP; consequentially, cytochrome c released from mitochondria activated caspase-9, and then caspase-9 activated caspase-3, which executed the apoptosis.	Flavonoids	8-18	caspase 8	Homo sapiens	29-38
29039326-6	2017	The two flavonoids activated caspase-8, which cleaved Bid into tBid; simultaneously, Bax transferred from cytosol into mitochondria to decrease MMP; consequentially, cytochrome c released from mitochondria activated caspase-9, and then caspase-9 activated caspase-3, which executed the apoptosis.	tBID	63-67	caspase 8	Homo sapiens	29-38
28701864-11	2017	Blockade of autophagy by hydroxychloroquine dramatically potentiated KG-135-induced FOXO3a and its downstream (FasL) ligand accompanied by the cleavage of caspase-8.	Hydroxychloroquine	25-43	caspase 8	Homo sapiens	155-164
28701864-14	2017	Both the KG-135-activated extrinsic FOXO3a/FasL/caspase-8 and intrinsic caspase-9 apoptotic pathways were potentiated by blockade of autophagy.	kg-135	9-15	caspase 8	Homo sapiens	48-57
28528544-0	2017	The New Chemical Reporter 6-Alkynyl-6-deoxy-GlcNAc Reveals O-GlcNAc Modification of the Apoptotic Caspases That Can Block the Cleavage/Activation of Caspase-8.	6-alkynyl-6-deoxy-glcnac	26-50	caspase 8	Homo sapiens	98-106
28528544-0	2017	The New Chemical Reporter 6-Alkynyl-6-deoxy-GlcNAc Reveals O-GlcNAc Modification of the Apoptotic Caspases That Can Block the Cleavage/Activation of Caspase-8.	6-alkynyl-6-deoxy-glcnac	26-50	caspase 8	Homo sapiens	149-158
28594322-5	2017	Here, we demonstrate that Caspase-8, through activation of NF-kB, enhances the expression and secretion of VEGF, IL-6, IL-8, IL-1beta and MCP-1, leading to neovascularization and increased resistance to Temozolomide.	Temozolomide	203-215	caspase 8	Homo sapiens	26-35
28638870-6	2017	However activity of caspase enzymes and translocation of cytochrome c were enhanced after treatment with epifriedelinol.	friedelinol	105-119	caspase 8	Homo sapiens	20-27
28638870-8	2017	CONCLUSION: Result of our study proves the anticancer activity of epifriedelinol in cervical cancer by inducing apoptosis as treatment with it enhances the production of oligonucleosomes, translocation of cytochrome c and activity caspase enzymes.	friedelinol	66-80	caspase 8	Homo sapiens	231-238
28664141-0	2017	Induction of apoptosis by Dae-Hwang-Mok-Dan-Tang in HCT-116 colon cancer cells through activation of caspases and inactivation of the phosphatidylinositol 3-kinase/Akt signaling.	o,p-dinitrophenyl aminoethyldiphosphate-beryllium trifluoride	26-29	caspase 8	Homo sapiens	101-109
28111999-8	2017	Furthermore, OZ pre-treatment promotes caspase-8 cleavage, Fas externalisation, caspase 3 activity and intracellular calcium ion levels.	5-7-oxo-zeaenol	13-15	caspase 8	Homo sapiens	39-48
28664142-10	2017	DOE treatment caused activation of caspase-8, -9, -3 and -7, reactive oxygen species production, and cleavage of cleavage of poly-ADP-ribose polymerase (PARP), the markers of apoptosis.	deoxyelephantopin	0-3	caspase 8	Homo sapiens	35-59
28238526-6	2017	Reactive oxygen species-induced mitochondrial DNA oxidative damage and BRCC36 deubiquitinating activity provide a missing link and mechanism by which innate immunity responds to environmental stress via caspase-8-involved NLRP3/NLRP6 inflammasomes.	Reactive Oxygen Species	0-23	caspase 8	Homo sapiens	203-212
28664141-9	2017	Moreover, DHMDT increased the levels of death receptor-associated ligands and enhanced activation of caspase-8 and cleavage of its substrate, Bid.	dhmdt	10-15	caspase 8	Homo sapiens	101-110
28664141-10	2017	However, the pan-caspase inhibitor could reverse DHMDT-induced apoptosis.	dhmdt	49-54	caspase 8	Homo sapiens	17-24
28542135-3	2017	In this study, we found that furanodienone significantly inhibited proliferation of RKO and HT-29 cells, induced mitochondrial dysfunction characterized by collapse of mitochondrial transmembrane potential and reduction of ATP level, and promoted the production of reactive oxygen species (ROS) that functions upstream of caspase-dependent apoptosis.	furanodienone	29-42	caspase 8	Homo sapiens	322-329
28240376-13	2017	Mechanistically, we demonstrate that apoptosis in response to enzalutamide and IAP antagonist requires activation of caspase-8, suggesting extrinsic/death receptor apoptosis signaling.	enzalutamide	62-74	caspase 8	Homo sapiens	117-126
28542135-8	2017	In conclusion, the results demonstrated that furanodienone-triggered ROS plays a pivotal role in apoptosis as an upstream molecule-modulating activity of caspases in mitochondrial pathway via stimulating MAPKs signaling pathway.	furanodienone	45-58	caspase 8	Homo sapiens	154-162
28542135-8	2017	In conclusion, the results demonstrated that furanodienone-triggered ROS plays a pivotal role in apoptosis as an upstream molecule-modulating activity of caspases in mitochondrial pathway via stimulating MAPKs signaling pathway.	Reactive Oxygen Species	69-72	caspase 8	Homo sapiens	154-162
28542135-6	2017	The specific inhibitors U0126, SP600125 and SB202190 attenuated the expression of MAPKs, and regulated the expression of cleaved caspase-8, -9 and -3.	U 0126	24-29	caspase 8	Homo sapiens	129-149
28542135-6	2017	The specific inhibitors U0126, SP600125 and SB202190 attenuated the expression of MAPKs, and regulated the expression of cleaved caspase-8, -9 and -3.	pyrazolanthrone	31-39	caspase 8	Homo sapiens	129-149
28542135-6	2017	The specific inhibitors U0126, SP600125 and SB202190 attenuated the expression of MAPKs, and regulated the expression of cleaved caspase-8, -9 and -3.	4-(4-fluorophenyl)-2-(4-hydroxyphenyl)-5-(4-pyridyl)imidazole	44-52	caspase 8	Homo sapiens	129-149
28331083-6	2017	This effect can be overcome by treating cells with the clinically approved BCL2 antagonist venetoclax, which prevents Casp8p41 from binding BCL2, thereby allowing Casp8p41 to bind Bak and kill the infected cell.	venetoclax	91-101	caspase 8	Homo sapiens	118-124
28331083-6	2017	This effect can be overcome by treating cells with the clinically approved BCL2 antagonist venetoclax, which prevents Casp8p41 from binding BCL2, thereby allowing Casp8p41 to bind Bak and kill the infected cell.	venetoclax	91-101	caspase 8	Homo sapiens	163-169
28522217-7	2017	In addition, celastrol inhibited the expression of CIP2A, c-MYC, and suppressed apoptotic proteins BAX and caspase-8 in human CS cells, on the other hand, it induced the expression of antiapoptotic protein Bcl-2.	celastrol	13-22	caspase 8	Homo sapiens	107-116
28938593-12	2017	After treatment with DOX, CRT and ER stress-related proteins p-PERK, p-eIF2alpha, caspase-8 and apoptosis were significantly increased in wild-type EC cells, but not in drug-resistant EC cells.	Doxorubicin	21-24	caspase 8	Homo sapiens	82-91
28938593-14	2017	The knockdown of PERK gene and addition of DOX resulted in significant decrease of cleaved-caspase 8 and p-eIF2alpha in sensitive EC cells.	Doxorubicin	43-46	caspase 8	Homo sapiens	91-100
28185768-5	2017	Our results demonstrated that PA showed significant anti-tumor activity on lung cancer in vitro; the mechanisms were involved in inducing mitochondria-mediated apoptosis via up-regulation of caspase-3, caspase-8, caspase-9, Bid, Bax, down-regulation of Bcl-2 and stimulating the release of Cyto-C from mitochondria.	paederosidic acid	30-32	caspase 8	Homo sapiens	202-211
28302628-3	2017	The experiments showed significantly increased releases of FADD, caspase-3, and caspase-8 after Fas stimulation.	ammonium ferrous sulfate	96-99	caspase 8	Homo sapiens	80-89
28365838-10	2017	CS produced significant higher activity of caspase-8 compared to control.	N-(p-coumaroyl)serotonin	0-2	caspase 8	Homo sapiens	43-52
28521469-7	2017	Treatment with Lico-E increased the expression of Fas ligand and the cleaved form of caspase-8 in FaDu cells.	licochalcone E	15-21	caspase 8	Homo sapiens	85-94
26953980-3	2017	24S-OHC induces necroptosis-like cell death in SH-SY5Y cells expressing little caspase-8.	24-hydroxycholesterol	0-7	caspase 8	Homo sapiens	79-88
26953980-4	2017	In the present study, 24S-OHC was found to induce apoptosis as determined by caspase-3 activation in all-trans-retinoic acid (atRA)-treated SH-SY5Y cells in which expression of caspase-8 was induced.	24-hydroxycholesterol	22-29	caspase 8	Homo sapiens	177-186
26953980-4	2017	In the present study, 24S-OHC was found to induce apoptosis as determined by caspase-3 activation in all-trans-retinoic acid (atRA)-treated SH-SY5Y cells in which expression of caspase-8 was induced.	Tretinoin	105-124	caspase 8	Homo sapiens	177-186
26953980-4	2017	In the present study, 24S-OHC was found to induce apoptosis as determined by caspase-3 activation in all-trans-retinoic acid (atRA)-treated SH-SY5Y cells in which expression of caspase-8 was induced.	Tretinoin	126-130	caspase 8	Homo sapiens	177-186
28107698-11	2017	The combination of the IC50 doses of apigenin (15muM) and cisplatin (7.5muM) for 48h significantly enhanced cisplatin"s cytotoxic and apoptotic effects through downregulation of Bcl-2, sharpin and survivin; and upregulation of caspase-8, Apaf-1 and p53 mRNA expression.	Apigenin	37-45	caspase 8	Homo sapiens	227-236
28154184-6	2017	More intriguingly, we find that it is sorafenib-induced ROS accumulation that enables TRAIL to activate caspase-8 in RCC.	Sorafenib	38-47	caspase 8	Homo sapiens	104-113
28154184-6	2017	More intriguingly, we find that it is sorafenib-induced ROS accumulation that enables TRAIL to activate caspase-8 in RCC.	Reactive Oxygen Species	56-59	caspase 8	Homo sapiens	104-113
28460471-5	2017	Moreover, Norcantharidin markedly enhanced Birinapant-triggered caspase-8/caspase-3 cascade.	norcantharidin	10-24	caspase 8	Homo sapiens	64-73
28460471-5	2017	Moreover, Norcantharidin markedly enhanced Birinapant-triggered caspase-8/caspase-3 cascade.	birinapant	43-53	caspase 8	Homo sapiens	64-73
28460471-6	2017	Inhibition of caspase-8 activity by a synthetic peptide Z-IETD-FMK significantly attenuated cell death induction by the combination, suggesting that caspase-8 plays a critical role in the anticancer action.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	56-66	caspase 8	Homo sapiens	14-23
28460471-6	2017	Inhibition of caspase-8 activity by a synthetic peptide Z-IETD-FMK significantly attenuated cell death induction by the combination, suggesting that caspase-8 plays a critical role in the anticancer action.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	56-66	caspase 8	Homo sapiens	149-158
28579903-4	2017	The results showed that the higher the dose, the higher the rate of apoptosis and that the rate of apoptosis was dependent on the dose; the relative protein activity of Fas, FasL, Caspase-8 and bid gradually rose with the increase of lycorine dosage and the activities revealed certain dose-independence.	lycorine	234-242	caspase 8	Homo sapiens	180-189
28107698-11	2017	The combination of the IC50 doses of apigenin (15muM) and cisplatin (7.5muM) for 48h significantly enhanced cisplatin"s cytotoxic and apoptotic effects through downregulation of Bcl-2, sharpin and survivin; and upregulation of caspase-8, Apaf-1 and p53 mRNA expression.	Cisplatin	58-67	caspase 8	Homo sapiens	227-236
27869161-2	2017	Here, we identify that Smac mimetics such as BV6, which antagonizes IAP proteins, elicit necroptosis in AML cells, in which apoptosis is inhibited pharmacologically by caspase inhibitors or genetically by caspase-8 knockdown.	BV6	45-48	caspase 8	Homo sapiens	205-214
28553347-6	2017	Mitomycin C upregulated the expression levels of Fas, DR4, DR5, cleaved caspase-8/9, Bax, Bim and cleaved caspase-3 proteins, and it downregulated Bcl-2 and Bcl-xL expression.	Mitomycin	0-11	caspase 8	Homo sapiens	72-83
28314692-6	2017	Further distinguishing features of this "CIMP-Atypical" subtype include an antiviral gene expression profile associated with pro-inflammatory M1 macrophages and CD8+ T cell infiltration, CASP8 mutations, and a well-differentiated state corresponding to normal SOX2 copy number and SOX2OT hypermethylation.	Cyclic IMP	41-45	caspase 8	Homo sapiens	187-192
28040581-5	2017	Western blot confirmed that EGCG induced apoptosis in SW780 cells by activation of caspases-8, -9 and -3, Bax, Bcl-2 and PARP.	epigallocatechin gallate	28-32	caspase 8	Homo sapiens	83-104
28553507-5	2017	The green and red fluorescence can be sequentially turned on when the peptide substrate is cleaved by the cascade activation of caspase-8 and caspase-3 in early apoptotic HeLa cells induced by hydrogen peroxide.	Hydrogen Peroxide	193-210	caspase 8	Homo sapiens	128-137
28177892-5	2017	Pevonedistat enhanced caspase-8 processing following death receptor ligation, and downmodulated cFLIP, a NFkappaB-regulated protease-deficient caspase homolog.	pevonedistat	0-12	caspase 8	Homo sapiens	22-31
28099148-11	2017	In conclusion, SAHA inhibited the growth of lung cancer cells via a G2/M phase arrest and caspase-dependent apoptosis.	Vorinostat	15-19	caspase 8	Homo sapiens	90-97
27993669-6	2017	Suppression of etoposide-induced cell death correlated with a downregulation of p53 expression, which, among other functions, regulates the expression of death receptor 5, one of the activators of caspase-8.	Etoposide	15-24	caspase 8	Homo sapiens	197-206
27993669-7	2017	In contrast, stimulation of cisplatin-induced cell death involved reactive oxygen species-mediated downregulation of FLIP-S, an inhibitor of caspase-8.	Cisplatin	28-37	caspase 8	Homo sapiens	141-150
27993669-7	2017	In contrast, stimulation of cisplatin-induced cell death involved reactive oxygen species-mediated downregulation of FLIP-S, an inhibitor of caspase-8.	Reactive Oxygen Species	66-89	caspase 8	Homo sapiens	141-150
27834952-4	2017	PolyI:C-induced inhibition of tumor growth was attributed to caspase-8/3 cascade activation in tumor cells that occurred independently of CD8alpha+/CD103+ dendritic cells (DCs) and CTLs.	Poly I-C	0-7	caspase 8	Homo sapiens	61-70
28230157-4	2017	Using caspase-3, caspase-7, caspase-8, neutrophil elastase, legumain, and two matrix metalloproteinases (MMP2 and MMP9), we demonstrated that substrates containing ACC/Lys(DNP) exhibit 7 to 10 times higher sensitivity than conventional 7-methoxy-coumarin-4-yl acetic acid (MCA)/Lys(DNP) substrates; thus, substantially lower amounts of substrate and enzyme can be used for each assay.	7-amino-4-carbamoylmethylcoumarin	164-167	caspase 8	Homo sapiens	28-37
28351307-4	2017	Furthermore, induction of apoptosis in A549 cells by coptisine was characterized by the activation of caspase 9, caspase 8, and caspase 3, and cleavage of poly adenosine diphosphate ribose polymerase.	coptisine	53-62	caspase 8	Homo sapiens	113-122
28230157-7	2017	Finally, we used IQF substrates to re-investigate the P1-Asp characteristic of caspases, thus demonstrating that some human caspases can also hydrolyze substrates after glutamic acid.	Glutamic Acid	169-182	caspase 8	Homo sapiens	79-87
28228218-9	2017	Western blotting indicated that compared with TRAIL group, expressions of Cleaved-caspase-8, Cleaved-PARP and DR5 increased significantly in combination group of TRAIL and thioridazine.	Thioridazine	172-184	caspase 8	Homo sapiens	82-91
28230157-7	2017	Finally, we used IQF substrates to re-investigate the P1-Asp characteristic of caspases, thus demonstrating that some human caspases can also hydrolyze substrates after glutamic acid.	Glutamic Acid	169-182	caspase 8	Homo sapiens	124-132
28031531-5	2017	Inhibiting the autophagy generation by 3-methyladenine (3-MA) increase cell viability but decrease the caspase 3/7 and caspase 8 activities in combination groups, and inhibiting apoptosis took the same effect.	3-methyladenine	39-54	caspase 8	Homo sapiens	119-128
28205610-5	2017	In addition, CR-LAAO promoted apoptosis of HL-60 and HepG2 tumor cells mediated by the release of hydrogen peroxide and activation of immune cells, resulting in oxidative stress and production of IL-6 and IL-1beta that triggered a series of events, such as activation of caspase 8, 9 and 3, and the expression of the pro-apoptotic gene BAX.	cr-laao	13-20	caspase 8	Homo sapiens	271-289
28246474-8	2017	CONCLUSION: ST ethanol extracts induced the apoptosis of hepatocellular carcinoma SMMC-7721 cells through up-regulated Fas, caspase-8, caspse-3 and p53, and down-regulated FasL and Bcl-2 in the mitochondrial pathway.	Ethanol	15-22	caspase 8	Homo sapiens	124-133
28182780-3	2017	FTS pretreatment significantly enhanced DHA/ARS-induced phosphatidylserine (PS) externalization, Bak/Bax activation, mitochondrial membrane depolarization, cytochrome c release, and caspase-8 and -9 activations, characteristics of the extrinsic and intrinsic apoptosis.	farnesylthiosalicylic acid	0-3	caspase 8	Homo sapiens	182-198
28182780-4	2017	Pretreatment with Z-IETD-FMK (caspase-8 inhibitor) potently prevented the cytotoxicity of the combination treatment of DHA/ARS and FTS, and pretreatment with Z-VAD-FMK (pan-caspase inhibitor) significantly inhibited the loss of DeltaPsim induced by DHA/ARS treatment or the combination treatment of DHA/ARS and FTS in HCC cells.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	18-28	caspase 8	Homo sapiens	30-39
28182780-4	2017	Pretreatment with Z-IETD-FMK (caspase-8 inhibitor) potently prevented the cytotoxicity of the combination treatment of DHA/ARS and FTS, and pretreatment with Z-VAD-FMK (pan-caspase inhibitor) significantly inhibited the loss of DeltaPsim induced by DHA/ARS treatment or the combination treatment of DHA/ARS and FTS in HCC cells.	artenimol	119-122	caspase 8	Homo sapiens	30-39
28182780-4	2017	Pretreatment with Z-IETD-FMK (caspase-8 inhibitor) potently prevented the cytotoxicity of the combination treatment of DHA/ARS and FTS, and pretreatment with Z-VAD-FMK (pan-caspase inhibitor) significantly inhibited the loss of DeltaPsim induced by DHA/ARS treatment or the combination treatment of DHA/ARS and FTS in HCC cells.	farnesylthiosalicylic acid	131-134	caspase 8	Homo sapiens	30-39
28031531-5	2017	Inhibiting the autophagy generation by 3-methyladenine (3-MA) increase cell viability but decrease the caspase 3/7 and caspase 8 activities in combination groups, and inhibiting apoptosis took the same effect.	3-methyladenine	56-60	caspase 8	Homo sapiens	119-128
27868169-0	2017	Articulatin-D induces apoptosis via activation of caspase-8 in acute T-cell leukemia cell line.	articulatin-d	0-13	caspase 8	Homo sapiens	50-59
28080141-9	2017	The mRNA expressions of superoxide dismutase (SOD), induced nitric oxide synthase (iNOS), interleukin-1beta, IL-12, COX-2, caspase-3 and caspase-8 were increased by 2.4, 2.2, 2.2, 2.3, 3.0, 2.6, and 2.5 fold, respectively, by LPS, and oleic acid pretreatment significantly potentiated the effect of LPS.	Oleic Acid	235-245	caspase 8	Homo sapiens	137-146
27879498-10	2017	The combination of anisomycin and mapatumumab also enhanced the activity of caspases 8 and 3, the downstream molecules of death receptors.	Anisomycin	19-29	caspase 8	Homo sapiens	76-92
27868169-9	2017	In conclusion, we provided evidence that Articulatin-D efficiently activates caspase-8 involved in extrinsic pathway of apoptosis induction, which ultimately results in caspase-3-dependent DNA fragmentation of Jurkat cells.	articulatin-d	41-54	caspase 8	Homo sapiens	77-86
27671304-9	2017	Moreover, the exposure of U87-MG cells to dehydroleucodine upregulated the protein levels of CDKN1A, BAX, TP53AIP1, CYLD, RIPK1, APG5L, and downregulated the CASP8 level.	dehydroleucodine	42-58	caspase 8	Homo sapiens	158-163
28184196-9	2017	In addition, the caspase-8 inhibitor z-IETD-fmk could significantly block AG36-triggered MCF-7 cells apoptosis.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	37-47	caspase 8	Homo sapiens	17-26
28184196-9	2017	In addition, the caspase-8 inhibitor z-IETD-fmk could significantly block AG36-triggered MCF-7 cells apoptosis.	ag36	74-78	caspase 8	Homo sapiens	17-26
27871859-9	2017	Interestingly, in HO8910PM cells with ST3Gal3 knockdown, the levels of caspase 8 and caspase 3 proteins increased, which was more obvious in cells treated with both ST3Gal3 knockdown and cisplatin, suggesting that ST3Gal3 knockdown synergistically enhanced cisplatin-induced apoptosis in ovarian cancer cells.	Cisplatin	187-196	caspase 8	Homo sapiens	71-80
27871859-9	2017	Interestingly, in HO8910PM cells with ST3Gal3 knockdown, the levels of caspase 8 and caspase 3 proteins increased, which was more obvious in cells treated with both ST3Gal3 knockdown and cisplatin, suggesting that ST3Gal3 knockdown synergistically enhanced cisplatin-induced apoptosis in ovarian cancer cells.	Cisplatin	257-266	caspase 8	Homo sapiens	71-80
28176915-10	2017	Caspase-8 inhibitor Ac-IETD-CHO significantly decreased the activation of caspase cascade, indicating that the extrinsic pathway may have a vital role in the apoptotic events induced by SiDcR3/TRAIL.	Ac-IETD-CHO	20-31	caspase 8	Homo sapiens	0-9
27198984-0	2017	Effect of PUFAs Oral Administration on the Amount of Apoptotic Caspases Enzymes in Gastric Cancer Patients Undergoing Chemotherapy.	Fatty Acids, Unsaturated	10-15	caspase 8	Homo sapiens	63-71
28011486-5	2017	We also found that hyperforin significantly induced accumulation of cells in sub-G1 phase, loss of mitochondrial membrane potential, and increased levels of active caspase-3, and caspase-8.	hyperforin	19-29	caspase 8	Homo sapiens	179-188
28000850-6	2017	The present study demonstrated that Fas was associated with gastric cancer and promoted the apoptosis of gastric cancer cells via caspase-8, caspase-3 and PARP1.	ammonium ferrous sulfate	36-39	caspase 8	Homo sapiens	130-139
28133573-7	2017	To identify the mechanism(s) underlying Jellyfish-HE-induced apoptosis in K562 cells, we examined the effects of Jellyfish-HE on activation of caspase and mitogen-activated protein kinases (MAPKs), which are responsible for cell cycle progression.	Helium	123-125	caspase 8	Homo sapiens	143-150
28068431-3	2017	Treatment of DLD-1 cells with CIL-102 resulted in triggering the extrinsic apoptosis pathway through the activation of Fas-L, caspase-8 and the induction of Bid cleavage and cytochrome c release in a time-dependent manner.	1-(4-(furo(2,3-b)quinolin-4-ylamino)phenyl)ethanone	30-37	caspase 8	Homo sapiens	126-135
28056970-3	2017	METHODS AND RESULTS: Q-PCR and Western blot results showed that alcohol exposure increased gene and active forms of caspase-3 and caspase-8, while decreased gene and protein of bcl-2.	Alcohols	64-71	caspase 8	Homo sapiens	130-139
28056970-4	2017	ChIP assay results showed that, alcohol exposure increased the acetylation of histone H3K9 near the promoter region of caspase-3 and caspase-8, and decreased the acetylation of histone H3K9 near the promoter region of bcl-2.	Alcohols	32-39	caspase 8	Homo sapiens	133-142
28056970-6	2017	In vitro experiments demonstrated that curcumin treatment could reverse the up-regulation of active forms of caspase-3 and caspase-8, and down-regulation of bcl-2 induced by alcohol treatment.	Curcumin	39-47	caspase 8	Homo sapiens	123-132
28231749-6	2017	Cleaved-caspase-3 protein levels in A549 cells after treatment with total flavonoids or total tannins were increased in a dose-dependent manner, followed by the activation of caspase-8 and caspase-9, finally triggering to PARP cleavage.	Flavonoids	74-84	caspase 8	Homo sapiens	175-184
26478521-8	2017	In addition, DHTI induced apoptosis of 143B cells through caspase pathways to activate caspase-3, caspase-8, caspase-9, Bax, and PARP cleavage but reduce the expression of Bcl-2.	dhts	13-17	caspase 8	Homo sapiens	58-65
26478521-8	2017	In addition, DHTI induced apoptosis of 143B cells through caspase pathways to activate caspase-3, caspase-8, caspase-9, Bax, and PARP cleavage but reduce the expression of Bcl-2.	dhts	13-17	caspase 8	Homo sapiens	98-107
28302032-5	2017	Furthermore, treatment with HH2O2 scavenger catalase significantly inhibited resveratrol-induced c-FLIP downregulation, caspase-8 activation and apoptosis.	hh2o2	28-33	caspase 8	Homo sapiens	120-129
29333445-8	2017	Experiments using the microtubule stabilizer Taxol showed that caspase-8 signaling is retrogradely transported by microtubules from the site of axotomy to the neuronal soma.	Paclitaxel	45-50	caspase 8	Homo sapiens	63-72
28302032-5	2017	Furthermore, treatment with HH2O2 scavenger catalase significantly inhibited resveratrol-induced c-FLIP downregulation, caspase-8 activation and apoptosis.	Resveratrol	77-88	caspase 8	Homo sapiens	120-129
28325143-7	2017	RESULTS: DBID inhibited the proliferation of HCT 116 cells with an IC50 of 9.32 microg/ml and significantly increased the levels of caspase -8, -9 and -3/7 in the treated cells compared to untreated cells.	dbid	9-13	caspase 8	Homo sapiens	132-153
26833863-9	2017	We also used cDNA microarray to confirm several gene expressions such as caspase -8, -3, -4, -6, and -7 that are affected by SFN.	sulforaphane	125-128	caspase 8	Homo sapiens	73-103
27310834-5	2017	There is a clear dose-dependent increase in superoxide production, caspase 8 and 9 activity, and apoptosis in HaCaTs after treatment with all three forms of TiO2; however, there is no consistent effect on cell viability and proliferation with either of these TiO2 particles.	titanium dioxide	157-161	caspase 8	Homo sapiens	67-76
27915154-0	2017	Lipopolysaccharides-stimulated macrophage products enhance Withaferin A-induced apoptosis via activation of caspases and inhibition of NF-kappaB pathway in human cancer cells.	withaferin A	59-71	caspase 8	Homo sapiens	108-116
27592797-5	2017	Using this SE model, we showed that arsenic initiated SUV39H2-mediated epigenetic modification of E2F1, which induced centrosome amplification in keratinocytes in 2 days; this, however, led to caspase-8-mediated apoptosis in 10 days.	Arsenic	36-43	caspase 8	Homo sapiens	193-202
27592797-7	2017	Tumor necrosis factor-alpha triggered anti-apoptotic signals via FLIP-associated caspase-8 inactivation in arsenic-treated keratinocytes, which in turn contributed to cell survival and aneuploidy.	Arsenic	107-114	caspase 8	Homo sapiens	81-90
29362666-8	2017	Further study demonstrated that VCAF attenuated the apoptosis of t-BHP-treated HepG2 cells by suppressing the activation of caspase-3 and caspase-8.	tert-Butylhydroperoxide	65-70	caspase 8	Homo sapiens	138-147
27245499-8	2017	This glial signaling pathway initiates a caspase-8-driven activation of IL-1beta that induces tryptophan-2,3-dioxygenase 2 (TDO2), an enzyme in the kynurenine pathway.	Kynurenine	148-158	caspase 8	Homo sapiens	41-50
27847202-6	2016	We found that EAEPT could induce the cleavage of the caspase 3, caspase 8, caspase 9 and Bid.	eaept	14-19	caspase 8	Homo sapiens	64-73
27812566-7	2016	The most evident effect of BC was the increase of the activity of caspase 8, leading to induction of extrinsic apoptosis.	Betacyanins	27-29	caspase 8	Homo sapiens	66-75
27705939-0	2016	The andean anticancer herbal product BIRM causes destabilization of androgen receptor and induces caspase-8 mediated-apoptosis in prostate cancer.	birm	37-41	caspase 8	Homo sapiens	98-107
27705939-9	2016	A synthetic inhibitor of Caspase-8 cleavage (IETD-CHO) aborted BIRM-induced apoptosis.	IETD-CHO	45-53	caspase 8	Homo sapiens	25-34
27705939-9	2016	A synthetic inhibitor of Caspase-8 cleavage (IETD-CHO) aborted BIRM-induced apoptosis.	birm	63-67	caspase 8	Homo sapiens	25-34
28462130-8	2016	AGRE induced apoptosis through the activation of caspase-3, caspase-8, and caspase-9.	agre	0-4	caspase 8	Homo sapiens	60-69
27693639-6	2016	Knockdown of FAT1 and CASP8 individually or in combination in OSCC cells led to increased cell migration and clonal growth, resistance to Staurosporine-induced apoptosis and, in some cases, increased terminal differentiation.	Staurosporine	138-151	caspase 8	Homo sapiens	22-27
28675694-0	2016	Benzyl isothiocyanate (BITC) induces apoptosis of GBM 8401 human brain glioblastoma multiforms cells via activation of caspase-8/Bid and the reactive oxygen species-dependent mitochondrial pathway.	benzyl isothiocyanate	0-21	caspase 8	Homo sapiens	119-128
28675694-0	2016	Benzyl isothiocyanate (BITC) induces apoptosis of GBM 8401 human brain glioblastoma multiforms cells via activation of caspase-8/Bid and the reactive oxygen species-dependent mitochondrial pathway.	benzyl isothiocyanate	23-27	caspase 8	Homo sapiens	119-128
28675694-6	2016	After cells were pretreated with Z-IETD-FMK, Z-LEHD-FMK, and Z-DEVD-FMK (caspase-8, -9, and -3 inhibitors, respectively) led to decrease in the activities of caspase-8, -9, and -3 and increased the percentage of viable GBM 8401 cells that indicated which BITC induced cell apoptosis through caspase-dependent pathways.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	33-43	caspase 8	Homo sapiens	73-94
28675694-6	2016	After cells were pretreated with Z-IETD-FMK, Z-LEHD-FMK, and Z-DEVD-FMK (caspase-8, -9, and -3 inhibitors, respectively) led to decrease in the activities of caspase-8, -9, and -3 and increased the percentage of viable GBM 8401 cells that indicated which BITC induced cell apoptosis through caspase-dependent pathways.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	33-43	caspase 8	Homo sapiens	158-179
28675694-6	2016	After cells were pretreated with Z-IETD-FMK, Z-LEHD-FMK, and Z-DEVD-FMK (caspase-8, -9, and -3 inhibitors, respectively) led to decrease in the activities of caspase-8, -9, and -3 and increased the percentage of viable GBM 8401 cells that indicated which BITC induced cell apoptosis through caspase-dependent pathways.	benzyloxycarbonyl-leucyl-glutamyl-histidyl-aspartic acid fluoromethyl ketone	45-55	caspase 8	Homo sapiens	73-94
28675694-6	2016	After cells were pretreated with Z-IETD-FMK, Z-LEHD-FMK, and Z-DEVD-FMK (caspase-8, -9, and -3 inhibitors, respectively) led to decrease in the activities of caspase-8, -9, and -3 and increased the percentage of viable GBM 8401 cells that indicated which BITC induced cell apoptosis through caspase-dependent pathways.	benzyloxycarbonyl-leucyl-glutamyl-histidyl-aspartic acid fluoromethyl ketone	45-55	caspase 8	Homo sapiens	158-179
28675694-6	2016	After cells were pretreated with Z-IETD-FMK, Z-LEHD-FMK, and Z-DEVD-FMK (caspase-8, -9, and -3 inhibitors, respectively) led to decrease in the activities of caspase-8, -9, and -3 and increased the percentage of viable GBM 8401 cells that indicated which BITC induced cell apoptosis through caspase-dependent pathways.	benzoylcarbonyl-aspartyl-glutamyl-valyl-aspartyl-fluoromethyl ketone	61-71	caspase 8	Homo sapiens	73-94
28675694-6	2016	After cells were pretreated with Z-IETD-FMK, Z-LEHD-FMK, and Z-DEVD-FMK (caspase-8, -9, and -3 inhibitors, respectively) led to decrease in the activities of caspase-8, -9, and -3 and increased the percentage of viable GBM 8401 cells that indicated which BITC induced cell apoptosis through caspase-dependent pathways.	benzoylcarbonyl-aspartyl-glutamyl-valyl-aspartyl-fluoromethyl ketone	61-71	caspase 8	Homo sapiens	158-179
28675694-6	2016	After cells were pretreated with Z-IETD-FMK, Z-LEHD-FMK, and Z-DEVD-FMK (caspase-8, -9, and -3 inhibitors, respectively) led to decrease in the activities of caspase-8, -9, and -3 and increased the percentage of viable GBM 8401 cells that indicated which BITC induced cell apoptosis through caspase-dependent pathways.	benzyl isothiocyanate	255-259	caspase 8	Homo sapiens	73-94
28675694-6	2016	After cells were pretreated with Z-IETD-FMK, Z-LEHD-FMK, and Z-DEVD-FMK (caspase-8, -9, and -3 inhibitors, respectively) led to decrease in the activities of caspase-8, -9, and -3 and increased the percentage of viable GBM 8401 cells that indicated which BITC induced cell apoptosis through caspase-dependent pathways.	benzyl isothiocyanate	255-259	caspase 8	Homo sapiens	158-179
28675694-7	2016	Western blotting indicated that BITC induced Fas, Fas-L, FADD, caspase-8, caspase -3, and pro-apoptotic protein (Bax, Bid, and Bak), but inhibited the ant-apoptotic proteins (Bcl-2 and Bcl-x) in GBM 8401 cells.	benzyl isothiocyanate	32-36	caspase 8	Homo sapiens	63-72
27779649-11	2016	Curcumin alone and combined with paclitaxel increased p53, Bid, caspase-3, caspase-8 and Bax gene expression in MDA-MB-231, whereas Bcl-xL decreased such expression in MDA-MB-231 cells.	Curcumin	0-8	caspase 8	Homo sapiens	75-84
27779649-11	2016	Curcumin alone and combined with paclitaxel increased p53, Bid, caspase-3, caspase-8 and Bax gene expression in MDA-MB-231, whereas Bcl-xL decreased such expression in MDA-MB-231 cells.	Paclitaxel	33-43	caspase 8	Homo sapiens	75-84
27192488-6	2016	We demonstrated that 3-HTMC treatment on both cell lines induced apoptotic process associated with overexpression of death receptor DR5, activation of caspase-8 and -3, PARP cleavage, and DNA fragmentation.	3-hydroxy-3',4,4',5'-tetramethoxychalcone	21-27	caspase 8	Homo sapiens	151-167
27699933-7	2016	We also showed for the first time that AKT3 suppressed BI 6727-induced caspase-8 activation and conferred resistance to PLKis.	BI 6727	55-62	caspase 8	Homo sapiens	71-80
27692344-8	2016	Subsequent ex vivo experiments showed the activation of carboplatin related TRAIL-dependent apoptosis through caspase 8 and a synergistic role of miR-155 in lung tissue infiltration by CD4+, and FoxP3+ lymphocytes.	Carboplatin	56-67	caspase 8	Homo sapiens	110-119
27748868-6	2016	Colorimetric assay analyses also showed that activities of caspase-3, caspase-8, caspase-9 and caspase-4 occurred in GdCl3-treated U-2 OS cells.	gadolinium chloride	117-122	caspase 8	Homo sapiens	70-79
28105237-6	2016	Furthermore, xanthohumol treatment (40 microM) induced SCC4 cell apoptosis, as indicated by the significant increase in activity and expression of caspase-3, caspase-8, caspase-9, PARP, p53 and AIF.	xanthohumol	13-24	caspase 8	Homo sapiens	158-167
27806731-9	2016	Spectrophotometric analysis of caspase 8 activity demonstrated that 2ME2 and ESE-15-ol both induced caspase 8 activation by 2- and 1.7-fold respectively indicating the induction of the apoptosis.	2-ethyl-3-O-sulphamoyl-estra-1,3,5(10),15-tetraen-17-ol	77-86	caspase 8	Homo sapiens	31-40
27748905-6	2016	Interestingly, pretreatment with z-IETD-fmk, a caspase-8 inhibitor, completely abolished 8-ADEQ-induced caspase-3 and -9 activation, and subsequent DNA fragmentation.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	33-43	caspase 8	Homo sapiens	47-56
27748905-6	2016	Interestingly, pretreatment with z-IETD-fmk, a caspase-8 inhibitor, completely abolished 8-ADEQ-induced caspase-3 and -9 activation, and subsequent DNA fragmentation.	(E)-8-acetoxy-2-(2-(3,4-diacetoxyphenyl)ethenyl)quinazoline	89-95	caspase 8	Homo sapiens	47-56
27748905-9	2016	Taken together, our data indicated that 8-ADEQ-stimulated apoptosis in HL-60 leukemia cells is due to a Fas-mediated caspase-8-dependent pathway via ROS generation, but also, to a lesser extent cytochrome c release and caspase-9 activation.	(E)-8-acetoxy-2-(2-(3,4-diacetoxyphenyl)ethenyl)quinazoline	40-46	caspase 8	Homo sapiens	117-126
27748905-9	2016	Taken together, our data indicated that 8-ADEQ-stimulated apoptosis in HL-60 leukemia cells is due to a Fas-mediated caspase-8-dependent pathway via ROS generation, but also, to a lesser extent cytochrome c release and caspase-9 activation.	ammonium ferrous sulfate	104-107	caspase 8	Homo sapiens	117-126
27748905-9	2016	Taken together, our data indicated that 8-ADEQ-stimulated apoptosis in HL-60 leukemia cells is due to a Fas-mediated caspase-8-dependent pathway via ROS generation, but also, to a lesser extent cytochrome c release and caspase-9 activation.	ros	149-152	caspase 8	Homo sapiens	117-126
27904697-3	2016	Treatment of human retinoblastoma (HXO-RB44) cells with bufalin induced apoptosis which was accompanied by a decrease in mitochondrial membrane potential, activation of caspase-9, caspase-8 and caspase-3, as well as changes in the expression of cytochrome C.	bufalin	56-63	caspase 8	Homo sapiens	180-189
27748905-3	2016	In addition, 8-ADEQ triggered activation of caspases-8, -9, -6 and -3 and cleavage of their substrates such as poly(ADP-ribose) polymerase (PARP).	(E)-8-acetoxy-2-(2-(3,4-diacetoxyphenyl)ethenyl)quinazoline	13-19	caspase 8	Homo sapiens	44-69
27738323-6	2016	Addition of the caspase-8 inhibitor z-IETD-FMK abolished the Sp1 reduction not only by panobinostat alone but also by its combination with bortezomib, suggesting caspase-8-mediated Sp1 degradation.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	36-46	caspase 8	Homo sapiens	16-25
27738323-6	2016	Addition of the caspase-8 inhibitor z-IETD-FMK abolished the Sp1 reduction not only by panobinostat alone but also by its combination with bortezomib, suggesting caspase-8-mediated Sp1 degradation.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	36-46	caspase 8	Homo sapiens	162-171
27738323-6	2016	Addition of the caspase-8 inhibitor z-IETD-FMK abolished the Sp1 reduction not only by panobinostat alone but also by its combination with bortezomib, suggesting caspase-8-mediated Sp1 degradation.	Panobinostat	87-99	caspase 8	Homo sapiens	16-25
27738323-6	2016	Addition of the caspase-8 inhibitor z-IETD-FMK abolished the Sp1 reduction not only by panobinostat alone but also by its combination with bortezomib, suggesting caspase-8-mediated Sp1 degradation.	Panobinostat	87-99	caspase 8	Homo sapiens	162-171
27738323-6	2016	Addition of the caspase-8 inhibitor z-IETD-FMK abolished the Sp1 reduction not only by panobinostat alone but also by its combination with bortezomib, suggesting caspase-8-mediated Sp1 degradation.	Bortezomib	139-149	caspase 8	Homo sapiens	16-25
27738323-6	2016	Addition of the caspase-8 inhibitor z-IETD-FMK abolished the Sp1 reduction not only by panobinostat alone but also by its combination with bortezomib, suggesting caspase-8-mediated Sp1 degradation.	Bortezomib	139-149	caspase 8	Homo sapiens	162-171
27738323-9	2016	Collectively, caspase-8-mediated post-translational Sp1 degradation appears to be among major mechanisms for synergistic anti-MM effects of panobinostat and proteasome inhibitors in combination.	Panobinostat	140-152	caspase 8	Homo sapiens	14-23
27886059-11	2016	Oleandrin also down-regulated the expression of bcl-2, but up-regulated bax, caspase-9, Fas, FasL, caspase-8 and caspase-3.	oleandrin	0-9	caspase 8	Homo sapiens	99-108
27863490-6	2016	Furthermore, at high concentrations (more than 5 muM), SAHA triggered apoptosis of GSCs accompanied by increases in both activation of caspase 8- and caspase 9-mediated pathways.	Vorinostat	55-59	caspase 8	Homo sapiens	135-144
27678524-6	2016	Subsequently, ABT-751 triggered apoptosis with marked downregulation of B-cell CLL/lymphoma 2, upregulation of mitochondrial BCL2 antagonist/killer 1 and BCL2 like 11 protein levels, and cleavages of caspase 8 (CASP8), CASP9, CASP3 and DNA fragmentation factor subunit alpha proteins.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	14-17	caspase 8	Homo sapiens	200-209
27678524-6	2016	Subsequently, ABT-751 triggered apoptosis with marked downregulation of B-cell CLL/lymphoma 2, upregulation of mitochondrial BCL2 antagonist/killer 1 and BCL2 like 11 protein levels, and cleavages of caspase 8 (CASP8), CASP9, CASP3 and DNA fragmentation factor subunit alpha proteins.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	14-17	caspase 8	Homo sapiens	211-216
27806731-9	2016	Spectrophotometric analysis of caspase 8 activity demonstrated that 2ME2 and ESE-15-ol both induced caspase 8 activation by 2- and 1.7-fold respectively indicating the induction of the apoptosis.	2-ethyl-3-O-sulphamoyl-estra-1,3,5(10),15-tetraen-17-ol	77-86	caspase 8	Homo sapiens	100-109
27473386-6	2016	Apigenin attenuated the proteasome inhibitors (MG132 and MG115)-induced decrease in the levels of Bid and Bcl-2, increase in the levels of Bax and p53, loss of the mitochondrial transmembrane potential, release of cytochrome c, activation of caspases (-8, -9 and -3), cleavage of PARP-1 and cell death in both cell lines.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	47-52	caspase 8	Homo sapiens	242-265
27469405-3	2016	We found that dinaciclib induced apoptosis through the activation of caspases 8 and 9, which was independent of the presence of cytokines to mimic the environment of proliferation centres or IGVH mutation status.	dinaciclib	14-24	caspase 8	Homo sapiens	69-85
27473386-6	2016	Apigenin attenuated the proteasome inhibitors (MG132 and MG115)-induced decrease in the levels of Bid and Bcl-2, increase in the levels of Bax and p53, loss of the mitochondrial transmembrane potential, release of cytochrome c, activation of caspases (-8, -9 and -3), cleavage of PARP-1 and cell death in both cell lines.	carbobenzoxy-leucyl-leucyl-norvalinal	57-62	caspase 8	Homo sapiens	242-265
27602962-4	2016	In this study, Polyphyllin G can potently induced apoptosis dependent on the activations of caspase-8, -3, and -9 and the changes of Bcl-2, Bcl-xL and Bax protein expression in different human NPC cell lines (HONE-1 and NPC-039).	polyphyllin VII	15-28	caspase 8	Homo sapiens	92-113
27896224-4	2016	FTIs also induced activation of caspase-3 and Fas-independent apoptosis, confirmed by the finding that inhibition of caspase-8 was not associated with the rescue of FTI-treated cells.	FTI	0-3	caspase 8	Homo sapiens	117-126
27644244-9	2016	In conclusion, these results demonstrated that PP-22 activated p38, inhibited cdc25B, increased p-cdc2 (Tyr15), and triggered S and G2/M phase arrest, as well as activated p53 through the p38-p53 pathway, inhibited the MAPK/ERK pathway, activated the caspase 8/caspase 3 pathway, and triggered the extrinsic apoptotic pathway in SCC-15 cells.	CHEMBL86597	47-52	caspase 8	Homo sapiens	251-260
27109099-0	2016	Caspase-8 tyrosine-380 phosphorylation inhibits CD95 DISC function by preventing procaspase-8 maturation and cycling within the complex.	Tyrosine	10-18	caspase 8	Homo sapiens	0-9
27109099-2	2016	However, the observation that caspase-8 is upregulated in many common tumour types led to the discovery of alternative non-apoptotic, pro-survival functions, many of which are contingent on phosphorylation of a tyrosine residue (Y380) found in the linker region between the two catalytic domains of the enzyme.	Tyrosine	211-219	caspase 8	Homo sapiens	30-39
27343853-7	2016	Selenoquinones 18, 21, 22 and 23 were selected to monitor the expression levels of caspase-8, Bcl-2 and Ki-67 molecular biomarkers.	selenoquinones	0-14	caspase 8	Homo sapiens	83-92
27393947-3	2016	In particular, it induced reactive oxygen species-mediated caspase-8/caspase-3-dependent apoptosis as revealed from the increased sub G1 cell population and changes in cell morphology.	Reactive Oxygen Species	26-49	caspase 8	Homo sapiens	59-68
27465521-9	2016	Hyperthermia-provoked apoptosis and potentiation by melatonin were abrogated by a broad-spectrum caspase inhibitor (z-VAD-fmk) as well as by specific inhibitors against caspase-8 or caspase-3.	Melatonin	52-61	caspase 8	Homo sapiens	169-178
27488900-4	2016	Furthermore, the apoptotic and cytotoxic effects of blank amphiphilic CDs were demonstrated by various mechanistic methods including Caspase-8 activity, lipid peroxidation assay, TUNEL assay, Tali( )-based image analysis, cholesterol assay, and gene expression studies.	Cyclodextrins	70-73	caspase 8	Homo sapiens	133-142
27746017-4	2016	Extensive assembly interfaces not predicted by the previously proposed linear DED chain model were uncovered, and were further confirmed by structure-based mutagenesis in filament formation in vitro and Fas-induced apoptosis and ASC-mediated caspase-8 recruitment in cells.	ammonium ferrous sulfate	203-206	caspase 8	Homo sapiens	242-251
27752362-8	2016	Regarding the inhibitors, z-VAD-fmk diminishes the cleaved caspase 8, RIP1, RIP3, and MLKL induced by Tan IIA, and reconstructs the ripoptosome complex, which marks cells moving from apoptosis to necroptosis.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	26-35	caspase 8	Homo sapiens	59-68
27695262-12	2016	Furthermore, KA-induced DNA fragmentation was abolished by pretreatment with z-VAD-FMK (a broad caspase inhibitor), z-DEVD-FMK (a caspase-3 inhibitor), and z-IETD-FMK (a caspase-8 inhibitor), but not by z-LEHD-FMK (a caspase-9 inhibitor) pretreatment.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	77-86	caspase 8	Homo sapiens	96-103
26666201-4	2016	A series of post-mortem brain tissue and in vitro experiments suggested SNX7 downregulation to result in a caspase-8-driven activation of interleukin-1beta and a subsequent induction of the brain kynurenine pathway.	Kynurenine	196-206	caspase 8	Homo sapiens	107-116
27351945-5	2016	In addition, the effect of MZO-2 on expression of caspases in Jurkat cells was determined.	mzo-2	27-32	caspase 8	Homo sapiens	50-58
27569589-6	2016	Apigenin induced apoptosis via an extrinsic caspase-dependent pathway by upregulating the mRNA expressions of caspases-8, -3 and TNF-alpha, but failed to regulate the intrinsic pathway as determined by the Bax, cytochrome c (Cyt-c) and APAF-1 in CSCs.	Apigenin	0-8	caspase 8	Homo sapiens	110-124
27474150-6	2016	The clinically relevant histone deacetylase (HDAC) inhibitors vorinostat and entinostat were subsequently found to sensitize a subset of NSCLC cell lines to IR in a manner that was dependent on their ability to suppress FLIP expression and promote activation of caspase-8.	Vorinostat	62-72	caspase 8	Homo sapiens	262-271
27695262-12	2016	Furthermore, KA-induced DNA fragmentation was abolished by pretreatment with z-VAD-FMK (a broad caspase inhibitor), z-DEVD-FMK (a caspase-3 inhibitor), and z-IETD-FMK (a caspase-8 inhibitor), but not by z-LEHD-FMK (a caspase-9 inhibitor) pretreatment.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	156-166	caspase 8	Homo sapiens	170-179
27565731-5	2016	Meanwhile, ONC201-induced TRAIL/death receptor-5 (DR-5) expression, caspase-8 activation and CRC cell apoptosis were also potentiated with AZD-8055 co-treatment.	(5-(2,4-bis((3S)-3-methylmorpholin-4-yl)pyrido(2,3-d)pyrimidin-7-yl)-2-methoxyphenyl)methanol	139-147	caspase 8	Homo sapiens	68-77
27465556-0	2016	Fibronectin protects lung cancer cells against docetaxel-induced apoptosis by promoting Src and caspase-8 phosphorylation.	Docetaxel	47-56	caspase 8	Homo sapiens	96-105
27465556-3	2016	Subsequently, we showed that fibronectin pretreatment could enhance cell viability and reduce apoptosis in docetaxel-treated lung cancer cells because fibronectin induced phosphorylated Src and caspase-8, rendering the later inactive, thus inhibiting docetaxel-induced apoptosis.	Docetaxel	107-116	caspase 8	Homo sapiens	194-203
27465556-7	2016	Inhibition of phospho-Src reduced phospho-caspase-8 and promoted caspase-8 activity, restoring apoptosis following docetaxel and fibronectin co-treatment.	Docetaxel	115-124	caspase 8	Homo sapiens	42-51
27465556-7	2016	Inhibition of phospho-Src reduced phospho-caspase-8 and promoted caspase-8 activity, restoring apoptosis following docetaxel and fibronectin co-treatment.	Docetaxel	115-124	caspase 8	Homo sapiens	65-74
27465556-9	2016	Our findings indicate that fibronectin promotes Src and caspase-8 phosphorylation in lung cancer cells, which decreases caspase-8 activation and protects tumor cells from docetaxel-induced apoptosis.	Docetaxel	171-180	caspase 8	Homo sapiens	56-65
27465556-10	2016	Therefore, the fibronectin/Src/caspase-8 pathway may play a crucial role in docetaxel resistance in lung cancer.	Docetaxel	76-85	caspase 8	Homo sapiens	31-40
27565731-6	2016	Reversely, TRAIL sequestering antibody RIK-2 or the caspase-8 specific inhibitor z-IETD-fmk attenuated AZD-8055 plus ONC201-induced CRC cell death.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	81-91	caspase 8	Homo sapiens	52-61
27565731-6	2016	Reversely, TRAIL sequestering antibody RIK-2 or the caspase-8 specific inhibitor z-IETD-fmk attenuated AZD-8055 plus ONC201-induced CRC cell death.	(5-(2,4-bis((3S)-3-methylmorpholin-4-yl)pyrido(2,3-d)pyrimidin-7-yl)-2-methoxyphenyl)methanol	103-111	caspase 8	Homo sapiens	52-61
27571890-0	2016	Baicalein induces apoptosis via ROS-dependent activation of caspases in human bladder cancer 5637 cells.	baicalein	0-9	caspase 8	Homo sapiens	60-68
27444344-11	2016	In addition, trifolin increased the levels of the death receptor involving the Fas/Fas ligand (FasL) and Fas-associated protein with the death domain (FADD), which consequently activated caspase-8, caspase-9, caspase-3, and the proteolytic cleavage of poly (ADP-ribose) polymerase (PARP).	kaempferol-3-O-galactoside	13-21	caspase 8	Homo sapiens	187-196
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	caspase 8	Homo sapiens	148-157
27448221-6	2016	In addition, western blot showed that 5Z-7-oxozeaenol enhanced HT-induced expressions of cleaved caspase-3, cleaved caspase-8, and HSP70 and decreased HT-induced expressions of Bcl-2, p-p38, p-JNK, and LC3.	5-7-oxo-zeaenol	38-53	caspase 8	Homo sapiens	116-125
27313093-6	2016	DCF-induced apoptotic effects were potentiated by TNF-alpha only in death receptor-expressing differentiated HepaRG and HepG2 cells and were associated with marked activation of caspase 8.	Diclofenac	0-3	caspase 8	Homo sapiens	178-187
27571890-0	2016	Baicalein induces apoptosis via ROS-dependent activation of caspases in human bladder cancer 5637 cells.	Reactive Oxygen Species	32-35	caspase 8	Homo sapiens	60-68
27571890-12	2016	In addition, the blocking of ROS generation decreases the apoptotic activity and antiproliferative effect of baicalein, indicating that baicalein induces apoptosis of 5637 cells through the ROS-dependent activation of caspases.	Reactive Oxygen Species	29-32	caspase 8	Homo sapiens	218-226
27571890-12	2016	In addition, the blocking of ROS generation decreases the apoptotic activity and antiproliferative effect of baicalein, indicating that baicalein induces apoptosis of 5637 cells through the ROS-dependent activation of caspases.	baicalein	109-118	caspase 8	Homo sapiens	218-226
27571890-12	2016	In addition, the blocking of ROS generation decreases the apoptotic activity and antiproliferative effect of baicalein, indicating that baicalein induces apoptosis of 5637 cells through the ROS-dependent activation of caspases.	baicalein	136-145	caspase 8	Homo sapiens	218-226
27571890-12	2016	In addition, the blocking of ROS generation decreases the apoptotic activity and antiproliferative effect of baicalein, indicating that baicalein induces apoptosis of 5637 cells through the ROS-dependent activation of caspases.	Reactive Oxygen Species	190-193	caspase 8	Homo sapiens	218-226
27473145-5	2016	However, combined treatment with GA and CDDP revealed a strong synergistic action between these drugs, and higher protein levels of the apoptosis-related factor Fas, cleaved caspase-8 and cleaved caspase-3 and lower expression of hypoxia-inducible factor (HIF)-1alpha are detected in both cell lines.	gambogic acid	33-35	caspase 8	Homo sapiens	174-183
27473145-5	2016	However, combined treatment with GA and CDDP revealed a strong synergistic action between these drugs, and higher protein levels of the apoptosis-related factor Fas, cleaved caspase-8 and cleaved caspase-3 and lower expression of hypoxia-inducible factor (HIF)-1alpha are detected in both cell lines.	Cisplatin	40-44	caspase 8	Homo sapiens	174-183
27462786-2	2016	In the present study we aimed to investigate the clinical relevance of Plk3 expression and phosphorylation of caspase-8 at T273 in patients with anal squamous cell carcinoma (SSC) treated with 5-fluorouracil and mitomycin C-based chemoradiotherapy (CRT).	Fluorouracil	193-207	caspase 8	Homo sapiens	110-119
27581364-4	2016	Physapubescin decreases the expression of HIF-2alpha and increases the expression of CCAAT/enhancer-binding protein homologus protein (CHOP), which leads to up-regulation of death receptor 5 (DR5), activation of caspase-8 and -3, cleavage of poly (ADP-Ribose) polymerase (PARP) and apoptosis.	physapubescin	0-13	caspase 8	Homo sapiens	212-228
27494891-6	2016	Mechanistic studies suggested that treatment of cells with PHPO or with PHPO + cisplatin differentially inhibited the PI3K/Akt, MAPK and ATM/Chk2 pathways, which consequently suppressed the anti-apoptotic factors Bcl-xL, Bcl-2 and XIAP, but activated the pro-apoptotic factors Bad, Bax, p53, caspase 9, caspase 8, caspase 7 and PARP.	phpo	59-63	caspase 8	Homo sapiens	303-312
27494891-6	2016	Mechanistic studies suggested that treatment of cells with PHPO or with PHPO + cisplatin differentially inhibited the PI3K/Akt, MAPK and ATM/Chk2 pathways, which consequently suppressed the anti-apoptotic factors Bcl-xL, Bcl-2 and XIAP, but activated the pro-apoptotic factors Bad, Bax, p53, caspase 9, caspase 8, caspase 7 and PARP.	phpo	72-76	caspase 8	Homo sapiens	303-312
27494891-6	2016	Mechanistic studies suggested that treatment of cells with PHPO or with PHPO + cisplatin differentially inhibited the PI3K/Akt, MAPK and ATM/Chk2 pathways, which consequently suppressed the anti-apoptotic factors Bcl-xL, Bcl-2 and XIAP, but activated the pro-apoptotic factors Bad, Bax, p53, caspase 9, caspase 8, caspase 7 and PARP.	Cisplatin	79-88	caspase 8	Homo sapiens	303-312
27378626-7	2016	Biochemical evidence of apoptosis came from elevating the intracellular ROS level that was accompanied by mitochondrial membrane potential loss, decreasing the expression profile of anti-apoptotic protein Bcl-2, whereas it augments cleavage of caspase-3 and PARP-1, activates caspase-8 and 9 with concomitant increase in expression of proapoptotic protein Bax in a dose dependent manner.	ros	72-75	caspase 8	Homo sapiens	276-285
27268964-8	2016	In addition, an increment in the levels of ROS, caspase-8, -9 and -3 was observed.	ros	43-46	caspase 8	Homo sapiens	48-68
27461934-4	2016	In addition, by using caspase-3, caspase-8 and caspase-9 activity assays and western blot analysis, the anticancer effects of triptolide against osteosarcoma growth were found to involve activation of the DR-5/p53/Bax/caspase-9/ caspase-3 signaling pathway and the DR-5/FADD/caspase-8/lysosomal/cathepsin B/caspase-3 signaling pathway in the MG-63 cells.	triptolide	126-136	caspase 8	Homo sapiens	33-42
27461934-4	2016	In addition, by using caspase-3, caspase-8 and caspase-9 activity assays and western blot analysis, the anticancer effects of triptolide against osteosarcoma growth were found to involve activation of the DR-5/p53/Bax/caspase-9/ caspase-3 signaling pathway and the DR-5/FADD/caspase-8/lysosomal/cathepsin B/caspase-3 signaling pathway in the MG-63 cells.	triptolide	126-136	caspase 8	Homo sapiens	275-284
27544395-9	2016	CONCLUSIONS: CASP8, MLH1, and RARB tumor suppressor genes were altered by copy number losses during PA progression to CXPA.	cxpa	118-122	caspase 8	Homo sapiens	13-18
27195913-0	2016	Dasatinib promotes paclitaxel-induced necroptosis in lung adenocarcinoma with phosphorylated caspase-8 by c-Src.	Dasatinib	0-9	caspase 8	Homo sapiens	93-102
27195913-0	2016	Dasatinib promotes paclitaxel-induced necroptosis in lung adenocarcinoma with phosphorylated caspase-8 by c-Src.	Paclitaxel	19-29	caspase 8	Homo sapiens	93-102
27195913-4	2016	The present study reported that phosphorylated caspase-8 at tyrosine 380 (p-Casp8) was characterized as a biomarker of chemoresistance to TP regimen (cisplatin and paclitaxel) in patients with resectable lung adenocarcinoma with significantly poorer 5-year disease-free survival (DFS) and overall survival (OS).	neotetrazolium	138-140	caspase 8	Homo sapiens	47-72
27195913-4	2016	The present study reported that phosphorylated caspase-8 at tyrosine 380 (p-Casp8) was characterized as a biomarker of chemoresistance to TP regimen (cisplatin and paclitaxel) in patients with resectable lung adenocarcinoma with significantly poorer 5-year disease-free survival (DFS) and overall survival (OS).	neotetrazolium	138-140	caspase 8	Homo sapiens	76-81
27195913-4	2016	The present study reported that phosphorylated caspase-8 at tyrosine 380 (p-Casp8) was characterized as a biomarker of chemoresistance to TP regimen (cisplatin and paclitaxel) in patients with resectable lung adenocarcinoma with significantly poorer 5-year disease-free survival (DFS) and overall survival (OS).	Cisplatin	150-159	caspase 8	Homo sapiens	47-72
27195913-4	2016	The present study reported that phosphorylated caspase-8 at tyrosine 380 (p-Casp8) was characterized as a biomarker of chemoresistance to TP regimen (cisplatin and paclitaxel) in patients with resectable lung adenocarcinoma with significantly poorer 5-year disease-free survival (DFS) and overall survival (OS).	Cisplatin	150-159	caspase 8	Homo sapiens	76-81
27195913-4	2016	The present study reported that phosphorylated caspase-8 at tyrosine 380 (p-Casp8) was characterized as a biomarker of chemoresistance to TP regimen (cisplatin and paclitaxel) in patients with resectable lung adenocarcinoma with significantly poorer 5-year disease-free survival (DFS) and overall survival (OS).	Paclitaxel	164-174	caspase 8	Homo sapiens	47-72
27195913-4	2016	The present study reported that phosphorylated caspase-8 at tyrosine 380 (p-Casp8) was characterized as a biomarker of chemoresistance to TP regimen (cisplatin and paclitaxel) in patients with resectable lung adenocarcinoma with significantly poorer 5-year disease-free survival (DFS) and overall survival (OS).	Paclitaxel	164-174	caspase 8	Homo sapiens	76-81
27195913-6	2016	Subsequently, we identified a novel mechanism by which paclitaxel induced necroptosis in lung adenocarcinoma cells that was dependent upon p-Casp8, receptor-interacting protein kinase 1 (RIPK1), and RIPK3.	Paclitaxel	55-65	caspase 8	Homo sapiens	141-146
27195913-7	2016	Moreover, dasatinib, a c-Src inhibitor, dephosphorylated caspase-8 to facilitate necroptosis, rather than apoptosis, in paclitaxel-treated p-Casp8-expressing lung adenocarcinoma cells.	Dasatinib	10-19	caspase 8	Homo sapiens	57-66
27195913-7	2016	Moreover, dasatinib, a c-Src inhibitor, dephosphorylated caspase-8 to facilitate necroptosis, rather than apoptosis, in paclitaxel-treated p-Casp8-expressing lung adenocarcinoma cells.	Dasatinib	10-19	caspase 8	Homo sapiens	141-146
27195913-7	2016	Moreover, dasatinib, a c-Src inhibitor, dephosphorylated caspase-8 to facilitate necroptosis, rather than apoptosis, in paclitaxel-treated p-Casp8-expressing lung adenocarcinoma cells.	Paclitaxel	120-130	caspase 8	Homo sapiens	57-66
27195913-7	2016	Moreover, dasatinib, a c-Src inhibitor, dephosphorylated caspase-8 to facilitate necroptosis, rather than apoptosis, in paclitaxel-treated p-Casp8-expressing lung adenocarcinoma cells.	Paclitaxel	120-130	caspase 8	Homo sapiens	141-146
27462786-2	2016	In the present study we aimed to investigate the clinical relevance of Plk3 expression and phosphorylation of caspase-8 at T273 in patients with anal squamous cell carcinoma (SSC) treated with 5-fluorouracil and mitomycin C-based chemoradiotherapy (CRT).	Mitomycin	212-223	caspase 8	Homo sapiens	110-119
27462786-5	2016	Patients with high scores of Plk3 and pT273 caspase-8 showed increased local control (p = 0.011; p = 0.001), increased CSS (p = 0.011; p = 0.013) and OS (p = 0.024; p = 0.001), while the levels of pT273 caspase-8 were significantly associated (p = 0.033) with distant metastases.	thiocysteine	119-122	caspase 8	Homo sapiens	44-53
27462786-7	2016	Moreover, a combined HPV16 DNA load and Plk3 or pT273 caspase-8 variable revealed a significant correlation to decreased local failure (p = 0.001; p = 0.009), increased CSS (p = 0.016; p = 0.023) and OS (p = 0.003; p = 0.003).	thiocysteine	169-172	caspase 8	Homo sapiens	54-63
27462786-7	2016	Moreover, a combined HPV16 DNA load and Plk3 or pT273 caspase-8 variable revealed a significant correlation to decreased local failure (p = 0.001; p = 0.009), increased CSS (p = 0.016; p = 0.023) and OS (p = 0.003; p = 0.003).	Osmium	200-202	caspase 8	Homo sapiens	54-63
27388162-0	2016	Developing Activity Localization Fluorescence Peptide Probe Using Thiol-Ene Click Reaction for Spatially Resolved Imaging of Caspase-8 in Live Cells.	2,3-Dihydrothiophene	66-75	caspase 8	Homo sapiens	125-134
27487939-0	2016	Ceramide mediates FasL-induced caspase 8 activation in colon carcinoma cells to enhance FasL-induced cytotoxicity by tumor-specific cytotoxic T lymphocytes.	Ceramides	0-8	caspase 8	Homo sapiens	31-40
27487939-7	2016	Ceramide enhances FasL-induced activation of the MAPK, NF-kappaB, and caspase 8 despite induction of potent tumor cell death.	Ceramides	0-8	caspase 8	Homo sapiens	70-79
26676947-10	2016	Additionally, activation of caspases 3, 8, and 9 and apoptotic nuclear morphological changes were found in primary rat hepatocytes exposed to MDPV, indicating that this cathinone derivative activates both intrinsic and extrinsic apoptotic death pathways.	cathinone	169-178	caspase 8	Homo sapiens	28-36
26810384-14	2016	Moreover, proapoptotic effects of TEO were mediated through the activation of TNF-alpha, caspases and mitochondrial pathway.	2a,-3a,-24-trihydroxyurs-12-en-28-oic acid	34-37	caspase 8	Homo sapiens	89-97
25640594-0	2016	Atrazine induces endoplasmic reticulum stress-mediated apoptosis of T lymphocytes via the caspase-8-dependent pathway.	Atrazine	0-8	caspase 8	Homo sapiens	90-99
27278553-6	2016	Results also indicated that Dox induced apoptosis by upregulating Bax, caspase-8 and caspase-3 and downregulation of Bcl-2 protein expression.	Doxorubicin	28-31	caspase 8	Homo sapiens	71-80
27278553-8	2016	It can be concluded that Dox activated apoptosis by inducing proteolytic processing of Bcl-2 family, caspases and simultaneously decreased oxidative stress by influencing ROS damage in MCF-7 and MDA-MB-231 cell lines.	Doxorubicin	25-28	caspase 8	Homo sapiens	101-109
26755433-6	2016	Fisetin inhibited TNBC cell division and induced apoptosis, which was associated with mitochondrial membrane permeabilization and the activation of caspase-9 and caspase-8, as well as the cleavage of poly(ADP-ribose) polymerase-1.	fisetin	0-7	caspase 8	Homo sapiens	162-171
27277541-6	2016	The induction of apoptosis by proteasome inhibitor MG132 was mainly through the extrinsic apoptotic pathways of caspase activation such as caspase-8, caspase-3 and PARP cleavage.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	51-56	caspase 8	Homo sapiens	139-148
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	caspase 8	Homo sapiens	123-132
27501765-4	2016	We evaluated the action of these PCN congeners on cell proliferation, DNA fragmentation and caspase-8,-9 activity.	PREGNENOLONE CARBONITRILE	33-36	caspase 8	Homo sapiens	92-104
27621815-8	2016	Caspase-8 was also inhibited using a caspase-8 inhibitor, z-IEDT.	z-iedt	58-64	caspase 8	Homo sapiens	0-9
27270451-5	2016	Sesamol increased the activity of caspase 8, 9, and 3/7, indicating that apoptotic cell death occurred through both extrinsic and intrinsic pathways.	sesamol	0-7	caspase 8	Homo sapiens	34-43
27501765-9	2016	None of the higher chlorinated PCNs affected cell proliferation but all higher chlorinated PCNs increased caspase-8 activity, and hexa PCNs also increased caspase-9 activity.	Pregnenolone Carbonitrile	91-95	caspase 8	Homo sapiens	106-115
27621815-8	2016	Caspase-8 was also inhibited using a caspase-8 inhibitor, z-IEDT.	z-iedt	58-64	caspase 8	Homo sapiens	37-46
27250033-4	2016	We found that LPS caused a mild increase in caspase-8 activity and that the caspase-8 inhibitor IETD-fmk partially decreased monocyte activation.	isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	96-104	caspase 8	Homo sapiens	76-85
27376261-1	2016	In this study we investigate the molecular mechanisms of caspases and mitochondria in the extrinsic and intrinsic signal apoptosis pathways in human leukemia HL-60 cells after in vitro exposure to 18alpha-glycyrrhetinic acid (18alpha-GA).	18alpha-glycyrrhetinic acid	197-224	caspase 8	Homo sapiens	57-65
27376261-1	2016	In this study we investigate the molecular mechanisms of caspases and mitochondria in the extrinsic and intrinsic signal apoptosis pathways in human leukemia HL-60 cells after in vitro exposure to 18alpha-glycyrrhetinic acid (18alpha-GA).	18alpha-glycyrrhetinic acid	226-236	caspase 8	Homo sapiens	57-65
27376261-3	2016	Cells treated with 18alpha-GA significantly inhibited cell proliferation and induced cell apoptosis in a dose-dependent manner, with an IC50 value of 100 muM at 48 h. The cell growth inhibition resulted in induction of apoptosis and decreased the mitochondria membrane potential (DeltaPsim) and increased caspase-8, -9 and -3 activities.	18alpha-glycyrrhetinic acid	19-29	caspase 8	Homo sapiens	305-325
27175602-12	2016	Quercetin induced caspase-dependent extrinsic apoptosis upregulating the levels of cleaved caspase-8 and cleaved caspase-3, and inducing the cleavage of poly(ADP-ribose) polymerase (PARP).	Quercetin	0-9	caspase 8	Homo sapiens	91-100
27259273-7	2016	The triazine-modified dendrimer efficiently stimulates the down-regulation of MDM2 gene in NSCLC PC9 cells, which induces significant cell apoptosis through the activation of apoptosis markers such as caspase-8 and poly(ADP-ribose) polymerase (PARP) cleavage.	Triazines	4-12	caspase 8	Homo sapiens	201-210
27176505-9	2016	The specific caspase-8 inhibitor, Z-IETD-FMK, identified the extrinsic pathway as the principal mode of apoptosis.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	34-44	caspase 8	Homo sapiens	13-22
27221553-0	2016	Hwang-Heuk-San induces apoptosis in HCT116 human colorectal cancer cells through the ROS-mediated activation of caspases and the inactivation of the PI3K/Akt signaling pathway.	Reactive Oxygen Species	85-88	caspase 8	Homo sapiens	112-120
27081867-13	2016	Furthermore, it increased cleavage of caspase-8, suggesting that noscapine-induced apoptosis is probably due to the involvement of extrinsic and intrinsic apoptosis pathways.	Noscapine	65-74	caspase 8	Homo sapiens	38-47
27129269-8	2016	The residues of Trp-354, Arg-359, Glu-355, Leu-363, and Glu-367 in DR5 death domain that are important for DR5 recruitment of FADD and caspase-8 for DISC formation to signal apoptosis also play an important role for CaM-DR5 binding.	Tryptophan	16-19	caspase 8	Homo sapiens	135-144
27129269-8	2016	The residues of Trp-354, Arg-359, Glu-355, Leu-363, and Glu-367 in DR5 death domain that are important for DR5 recruitment of FADD and caspase-8 for DISC formation to signal apoptosis also play an important role for CaM-DR5 binding.	Arginine	25-28	caspase 8	Homo sapiens	135-144
27129269-8	2016	The residues of Trp-354, Arg-359, Glu-355, Leu-363, and Glu-367 in DR5 death domain that are important for DR5 recruitment of FADD and caspase-8 for DISC formation to signal apoptosis also play an important role for CaM-DR5 binding.	Glutamic Acid	34-37	caspase 8	Homo sapiens	135-144
27129269-8	2016	The residues of Trp-354, Arg-359, Glu-355, Leu-363, and Glu-367 in DR5 death domain that are important for DR5 recruitment of FADD and caspase-8 for DISC formation to signal apoptosis also play an important role for CaM-DR5 binding.	Leucine	43-46	caspase 8	Homo sapiens	135-144
27129269-8	2016	The residues of Trp-354, Arg-359, Glu-355, Leu-363, and Glu-367 in DR5 death domain that are important for DR5 recruitment of FADD and caspase-8 for DISC formation to signal apoptosis also play an important role for CaM-DR5 binding.	Glutamic Acid	56-59	caspase 8	Homo sapiens	135-144
27514549-5	2016	The L02 cells in the 0.8~3.2 mmol/L trichloroethylene groups showed significant increases in the expression of the apoptosis genes caspase-3, caspase-8, and caspase-9 (P&lt;0.05) , as well as the oncogenes c-myc, c-fos, and k-ras (P&lt;0.05).	Trichloroethylene	36-53	caspase 8	Homo sapiens	142-151
27082017-7	2016	Results indicated that curcumin decreased expression of EMT-related genes in Tumor2 cell line when compared to its counterpart as E-cadherin, N-cadherin, ZEB2, Twist1, Slug, Axl, vimentin, STAT-3, fibronectin; and genes p53 and caveolin-1, as well as apoptotic genes caspase-3, caspase-8, and others such as cyclin D1 and NFkappaB.	Curcumin	23-31	caspase 8	Homo sapiens	278-287
27053107-7	2016	By generating Bid/Bax/Bak-deficient (TKO) cells, we demonstrated that Bid is primarily cleaved by caspase 8, not by effector caspases, to give rise to truncated Bid (tBid) upon TRAIL treatment.	tBID	166-170	caspase 8	Homo sapiens	98-107
27468551-10	2016	In addition, evodiamine treatment led to the activation of caspase-8, caspase-9, and caspase-3 and the cleavage of poly (ADP-ribose)-polymerase (PARP).	evodiamine	13-23	caspase 8	Homo sapiens	59-68
26912071-8	2016	Addition of the broad-range caspase inhibitor N-benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone (zVAD.fmk) significantly protects RCC cells against BV6/IFNalpha-induced apoptosis, demonstrating that caspase activity is required for apoptosis.	Caspase Inhibitor VI	46-96	caspase 8	Homo sapiens	28-35
26912071-8	2016	Addition of the broad-range caspase inhibitor N-benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone (zVAD.fmk) significantly protects RCC cells against BV6/IFNalpha-induced apoptosis, demonstrating that caspase activity is required for apoptosis.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	98-106	caspase 8	Homo sapiens	28-35
27194727-0	2016	The caspase-8 inhibitor emricasan combines with the SMAC mimetic birinapant to induce necroptosis and treat acute myeloid leukemia.	3-(2-(2-tert-butylphenylaminooxalyl)aminopropionylamino)-4-oxo-5-(2,3,5,6-tetrafluorophenoxy)pentanoic acid	24-33	caspase 8	Homo sapiens	4-13
27194727-0	2016	The caspase-8 inhibitor emricasan combines with the SMAC mimetic birinapant to induce necroptosis and treat acute myeloid leukemia.	birinapant	65-75	caspase 8	Homo sapiens	4-13
27194727-4	2016	Deletion of caspase-8 sensitized AML to birinapant, whereas combined loss of caspase-8 and the necroptosis effector MLKL (mixed lineage kinase domain-like) prevented birinapant/IDN-6556-induced death, showing that inhibition of caspase-8 sensitizes AML cells to birinapant-induced necroptosis.	birinapant	166-176	caspase 8	Homo sapiens	77-86
27194727-4	2016	Deletion of caspase-8 sensitized AML to birinapant, whereas combined loss of caspase-8 and the necroptosis effector MLKL (mixed lineage kinase domain-like) prevented birinapant/IDN-6556-induced death, showing that inhibition of caspase-8 sensitizes AML cells to birinapant-induced necroptosis.	birinapant	166-176	caspase 8	Homo sapiens	77-86
27194727-4	2016	Deletion of caspase-8 sensitized AML to birinapant, whereas combined loss of caspase-8 and the necroptosis effector MLKL (mixed lineage kinase domain-like) prevented birinapant/IDN-6556-induced death, showing that inhibition of caspase-8 sensitizes AML cells to birinapant-induced necroptosis.	birinapant	166-176	caspase 8	Homo sapiens	77-86
27194727-4	2016	Deletion of caspase-8 sensitized AML to birinapant, whereas combined loss of caspase-8 and the necroptosis effector MLKL (mixed lineage kinase domain-like) prevented birinapant/IDN-6556-induced death, showing that inhibition of caspase-8 sensitizes AML cells to birinapant-induced necroptosis.	birinapant	166-176	caspase 8	Homo sapiens	77-86
27164070-4	2016	These results provide evidence that 5r-induced apoptosis in HepG2 cell is caspase-8-dependent.	CHEMBL3741454	36-38	caspase 8	Homo sapiens	74-83
27064011-8	2016	In parallel, honokiol induced activations of caspase-8, -9, and -3, apoptosis, and G1 cell cycle arrest.	honokiol	13-21	caspase 8	Homo sapiens	45-66
27226712-9	2016	In addition, both catechin extract and nanoemulsion could induce apoptosis of PC-3 cells through decrease in B-cell lymphoma 2 (bcl-2) expression and increase in cytochrome c expression for activation of caspase-3, caspase-8, and caspase-9.	Catechin	18-26	caspase 8	Homo sapiens	215-224
26448608-3	2016	Chal-24 treatment significantly enhanced TRAIL-induced activation of caspase-8 and caspase-3, and the cytotoxicity induced by combination of these agents was effectively suppressed by the pan-caspase inhibitor z-VAD-fmk.	3-(3-hydroxy-4-methoxyphenyl)-1-(3,4,5-trimethoxyphenyl)prop-2-en-1-one	0-7	caspase 8	Homo sapiens	69-78
27013583-6	2016	Both downregulated PLAG1 and elevated expression of miR-424&amp;27a led to Bcl2 downregulation and augmented cleavage of Caspase8, Caspase3 and PARP in the presence of TRAIL.	Adenosine Monophosphate	60-63	caspase 8	Homo sapiens	121-129
26984266-7	2016	The caspase signals, including caspase-8, -9 and -3, were time-dependently activated in HUVECs after kaempferol exposure.	kaempferol	101-111	caspase 8	Homo sapiens	4-11
26984266-7	2016	The caspase signals, including caspase-8, -9 and -3, were time-dependently activated in HUVECs after kaempferol exposure.	kaempferol	101-111	caspase 8	Homo sapiens	31-51
26984266-8	2016	Furthermore, pre-treatment with a specific inhibitor of caspase-8 (Z-IETD-FMK) significantly reduced the activity of caspase-8, -9 and -3, indicating that extrinsic pathway is a major signaling pathway in kaempferol-treated HUVECs.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	67-77	caspase 8	Homo sapiens	56-65
26984266-8	2016	Furthermore, pre-treatment with a specific inhibitor of caspase-8 (Z-IETD-FMK) significantly reduced the activity of caspase-8, -9 and -3, indicating that extrinsic pathway is a major signaling pathway in kaempferol-treated HUVECs.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	67-77	caspase 8	Homo sapiens	117-137
26984266-8	2016	Furthermore, pre-treatment with a specific inhibitor of caspase-8 (Z-IETD-FMK) significantly reduced the activity of caspase-8, -9 and -3, indicating that extrinsic pathway is a major signaling pathway in kaempferol-treated HUVECs.	kaempferol	205-215	caspase 8	Homo sapiens	56-65
26984266-8	2016	Furthermore, pre-treatment with a specific inhibitor of caspase-8 (Z-IETD-FMK) significantly reduced the activity of caspase-8, -9 and -3, indicating that extrinsic pathway is a major signaling pathway in kaempferol-treated HUVECs.	kaempferol	205-215	caspase 8	Homo sapiens	117-137
26448608-4	2016	Chal-24 and TRAIL combination suppressed expression of cellular FLICE (FADD-like IL-1beta-converting enzyme)-inhibitory protein large (c-FLIP(L)) and cellular inhibitor of apoptosis proteins (c-IAPs), and ectopic expression of c-FLIP(L) and c-IAPs inhibited the potentiated cytotoxicity.	3-(3-hydroxy-4-methoxyphenyl)-1-(3,4,5-trimethoxyphenyl)prop-2-en-1-one	0-7	caspase 8	Homo sapiens	64-69
26448608-4	2016	Chal-24 and TRAIL combination suppressed expression of cellular FLICE (FADD-like IL-1beta-converting enzyme)-inhibitory protein large (c-FLIP(L)) and cellular inhibitor of apoptosis proteins (c-IAPs), and ectopic expression of c-FLIP(L) and c-IAPs inhibited the potentiated cytotoxicity.	3-(3-hydroxy-4-methoxyphenyl)-1-(3,4,5-trimethoxyphenyl)prop-2-en-1-one	0-7	caspase 8	Homo sapiens	71-107
26448608-3	2016	Chal-24 treatment significantly enhanced TRAIL-induced activation of caspase-8 and caspase-3, and the cytotoxicity induced by combination of these agents was effectively suppressed by the pan-caspase inhibitor z-VAD-fmk.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	210-219	caspase 8	Homo sapiens	69-78
30133211-6	2016	The result of Western blot confirmed that mulberry anthocyanins can increase the ratio of LC3-II /LC3-I,BAX / BCL-2 ratio and the expression of Caspase-8,Beclin1 of SGC-7901 cells.	Anthocyanins	51-63	caspase 8	Homo sapiens	144-153
26460589-4	2016	Co-treatment with resveratrol, IC50 values of bestatin in K562/ADR cells significantly decreased and activation of caspase-3 and caspase-8 increased, which indicated that resveratrol potentiated bestatin-induced apoptosis.	Resveratrol	171-182	caspase 8	Homo sapiens	129-138
26998763-4	2016	Activation of T cell antigen receptors induced expression of pro-IL-1beta, whereas ATP stimulation triggered T cell production of IL-1beta via ASC-NLRP3-dependent caspase-8 activation.	Adenosine Triphosphate	83-86	caspase 8	Homo sapiens	163-172
26662956-0	2016	Synergistic effect of fisetin combined with sorafenib in human cervical cancer HeLa cells through activation of death receptor-5 mediated caspase-8/caspase-3 and the mitochondria-dependent apoptotic pathway.	fisetin	22-29	caspase 8	Homo sapiens	138-147
26662956-0	2016	Synergistic effect of fisetin combined with sorafenib in human cervical cancer HeLa cells through activation of death receptor-5 mediated caspase-8/caspase-3 and the mitochondria-dependent apoptotic pathway.	Sorafenib	44-53	caspase 8	Homo sapiens	138-147
26662956-7	2016	Our study showed that the combination of fisetin and sorafenib exerted better synergistic effects in vitro and in vivo than either agent used alone against human cervical cancer, and this synergism was based on apoptotic potential through a mitochondrial- and DR5-dependent caspase-8/caspase-3 signaling pathway.	fisetin	41-48	caspase 8	Homo sapiens	274-283
26662956-7	2016	Our study showed that the combination of fisetin and sorafenib exerted better synergistic effects in vitro and in vivo than either agent used alone against human cervical cancer, and this synergism was based on apoptotic potential through a mitochondrial- and DR5-dependent caspase-8/caspase-3 signaling pathway.	Sorafenib	53-62	caspase 8	Homo sapiens	274-283
27101103-0	2016	Tyrosine Phosphorylation of Caspase-8 Abrogates Its Apoptotic Activity and Promotes Activation of c-Src.	Tyrosine	0-8	caspase 8	Homo sapiens	28-37
27101103-9	2016	Finally, we demonstrate that caspase-8 activity prevents its own tyrosine phosphorylation by Src.	Tyrosine	65-73	caspase 8	Homo sapiens	29-38
27101103-11	2016	Specifically, tyrosine phosphorylation by Src renders caspase-8 uncleavable and thereby inactive, and at the same time converts it to a Src activator.	Tyrosine	14-22	caspase 8	Homo sapiens	54-63
27064569-11	2016	Pre-treatment with caspase-8 inhibitor Z-IETD-FMK, or caspase-9 inhibitor Z-LEHD-FMK, attenuated the growth-inhibitory and apoptosis-inducing effects of DMQ and the fraction on HepG2 cells.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	39-49	caspase 8	Homo sapiens	19-28
27104510-6	2016	The western blot results revealed that exposure to UA was associated with decreased expression of the anti-apoptotic proteins Mcl-1, Bcl-xL, Bcl-2, and TCTP and increased expression of apoptosis-related proteins TNF-alpha, Fas, FADD, Bax, cleaved caspase-3, caspase-8, caspase-9, and PARP.	ursolic acid	51-53	caspase 8	Homo sapiens	258-267
27162720-8	2016	Moreover, FCM and ELISA assays revealed that 2.5 g/L pilocarpine also induced S phase arrest, PS externalization, MTP disruption, and caspase-8, -9 and -3 activation of the cells.	Pilocarpine	53-64	caspase 8	Homo sapiens	134-154
27064569-11	2016	Pre-treatment with caspase-8 inhibitor Z-IETD-FMK, or caspase-9 inhibitor Z-LEHD-FMK, attenuated the growth-inhibitory and apoptosis-inducing effects of DMQ and the fraction on HepG2 cells.	rubiadin	153-156	caspase 8	Homo sapiens	19-28
26769704-5	2016	Further studies showed that FBRA extract induced the cleavage of caspase-8, -9, and -3, and decreased Bcl-2 protein expression.	fbra	28-32	caspase 8	Homo sapiens	65-86
26894857-5	2016	In this study, we investigated the molecular mechanism of 14-3-3sigma function in gemcitabine resistance and found that 14-3-3sigma up-regulates YAP1 expression and then binds to YAP1 to inhibit gemcitabine-induced caspase 8 activation and apoptosis.	gemcitabine	82-93	caspase 8	Homo sapiens	215-224
26894857-5	2016	In this study, we investigated the molecular mechanism of 14-3-3sigma function in gemcitabine resistance and found that 14-3-3sigma up-regulates YAP1 expression and then binds to YAP1 to inhibit gemcitabine-induced caspase 8 activation and apoptosis.	gemcitabine	195-206	caspase 8	Homo sapiens	215-224
26769704-6	2016	Moreover, the expression of tBid, DR5, and Fas proteins was enhanced by FBRA extract, and the pretreatment with caspase-8 inhibitor, but not caspase-9 inhibitor, restored the reduction of the cell viability induced by FBRA extract.	tBID	28-32	caspase 8	Homo sapiens	112-121
26769704-6	2016	Moreover, the expression of tBid, DR5, and Fas proteins was enhanced by FBRA extract, and the pretreatment with caspase-8 inhibitor, but not caspase-9 inhibitor, restored the reduction of the cell viability induced by FBRA extract.	fbra	218-222	caspase 8	Homo sapiens	112-121
25266202-0	2016	Tetrandrine induces apoptosis Via caspase-8, -9, and -3 and poly (ADP ribose) polymerase dependent pathways and autophagy through beclin-1/ LC3-I, II signaling pathways in human oral cancer HSC-3 cells.	tetrandrine	0-11	caspase 8	Homo sapiens	34-55
26803534-7	2016	Caspase-8 activation subsequently results in cleavage of BH3 interacting-domain death agonist and loss of mitochondrial membrane potential causing secondary activation of caspase-9.	BH 3	57-60	caspase 8	Homo sapiens	0-9
27073499-0	2016	Hyperoside and rutin of Nelumbo nucifera induce mitochondrial apoptosis through a caspase-dependent mechanism in HT-29 human colon cancer cells.	hyperoside	0-10	caspase 8	Homo sapiens	82-89
26785286-10	2016	CONCLUSION: These data reveal that 5-FU-induced cellular apoptosis in corneal epithelial cells may be mediated through caspase-8, caspase-9, and mitochondria-regulated pathways, as well as by upregulation of p21 and downregulation of Bcl-2-dependent signal transduction pathways.	Fluorouracil	35-39	caspase 8	Homo sapiens	119-128
26995783-5	2016	Results from the molecular dynamics simulations show that the simulated mutants induce conformational, dynamical motions and interactions changes in the DR5 DD-FADD tetramer complex, including changes in a protein"s backbone flexibility, less exposure of FADD DED"s caspase-8 binding site, reduced H-bonding and hydrophobic contacts at the DR5 DD-FADD DD binding, altered distribution of the electrostatic potentials and correlated motions of residues, and reduced binding affinity of DR5 DD binding to FADD.	dd-fadd	157-164	caspase 8	Homo sapiens	266-275
26995783-5	2016	Results from the molecular dynamics simulations show that the simulated mutants induce conformational, dynamical motions and interactions changes in the DR5 DD-FADD tetramer complex, including changes in a protein"s backbone flexibility, less exposure of FADD DED"s caspase-8 binding site, reduced H-bonding and hydrophobic contacts at the DR5 DD-FADD DD binding, altered distribution of the electrostatic potentials and correlated motions of residues, and reduced binding affinity of DR5 DD binding to FADD.	fadd	160-164	caspase 8	Homo sapiens	266-275
26995783-5	2016	Results from the molecular dynamics simulations show that the simulated mutants induce conformational, dynamical motions and interactions changes in the DR5 DD-FADD tetramer complex, including changes in a protein"s backbone flexibility, less exposure of FADD DED"s caspase-8 binding site, reduced H-bonding and hydrophobic contacts at the DR5 DD-FADD DD binding, altered distribution of the electrostatic potentials and correlated motions of residues, and reduced binding affinity of DR5 DD binding to FADD.	dd-fadd	344-351	caspase 8	Homo sapiens	266-275
26995783-5	2016	Results from the molecular dynamics simulations show that the simulated mutants induce conformational, dynamical motions and interactions changes in the DR5 DD-FADD tetramer complex, including changes in a protein"s backbone flexibility, less exposure of FADD DED"s caspase-8 binding site, reduced H-bonding and hydrophobic contacts at the DR5 DD-FADD DD binding, altered distribution of the electrostatic potentials and correlated motions of residues, and reduced binding affinity of DR5 DD binding to FADD.	fadd	255-259	caspase 8	Homo sapiens	266-275
27150997-13	2016	CONCLUSION: The magnolol can significantly inhibit the proliferation of HL-60 cells and induce the apoptosis of HL-60 cells, which may occur through up-regulation of BAX, down-regulation of BCL-2 and the activation of caspases.	magnolol	16-24	caspase 8	Homo sapiens	218-226
26953890-5	2016	In addition, treatment with rubropunctatin alone or under light irradiation was found to induce apoptosis in HeLa cells via the mitochondrial pathway, including loss of mitochondrial membrane potential, activation of caspase-3, caspase-8, and caspase-9, and increase of the level of intracellular reactive oxygen species (ROS).	rubropunctatin	28-42	caspase 8	Homo sapiens	228-237
26842479-10	2016	Antagonizing BCL-2 with venetoclax derepresses this antagonism, resulting in death, preferentially in HIV DNA containing cells, since only these cells generate Casp8p41.	venetoclax	24-34	caspase 8	Homo sapiens	160-165
26375985-7	2016	A pan inhibitor of caspases, Z-VAD-FMK (20 muM), blocked caspase-mediated mitochondrial membrane depolarization.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	29-38	caspase 8	Homo sapiens	19-27
26757822-6	2016	Treatment with the deubiquitinase inhibitor PR-619 increased caspase-8 ubiquitination and caspase-8 enzymatic activity and sensitized normal fibroblasts to TRAIL-mediated apoptosis.	2,6-diaminopyridine-3,5-bis(thiocyanate)	44-50	caspase 8	Homo sapiens	61-70
26757822-6	2016	Treatment with the deubiquitinase inhibitor PR-619 increased caspase-8 ubiquitination and caspase-8 enzymatic activity and sensitized normal fibroblasts to TRAIL-mediated apoptosis.	2,6-diaminopyridine-3,5-bis(thiocyanate)	44-50	caspase 8	Homo sapiens	90-99
26960190-8	2016	Furthermore, CTS treatment activated caspase-3/caspase-8 and cleavage of poly (ADP-ribose) polymerase (PARP).	castanospermine	13-16	caspase 8	Homo sapiens	47-56
26971531-3	2016	Baicalein stimulated the expression of DR5, FasL, and FADD, and activated caspase-8 by reducing the levels of FLIPs (FLICE-inhibitory proteins).	baicalein	0-9	caspase 8	Homo sapiens	74-83
26971531-6	2016	In turn, baicalein increased the generation of reactive oxygen species (ROS); however, an ROS scavenger, N-acetylcysteine, notably attenuated baicalein-mediated loss of MMP and activation of caspases.	Reactive Oxygen Species	90-93	caspase 8	Homo sapiens	191-199
26971531-6	2016	In turn, baicalein increased the generation of reactive oxygen species (ROS); however, an ROS scavenger, N-acetylcysteine, notably attenuated baicalein-mediated loss of MMP and activation of caspases.	Acetylcysteine	105-121	caspase 8	Homo sapiens	191-199
26971531-6	2016	In turn, baicalein increased the generation of reactive oxygen species (ROS); however, an ROS scavenger, N-acetylcysteine, notably attenuated baicalein-mediated loss of MMP and activation of caspases.	baicalein	142-151	caspase 8	Homo sapiens	191-199
26800624-11	2016	The TPP-BLM treatment synergistically induced apoptosis through caspase-3, caspase-8 and caspase-9 activation, Bcl-2 upregulation and p53 overexpression.	tpp-blm	4-11	caspase 8	Homo sapiens	75-84
26883800-5	2016	Kaempferol was found to decrease the expression of Bcl-2 and increase the expressions of Bax, Fas, cleaved-caspase 3, cleaved-caspase 8, cleaved-caspase 9, and cleaved-PARP.	kaempferol	0-10	caspase 8	Homo sapiens	126-135
26718494-7	2016	The results showed that both BNMPH and its copper complex induced reactive oxygen species (ROS) generation, and caused upregulation of caspase 8 and Bax as well as the downregulation of Bcl-2, indicating that apoptosis was involved in the cytotoxic effects.	bnmph	29-34	caspase 8	Homo sapiens	135-144
26859520-7	2016	The decrease of sphingolipids reflected the lesions of cell membrane, and the up-regulation of sphingosine-1-phosphate indicated that TRAF2 and caspase-8 were likely to be activated by flexibilide and further caused cell apoptosis.	sphingosine 1-phosphate	95-118	caspase 8	Homo sapiens	144-153
26859520-7	2016	The decrease of sphingolipids reflected the lesions of cell membrane, and the up-regulation of sphingosine-1-phosphate indicated that TRAF2 and caspase-8 were likely to be activated by flexibilide and further caused cell apoptosis.	flexibilide	185-196	caspase 8	Homo sapiens	144-153
26332363-7	2016	MEAG also caused an increase in truncated Bid (t-Bid), cleaved caspase-8, and death receptor 5 (DR5).	meag	0-4	caspase 8	Homo sapiens	63-72
26332363-8	2016	Interestingly, withaferin A (WA), a bioactive component of MEAG, clearly induced apoptosis accompanied by upregulation of Bim, t-Bid, caspase-8, and DR5 similar to the effects of MEAG.	withaferin A	15-27	caspase 8	Homo sapiens	134-143
25502462-5	2016	Furthermore, UDCA amended alterations in Bax and Bcl-2 and reduced the activities of caspase-8, caspase-9, and caspase-3, indicating that it suppressed rotenone-induced apoptosis via modulating both intrinsic and extrinsic pathways.	Ursodeoxycholic Acid	13-17	caspase 8	Homo sapiens	85-94
26718494-7	2016	The results showed that both BNMPH and its copper complex induced reactive oxygen species (ROS) generation, and caused upregulation of caspase 8 and Bax as well as the downregulation of Bcl-2, indicating that apoptosis was involved in the cytotoxic effects.	Copper	43-49	caspase 8	Homo sapiens	135-144
26952131-4	2016	Furthermore, the activities of caspase-3, caspase-8 and caspase-9 and the levels of ROS and cytochrome c were gradually decreased with increasing concentrations of Ala, Cit, Pro and Ala10Pro4Cit1 (0.175-1.400 mM) in the  OH-induced carp erythrocytes.	Citrulline	169-172	caspase 8	Homo sapiens	42-51
26911899-6	2016	ALA-SDT activated the caspase-3 and caspase-8 pathways in foam cells, which is responsible for the switch from necroptosis to apoptosis.	ala-sdt	0-7	caspase 8	Homo sapiens	36-45
26911899-7	2016	The inhibition of either caspase-8 or caspase-3 abolished the anti-necroptotic effect of ALA-SDT.	ala-sdt	89-96	caspase 8	Homo sapiens	25-34
26911899-9	2016	Taken together, our data indicate that ALA-SDT mediates the switch from necroptosis to apoptosis by activating the caspase-3 and caspase-8 pathways and may improve the prognosis of atherosclerosis.	ala-sdt	39-46	caspase 8	Homo sapiens	129-138
26952131-0	2016	Data in the activities of caspases and the levels of reactive oxygen species and cytochrome c in the  OH-induced fish erythrocytes treated with alanine, citrulline, proline and their combination.	Alanine	144-151	caspase 8	Homo sapiens	26-34
26952131-0	2016	Data in the activities of caspases and the levels of reactive oxygen species and cytochrome c in the  OH-induced fish erythrocytes treated with alanine, citrulline, proline and their combination.	Citrulline	153-163	caspase 8	Homo sapiens	26-34
26952131-4	2016	Furthermore, the activities of caspase-3, caspase-8 and caspase-9 and the levels of ROS and cytochrome c were gradually decreased with increasing concentrations of Ala, Cit, Pro and Ala10Pro4Cit1 (0.175-1.400 mM) in the  OH-induced carp erythrocytes.	Proline	174-177	caspase 8	Homo sapiens	42-51
26952131-0	2016	Data in the activities of caspases and the levels of reactive oxygen species and cytochrome c in the  OH-induced fish erythrocytes treated with alanine, citrulline, proline and their combination.	Proline	165-172	caspase 8	Homo sapiens	26-34
26952131-1	2016	The present study explored the effects of alanine (Ala), citrulline (Cit), proline (Pro) and their combination (Ala10Pro4Cit1) on the activities of caspases and levels of reactive oxygen species (ROS) and cytochrome c in hydroxyl radicals ( OH)-induced carp erythrocytes.	Alanine	42-49	caspase 8	Homo sapiens	148-156
26952131-4	2016	Furthermore, the activities of caspase-3, caspase-8 and caspase-9 and the levels of ROS and cytochrome c were gradually decreased with increasing concentrations of Ala, Cit, Pro and Ala10Pro4Cit1 (0.175-1.400 mM) in the  OH-induced carp erythrocytes.	ala10pro4cit1	182-195	caspase 8	Homo sapiens	42-51
26952131-1	2016	The present study explored the effects of alanine (Ala), citrulline (Cit), proline (Pro) and their combination (Ala10Pro4Cit1) on the activities of caspases and levels of reactive oxygen species (ROS) and cytochrome c in hydroxyl radicals ( OH)-induced carp erythrocytes.	Alanine	51-54	caspase 8	Homo sapiens	148-156
26952131-1	2016	The present study explored the effects of alanine (Ala), citrulline (Cit), proline (Pro) and their combination (Ala10Pro4Cit1) on the activities of caspases and levels of reactive oxygen species (ROS) and cytochrome c in hydroxyl radicals ( OH)-induced carp erythrocytes.	Citrulline	57-67	caspase 8	Homo sapiens	148-156
26952131-1	2016	The present study explored the effects of alanine (Ala), citrulline (Cit), proline (Pro) and their combination (Ala10Pro4Cit1) on the activities of caspases and levels of reactive oxygen species (ROS) and cytochrome c in hydroxyl radicals ( OH)-induced carp erythrocytes.	Citrulline	69-72	caspase 8	Homo sapiens	148-156
26952131-5	2016	These data demonstrated that the 50% inhibitory doses (ID50) of Ala10Pro4Cit1 on the activities of caspase-8, caspase-9 and caspase-3 and levels of ROS and cytochrome c were respectively estimated to be the minimum values among amino acids examined so far.	ala10pro4cit1	64-77	caspase 8	Homo sapiens	99-108
26952131-1	2016	The present study explored the effects of alanine (Ala), citrulline (Cit), proline (Pro) and their combination (Ala10Pro4Cit1) on the activities of caspases and levels of reactive oxygen species (ROS) and cytochrome c in hydroxyl radicals ( OH)-induced carp erythrocytes.	Proline	75-82	caspase 8	Homo sapiens	148-156
26952131-1	2016	The present study explored the effects of alanine (Ala), citrulline (Cit), proline (Pro) and their combination (Ala10Pro4Cit1) on the activities of caspases and levels of reactive oxygen species (ROS) and cytochrome c in hydroxyl radicals ( OH)-induced carp erythrocytes.	Proline	84-87	caspase 8	Homo sapiens	148-156
26952131-1	2016	The present study explored the effects of alanine (Ala), citrulline (Cit), proline (Pro) and their combination (Ala10Pro4Cit1) on the activities of caspases and levels of reactive oxygen species (ROS) and cytochrome c in hydroxyl radicals ( OH)-induced carp erythrocytes.	ala10pro4cit1	112-125	caspase 8	Homo sapiens	148-156
26952131-3	2016	However, Ala, Cit, Pro and Ala10Pro4Cit1 effectively suppressed the  OH-induced increases in the activities of caspase-3, caspase-8 and caspase-9 and the levels of ROS and cytochrome c in carp erythrocytes.	Alanine	9-12	caspase 8	Homo sapiens	122-131
26952131-3	2016	However, Ala, Cit, Pro and Ala10Pro4Cit1 effectively suppressed the  OH-induced increases in the activities of caspase-3, caspase-8 and caspase-9 and the levels of ROS and cytochrome c in carp erythrocytes.	Citrulline	14-17	caspase 8	Homo sapiens	122-131
26952131-6	2016	The 5% inhibitory doses (ID5) of Ala, Cit, Pro and Ala10Pro4Cit1 on the activities of caspase-8, caspase-9 and caspase-3 and levels of ROS and cytochrome c were estimated to be at their physiological concentrations in mammalian.	Alanine	33-36	caspase 8	Homo sapiens	86-95
26952131-3	2016	However, Ala, Cit, Pro and Ala10Pro4Cit1 effectively suppressed the  OH-induced increases in the activities of caspase-3, caspase-8 and caspase-9 and the levels of ROS and cytochrome c in carp erythrocytes.	Proline	19-22	caspase 8	Homo sapiens	122-131
26952131-3	2016	However, Ala, Cit, Pro and Ala10Pro4Cit1 effectively suppressed the  OH-induced increases in the activities of caspase-3, caspase-8 and caspase-9 and the levels of ROS and cytochrome c in carp erythrocytes.	ala10pro4cit1	27-40	caspase 8	Homo sapiens	122-131
26952131-6	2016	The 5% inhibitory doses (ID5) of Ala, Cit, Pro and Ala10Pro4Cit1 on the activities of caspase-8, caspase-9 and caspase-3 and levels of ROS and cytochrome c were estimated to be at their physiological concentrations in mammalian.	Citrulline	38-41	caspase 8	Homo sapiens	86-95
26952131-4	2016	Furthermore, the activities of caspase-3, caspase-8 and caspase-9 and the levels of ROS and cytochrome c were gradually decreased with increasing concentrations of Ala, Cit, Pro and Ala10Pro4Cit1 (0.175-1.400 mM) in the  OH-induced carp erythrocytes.	Alanine	164-167	caspase 8	Homo sapiens	42-51
26952131-6	2016	The 5% inhibitory doses (ID5) of Ala, Cit, Pro and Ala10Pro4Cit1 on the activities of caspase-8, caspase-9 and caspase-3 and levels of ROS and cytochrome c were estimated to be at their physiological concentrations in mammalian.	Proline	43-46	caspase 8	Homo sapiens	86-95
26952131-6	2016	The 5% inhibitory doses (ID5) of Ala, Cit, Pro and Ala10Pro4Cit1 on the activities of caspase-8, caspase-9 and caspase-3 and levels of ROS and cytochrome c were estimated to be at their physiological concentrations in mammalian.	ala10pro4cit1	51-64	caspase 8	Homo sapiens	86-95
26796280-2	2016	Cisplatin may initiate p73-dependent apoptosis in p53 mutant cell lines through Fas trimerization and Caspase-8 activation and Bax up regulation and subsequent Caspase-9 activation.	Cisplatin	0-9	caspase 8	Homo sapiens	102-111
26692089-9	2016	Danazol had a caspase-dependent pro-apoptotic and cytotoxic effect on leukemic cells in a tumor-specific manner.	Danazol	0-7	caspase 8	Homo sapiens	14-21
26725849-3	2016	In addition, SH-6 induced an early apoptotic effect and activation of caspases as well as the cleavage of PARP, which is a hallmark of apoptosis.	sanguiin H 6	13-17	caspase 8	Homo sapiens	70-78
26796280-3	2016	The triple-negative breast cancer, MDA-MB-231, overexpresses the protein Lifeguard, which inhibits Fas-mediated apoptosis by inhibiting Caspase-8 activation after Fas trimerization.	ammonium ferrous sulfate	99-102	caspase 8	Homo sapiens	136-145
26796280-3	2016	The triple-negative breast cancer, MDA-MB-231, overexpresses the protein Lifeguard, which inhibits Fas-mediated apoptosis by inhibiting Caspase-8 activation after Fas trimerization.	ammonium ferrous sulfate	163-166	caspase 8	Homo sapiens	136-145
26796280-7	2016	Higher Caspase-8 activity in the Lifeguard knockdown MDA after cisplatin administration could explain the significant decrease in cell viability from 24 to 48h.	Cisplatin	63-72	caspase 8	Homo sapiens	7-16
26707875-8	2016	We observed that NDMP generation was dependent on the extrinsic caspase apoptotic pathway (caspase 3 and caspase 8), cAMP activation of PKA but not of Epac, and on activation of MLCK.	N-desmethylmethoxyphenamine	17-21	caspase 8	Homo sapiens	105-114
26676928-5	2016	The results demonstrated that the lower concentration of oridonin in combination with lower concentration of VPA synergistically inhibited the proliferation of HL-60 cells, and induced obvious caspase-dependent apoptosis through activation of the intrinsic apoptosis pathway, which is involved in the downregulation of Bcl-2/Bax ratio, release of cytochrome c to cytosol and caspase-9 activation, as well as through the extrinsic apoptosis pathway mediated by Fas/FasL and caspase-8 activation.	oridonin	57-65	caspase 8	Homo sapiens	473-482
26578299-7	2016	Besides its well-known inhibition on the mitochondria-dependent or intrinsic apoptotic pathway, isorhamnetin also reduced activation of the extrinsic apoptotic pathway, as characterized by the decreased expression and activity of caspase 3 and caspase 8.	3-methylquercetin	96-108	caspase 8	Homo sapiens	244-253
27627923-7	2016	The flow cytometric assay also showed that SFN induced the generation of reactive oxygen species (ROS) and Ca[Formula: see text] and decreased mitochondria membrane potential and increased caspase-8, -9 and -3 activities in HCT 116 cell.	sulforaphane	43-46	caspase 8	Homo sapiens	189-209
26794656-6	2016	Both compounds clearly inhibited the ability of E6 to bind in vitro to both caspase 8 and E6AP, the protein that mediates p53 degradation.	Polyurethane Y-290	48-50	caspase 8	Homo sapiens	76-85
27551490-7	2016	DBME induced G2/M phase arrest and apoptosis in MCF-7 cells by suppressing the expression of cyclin A1, cyclin B1 and Cdk-1 and increasing the expression of p53, Bax/Bcl-2 ratio leading to activation of caspases and PARP degradation.	dbme	0-4	caspase 8	Homo sapiens	203-211
27551490-8	2016	Presence of caspase-8 (Z-IETD-fmk) and caspase-9 (Z-LEHD-fmk) inhibitors alone did prevent the apoptosis partially while apoptosis prevention was significantly observed when used in combination, suggesting vital role of caspases in DBME-induced apoptosis in MCF-7 cells.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	23-33	caspase 8	Homo sapiens	12-21
27551490-8	2016	Presence of caspase-8 (Z-IETD-fmk) and caspase-9 (Z-LEHD-fmk) inhibitors alone did prevent the apoptosis partially while apoptosis prevention was significantly observed when used in combination, suggesting vital role of caspases in DBME-induced apoptosis in MCF-7 cells.	dbme	232-236	caspase 8	Homo sapiens	12-21
26711147-4	2016	Furthermore, ASA could up-regulate TNF-R1 and DR5 via activation of p38 MAPK, thereby activating caspase 8, revealing the death receptor pathway was also involved in this process.	Aspirin	13-16	caspase 8	Homo sapiens	97-106
27509924-0	2016	15d-PGJ2 Induces Apoptosis of MCF-7 and MDA-MB-231 Cells via Increased Intracellular Calcium and Activation of Caspases, Independent of ERalpha and ERbeta.	15-deoxyprostaglandin J2	0-8	caspase 8	Homo sapiens	111-119
25926385-6	2016	In contrast to LSGs, stimulation of SGECs with polyinosinic:cytidylic acid (poly I:C) significantly induced the expression of RIPK3, p-FADD, and cleaved caspase-8 by immunofluorescence and RIPK3, p-FADD, and cleaved caspase-3 by WB.	poly I:C	76-84	caspase 8	Homo sapiens	153-162
26204498-9	2016	The increased expression of CD95/CD95L and caspase-8 activity was abolished by Nomega-nitro-l-arginine methyl ester hydrochloride, p53 and CD95 small interfering RNA.	L-NAME hydrochloride	79-129	caspase 8	Homo sapiens	43-52
27404955-4	2016	6-Propargyl-9-trifluoromethylquinobenzothiazine was shown to block caspase 3 expression and inhibit expression of caspase 8 and 9 in Jurkat cells indicating its possible mechanism of action.	6-propargyl-9-trifluoromethylquinobenzothiazine	0-47	caspase 8	Homo sapiens	114-123
25926385-6	2016	In contrast to LSGs, stimulation of SGECs with polyinosinic:cytidylic acid (poly I:C) significantly induced the expression of RIPK3, p-FADD, and cleaved caspase-8 by immunofluorescence and RIPK3, p-FADD, and cleaved caspase-3 by WB.	polyinosinic	47-59	caspase 8	Homo sapiens	153-162
25926385-6	2016	In contrast to LSGs, stimulation of SGECs with polyinosinic:cytidylic acid (poly I:C) significantly induced the expression of RIPK3, p-FADD, and cleaved caspase-8 by immunofluorescence and RIPK3, p-FADD, and cleaved caspase-3 by WB.	Cytidine Monophosphate	60-74	caspase 8	Homo sapiens	153-162
27509965-9	2016	There was an increased expression of truncated Bid (tBid), which indicated caspase8 proteolysis activity in Bid cleavage as its substrate in the extrinsic pathway.	tBID	52-56	caspase 8	Homo sapiens	75-83
27509965-10	2016	In conclusion, naringin induces human hepatocellular carcinoma HepG2 cell apoptosis via mitochondriamediated activation of caspase9 and caspase8mediated proteolysis of Bid.	naringin	15-23	caspase 8	Homo sapiens	136-144
26628086-5	2016	Treatment with d28O-CM restrained cell cycle progression through G2 phase, elicited a caspase-8-driven apoptotic effect already after 5 h of culture, and down-regulated autophagosome accumulation and beclin-1 expression.	d28o	15-19	caspase 8	Homo sapiens	86-95
29431086-5	2016	Sorafenib reduces S-nitrosation of cell death receptors and caspase-3, triggering a switch to caspase-3 from caspase-8.	Sorafenib	0-9	caspase 8	Homo sapiens	109-118
26446980-5	2016	Mechanistic investigations revealed that ML-7 and quinocetone act in concert to trigger the cleavage of caspase-8 as well as Bax/Bcl-2 ratio up-regulation and subsequent cleavage of Bid, capsases-9 and -3.	quinocetone	50-61	caspase 8	Homo sapiens	104-113
26802648-8	2016	In conclusion, curcumin may act synergistically with the chemotherapeutic regimen FOLFOX in gastric cancer in vitro and in vivo by inducing apoptosis via Bcl/Bax-caspase 8,9-caspase 3 pathway.	Curcumin	15-23	caspase 8	Homo sapiens	162-171
26549417-0	2016	Harmine Hydrochloride Triggers G2 Phase Arrest and Apoptosis in MGC-803 Cells and SMMC-7721 Cells by Upregulating p21, Activating Caspase-8/Bid, and Downregulating ERK/Bad Pathway.	Harmine Hydrochloride	0-21	caspase 8	Homo sapiens	130-139
27259314-4	2015	Anisodamine treatment decreases the expression of caspase-3 and caspase-8, and increases Bcl-2/Bax ratio in cardiomyocytes.	anisodamine	0-11	caspase 8	Homo sapiens	64-73
26254612-0	2016	Ethylacetate extract from Tetrastigma hemsleyanum induces apoptosis via the mitochondrial caspase-dependent intrinsic pathway in HepG2 cells.	ethyl acetate	0-12	caspase 8	Homo sapiens	90-97
26469741-8	2015	Induction of apoptosis by SA-BA treatment increased pro-inflammatory cytokines, specifically potentiated TNF-alpha mediated cell death, confirmed by expression of caspase-8 and caspage-3 by immunocytochemistry.	sa-ba	26-31	caspase 8	Homo sapiens	163-172
26714174-7	2015	Pretreatment of the animals with ethylene glycol-bis-(b-aminoethyl ether)-N,N,N",N"-tetraacetic acid (EGTA), Ca2+ chelator, inhibited Cd-induced activation of caspases-3, -8 and -9 as well as blocked the Cd-triggered apoptotic DNA fragmentation.	ethylene glycol-bis-(b-aminoethyl ether)-n,n,n",n"-tetraacetic acid	33-100	caspase 8	Homo sapiens	159-180
26692822-13	2015	In addition, As2O3 in combination with 5-FU treatment caused up-regulation of DR5, caspase 3, caspase 8, and caspase 9, and down-regulation of BCL-2, but had no effect of DR4.	Arsenic Trioxide	13-18	caspase 8	Homo sapiens	94-103
26692822-13	2015	In addition, As2O3 in combination with 5-FU treatment caused up-regulation of DR5, caspase 3, caspase 8, and caspase 9, and down-regulation of BCL-2, but had no effect of DR4.	Fluorouracil	39-43	caspase 8	Homo sapiens	94-103
26456076-5	2015	Marizomib plus pomalidomide-induced apoptosis is associated with: (i) activation of caspase-8, caspase-9, caspase-3 and PARP cleavage, (ii) downregulation of cereblon (CRBN), IRF4, MYC and MCL1, and (iii) suppression of chymotrypsin-like, caspase-like, and trypsin-like proteasome activities.	marizomib	0-9	caspase 8	Homo sapiens	84-93
26456076-5	2015	Marizomib plus pomalidomide-induced apoptosis is associated with: (i) activation of caspase-8, caspase-9, caspase-3 and PARP cleavage, (ii) downregulation of cereblon (CRBN), IRF4, MYC and MCL1, and (iii) suppression of chymotrypsin-like, caspase-like, and trypsin-like proteasome activities.	pomalidomide	15-27	caspase 8	Homo sapiens	84-93
26502896-7	2015	Quantitative real-time PCR and western blotting found that beta-asarone significantly activated caspase-3, caspase-8, caspase-9, Bax, Bak and suppressed Bcl-2, Bcl-xL and survivin activity.	asarone	59-71	caspase 8	Homo sapiens	107-116
26706948-10	2015	In the mean time, thioridazine promoted the activities of Caspase-3, Caspase-8 and Caspase-9 (P&lt;0.01).	Thioridazine	18-30	caspase 8	Homo sapiens	69-78
26503508-4	2015	Berberine also induced the upregulation of apoptotic ligands, such as FasL and TNF-related apoptosis-inducing ligand, and triggered the activation of caspase-8, -7 and -3, and poly(ADP ribose) polymerase, characteristic of death receptor-dependent extrinsic apoptosis.	Berberine	0-9	caspase 8	Homo sapiens	150-170
26225731-8	2015	It depended on singlet oxygen-dependent activation of the FAS receptor and caspase-8, followed by caspase-8-mediated enhancement of NOX activity.	Singlet Oxygen	15-29	caspase 8	Homo sapiens	75-84
25916999-7	2015	Annexin V-PI staining and Western blot assays on PARP cleavage and caspase-8 and caspase-3 revealed that BIBR1532 in combination with paclitaxel was more potent than either agent alone in promoting MCF-7 cell apoptosis.	BIBR 1532	105-113	caspase 8	Homo sapiens	67-76
26884946-5	2015	The studies showed that Crocin induced apoptosis of MCF-7 cells partially through caspase-8 mediated mitochondrial pathway.	crocin	24-30	caspase 8	Homo sapiens	82-91
26517515-4	2015	GOS and VPA co-treatment induced robust apoptosis as evidenced by caspase-8/-9/-3 activation, PARP cleavage, and nuclear fragmentation.	Valproic Acid	8-11	caspase 8	Homo sapiens	66-75
27551472-9	2015	Combination treatment caused a synergistic downregulation of glutathione levels and increased DNA damage, driving apoptosis via caspase 8 and 9 activation.	Glutathione	61-72	caspase 8	Homo sapiens	128-137
26451628-7	2015	PCB29-pQ also induces apoptosis via the up-regulation of Fas/FasL and the activation of caspase 8/3.	2,3,5-trichloro-6-phenyl-(1,4)benzoquinone	0-8	caspase 8	Homo sapiens	88-97
24840272-8	2015	Results showed that cleavage of caspase-8 was inhibited by the presence of the inhibitor, Z-IETD-FMK, and this suggested the presence of Ni(2+)-induced U937 cell death through a death receptor-mediated pathway.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	90-100	caspase 8	Homo sapiens	32-41
26528725-4	2015	Salinomycin significantly induced anoikis-sensitivity, accompanied by caspase-3 and caspase-8 activation and PARP cleavage, during anchorage-independent growth.	salinomycin	0-11	caspase 8	Homo sapiens	84-93
26544184-5	2015	The decreased flux of glucose associated to caffeic acid affected HG induced apoptosis by down-regulating the expression of initiator (caspase 8 and 9) and effector caspases (caspase 7 and 3) and by increasing the levels of phosphorylated Bcl-2.	Glucose	22-29	caspase 8	Homo sapiens	135-190
26544184-5	2015	The decreased flux of glucose associated to caffeic acid affected HG induced apoptosis by down-regulating the expression of initiator (caspase 8 and 9) and effector caspases (caspase 7 and 3) and by increasing the levels of phosphorylated Bcl-2.	caffeic acid	44-56	caspase 8	Homo sapiens	135-190
26232616-0	2015	Ceramide generation during curcumin-induced apoptosis is controlled by crosstalk among Bcl-2, Bcl-xL, caspases and glutathione.	Ceramides	0-8	caspase 8	Homo sapiens	102-110
26232616-0	2015	Ceramide generation during curcumin-induced apoptosis is controlled by crosstalk among Bcl-2, Bcl-xL, caspases and glutathione.	Curcumin	27-35	caspase 8	Homo sapiens	102-110
26232616-5	2015	These data place nSMase activation downstream of caspase-8 and Bcl-xL and indicate a mutual regulation between nSMase and caspase-3 activity on one hand, and Bcl-2 level on the other hand in curcumin-treated cells.	Curcumin	191-199	caspase 8	Homo sapiens	49-58
26410814-6	2015	The fluorescence intensity of ROS and the activities of Caspase-3, Caspase-8, and Caspase-9 were increased.	ros	30-33	caspase 8	Homo sapiens	67-76
24840272-8	2015	Results showed that cleavage of caspase-8 was inhibited by the presence of the inhibitor, Z-IETD-FMK, and this suggested the presence of Ni(2+)-induced U937 cell death through a death receptor-mediated pathway.	Nickel(2+)	137-143	caspase 8	Homo sapiens	32-41
26485709-11	2015	According to the results, trabectedin induced cytotoxicity and apoptosis at the IC50 dose, resulting in a significant increase expression of caspase-3, caspase-8, caspase-9, p53 and decrease expression of bcl-2 in dose-dependent manner.	Trabectedin	26-37	caspase 8	Homo sapiens	152-161
26324225-5	2015	Furthermore, reverse transcription quantitative polymerase chain reaction and western blot analyses indicated that treatment with fucoidan (100 microg/ml for 48 h) activated Fas and caspase-8 in SKM-1 cells, which are critical for the extrinsic apoptotic pathway; furthermore, caspase-9 was activated via decreases in phosphoinositide-3 kinase/Akt signaling as indicated by reduced levels of phosphorylated Akt, suggesting the involvement of the intrinsic apoptotic pathway.	fucoidan	130-138	caspase 8	Homo sapiens	182-191
26352862-5	2015	The combination of genistein and TRAIL increased LC3-II, p62, activated caspase-3 and activated caspase-8 accumulation, confirming the inhibition of autophagic flux.	Genistein	19-28	caspase 8	Homo sapiens	96-105
26302991-3	2015	Our previous work shows that the apoptotic resistance of CTCL correlates with low expression of death receptors like Fas cell surface death receptor (FAS), and that methotrexate upregulates FAS by inhibiting the methylation of its promoter, acting as an epigenetic derepressor that restores the susceptibility of FAS-low CTCL to caspase-8-mediated apoptosis.	Methotrexate	165-177	caspase 8	Homo sapiens	329-338
26084607-5	2015	Reversely, the pan caspase inhibitor z-VAD-fmk and the caspase-8 inhibitor z-ITED-fmk alleviated ST-3595-mediated anti-pancreatic cancer activity in vitro.	z-ited-fmk	75-85	caspase 8	Homo sapiens	55-64
26084607-5	2015	Reversely, the pan caspase inhibitor z-VAD-fmk and the caspase-8 inhibitor z-ITED-fmk alleviated ST-3595-mediated anti-pancreatic cancer activity in vitro.	CHEMBL561209	97-104	caspase 8	Homo sapiens	55-64
26055088-4	2015	There is evidence that two single nucleotide polymorphisms (SNPs) within the CASP8 gene are associated with ATP, but only in populations from the Southern Hemisphere.	Adenosine Triphosphate	108-111	caspase 8	Homo sapiens	77-82
26055088-6	2015	We additionally sought to determine whether copy number variation (CNV) within the CASP8 gene was associated with ATP.	Adenosine Triphosphate	114-117	caspase 8	Homo sapiens	83-88
26500281-7	2015	Apigenin-induced extrinsic a caspase-dependent apoptosis up-regulating the levels of cleaved caspase-8 and cleaved caspase-3, and inducing the cleavage of poly (ADP-ribose) polymerase (PARP).	Apigenin	0-8	caspase 8	Homo sapiens	93-102
26492346-8	2015	PNAP-6h induced apoptosis, most likely by the promotion of Fas expression, increased PARP activity, caspase-7, caspase-8, and caspase-9 expression, the Bax/Bcl-2 ratio, and the phosphorylation of p38, and decreased the phosphorylation of ERK.	6H	5-7	caspase 8	Homo sapiens	111-120
26458812-10	2015	When compared within the control group, CASP8 -652 6 N ins + FasR-1377A showed a reduced risk (P = 0.023, CPS = -2.28) of HSV-2 infection in both black African and mixed-ancestry population.	cps	106-109	caspase 8	Homo sapiens	40-45
26102991-9	2015	The colchicine competition-binding experiments and computer modelling results suggested that WTC-01 causes microtubule disruption via binding to the colchicine-binding site of tubulin resulting in mitochondrial membrane damage and cell apoptosis via activation of caspase-9/-3 without noticeable activation of the caspase-8.	Colchicine	149-159	caspase 8	Homo sapiens	314-323
26426685-9	2015	This suggested that failure of the TRAIL receptor complex to transduce the death signal to Caspase-8 underlies AZD5582+TRAIL resistance.	N,N'-(2,2'-(hexa-2,4-diyne-1,6-diylbis(oxy))bis(2,3-dihydro-1H-indene-2,1-diyl))bis(1-(2-cyclohexyl-2-(2-(methylamino)propanamido)acetyl)pyrrolidine-2-carboxamide)	111-119	caspase 8	Homo sapiens	91-100
25916730-10	2015	CONCLUSIONS: A down-regulated expression of Casp8 compared with controls was observed (p = .014) in patients treated with bisphosphonates.	Diphosphonates	122-137	caspase 8	Homo sapiens	44-49
26300346-8	2015	Bufadienolide proscillaridin A, arenobufagin, and cardenolides evomonoside, convallatoxol and ouabain waged strongest apoptotic induction, associated with breakdown of mitochondrial membrane potential and activation of caspases -8 and -9.	bufadienolide	0-13	caspase 8	Homo sapiens	219-237
26300346-8	2015	Bufadienolide proscillaridin A, arenobufagin, and cardenolides evomonoside, convallatoxol and ouabain waged strongest apoptotic induction, associated with breakdown of mitochondrial membrane potential and activation of caspases -8 and -9.	Proscillaridin	14-30	caspase 8	Homo sapiens	219-237
26300346-8	2015	Bufadienolide proscillaridin A, arenobufagin, and cardenolides evomonoside, convallatoxol and ouabain waged strongest apoptotic induction, associated with breakdown of mitochondrial membrane potential and activation of caspases -8 and -9.	arenobufagin	32-44	caspase 8	Homo sapiens	219-237
26300346-8	2015	Bufadienolide proscillaridin A, arenobufagin, and cardenolides evomonoside, convallatoxol and ouabain waged strongest apoptotic induction, associated with breakdown of mitochondrial membrane potential and activation of caspases -8 and -9.	Cardenolides	50-62	caspase 8	Homo sapiens	219-237
26300346-8	2015	Bufadienolide proscillaridin A, arenobufagin, and cardenolides evomonoside, convallatoxol and ouabain waged strongest apoptotic induction, associated with breakdown of mitochondrial membrane potential and activation of caspases -8 and -9.	evomonoside	63-74	caspase 8	Homo sapiens	219-237
26164631-5	2015	On the other hand, high concentrations of 24S-OHC have been found to induce a type of nonapoptotic programmed cell death in neuronal cells expressing little caspase-8.	24-hydroxycholesterol	42-49	caspase 8	Homo sapiens	157-166
26300346-8	2015	Bufadienolide proscillaridin A, arenobufagin, and cardenolides evomonoside, convallatoxol and ouabain waged strongest apoptotic induction, associated with breakdown of mitochondrial membrane potential and activation of caspases -8 and -9.	Convallatoxol	76-89	caspase 8	Homo sapiens	219-237
26300346-8	2015	Bufadienolide proscillaridin A, arenobufagin, and cardenolides evomonoside, convallatoxol and ouabain waged strongest apoptotic induction, associated with breakdown of mitochondrial membrane potential and activation of caspases -8 and -9.	Ouabain	94-101	caspase 8	Homo sapiens	219-237
26112902-6	2015	Finally, the influence of novel platinum(II) complex (Pt12) used with anti-MUC1 on the concentration of selected markers of apoptosis such as Bax, caspase-8, -9, and caspase-3 was performed using ELISA.	pt12	54-58	caspase 8	Homo sapiens	147-160
26228523-6	2015	Apoptosis triggered by D-homoestrone develops through activation of the intrinsic pathway, as demonstrated by determination of the activities of caspase-8 and -9.	D-homoestrone	23-36	caspase 8	Homo sapiens	145-161
26216939-4	2015	Fingolimod also induces typical apoptotic features, including rapid externalization of phosphatidylserine and activation of caspase-8.	Fingolimod Hydrochloride	0-10	caspase 8	Homo sapiens	124-133
24962868-6	2015	6SG induced apoptosis as characterized by cleavage of PARP, accumulation of cells in subG1 phase, positive Annexin V binding, down-regulation of STAT3-regulated proteins, and activation of caspase-8, -9, -3 in both MDA-MB231 cells.	shogaol	0-3	caspase 8	Homo sapiens	189-198
26074357-0	2015	miR-130a activates apoptotic signaling through activation of caspase-8 in taxane-resistant prostate cancer cells.	taxane	74-80	caspase 8	Homo sapiens	61-70
26224159-5	2015	These results suggest that 3,4,5-tricaffeoylquinic acid may reduce TRAIL-induced apoptosis in human keratinocytes by suppressing the activation of the caspase-8 and Bid pathways and the mitochondria-mediated cell death pathway.	caffeoylquinic acid	27-55	caspase 8	Homo sapiens	151-160
26504757-0	2015	Doxorubicin Changes Bax /Bcl-xL Ratio, Caspase-8 and 9 in Breast Cancer Cells.	Doxorubicin	0-11	caspase 8	Homo sapiens	39-54
26052022-4	2015	All HAAs studied, and DCAA and DBAA in particular (at lower concentrations than those, which caused necrosis) induced apoptotic changes, which was confirmed by analysis of alterations in cell membrane permeability and caspase 8, 9 and 3 activation.	Dichloroacetic Acid	22-26	caspase 8	Homo sapiens	218-227
26052022-4	2015	All HAAs studied, and DCAA and DBAA in particular (at lower concentrations than those, which caused necrosis) induced apoptotic changes, which was confirmed by analysis of alterations in cell membrane permeability and caspase 8, 9 and 3 activation.	dibromoacetic acid	31-35	caspase 8	Homo sapiens	218-227
26491348-10	2015	The protein expressions of caspase-8, -3, and -9 were decreased in human anti-DR5 mAb-treated FLS in a dose-dependent manner through exposure to a caspase inhibitor, indicating that anti-DR5 mAb induction of apoptosis is through the caspase pathway.	CHEMBL1232769	94-97	caspase 8	Homo sapiens	27-48
26390405-5	2015	Moreover, the nucleosides were able to induce apoptosis as measured by an increase in caspase 8 and caspase 3 activity above that of the control.	Nucleosides	14-25	caspase 8	Homo sapiens	86-95
26393583-6	2015	The expression of Fas Ligand (FasL) protein was up-regulated dose dependently in Poncirin-treated AGS cells Moreover, Poncirin in AGS cells induced activation of Caspase-8 and -3, and subsequent cleavage of poly(ADP-ribose) polymerase (PARP).	poncirin	81-89	caspase 8	Homo sapiens	162-178
26337205-9	2015	Inhibiting glycolysis increased superoxide and blocked autophagy in apoptosis-resistant cells, causing p62-dependent caspase-8 activation.	Superoxides	32-42	caspase 8	Homo sapiens	117-126
26367393-12	2015	Meanwhile, both cleaved caspse-3 and caspase-8 are dramatically enhanced in SDT groups.	3,4-Dihydroxy-9,10-secoandrosta-1,3,5(10)-triene-9,17-dione	76-79	caspase 8	Homo sapiens	37-46
26504757-3	2015	The present study describes Bax, Bcl-xL gene expression and Caspase-8 and 9 protein levels in MCF-7 cells incubated with doxorubicin at different doses an incubation times.	Doxorubicin	121-132	caspase 8	Homo sapiens	60-75
26299580-5	2015	Mechanistic studies showed that anticancer activity of curcumin is associated with decrease in migration of HNSCC and associated angiogenesis through activating of intrinsic apoptotic pathway (caspase-9) and extrinsic apoptotic pathway (caspase-8).	Curcumin	55-63	caspase 8	Homo sapiens	237-246
26062076-8	2015	Furthermore, treatment with 6-acetoxy cyperene stimulated the activation of caspase-3, caspase-8 and caspase-9 and poly(ADP-ribose)polymerase in a dose-dependent manner.	6-acetoxy cyperene	28-46	caspase 8	Homo sapiens	87-96
26372842-3	2015	Data showed that H2 O2 enhanced Bax, caspase-3 and caspase-8 expression, and declined Bcl-2 expression.	Hydrogen Peroxide	17-22	caspase 8	Homo sapiens	51-60
26327534-8	2015	ACE/CS and ACE/S could also increase reactive oxygen species (ROS) generation, induce Fas/APO-1 (apoptosis antigen 1) expression and elevate the proteolytic activities of caspase-3, caspase-8 and caspase-9 in Hep G2 cells.	Cesium	4-6	caspase 8	Homo sapiens	182-191
26327534-8	2015	ACE/CS and ACE/S could also increase reactive oxygen species (ROS) generation, induce Fas/APO-1 (apoptosis antigen 1) expression and elevate the proteolytic activities of caspase-3, caspase-8 and caspase-9 in Hep G2 cells.	Sulfur	5-6	caspase 8	Homo sapiens	182-191
26287184-3	2015	Culture studies found that methyl sartortuoate inhibited colon cancer cell (LoVo and RKO) growth and caused apoptotic death in a concentration- and time-dependent manner, by activation of caspase-8, caspase-9, caspase-3, p53 and Bax, and inactivation of B-cell lymphoma 2 (Bcl-2) apoptosis regulating proteins.	methyl sartortuoate	27-46	caspase 8	Homo sapiens	188-197
26295969-6	2015	Quantitative PCR and Western Blot analysis showed that the two saponins significantly increased mRNA expression of FADD and BID as well as induced caspase-8 via increased of procaspase-8 processing in the treated cells.	Saponins	63-71	caspase 8	Homo sapiens	147-156
26287184-9	2015	Taken together, these findings suggest that methyl sartortuoate is capable of leading to activation of caspase-8, -9, -3, increasing p53 and Bax/Bcl-2 ratio apoptosis through MAPK-dependent apoptosis and results in G2-M phase arrest in LoVo and RKO cells.	methyl sartortuoate	44-63	caspase 8	Homo sapiens	103-120
26036637-4	2015	Sequential application of erlotinib and doxorubicin increased activated caspase-8 by promoting pro-caspase-8 homodimerization and autocatalytical cleavage, whereas coadministration did not.	Erlotinib Hydrochloride	26-35	caspase 8	Homo sapiens	72-81
26043797-6	2015	Apoptosis induced by MHY218 was involved in the activation of caspase-8, -9, and -3, and it was blocked by the addition of Z-VAD-FMK, a pan-caspase inhibitor.	N1-hydroxy-N8-(4-phenoxyphenyl)octanediamide	21-27	caspase 8	Homo sapiens	62-83
26043797-6	2015	Apoptosis induced by MHY218 was involved in the activation of caspase-8, -9, and -3, and it was blocked by the addition of Z-VAD-FMK, a pan-caspase inhibitor.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	123-132	caspase 8	Homo sapiens	62-83
25684371-4	2015	Caspase-8 was also activated after both MWCNTs exposure, indicating extrinsic apoptotic pathway was involved in the apoptosis induced by MWCNTs exposure, more importantly, MWCNTs-COOH significantly reduced the activation of caspase-8 as compared with p-MWCNTs.	Carbonic Acid	179-183	caspase 8	Homo sapiens	0-9
25684371-4	2015	Caspase-8 was also activated after both MWCNTs exposure, indicating extrinsic apoptotic pathway was involved in the apoptosis induced by MWCNTs exposure, more importantly, MWCNTs-COOH significantly reduced the activation of caspase-8 as compared with p-MWCNTs.	Carbonic Acid	179-183	caspase 8	Homo sapiens	224-233
26314429-0	2015	[Effect of Recombinant Adenovirus AdE-SH2-Caspase 8 on the Apoptosis of Imatinib-resistant K562/G01 Cell Line].	Imatinib Mesylate	72-80	caspase 8	Homo sapiens	42-51
26314429-1	2015	OBJECTIVE: To investigate the effect of SH2-Caspase 8 fusion protein expressed by recombinant adenovirus AdE-SH2-Caspase8-HA-GFP (SC) on the apoptosis of K562/G01 cell line, which is a BCR/ABL positive chronic myeloid leukemia cell line and resistant to imatinib.	Imatinib Mesylate	254-262	caspase 8	Homo sapiens	44-53
26220626-14	2015	CONCLUSION: The current study strongly reveals that rosamultic acid inhibits gastric cancer proliferation by inducing apoptosis mediated through cell cycle arrest, downregulation of cell cycle related protein expressions, inhibition of cell migration, DNA damage, and activation of caspases.	rosamultic acid	52-67	caspase 8	Homo sapiens	282-290
26013168-10	2015	Although gemcitabine activated both caspase-8 (CASP8) and caspase-9 (CASP9), the effect of PTK6 on gemcitabine-induced apoptosis required CASP8 but not CASP9.	gemcitabine	9-20	caspase 8	Homo sapiens	36-45
26013168-10	2015	Although gemcitabine activated both caspase-8 (CASP8) and caspase-9 (CASP9), the effect of PTK6 on gemcitabine-induced apoptosis required CASP8 but not CASP9.	gemcitabine	9-20	caspase 8	Homo sapiens	47-52
26013168-10	2015	Although gemcitabine activated both caspase-8 (CASP8) and caspase-9 (CASP9), the effect of PTK6 on gemcitabine-induced apoptosis required CASP8 but not CASP9.	gemcitabine	99-110	caspase 8	Homo sapiens	138-143
26622554-6	2015	Furthermore, the caspase-3, caspase-8 and caspase-9 activities in etoposide-induced apoptosis demonstrated a greater increase upon neuraminidase pretreatment compared with no neuraminidase pretreatment.	Etoposide	66-75	caspase 8	Homo sapiens	28-37
25930665-6	2015	alpha-H induced activation of caspase-8 and caspase-9 and also increased levels of the proapoptotic protein Bax, decreasing antiapoptotic proteins (Bcl-2, X-IAP and IAP-1) in HepG2 cells.	alpha-h	0-7	caspase 8	Homo sapiens	30-39
25930665-7	2015	Specific inhibition of caspase-8 abrogated the cascade of caspase activation, suggesting that the extrinsic pathway has a critical role in the apoptotic events induced by alpha-H.	alpha-h	171-178	caspase 8	Homo sapiens	23-32
25930665-7	2015	Specific inhibition of caspase-8 abrogated the cascade of caspase activation, suggesting that the extrinsic pathway has a critical role in the apoptotic events induced by alpha-H.	alpha-h	171-178	caspase 8	Homo sapiens	23-30
25930665-8	2015	Furthermore, combined treatment of alpha-H with TRAIL enhanced apoptosis in HepG2 cells, activating caspase-8 and caspase-9.	alpha-h	35-42	caspase 8	Homo sapiens	100-109
25930665-11	2015	Our results demonstrate that alpha-H induced apoptosis in the human hepatocellular carcinoma cell line HepG2 through activation of caspases and induction of the death receptor pathway.	alpha-h	29-36	caspase 8	Homo sapiens	131-139
26226135-5	2015	GBM-ganglioside induced activation of the effector caspase-3 along with both initiator caspases (-9 and -8) in T cells while both the caspase-8 and -9 inhibitors were equally effective in blocking apoptosis (60% protection) confirming the role of caspases in the apoptotic process.	gbm-ganglioside	0-15	caspase 8	Homo sapiens	87-95
26226135-9	2015	Thus, GBM-ganglioside can mediate T cell apoptosis by interacting with the TNF receptor followed by activation of both the extrinsic and the intrinsic pathway of caspases.	gbm-ganglioside	6-21	caspase 8	Homo sapiens	162-170
26205793-9	2015	Protein analysis using Western blotting confirmed that FasL-induced cleavage/activation of caspase-8 and caspase-3, were inhibited by DC treatment at low concentration (0.5 microg/mL).	Doxycycline	134-136	caspase 8	Homo sapiens	91-100
26379864-7	2015	Further Western blot assays showed that rapamycin induced activation of caspase-9 and caspase-8 and the cleavage of caspase-3.	Sirolimus	40-49	caspase 8	Homo sapiens	86-95
26036637-4	2015	Sequential application of erlotinib and doxorubicin increased activated caspase-8 by promoting pro-caspase-8 homodimerization and autocatalytical cleavage, whereas coadministration did not.	Erlotinib Hydrochloride	26-35	caspase 8	Homo sapiens	99-108
26036637-4	2015	Sequential application of erlotinib and doxorubicin increased activated caspase-8 by promoting pro-caspase-8 homodimerization and autocatalytical cleavage, whereas coadministration did not.	Doxorubicin	40-51	caspase 8	Homo sapiens	72-81
26036637-4	2015	Sequential application of erlotinib and doxorubicin increased activated caspase-8 by promoting pro-caspase-8 homodimerization and autocatalytical cleavage, whereas coadministration did not.	Doxorubicin	40-51	caspase 8	Homo sapiens	99-108
25138434-3	2015	Results from Western blot and flow cytometric assays revealed that quercetin significantly induced caspase-8, caspase-9, and caspase-3 activation, poly ADP-ribose polymerase (PARP) cleavage, and mitochondrial membrane depolarization in HL-60 AML cells.	Quercetin	67-76	caspase 8	Homo sapiens	99-108
25894537-6	2015	Increased caspase-8 and -9 activation was induced by cisplatin in C2 as compared to NT3 cells.	Cisplatin	53-62	caspase 8	Homo sapiens	10-26
25740014-6	2015	Treatment of SK-N-BE2 and IMR-32 cells with 75 muMu wogonin for 48 h significantly promoted apoptosis, the release of cytochrome c, altered the expression of certain members of Bcl-2 family (Bcl-2, Bax and Bid), and increased the activation of caspase-3, caspase-8, caspase-9, and PARP-1, which demonstrated that the cytotoxic effect of wogonin in SK-N-BE2 and IMR-32 cells is mediated by mitochondrial dysfunction.	sk-n-be2	13-21	caspase 8	Homo sapiens	255-264
26339347-7	2015	In SU1498 treated cells, caspase 3 activity was detected 3 hours after the treatment, while activation of caspase 8 and 9 was detected 48 hours later.	SU 1498	3-9	caspase 8	Homo sapiens	106-121
25740014-6	2015	Treatment of SK-N-BE2 and IMR-32 cells with 75 muMu wogonin for 48 h significantly promoted apoptosis, the release of cytochrome c, altered the expression of certain members of Bcl-2 family (Bcl-2, Bax and Bid), and increased the activation of caspase-3, caspase-8, caspase-9, and PARP-1, which demonstrated that the cytotoxic effect of wogonin in SK-N-BE2 and IMR-32 cells is mediated by mitochondrial dysfunction.	wogonin	52-59	caspase 8	Homo sapiens	255-264
25954945-4	2015	The activation of caspase-8 and -9 was observed as early as 1-h post-exposure to delphinidin, followed by the activation of caspase-3 from 3-h post-exposure.	delphinidin	81-92	caspase 8	Homo sapiens	18-34
25815518-9	2015	VPA and ATO had synergistic effects on the proliferation of RPMI8226 cells, which may have been associated with the decreased expression of Bcl-2 and the increased expression levels of Bcl-2-associated X protein, Caspase 8 and Caspase 9.	Valproic Acid	0-3	caspase 8	Homo sapiens	213-222
25815518-9	2015	VPA and ATO had synergistic effects on the proliferation of RPMI8226 cells, which may have been associated with the decreased expression of Bcl-2 and the increased expression levels of Bcl-2-associated X protein, Caspase 8 and Caspase 9.	Arsenic Trioxide	8-11	caspase 8	Homo sapiens	213-222
25697054-2	2015	We have previously reported that 24S-OHC induces a type of non-apoptotic programmed necrosis in neuronal cells expressing little caspase-8.	24-hydroxycholesterol	33-40	caspase 8	Homo sapiens	129-138
26171069-7	2015	Furthermore, enhanced protein expression of caspase-8 and -9, in line with the significantly increased caspase-3 activation, was detected when the cells were treated with a combination of cisplatin and bortezomib, compared with that of either agent alone.	Cisplatin	188-197	caspase 8	Homo sapiens	44-60
26171069-7	2015	Furthermore, enhanced protein expression of caspase-8 and -9, in line with the significantly increased caspase-3 activation, was detected when the cells were treated with a combination of cisplatin and bortezomib, compared with that of either agent alone.	Bortezomib	202-212	caspase 8	Homo sapiens	44-60
26122204-0	2015	Water extract of brewers" rice induces apoptosis in human colorectal cancer cells via activation of caspase-3 and caspase-8 and downregulates the Wnt/beta-catenin downstream signaling pathway in brewers" rice-treated rats with azoxymethane-induced colon carcinogenesis.	Water	0-5	caspase 8	Homo sapiens	114-123
25978330-9	2015	In addition, SA and SB also prevented UVB-induced cell apoptosis and the cleavage of caspase-3, caspase-8 and caspase-9.	2-chloro-10-(4'(N-beta-hydroxyethyl)piperazinyl-1')acetylphenothiazine	13-15	caspase 8	Homo sapiens	96-105
26111690-9	2015	Western blotting showed that lonidamine up-regulated the expression of GRP78, down-regulated the expression of cIAP1 and promoted caspase-8 activation as the treatment time extended.	lonidamine	29-39	caspase 8	Homo sapiens	130-139
26111690-10	2015	CONCLUSION: Lonidamine can inhibit the proliferation and induce apoptosis in MCF-7 cells, and these effects are probably mediated by reducing ATP level, inducing endoplasmic reticulum stress response, down-regulating cIAP1, and promoting caspase-8 activation in the cells.	lonidamine	12-22	caspase 8	Homo sapiens	238-247
26034354-12	2015	Levels of caspase-8, -9 and -3 mRNAs were significantly increased after treatment with GA (1.25, 2.50 or 5.00 mumol/L) for 48 h (P &lt; 0.05 for all).	gambogic acid	87-89	caspase 8	Homo sapiens	10-30
25639670-0	2015	Cobalt oxide nanoparticles induced oxidative stress linked to activation of TNF-alpha/caspase-8/p38-MAPK signaling in human leukemia cells.	cobalt oxide	0-12	caspase 8	Homo sapiens	86-95
25639670-8	2015	This study showed that CoO NPs induced oxidative stress and activated the signaling pathway of TNF-alpha-Caspase-8-p38-Caspase-3 to cancer cells.	coo nps	23-30	caspase 8	Homo sapiens	105-114
25978330-9	2015	In addition, SA and SB also prevented UVB-induced cell apoptosis and the cleavage of caspase-3, caspase-8 and caspase-9.	schizandrin B	20-22	caspase 8	Homo sapiens	96-105
24249517-0	2015	Osteopontin mediates tumorigenic transformation of a preneoplastic murine cell line by suppressing anoikis: an Arg-Gly-Asp-dependent-focal adhesion kinase-caspase-8 axis.	Arginine	111-114	caspase 8	Homo sapiens	155-164
25939870-4	2015	This involves the depletion of the ubiquitine ligases cIAP2 and XIAP and leads to the association of RIP1 to caspase-8 and FADD.	ubiquitine	35-45	caspase 8	Homo sapiens	109-118
25751739-5	2015	Additionally, galactose enhanced expression of the anti-apoptotic genes, c-IAP1 and A20, and inhibited cleavage of caspase-8 and caspase-3.	Galactose	14-23	caspase 8	Homo sapiens	115-124
25770930-5	2015	In addition, combination of chrysin and cisplatin promoted both extrinsic apoptosis by activating caspase-8 and intrinsic apoptosis by increasing the release of cytochrome c and activating caspase-9 in Hep G2 cells.	Cisplatin	40-49	caspase 8	Homo sapiens	98-107
25951128-0	2015	Anticancer Effect of Ursodeoxycholic Acid in Human Oral Squamous Carcinoma HSC-3 Cells through the Caspases.	Ursodeoxycholic Acid	21-41	caspase 8	Homo sapiens	99-107
25829127-6	2015	Through Western blotting, activity analysis of caspase-3, caspase-8 and caspase-9 and mitochondrial membrane potential measurement, the apoptosis induced by PEN-mediated p53 transfection was conducted in a mitochondria-dependent apoptosis pathway.	Polyethyleneimine	157-160	caspase 8	Homo sapiens	58-67
24249517-0	2015	Osteopontin mediates tumorigenic transformation of a preneoplastic murine cell line by suppressing anoikis: an Arg-Gly-Asp-dependent-focal adhesion kinase-caspase-8 axis.	Aspartic Acid	119-122	caspase 8	Homo sapiens	155-164
24249517-9	2015	Transfection studies with wild-type and mutant focal adhesion kinases (FAK) and Western blot analyses suggest that OPN suppression of caspase-8 activation is mediated through phosphorylation of FAK at Tyr(861).	Tyrosine	201-204	caspase 8	Homo sapiens	134-143
25915766-7	2015	Similar to cell proliferation, GSH, NAC and L-cysteine but not D-cysteine, completely restored the processing of caspase-8 and caspase-3 to their respective subunits in z-FA-FMK-treated activated T cells.	Glutathione	31-34	caspase 8	Homo sapiens	113-122
25915766-7	2015	Similar to cell proliferation, GSH, NAC and L-cysteine but not D-cysteine, completely restored the processing of caspase-8 and caspase-3 to their respective subunits in z-FA-FMK-treated activated T cells.	Acetylcysteine	36-39	caspase 8	Homo sapiens	113-122
25915766-7	2015	Similar to cell proliferation, GSH, NAC and L-cysteine but not D-cysteine, completely restored the processing of caspase-8 and caspase-3 to their respective subunits in z-FA-FMK-treated activated T cells.	Cysteine	44-54	caspase 8	Homo sapiens	113-122
25915766-7	2015	Similar to cell proliferation, GSH, NAC and L-cysteine but not D-cysteine, completely restored the processing of caspase-8 and caspase-3 to their respective subunits in z-FA-FMK-treated activated T cells.	MDL 201053	169-177	caspase 8	Homo sapiens	113-122
25906152-6	2015	5-FU treatment led to the formation of a z-VAD-resistant pro-caspase-8/RIP1/FADD complex, which was strongly stabilized by caspase-3 KO.	Fluorouracil	0-4	caspase 8	Homo sapiens	61-70
25906152-6	2015	5-FU treatment led to the formation of a z-VAD-resistant pro-caspase-8/RIP1/FADD complex, which was strongly stabilized by caspase-3 KO.	z-vad	41-46	caspase 8	Homo sapiens	61-70
25897357-11	2015	Antioxidants, such as thioredoxin, which inhibits the ASK1-FoxO3a-caspase 8 pathway or ER stress inhibitors, may prevent PGD-induced birth defects.	pgd	121-124	caspase 8	Homo sapiens	66-75
25670618-5	2015	CIB activated both intrinsic and extrinsic pathways of apoptosis via caspase-9 and caspase-8 activation respectively, followed by caspase-3 activation, apoptotic body, nucleosomal ladder formation and sub-G1 accumulation.	cib	0-3	caspase 8	Homo sapiens	83-92
25960227-5	2015	Alternatively, caspases inhibitors could lead to the disappearance of MHMD-eliciting nuclei fragmentation by Hoechst 33342 staining.	bisbenzimide ethoxide trihydrochloride	109-122	caspase 8	Homo sapiens	15-23
25647297-0	2015	(-)-Epigallocatechingallate induces apoptosis in B lymphoma cells via caspase-dependent pathway and Bcl-2 family protein modulation.	epigallocatechin gallate	0-27	caspase 8	Homo sapiens	70-77
25619142-6	2015	Singlet-oxygen-dependent activation of the FAS receptor and caspase-8 increased superoxide anion generation by NOX1 and amplification of singlet oxygen generation, which allowed singlet-oxygen-dependent inactivation of catalase.	singlet	0-7	caspase 8	Homo sapiens	60-69
25619142-6	2015	Singlet-oxygen-dependent activation of the FAS receptor and caspase-8 increased superoxide anion generation by NOX1 and amplification of singlet oxygen generation, which allowed singlet-oxygen-dependent inactivation of catalase.	Oxygen	8-14	caspase 8	Homo sapiens	60-69
25619142-6	2015	Singlet-oxygen-dependent activation of the FAS receptor and caspase-8 increased superoxide anion generation by NOX1 and amplification of singlet oxygen generation, which allowed singlet-oxygen-dependent inactivation of catalase.	Superoxides	80-96	caspase 8	Homo sapiens	60-69
25619142-6	2015	Singlet-oxygen-dependent activation of the FAS receptor and caspase-8 increased superoxide anion generation by NOX1 and amplification of singlet oxygen generation, which allowed singlet-oxygen-dependent inactivation of catalase.	Singlet Oxygen	137-151	caspase 8	Homo sapiens	60-69
25619142-6	2015	Singlet-oxygen-dependent activation of the FAS receptor and caspase-8 increased superoxide anion generation by NOX1 and amplification of singlet oxygen generation, which allowed singlet-oxygen-dependent inactivation of catalase.	singlet	137-144	caspase 8	Homo sapiens	60-69
25619142-6	2015	Singlet-oxygen-dependent activation of the FAS receptor and caspase-8 increased superoxide anion generation by NOX1 and amplification of singlet oxygen generation, which allowed singlet-oxygen-dependent inactivation of catalase.	Oxygen	145-151	caspase 8	Homo sapiens	60-69
25434584-10	2015	Icaritin also activated the Fas-mediated apoptosis pathway, as was evident by the increased expression levels of Fas and activation of caspase-8.	icaritin	0-8	caspase 8	Homo sapiens	135-144
25434584-10	2015	Icaritin also activated the Fas-mediated apoptosis pathway, as was evident by the increased expression levels of Fas and activation of caspase-8.	ammonium ferrous sulfate	28-31	caspase 8	Homo sapiens	135-144
25886453-8	2015	Moreover, co-activation of the caspase-8/cellular FLICE-inhibitory protein (cFLIP)- and caspase-9/p-PTEN/p-AKT-dependent apoptotic pathways by aloperine caused irreversible inhibition of clonogenic survival.	aloperine	143-152	caspase 8	Homo sapiens	31-40
25653236-9	2015	This allows the formation of extracellular singlet oxygen through the reaction between H(2)O(2) and peroxynitrite, amplification through a caspase8-dependent step and subsequent singlet oxygen-mediated inactivation of catalase.	Singlet Oxygen	43-57	caspase 8	Homo sapiens	139-147
25521557-8	2015	The release of caspase-3, caspase-8, and caspase-9 was stimulated by AG4 in CNE, and the decreased proliferation induced by AG4 was blocked by the inhibitor of pan caspase (Z-VAD-FMK).	CHEMBL1099124	69-72	caspase 8	Homo sapiens	26-35
25521557-8	2015	The release of caspase-3, caspase-8, and caspase-9 was stimulated by AG4 in CNE, and the decreased proliferation induced by AG4 was blocked by the inhibitor of pan caspase (Z-VAD-FMK).	CHEMBL1099124	69-72	caspase 8	Homo sapiens	15-22
25521557-8	2015	The release of caspase-3, caspase-8, and caspase-9 was stimulated by AG4 in CNE, and the decreased proliferation induced by AG4 was blocked by the inhibitor of pan caspase (Z-VAD-FMK).	CHEMBL1099124	124-127	caspase 8	Homo sapiens	15-22
25521557-8	2015	The release of caspase-3, caspase-8, and caspase-9 was stimulated by AG4 in CNE, and the decreased proliferation induced by AG4 was blocked by the inhibitor of pan caspase (Z-VAD-FMK).	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	173-182	caspase 8	Homo sapiens	26-35
25521557-8	2015	The release of caspase-3, caspase-8, and caspase-9 was stimulated by AG4 in CNE, and the decreased proliferation induced by AG4 was blocked by the inhibitor of pan caspase (Z-VAD-FMK).	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	173-182	caspase 8	Homo sapiens	15-22
25653236-9	2015	This allows the formation of extracellular singlet oxygen through the reaction between H(2)O(2) and peroxynitrite, amplification through a caspase8-dependent step and subsequent singlet oxygen-mediated inactivation of catalase.	Hydrogen Peroxide	87-95	caspase 8	Homo sapiens	139-147
25653236-9	2015	This allows the formation of extracellular singlet oxygen through the reaction between H(2)O(2) and peroxynitrite, amplification through a caspase8-dependent step and subsequent singlet oxygen-mediated inactivation of catalase.	Peroxynitrous Acid	100-113	caspase 8	Homo sapiens	139-147
25653236-9	2015	This allows the formation of extracellular singlet oxygen through the reaction between H(2)O(2) and peroxynitrite, amplification through a caspase8-dependent step and subsequent singlet oxygen-mediated inactivation of catalase.	Singlet Oxygen	178-192	caspase 8	Homo sapiens	139-147
26045757-12	2015	Moreover, PAL administration significantly decreased the mRNA and proteins expression of Bcl-2 as well as increased the mRNA expression of BAX and the protein expression of caspase-3 and caspase-8 as compare to those of control group, but APS treatment could reverse PA-induced HCMs apoptosis.	Protactinium	10-12	caspase 8	Homo sapiens	187-196
25721485-12	2015	In summary, we report that Epothilone B induces apoptosis in OV-90 cells via a TRAIL and caspase 8-dependent pathway.	epothilone B	27-39	caspase 8	Homo sapiens	89-98
25586525-10	2015	Inhibition of p38 MAPK decreased ROS production, and inhibition of either p38 MAPK or ROS production attenuated apoptotic cell death and activation of caspase-8 and -9.	Reactive Oxygen Species	86-89	caspase 8	Homo sapiens	151-167
25373554-6	2015	The results demonstrated that baicalein inhibits the proliferation of HeLa cells and induces apoptosis in a caspase-3-dependent pathway, through downregulation of the B-cell lymphoma 2 (Bcl-2) protein and upregulation of the Bcl-2-associated X protein (Bax), Fas, Fas ligand (FasL) and caspase-8.	baicalein	30-39	caspase 8	Homo sapiens	286-295
26273359-8	2015	Furthermore, the treatment of A549 cells with TSA and cisplatin resulted in a significant decrease of pro-caspase-8 and a significant increase of caspase-8.	trichostatin A	46-49	caspase 8	Homo sapiens	106-115
25330024-0	2015	Nuclear receptor subfamily 4, group A, member 1 inhibits extrinsic apoptosis and reduces caspase-8 activity in H2O2-induced human HUC-F2 fibroblasts.	Hydrogen Peroxide	111-115	caspase 8	Homo sapiens	89-98
25330024-11	2015	Moreover inhibition of NR4A1 with specific siRNA in HUC-F2 cells triggered an increase in apoptosis and caspase-8 and -3 activities following the addition of H2O2.	Hydrogen Peroxide	158-162	caspase 8	Homo sapiens	104-120
25384757-7	2015	Characterization of polysaccharide-treated MDA-MB-231 cell death revealed that induction of apoptosis occurred via the activation of the extrinsic apoptotic caspase-8 gene.	Polysaccharides	20-34	caspase 8	Homo sapiens	157-166
26273359-8	2015	Furthermore, the treatment of A549 cells with TSA and cisplatin resulted in a significant decrease of pro-caspase-8 and a significant increase of caspase-8.	trichostatin A	46-49	caspase 8	Homo sapiens	146-155
26273359-8	2015	Furthermore, the treatment of A549 cells with TSA and cisplatin resulted in a significant decrease of pro-caspase-8 and a significant increase of caspase-8.	Cisplatin	54-63	caspase 8	Homo sapiens	106-115
26273359-8	2015	Furthermore, the treatment of A549 cells with TSA and cisplatin resulted in a significant decrease of pro-caspase-8 and a significant increase of caspase-8.	Cisplatin	54-63	caspase 8	Homo sapiens	146-155
25695505-11	2015	Collectively, these data suggest that caspase-4 activity is required for Fas-induced cell apoptosis and caspase-4 may act upstream of PARP and caspase-3 and downstream of caspase-8.	ammonium ferrous sulfate	73-76	caspase 8	Homo sapiens	171-180
25759589-4	2015	Treatment with EGCG activates the expression of the BAD, BAK, FAS, IGF1R, WNT11, and ZEB1 genes and inhibits CASP8, MYC, and TP53.	epigallocatechin gallate	15-19	caspase 8	Homo sapiens	109-114
25685064-4	2015	METHODS AND RESULTS: Using western blot analysis we demonstrated the activation of initiator caspase-8 and -9 as well as executioner caspase-6 and -7 in both tested cell lines after application of taxanes (paclitaxel, SB-T-1216) at death-inducing concentrations.	Taxoids	197-204	caspase 8	Homo sapiens	93-109
25685064-4	2015	METHODS AND RESULTS: Using western blot analysis we demonstrated the activation of initiator caspase-8 and -9 as well as executioner caspase-6 and -7 in both tested cell lines after application of taxanes (paclitaxel, SB-T-1216) at death-inducing concentrations.	CHEMBL204644	218-227	caspase 8	Homo sapiens	93-109
25665064-0	2015	Silver nanoparticles biosynthesized using Achillea biebersteinii flower extract: apoptosis induction in MCF-7 cells via caspase activation and regulation of Bax and Bcl-2 gene expression.	Silver	0-6	caspase 8	Homo sapiens	120-127
25242579-8	2015	Deguelin induced differentiation of OCI-AML3 cells at a nontoxic concentration which was associated with a decrease in expression of activated caspase-8, p53, p21, and the 30-kD form of CCAAT/enhancer binding protein alpha (C/EBPalpha), whereas no effects were found in OCIM2 cells expressing NPM-wt.	deguelin	0-8	caspase 8	Homo sapiens	143-152
25448810-7	2015	Ectopic expression of p16(INK4A) abolished the overgrowth of uveal melanoma cells in response to Cd and the overexpression of caspase 8 drastically increased the apoptotic rate of Cd-treated cutaneous melanoma cells.	Cadmium	180-182	caspase 8	Homo sapiens	126-135
25370004-5	2015	The H2O2 group showed significantly decreased cell viability, increased apoptosis as well as upregulation of caspases (cleaved caspase-3, -8 and -9) and ERS protein markers compared with those of the control group.	Hydrogen Peroxide	4-8	caspase 8	Homo sapiens	109-117
25370004-8	2015	In conclusion, relaxin-3 was shown to protect hepatocytes from H2O2-induced apoptosis via downregulation of cleaved caspase-8 and -9, as well as inhibition of the ERS pathway.	Hydrogen Peroxide	63-67	caspase 8	Homo sapiens	116-132
25125499-5	2015	Interestingly, ursodeoxycholyl lysophosphatidylethanolamide was able to increase expression of antiapoptotic cellular FLICE-inhibitory protein in both cell types.	ursodeoxycholyl lysophosphatidylethanolamide	15-59	caspase 8	Homo sapiens	118-123
25125499-8	2015	Hence, ursodeoxycholyl lysophosphatidylethanolamide mediated cytoprotection against apoptosis during toxic bile-acid and ischemic stresses by a mechanism involving accumulation of cellular FLICE-inhibitory protein, myeloid cell leukemia sequence-1 and cellular inhibitor of apoptosis 2 proteins.	ursodeoxycholyl lysophosphatidylethanolamide	7-51	caspase 8	Homo sapiens	189-194
25448810-8	2015	In conclusion, our data suggest that hypermethylation of p16(INK4A) and caspase 8 represents the most common event linked to Cd-induced stimulation of cell growth and inhibition of cell death pathway in melanoma.	Cadmium	125-127	caspase 8	Homo sapiens	72-81
25778894-8	2015	Moreover, ursolic acid could up-regulate expression of caspase-8, caspase-3 and caspase-9 protein (P&lt;0.01).	ursolic acid	10-22	caspase 8	Homo sapiens	55-64
25687050-6	2015	Furthermore, sorafenib treatment resulted in the obvious increase of the Caspase-3 and Caspase-8 protein and mRNA expressions, and down-regulated the MCL-1 protein and mRNA expressions in NB4 cells.	Sorafenib	13-22	caspase 8	Homo sapiens	87-96
25687050-7	2015	CONCLUSION: Sorafenib can inhibit proliferation and induce apopotosis of human acute promyelocytic leukemia cell NB4 through the expression of Caspase-3 and Caspase-8, and down-regulation of the expression of MCL-1.	Sorafenib	12-21	caspase 8	Homo sapiens	157-166
25513960-4	2015	Treatment of MKN28 cells with TNF-alpha plus CHX induced degradation of survivin and activation of caspase-8 and -3, followed by degradation of cIAP1 and XIAP and apoptosis.	Cycloheximide	45-48	caspase 8	Homo sapiens	99-115
25682199-7	2015	Furthermore, the cisplatin and Chal-24 combination induced dramatic degradation of cellular FLICE (FADD-like IL-1beta-converting enzyme)-inhibitory protein large (cFLIPL) which suppresses Ripoptosome-mediated apoptosis activation.	Cisplatin	17-26	caspase 8	Homo sapiens	92-97
25682199-7	2015	Furthermore, the cisplatin and Chal-24 combination induced dramatic degradation of cellular FLICE (FADD-like IL-1beta-converting enzyme)-inhibitory protein large (cFLIPL) which suppresses Ripoptosome-mediated apoptosis activation.	Cisplatin	17-26	caspase 8	Homo sapiens	99-135
25682199-7	2015	Furthermore, the cisplatin and Chal-24 combination induced dramatic degradation of cellular FLICE (FADD-like IL-1beta-converting enzyme)-inhibitory protein large (cFLIPL) which suppresses Ripoptosome-mediated apoptosis activation.	3-(3-hydroxy-4-methoxyphenyl)-1-(3,4,5-trimethoxyphenyl)prop-2-en-1-one	31-38	caspase 8	Homo sapiens	92-97
25682199-7	2015	Furthermore, the cisplatin and Chal-24 combination induced dramatic degradation of cellular FLICE (FADD-like IL-1beta-converting enzyme)-inhibitory protein large (cFLIPL) which suppresses Ripoptosome-mediated apoptosis activation.	3-(3-hydroxy-4-methoxyphenyl)-1-(3,4,5-trimethoxyphenyl)prop-2-en-1-one	31-38	caspase 8	Homo sapiens	99-135
25446602-15	2015	Procyanidin B1, as well as yokukansan, Glycyrrhiza, and Uncaria Hook, may attenuate the activation of caspase-3 by inhibiting that of caspase-8 and -9.	procyanidin B1	0-14	caspase 8	Homo sapiens	134-150
26645326-8	2015	We observed that the CD25 expression exclusively on the CD3(-)CD56(+)CD25(+) NK cells was positively correlated with their cytotoxic function evaluated by the MTT test (r = 0.68), the upregulation of granzyme B (r = 0.89), IL-2 (r = 0.78) and IFN-gamma (r = 0.57), however, it was not positively correlated with FasL and caspase-8.	monooxyethylene trimethylolpropane tristearate	159-162	caspase 8	Homo sapiens	321-330
26266085-11	2015	Caspase-3, caspase-8, and caspase-9 were activated in cells treated with CRS Type 5 plasma compared to controls.	Chromium	73-76	caspase 8	Homo sapiens	11-20
25434989-9	2015	Furthermore, DMAS resulted in loss of mitochondrial membrane potential and release of cytochrome c in the cells, and activated caspase-9, caspase-8, and caspase-3, and subsequently cleaved PARP, which was abolished by pretreatment with Z-VAD-FMK, a pan-caspase inhibitor.	Dimethyl acetylsuccinate	13-17	caspase 8	Homo sapiens	138-147
26477797-13	2015	Specific caspase inhibitors (caspase-8 inhibitor: Z-IETD-FMK; caspase-9 inhibitor: Z-LEHD-FMK and caspase-3 inhibitor: Z-DEVD-FMK) for caspase-8, -9, and -3 blocked SLE-activated caspase-8, -9, and -3 activities which were associated with an increase in the percentage of viable cells.	benzyloxycarbonyl-leucyl-glutamyl-histidyl-aspartic acid fluoromethyl ketone	83-93	caspase 8	Homo sapiens	135-156
25593641-5	2015	Combined treatment with TSA and TRAIL significantly reduced the levels of the cellular Fas-associated death domain (FADD)-like interleukin-1beta-converting enzyme (FLICE) inhibitory protein (c-FLIP), whereas those of death receptor (DR) 4, DR5, and FADD remained unchanged.	trichostatin A	24-27	caspase 8	Homo sapiens	164-169
25666501-10	2015	Concurrent incubation with TRAIL and epoxomicin for 24 hour significantly increased caspase-3, caspase-8, caspase-9 activities and Bax protein levels.	epoxomicin	37-47	caspase 8	Homo sapiens	95-104
26745109-10	2015	DOX led to the activation of all tested caspases, 8, 9 and 3, whereas WP 631 only induced an increase in caspase 8 activity after 24h of treatment and consequently led to the cleavage of PARP.	Doxorubicin	0-3	caspase 8	Homo sapiens	40-48
26434906-8	2015	Western blot analysis of pro-apoptotic markers revealed that as opposed to capsaicin, eugenol could induce caspase-8 and caspase-3 even in the absence of p53.	Eugenol	86-93	caspase 8	Homo sapiens	107-116
25469259-0	2015	Induction of caspase cascade pathway by kaempferol-3-O-rhamnoside in LNCaP prostate cancer cell lines.	kaempferol 3-O-rhamnoside	40-65	caspase 8	Homo sapiens	13-20
25469259-5	2015	The results showed that kaempferol-3-O-rhamnoside inhibits the proliferation of LNCaP cells in a dose-dependent manner by upregulating the expression of caspase-8, caspase-9, caspase-3 and poly (ADP-ribose) polymerase proteins.	kaempferol 3-O-rhamnoside	24-49	caspase 8	Homo sapiens	153-162
25714978-4	2015	The interaction of leucine-rich repeat kinase and Fas- Associated protein with Death Domain has been implicated in the switching-on of the extrinsic apoptotic pathway via caspase-8 activation, while deficiency in PTEN induced putative kinase 1 has been shown to cause Ca2+ accumulation in mitochondria, increased generation of reactive oxygen species and intrinsic cell death.	Leucine	19-26	caspase 8	Homo sapiens	171-180
25714978-4	2015	The interaction of leucine-rich repeat kinase and Fas- Associated protein with Death Domain has been implicated in the switching-on of the extrinsic apoptotic pathway via caspase-8 activation, while deficiency in PTEN induced putative kinase 1 has been shown to cause Ca2+ accumulation in mitochondria, increased generation of reactive oxygen species and intrinsic cell death.	Oxygen	336-342	caspase 8	Homo sapiens	171-180
25262359-0	2015	Curcumin induces apoptosis through mitochondrial pathway and caspases activation in human melanoma cells.	Curcumin	0-8	caspase 8	Homo sapiens	61-69
25367763-6	2015	Our study has also pointed to essential role of caspase 8 in bortezomib-induced cleavage of HSP90beta in both HL-60 and K562 cells.	Bortezomib	61-71	caspase 8	Homo sapiens	48-57
25976336-8	2015	Rapamycin slightly induced cell apoptosis but significantly enhanced the effect of oxaliplatin in soliciting apoptosis of A2780cis cells, which might be ascribed to its ability in further increasing the levels of cleaved caspase-8 and -3 and PARP induced by oxaliplatin.	Sirolimus	0-9	caspase 8	Homo sapiens	221-237
25976336-8	2015	Rapamycin slightly induced cell apoptosis but significantly enhanced the effect of oxaliplatin in soliciting apoptosis of A2780cis cells, which might be ascribed to its ability in further increasing the levels of cleaved caspase-8 and -3 and PARP induced by oxaliplatin.	Oxaliplatin	83-94	caspase 8	Homo sapiens	221-237
25262359-10	2015	During curcumin treatment, caspase-8 and Caspase-3 were cleaved in time and dose-dependent manners.	Curcumin	7-15	caspase 8	Homo sapiens	27-36
25333675-9	2015	Further investigation of the mechanism underlying these effects revealed that the evodiamine + TRAIL effect is associated with the increased expression of death receptor (DR)4, DR5, caspase-8 and cleaved caspase-3.	evodiamine	82-92	caspase 8	Homo sapiens	182-191
25333816-0	2015	Rocaglamide overcomes tumor necrosis factor-related apoptosis-inducing ligand resistance in hepatocellular carcinoma cells by attenuating the inhibition of caspase-8 through cellular FLICE-like-inhibitory protein downregulation.	rocaglamide	0-11	caspase 8	Homo sapiens	156-165
25333816-7	2015	Rocaglamide significantly sensitized the TRAIL-resistant HCC cells to apoptosis by TRAIL, which resulted from the rocaglamide-mediated downregulation of cellular FLICE-like inhibitory protein and subsequent caspase-8 activation.	rocaglamide	0-11	caspase 8	Homo sapiens	207-216
25339540-6	2015	In addition, treatment of K562/ADR cells with quercetin alone or in combination with ADR resulted in loss of mitochondrial membrane potential, activation of caspase-8, -9 and -3, reduced expression of the anti-apoptotic proteins B-cell lymphoma (Bcl)-2 and Bcl-extra large and enhanced expression of the pro-apoptotic proteins Bcl-2-interacting mediator of cell death, Bcl-2-associated death promoter and Bcl-2-associated X protein in the cells.	Quercetin	46-55	caspase 8	Homo sapiens	157-177
25333816-7	2015	Rocaglamide significantly sensitized the TRAIL-resistant HCC cells to apoptosis by TRAIL, which resulted from the rocaglamide-mediated downregulation of cellular FLICE-like inhibitory protein and subsequent caspase-8 activation.	rocaglamide	114-125	caspase 8	Homo sapiens	207-216
26278147-7	2015	Cells that were sequentially exposed to rapamycin and topotecan had significantly higher levels of cleaved caspase-8, -3, and PARP compared to those treated with topotecan alone.	Sirolimus	40-49	caspase 8	Homo sapiens	107-116
25866222-4	2015	Deltonin treatment selectively prevents proliferation of FaDu cells by cell-cycle arrest and induction of apoptosis, via activating checkpoint kinase Chk1and Chk2 as well as caspases 8, 9 and 3.	deltonin	0-8	caspase 8	Homo sapiens	174-193
25726174-12	2015	The present results indicate that 6-PSA induces cytotoxicity and moderate genotoxicity, together with an increase in the apoptosis rate, in a caspase 8-dependent manner in gastric cancer cells.	anacardic acid	34-39	caspase 8	Homo sapiens	142-151
25738310-11	2015	Sorafenib and irinotecan sequential treatment significantly increased the levels of cleaved caspase-8, -3, and PARP in HepG2 cells.	Sorafenib	0-9	caspase 8	Homo sapiens	92-101
25738310-11	2015	Sorafenib and irinotecan sequential treatment significantly increased the levels of cleaved caspase-8, -3, and PARP in HepG2 cells.	Irinotecan	14-24	caspase 8	Homo sapiens	92-101
26278147-7	2015	Cells that were sequentially exposed to rapamycin and topotecan had significantly higher levels of cleaved caspase-8, -3, and PARP compared to those treated with topotecan alone.	Topotecan	54-63	caspase 8	Homo sapiens	107-116
25091578-8	2014	Significant concentrations of 15d-PGJ2 were reached in the medium of melanoma cells, which were sufficient to activate caspase 8 and the mitochondrial pathway of apoptosis.	15-deoxyprostaglandin J2	30-38	caspase 8	Homo sapiens	119-128
25447764-8	2015	In this work we demonstrate that after 8 h of incubation with deoxyadenosine and deoxycoformycin, caspase-8 is activated, mitochondrial mass increases and mitochondrial reactive oxygen species decrease.	2'-deoxyadenosine	62-76	caspase 8	Homo sapiens	98-107
25447764-8	2015	In this work we demonstrate that after 8 h of incubation with deoxyadenosine and deoxycoformycin, caspase-8 is activated, mitochondrial mass increases and mitochondrial reactive oxygen species decrease.	Pentostatin	81-96	caspase 8	Homo sapiens	98-107
25447764-8	2015	In this work we demonstrate that after 8 h of incubation with deoxyadenosine and deoxycoformycin, caspase-8 is activated, mitochondrial mass increases and mitochondrial reactive oxygen species decrease.	Reactive Oxygen Species	169-192	caspase 8	Homo sapiens	98-107
26180579-0	2015	Impact of Procyanidins from Different Berries on Caspase 8 Activation in Colon Cancer.	Proanthocyanidins	10-22	caspase 8	Homo sapiens	49-58
26180579-6	2015	In Pcys-treated gut cell lines, caspase 8 (apoptosis extrinsic pathway) but not caspase 9 (apoptosis intrinsic pathway) is activated after 3 hours through P38 phosphorylation (90 min), emphasizing the potency of lowbush blueberry Pcys to eradicate gut TRAIL-resistant cancer cells.	Proanthocyanidins	3-7	caspase 8	Homo sapiens	32-41
25531367-7	2014	Maduramicin also induced expression of BAK, BAD, DR4, TRADD and TRAIL, leading to activation of caspases 8, 9 and 3 as well as cleavage of poly ADP ribose polymerase (PARP).	maduramicin	0-11	caspase 8	Homo sapiens	96-115
25465706-11	2015	AEA-treated cells showed increased caspase-8 activation and formation of t-Bid, suggesting the interplay between intrinsic and extrinsic apoptotic pathways.	anandamide	0-3	caspase 8	Homo sapiens	35-44
25553350-2	2014	CASP8 D302H (rs1045485) (D, Aspartate; H, Histidine) and CASP8 -652 6N del (rs3834129) polymorphisms have been reported to be associated with Cancer susceptibility.	Aspartic Acid	28-37	caspase 8	Homo sapiens	0-5
25553350-2	2014	CASP8 D302H (rs1045485) (D, Aspartate; H, Histidine) and CASP8 -652 6N del (rs3834129) polymorphisms have been reported to be associated with Cancer susceptibility.	Histidine	42-51	caspase 8	Homo sapiens	0-5
25310109-2	2014	In the present study, we reported that celastrol potentiated tumor necrosis factor-alpha (TNF-alpha)-induced apoptosis, affected activation of caspase-8, caspase-3 and PARP cleavage, and inhibited the expression of anti-apoptotic proteins such as cellular inhibitor of apoptosis protein 1 and 2 (cIAP1 and cIAP2), cellular FLICE-inhibitory protein (FLIP), and B-cell lymphoma 2 (Bcl-2).	celastrol	39-48	caspase 8	Homo sapiens	143-152
25251038-7	2014	Furthermore, we demonstrate that AS-06 and AS-29 induce apoptosis through the caspase-8 and caspase-9 cascades.	as-06	33-38	caspase 8	Homo sapiens	78-87
25251038-7	2014	Furthermore, we demonstrate that AS-06 and AS-29 induce apoptosis through the caspase-8 and caspase-9 cascades.	N,N-dimethyl-3,3-diphenyl-1-methylallylamine	43-48	caspase 8	Homo sapiens	78-87
25200008-5	2014	Using the HCT116 colorectal cancer model, we show that following binding to DR5, the nanoparticles activate caspase 8, enhancing the anti-tumor activity of the camptothecin payload both in vitro and in vivo.	Camptothecin	160-172	caspase 8	Homo sapiens	108-117
25273175-0	2014	Rotundarpene prevents TRAIL-induced apoptosis in human keratinocytes by suppressing the caspase-8- and Bid-pathways and the mitochondrial pathway.	rotundarpene	0-12	caspase 8	Homo sapiens	88-106
25273175-6	2014	These results suggest that rotundarpene may reduce TRAIL-induced apoptosis in human keratinocytes by suppressing the activation of the caspase-8- and Bid-pathways and the mitochondria-mediated cell death pathway, which is associated with the formation of reactive oxygen species and reactive nitrogen species.	rotundarpene	27-39	caspase 8	Homo sapiens	135-153
25241797-0	2014	Induction of apoptosis in MDA-MB-231 human breast carcinoma cells with an ethanol extract of Cyperus rotundus L. by activating caspases.	Ethanol	74-81	caspase 8	Homo sapiens	127-135
25388371-5	2014	Mechanistic differences in apoptotic responses were observed as differential patterns of DNA fragmentation and levels of BAX, BCL-XL, CASP8, and p-ERK in response to GSNO and STS treatment.	S-Nitrosoglutathione	166-170	caspase 8	Homo sapiens	134-139
23776099-10	2014	In conclusion, these benzene metabolites could induce apoptosis of K562 cells mainly through caspase-8-dependent pathway and ROS production, and sialic acid metabolism might play a role in the apoptotic process.	Benzene	21-28	caspase 8	Homo sapiens	93-102
25148872-3	2014	These stimulatory effects on calcium signals were followed by intracellular ROS production and mitochondria membrane depolarization, as well as a time-dependent increase in caspase-8 and -9 activities.	Calcium	29-36	caspase 8	Homo sapiens	173-189
25537896-3	2014	The expression of phosphorylated caspase-8 at 380 tyrosine by Src was detected using Western blotting.	Tyrosine	50-58	caspase 8	Homo sapiens	33-42
25333266-9	2014	Interestingly, although ABT-263 activated caspase-9 in PC3 cells, inhibition of caspase-9 unexpectedly promoted ABT-263-induced apoptosis in a caspase-8-dependent manner.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	112-115	caspase 8	Homo sapiens	143-152
25164609-0	2014	Nobiletin suppresses the proliferation and induces apoptosis involving MAPKs and caspase-8/-9/-3 signals in human acute myeloid leukemia cells.	nobiletin	0-9	caspase 8	Homo sapiens	81-90
25164609-6	2014	Furthermore, nobiletin effectively induced apoptosis of HL-60 cells through caspase-8, caspase-9, and caspases-3 activation concomitantly with a marked induction of p38 mitogen-activated protein kinase (MAPK) activation, but without affecting expression levels of Bcl-2, Bax, or Bid.	nobiletin	13-22	caspase 8	Homo sapiens	76-85
25506265-0	2014	Upregulation of death receptor 5 and activation of caspase 8/3 play a critical role in ergosterol peroxide induced apoptosis in DU 145 prostate cancer cells.	ergosterol-5,8-peroxide	87-106	caspase 8	Homo sapiens	51-60
25216351-13	2014	Flavopiridol induced growth inhibition and apoptosis at the IC(50) dose (500 nM), resulting in a significant increase in immunofluorescence staining of caspase-3, caspase-8 and p53.	alvocidib	0-12	caspase 8	Homo sapiens	163-172
25506265-9	2014	Conversely, caspase 8 inhibitor Z-IETD-FMK blocked the apoptotic ability of EP to cleave PARP and an increase of sub G1 population in DU 145 prostate cancer cells.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	32-42	caspase 8	Homo sapiens	12-21
25506265-11	2014	CONCLUSION: Overall, our findings suggest that ergosterol peroxide induces apoptosis via activation of death receptor 5 and caspase 8/3 in DU 145 prostate cancer cells as a cancer chemopreventive agent or dietary factor.	ergosterol-5,8-peroxide	47-66	caspase 8	Homo sapiens	124-133
25132643-0	2014	Mechanism of 2",3"-dimethoxyflavanone-induced apoptosis in breast cancer stem cells: role of ubiquitination of caspase-8 and LC3.	2',3'-dimethoxyflavanone	13-37	caspase 8	Homo sapiens	111-120
25132643-7	2014	We found that 2",3"-DMF induces the ubiquitination of caspase-8, this resulted in an interaction between caspase-8 and LC3, which led to the aggregation and activation of caspase-8.	2',3'-dimethoxyflavanone	14-23	caspase 8	Homo sapiens	54-63
25132643-7	2014	We found that 2",3"-DMF induces the ubiquitination of caspase-8, this resulted in an interaction between caspase-8 and LC3, which led to the aggregation and activation of caspase-8.	2',3'-dimethoxyflavanone	14-23	caspase 8	Homo sapiens	105-114
25132643-7	2014	We found that 2",3"-DMF induces the ubiquitination of caspase-8, this resulted in an interaction between caspase-8 and LC3, which led to the aggregation and activation of caspase-8.	2',3'-dimethoxyflavanone	14-23	caspase 8	Homo sapiens	105-114
25132643-8	2014	Co-treating cells with 2",3"-DMF and 3-methyladenine, an inhibitor of LC3 lipidation, reduced the activation of caspase-8.	2',3'-dimethoxyflavanone	23-32	caspase 8	Homo sapiens	112-121
25132643-8	2014	Co-treating cells with 2",3"-DMF and 3-methyladenine, an inhibitor of LC3 lipidation, reduced the activation of caspase-8.	3-methyladenine	37-52	caspase 8	Homo sapiens	112-121
25132643-9	2014	These findings provide novel insights into the anti-cancer effects of 2",3"-DMF in breast cancer stem cells by revealing that it induced apoptosis in accompany with the activation of caspase-8 mediated by LC3 conversion.	2',3'-dimethoxyflavanone	70-79	caspase 8	Homo sapiens	183-192
25421516-5	2014	RESULTS: Alcohol subjects had significantly higher levels of the 14 kDa C8 fragment (C8-14), an indicator of C8 activation.	Alcohols	9-16	caspase 8	Homo sapiens	72-74
25421516-5	2014	RESULTS: Alcohol subjects had significantly higher levels of the 14 kDa C8 fragment (C8-14), an indicator of C8 activation.	Alcohols	9-16	caspase 8	Homo sapiens	85-87
25411798-9	2014	Se-methylselenocysteine (MSC) at an optimum concentration of 1 muM could reverse the alteration in antioxidative capacity, Bcl2/Bax ratio and caspase-8 activity caused by Clu-knockdown, thus inhibiting apoptosis and maintaining cell viability.	Se-methylselenocysteine	0-23	caspase 8	Homo sapiens	142-151
25338206-6	2014	The induction of apoptosis by HS-133 was confirmed by the increases of the cleaved PARP, caspase-3, and caspase-8.	Keggin peroxo polyoxometalate	30-36	caspase 8	Homo sapiens	104-113
24905183-4	2014	Moreover, honokiol elicited the extrinsic death receptor pathway of DR5 and caspase 8 and the intrinsic pathway of caspase 9.	honokiol	10-18	caspase 8	Homo sapiens	76-85
25108184-8	2014	All of these molecules activate caspase-9 and caspase-3, while caspase-8 activity is significantly induced by both cinnamaldehyde metal complexes.	cinnamaldehyde	115-129	caspase 8	Homo sapiens	63-72
25108184-8	2014	All of these molecules activate caspase-9 and caspase-3, while caspase-8 activity is significantly induced by both cinnamaldehyde metal complexes.	Metals	130-135	caspase 8	Homo sapiens	63-72
25085582-9	2014	The enhanced antitumor effects in vitro elicited by Ad/PSCAE/UPII/E1A plus cisplatin were closely related to the increased Fas expression and cleavage of caspase-8 and Bid and decrease in the ratio of anti- to pro-apoptotic proteins followed by activation of caspase-9 and caspase-3, which may contribute to the activation of extrinsic and intrinsic apoptotic pathways.	Cisplatin	75-84	caspase 8	Homo sapiens	154-163
25356873-8	2014	Interestingly, Beclin-1 phosphorylated at Ser 93/96 is sufficient to induce Beclin-1 cleavage by caspase-8, which switches off autophagy to achieve the synergistic induction of apoptosis.	Serine	42-45	caspase 8	Homo sapiens	97-106
25330190-8	2014	In the brain, hierarchical clustering has revealed that the expression of regulative apoptotic caspases (CASP2, CASP8 CASP9, CASP10) and of the inflammatory CASP1 is linked to several genes involved in cholesterol homeostasis.	Cholesterol	202-213	caspase 8	Homo sapiens	112-117
25226230-8	2014	Imaging and scWestern analysis of single glioblastoma cells dosed with the chemotherapeutic daunomycin showed both apoptotic (cleaved caspase 8- and annexin V-positive) and living cells.	Daunorubicin	92-102	caspase 8	Homo sapiens	134-143
25341043-0	2014	Bortezomib sensitises TRAIL-resistant HPV-positive head and neck cancer cells to TRAIL through a caspase-dependent, E6-independent mechanism.	Bortezomib	0-10	caspase 8	Homo sapiens	97-104
25341043-6	2014	Bortezomib-mediated sensitisation to TRAIL was associated with enhanced activation of caspase-8, -9 and -3, elevated membrane expression levels of TRAIL-R2, cytochrome c release and G2/M arrest.	Bortezomib	0-10	caspase 8	Homo sapiens	86-106
25330300-11	2014	Caspase-8 and -3 levels were increased in cells exposed to MTX, but the modulation of these genes, as well as that of the Bax and Bcl-2 genes involved in the apoptosis pathway, presented a modulation that was dependent on the SOD2 genotype.	Methotrexate	59-62	caspase 8	Homo sapiens	0-16
25604189-4	2014	One of these, an interaction between CASP8-rs1045485 and alcohol consumption has been replicated, but others have not, including LSP1- rs3817198 and parity, and 1p11.2-rs11249433 and ever being parous.	Alcohols	57-64	caspase 8	Homo sapiens	37-42
25196075-10	2014	However, inhibition of caspases by Z-VAD-FMK reversed the down-regulatory effect of P16 on pAKT (S473) and pP70S6K, as evident by the cell viability assay and flow cytometric analysis but this inhibition did not completely reverse the antiproliferative effect of P16, thereby indicating the role of additional factors apart from caspases in P16 induced apoptosis in MOLT-4 cells.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	35-44	caspase 8	Homo sapiens	23-31
24805111-0	2014	p62/SQSTM1 is involved in caspase-8 associated cell death induced by proteasome inhibitor MG132 in U87MG cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	90-95	caspase 8	Homo sapiens	26-35
25456851-0	2014	Antiproliferation and induction of caspase-8-dependent mitochondria-mediated apoptosis by beta-tocotrienol in human lung and brain cancer cell lines.	tocotrienol, beta	90-106	caspase 8	Homo sapiens	35-44
25456851-7	2014	beta-Tocotrienol is said to induce activation of caspase-8 in both A549 and U87MG cells guided by no activation when caspase-8 inhibitor, z-IETD-fmk was added.	tocotrienol, beta	0-16	caspase 8	Homo sapiens	49-58
25456851-7	2014	beta-Tocotrienol is said to induce activation of caspase-8 in both A549 and U87MG cells guided by no activation when caspase-8 inhibitor, z-IETD-fmk was added.	tocotrienol, beta	0-16	caspase 8	Homo sapiens	117-126
25456851-7	2014	beta-Tocotrienol is said to induce activation of caspase-8 in both A549 and U87MG cells guided by no activation when caspase-8 inhibitor, z-IETD-fmk was added.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	138-148	caspase 8	Homo sapiens	49-58
25275027-4	2014	The FAS receptor and caspase-8 are required for amplification of ROS signaling triggered by individual compounds, but are dispensable when the synergistic effect is established.	Reactive Oxygen Species	65-68	caspase 8	Homo sapiens	21-30
24938188-4	2014	A portion of the neuronal death induced by CysDA was preceded by a rapid uptake and intracellular oxidation of CysDA, leading to an acute and transient activation of ERK2 (extracellular-signal-regulated kinase 2) and caspase 8.	5-S-cysteinyldopamine	43-48	caspase 8	Homo sapiens	217-226
24938188-4	2014	A portion of the neuronal death induced by CysDA was preceded by a rapid uptake and intracellular oxidation of CysDA, leading to an acute and transient activation of ERK2 (extracellular-signal-regulated kinase 2) and caspase 8.	5-S-cysteinyldopamine	111-116	caspase 8	Homo sapiens	217-226
24938188-5	2014	The oxidation of CysDA also induced the activation of apoptosis signal-regulating kinase 1 via its de-phosphorylation at Ser967, the phosphorylation of JNK (c-Jun N-terminal kinase) and c-Jun (Ser73) as well as the activation of p38, caspase 3, caspase 8, caspase 7 and caspase 9.	5-S-cysteinyldopamine	17-22	caspase 8	Homo sapiens	245-254
25018064-1	2014	Our recent studies have demonstrated the key roles of reactive oxygen species (ROS)-mediated caspase-8- and Bax-dependent apoptotic pathways in dihydroartemisinin (DHA)-induced apoptosis of A549 cells.	Reactive Oxygen Species	54-77	caspase 8	Homo sapiens	93-102
25018064-1	2014	Our recent studies have demonstrated the key roles of reactive oxygen species (ROS)-mediated caspase-8- and Bax-dependent apoptotic pathways in dihydroartemisinin (DHA)-induced apoptosis of A549 cells.	Reactive Oxygen Species	79-82	caspase 8	Homo sapiens	93-102
25018064-1	2014	Our recent studies have demonstrated the key roles of reactive oxygen species (ROS)-mediated caspase-8- and Bax-dependent apoptotic pathways in dihydroartemisinin (DHA)-induced apoptosis of A549 cells.	artenimol	144-162	caspase 8	Homo sapiens	93-102
25018064-1	2014	Our recent studies have demonstrated the key roles of reactive oxygen species (ROS)-mediated caspase-8- and Bax-dependent apoptotic pathways in dihydroartemisinin (DHA)-induced apoptosis of A549 cells.	artenimol	164-167	caspase 8	Homo sapiens	93-102
25018064-7	2014	Furthermore, NAC pretreatment potently prevented DHA-induced ROS generation and loss of DeltaPsim as well as apoptosis, and silencing Bax by shRNA or inhibition of one of caspase-3, -8 and -9 also significantly prevented DHA-induced apoptosis in both cell lines, indicating the key roles of ROS and Bax as well as the caspases.	artenimol	49-52	caspase 8	Homo sapiens	318-326
25018064-8	2014	Collectively, DHA presents more potent proapoptotic actions in A549GR cells preferentially over normal A549 cells via ROS-dependent apoptotic pathway, in which Bax and caspases are involved.	artenimol	14-17	caspase 8	Homo sapiens	168-176
25070834-12	2014	The DNA fragmentation was inhibited in the presence of caspase 8 inhibitor (Z-IETD-FMK).	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	76-86	caspase 8	Homo sapiens	55-64
24805111-3	2014	We treated U87MG cells with the proteasome inhibitor MG132 and found that cell death correlated with caspase-8 activation and autophagy protein p62/SQSTM1.To explore the role of autophagy and p62/SQSTM1 in MG132-induced cancer cell death, we measured the alteration of MG132"s cytotoxicity by autophagy inhibition, autophagy induction or variation of p62/SQSTM1 gene expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	53-58	caspase 8	Homo sapiens	101-110
25018064-8	2014	Collectively, DHA presents more potent proapoptotic actions in A549GR cells preferentially over normal A549 cells via ROS-dependent apoptotic pathway, in which Bax and caspases are involved.	Reactive Oxygen Species	118-121	caspase 8	Homo sapiens	168-176
24927175-0	2014	Tazarotene induces apoptosis in human basal cell carcinoma via activation of caspase-8/t-Bid and the reactive oxygen species-dependent mitochondrial pathway.	tazarotene	0-10	caspase 8	Homo sapiens	77-86
25228008-0	2014	Gefitinib induces cytoplasmic translocation of the CDK inhibitor p27 and its binding to a cleaved intermediate of caspase 8 in non-small cell lung cancer cells.	Gefitinib	0-9	caspase 8	Homo sapiens	114-123
25228008-6	2014	RESULTS: We found that gefitinib treatment caused the NSCLC cells to undergo apoptosis following activation of the caspase 8 cascade.	Gefitinib	23-32	caspase 8	Homo sapiens	115-124
25228008-8	2014	Moreover, we found that cytoplasmic p27 bound to a cleaved intermediate (p43/p41) of caspase 8 and that inhibition of cytoplasmic translocation of p27 reduced gefitinib-induced cell death in HCC827 cells.	Gefitinib	159-168	caspase 8	Homo sapiens	85-94
25228008-9	2014	CONCLUSION: Based on our results, we conclude that gefitinib-induced apoptosis is mediated by the interaction of p27 and caspase 8 in NSCLC cells carrying an activating EGFR mutation.	Gefitinib	51-60	caspase 8	Homo sapiens	121-130
24927175-4	2014	Our results are the first to demonstrate that tazarotene induces mitochondria-dependent cleavage of caspase-9 and -3 and PARP in BCC cells by producing reactive oxygen species (ROS) and activating caspase-8 through both ROS and death receptor signaling.	tazarotene	46-56	caspase 8	Homo sapiens	197-206
24927175-4	2014	Our results are the first to demonstrate that tazarotene induces mitochondria-dependent cleavage of caspase-9 and -3 and PARP in BCC cells by producing reactive oxygen species (ROS) and activating caspase-8 through both ROS and death receptor signaling.	Reactive Oxygen Species	220-223	caspase 8	Homo sapiens	197-206
24927175-6	2014	Furthermore, our results presented for the first time that tazarotene triggers a convergence of the intrinsic and extrinsic apoptotic pathways via the caspase-8-truncated Bid signaling pathway.	tazarotene	59-69	caspase 8	Homo sapiens	151-160
25112602-0	2014	Cartilage polysaccharide induces apoptosis in K562 cells through a reactive oxygen species-mediated caspase pathway.	Polysaccharides	10-24	caspase 8	Homo sapiens	100-107
25112602-0	2014	Cartilage polysaccharide induces apoptosis in K562 cells through a reactive oxygen species-mediated caspase pathway.	Reactive Oxygen Species	67-90	caspase 8	Homo sapiens	100-107
25116791-0	2014	Xanthoceraside induces apoptosis in melanoma cells through the activation of caspases and the suppression of the IGF-1R/Raf/MEK/ERK signaling pathway.	xanthoceraside	0-14	caspase 8	Homo sapiens	77-85
25103559-5	2014	Expression of the mitochondrial protective protein BCL-XL or the caspase-8 inhibitor c-FLIP-s, or knockdown of death receptor CD95 or the death receptor caspase-8 linker protein FADD, suppressed killing by [OSU-03012 + PDE5 inhibitor] treatment.	OSU 03012	207-216	caspase 8	Homo sapiens	153-162
25050836-7	2014	The results revealed that CXB sensitized TRAIL-resistant MG-63 OS cells to TRAIL-induced apoptosis through downregulation of cellular B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein, caspase-8 and caspase-3.	Celecoxib	26-29	caspase 8	Homo sapiens	189-198
25070748-4	2014	Phloroglucinol treatment of HT-29 cells resulted in characteristic apoptosis-related changes: altered Bcl-2 family proteins, cytochrome c release, and activation of caspase-3 and caspase-8.	Phloroglucinol	0-14	caspase 8	Homo sapiens	179-188
25533359-4	2014	Caspase-3, Caspase-8 and caspase-9 mRNA expression increased by 30%~600% in CYP2E1-overexpressing cells at doses of 0.5~4.0 mmol/L TCE when compared with L02 cells (P &lt; 0.01).	Trichloroethylene	131-134	caspase 8	Homo sapiens	11-20
24930757-5	2014	Ilimaquinone pretreatment significantly enhanced TRAIL-induced apoptosis in HCT 116 cells and sensitized colon cancer cells to TRAIL-induced apoptosis through increased caspase-8, -3 activation, PARP cleavage, and DNA damage.	ilimaquinone	0-12	caspase 8	Homo sapiens	169-178
25227113-8	2014	Immunoblots and assays with a panel of caspase inhibitors revealed that poly(I:C) transfection-induced apoptosis was dependent on caspase-8 and -9, as well as caspase-2.	Poly I-C	72-80	caspase 8	Homo sapiens	130-146
25036791-4	2014	In A549 cells, 31h decreased phosphorylation of histone H3, triggered polyploidy, induced expression of pro-apoptotic Fas and FasL with subsequent activation of caspase 8, resulting into apoptosis.	31h	15-18	caspase 8	Homo sapiens	161-170
23239598-8	2014	CECF-stimulated activities of caspase-8, caspase-9, and caspase-3, ROS, and Ca(2+) production, decreased DeltaPsim levels of in U-2 OS cells.	cecf	0-4	caspase 8	Homo sapiens	30-39
25221997-5	2014	In the HL-60 cells, A398 induced apoptosis in a time and concentration-dependent manner, promoting mitochondrial depolarization, inhibition of Bcl-2, phosphatidylserine exposure, activation of caspases -8, -9 and -3, and DNA fragmentation.	a398	20-24	caspase 8	Homo sapiens	193-215
25202081-8	2014	Pre-treatment with N-acetylcysteine blocked loss of MMP, caused increase of Bcl-2-associated X protein (Bax)/B-cell lymphoma 2 (Bcl-2) ratio, caspase-8 activation, and apoptosis induced by equol.	Acetylcysteine	19-35	caspase 8	Homo sapiens	142-151
24867094-6	2014	In addition, crebanine affected TNF-alpha-induced activation of caspase-8, caspase-3, and poly(ADP-ribose) polymerase cleavage, indicating that the apoptotic effects of TNF-alpha were enhanced by crebanine.	crebanine	13-22	caspase 8	Homo sapiens	64-73
25036608-0	2014	A polysaccharide from Sanguisorbae radix induces caspase-dependent apoptosis in human leukemia HL-60 cells.	Polysaccharides	2-16	caspase 8	Homo sapiens	49-56
26331107-12	2014	Although DMC did not affect DR5 expression in the GBM cells, it increased TRAIL-induced caspase-8 activation in both TRAIL-sensitive and -resistant cells, indicating that DMC potentiates initiator caspase activation in these cells.	2,5-dimethylcelecoxib	9-12	caspase 8	Homo sapiens	88-97
26331107-12	2014	Although DMC did not affect DR5 expression in the GBM cells, it increased TRAIL-induced caspase-8 activation in both TRAIL-sensitive and -resistant cells, indicating that DMC potentiates initiator caspase activation in these cells.	2,5-dimethylcelecoxib	9-12	caspase 8	Homo sapiens	88-95
23047612-0	2014	The effects of cytotoxicity and genotoxicity induced by 2,2-bis[4-(acryloxypropoxy)phenyl]propane via caspases in human gingival fibroblasts.	2,2-bis[4-(acryloxypropoxy)phenyl]propane	56-97	caspase 8	Homo sapiens	102-110
24879465-6	2014	The results suggest that menadione may induce apoptotic cell death in ovarian carcinoma cell lines by activating the mitochondrial pathway and the caspase-8- and Bid-dependent pathways.	Vitamin K 3	25-34	caspase 8	Homo sapiens	147-165
25105597-11	2014	Caspase activity assays suggested that PDT with Na-pheophorbide A induced an apoptotic change in HuO9 cells, mainly via activation of mitochondrial caspase -9 and -3 pathways.	Na-Pheophorbide a	48-65	caspase 8	Homo sapiens	0-7
25011914-4	2014	Western blot and RT-PCR analysis have indicated that isosclerone induce cancer cells apoptosis through down-regulated Bcl-2 family and up-regulated caspases, and activating the NF-kappa-B signaling pathway.	isosclerone	53-64	caspase 8	Homo sapiens	148-156
25216531-5	2014	Apollon knockdown also enhanced cisplatin/docetaxel-induced activation of caspase-8 (extrinsic pathway) and caspase-9 (intrinsic pathway) in ESCC cells and xenograft tumor models.	Cisplatin	32-41	caspase 8	Homo sapiens	74-83
25216531-5	2014	Apollon knockdown also enhanced cisplatin/docetaxel-induced activation of caspase-8 (extrinsic pathway) and caspase-9 (intrinsic pathway) in ESCC cells and xenograft tumor models.	Docetaxel	42-51	caspase 8	Homo sapiens	74-83
25023790-8	2014	RESULTS: beta-OH-S infusion prior to reperfusion reduced coronary and cardiac oxidative DNA-damage, diminished neutrophil infiltration at the site of ischemia, preserved mitochondrial membrane potential and reduced apoptosis in the ischemic myocardium (lower mRNA levels of Fas, casp8, p53, and casp3 and mitochondrial-p-Bcl2; and reduced TUNEL and active caspase-3; p&lt;0.05 vs. vehicle/control).	beta-oh-s	9-18	caspase 8	Homo sapiens	279-284
25011914-5	2014	Our data demonstrate that isosclerone specifically binds to crystal structure of apoptosis regulator BCL-2 and pseudo-activated procaspase-3 proteins through down-regulated Bcl-2 family and up-regulated caspases, and activating the NF-kappa-B signaling pathway.	isosclerone	26-37	caspase 8	Homo sapiens	203-211
25087893-7	2014	Acute ablation of D-cyclins upregulated these proapoptotic genes and led to Fas- and caspase 8-dependent apoptosis.	d-cyclins	18-27	caspase 8	Homo sapiens	85-94
25337187-10	2014	Furthermore, FADD and cleaved caspase-8 expression were up-regulated by thiostrepton or FoxM1 siRNA, and expression of cIAP1 and XIAP was inhibited by thiostrepton.	Thiostrepton	72-84	caspase 8	Homo sapiens	30-39
24919588-8	2014	Minocycline caused S phase cell cycle arrest and an increase in the apoptotic rate associated with upregulation of p27, cleaved-caspase8, cleaved-caspase3 and cleaved-PRAP-1.	Minocycline	0-11	caspase 8	Homo sapiens	128-136
25100434-5	2014	By RT-PCR and western blot assays, Kuding tea polyphenol significantly induced apoptosis in BcaCD885 cancer cells (p &lt; 0.05) by upregulating caspase-3, caspase-8, caspase-9, Fas/FasL, Bax, p53, p21, E2F1, p73 and downregulating Bcl-2, Bcl-xL, HIAP-1, and HIAP-2 mRNA and protein expressions.	Polyphenols	46-56	caspase 8	Homo sapiens	155-164
25013479-5	2014	Moreover, the increased activities of caspase 8 and 9 strongly indicated that pregnenolone activated the extrinsic and intrinsic pathways of apoptosis.	Pregnenolone	78-90	caspase 8	Homo sapiens	38-47
25089613-8	2014	Under hypoxia, downregulation of HIF-1alpha and upregulation of caspase-3, caspase-8, caspase-9, LC3 and Beclin-1 were observed when paclitaxel was combined with oxygen-CNT.	Paclitaxel	133-143	caspase 8	Homo sapiens	75-84
25066322-6	2014	G226 induced dose-dependent apoptosis of MDA-MB-231 and MCF-7 cells, accompanied by markedly increased activities of caspase-8 and caspase-3/7, which were abolished by caspase inhibitors zVAD or zIETD.	Lovastatin	0-4	caspase 8	Homo sapiens	117-126
25066322-6	2014	G226 induced dose-dependent apoptosis of MDA-MB-231 and MCF-7 cells, accompanied by markedly increased activities of caspase-8 and caspase-3/7, which were abolished by caspase inhibitors zVAD or zIETD.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	187-191	caspase 8	Homo sapiens	117-126
25066322-8	2014	Moreover, G226 dose-dependently enhanced the autophagy marker LC3-II and autophagy substrate p62 accumulation in the cells, which were co-localized with caspase-8.	Lovastatin	10-14	caspase 8	Homo sapiens	153-162
25219839-6	2014	When incubated with Ang-II, (inhibited by losartan) the improvement was observed in the expression of caspase-3 and caspase-8.	Losartan	42-50	caspase 8	Homo sapiens	116-125
24865236-4	2014	SNS-032 had a direct apoptosis-inducing effect through both the extrinsic and intrinsic apoptotic pathways in breast cancer cells as shown by a dose-dependent increase in Annexin V-positive cells and terminal deoxynucleotidyl transferase-mediated dUTP nick?end labeling (TUNEL)-positive cells, as well as activation of caspase-8, -9 and poly(ADP-ribose) polymerase (PARP).	N-(5-(((5-(1,1-dimethylethyl)-2-oxazolyl)methyl)thio)-2-thiazolyl)-4-piperidinecarboxamide	0-7	caspase 8	Homo sapiens	319-332
24919794-7	2014	In addition, extrinsic caspase signaling (caspase-8 and -3) was activated in the HMJ-30-treated HUVECs and their inhibitors were applied to assess the signal transduction.	6-fluoro-2-(3-fluorophenyl)-4-(cyanoanilino)quinazoline	81-87	caspase 8	Homo sapiens	42-58
25130820-9	2014	It is concluded that VPA can enhance the sensitivity of RPMI 8226 cells to ATO-induced apoptosis, which may be associated with decreasing the BCL-2 expression and increasing the BAX, caspase-8 and caspase-9 gene expression.	Valproic Acid	21-24	caspase 8	Homo sapiens	183-192
25077544-2	2014	Its function in apoptosis is associated with the proteolytic cleavage to the truncated form tBid, mainly by caspase-8.	tBID	92-96	caspase 8	Homo sapiens	108-117
25130820-9	2014	It is concluded that VPA can enhance the sensitivity of RPMI 8226 cells to ATO-induced apoptosis, which may be associated with decreasing the BCL-2 expression and increasing the BAX, caspase-8 and caspase-9 gene expression.	Arsenic Trioxide	75-78	caspase 8	Homo sapiens	183-192
25015549-3	2014	Comibination of Tanshinone I and TRAIL exerted synergistic cytotoxicity, increased cleaved PARP, sub G1 population, the number of TUNELpositive cells, activated caspase 8, 9 and ROS production in PC-3 and DU145 cells.	tanshinone	16-28	caspase 8	Homo sapiens	161-170
25034326-12	2014	SCS further promoted the tamoxifen-induced apoptosis that was associated with modulation of mitochondrial membrane potential and activation of caspase-8 and caspase-9, suggesting the involvement of intrinsic and extrinsic signaling pathways.	Tamoxifen	25-34	caspase 8	Homo sapiens	143-152
24855207-6	2014	We identify a novel mechanism by showing that BV6 and dexamethasone cooperate to deplete cIAP1, cIAP2, and XIAP, thereby promoting assembly of the ripoptosome, a RIP1/FADD/caspase-8-containing complex.	BV6	46-49	caspase 8	Homo sapiens	172-181
25221599-4	2014	Peroxynitrite triggered apoptosis in these cells, and increased the expression of Fas-associated death domain, Bax, caspa-se-8 and Bcl-2.	Peroxynitrous Acid	0-13	caspase 8	Homo sapiens	116-126
24855207-6	2014	We identify a novel mechanism by showing that BV6 and dexamethasone cooperate to deplete cIAP1, cIAP2, and XIAP, thereby promoting assembly of the ripoptosome, a RIP1/FADD/caspase-8-containing complex.	Dexamethasone	54-67	caspase 8	Homo sapiens	172-181
24519546-8	2014	Cisplatin sensitivity analysis and cisplatin-induced activation of caspase 8 analysis were also performed.	Cisplatin	35-44	caspase 8	Homo sapiens	67-76
25002129-7	2014	Employing flow cytometric, DNA fragmentation and caspase activation analyses, demonstrated that the cytotoxic effect of the oils is mediated by a caspase-dependent apoptosis.	Oils	124-128	caspase 8	Homo sapiens	49-56
25002129-7	2014	Employing flow cytometric, DNA fragmentation and caspase activation analyses, demonstrated that the cytotoxic effect of the oils is mediated by a caspase-dependent apoptosis.	Oils	124-128	caspase 8	Homo sapiens	146-153
24973666-6	2014	Cordycepin-induced cell death was also associated with induction of Fas and death receptor 5, activation of caspase-8, and truncation of Bid (tBid), suggesting that tBid might serve to connect activation of both the mitochondrial-mediated intrinsic and death receptor-mediated extrinsic apoptotic pathways.	cordycepin	0-10	caspase 8	Homo sapiens	108-117
24973666-7	2014	The general caspase inhibitor, z-VAD-fmk, completely abolished cordycepin-induced cell death, demonstrating that cordycepin-induced apoptosis was dependent on the activation of caspases.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	31-40	caspase 8	Homo sapiens	177-185
24973666-7	2014	The general caspase inhibitor, z-VAD-fmk, completely abolished cordycepin-induced cell death, demonstrating that cordycepin-induced apoptosis was dependent on the activation of caspases.	cordycepin	63-73	caspase 8	Homo sapiens	177-185
24973666-7	2014	The general caspase inhibitor, z-VAD-fmk, completely abolished cordycepin-induced cell death, demonstrating that cordycepin-induced apoptosis was dependent on the activation of caspases.	cordycepin	113-123	caspase 8	Homo sapiens	177-185
25002129-11	2014	CONCLUSIONS: The results demonstrate that the EO-induced apoptosis in HL-60 cells is mediated by caspase-dependent pathways, involving caspases-3, -9, and -8, which are initiated by Bcl-2/Bax/Bid-dependent loss of DeltaPsim leading to release of cytochrome c to the cytoplasm to activate the caspase cascade.	Oils, Volatile	46-48	caspase 8	Homo sapiens	97-104
25261647-1	2014	PURPOSE: Our previous data have shown that emodin azide methyl anthraquinone derivative (AMAD) triggered mitochondrial- dependent cell apoptosis involving caspase-8-mediated Bid cleavage, and induced proteasomal degradation of HER2/neu by blocking Her2/neu binding to Hsp90.	azide methyl anthraquinone	50-76	caspase 8	Homo sapiens	155-164
24662747-3	2014	Triptolide increases levels of death receptor DR5 and decreases the pro-survival FLICE-like inhibitory protein (c-FLIP), which contribute to the activation of caspase-8.	triptolide	0-10	caspase 8	Homo sapiens	159-168
24858270-5	2014	The presence of cleaved caspase-3/-7, caspase-8 and caspase-9 in the cubelin treated population indicated the potential of the compound to induce apoptosis in HeLa cells via both intrinsic and extrinsic pathways.	6-(4-hydroxy-4-methyl-2-pentenoyl)-4,6-dimethyl-5-(3-methyl-2-butenyl)-1,3-cyclohexadienecarbaldehyde	69-76	caspase 8	Homo sapiens	38-47
24917907-7	2014	RESULTS: The expression ratios of FasL, activated form of caspase-8, caspase-9, and caspase-3 were significantly higher in DEX-treated polyps (P&lt;0.01).	Dexamethasone	123-126	caspase 8	Homo sapiens	58-67
24894297-0	2014	Targeting Notch1 signaling pathway positively affects the sensitivity of osteosarcoma to cisplatin by regulating the expression and/or activity of Caspase family.	Cisplatin	89-98	caspase 8	Homo sapiens	147-154
24894297-10	2014	Further mechanism investigation revealed that activation/inhibition of Notch1 sensitized/desensitized cisplatin-induced apoptosis, which probably depended on the changes in the activity of Caspase family, including Caspase 3, Caspase 8 and Caspase 9 in these cells.	Cisplatin	102-111	caspase 8	Homo sapiens	189-196
24894297-10	2014	Further mechanism investigation revealed that activation/inhibition of Notch1 sensitized/desensitized cisplatin-induced apoptosis, which probably depended on the changes in the activity of Caspase family, including Caspase 3, Caspase 8 and Caspase 9 in these cells.	Cisplatin	102-111	caspase 8	Homo sapiens	226-235
24535941-3	2014	In this study, we investigated the association of four polymorphisms (FAS -1377G&gt;A, -670A&gt;G, FASL -844C&gt;T, and CASP8 -652 6N ins&gt;del) with the clinical outcome of 940 gastric cancer patients in a Chinese population.	ammonium ferrous sulfate	70-73	caspase 8	Homo sapiens	120-125
24519064-6	2014	We also found that DHA decreased the mitochondrial membrane potential; activated the caspase-3, caspase-8, and caspase-9; and increased the ratio of Bax/Bcl-2.	artenimol	19-22	caspase 8	Homo sapiens	96-105
24594218-5	2014	RESULTS: HA22T/VGH cells treated with epirubicin increased the production of reactive oxygen species and nitric oxide, the expression of Fas, FasL, and Fas-associated death domain, and the activities of caspase-8 and caspase-3.	Epirubicin	38-48	caspase 8	Homo sapiens	203-212
24484936-6	2014	Using an RNAi-based strategy we could demonstrate that the extrinsic cell death is increased upon Fas-stimulation when endogenous caspase-8 is replaced by a mutant (S305A) mimicking the non-phosphorylated form.	ammonium ferrous sulfate	98-101	caspase 8	Homo sapiens	130-139
25009698-4	2014	Treatment with beta-lapachone caused mitochondrial transmembrane potential dissipation, stimulated the mitochondria-mediated intrinsic apoptotic pathway, as indicated by caspase-9 activation, cytochrome c release, Bcl-2 downregulation and Bax upregulation, as well as death receptor-mediated extrinsic apoptotic pathway, as indicated by activation of caspase-8 and truncation of Bid.	beta-lapachone	15-29	caspase 8	Homo sapiens	351-360
25195260-6	2014	RESULT: MTT results showed significant inhibitory action of matrine on CNE2 cells proliferation in does-dependent manner, which could up-regulate the expression of Caspase-3 mRNA and Caspase-3, Caspase-8, Caspase-9 protein in a dose-dependent manner.	monooxyethylene trimethylolpropane tristearate	8-11	caspase 8	Homo sapiens	194-203
22926505-7	2014	Apoptosis in reversine-treated cells was exhibited with PARP cleavage and caspase-3 and caspase-8 activation, but not caspase-9 activation, indicating that caspase-dependent apoptosis mediated by an extrinsic pathway took place in reversine-treated cells.	2-(4-morpholinoanilino)-6-cyclohexylaminopurine	13-22	caspase 8	Homo sapiens	88-97
24627148-0	2014	Anti-apoptotic effect of caspase inhibitors on H2O2-treated HeLa cells through early suppression of its oxidative stress.	Hydrogen Peroxide	47-51	caspase 8	Homo sapiens	25-32
24627148-7	2014	H2O2 also increased the ROS level at 1 h, and several caspase inhibitors attenuated the increased level at 1 h but not at 6, 12 and 24 h. H2O2 decreased the GSH level in HeLa cells at 1 h, and several caspase inhibitors attenuated the decreased level of GSH at this time.	Hydrogen Peroxide	0-4	caspase 8	Homo sapiens	201-208
24604218-9	2014	The curcumin- or EF-24-induced apoptosis in the Saos2 cells was mediated by the expression of Fas and activation of caspase-8, caspase-3 and poly(ADP-ribose) polymerase.	Curcumin	4-12	caspase 8	Homo sapiens	116-125
24604218-0	2014	Induction of apoptosis by diphenyldifluoroketone in osteogenic sarcoma cells is associated with activation of caspases.	diphenyldifluoroketone	26-48	caspase 8	Homo sapiens	110-118
24966519-2	2014	It is well known that apoptosis is regulated by some intracellular proteases, such as, Caspases (cysteine-dependent, aspartate-specific proteases).	Cysteine	97-105	caspase 8	Homo sapiens	87-95
24627148-7	2014	H2O2 also increased the ROS level at 1 h, and several caspase inhibitors attenuated the increased level at 1 h but not at 6, 12 and 24 h. H2O2 decreased the GSH level in HeLa cells at 1 h, and several caspase inhibitors attenuated the decreased level of GSH at this time.	Hydrogen Peroxide	138-142	caspase 8	Homo sapiens	54-61
24627148-7	2014	H2O2 also increased the ROS level at 1 h, and several caspase inhibitors attenuated the increased level at 1 h but not at 6, 12 and 24 h. H2O2 decreased the GSH level in HeLa cells at 1 h, and several caspase inhibitors attenuated the decreased level of GSH at this time.	Hydrogen Peroxide	138-142	caspase 8	Homo sapiens	201-208
24627148-7	2014	H2O2 also increased the ROS level at 1 h, and several caspase inhibitors attenuated the increased level at 1 h but not at 6, 12 and 24 h. H2O2 decreased the GSH level in HeLa cells at 1 h, and several caspase inhibitors attenuated the decreased level of GSH at this time.	Glutathione	157-160	caspase 8	Homo sapiens	54-61
24627148-7	2014	H2O2 also increased the ROS level at 1 h, and several caspase inhibitors attenuated the increased level at 1 h but not at 6, 12 and 24 h. H2O2 decreased the GSH level in HeLa cells at 1 h, and several caspase inhibitors attenuated the decreased level of GSH at this time.	Glutathione	157-160	caspase 8	Homo sapiens	201-208
24627148-7	2014	H2O2 also increased the ROS level at 1 h, and several caspase inhibitors attenuated the increased level at 1 h but not at 6, 12 and 24 h. H2O2 decreased the GSH level in HeLa cells at 1 h, and several caspase inhibitors attenuated the decreased level of GSH at this time.	Glutathione	254-257	caspase 8	Homo sapiens	54-61
24627159-7	2014	We also confirmed the anti-NF-kappaB activity of As4O6 with synergism with TNF-alpha by augmenting caspase-8 activation.	Arsenic Trioxide	49-54	caspase 8	Homo sapiens	99-108
24525192-7	2014	Moreover, immunoblotting analysis also showed that the co-administration of luteolin and paclitaxel activated caspase-8 and caspase-3 and increased the expression of Fas.	Paclitaxel	89-99	caspase 8	Homo sapiens	110-119
24604290-6	2014	Moreover, thioridazine induced gastric cancer cell apoptosis in a caspase-dependent manner, as shown by a decrease in the precursors of casapse-9, caspase-8 and caspase-3, and by the ability of the caspase inhibitor Z-VAD-FMK to reverse the cytotoxic effect of thioridazine.	Thioridazine	10-22	caspase 8	Homo sapiens	147-156
24966519-8	2014	Out of all the selected compounds, rosmarinic acid and curcumin proved to be the most potent inhibitors of Caspase-8 with binding energy (DeltaG) of -7.10 Kcal/mol and -7.08 Kcal/mol, respectively.	rosmarinic acid	35-50	caspase 8	Homo sapiens	107-116
24966519-8	2014	Out of all the selected compounds, rosmarinic acid and curcumin proved to be the most potent inhibitors of Caspase-8 with binding energy (DeltaG) of -7.10 Kcal/mol and -7.08 Kcal/mol, respectively.	Curcumin	55-63	caspase 8	Homo sapiens	107-116
24589337-4	2014	Caspase-8 was constitutively tyrosine phosphorylated in a panel of resting epithelial cells, but underwent SHP-1-dependent dephosphorylation in response to hydrogen peroxide, activated neutrophils, or inhibition of Src kinases.	Hydrogen Peroxide	156-173	caspase 8	Homo sapiens	0-9
24566867-8	2014	Concordantly, MC2392 induced rapid and massive, caspase-8-dependent cell death accompanied by RIP1 induction and ROS production.	mc2392	14-20	caspase 8	Homo sapiens	48-57
24530911-5	2014	On the other hand, we found that high concentrations of 24S-OHC induced apoptosis in T-lymphoma Jurkat cells which endogenously expressed caspase-8, and induced necroptosis - a form of programmed necrosis - in neuronal SH-SY5Y cells which expressed no caspase-8.	24-hydroxycholesterol	56-63	caspase 8	Homo sapiens	138-147
24530911-5	2014	On the other hand, we found that high concentrations of 24S-OHC induced apoptosis in T-lymphoma Jurkat cells which endogenously expressed caspase-8, and induced necroptosis - a form of programmed necrosis - in neuronal SH-SY5Y cells which expressed no caspase-8.	24-hydroxycholesterol	56-63	caspase 8	Homo sapiens	252-261
24589337-0	2014	Activated neutrophils induce epithelial cell apoptosis through oxidant-dependent tyrosine dephosphorylation of caspase-8.	Tyrosine	81-89	caspase 8	Homo sapiens	111-120
24589337-5	2014	Cells transfected with a mutant caspase-8 in which tyrosine residues at Tyr397 or Tyr465 are replaced by nonphosphorylatable phenylalanine underwent accelerated apoptosis, whereas either mutation of these residues to phosphomimetic glutamic acid or transfection with the Src kinases Lyn or c-Src inhibited hydrogen peroxide-induced apoptosis.	Phenylalanine	125-138	caspase 8	Homo sapiens	32-41
24589337-4	2014	Caspase-8 was constitutively tyrosine phosphorylated in a panel of resting epithelial cells, but underwent SHP-1-dependent dephosphorylation in response to hydrogen peroxide, activated neutrophils, or inhibition of Src kinases.	Tyrosine	29-37	caspase 8	Homo sapiens	0-9
24589337-5	2014	Cells transfected with a mutant caspase-8 in which tyrosine residues at Tyr397 or Tyr465 are replaced by nonphosphorylatable phenylalanine underwent accelerated apoptosis, whereas either mutation of these residues to phosphomimetic glutamic acid or transfection with the Src kinases Lyn or c-Src inhibited hydrogen peroxide-induced apoptosis.	Glutamic Acid	232-245	caspase 8	Homo sapiens	32-41
24589337-5	2014	Cells transfected with a mutant caspase-8 in which tyrosine residues at Tyr397 or Tyr465 are replaced by nonphosphorylatable phenylalanine underwent accelerated apoptosis, whereas either mutation of these residues to phosphomimetic glutamic acid or transfection with the Src kinases Lyn or c-Src inhibited hydrogen peroxide-induced apoptosis.	Hydrogen Peroxide	306-323	caspase 8	Homo sapiens	32-41
24589337-6	2014	Exposure to either hydrogen peroxide or lipopolysaccharide-stimulated neutrophils increased phosphorylation and activity of the phosphatase SHP-1, increased activity of caspases 8 and 3, and accelerated epithelial cell apoptosis.	Hydrogen Peroxide	19-36	caspase 8	Homo sapiens	169-185
24337869-6	2014	Collectively, the present study demonstrates a strong synergistic action of the combined treatment with Gem and DHA in inducing apoptosis of A549 cells via both the Bak-mediated intrinsic pathway and the Fas-caspase-8-mediated extrinsic pathway.	gemcitabine	104-107	caspase 8	Homo sapiens	208-217
24292505-8	2014	Finally, we found that extracellular NAD(+) inhibited spontaneous activation of caspase-9, but not caspase-8, and the pro-survival effect of extracellular NAD(+) was abrogated by the inhibitor of caspase-9, but not by the inhibitor of caspase-8.	NAD	37-43	caspase 8	Homo sapiens	235-244
24292505-8	2014	Finally, we found that extracellular NAD(+) inhibited spontaneous activation of caspase-9, but not caspase-8, and the pro-survival effect of extracellular NAD(+) was abrogated by the inhibitor of caspase-9, but not by the inhibitor of caspase-8.	NAD	155-161	caspase 8	Homo sapiens	235-244
24213561-6	2014	Finally, we highlight that two separate pathways are activated during the apoptotic death of GBM cells treated with a combination of TRAIL and R-roscovitine, one which leads to caspase-8 and caspase-3 activation and a second pathway, involving a Mcl-1:Noxa axis.	Roscovitine	143-156	caspase 8	Homo sapiens	177-186
24337869-6	2014	Collectively, the present study demonstrates a strong synergistic action of the combined treatment with Gem and DHA in inducing apoptosis of A549 cells via both the Bak-mediated intrinsic pathway and the Fas-caspase-8-mediated extrinsic pathway.	artenimol	112-115	caspase 8	Homo sapiens	208-217
24530510-1	2014	A previous study demonstrated that disaccharides, antioxidants, and caspase inhibitors can be used in freezing solutions to reduce the concentration of Me2SO from the current standard of 10% (v/v) to 5% (v/v) or 2.5% and to eliminate fetal bovine serum (FBS) for the cryopreservation of human amniotic fluid-derived stem cells (AFSCs).	me2so	152-157	caspase 8	Homo sapiens	68-75
24530510-2	2014	Hence, this study investigated whether an irreversible inhibitor of caspase enzymes, benzyloxycarbonyl-Val-Ala-dl-Asp-fluoromethylketone (zVAD-fmk), could be used in post-thaw culture media to increase the survival rate of AFSCs.	benzyloxycarbonyl-Val-Ala-DL-Asp-fluoromethylketone	85-136	caspase 8	Homo sapiens	68-75
24442508-7	2014	RESULTS: hIAPP treatment induced activation of caspase-8 and -3 in islet beta cells (via Fas upregulation), resulting in apoptosis, which was markedly reduced by blocking caspase-8, Fas or amyloid.	ammonium ferrous sulfate	89-92	caspase 8	Homo sapiens	47-63
24530510-2	2014	Hence, this study investigated whether an irreversible inhibitor of caspase enzymes, benzyloxycarbonyl-Val-Ala-dl-Asp-fluoromethylketone (zVAD-fmk), could be used in post-thaw culture media to increase the survival rate of AFSCs.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	138-146	caspase 8	Homo sapiens	68-75
24442508-7	2014	RESULTS: hIAPP treatment induced activation of caspase-8 and -3 in islet beta cells (via Fas upregulation), resulting in apoptosis, which was markedly reduced by blocking caspase-8, Fas or amyloid.	ammonium ferrous sulfate	89-92	caspase 8	Homo sapiens	47-56
23894007-4	2014	In addition to upregulation of Fas receptor mRNA, the activities of caspase-8 and -3 were significantly increased by LPC treatment.	Lysophosphatidylcholines	117-120	caspase 8	Homo sapiens	68-84
24651472-1	2014	We have recently demonstrated that histone deacetylase inhibitor, Vorinostat, applied as a single therapy or in combination with caspase-8 downregulation exhibits high anti-tumoral activity on endometrial carcinoma cell lines.	Vorinostat	66-76	caspase 8	Homo sapiens	129-138
24641804-9	2014	This iron-induced apoptosis was linked to enhanced caspase 8, reduced Bcl-2, Bcl-xL, phosphorylated Akt and GATA-4.	Iron	5-9	caspase 8	Homo sapiens	51-60
24641804-11	2014	In iron pretreated cardiomyocytes, the siRNA2 transfection further increased caspase 8 expression and decreased the expression of GATA-4, Bcl-2, Bcl-xL and phosphorylated Akt than iron pretreatment alone, but caspase 9 levels remained unchanged.	Iron	3-7	caspase 8	Homo sapiens	77-86
24365254-7	2014	In our study, BDMC-A exerted more potent effect on the modulation of selective apoptotic markers (intrinsic pathway: p53, Bcl-2, Bax, cyt c, Apaf-1, caspase-9, 3, PARP; extrinsic pathway: FasL, caspase 8) compared to curcumin.	BDMC-A	14-20	caspase 8	Homo sapiens	194-203
24330236-5	2014	It reduced the formation of reactive oxygen species in the cells, increased the catalase (CAT) and glutathione (GSH) concentrations, suppressed the DU-induced soluble Fas receptor (sFasR) and soluble Fas ligand (sFasL) overexpression, suppressed the release of cytochrome c and apoptosis inhibitor factor (AIF) from mitochondria to cytoplasm, inhibited the activation of caspase-9, caspase-8 and caspase-3, and induced metallothionein (MT) expression.	du	148-150	caspase 8	Homo sapiens	382-391
24330236-8	2014	Through independent mechanisms, such as indirect antioxidant effects, inhibition of the activation of caspase-9, caspase-8 and caspase-3, and induction of MT expression, Zn inhibits DU-induced apoptosis.	du	182-184	caspase 8	Homo sapiens	113-122
23981054-6	2014	RSV decreased hepatocyte apoptosis by reducing caspase 8 and caspase 3 but not Bax and Bcl-xL.	Resveratrol	0-3	caspase 8	Homo sapiens	47-56
24480042-4	2014	alpha-Mangostin also activated caspases-8, -9, and -7; increased the protein levels of Bax, p53, and cytosolic cytochrome c; and induced PARP cleavage while reducing Bid and Bcl-2 protein expression.	mangostin	0-15	caspase 8	Homo sapiens	31-53
24481288-0	2014	Corosolic acid induces apoptotic cell death in HCT116 human colon cancer cells through a caspase-dependent pathway.	corosolic acid	0-14	caspase 8	Homo sapiens	89-96
24481288-7	2014	The apoptotic cell death induced by CA was accompanied by the activation of caspase-8, -9 and -3, which was completely abrogated by the pan-caspase inhibitor, z-VAD-FMK.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	159-168	caspase 8	Homo sapiens	76-96
24481288-7	2014	The apoptotic cell death induced by CA was accompanied by the activation of caspase-8, -9 and -3, which was completely abrogated by the pan-caspase inhibitor, z-VAD-FMK.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	159-168	caspase 8	Homo sapiens	76-83
24442640-1	2014	Caspase-8 is a cysteine directed aspartate-specific protease that is activated at the cytosolic face of the cell membrane upon receptor ligation.	Cysteine	15-23	caspase 8	Homo sapiens	0-9
24655592-12	2014	Inhibition of autophagic flux using chloroquine prevented clearance of p62 aggregates, leading to caspase-8 activation and cell death in C4-2 cells.	Chloroquine	36-47	caspase 8	Homo sapiens	98-107
23524581-12	2014	Recent studies have shown that PTX-stabilized microtubules serves as a scaffold for pro-caspase-8 binding and induction of apoptosis downstream of induced-proximity activation of caspase-8.	Paclitaxel	31-34	caspase 8	Homo sapiens	88-97
23524581-12	2014	Recent studies have shown that PTX-stabilized microtubules serves as a scaffold for pro-caspase-8 binding and induction of apoptosis downstream of induced-proximity activation of caspase-8.	Paclitaxel	31-34	caspase 8	Homo sapiens	179-188
24618889-7	2014	Apoptosis resistance was caused by reduced expression of caspase-8 and DR 4/TRAIL-R1 in ESS-1 and MES-SA cells, respectively, due to epigenetic silencing by DNA hypermethylation of gene promoter sequences.	2-(N-morpholino)ethanesulfonic acid	98-101	caspase 8	Homo sapiens	57-66
24618889-7	2014	Apoptosis resistance was caused by reduced expression of caspase-8 and DR 4/TRAIL-R1 in ESS-1 and MES-SA cells, respectively, due to epigenetic silencing by DNA hypermethylation of gene promoter sequences.	2-chloro-10-(4'(N-beta-hydroxyethyl)piperazinyl-1')acetylphenothiazine	102-104	caspase 8	Homo sapiens	57-66
24547878-9	2014	The autophagy inhibitor bafilomycin A1 (BaF) decreased 1-induced cell viability and increased pp38, pJNK, FasL, caspase-8 activation, and caspase-3 activation.	bafilomycin A1	24-38	caspase 8	Homo sapiens	112-121
24462874-4	2014	H2O2 increased the activated caspase-8 sequestered in the mitochondria thereby decreasing cell death through the extrinsic apoptotic pathway.	Hydrogen Peroxide	0-4	caspase 8	Homo sapiens	29-38
24549175-8	2014	Additionally, kaempferol increased the levels of membrane-bound FAS ligand, decreased those of uncleaved caspase-8 and intact Bid and increased caspase-8 activity.	kaempferol	14-24	caspase 8	Homo sapiens	105-114
24549175-8	2014	Additionally, kaempferol increased the levels of membrane-bound FAS ligand, decreased those of uncleaved caspase-8 and intact Bid and increased caspase-8 activity.	kaempferol	14-24	caspase 8	Homo sapiens	144-153
24398693-4	2014	The caspase inhibitor benzyloxycarbonyl-Val-Ala-Asp(OMe)-fluoromethylketone greatly diminished caspase 8-dependent NF-kappaB activation induced by Fas ligand (FasL) when c-FLIPL, but not its N-terminal fragment c-FLIP(p43), was expressed.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	22-75	caspase 8	Homo sapiens	95-104
24507386-14	2014	The tumor tissues were harvested after treatment, and ACBP-L and Cisplatin treatment suppressed Bcl-2, and induced Bax, Caspase 3, and Caspase 8 molecules as detected by RT-PCR and immunohistochemistry.	Cisplatin	65-74	caspase 8	Homo sapiens	135-144
24577083-7	2014	Collectively, our findings demonstrate that selenite caused CYLD upregulation via LEF1 and cIAP downregulation, both of which contribute to the degradation of ubiquitin chains on RIP1 and subsequent caspase-8 activation and apoptosis.	Selenious Acid	44-52	caspase 8	Homo sapiens	199-208
24586490-6	2014	In a post-hoc analysis, plaque caspase-3 (P&lt;0.001) and caspase-8 (P&lt;0.05) activity were found to be significantly lower in the darapladib 80-mg group versus placebo.	darapladib 80	133-146	caspase 8	Homo sapiens	58-67
24523856-7	2014	The results showed that exposure of the cells to BP-C1 for 48 h, significantly (P&lt;0.001) reduced cell viability, induced apoptosis and activated caspase 8 and caspace 9.	bp-c1	49-54	caspase 8	Homo sapiens	148-157
24286513-7	2014	The acetyl-L-carnitine-cisplatin combination caused reduced expression of genes Casp8, Fas, Casp1, Tnfrsf11b, Tnfrsf10b induced by cisplatin.	Acetylcarnitine	4-22	caspase 8	Homo sapiens	80-85
24291674-6	2014	More specifically, we found that HIMOXOL was able to activate the extrinsic apoptotic pathway, which was proven by observation of caspase-8, caspase-3 and PARP-1 protein activation in Western blot analysis.	himoxol	33-40	caspase 8	Homo sapiens	130-139
24286513-6	2014	Genes displaying increase in expression of apoptosis, related to cisplatin treatment, were Casp8, Bcl10, Bcl2, Bcl2l1, Bcl2l2, Bid, Naip1, Bnip3l, Card6, Pak7, Cd40, Trp 53inp1, Cideb and Cd70.	Cisplatin	65-74	caspase 8	Homo sapiens	91-96
24516579-8	2014	Etodolac induced apoptosis of FMS-1 cells through the activation of caspase-8, -9, and -3.	Etodolac	0-8	caspase 8	Homo sapiens	68-89
24516579-9	2014	Moreover, several caspase inhibitors significantly inhibited etodolac-induced apoptosis.	Etodolac	61-69	caspase 8	Homo sapiens	18-25
24270406-10	2014	Finally, caspase-8 is involved in glucocortocoid-induced thymocyte apoptosis through an activation loop with the protein GILZ.	glucocortocoid	34-48	caspase 8	Homo sapiens	9-18
24286513-7	2014	The acetyl-L-carnitine-cisplatin combination caused reduced expression of genes Casp8, Fas, Casp1, Tnfrsf11b, Tnfrsf10b induced by cisplatin.	Cisplatin	23-32	caspase 8	Homo sapiens	80-85
24286513-7	2014	The acetyl-L-carnitine-cisplatin combination caused reduced expression of genes Casp8, Fas, Casp1, Tnfrsf11b, Tnfrsf10b induced by cisplatin.	Cisplatin	131-140	caspase 8	Homo sapiens	80-85
24128051-8	2014	Moreover, gemcitabine increased CH11-induced caspase-8 and caspase-3 cleavage and proteolytic activity.	gemcitabine	10-21	caspase 8	Homo sapiens	45-54
24296129-4	2014	Sulforaphane-induced apoptosis was associated with the activation of caspase-8 and -9, the initiators caspases of the extrinsic and intrinsic apoptotic pathways, respectively, and activation of effector caspase-3 and cleavage of poly (ADP-ribose) polymerase.	sulforaphane	0-12	caspase 8	Homo sapiens	69-85
24128051-8	2014	Moreover, gemcitabine increased CH11-induced caspase-8 and caspase-3 cleavage and proteolytic activity.	4-dimethylamino-3',4'-dimethoxychalcone	32-36	caspase 8	Homo sapiens	45-54
24128051-10	2014	These results demonstrate that gemcitabine: (i) induces up-regulation of FasL in lung cancer cells triggering cell apoptosis via an autocrine/paracrine loop; (ii) induces a Fas-dependent apoptosis mediated by caspase-8 and caspase-3 activation; (iii) enhances the sensitivity of lung cancer cells to cytotoxic activity of LAK cells and malignant pleural fluid lymphocytes, partially via Fas/FasL pathway.	gemcitabine	31-42	caspase 8	Homo sapiens	209-218
24337492-0	2014	Licochalcone A induces apoptosis in KB human oral cancer cells via a caspase-dependent FasL signaling pathway.	licochalcone A	0-14	caspase 8	Homo sapiens	69-76
24526787-7	2014	Birinapant induced death receptor-/caspase-8-mediated apoptosis in AML cells, including in AML stem/progenitor cells, but not in normal CD34(+) cells.	birinapant	0-10	caspase 8	Homo sapiens	35-44
23709189-10	2014	The cytotoxicity of the most potent ring-DIM, 4,4"-dibromoDIM, but not the other compounds was decreased by an inhibitor of caspase -3.	4,4"-dibromodim	46-61	caspase 8	Homo sapiens	124-131
24337492-8	2014	Additionally, Lico-A-induced apoptosis in KB oral cancer cells was mediated by the expression of factor associated suicide ligand (FasL) and activated caspase-8 and -3 and poly(ADP-ribose) polymerase (PARP).	licochalcone A	14-20	caspase 8	Homo sapiens	151-167
24337492-9	2014	Furthermore, in the KB oral cancer cells co-stimulation with a caspase inhibitor (Z-VAD-fmk) and Lico-A significantly abolished the apoptotic phenomena.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	82-91	caspase 8	Homo sapiens	63-70
24337492-10	2014	Our findings demonstrated that Lico-A-induced apoptosis in KB oral cancer cells involves the extrinsic apoptotic signaling pathway, which involves a caspase-dependent FasL-mediated death receptor pathway.	licochalcone A	31-37	caspase 8	Homo sapiens	149-156
24194395-6	2014	Pretreatment of the HepG2 cells with caspase-3, caspase-8, and caspase-9 inhibitors partially but significantly reduced the release of lactate dehydrogenase, indicating that sertraline-induced apoptosis is mediated by both intrinsic and extrinsic apoptotic pathways.	Sertraline	174-184	caspase 8	Homo sapiens	48-57
24407243-8	2014	24S-OHC induced apoptosis in T-lymphoma Jurkat cells, which endogenously expressed caspase-8, but did not induce apoptosis in SH-SY5Y cells, which expressed no caspase-8.	24-hydroxycholesterol	0-7	caspase 8	Homo sapiens	83-92
24460687-15	2014	Rm-HE induced apoptosis was partially JNK-dependent and characterized by an increase in Fas-L levels together with activation of caspases 8, 3, 7 and 9, whereas neither the pro-apoptotic nor anti-apoptotic mitochondrial membrane proteins analyzed were significantly altered.	rm-he	0-5	caspase 8	Homo sapiens	129-151
24364735-1	2014	Our previous study showed that trans-fatty acids can cause apoptosis of endothelial cells through the caspase pathway and the mitochondrial pathway.	Trans Fatty Acids	31-48	caspase 8	Homo sapiens	102-109
24413065-5	2014	Caspase 8-negative I9.2 cells were considerably more resistant to [Gem+Clo+Ed] than caspase 8-positive cells.	Clofarabine	71-74	caspase 8	Homo sapiens	0-9
24407243-9	2014	In Jurkat cells treated with the pan-caspase inhibitor ZVAD and in caspase-8-deficient Jurkat cells, 24S-OHC was found to induce caspase-independent cell death, and this was partially but significantly inhibited by Necrostatin-1.	24-hydroxycholesterol	101-108	caspase 8	Homo sapiens	67-76
24407243-9	2014	In Jurkat cells treated with the pan-caspase inhibitor ZVAD and in caspase-8-deficient Jurkat cells, 24S-OHC was found to induce caspase-independent cell death, and this was partially but significantly inhibited by Necrostatin-1.	necrostatin-1	215-228	caspase 8	Homo sapiens	67-76
25124618-5	2014	Additionally, MBS treatment led to activation of caspase-9, caspase-8 and caspase-3, and cleavage of PARP, which was abolished by pretreatment with the pan-caspase inhibitor Z-VAD-FMK.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	174-183	caspase 8	Homo sapiens	60-69
24913659-0	2014	Caspases and ROS - dependent mechanism of action mediated by combination of WP 631 and epothilone B.	epothilone B	87-99	caspase 8	Homo sapiens	0-8
25292102-4	2014	Our findings indicated that IFN-gamma treatment caused a time-dependent reduction in cell viability and induced apoptosis through a FADD-mediated caspase-8/tBid/mitochondria-dependent pathway in both cell lines.	tBID	156-160	caspase 8	Homo sapiens	146-155
24146141-9	2014	Interestingly, stimulation of GSH loss by MK571 also enhanced the initiator phase of apoptosis by stimulating initiator caspase 8 and 9 activity and pro-apoptotic BCL-2 interacting domain cleavage.	Glutathione	30-33	caspase 8	Homo sapiens	120-129
24146141-9	2014	Interestingly, stimulation of GSH loss by MK571 also enhanced the initiator phase of apoptosis by stimulating initiator caspase 8 and 9 activity and pro-apoptotic BCL-2 interacting domain cleavage.	verlukast	42-47	caspase 8	Homo sapiens	120-129
25374178-0	2014	Roles of the Bcl-2/Bax ratio, caspase-8 and 9 in resistance of breast cancer cells to paclitaxel.	Paclitaxel	86-96	caspase 8	Homo sapiens	30-39
24211971-11	2014	Fucosterol also increased the protein expression of Fas, FasL, Fadd and Caspase-8.	fucosterol	0-10	caspase 8	Homo sapiens	72-81
24583858-6	2014	Glionitrin A activated caspase-8, -9 and -3 and also released endonuclease G from the mitochondria to the nucleus in a dose-dependent manner.	glionitrin A	0-12	caspase 8	Homo sapiens	23-43
24716979-0	2014	Curcumin inhibits MHCC97H liver cancer cells by activating ROS/TLR-4/caspase signaling pathway.	Curcumin	0-8	caspase 8	Homo sapiens	69-76
24716979-0	2014	Curcumin inhibits MHCC97H liver cancer cells by activating ROS/TLR-4/caspase signaling pathway.	Reactive Oxygen Species	59-62	caspase 8	Homo sapiens	69-76
24716979-3	2014	Also, we showed that increased intracellular ROS formation activated the TLR-4/MyD-88 signaling pathway, resulting in activation of caspase-8 and caspase-3, which eventually led to apoptosis in MHCC97H cells.	Reactive Oxygen Species	45-48	caspase 8	Homo sapiens	132-141
25036678-6	2014	Taken together, these results suggest that DHS-induced apoptosis is mediated by a caspase-dependent pathway in human HeLa cells.	Silybin	43-46	caspase 8	Homo sapiens	82-89
24895574-4	2014	We further found that icaritin could significantly inhibit Raji cells proliferation with S-phase arrest of cell cycle and induced cell apoptosis accompanied by activation of caspase-8 and caspase-9 and cleavage of PARP.	icaritin	22-30	caspase 8	Homo sapiens	174-183
25036678-0	2014	Induction of apoptosis by 2,3-dehydrosilybin via a caspase-dependent pathway in human HeLa cells.	Silybin	26-44	caspase 8	Homo sapiens	51-58
25036678-5	2014	Furthermore, z-VAD-fmk (a pan-caspase inhibitor) and z-IETD-fmk (a specific caspase-8 inhibitor) abolished the DHS-induced activation of the caspase-8, -9, and -3, cleavage of PARP, the depolarization of Deltapsim, the release of cytochrome c, the cleavage of Bid, and the downregulation of Bcl-2.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	13-22	caspase 8	Homo sapiens	30-37
24065392-5	2014	The results suggest that parthenolide may induce apoptotic cell death in ovarian carcinoma cell lines by activating the mitochondrial pathway and the caspase-8- and Bid-dependent pathways.	parthenolide	25-37	caspase 8	Homo sapiens	150-168
25036678-5	2014	Furthermore, z-VAD-fmk (a pan-caspase inhibitor) and z-IETD-fmk (a specific caspase-8 inhibitor) abolished the DHS-induced activation of the caspase-8, -9, and -3, cleavage of PARP, the depolarization of Deltapsim, the release of cytochrome c, the cleavage of Bid, and the downregulation of Bcl-2.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	13-22	caspase 8	Homo sapiens	141-162
25036678-5	2014	Furthermore, z-VAD-fmk (a pan-caspase inhibitor) and z-IETD-fmk (a specific caspase-8 inhibitor) abolished the DHS-induced activation of the caspase-8, -9, and -3, cleavage of PARP, the depolarization of Deltapsim, the release of cytochrome c, the cleavage of Bid, and the downregulation of Bcl-2.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	53-63	caspase 8	Homo sapiens	76-85
25036678-5	2014	Furthermore, z-VAD-fmk (a pan-caspase inhibitor) and z-IETD-fmk (a specific caspase-8 inhibitor) abolished the DHS-induced activation of the caspase-8, -9, and -3, cleavage of PARP, the depolarization of Deltapsim, the release of cytochrome c, the cleavage of Bid, and the downregulation of Bcl-2.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	53-63	caspase 8	Homo sapiens	141-162
25036678-5	2014	Furthermore, z-VAD-fmk (a pan-caspase inhibitor) and z-IETD-fmk (a specific caspase-8 inhibitor) abolished the DHS-induced activation of the caspase-8, -9, and -3, cleavage of PARP, the depolarization of Deltapsim, the release of cytochrome c, the cleavage of Bid, and the downregulation of Bcl-2.	Silybin	111-114	caspase 8	Homo sapiens	30-37
25036678-5	2014	Furthermore, z-VAD-fmk (a pan-caspase inhibitor) and z-IETD-fmk (a specific caspase-8 inhibitor) abolished the DHS-induced activation of the caspase-8, -9, and -3, cleavage of PARP, the depolarization of Deltapsim, the release of cytochrome c, the cleavage of Bid, and the downregulation of Bcl-2.	Silybin	111-114	caspase 8	Homo sapiens	76-85
25036678-5	2014	Furthermore, z-VAD-fmk (a pan-caspase inhibitor) and z-IETD-fmk (a specific caspase-8 inhibitor) abolished the DHS-induced activation of the caspase-8, -9, and -3, cleavage of PARP, the depolarization of Deltapsim, the release of cytochrome c, the cleavage of Bid, and the downregulation of Bcl-2.	Silybin	111-114	caspase 8	Homo sapiens	141-162
24558306-5	2014	Ginsenoside 20(S)-Rg3 induced apoptosis through activation of caspase-3, caspase-8, and caspase-9, as well as regulation of Bcl-2 and Bax expression.	ginsenoside 20	0-14	caspase 8	Homo sapiens	73-82
24558306-5	2014	Ginsenoside 20(S)-Rg3 induced apoptosis through activation of caspase-3, caspase-8, and caspase-9, as well as regulation of Bcl-2 and Bax expression.	Sulfur	14-17	caspase 8	Homo sapiens	73-82
24558306-6	2014	Taken together, these findings suggest that heat-processing serves as an increase in the antitumor activity of American ginseng in AGS cells, and ginsenoside 20(S)-Rg3, the active component produced by heat-processing, induces the activation of caspase-3, caspase-8, and caspase-9, which contributes to the apoptotic cell death.	Ginsenosides	146-157	caspase 8	Homo sapiens	256-265
23564030-6	2014	Mechanically, activation of caspase-8, caspase-9, and caspase-3 and increasing expression of cell cycle regulatory protein p21(WAF1/CIP1) and p27(KIP1) were observed in tetrandrine-treated RCC cells.	tetrandrine	169-180	caspase 8	Homo sapiens	28-37
25301502-5	2014	The results of the present study indicate that naftopidil induces apoptosis of NCI-H2052 cells by upregulating the expression of TNF-alpha and stimulating the secretion of FasL, a ligand for the death receptor Fas, both to activate caspase-8 and the effector caspase-3, leading to the suppression of NCI-H2052 cell proliferation in vivo.	naftopidil	47-57	caspase 8	Homo sapiens	232-241
23802642-10	2014	RESULTS: HPFs exposed to TEGDMA showed significant increases in multiple pro-apoptotic proteins such as Bid, Bim, Caspase 3, Caspase 8, and Cytochrome c at 24 hours.	triethylene glycol dimethacrylate	25-31	caspase 8	Homo sapiens	125-134
23948751-0	2013	Reversal of boswellic acid analog BA145 induced caspase dependent apoptosis by PI3K inhibitor LY294002 and MEK inhibitor PD98059.	boswellic acid	12-26	caspase 8	Homo sapiens	48-55
24368570-9	2013	Gliotoxin-induced activation of caspase-3, caspase-8 and caspase-9, down-regulation of Bcl-2, up-regulation of Bax and cytochromec (cyt c) release showed evidence for the gliotoxin activity on apoptosis.	Gliotoxin	0-9	caspase 8	Homo sapiens	43-52
24189055-6	2013	However, use of selective caspase inhibitors revealed that the caspase-8-dependent pathway is the major contributor to 15a-induced apoptosis.	15a	119-122	caspase 8	Homo sapiens	63-72
24317430-4	2013	In addition, the up-regulation of caspase-3 and -8 expression and activation of both caspases may also contribute to the apoptotic cell death of human colorectal adenocarcinoma HT-29 cells when exposed to IP6.	Phytic Acid	205-208	caspase 8	Homo sapiens	85-93
24317430-5	2013	Collectively, this present study has shown that rice bran IP6 induces apoptosis, by regulating the pro- and anti-apoptotic markers; Bax and Bcl-xl and via the activation of caspase molecules (caspase-3 and -8).	Phytic Acid	58-61	caspase 8	Homo sapiens	192-208
23982257-11	2013	SP600125 remarkably reduced the expression of cleaved caspase-8, -3, and PARP and the phosphorylation of FADD and c-Jun, as well as apoptotic cell death.	pyrazolanthrone	0-8	caspase 8	Homo sapiens	54-63
23726389-8	2013	It also inhibited Fas, caspase-3, caspase-8 and integrin alphavbeta6 (alphavbeta6) gene expressions in the NAC-treated piglets.	Acetylcysteine	107-110	caspase 8	Homo sapiens	34-43
24309938-7	2013	In addition, HDAC inhibitors synergized with TRAIL and cisplatin in NSCLC cells in a FLIP- and caspase-8-dependent manner.	Cisplatin	55-64	caspase 8	Homo sapiens	95-104
23948751-0	2013	Reversal of boswellic acid analog BA145 induced caspase dependent apoptosis by PI3K inhibitor LY294002 and MEK inhibitor PD98059.	ba145	34-39	caspase 8	Homo sapiens	48-55
23948751-0	2013	Reversal of boswellic acid analog BA145 induced caspase dependent apoptosis by PI3K inhibitor LY294002 and MEK inhibitor PD98059.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	94-102	caspase 8	Homo sapiens	48-55
23948751-0	2013	Reversal of boswellic acid analog BA145 induced caspase dependent apoptosis by PI3K inhibitor LY294002 and MEK inhibitor PD98059.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	121-128	caspase 8	Homo sapiens	48-55
23948751-7	2013	Besides, LY and PD also reversed the caspase dependent DNA damage induced by BA145.	ba145	77-82	caspase 8	Homo sapiens	37-44
23948751-8	2013	Further studies revealed that LY and PD significantly reversed the inhibitory effect of BA145 on cell cycle regulatory proteins by upregulating hyperphosphorylated retinoblastoma, pRB (S795) and downregulating p21 and cyclin E. More importantly, all these events were reversed by caspase inhibition by Z-VAD-fmk, suggesting that both LY and PD act at the level of caspases to diminish the apoptosis induced by BA145.	ba145	88-93	caspase 8	Homo sapiens	280-287
23948751-8	2013	Further studies revealed that LY and PD significantly reversed the inhibitory effect of BA145 on cell cycle regulatory proteins by upregulating hyperphosphorylated retinoblastoma, pRB (S795) and downregulating p21 and cyclin E. More importantly, all these events were reversed by caspase inhibition by Z-VAD-fmk, suggesting that both LY and PD act at the level of caspases to diminish the apoptosis induced by BA145.	ba145	88-93	caspase 8	Homo sapiens	364-372
24161692-4	2013	Quinocetone-induced apoptosis in HepG2 cells was characterized by cell and nuclei morphology change, cell membrane phosphatidylserine translocation, DNA fragmentation, cleavage of poly (ADP-ribose) polymerase (PARP) and a cascade activation of caspase-8, caspase-9 and caspase-3.	quinocetone	0-11	caspase 8	Homo sapiens	244-253
24161692-8	2013	Both soluble TNFR1 receptors and caspase inhibitors suppressed quinocetone-induced apoptosis.	quinocetone	63-74	caspase 8	Homo sapiens	33-40
24161692-10	2013	Taken together, quinocetone induced apoptosis in HepG2 cells via activation of caspase, interaction of TNF-alpha and TNFR1 and modulation of the protein levels of Bid, Bax and Bcl-2, involving the participation of p53, p38 and JNK.	quinocetone	16-27	caspase 8	Homo sapiens	79-86
23794119-13	2013	Curcumin effect was mediated through activation of TNFR, CASP 8, CASP3, BID, BAX, and down-regulation of NFkappaB, NDRG 1, and BCL2L10 genes.	Curcumin	0-8	caspase 8	Homo sapiens	57-63
22821714-6	2013	Subsequently, pretreatment with specific inhibitor of caspase-8 Z-LEHD-FMK and caspase-9 Z-LEHD-FMK significantly attenuated caspase-3 activity, the cleavage of caspase-3 and PARP, meanwhile increased the cell viability.	benzyloxycarbonyl-leucyl-glutamyl-histidyl-aspartic acid fluoromethyl ketone	64-74	caspase 8	Homo sapiens	54-63
22821714-6	2013	Subsequently, pretreatment with specific inhibitor of caspase-8 Z-LEHD-FMK and caspase-9 Z-LEHD-FMK significantly attenuated caspase-3 activity, the cleavage of caspase-3 and PARP, meanwhile increased the cell viability.	benzyloxycarbonyl-leucyl-glutamyl-histidyl-aspartic acid fluoromethyl ketone	89-99	caspase 8	Homo sapiens	54-63
24121507-0	2013	p62/sequestosome-1 up-regulation promotes ABT-263-induced caspase-8 aggregation/activation on the autophagosome.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	42-45	caspase 8	Homo sapiens	58-67
24064712-0	2013	Valproic acid inhibits the growth of HeLa cervical cancer cells via caspase-dependent apoptosis.	Valproic Acid	0-13	caspase 8	Homo sapiens	68-75
24121507-4	2013	Here, we demonstrate that p62 can regulate a caspase-8-dependent apoptosis in response to the BH3 mimetic agent, ABT-263.	BH 3	94-97	caspase 8	Homo sapiens	45-54
24121507-4	2013	Here, we demonstrate that p62 can regulate a caspase-8-dependent apoptosis in response to the BH3 mimetic agent, ABT-263.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	113-116	caspase 8	Homo sapiens	45-54
24121507-5	2013	Up-regulation of p62 was shown to enhance ABT-263-induced caspase-8 activation that was Bax-dependent and resulted from mitochondrial amplification.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	42-45	caspase 8	Homo sapiens	58-67
24121507-8	2013	Endogenous p62 co-localized with caspase-8 in the presence of ABT-263 plus an autophagy inhibitor.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	62-65	caspase 8	Homo sapiens	33-42
24121507-12	2013	A direct activator of caspase-8, i.e., TRAIL, alone or combined with ABT-263, induced caspase-8 aggregation and co-localization with p62 that was associated with a synergistic drug interaction.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	69-72	caspase 8	Homo sapiens	22-31
24121507-12	2013	A direct activator of caspase-8, i.e., TRAIL, alone or combined with ABT-263, induced caspase-8 aggregation and co-localization with p62 that was associated with a synergistic drug interaction.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	69-72	caspase 8	Homo sapiens	86-95
24245877-9	2013	PEEP also induced significant Fas and FasL activation, and cleavage of caspase-8.	peep	0-4	caspase 8	Homo sapiens	71-80
24236158-6	2013	In contrast, SAHA increased expression of Caspase-3, p21 and p53 mRNA, and upregulated acetyl-Histones H3 and H4, Caspase-8, and p53 proteins.	Vorinostat	13-17	caspase 8	Homo sapiens	114-123
24260465-9	2013	In HaCaT cells resveratrol pretreatment: reduces UVB-induced ROS formation, enhances the detrimental effect of UVB on HaCaT cell vitality, increases UVB-induced caspase 8, PARP cleavage, and induces autophagy.	Resveratrol	15-26	caspase 8	Homo sapiens	161-170
24100030-5	2013	We also show that upon TRAIL treatment, Src, caspase-8, and PP2A/C (a catalytic subunit of the PP2A phosphatase) are redistributed into lipid rafts, a microdomain of the plasma membrane enriched with cholesterol, where PP2A dephosphorylates Src at tyrosine 418 and in turn inhibits caspase-8 phosphorylation.	Cholesterol	200-211	caspase 8	Homo sapiens	45-54
24100030-5	2013	We also show that upon TRAIL treatment, Src, caspase-8, and PP2A/C (a catalytic subunit of the PP2A phosphatase) are redistributed into lipid rafts, a microdomain of the plasma membrane enriched with cholesterol, where PP2A dephosphorylates Src at tyrosine 418 and in turn inhibits caspase-8 phosphorylation.	Tyrosine	248-256	caspase 8	Homo sapiens	45-54
24244715-4	2013	Triptolide induces HEp-2 cell cycle arrest at the G1 phase and apoptosis through intrinsic and extrinsic pathways since both caspase-8 and -9 are activated.	triptolide	0-10	caspase 8	Homo sapiens	125-141
24100030-4	2013	Specifically, we show that TRAIL treatment activates the tyrosine kinase Src, which subsequently phosphorylates caspase-8 at tyrosine 380, leading to the inhibition of caspase-8 activation.	Tyrosine	57-65	caspase 8	Homo sapiens	112-121
24100030-4	2013	Specifically, we show that TRAIL treatment activates the tyrosine kinase Src, which subsequently phosphorylates caspase-8 at tyrosine 380, leading to the inhibition of caspase-8 activation.	Tyrosine	57-65	caspase 8	Homo sapiens	168-177
24195809-6	2013	Subsequently, the expression of proteins relating to TLR3 signaling pathway, such as NF-kappaB, caspase 8 survivin, bcl-2 and PCNA affected by BM-06, sorafenib alone or in combination, was compared.	Sorafenib	150-159	caspase 8	Homo sapiens	96-105
23992829-11	2013	In addition, NaHS increased the phosphorylation of Akt and decreased the expression of Caspase 8 and Bax in hiPSC-MSCs.	sodium bisulfide	13-17	caspase 8	Homo sapiens	87-96
23826964-5	2013	The results suggest that brefeldin A may induce apoptotic cell death in ovarian carcinoma cell lines by activating the mitochondrial pathway and the caspase-8- and Bid-dependent pathways.	Brefeldin A	25-36	caspase 8	Homo sapiens	149-167
23826964-6	2013	The apoptotic effect of brefeldin A seems to be mediated by formation of reactive oxygen species and depletion of GSH, which results in the activation of apoptotic caspases.	Brefeldin A	24-35	caspase 8	Homo sapiens	164-172
23826964-6	2013	The apoptotic effect of brefeldin A seems to be mediated by formation of reactive oxygen species and depletion of GSH, which results in the activation of apoptotic caspases.	Reactive Oxygen Species	73-96	caspase 8	Homo sapiens	164-172
23826964-6	2013	The apoptotic effect of brefeldin A seems to be mediated by formation of reactive oxygen species and depletion of GSH, which results in the activation of apoptotic caspases.	Glutathione	114-117	caspase 8	Homo sapiens	164-172
23994488-10	2013	In addition, our results also indicated that Pc13 induced a caspase-dependent apoptotic response, being activation of caspase-8, -9 and -3 the result of a post-mitochondrial event.	PC13	45-49	caspase 8	Homo sapiens	118-138
24044897-7	2013	Addition of ceramide analog induced caspase-8 activation leading to caspase-3 activation and apoptotic neuronal death.	Ceramides	12-20	caspase 8	Homo sapiens	36-45
23292890-8	2013	In addition, caspase-8 inhibitor (z-IETD-fmk, 50 muMu) was found to reverse andrographolide-induced caspase-8 activation, whereas the antagonistic anti-Fas receptor (ZB4, 500 ng/mL) and anti-tumor necrosis factor-R1 (H398, 10 microg/mL) monoclonal antibodies did not.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	34-44	caspase 8	Homo sapiens	13-22
23292890-8	2013	In addition, caspase-8 inhibitor (z-IETD-fmk, 50 muMu) was found to reverse andrographolide-induced caspase-8 activation, whereas the antagonistic anti-Fas receptor (ZB4, 500 ng/mL) and anti-tumor necrosis factor-R1 (H398, 10 microg/mL) monoclonal antibodies did not.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	34-44	caspase 8	Homo sapiens	100-109
23292890-8	2013	In addition, caspase-8 inhibitor (z-IETD-fmk, 50 muMu) was found to reverse andrographolide-induced caspase-8 activation, whereas the antagonistic anti-Fas receptor (ZB4, 500 ng/mL) and anti-tumor necrosis factor-R1 (H398, 10 microg/mL) monoclonal antibodies did not.	andrographolide	76-91	caspase 8	Homo sapiens	13-22
23292890-8	2013	In addition, caspase-8 inhibitor (z-IETD-fmk, 50 muMu) was found to reverse andrographolide-induced caspase-8 activation, whereas the antagonistic anti-Fas receptor (ZB4, 500 ng/mL) and anti-tumor necrosis factor-R1 (H398, 10 microg/mL) monoclonal antibodies did not.	andrographolide	76-91	caspase 8	Homo sapiens	100-109
23292890-9	2013	In conclusion, this study for the first time demonstrated that andrographolide might limit platelet lifespan by initiating the caspase-8-dependent extrinsic apoptotic pathway, in spite of no direct evidence that death receptors are involved in this process proved.	andrographolide	63-78	caspase 8	Homo sapiens	127-136
24093560-0	2013	Hispolon induces apoptosis through JNK1/2-mediated activation of a caspase-8, -9, and -3-dependent pathway in acute myeloid leukemia (AML) cells and inhibits AML xenograft tumor growth in vivo.	hispolon	0-8	caspase 8	Homo sapiens	67-88
23661289-1	2013	This report is designed to explore the roles of caspase-8, -9 and -3 in artemisinin (ARTE)-induced apoptosis in non-small cell lung cancer cells (A549 cells).	artemisinin	72-83	caspase 8	Homo sapiens	48-68
23661289-1	2013	This report is designed to explore the roles of caspase-8, -9 and -3 in artemisinin (ARTE)-induced apoptosis in non-small cell lung cancer cells (A549 cells).	artemisinin	85-89	caspase 8	Homo sapiens	48-68
23688633-7	2013	In particular, the autophagic process induced by gAcrp was involved in the suppression of ethanol-induced activation of caspase-8 and expression of Bax.	Ethanol	90-97	caspase 8	Homo sapiens	120-129
24123010-8	2013	Citric acid also activated death receptors and increased the levels of caspase-8, activated BH3 interacting-domain death agonist (BID) protein, Apoptosis-inducing factor (AIF), and Endonuclease G (EndoG).	Citric Acid	0-11	caspase 8	Homo sapiens	71-80
23892367-10	2013	In contrast, RIPK3 participates in caspase-8 activation by acting downstream of the cytosolic death complex assembly, possibly via reactive oxygen species generation.	Reactive Oxygen Species	131-154	caspase 8	Homo sapiens	35-44
23307628-0	2013	In vitro changes in mitochondrial potential, aggresome formation and caspase activity by a novel 17-beta-estradiol analogue in breast adenocarcinoma cells.	Estradiol	97-114	caspase 8	Homo sapiens	69-76
24015987-7	2013	OkA resulted in the generation of reactive oxygen species, and exogenous antioxidant prevented activation of the indicated caspases.	Okadaic Acid	0-3	caspase 8	Homo sapiens	123-131
23494753-5	2013	Here we show that high dose of salicylate trigger an apoptotic response in spiral ganglion neurons characterized morphologically by soma shrinkage and nuclear condensation and fragmentation plus activation of extrinsic initiator caspase-8 and intrinsic initiator caspase-9 several days after the onset of drug treatment.	Salicylates	31-41	caspase 8	Homo sapiens	229-238
23504627-6	2013	Compared to untreated cells, pretreatment of tumor cells with DOX showed increased processing and activation of caspase-8 on coculture with NK or T cells.	Doxorubicin	62-65	caspase 8	Homo sapiens	112-121
23993302-7	2013	The depletion of CD4(+)FOXP3(high) cells and activation of Caspase 8 in CD4(+)FOXP3(high) cells was attenuated by Fas antagonist antibody, ZB4, in short-term culture.	N-{(1S,2S)-2-[4-(2-methoxyphenyl)piperazin-1-yl]cyclohexyl}benzenesulfonamide	139-142	caspase 8	Homo sapiens	59-68
24436715-11	2013	In the human NP cells, NCCM inhibits Etoposide- mediated apoptosis via suppression of activated caspase-8, caspase-9, and mainly caspase-3/7.	Etoposide	37-46	caspase 8	Homo sapiens	96-105
24436715-12	2013	CDCM demonstrated an inhibitory effect on Etoposide-mediated apoptosis via suppression of activated caspase-8, caspase-9, and mainly caspase-3/7, though not as effective as NCCM (Fig.	cdcm	0-4	caspase 8	Homo sapiens	100-109
23994633-6	2013	The results indicated that combination of MG132 and TRAIL had the effect of up-regulating expression of DR5, caspase-3, caspase-8 and p27(kip1), down-regulating expression of MMP-9 and inducing apoptosis as well as suppressing the ability of invasion of OS732 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	42-47	caspase 8	Homo sapiens	120-129
23912708-9	2013	Moreover, the induction of apoptosis by TRAIL plus cisplatin was accompanied by the downregulation of cFLIP and BCL2L1, and simultaneously robust enzymatic activation of caspase-8, culminating in decreased cancer cell survival.	Cisplatin	51-60	caspase 8	Homo sapiens	170-179
23917535-3	2013	The activation of caspase-9 and -3 was observed in both cell lines following treatment with 50 microM Pg for 24 h. In addition, the activation of caspase-8 was observed in A3 cells.	Progesterone	102-104	caspase 8	Homo sapiens	146-155
24039967-5	2013	Indeed, GB elicited an increase of TNF-alpha production, caspase-8 and caspase-3 activation, and PARP-1 cleavage within pre-B acute lymphoblastic leukemia Nalm-6 cells.	gb	8-10	caspase 8	Homo sapiens	57-66
23926306-4	2013	According to the gene profile, the downregulation of caspase-8 and caspase-10, and upregulation of oct3/4 and tgf-beta1, may be associated with THD modulation.	Thalidomide	144-147	caspase 8	Homo sapiens	53-62
23108402-3	2013	Current knowledge states that in certain cell types, 5-FU-induced stress is signaling through a p53-dependent induction of tumor necrosis factor-receptor oligomerization required for death-inducing signaling complex formation and caspase-8 activation.	Fluorouracil	53-57	caspase 8	Homo sapiens	230-239
24039967-6	2013	Moreover, caspase-8 and caspase-3 activation and PARP-1 cleavage were strongly inhibited/blocked by the addition of the specific caspase inhibitors Z-VAD-FMK and Ac-DEVD-CHO.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	148-157	caspase 8	Homo sapiens	10-19
24039967-6	2013	Moreover, caspase-8 and caspase-3 activation and PARP-1 cleavage were strongly inhibited/blocked by the addition of the specific caspase inhibitors Z-VAD-FMK and Ac-DEVD-CHO.	acetyl-aspartyl-glutamyl-valyl-aspartal	162-173	caspase 8	Homo sapiens	10-19
24039967-8	2013	Taken together, these findings indicate that GB induced preferential anti-proliferative and pro-apoptotic signals within B-lineage leukemia/lymphoma cells, as determined by the following biochemical hallmarks of apoptosis: PS externalization, enhanced release of TNF-alpha, caspase-8 and caspase-3 activation, PARP-1 cleavage and DNA fragmentation Our observations reveal that GB has potential as an anti-leukemia/lymphoma agent alone or in combination with standard cancer therapies and thus warrants further evaluation in vivo to support these findings.	gb	45-47	caspase 8	Homo sapiens	274-283
23784310-8	2013	However, a pan-caspase inhibitor, z-VED-fmk, significantly inhibited EEDM-induced U937 cell apoptosis indicating that the caspases were key regulators of apoptosis in response to EEDM in U937 cells.	z-ved-fmk	34-43	caspase 8	Homo sapiens	15-22
23708311-4	2013	In particular, activation of caspas-3 and caspase-8 as well as release of cytochrome c were significantly enhanced in response to the combined treatment with VA and TNF-alpha (VA/TNF-alpha) and the pan-caspase inhibitor z-VAD-fmk completely reversed the apoptosis, suggesting that caspases are the main effector molecules in VA/TNF-alpha-induced apoptosis via the intrinsic and extrinsic pathway.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	220-229	caspase 8	Homo sapiens	42-51
23708311-4	2013	In particular, activation of caspas-3 and caspase-8 as well as release of cytochrome c were significantly enhanced in response to the combined treatment with VA and TNF-alpha (VA/TNF-alpha) and the pan-caspase inhibitor z-VAD-fmk completely reversed the apoptosis, suggesting that caspases are the main effector molecules in VA/TNF-alpha-induced apoptosis via the intrinsic and extrinsic pathway.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	220-229	caspase 8	Homo sapiens	42-49
23906331-6	2013	Further colorimetric TUNEL assay, Hoechst staining and flow cytometric assay indicated a time-dependent apoptosis in which the activities of caspase-8 and caspase-3 were both regulated via CXXC5 according to enzymatic activity assay, Hoechst staining and Western blotting.	hoechst	234-241	caspase 8	Homo sapiens	141-150
23784310-8	2013	However, a pan-caspase inhibitor, z-VED-fmk, significantly inhibited EEDM-induced U937 cell apoptosis indicating that the caspases were key regulators of apoptosis in response to EEDM in U937 cells.	z-ved-fmk	34-43	caspase 8	Homo sapiens	122-130
23751424-5	2013	Administration of DB, induced apoptosis via death receptor pathway activating Fas associated death domain (FADD), caspase 8 and caspase 3, and suppressed the cell growth.	destruxin B	18-20	caspase 8	Homo sapiens	114-123
23878197-6	2013	K-7174 induces transcriptional repression of class I histone deacetylases (HDAC1, -2, and -3) via caspase-8-dependent degradation of Sp1, the most potent transactivator of class I HDAC genes.	K 7174	0-6	caspase 8	Homo sapiens	98-107
23830991-10	2013	The results suggested that combination of crocin and cisplatin has a strong killing effect on osteosarcoma cells and suppresses the ability of invasion of MG63 and OS732 cells which might be related to up-regulate the expression of caspase-3 and caspase-8.	Cisplatin	53-62	caspase 8	Homo sapiens	246-255
23711929-0	2013	Quercetin-3-O-(2"-galloyl)-alpha-l-rhamnopyranoside prevents TRAIL-induced apoptosis in human keratinocytes by suppressing the caspase-8- and Bid-pathways and the mitochondrial pathway.	quercetin 3-O-beta-(2''-galloyl)-rhamnopyranoside	0-51	caspase 8	Homo sapiens	127-145
23865778-5	2013	This was prevented by the nonspecific caspase inhibitor Z-VAD-FMK and, in the case of compounds 14 and 15, reduced by the selective caspase-8 inhibitor Z-IETD-FMK.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	152-162	caspase 8	Homo sapiens	132-141
23940767-4	2013	The caspase-8 inhibitor Z-IETD-FMK strongly attenuated apoptosis in Phe-treated neurons (0.9 mM, 18 h), suggesting involvement of the Fas receptor (FasR)-mediated cell death receptor pathway in Phe toxicity.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	24-34	caspase 8	Homo sapiens	4-13
23769740-5	2013	Broussoflavonol B also induced apoptotic cell death characterized by accumulation of the annexin V- and propidium iodide-positive cells, and cleavage of caspases 8, 9 and 3.	broussoflavonol B	0-17	caspase 8	Homo sapiens	153-172
23940835-4	2013	In LNCaP and PC-3 cells, LCA triggered the extrinsic pathway of apoptosis and cell death induced by LCA was partially dependent on the activation of caspase-8 and -3.	Lithocholic Acid	25-28	caspase 8	Homo sapiens	149-165
23940835-4	2013	In LNCaP and PC-3 cells, LCA triggered the extrinsic pathway of apoptosis and cell death induced by LCA was partially dependent on the activation of caspase-8 and -3.	Lithocholic Acid	100-103	caspase 8	Homo sapiens	149-165
23940767-4	2013	The caspase-8 inhibitor Z-IETD-FMK strongly attenuated apoptosis in Phe-treated neurons (0.9 mM, 18 h), suggesting involvement of the Fas receptor (FasR)-mediated cell death receptor pathway in Phe toxicity.	Phenylalanine	68-71	caspase 8	Homo sapiens	4-13
23940767-4	2013	The caspase-8 inhibitor Z-IETD-FMK strongly attenuated apoptosis in Phe-treated neurons (0.9 mM, 18 h), suggesting involvement of the Fas receptor (FasR)-mediated cell death receptor pathway in Phe toxicity.	Phenylalanine	194-197	caspase 8	Homo sapiens	4-13
23652278-8	2013	Further studies with caspase-9-specific and caspase-8-specific inhibitors (z-LEHDfmk and z-IETDfmk, respectively) pointed toward the involvement of the caspase-9 pathway, but not the caspase-8 pathway, in the execution of OSU-03012-induced apoptosis.	benzyloxycarbonyl-leucyl-glutamyl-histidyl-aspartic acid fluoromethyl ketone	75-84	caspase 8	Homo sapiens	44-53
23652278-8	2013	Further studies with caspase-9-specific and caspase-8-specific inhibitors (z-LEHDfmk and z-IETDfmk, respectively) pointed toward the involvement of the caspase-9 pathway, but not the caspase-8 pathway, in the execution of OSU-03012-induced apoptosis.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	89-98	caspase 8	Homo sapiens	44-53
23690229-5	2013	Caspase-8 was seen only at higher (100 mM) EtOH concentration.	Ethanol	43-47	caspase 8	Homo sapiens	0-9
23659359-5	2013	Moreover, forced expression of wild-type CASP8 suppressed the growth of T3M-1 Cl-10 cells without notable effects on apoptosis.	cl-10	78-83	caspase 8	Homo sapiens	41-46
24137193-7	2013	However, the apoptosis induced by sarijang was significantly inhibited by z-VED-fmk, a pan-caspase inhibitor, which demonstrated the importance of caspases in the process.	z-ved-fmk	74-83	caspase 8	Homo sapiens	91-98
24137193-7	2013	However, the apoptosis induced by sarijang was significantly inhibited by z-VED-fmk, a pan-caspase inhibitor, which demonstrated the importance of caspases in the process.	z-ved-fmk	74-83	caspase 8	Homo sapiens	147-155
23590818-4	2013	Vorinostat-induced the activation of caspase-8 and -9, the initiators caspases of the extrinsic and the intrinsic apoptotic pathways, respectively.	Vorinostat	0-10	caspase 8	Homo sapiens	37-53
23590818-4	2013	Vorinostat-induced the activation of caspase-8 and -9, the initiators caspases of the extrinsic and the intrinsic apoptotic pathways, respectively.	Vorinostat	0-10	caspase 8	Homo sapiens	70-78
23590818-8	2013	To further investigate the role of extrinsic apoptotic pathway in Vorinostat-induced apoptosis, we performed an shRNA-mediated knock-down of caspase-8.	Vorinostat	66-76	caspase 8	Homo sapiens	141-150
24137229-7	2013	Gene expression analyses revealed that propranolol treatment led to a marked increase in the expression of caspase-8, cytochrome c, apoptosis-inducing factor, caspase-3 and poly (ADP-ribose) polymerase 1, as well as a concomitant reduction in lamin B1 expression.	Propranolol	39-50	caspase 8	Homo sapiens	107-116
23754197-4	2013	We demonstrated that Asp induced cell death through the activation of TRAIL DR4/DR5 death receptors leading to the activation of caspase-8 and caspase-3 and to cell apoptosis.	Aspartic Acid	21-24	caspase 8	Homo sapiens	129-138
23926438-6	2013	Furthermore, cordycepin or cisplatin induced caspase-8, caspase-9, caspase-3, and poly adenosine diphosphate-ribose polymerase protein cleavages, and stimulated c-Jun NH2-terminal kinase, extracellular signal-regulated kinase, and p38 protein phosphorylations.	Cisplatin	27-36	caspase 8	Homo sapiens	45-54
23998584-9	2013	It is concluded that high dose of MG132 can induce the apoptosis of HL-60 cells, and has direct killing effect on HL-60 cells, but this inducing apoptotic effect on HL-60 cells can not be realized through caspase-8 and caspase-9 pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	34-39	caspase 8	Homo sapiens	205-214
23459296-5	2013	An apoptotic-ELISA and western blot assays on PARP cleavage and caspase-8 and caspase-3 revealed that bendamustine in combination with entinostat exhibited a much more potent activity than either agent alone to promote the MM cells undergoing apoptosis in a dose-dependent manner.	Bendamustine Hydrochloride	102-114	caspase 8	Homo sapiens	64-73
23926438-6	2013	Furthermore, cordycepin or cisplatin induced caspase-8, caspase-9, caspase-3, and poly adenosine diphosphate-ribose polymerase protein cleavages, and stimulated c-Jun NH2-terminal kinase, extracellular signal-regulated kinase, and p38 protein phosphorylations.	cordycepin	13-23	caspase 8	Homo sapiens	45-54
23874836-6	2013	In addition, upon oxaliplatin treatment of Pokemon-silenced cells, the FAS receptor, FADD and their downstream targets caspase-10 and caspase-8 were activated, causing increased release of caspase-8 active fragments p18 and p10.	Oxaliplatin	18-29	caspase 8	Homo sapiens	134-143
23868066-6	2013	Further analyses revealed that MPM cells were sensitized to SMC-induced apoptosis by siRNA-mediated downregulation of the caspase 8 inhibitor FLIP, an antiapoptotic protein overexpressed in several cancer types including MPM.	S-Methyl-L-cysteine	60-63	caspase 8	Homo sapiens	122-131
23868066-9	2013	Although treatment with SMC in the presence of TNFalpha promoted interaction between caspase 8 and the necrosis-promoting RIPK1, the cell death induced by combined treatment with SAHA and SMC was apoptotic and mediated by caspase 8.	S-Methyl-L-cysteine	24-27	caspase 8	Homo sapiens	85-94
23868066-9	2013	Although treatment with SMC in the presence of TNFalpha promoted interaction between caspase 8 and the necrosis-promoting RIPK1, the cell death induced by combined treatment with SAHA and SMC was apoptotic and mediated by caspase 8.	S-Methyl-L-cysteine	24-27	caspase 8	Homo sapiens	222-231
23868066-9	2013	Although treatment with SMC in the presence of TNFalpha promoted interaction between caspase 8 and the necrosis-promoting RIPK1, the cell death induced by combined treatment with SAHA and SMC was apoptotic and mediated by caspase 8.	Vorinostat	179-183	caspase 8	Homo sapiens	222-231
23868066-9	2013	Although treatment with SMC in the presence of TNFalpha promoted interaction between caspase 8 and the necrosis-promoting RIPK1, the cell death induced by combined treatment with SAHA and SMC was apoptotic and mediated by caspase 8.	S-Methyl-L-cysteine	188-191	caspase 8	Homo sapiens	85-94
23868066-9	2013	Although treatment with SMC in the presence of TNFalpha promoted interaction between caspase 8 and the necrosis-promoting RIPK1, the cell death induced by combined treatment with SAHA and SMC was apoptotic and mediated by caspase 8.	S-Methyl-L-cysteine	188-191	caspase 8	Homo sapiens	222-231
23874836-6	2013	In addition, upon oxaliplatin treatment of Pokemon-silenced cells, the FAS receptor, FADD and their downstream targets caspase-10 and caspase-8 were activated, causing increased release of caspase-8 active fragments p18 and p10.	Oxaliplatin	18-29	caspase 8	Homo sapiens	189-198
22890322-4	2013	RIP1 is required for the formation of a RIP1/FADD/caspase-8 complex that drives caspase-8 activation, cleavage of Bid into tBid, mitochondrial outer membrane permeabilization, full activation of caspase-3 and caspase-dependent apoptosis.	tBID	123-127	caspase 8	Homo sapiens	50-59
23699387-8	2013	Apoptotic parameters like PARP and caspase 8 cleavages, BAX, and BCLXs increased in KGN cells cultured with DAPT, whereas others such as BCL2, BCLXl, FAS, and FAS ligand did not change.	dapt	108-112	caspase 8	Homo sapiens	35-44
23618862-0	2013	YM155 induces caspase-8 dependent apoptosis through downregulation of survivin and Mcl-1 in human leukemia cells.	YM 155	0-5	caspase 8	Homo sapiens	14-23
23660334-3	2013	Sanguinarine also promoted the activation of caspase-8 and truncation of Bid (tBid).	sanguinarine	0-12	caspase 8	Homo sapiens	45-54
23660334-4	2013	However, the quenching of ROS generation by N-acetyl-l-cysteine, a scavenger of ROS, reversed the sanguinarine-induced apoptosis effects via inhibition of the MMP collapse, tBid expression, and activation of caspases.	Acetylcysteine	44-63	caspase 8	Homo sapiens	208-216
23660334-4	2013	However, the quenching of ROS generation by N-acetyl-l-cysteine, a scavenger of ROS, reversed the sanguinarine-induced apoptosis effects via inhibition of the MMP collapse, tBid expression, and activation of caspases.	sanguinarine	98-110	caspase 8	Homo sapiens	208-216
23685456-5	2013	Dex-dependent activation of caspase-8 was blocked by the specific caspase-9 inhibitor, z-LEHD-fmk.	Dexamethasone	0-3	caspase 8	Homo sapiens	28-37
23685456-5	2013	Dex-dependent activation of caspase-8 was blocked by the specific caspase-9 inhibitor, z-LEHD-fmk.	benzyloxycarbonyl-leucyl-glutamyl-histidyl-aspartic acid fluoromethyl ketone	87-97	caspase 8	Homo sapiens	28-37
23685456-11	2013	These results demonstrated that Dex-mediated activation of caspase-9 via ROS generation and ERK1/2 pathway activation resulted in the activation of caspase-8 and the increment of XAF1, thereby induced apoptosis of EBV-transformed B cells.	Dexamethasone	32-35	caspase 8	Homo sapiens	148-157
23430060-9	2013	GP7- or etoposide-induced apoptotic DNA fragmentation of human OS cells was inhibited by the pan caspase inhibitor and caspase-9 inhibitor, not by caspase-8 inhibitor whereas it was not inhibited by the pan caspase inhibitor in mouse OS cells.	Etoposide	8-17	caspase 8	Homo sapiens	147-156
23348695-2	2013	In combination treatment with nafamostat mesilate and oxaliplatin, NF-kappaB activation was inhibited by suppressing IkappaBalpha phosphorylation, and caspase-8-mediated apoptosis was more prominent than that treated with oxaliplatin alone, both in vitro and in vivo.	nafamostat	30-49	caspase 8	Homo sapiens	151-160
23348695-2	2013	In combination treatment with nafamostat mesilate and oxaliplatin, NF-kappaB activation was inhibited by suppressing IkappaBalpha phosphorylation, and caspase-8-mediated apoptosis was more prominent than that treated with oxaliplatin alone, both in vitro and in vivo.	Oxaliplatin	54-65	caspase 8	Homo sapiens	151-160
23348695-2	2013	In combination treatment with nafamostat mesilate and oxaliplatin, NF-kappaB activation was inhibited by suppressing IkappaBalpha phosphorylation, and caspase-8-mediated apoptosis was more prominent than that treated with oxaliplatin alone, both in vitro and in vivo.	Oxaliplatin	222-233	caspase 8	Homo sapiens	151-160
23647679-5	2013	Significantly lower caspase-3 and caspase-8 activity was also observed in the response of these cells to CO1 compared with DOX treatment.	Doxorubicin	123-126	caspase 8	Homo sapiens	34-43
23685456-11	2013	These results demonstrated that Dex-mediated activation of caspase-9 via ROS generation and ERK1/2 pathway activation resulted in the activation of caspase-8 and the increment of XAF1, thereby induced apoptosis of EBV-transformed B cells.	Reactive Oxygen Species	73-76	caspase 8	Homo sapiens	148-157
23828551-6	2013	Whereas dnFADD partially inhibited cell death, CrmA and dnBID efficiently rescued ALL cells after FOXO3 activation, suggesting a caspase-8 amplifying feedback loop downstream of FADD.	crma	47-51	caspase 8	Homo sapiens	129-138
23618270-8	2013	Simultaneously, the apoptotic mechanism of HepG2 cells induced by S-GFB was associated with down regulation of FLIP, and activation of caspase-3 and caspase-8.	s-gfb	66-71	caspase 8	Homo sapiens	149-158
23481040-5	2013	The flavone"s apoptotic action in U937 cells was associated with recruitment of mitochondria, Bax activation, Bad dephosphorylation (at Ser(136)), activation of caspases -8, -9, and -3 and cleavage of the caspase substrate PARP-1.	flavone	4-11	caspase 8	Homo sapiens	161-184
23618862-6	2013	Treatment of HL-60 and U937 cells with YM155 induced apoptosis concomitant with the activation of caspase-8 and caspase-3.	YM 155	39-44	caspase 8	Homo sapiens	98-107
23618862-7	2013	Interestingly, we have found that caspase-8 inhibitor Z-IETD-FMK strongly inhibited YM155-induced apoptosis in HL-60 and U937 cells.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	54-64	caspase 8	Homo sapiens	34-43
23618862-7	2013	Interestingly, we have found that caspase-8 inhibitor Z-IETD-FMK strongly inhibited YM155-induced apoptosis in HL-60 and U937 cells.	YM 155	84-89	caspase 8	Homo sapiens	34-43
23618862-8	2013	When cells were pretreated with Z-IETD-FMK, the activation of caspase-3 was completely abolished, suggesting that caspase-8 may be involved in the activation of caspase-3 during YM155-induced apoptosis.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	32-42	caspase 8	Homo sapiens	114-123
23618862-8	2013	When cells were pretreated with Z-IETD-FMK, the activation of caspase-3 was completely abolished, suggesting that caspase-8 may be involved in the activation of caspase-3 during YM155-induced apoptosis.	YM 155	178-183	caspase 8	Homo sapiens	114-123
23618862-9	2013	We demonstrated for the first time that YM155 induces caspase-8 dependent apoptosis through downregulation of survivin and Mcl-1 in human leukemia cells.	YM 155	40-45	caspase 8	Homo sapiens	54-63
23826494-0	2013	Synergistic Effect of Subtoxic-dose Cisplatin and TRAIL to Mediate Apoptosis by Down-regulating Decoy Receptor 2 and Up-regulating Caspase-8, Caspase-9 and Bax Expression on NCI-H460 and A549 Cells.	Cisplatin	36-45	caspase 8	Homo sapiens	131-140
23329180-3	2013	Here we showed that theaflavins, the bioactive components of black tea, successfully induced apoptosis in human MTC cell line, TT, by inversely modulating two molecular pathways: (i) stalling PI3K/Akt/Bad pathway that resulted in mitochondrial transmembrane potential (MTP) loss, cytochrome-c release and activation of the executioner caspases-9 and -3, and (ii) upholding p38MAPK/caspase-8/caspase-3 pathway via inhibition of Ras/Raf/ERK.	theaflavin	20-31	caspase 8	Homo sapiens	381-390
23494867-8	2013	The results demonstrated that altholactone was cytotoxic to HeLa (IC50  = 9.6 mug/mL), and apoptotic cell death was manifested by appearance of chromatin condensation and caspase-3 activation, which was inhibited by specific inhibitors of both caspase-8 and -9.	altholactone	30-42	caspase 8	Homo sapiens	244-260
23212307-7	2013	JNK inhibitor abolished the DPQZ-induced increase in the phosphorylation of Bcl-2 and the protein levels of proform caspase-3, caspase-8, and caspase-9, indicating that JNK is an upstream activator of Bcl-2 and caspase family members and plays a key role in DPQZ-induced HSC-3 cell apoptosis.	6-(N,N-dimethylamino)-2-(naphthalene-1-yl)-4-quinazolinone	28-32	caspase 8	Homo sapiens	127-136
23212307-7	2013	JNK inhibitor abolished the DPQZ-induced increase in the phosphorylation of Bcl-2 and the protein levels of proform caspase-3, caspase-8, and caspase-9, indicating that JNK is an upstream activator of Bcl-2 and caspase family members and plays a key role in DPQZ-induced HSC-3 cell apoptosis.	6-(N,N-dimethylamino)-2-(naphthalene-1-yl)-4-quinazolinone	28-32	caspase 8	Homo sapiens	116-123
23589036-13	2013	Western blot analyses showed that selenite-induced apoptosis was accompanied by activation of caspase-8 and specific proteolytic cleavage of PARP.	Selenious Acid	34-42	caspase 8	Homo sapiens	94-103
23397952-6	2013	Cells were treated with TNF-alpha alone or in the presence of cycloheximide (CHX), which promotes caspase-8 activation by eliminating the endogenous caspase-8 inhibitor, c-FLIP.	Cycloheximide	62-75	caspase 8	Homo sapiens	98-107
23397952-6	2013	Cells were treated with TNF-alpha alone or in the presence of cycloheximide (CHX), which promotes caspase-8 activation by eliminating the endogenous caspase-8 inhibitor, c-FLIP.	Cycloheximide	62-75	caspase 8	Homo sapiens	149-158
23397952-6	2013	Cells were treated with TNF-alpha alone or in the presence of cycloheximide (CHX), which promotes caspase-8 activation by eliminating the endogenous caspase-8 inhibitor, c-FLIP.	Cycloheximide	77-80	caspase 8	Homo sapiens	98-107
23397952-6	2013	Cells were treated with TNF-alpha alone or in the presence of cycloheximide (CHX), which promotes caspase-8 activation by eliminating the endogenous caspase-8 inhibitor, c-FLIP.	Cycloheximide	77-80	caspase 8	Homo sapiens	149-158
23434428-5	2013	The combination of simvastatin and thalidomide augmented caspase 8 and 3 activation, and the additional application of p38 MAPK inhibitor resulted in enhanced apoptosis of MM cells concomitant with increased caspase 9 and 3 activation, as well as JNK phosphorylation.	Simvastatin	19-30	caspase 8	Homo sapiens	57-66
23434428-5	2013	The combination of simvastatin and thalidomide augmented caspase 8 and 3 activation, and the additional application of p38 MAPK inhibitor resulted in enhanced apoptosis of MM cells concomitant with increased caspase 9 and 3 activation, as well as JNK phosphorylation.	Thalidomide	35-46	caspase 8	Homo sapiens	57-66
23396089-7	2013	However, fenretinide specifically induced Fas/TNFalpha-mediated apoptosis by increasing the expression of pro-apoptotic genes i.e., DEDD2, CASP8, CASP4, and HSPA1A/B; whereas, ATRA induced the expression of BIRC3 and TNFAIP3, which inhibit apoptosis by interacting with TRAF2.	Fenretinide	9-20	caspase 8	Homo sapiens	139-144
23540413-0	2013	Caspase-2 and caspase-8 trigger caspase-3 activation following 6-OHDA-induced stress in human dopaminergic neurons differentiated from ReNVM stem cells.	Oxidopamine	63-69	caspase 8	Homo sapiens	14-23
23485651-7	2013	Extrinsic apoptotic pathway markers such as Fas levels and caspase-8 activity increased as a result of CdTe-QD exposure.	cadmium telluride	103-107	caspase 8	Homo sapiens	59-68
23426995-6	2013	The results suggest that both the caspases in the extrinsic death receptor pathway and the mitochondrial-dependent pathway are involved in the GA-induced cell apoptosis.	gambogic acid	143-145	caspase 8	Homo sapiens	34-42
23638002-6	2013	Further examination indicated that nickel released from 316L SS triggered the cell apoptosis via Fas-Caspase8-Caspase3 exogenous pathway.	Nickel	35-41	caspase 8	Homo sapiens	101-109
23499692-11	2013	In conclusion, rolipram protects against apoptosis of MRC-5 cells through inhibition of caspase-3 and caspase-8.	Rolipram	15-23	caspase 8	Homo sapiens	102-111
23564782-7	2013	Collectively, these results suggest that beta-elemene augments the antitumor activity of cisplatin in human bladder cancer by enhancing the induction of cellular apoptosis via a caspase-dependent mechanism.	beta-elemene	41-53	caspase 8	Homo sapiens	178-185
23564782-7	2013	Collectively, these results suggest that beta-elemene augments the antitumor activity of cisplatin in human bladder cancer by enhancing the induction of cellular apoptosis via a caspase-dependent mechanism.	Cisplatin	89-98	caspase 8	Homo sapiens	178-185
23564786-9	2013	Salinomycin increased the expression of death receptor-5 (DR5), caspase-8 and Fas-associated protein with death domain (FADD).	salinomycin	0-11	caspase 8	Homo sapiens	64-73
23564786-12	2013	CONCLUSION: These findings provide important insights regarding the activation of caspase-8 and DR5, to our knowledge, for the first time in salinomycin-treated cisplatin-resistant ovarian cancer and demonstrate that salinomycin could be a prominent anticancer agent.	salinomycin	141-152	caspase 8	Homo sapiens	82-91
23564786-12	2013	CONCLUSION: These findings provide important insights regarding the activation of caspase-8 and DR5, to our knowledge, for the first time in salinomycin-treated cisplatin-resistant ovarian cancer and demonstrate that salinomycin could be a prominent anticancer agent.	Cisplatin	161-170	caspase 8	Homo sapiens	82-91
23564786-12	2013	CONCLUSION: These findings provide important insights regarding the activation of caspase-8 and DR5, to our knowledge, for the first time in salinomycin-treated cisplatin-resistant ovarian cancer and demonstrate that salinomycin could be a prominent anticancer agent.	salinomycin	217-228	caspase 8	Homo sapiens	82-91
23462961-6	2013	F-L-DOX inhibited proliferation of NFPA cells and promoted apoptosis through activation of caspase-8, caspase-9, and caspase-3/7 more effectively than L-DOX.	f-l-dox	0-7	caspase 8	Homo sapiens	91-100
23462961-6	2013	F-L-DOX inhibited proliferation of NFPA cells and promoted apoptosis through activation of caspase-8, caspase-9, and caspase-3/7 more effectively than L-DOX.	l-dox	2-7	caspase 8	Homo sapiens	91-100
23599794-0	2013	Pseudomonas aeruginosa-mannose-sensitive hemagglutinin inhibits proliferation and induces apoptosis in a caspase-dependent manner in human bladder cancer cell lines.	Mannose	23-30	caspase 8	Homo sapiens	105-112
23294316-6	2013	Although anthocyanins induced apoptosis in some leukaemia cell lines, the level of caspase-3, caspase-8 and caspase-9 was significantly lower compared with imatinib and 6-MP.	Anthocyanins	9-21	caspase 8	Homo sapiens	94-103
23599794-10	2013	PA-MSHA inhibits proliferation and induces apoptosis in the T24 and 5637 bladder cancer cell lines by modulating caspase family proteins and affecting the cell cycle regulation machinery.	pa-msha	0-7	caspase 8	Homo sapiens	113-120
23338718-5	2013	Pan-caspase inhibitor (Z-VAD) and caspase-8 inhibitor (Z-IETD) significantly rescued some cells from Zeb-induced Calu-6 cell death.	z-ietd	55-61	caspase 8	Homo sapiens	34-43
23338718-5	2013	Pan-caspase inhibitor (Z-VAD) and caspase-8 inhibitor (Z-IETD) significantly rescued some cells from Zeb-induced Calu-6 cell death.	pyrimidin-2-one beta-ribofuranoside	101-104	caspase 8	Homo sapiens	34-43
23345169-5	2013	In addition, 5-geranyloxy-7-methoxycoumarin arrested cells at the G0/G1 phase, and induction of apoptosis was demonstrated through the activation of tumour suppressor gene p53, caspase8/3, regulation of Bcl2, and inhibition of p38 MAPK phosphorylation.	5-geranyloxy-7-methoxycoumarin	13-43	caspase 8	Homo sapiens	177-185
23410748-1	2013	TNF has been reported to induce caspase-independent necroptosis in the presence of Z-VAD-fmk, a pan-caspase inhibitor.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	83-92	caspase 8	Homo sapiens	32-39
23410748-1	2013	TNF has been reported to induce caspase-independent necroptosis in the presence of Z-VAD-fmk, a pan-caspase inhibitor.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	83-92	caspase 8	Homo sapiens	100-107
23410748-3	2013	TNF-induced necroptosis was detected in the presence of Z-DEVD-fmk, which is commonly used as a caspase-3-specific inhibitor, but not in the presence of Z-Asp-CH2-DCB, which was reported to be a pan-caspase inhibitor.	benzoylcarbonyl-aspartyl-glutamyl-valyl-aspartyl-fluoromethyl ketone	56-66	caspase 8	Homo sapiens	96-103
23410748-7	2013	The cleavage of RIP1, which plays a crucial role in TNF-induced necroptosis and is cleaved by caspase-8, was completely inhibited by Z-VAD-fmk or Z-DEVD-fmk, whereas the partial degradation of RIP1 was detected in the presence of Z-Asp-CH2-DCB.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	133-142	caspase 8	Homo sapiens	94-103
23410748-7	2013	The cleavage of RIP1, which plays a crucial role in TNF-induced necroptosis and is cleaved by caspase-8, was completely inhibited by Z-VAD-fmk or Z-DEVD-fmk, whereas the partial degradation of RIP1 was detected in the presence of Z-Asp-CH2-DCB.	benzoylcarbonyl-aspartyl-glutamyl-valyl-aspartyl-fluoromethyl ketone	146-156	caspase 8	Homo sapiens	94-103
23410748-7	2013	The cleavage of RIP1, which plays a crucial role in TNF-induced necroptosis and is cleaved by caspase-8, was completely inhibited by Z-VAD-fmk or Z-DEVD-fmk, whereas the partial degradation of RIP1 was detected in the presence of Z-Asp-CH2-DCB.	benzyloxycarbonyl-Asp-CH2OC(O)-2,6-dichlorobenzene	230-243	caspase 8	Homo sapiens	94-103
23410748-8	2013	These results suggest that the partial activation of caspase-8 in the presence of Z-Asp-CH2-DCB may suppress TNF-induced necroptosis via the cleavage of RIP1, and also suggest that Z-Asp-CH2-DCB, but not Z-DEVD-fmk, may be used as a caspase-3-specific inhibitor in cells.	benzyloxycarbonyl-Asp-CH2OC(O)-2,6-dichlorobenzene	82-95	caspase 8	Homo sapiens	53-62
23410748-8	2013	These results suggest that the partial activation of caspase-8 in the presence of Z-Asp-CH2-DCB may suppress TNF-induced necroptosis via the cleavage of RIP1, and also suggest that Z-Asp-CH2-DCB, but not Z-DEVD-fmk, may be used as a caspase-3-specific inhibitor in cells.	benzyloxycarbonyl-Asp-CH2OC(O)-2,6-dichlorobenzene	181-194	caspase 8	Homo sapiens	53-62
23410748-8	2013	These results suggest that the partial activation of caspase-8 in the presence of Z-Asp-CH2-DCB may suppress TNF-induced necroptosis via the cleavage of RIP1, and also suggest that Z-Asp-CH2-DCB, but not Z-DEVD-fmk, may be used as a caspase-3-specific inhibitor in cells.	benzoylcarbonyl-aspartyl-glutamyl-valyl-aspartyl-fluoromethyl ketone	204-214	caspase 8	Homo sapiens	53-62
23482760-10	2013	CONCLUSION: Equol enhances TRAIL-induced apoptosis of HeLa cells through a death receptor-mediated caspase pathway.	Equol	12-17	caspase 8	Homo sapiens	99-106
23404469-7	2013	Measuring the modulation of regulators in the cell cycle, apoptosis and signal transductions by western blot analysis showed that the effect of Dasatinib was due to suppression of the expression of Bax, Bcl-2, Caspase-3, and Caspase-8.	Dasatinib	144-153	caspase 8	Homo sapiens	225-234
23338568-6	2013	Consistently, blockage of caspase activation, through treatment with a caspase inhibitor, z-VAD-fmk, inhibited apoptosis and abrogated Tat-SmacN7 radiosensitization.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	90-99	caspase 8	Homo sapiens	26-33
23338568-6	2013	Consistently, blockage of caspase activation, through treatment with a caspase inhibitor, z-VAD-fmk, inhibited apoptosis and abrogated Tat-SmacN7 radiosensitization.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	90-99	caspase 8	Homo sapiens	71-78
23841272-13	2013	PUVA could induce the apoptosis of NB4 cells and in vitro activate Caspase-3 and Caspase-8 genes.	puva	0-4	caspase 8	Homo sapiens	81-90
23408429-7	2013	In MDA-MB-231 breast cancer cells, sensitization to TRAIL upon MTDH down-regulation was inhibited by the caspase inhibitor Z-VAD-fmk (benzyloxycarbonyl-VAD-fluoromethyl ketone), suggesting that MTDH depletion stimulates activation of caspases.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	123-132	caspase 8	Homo sapiens	234-242
23408429-7	2013	In MDA-MB-231 breast cancer cells, sensitization to TRAIL upon MTDH down-regulation was inhibited by the caspase inhibitor Z-VAD-fmk (benzyloxycarbonyl-VAD-fluoromethyl ketone), suggesting that MTDH depletion stimulates activation of caspases.	benzyloxycarbonyl-vad-fluoromethyl ketone	134-175	caspase 8	Homo sapiens	234-242
23482758-11	2013	CONCLUSION: Naftopidil, as well as prazosin, has the potential to induce apoptosis in malignant mesothelioma cells by activating caspase-8 and the effector caspase-3, regardless of alpha1-adrenoceptor blocking.	naftopidil	12-22	caspase 8	Homo sapiens	129-138
23319430-3	2013	The techniques used were the MTT assay, flow cytometry, real-time PCR to assess miR-199a expression, as also caspase-8 and caspase-9 activity in HepG2 cells treated with Propofol.	Propofol	170-178	caspase 8	Homo sapiens	109-118
23319430-7	2013	Activation of caspase-8 and caspase-9 suggested that both extrinsic and intrinsic pathways are involved in Propofol-induced apoptosis.	Propofol	107-115	caspase 8	Homo sapiens	14-23
23319430-8	2013	Anti-miR-199a reversed the effect of Propofol on apoptosis and activation of caspase-8 and caspase-9 in HepG2 cells.	Propofol	37-45	caspase 8	Homo sapiens	77-86
23246691-6	2013	The presence of betaine (at 5 or 10 mM) significantly reduced the activity of caspase-8, -9 and -3/7 and release of TNF-alpha was also reduced by 34% or 55% after exposure of HCLE to 500 mOsm in the presence of 5 or 10 mM betaine, respectively.	Betaine	16-23	caspase 8	Homo sapiens	78-112
23246691-6	2013	The presence of betaine (at 5 or 10 mM) significantly reduced the activity of caspase-8, -9 and -3/7 and release of TNF-alpha was also reduced by 34% or 55% after exposure of HCLE to 500 mOsm in the presence of 5 or 10 mM betaine, respectively.	hcle	175-179	caspase 8	Homo sapiens	78-112
23246691-6	2013	The presence of betaine (at 5 or 10 mM) significantly reduced the activity of caspase-8, -9 and -3/7 and release of TNF-alpha was also reduced by 34% or 55% after exposure of HCLE to 500 mOsm in the presence of 5 or 10 mM betaine, respectively.	Betaine	222-229	caspase 8	Homo sapiens	78-112
22469979-3	2013	BV6 and TMZ synergistically reduce cell viability and trigger apoptosis in glioblastoma cells (combination index &lt;0.4-0.8), which is accompanied by increased loss of mitochondrial-membrane potential, cytochrome c release, caspase activation and caspase-dependent apoptosis.	Temozolomide	8-11	caspase 8	Homo sapiens	225-232
22469979-3	2013	BV6 and TMZ synergistically reduce cell viability and trigger apoptosis in glioblastoma cells (combination index &lt;0.4-0.8), which is accompanied by increased loss of mitochondrial-membrane potential, cytochrome c release, caspase activation and caspase-dependent apoptosis.	Temozolomide	8-11	caspase 8	Homo sapiens	248-255
23239672-9	2013	Surprisingly, caspase-8 exhibited a transient decrease in activity after LY30 treatment, prior to strong activation.	LY 303511	73-77	caspase 8	Homo sapiens	14-23
23238299-8	2013	Treatment of Caco-2 cells with 50 mug/ml alkaloid extract and 50 muM chelidonine for up to 48 h resulted in a significant decrease in mRNA levels of P-gp/MDR1, MRP1, BCRP, CYP3A4, GST, and hPXR and in a significant increase in caspase-3 and caspase-8 mRNA.	Alkaloids	41-49	caspase 8	Homo sapiens	241-250
23238299-8	2013	Treatment of Caco-2 cells with 50 mug/ml alkaloid extract and 50 muM chelidonine for up to 48 h resulted in a significant decrease in mRNA levels of P-gp/MDR1, MRP1, BCRP, CYP3A4, GST, and hPXR and in a significant increase in caspase-3 and caspase-8 mRNA.	chelidonine	69-80	caspase 8	Homo sapiens	241-250
23239672-10	2013	cFLIP, an inhibitor of caspase-8 activation, was up-regulated briefly after 30 min of LY30 treatment, followed by a significant down-regulation over prolonged exposure.	LY 303511	86-90	caspase 8	Homo sapiens	23-32
23590971-7	2013	Although the ligation of Fas results in caspase-8 cleavage and ERK1/2 phosphorylation, inhibitors for caspase-8 and MEK have no effect on the expressions of RORgammat, IL-17A, and IL-17F.	ammonium ferrous sulfate	25-28	caspase 8	Homo sapiens	40-49
22961085-6	2013	In embryos cultured under high-glucose conditions (20 mmol/L), the use of 4-phenylbutyric acid (4-PBA), an ER chemical chaperone, diminished ER stress markers and abolished the activation of JNK1/2 and its downstream transcription factors, caspase 3 and caspase 8, and Sox1 neural progenitor apoptosis.	4-phenylbutyric acid	74-94	caspase 8	Homo sapiens	254-263
22961085-6	2013	In embryos cultured under high-glucose conditions (20 mmol/L), the use of 4-phenylbutyric acid (4-PBA), an ER chemical chaperone, diminished ER stress markers and abolished the activation of JNK1/2 and its downstream transcription factors, caspase 3 and caspase 8, and Sox1 neural progenitor apoptosis.	4-phenylbutyric acid	96-101	caspase 8	Homo sapiens	254-263
22992806-6	2013	The resulting increase in nitric oxide significantly upregulates keratinocyte FasL expression, resulting in Fas- and caspase-8-mediated keratinocyte cell death.	Nitric Oxide	26-38	caspase 8	Homo sapiens	117-126
22992806-6	2013	The resulting increase in nitric oxide significantly upregulates keratinocyte FasL expression, resulting in Fas- and caspase-8-mediated keratinocyte cell death.	ammonium ferrous sulfate	78-81	caspase 8	Homo sapiens	117-126
23243059-9	2013	The combination of Y15 with temozolomide was more effective than either agent alone in decreasing viability and activating caspase-8 in DBTRG and U87 cells in vitro.	Temozolomide	28-40	caspase 8	Homo sapiens	123-132
22806078-0	2013	FasL-triggered death of Jurkat cells requires caspase 8-induced, ATP-dependent cross-talk between Fas and the purinergic receptor P2X(7).	Adenosine Triphosphate	65-68	caspase 8	Homo sapiens	46-55
22806078-0	2013	FasL-triggered death of Jurkat cells requires caspase 8-induced, ATP-dependent cross-talk between Fas and the purinergic receptor P2X(7).	ammonium ferrous sulfate	0-3	caspase 8	Homo sapiens	46-55
22806078-1	2013	Fas ligation via the ligand FasL activates the caspase-8/caspase-3-dependent extrinsic death pathway.	ammonium ferrous sulfate	0-3	caspase 8	Homo sapiens	47-56
22806078-5	2013	Here, we evaluated the possibility that ATP release downstream of caspase-8 via pannexin1 hemichannels (Panx1 HCs) and subsequent activation of P2X(7)Rs participate in FasL-stimulated cell death.	Adenosine Triphosphate	40-43	caspase 8	Homo sapiens	66-75
22806078-6	2013	Indeed, upon FasL stimulation, ATP was released from Jurkat cells in a time- and caspase-8-dependent manner.	Adenosine Triphosphate	31-34	caspase 8	Homo sapiens	81-90
22806078-10	2013	These results represent the first evidence indicating that the two death receptors, Fas and P2X(7)R connect functionally via caspase-8 and Panx1 HC-mediated ATP release to promote caspase-9/caspase-3-dependent cell death in lymphoid cells.	Adenosine Triphosphate	157-160	caspase 8	Homo sapiens	125-134
22310289-3	2013	Here, we report that hispanolone derivatives, a group of labdane diterpenoids, induce apoptosis in different tumor cell lines by activating caspase-8 with subsequent participation of mitochondrial signaling.	hispanolone	21-32	caspase 8	Homo sapiens	140-149
22951949-5	2013	The mechanism of DEDTC-induced apoptosis in neuronal model cells is thought to occur through the death receptor signaling triggered by DEDTC-copper complex in low concentration that is associated with the activation of caspase 8.	SODIUM DIETHYLDITHIOCARBAMATE	17-22	caspase 8	Homo sapiens	219-228
22951949-5	2013	The mechanism of DEDTC-induced apoptosis in neuronal model cells is thought to occur through the death receptor signaling triggered by DEDTC-copper complex in low concentration that is associated with the activation of caspase 8.	SODIUM DIETHYLDITHIOCARBAMATE	135-140	caspase 8	Homo sapiens	219-228
22951949-5	2013	The mechanism of DEDTC-induced apoptosis in neuronal model cells is thought to occur through the death receptor signaling triggered by DEDTC-copper complex in low concentration that is associated with the activation of caspase 8.	Copper	141-147	caspase 8	Homo sapiens	219-228
23065354-9	2013	Addition of specific inhibitors of caspase-8 (z-IETD-fmk) and caspase-9 (z-LEHD-fmk) to HUVEC was found to completely inhibit 9t,12t-C18:2-induced activation of caspase-3, and z-IETD-fmk inhibited the activation of caspase-9.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	46-56	caspase 8	Homo sapiens	35-44
23065354-9	2013	Addition of specific inhibitors of caspase-8 (z-IETD-fmk) and caspase-9 (z-LEHD-fmk) to HUVEC was found to completely inhibit 9t,12t-C18:2-induced activation of caspase-3, and z-IETD-fmk inhibited the activation of caspase-9.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	176-186	caspase 8	Homo sapiens	35-44
22310289-3	2013	Here, we report that hispanolone derivatives, a group of labdane diterpenoids, induce apoptosis in different tumor cell lines by activating caspase-8 with subsequent participation of mitochondrial signaling.	labdane	57-64	caspase 8	Homo sapiens	140-149
22310289-3	2013	Here, we report that hispanolone derivatives, a group of labdane diterpenoids, induce apoptosis in different tumor cell lines by activating caspase-8 with subsequent participation of mitochondrial signaling.	Diterpenes	65-77	caspase 8	Homo sapiens	140-149
22310289-4	2013	Activation of caspase-8 by hispanolone derivatives was followed by a decrease in mitochondrial membrane potential, the release of apoptotic factors from mitochondria to the cytosol, and activation of caspases-9 and 3.	hispanolone	27-38	caspase 8	Homo sapiens	14-23
22310289-6	2013	Inhibition of caspase-8 abrogated these processes, suggesting that the death receptor pathway has a critical role in the apoptotic events induced by hispanolone derivatives.	hispanolone	149-160	caspase 8	Homo sapiens	14-23
23173123-4	2013	Co-IP experiments also showed that Vps41 binds to the p18 subunit of caspase-8 through its WD40 region and RING-finger motif.	co-ip	0-5	caspase 8	Homo sapiens	69-78
23336515-7	2013	Oridonin triggered the reduction of Bcl-2/Bax ratio, caspase-8, NF-kappaB (p65), IKKalpha, IKKbeta, phospho-mTOR, and increased expression level of cleaved PARP, Fas and PPARgamma in a time-dependent manner.	oridonin	0-8	caspase 8	Homo sapiens	53-62
23390564-8	2013	An apoptotic-ELISA and western blot assays of PARP cleavage and activation of caspase-8 and caspase-3 indicated that cladribine or bendamustine induced apoptosis in both cell lines.	Cladribine	117-127	caspase 8	Homo sapiens	78-87
23390564-8	2013	An apoptotic-ELISA and western blot assays of PARP cleavage and activation of caspase-8 and caspase-3 indicated that cladribine or bendamustine induced apoptosis in both cell lines.	Bendamustine Hydrochloride	131-143	caspase 8	Homo sapiens	78-87
23406595-7	2013	RESULTS: MTX-treated NPs contained significantly increased amounts of the active forms of caspase 8, caspase 9, and caspase 3 and displayed increased cleavage of poly(ADP-ribose) polymerase.	Methotrexate	9-12	caspase 8	Homo sapiens	90-99
23701310-9	2013	Oppositely, GF109203X does not modify CCT129202-induced apoptosis through the caspase-8 pathway whereas Go6976 treatment abolishes the increase on caspase-8 activity due to CCT129202.	Go 6976	104-110	caspase 8	Homo sapiens	147-156
22931421-9	2013	AZT up-regulated the expression of tumor suppressor gene FOXP1 and the pro-apoptotic genes encoding BID, Bcl-10, and caspase-8.	Zidovudine	0-3	caspase 8	Homo sapiens	117-126
24460330-8	2013	The apoptotic response to terpinen-4-ol in HL-60 cells was due to induction of cytochrome c release from mitochondria and cleavage of Bid protein after the stimulation of caspase-8.	terpinenol-4	26-39	caspase 8	Homo sapiens	171-180
24377552-10	2013	Therefore, bortezomib can enhance ATO actions to induce apoptosis in RPMI 8266 cells, with decrease in expression of bcl-2 and increase of caspase-3, caspase-8 and caspase-9 proteins.	Bortezomib	11-21	caspase 8	Homo sapiens	150-159
23991959-0	2013	Autophagic degradation of caspase-8 protects U87MG cells against H2O2-induced oxidative stress.	Hydrogen Peroxide	65-69	caspase 8	Homo sapiens	26-35
23725188-7	2013	In conclusion, DMMA-induced activation of caspase-8 and -9 resulted in execution of apoptotic cell death in human leukemic HL-60 and MOLT-4 cell lines via extrinsic and intrinsic pathways.	6,8-dihydroxy-7-methoxy-1-methyl-azafluorenone	15-19	caspase 8	Homo sapiens	42-58
23725188-0	2013	6,8-dihydroxy-7-methoxy-1-methyl-azafluorenone induces caspase-8- and -9-mediated apoptosis in human cancer cells.	6,8-dihydroxy-7-methoxy-1-methyl-azafluorenone	0-46	caspase 8	Homo sapiens	55-72
23991959-1	2013	Oxidative stress induces apoptosis in many cellular systems including glioblastoma cells, with caspase-8 activation was regarded as a major contribution to H2O2-induced cell death.	Hydrogen Peroxide	156-160	caspase 8	Homo sapiens	95-104
23991959-4	2013	We found that H2O2 -induced U87MG cell death was correlated with caspase-8.	Hydrogen Peroxide	14-18	caspase 8	Homo sapiens	65-74
23991959-7	2013	In addition, inhibition of autophagy promoted p62 and active caspase-8 increasing H2O2 -induced apoptosis while induction of autophagy manifested the opposite effect.	Hydrogen Peroxide	82-86	caspase 8	Homo sapiens	61-70
23991959-8	2013	We further demonstrated that the function of p62/SQSTM1 required its C-terminus UBA domain to attenuate H2O2 cytotoxity by inhibition of caspase-8 activity.	Hydrogen Peroxide	104-108	caspase 8	Homo sapiens	137-146
24168763-13	2013	MM-121 enhances paclitaxel-induced poly(ADP-ribose) polymerase (PARP) cleavage, activation of caspase-8 and -3, and apoptosis in both paclitaxel-sensitive and -resistant cells.	Paclitaxel	16-26	caspase 8	Homo sapiens	94-110
24175297-3	2013	alpha-Mangostin (7.5  mug/mL) activated caspase activity, with a 3-fold and 4-fold increased caspase 8 and 9 activity, respectively.	mangostin	0-15	caspase 8	Homo sapiens	40-47
24175297-3	2013	alpha-Mangostin (7.5  mug/mL) activated caspase activity, with a 3-fold and 4-fold increased caspase 8 and 9 activity, respectively.	mangostin	0-15	caspase 8	Homo sapiens	93-102
24564733-3	2013	RESULTS: We show that coffee component HHQ has significant apoptotic effect on MDA-MB-231 and MCF-7 cells in vitro, and that ROS generation, change in mitochondrial membrane permeability, upregulation of Bax and Caspase-8 as well as down regulation of PGK1 and PKM2 expression may be important apoptosis-inducing mechanisms.	MY 12-62c	39-42	caspase 8	Homo sapiens	212-221
23476680-5	2013	Furthermore, our results present for the first time that baicalein triggers a convergence of the intrinsic and extrinsic apoptotic pathways via the death receptor-caspase 8-tBid signaling cascade in CCRF-CEM cells.	baicalein	57-66	caspase 8	Homo sapiens	163-172
23476680-5	2013	Furthermore, our results present for the first time that baicalein triggers a convergence of the intrinsic and extrinsic apoptotic pathways via the death receptor-caspase 8-tBid signaling cascade in CCRF-CEM cells.	tBID	173-177	caspase 8	Homo sapiens	163-172
24168111-6	2013	We further found that lupulone derivatives induced caspase-dependent apoptosis that is associated with activation of caspases 8, 9, and 3.	lupulon	22-30	caspase 8	Homo sapiens	117-137
23573140-3	2013	Mechanistic studies on human cutaneous squamous cell carcinoma (SCC) cell line SCC12 highlighted the involvement of apoptosis in subamolide B-induced cytotoxicity, as evidenced by the activation of caspases-8, -9, -4, and -3, the increase in annexin V-positive population, and the partial restoration of cell viability by cotreatment with the pan-caspase inhibitor z-VAD-fmk.	subamolide B	129-141	caspase 8	Homo sapiens	198-224
22903547-0	2013	EPA, an omega-3 fatty acid, induces apoptosis in human pancreatic cancer cells: role of ROS accumulation, caspase-8 activation, and autophagy induction.	Eicosapentaenoic Acid	0-3	caspase 8	Homo sapiens	106-115
22903547-1	2013	In a recent study, we showed that eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), two common omega-3 fatty acids, can cause ROS accumulation and subsequently induce caspase-8-dependent apoptosis in human breast cancer cells (Kang et al.	Eicosapentaenoic Acid	34-55	caspase 8	Homo sapiens	177-186
22903547-1	2013	In a recent study, we showed that eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), two common omega-3 fatty acids, can cause ROS accumulation and subsequently induce caspase-8-dependent apoptosis in human breast cancer cells (Kang et al.	Eicosapentaenoic Acid	57-60	caspase 8	Homo sapiens	177-186
22903547-1	2013	In a recent study, we showed that eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), two common omega-3 fatty acids, can cause ROS accumulation and subsequently induce caspase-8-dependent apoptosis in human breast cancer cells (Kang et al.	Docosahexaenoic Acids	66-86	caspase 8	Homo sapiens	177-186
22903547-1	2013	In a recent study, we showed that eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), two common omega-3 fatty acids, can cause ROS accumulation and subsequently induce caspase-8-dependent apoptosis in human breast cancer cells (Kang et al.	Docosahexaenoic Acids	88-91	caspase 8	Homo sapiens	177-186
22903547-1	2013	In a recent study, we showed that eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), two common omega-3 fatty acids, can cause ROS accumulation and subsequently induce caspase-8-dependent apoptosis in human breast cancer cells (Kang et al.	Fatty Acids, Omega-3	105-124	caspase 8	Homo sapiens	177-186
22903547-1	2013	In a recent study, we showed that eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), two common omega-3 fatty acids, can cause ROS accumulation and subsequently induce caspase-8-dependent apoptosis in human breast cancer cells (Kang et al.	ros	136-139	caspase 8	Homo sapiens	177-186
22903547-5	2013	EPA and DHA were found to induce ROS accumulation and caspase-8-dependent cell death in human pancreatic cancer cells (MIA-PaCa-2 and Capan-2) in vitro.	Eicosapentaenoic Acid	0-3	caspase 8	Homo sapiens	54-63
22903547-5	2013	EPA and DHA were found to induce ROS accumulation and caspase-8-dependent cell death in human pancreatic cancer cells (MIA-PaCa-2 and Capan-2) in vitro.	Docosahexaenoic Acids	8-11	caspase 8	Homo sapiens	54-63
25945102-5	2013	Moreover, TPL-induced apoptosis in SK-MEL-2 cells was mediated through dephosphorylation of focal adhesion kinase (FAK) and its cleavage by caspase-8-mediated caspase-3 activation via upregulation of Fas expression.	triptolide	10-13	caspase 8	Homo sapiens	140-149
23138847-4	2013	Moreover, the DHA treatment dramatically increased the protein expression of caspase-8,             cleaved caspase-9, activated Bid and induced the release of cytochrome c from             mitochondria into the cytosol.	artenimol	14-17	caspase 8	Homo sapiens	77-86
22476654-5	2013	Treatment with tagitinin C isolated from TDM resulted in activation of both caspase 3 and caspase 8 which suggested that the antiproliferative effect of this compound was caspase-dependent apoptosis.	tagitinin	15-26	caspase 8	Homo sapiens	90-99
23255955-7	2013	PA induced the activation of caspase-8, -9 and -3, critical mediators of apoptosis signaling.	pomolic acid	0-2	caspase 8	Homo sapiens	29-49
24168111-7	2013	Furthermore, caspase 8 inhibitor Z-IETD-fmk reduced cell death induced by lupulone derivatives, suggesting that apoptosis is mediated by caspase 8.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	33-43	caspase 8	Homo sapiens	13-22
23255955-9	2013	In addition, PA increased the expression of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-mediated apoptosis signaling-related death receptor 5 (DR5), mediating caspase-8-involved extrinsic pathway.	pomolic acid	13-15	caspase 8	Homo sapiens	179-188
24168111-7	2013	Furthermore, caspase 8 inhibitor Z-IETD-fmk reduced cell death induced by lupulone derivatives, suggesting that apoptosis is mediated by caspase 8.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	33-43	caspase 8	Homo sapiens	137-146
24168111-7	2013	Furthermore, caspase 8 inhibitor Z-IETD-fmk reduced cell death induced by lupulone derivatives, suggesting that apoptosis is mediated by caspase 8.	lupulon	74-82	caspase 8	Homo sapiens	13-22
24168111-7	2013	Furthermore, caspase 8 inhibitor Z-IETD-fmk reduced cell death induced by lupulone derivatives, suggesting that apoptosis is mediated by caspase 8.	lupulon	74-82	caspase 8	Homo sapiens	137-146
23536891-0	2013	Ionizing radiation potentiates dihydroartemisinin-induced apoptosis of A549 cells via a caspase-8-dependent pathway.	artenimol	31-49	caspase 8	Homo sapiens	88-97
23544014-7	2013	We replicated previously reported potential interactions between LSP1-rs3817198 and parity (Pinteraction = 2.4 x 10(-6)) and between CASP8-rs17468277 and alcohol consumption (Pinteraction = 3.1 x 10(-4)).	Alcohols	154-161	caspase 8	Homo sapiens	133-138
23544014-9	2013	For CASP8-rs17468277, the per-allele OR was 0.91 (0.85-0.98) in those with an alcohol intake of &lt;20 g/day and 1.45 (1.14-1.85) in those who drank &gt;= 20 g/day.	Alcohols	78-85	caspase 8	Homo sapiens	4-9
23921841-0	2013	Licochalcone A enhances geldanamycin-induced apoptosis through reactive oxygen species-mediated caspase activation.	licochalcone A	0-14	caspase 8	Homo sapiens	96-103
23921841-0	2013	Licochalcone A enhances geldanamycin-induced apoptosis through reactive oxygen species-mediated caspase activation.	geldanamycin	24-36	caspase 8	Homo sapiens	96-103
23921841-0	2013	Licochalcone A enhances geldanamycin-induced apoptosis through reactive oxygen species-mediated caspase activation.	Reactive Oxygen Species	63-86	caspase 8	Homo sapiens	96-103
23921841-4	2013	RESULTS: Geldanamycin induced changes in apoptosis-related protein levels, loss of the mitochondrial transmembrane potential, release of cytochrome c, activation of caspases, cleavage of PARP-1, formation of reactive oxygen species and depletion of glutathione (GSH).	geldanamycin	9-21	caspase 8	Homo sapiens	165-173
23921841-5	2013	Licochalcone A enhanced geldanamycin-induced apoptosis-related protein activation, formation of reactive oxygen species, caspase activation and cell death.	licochalcone A	0-14	caspase 8	Homo sapiens	121-128
23921841-5	2013	Licochalcone A enhanced geldanamycin-induced apoptosis-related protein activation, formation of reactive oxygen species, caspase activation and cell death.	geldanamycin	24-36	caspase 8	Homo sapiens	121-128
23921841-7	2013	CONCLUSIONS: Licochalcone A may potentiate the apoptotic effect of geldanamycin on ovarian carcinoma cell lines by the activation of the caspase-8- and Bid-dependent pathways and the mitochondria-mediated apoptotic pathway.	licochalcone A	13-27	caspase 8	Homo sapiens	137-155
23921841-7	2013	CONCLUSIONS: Licochalcone A may potentiate the apoptotic effect of geldanamycin on ovarian carcinoma cell lines by the activation of the caspase-8- and Bid-dependent pathways and the mitochondria-mediated apoptotic pathway.	geldanamycin	67-79	caspase 8	Homo sapiens	137-155
23921841-8	2013	The apoptosis-promoting effect of licochalcone A may be mediated by its stimulatory action on the formation of reactive oxygen species and the depletion of GSH, which results in the activation of caspases.	licochalcone	34-46	caspase 8	Homo sapiens	196-204
23921841-8	2013	The apoptosis-promoting effect of licochalcone A may be mediated by its stimulatory action on the formation of reactive oxygen species and the depletion of GSH, which results in the activation of caspases.	Glutathione	156-159	caspase 8	Homo sapiens	196-204
23536891-2	2013	DHA treatment induced a concentration- and time-dependent reactive oxygen species (ROS)-mediated cell death with typical apoptotic characteristics such as breakdown of mitochondrial membrane potential (Deltapsim), caspases activation, DNA fragmentation and phosphatidylserine (PS) externalization.	artenimol	0-3	caspase 8	Homo sapiens	214-222
23536891-2	2013	DHA treatment induced a concentration- and time-dependent reactive oxygen species (ROS)-mediated cell death with typical apoptotic characteristics such as breakdown of mitochondrial membrane potential (Deltapsim), caspases activation, DNA fragmentation and phosphatidylserine (PS) externalization.	Reactive Oxygen Species	58-81	caspase 8	Homo sapiens	214-222
23536891-2	2013	DHA treatment induced a concentration- and time-dependent reactive oxygen species (ROS)-mediated cell death with typical apoptotic characteristics such as breakdown of mitochondrial membrane potential (Deltapsim), caspases activation, DNA fragmentation and phosphatidylserine (PS) externalization.	Reactive Oxygen Species	83-86	caspase 8	Homo sapiens	214-222
23536891-3	2013	Inhibition of caspase-8 or -9 significantly blocked DHA-induced decrease of cell viability and activation of caspase-3, suggesting the dominant roles of caspase-8 and -9 in DHA-induced apoptosis.	artenimol	52-55	caspase 8	Homo sapiens	14-23
23536891-3	2013	Inhibition of caspase-8 or -9 significantly blocked DHA-induced decrease of cell viability and activation of caspase-3, suggesting the dominant roles of caspase-8 and -9 in DHA-induced apoptosis.	artenimol	52-55	caspase 8	Homo sapiens	153-169
23536891-3	2013	Inhibition of caspase-8 or -9 significantly blocked DHA-induced decrease of cell viability and activation of caspase-3, suggesting the dominant roles of caspase-8 and -9 in DHA-induced apoptosis.	artenimol	173-176	caspase 8	Homo sapiens	14-23
23536891-3	2013	Inhibition of caspase-8 or -9 significantly blocked DHA-induced decrease of cell viability and activation of caspase-3, suggesting the dominant roles of caspase-8 and -9 in DHA-induced apoptosis.	artenimol	173-176	caspase 8	Homo sapiens	153-169
23536891-7	2013	More importantly, IR synergistically potentiated DHA-induced generation of ROS, activation of caspase-8 and -3, irreparable G2/M arrest and apoptosis, but did not enhance DHA-induced loss of Deltapsim and activation of caspase-9.	artenimol	49-52	caspase 8	Homo sapiens	94-110
23536891-8	2013	Taken together, our results strongly demonstrate the remarkable synergistic efficacy of combination treatment with DHA and low-dose IR for A549 cells in which IR potentiates DHA-induced apoptosis largely by enhancing the caspase-8-mediated extrinsic pathway.	artenimol	115-118	caspase 8	Homo sapiens	221-230
23536891-8	2013	Taken together, our results strongly demonstrate the remarkable synergistic efficacy of combination treatment with DHA and low-dose IR for A549 cells in which IR potentiates DHA-induced apoptosis largely by enhancing the caspase-8-mediated extrinsic pathway.	artenimol	174-177	caspase 8	Homo sapiens	221-230
23451189-9	2013	Curcumin potentiated 5-FU-induced expression or cleavage of pro-apoptotic proteins (caspase-8, -9, -3, PARP and Bax), and down-regulated anti-apoptotic (Bcl-xL) and proliferative (cyclin D1) proteins.	Curcumin	0-8	caspase 8	Homo sapiens	84-101
23451128-8	2013	In addition, alpha-santalol induced extrinsic and intrinsic pathways of apoptosis in both cells with activation of caspase-8 and caspase-9.	a-santalol	13-27	caspase 8	Homo sapiens	115-124
23451065-7	2013	On the other hand, higher concentrations of OME (450 and 600 microg/mL) triggered a massive apoptosis through the extrinsic pathway, including the activation of tumor necrosis factor-alpha (TNF-alpha), caspase 8, caspase 3, and cleavage of PARP, downregulation of survivin as well as depletion of the mutant p53 in MDA-MB-231 cells.	ome	44-47	caspase 8	Homo sapiens	202-211
23451189-9	2013	Curcumin potentiated 5-FU-induced expression or cleavage of pro-apoptotic proteins (caspase-8, -9, -3, PARP and Bax), and down-regulated anti-apoptotic (Bcl-xL) and proliferative (cyclin D1) proteins.	Fluorouracil	21-25	caspase 8	Homo sapiens	84-101
23534290-6	2013	At the same time, the combined effect of radiation and Ptx enhanced antiapoptotic Bcl-2 phosphorylation, caspases activation and survivin expression.	Paclitaxel	55-58	caspase 8	Homo sapiens	105-113
23254292-0	2012	Acquired differential regulation of caspase-8 in cisplatin-resistant non-small-cell lung cancer.	Cisplatin	49-58	caspase 8	Homo sapiens	36-45
23142077-6	2012	This modification destines activated caspase-8 molecules to rapid proteasomal degradation upon autoprocessing and cytoplasmic translocation.	destines	18-26	caspase 8	Homo sapiens	37-46
23254292-5	2012	In H460 NSCLC cells, caspase-8 cleavage was shown to be induced by cisplatin and is dependent on death receptor 4, death receptor 5, Fas-associated protein with death domain, acid sphingomyelinase and ceramide synthesis.	Cisplatin	67-76	caspase 8	Homo sapiens	21-30
23254292-5	2012	In H460 NSCLC cells, caspase-8 cleavage was shown to be induced by cisplatin and is dependent on death receptor 4, death receptor 5, Fas-associated protein with death domain, acid sphingomyelinase and ceramide synthesis.	Ceramides	201-209	caspase 8	Homo sapiens	21-30
23254292-7	2012	Accordingly, caspase-8 activation block acquired during cisplatin resistance, can be bypassed by death receptor agonism.	Cisplatin	56-65	caspase 8	Homo sapiens	13-22
23144495-0	2012	Cutting edge: FAS (CD95) mediates noncanonical IL-1beta and IL-18 maturation via caspase-8 in an RIP3-independent manner.	ammonium ferrous sulfate	14-17	caspase 8	Homo sapiens	81-90
23123647-10	2012	In RPMI-8226 cells pretreated with ManNPr, however, the mAb significantly inhibited the cell proliferation, decreased the viability, and induced apoptosis, which was associated with cleavage of caspase-3, caspase-8, caspase-9, and poly(ADP-ribose) polymerase.	mannpr	35-41	caspase 8	Homo sapiens	205-214
22562160-8	2012	We found half of the lethal dose (LD(50)) of bleomycin on NCCIT cell viability as 120 mug/ml after incubation for 72 h. Incubation with bleomycin (LD(50)) induced increases in caspase-3, caspase-8, and caspase-9 activities and Cyt-c and Bax protein levels and a decrease in Bcl-2 level.	Bleomycin	45-54	caspase 8	Homo sapiens	187-196
23194187-5	2012	Furthermore, GA induced PARP cleavage, activation of caspase-3, caspase-8, and caspase-9, as well as an increased ratio of Bax/Bcl-2.	gambogic acid	13-15	caspase 8	Homo sapiens	64-73
23025479-5	2012	These data suggest that (i) caspase-8 activation is triggered in ABT-737- and A23187-treated anucleate platelets through the mitochondria-initiated caspase activation cascade bypassing the death receptors, and (ii) ABT-737-treated platelets are a useful experimental tool for discerning the role of platelet apoptosis in platelet function and survival.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	65-68	caspase 8	Homo sapiens	28-37
23025479-5	2012	These data suggest that (i) caspase-8 activation is triggered in ABT-737- and A23187-treated anucleate platelets through the mitochondria-initiated caspase activation cascade bypassing the death receptors, and (ii) ABT-737-treated platelets are a useful experimental tool for discerning the role of platelet apoptosis in platelet function and survival.	Calcimycin	78-84	caspase 8	Homo sapiens	28-37
23025479-5	2012	These data suggest that (i) caspase-8 activation is triggered in ABT-737- and A23187-treated anucleate platelets through the mitochondria-initiated caspase activation cascade bypassing the death receptors, and (ii) ABT-737-treated platelets are a useful experimental tool for discerning the role of platelet apoptosis in platelet function and survival.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	215-218	caspase 8	Homo sapiens	28-37
23052210-9	2012	Caspase-8 is activated by proximity-induced dimerization, which might be facilitated by citrate through the stabilization of intermolecular interactions between the proteins.	Citric Acid	88-95	caspase 8	Homo sapiens	0-9
23025479-0	2012	Activation of caspases-9, -3 and -8 in human platelets triggered by BH3-only mimetic ABT-737 and calcium ionophore A23187: caspase-8 is activated via bypass of the death receptors.	BH 3	68-71	caspase 8	Homo sapiens	123-132
23025479-0	2012	Activation of caspases-9, -3 and -8 in human platelets triggered by BH3-only mimetic ABT-737 and calcium ionophore A23187: caspase-8 is activated via bypass of the death receptors.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	85-88	caspase 8	Homo sapiens	123-132
23025479-0	2012	Activation of caspases-9, -3 and -8 in human platelets triggered by BH3-only mimetic ABT-737 and calcium ionophore A23187: caspase-8 is activated via bypass of the death receptors.	Calcium	97-104	caspase 8	Homo sapiens	123-132
23025479-0	2012	Activation of caspases-9, -3 and -8 in human platelets triggered by BH3-only mimetic ABT-737 and calcium ionophore A23187: caspase-8 is activated via bypass of the death receptors.	Calcimycin	115-121	caspase 8	Homo sapiens	123-132
23025479-3	2012	We found that ABT-737 predominantly induced activation of caspases-9, -3 and -8 rather than CD62 exposure, whereas A23187 induces both caspases activation and CD62 exposure.	ABT-737	14-21	caspase 8	Homo sapiens	58-66
22722337-2	2012	However, we show that inhibition of EGFR signaling in non-transformed breast epithelial cells by EGF deprivation or gefitinib, an inhibitor of EGFR tyrosine kinase, causes the upregulation of the long isoform of caspase-8 inhibitor FLICE-inhibitory protein (FLIP(L)) and makes these cells more resistant to the tumor necrosis factor-related apoptosis-inducing ligand (TRAIL).	Gefitinib	116-125	caspase 8	Homo sapiens	212-221
23052210-5	2012	The lethal effect of citrate was found to be related to the activation of apical caspases-8 and -2, rather than to the inhibition of cellular energy metabolism.	Citric Acid	21-28	caspase 8	Homo sapiens	81-98
22562160-8	2012	We found half of the lethal dose (LD(50)) of bleomycin on NCCIT cell viability as 120 mug/ml after incubation for 72 h. Incubation with bleomycin (LD(50)) induced increases in caspase-3, caspase-8, and caspase-9 activities and Cyt-c and Bax protein levels and a decrease in Bcl-2 level.	Bleomycin	136-145	caspase 8	Homo sapiens	187-196
22923501-6	2012	These interactions were associated with death receptor 5 (DR5) up-regulation and caspase-8 activation, whereas cells expressing dominant-negative caspase-8 were substantially protected from resveratrol/HDACI treatment, which suggests a significant functional role for the extrinsic apoptotic pathway in lethality.	Resveratrol	190-201	caspase 8	Homo sapiens	146-155
22923501-8	2012	The free radical scavenger Mn(III)tetrakis(4-benzoic acid)porphyrin chloride blocked ROS generation, DR5 up-regulation, caspase-8 activation, DNA damage, and apoptosis, which indicates a primary role for oxidative injury in lethality.	mn(iii)tetrakis(4-benzoic acid)porphyrin chloride	27-76	caspase 8	Homo sapiens	120-129
23089555-9	2012	Nimbolide induces the cleavage of pro-caspase-8, pro-caspase-3 and PARP.	nimbolide	0-9	caspase 8	Homo sapiens	38-47
23096116-0	2012	Intrinsic caspase-8 activation mediates sensitization of erlotinib-resistant tumor cells to erlotinib/cell-cycle inhibitors combination treatment.	Erlotinib Hydrochloride	57-66	caspase 8	Homo sapiens	10-19
22310286-6	2012	Also, 2DG sensitised Z138 cells to TRAIL and induced a marked decrease in caspase-8, -3, cFLIP(S), Bid and Mcl-1 expression but Bak remained unchanged, altering the Mcl-1/Bak ratio, facilitating cytochrome c release and cell death.	Deoxyglucose	6-9	caspase 8	Homo sapiens	74-83
22922338-4	2012	Capsazepine potentiated the effect of TRAIL, as shown by its effect on intracellular esterase activity; activation of caspase-8,-9, and -3; and colony-formation assay.	capsazepine	0-11	caspase 8	Homo sapiens	118-138
22895075-5	2012	A3D8-induced apoptosis is abrogated by the lipid raft disrupting agent methyl-beta-cyclodextrin and the caspase-8 inhibitor Z-IETD-fmk.	a3d8	0-4	caspase 8	Homo sapiens	104-113
22895075-5	2012	A3D8-induced apoptosis is abrogated by the lipid raft disrupting agent methyl-beta-cyclodextrin and the caspase-8 inhibitor Z-IETD-fmk.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	124-134	caspase 8	Homo sapiens	104-113
23132899-4	2012	RESULTS: We found that STC induces apoptosis in these cells in a dose-dependent manner and leads to the activation of Fas and caspase-8, cleavage of Bid, mitochondrial damage, and activation of caspase-3.	stichoposide	23-26	caspase 8	Homo sapiens	126-135
22865487-7	2012	The results suggest that 18beta-glycyrrhetinic acid may potentiate the Hsp90 inhibition-induced apoptosis in ovarian carcinoma cell lines via the activation of the caspase-8- and Bid-dependent pathways and the mitochondria-mediated cell death pathway, leading to activation of caspases.	18alpha-glycyrrhetinic acid	25-51	caspase 8	Homo sapiens	164-182
22865487-7	2012	The results suggest that 18beta-glycyrrhetinic acid may potentiate the Hsp90 inhibition-induced apoptosis in ovarian carcinoma cell lines via the activation of the caspase-8- and Bid-dependent pathways and the mitochondria-mediated cell death pathway, leading to activation of caspases.	18alpha-glycyrrhetinic acid	25-51	caspase 8	Homo sapiens	277-285
23096116-0	2012	Intrinsic caspase-8 activation mediates sensitization of erlotinib-resistant tumor cells to erlotinib/cell-cycle inhibitors combination treatment.	Erlotinib Hydrochloride	92-101	caspase 8	Homo sapiens	10-19
22116711-5	2012	Our results showed that OC induced a caspase-dependent apoptosis by triggering a series of events in HeLa cells including Bax translocation, cytochrome c release, caspase-3 activation, chromosome fragmentation followed by caspase-8 activation, Bid cleavage and eventually cell death.	oblongifolin C	24-26	caspase 8	Homo sapiens	222-231
23047484-7	2012	In summary, our resultsindicate that 10-acetylirciformonin B treatment causes apoptosis in leukaemia cells; probably through a caspase-dependent regulatory pathway.	10-acetylirciformonin B	37-60	caspase 8	Homo sapiens	127-134
23298479-8	2012	Ziram increased the intracellular levels of active caspases 3, 3/7, 8, and 9 and pan-caspase in a dose-dependent manner, and a caspase-3 inhibitor, Z-DEVD-FMK, and a general caspase inhibitor, Z-VAD-FMK, partially but significantly inhibited the apoptosis.	Ziram	0-5	caspase 8	Homo sapiens	51-58
23298479-8	2012	Ziram increased the intracellular levels of active caspases 3, 3/7, 8, and 9 and pan-caspase in a dose-dependent manner, and a caspase-3 inhibitor, Z-DEVD-FMK, and a general caspase inhibitor, Z-VAD-FMK, partially but significantly inhibited the apoptosis.	Ziram	0-5	caspase 8	Homo sapiens	85-92
23298479-10	2012	These findings indicate that ziram can induce apoptosis in human NK cells, and the apoptosis is at least mediated by both the caspase-cascade and the mitochondria/cytochrome-c pathways.	Ziram	29-34	caspase 8	Homo sapiens	126-133
22761256-3	2012	We found that caspase 8-cleaved Bid (tBid) could result in LMP directly.	tBID	37-41	caspase 8	Homo sapiens	14-23
22766766-5	2012	In addition, angelicin dose-dependently downregulated the expression of anti-apoptotic proteins including Bcl-2, Bcl-xL, and Mcl-1 suggesting the involvement of the intrinsic mitochondria-mediated apoptotic pathway which did not participate in Fas/FasL-induced caspase-8-mediated extrinsic, MAP kinases, and PI3K/AKT/GSK-3beta pathway.	angelicin	13-22	caspase 8	Homo sapiens	261-270
22359244-7	2012	Activation of caspase-8 and caspase-3, critical mediators of extrinsic apoptosis signaling, was also increased by 3-O-acetyloleanolic acid.	oleanolic acid 3-acetate	114-138	caspase 8	Homo sapiens	14-23
22998498-16	2012	The best of tested GOBA scores achieved 0.74 and 0.8 as a mean Pearson correlation to the observed quality of models in our CASP8 and CASP9-based validation sets.	goba	19-23	caspase 8	Homo sapiens	124-129
22998498-17	2012	GOBA also obtained the best result for two targets of CASP8, and one of CASP9, compared to the contest participants.	goba	0-4	caspase 8	Homo sapiens	54-59
22824956-6	2012	The prevention             of MEK by the pharmacologic inhibitors PD98059 and U0126, resulted in decreased             UDCA-induced apoptosis as shown by the reduction of apoptotic body formation,             caspase-8 activity, and caspase-3, -6 and PARP cleavage, indicating that ERK exerts             pro-apoptotic activity upon exposure to UDCA.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	66-73	caspase 8	Homo sapiens	209-218
22824956-6	2012	The prevention             of MEK by the pharmacologic inhibitors PD98059 and U0126, resulted in decreased             UDCA-induced apoptosis as shown by the reduction of apoptotic body formation,             caspase-8 activity, and caspase-3, -6 and PARP cleavage, indicating that ERK exerts             pro-apoptotic activity upon exposure to UDCA.	U 0126	78-83	caspase 8	Homo sapiens	209-218
22974127-10	2012	Simvastatin treatment resulted in increased mRNA and protein expression of molecules such as TNF, Fas-L, Traf1 and cleaved caspase 8, major mediators of intrinsic apoptosis pathway and reduced protein levels of pro-survival genes Lhx4 and Nme5.	Simvastatin	0-11	caspase 8	Homo sapiens	123-132
22828439-5	2012	Furthermore, calactin induced extracellular signal-regulated kinase (ERK) phosphorylation, activation of caspase-3, caspase-8, and caspase-9, and PARP cleavage.	Calactin	13-21	caspase 8	Homo sapiens	116-125
22433057-7	2012	The results suggest that parthenolide may potentiate the apoptotic effect of geldanamycin on ovarian carcinoma cell lines by the activation of the caspase-8- and Bid-dependent pathway and the mitochondria-mediated apoptotic pathway.	parthenolide	25-37	caspase 8	Homo sapiens	147-165
22433057-7	2012	The results suggest that parthenolide may potentiate the apoptotic effect of geldanamycin on ovarian carcinoma cell lines by the activation of the caspase-8- and Bid-dependent pathway and the mitochondria-mediated apoptotic pathway.	geldanamycin	77-89	caspase 8	Homo sapiens	147-165
22783925-11	2012	The antitumor activity of RAAP was associated with its role in inducing caspase-3 and caspase-8 expression as well as downregulating MMP-2 expression.	raap	26-30	caspase 8	Homo sapiens	86-95
22705147-7	2012	The induction of PGD(2)-CRTH2 dependent apoptosis was associated with the activation of caspase-9, but not caspase-8, leading to caspase-3 cleavage.	Prostaglandin D2	17-23	caspase 8	Homo sapiens	107-116
22492309-0	2012	Sulfuretin from heartwood of Rhus verniciflua triggers apoptosis through activation of Fas, Caspase-8, and the mitochondrial death pathway in HL-60 human leukemia cells.	sulfuretin	0-10	caspase 8	Homo sapiens	92-101
22613808-6	2012	Phlorofucofuroeckol A inhibited the phosphorylation of JNK and the expression of Fas-mediated apoptotic proteins including Fas ligand, cleaved caspase-8, cleaved caspase-3, and poly (ADP-ribose) polymerase.	phlorofucofuroeckol A	0-21	caspase 8	Homo sapiens	143-152
22735465-15	2012	Co-treatment with TRAIL and artepillin C induced the significant             activation of caspase-8 and caspase-3, as well as the disruption of  psim.	artepillin C	28-40	caspase 8	Homo sapiens	91-100
22492309-2	2012	In this study, sulfuretin induced apoptosis by activating caspases-8, -9, and -3 as well as cleavage of poly(ADP-ribose) polymerase.	sulfuretin	15-25	caspase 8	Homo sapiens	58-80
22492309-4	2012	Sulfuretin also activated the extrinsic apoptosis pathway, that is, it increased the expressions of Fas and FasL, the activation of caspase-8, and the cleavage of Bid.	sulfuretin	0-10	caspase 8	Homo sapiens	132-141
22492309-6	2012	The therapeutical effect of sulfuretin in leukemia is due to its potent apoptotic activity through the extrinsic pathway driven by a Fas-mediated caspase-8-dependent pathway.	sulfuretin	28-38	caspase 8	Homo sapiens	146-155
22492309-6	2012	The therapeutical effect of sulfuretin in leukemia is due to its potent apoptotic activity through the extrinsic pathway driven by a Fas-mediated caspase-8-dependent pathway.	ammonium ferrous sulfate	133-136	caspase 8	Homo sapiens	146-155
22653966-3	2012	Curcumin induces the activation of caspase-8, -2, and -9, alteration of mitochondrial membrane potential, release of cytochrome c, and activation of caspase-3 and concomitant PARP cleavage, but the addition of caspase inhibitors only partially blocked the curcumin-mediated apoptosis.	Curcumin	0-8	caspase 8	Homo sapiens	35-56
23019417-5	2012	In addition, apicidin and docetaxel co-treatment specifically stimulates apoptosis, characterized by an increased Bax/Bcl-2 ratio and caspase-8 activation.	apicidin	13-21	caspase 8	Homo sapiens	134-143
23019417-5	2012	In addition, apicidin and docetaxel co-treatment specifically stimulates apoptosis, characterized by an increased Bax/Bcl-2 ratio and caspase-8 activation.	Docetaxel	26-35	caspase 8	Homo sapiens	134-143
23086637-10	2012	CONCLUSION: Combining HDAC inhibitor SAHA with imatinib can kill CML cells synergistically by inhibiting cell growth and inducing apoptosis, which is associated with activation of Caspase pathway and regulation of anti-apoptotic proteins.	Vorinostat	37-41	caspase 8	Homo sapiens	180-187
22766785-11	2012	Although it did not suppress cell proliferation, IFNlambda             signaling via 10R1/lambdaR1 receptor induced cell cycle arrest, externalization of             phosphatidylserine, DNA fragmentation, activation of caspase-3, caspase-8 and             caspase-9.	ifnlambda	49-58	caspase 8	Homo sapiens	230-239
23086645-12	2012	CONCLUSION: The polysaccharide of snakegourd root can induce the apoptosis of MCF-7 cells,which is associated with the activation of intracellular Caspase-3 and Caspase-8.	Polysaccharides	16-30	caspase 8	Homo sapiens	161-170
23086637-10	2012	CONCLUSION: Combining HDAC inhibitor SAHA with imatinib can kill CML cells synergistically by inhibiting cell growth and inducing apoptosis, which is associated with activation of Caspase pathway and regulation of anti-apoptotic proteins.	Imatinib Mesylate	47-55	caspase 8	Homo sapiens	180-187
23086640-7	2012	Enhanced apoptosis was observed in SHBA group evidenced by strong activation of Caspase-9, Caspase-8 and Caspase-3.	shba	35-39	caspase 8	Homo sapiens	91-100
22739412-14	2012	The results demonstrated that PA induced apoptosis of MCF7 cells through NF-kappaB and Bcl2/Bax signaling pathways with the involvement of caspases.	pyranocycloartobiloxanthone A	30-32	caspase 8	Homo sapiens	139-147
22929310-12	2012	The mechanism of tumor cell death induced by the S20-3 peptide was associated with activation of caspases, but this activity was only partially inhibited by the pan-caspase inhibitor z-VAD.	z-vad	183-188	caspase 8	Homo sapiens	97-105
22929310-12	2012	The mechanism of tumor cell death induced by the S20-3 peptide was associated with activation of caspases, but this activity was only partially inhibited by the pan-caspase inhibitor z-VAD.	z-vad	183-188	caspase 8	Homo sapiens	97-104
24024120-3	2012	Here we show that switching off the Fas pathway using Fas apoptotic inhibitory protein (Faim/TOSO), which regulates apoptosis upstream of caspase 8, blocked beta-cell apoptosis and increased proliferation in human islets.	ammonium ferrous sulfate	36-39	caspase 8	Homo sapiens	138-147
22617025-7	2012	Furthermore, berberine inhibited caspase-8 mediated angiogenesis, as confirmed through expression of tumor necrotic factor related apoptosis-inducing ligand (TRAIL), vascular endothelial growth factor (VEGF) and survivin.	Berberine	13-22	caspase 8	Homo sapiens	33-42
22644571-4	2012	Both, tumor necrosis factor alpha and tumor necrosis factor-related apoptosis inducing ligand induced cell death was accompanied by Atg3 cleavage and this event was inhibited by a pan-caspase inhibitor (zVAD) or a caspase-8-specific inhibitor (zIETD).	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	203-207	caspase 8	Homo sapiens	184-191
22771329-3	2012	PGG increased the number of TUNEL-positive cells and the sub-G1 cell population as well as activated caspase cascades including caspase-8, -9 and -3 in K562 cells.	beta-penta-O-galloyl-glucose	0-3	caspase 8	Homo sapiens	128-148
22843888-5	2012	Moreover, pre-treatment of Caki-1 (wild-type VHL) and 786-O (mutant VHL) with HDACIs followed by sorafenib reduced cell viability synergistically via activation of caspases and downregulation of the levels of myeloid leukemia cell differentiation protein (MCL1), phospho-extracellular signal-regulated kinase (ERK), and secreted vascular endothelial growth factor (VEGF).	Sorafenib	97-106	caspase 8	Homo sapiens	164-172
22644571-4	2012	Both, tumor necrosis factor alpha and tumor necrosis factor-related apoptosis inducing ligand induced cell death was accompanied by Atg3 cleavage and this event was inhibited by a pan-caspase inhibitor (zVAD) or a caspase-8-specific inhibitor (zIETD).	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	203-207	caspase 8	Homo sapiens	214-223
22644571-4	2012	Both, tumor necrosis factor alpha and tumor necrosis factor-related apoptosis inducing ligand induced cell death was accompanied by Atg3 cleavage and this event was inhibited by a pan-caspase inhibitor (zVAD) or a caspase-8-specific inhibitor (zIETD).	zietd	244-249	caspase 8	Homo sapiens	184-191
22644571-4	2012	Both, tumor necrosis factor alpha and tumor necrosis factor-related apoptosis inducing ligand induced cell death was accompanied by Atg3 cleavage and this event was inhibited by a pan-caspase inhibitor (zVAD) or a caspase-8-specific inhibitor (zIETD).	zietd	244-249	caspase 8	Homo sapiens	214-223
22322857-4	2012	Using in vitro and in vivo colorectal cancer models, we further demonstrated that SAHA-induced apoptosis is dependant on FLIP downregulation and caspase 8 activation.	Vorinostat	82-86	caspase 8	Homo sapiens	145-154
22573342-11	2012	Correspondingly, in the RAP80 siRNA combined with gemcitabine group, both Bax and cleaved caspase-8 protein levels were increased (P &lt; 0.01), whereas Bcl-2 protein decreased significantly (P &lt; 0.01).	gemcitabine	50-61	caspase 8	Homo sapiens	90-99
21633925-3	2012	In the present study, we show that retinoic acid enhances the cytostatic and apoptogenic properties of the novel adamantyl retinoid ST1926 in a panel of neuroblastoma cells with different p53 status and caspase 8 expression, resulting in synergistic effects as assessed by Combination Index and Isobologram analysis.	Tretinoin	35-48	caspase 8	Homo sapiens	203-212
21633925-3	2012	In the present study, we show that retinoic acid enhances the cytostatic and apoptogenic properties of the novel adamantyl retinoid ST1926 in a panel of neuroblastoma cells with different p53 status and caspase 8 expression, resulting in synergistic effects as assessed by Combination Index and Isobologram analysis.	adamantyl	113-122	caspase 8	Homo sapiens	203-212
21809024-7	2012	At a concentration of 5 muM ABITC generated an excess amount of reactive oxygen species (ROS) and displayed pro-apoptotic signaling such as activation of caspase-8, JNK-SAPK and deactivation of PARP-1.	abietyl-isothiocyanate	28-33	caspase 8	Homo sapiens	154-163
22453599-4	2012	Apoptosis was attenuated upon pretreatment with specific inhibitors of caspase-8 (Z-IETD-fmk) and caspase-9 (Z-LEHD-fmk) suggesting the involvement of both intrinsic and extrinsic apoptotic cascades.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	82-92	caspase 8	Homo sapiens	71-80
22931640-10	2012	In addition, the expression of cleaved caspase-8 protein was induced significantly after treated with baicalin.	baicalin	102-110	caspase 8	Homo sapiens	39-48
22623731-7	2012	The histone deacetylase inhibitors (HDACi), droxinostat and SAHA, also downregulated c-FLIP expression, induced caspase-8- and caspase-3/7-mediated apoptosis, and increased apoptosis in bicalutamide-treated cells.	4-(4-chloro-2-methylphenoxy)-N-hydroxybutanamide	44-55	caspase 8	Homo sapiens	112-136
22348919-0	2012	5-epi-Sinuleptolide induces cell cycle arrest and apoptosis through tumor necrosis factor/mitochondria-mediated caspase signaling pathway in human skin cancer cells.	5-episinuleptolide	0-19	caspase 8	Homo sapiens	112-119
22348919-9	2012	5-epi-Sinuleptolide also up-regulated tBid, which is associated with up-regulation of tumor necrosis factor-alpha (TNF-alpha) and Fas ligand (FasL) and their cognate receptors (i.e., TNF-RI, TNF-R2 and Fas), downstream adaptor TNF-R1-associated death domain (TRADD) and Fas-associated death domain (FADD), and activated caspase-8 in SCC25 cells.	5-episinuleptolide	0-19	caspase 8	Homo sapiens	320-329
22348919-9	2012	5-epi-Sinuleptolide also up-regulated tBid, which is associated with up-regulation of tumor necrosis factor-alpha (TNF-alpha) and Fas ligand (FasL) and their cognate receptors (i.e., TNF-RI, TNF-R2 and Fas), downstream adaptor TNF-R1-associated death domain (TRADD) and Fas-associated death domain (FADD), and activated caspase-8 in SCC25 cells.	tBID	38-42	caspase 8	Homo sapiens	320-329
22538414-0	2012	Amphotericin B up-regulates lipid A-induced IL-6 production via caspase-8.	Amphotericin B	0-14	caspase 8	Homo sapiens	64-73
22538414-0	2012	Amphotericin B up-regulates lipid A-induced IL-6 production via caspase-8.	Lipid A	28-35	caspase 8	Homo sapiens	64-73
22538414-8	2012	Amphotericin B activated caspase-8.	Amphotericin B	0-14	caspase 8	Homo sapiens	25-34
22538414-9	2012	In addition, a caspase-8 inhibitor inhibited IL-6 production by amphotericin B and lipid A.	Amphotericin B	64-78	caspase 8	Homo sapiens	15-24
22538414-9	2012	In addition, a caspase-8 inhibitor inhibited IL-6 production by amphotericin B and lipid A.	Lipid A	83-90	caspase 8	Homo sapiens	15-24
22538414-10	2012	This suggests that caspase-8 is required for the synergistic production of IL-6 by amphotericin B and lipid A.	Amphotericin B	83-97	caspase 8	Homo sapiens	19-28
22538414-10	2012	This suggests that caspase-8 is required for the synergistic production of IL-6 by amphotericin B and lipid A.	Lipid A	102-109	caspase 8	Homo sapiens	19-28
22552576-7	2012	This elevation of cleaved caspase-8 or caspase-3 and caspase-9             or caspase-3 decreased in the presence of caspase-8 inhibitor Z-IETD-FMK or caspase-9             inhibitor Z-LEHD-FMK, respectively.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	137-147	caspase 8	Homo sapiens	26-35
22644961-3	2012	Although treatment with resveratrol alone did not induce caspase-8 activation, cotreatment with both SB203580 and resveratrol not only enhanced FasL cleavage but also activated caspase-8, indicating that the extrinsic apoptotic pathway may be involved in the synergistic effect.	SB 203580	101-109	caspase 8	Homo sapiens	177-186
22644961-3	2012	Although treatment with resveratrol alone did not induce caspase-8 activation, cotreatment with both SB203580 and resveratrol not only enhanced FasL cleavage but also activated caspase-8, indicating that the extrinsic apoptotic pathway may be involved in the synergistic effect.	Resveratrol	114-125	caspase 8	Homo sapiens	177-186
22552576-7	2012	This elevation of cleaved caspase-8 or caspase-3 and caspase-9             or caspase-3 decreased in the presence of caspase-8 inhibitor Z-IETD-FMK or caspase-9             inhibitor Z-LEHD-FMK, respectively.	benzyloxycarbonyl-leucyl-glutamyl-histidyl-aspartic acid fluoromethyl ketone	183-193	caspase 8	Homo sapiens	117-126
22552576-7	2012	This elevation of cleaved caspase-8 or caspase-3 and caspase-9             or caspase-3 decreased in the presence of caspase-8 inhibitor Z-IETD-FMK or caspase-9             inhibitor Z-LEHD-FMK, respectively.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	137-147	caspase 8	Homo sapiens	117-126
22552576-8	2012	Both inhibitors also rescued cell growth,             and the caspase-8 inhibitor Z-IETD-FMK prevented apoptotic phenomena including             the TUNEL signal.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	82-92	caspase 8	Homo sapiens	62-71
22552576-7	2012	This elevation of cleaved caspase-8 or caspase-3 and caspase-9             or caspase-3 decreased in the presence of caspase-8 inhibitor Z-IETD-FMK or caspase-9             inhibitor Z-LEHD-FMK, respectively.	benzyloxycarbonyl-leucyl-glutamyl-histidyl-aspartic acid fluoromethyl ketone	183-193	caspase 8	Homo sapiens	26-35
22477067-6	2012	Reversine induced apoptosis in PDTC cells with caspase-3 and caspase-8 activation, but not caspase-9.	2-(4-morpholinoanilino)-6-cyclohexylaminopurine	0-9	caspase 8	Homo sapiens	61-70
22309674-8	2012	This result was confirmed by blockage of PEITC-induced cleavages of Poly(ADP-ribose) Polymerase, caspase-3, caspase-8, and DR5 by p38 MAPK inhibitor, SB203580.	phenethyl isothiocyanate	41-46	caspase 8	Homo sapiens	108-117
22309674-8	2012	This result was confirmed by blockage of PEITC-induced cleavages of Poly(ADP-ribose) Polymerase, caspase-3, caspase-8, and DR5 by p38 MAPK inhibitor, SB203580.	SB 203580	150-158	caspase 8	Homo sapiens	108-117
22994042-4	2012	RESULTS: Compared with the 0 micromol/L control group, the 25, 50 and 100 micromol/L dihydroartemisinin groups showed significantly increased apoptosis of PC-3M cells ([2.92 +/- 0.45]% vs [8.85 +/- 0.74]%, [12.83 +/- 0.84]% and [18.65 +/- 1.24]%, P &lt; 0.01), and dose-dependent increase in the activities of caspase-8 ([0.47 +/- 0.05 ] U/microg vs [1.22 +/- 0.15], [1.76 +/- 0.07] and [2.91 +/- 0.24] U/microg, P &lt; 0.01) and caspase-3 ([0.44 +/- 0.07] U/microg vs [0.95 +/- 0.08], [1.48 +/- 0.14] and [2.92 +/- 0.45] U/microg, P &lt; 0.01).	artenimol	85-103	caspase 8	Homo sapiens	310-319
22523229-7	2012	In contrast, PJ-34 potentiated TGHQ-induced caspase-8 activation, suggesting that PARP-1 plays a dual role in regulating TGHQ-induced apoptosis via opposing effects on the intrinsic (mitochondrial) and extrinsic (death-receptor) pathways.	2,3,5-(triglutathion-S-yl)hydroquinone	31-35	caspase 8	Homo sapiens	44-53
23124518-6	2012	Moreover, pretreatment with etoposide increased TRAIL-induced apoptosis in caspase 8 restored IMR-32 cells through activation of a caspase cascade that included caspases 8, 9 and 3.	Etoposide	28-37	caspase 8	Homo sapiens	75-84
22609468-3	2012	Rapid doxorubicin-induced cell death in Jurkat cells was mediated by caspase activation.	Doxorubicin	6-17	caspase 8	Homo sapiens	69-76
22609468-6	2012	Other drugs containing quinone groups, such as menadione and adaphostin, were also tested on HLTC and both were toxic by a caspase-independent mechanism.	Vitamin K 3	47-56	caspase 8	Homo sapiens	123-130
22609468-6	2012	Other drugs containing quinone groups, such as menadione and adaphostin, were also tested on HLTC and both were toxic by a caspase-independent mechanism.	NSC 680410	61-71	caspase 8	Homo sapiens	123-130
23124518-0	2012	Etoposide sensitizes neuroblastoma cells expressing caspase 8 to TRAIL.	Etoposide	0-9	caspase 8	Homo sapiens	52-61
23124518-2	2012	We provide evidence that pretreatment with etoposide significantly enhanced TRAIL-mediated apoptosis via up-regulation of DR5 (death receptor 5 or TRAIL-R2) expression in the caspase 8 expressing neuroblastoma cell line, SK-N-MC.	Etoposide	43-52	caspase 8	Homo sapiens	175-184
23124518-6	2012	Moreover, pretreatment with etoposide increased TRAIL-induced apoptosis in caspase 8 restored IMR-32 cells through activation of a caspase cascade that included caspases 8, 9 and 3.	Etoposide	28-37	caspase 8	Homo sapiens	161-180
23124518-7	2012	These results indicate that the etoposide-mediated sensitization of neuroblastoma cells to TRAIL is associated with an increase in TRAIL-R2 expression and requires caspase 8 expression.	Etoposide	32-41	caspase 8	Homo sapiens	164-173
22611243-0	2012	Signal-transducing adaptor protein-2 modulates Fas-mediated T cell apoptosis by interacting with caspase-8.	ammonium ferrous sulfate	47-50	caspase 8	Homo sapiens	97-106
22528489-8	2012	Moreover, the main caspase-8 fragment generated by cathepsin D cleavage could be affinity-labeled with the active site probe biotin-VAD-fluoromethyl ketone, suggesting that this fragment is enzymatically active.	biotin-vad-fluoromethyl ketone	125-155	caspase 8	Homo sapiens	19-28
22611243-4	2012	Moreover, STAP-2 protein has a consensus caspase-8 cleavage sequence, VEAD, in its C-terminal domain, and processing of STAP-2 by caspase-8 was crucial for Fas-induced apoptosis.	ammonium ferrous sulfate	156-159	caspase 8	Homo sapiens	41-50
22611243-4	2012	Moreover, STAP-2 protein has a consensus caspase-8 cleavage sequence, VEAD, in its C-terminal domain, and processing of STAP-2 by caspase-8 was crucial for Fas-induced apoptosis.	ammonium ferrous sulfate	156-159	caspase 8	Homo sapiens	130-139
22311471-6	2012	The treatment with 2-DCB and PA resulted in the loss of mitochondrial membrane potential, and Fas, caspase-8 and caspase-3 activation.	2-dodecylcyclobutanone	19-24	caspase 8	Homo sapiens	99-108
22571975-10	2012	The alpha-santalol-induced apoptotic cell death and activation of caspase-3 was significantly attenuated in the presence of pharmacological inhibitors of caspase-8 and caspase-9.	a-santalol	4-18	caspase 8	Homo sapiens	154-163
22114764-8	2012	Pretreatment of cells with caspase inhibitor (Z-VAD-FMK) blocked butein-induced activation of caspases.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	46-55	caspase 8	Homo sapiens	94-102
22114764-8	2012	Pretreatment of cells with caspase inhibitor (Z-VAD-FMK) blocked butein-induced activation of caspases.	butein	65-71	caspase 8	Homo sapiens	94-102
22289270-10	2012	The other pathway includes increase in ROS, which resulted in activation of NF-kappaB, expression of FasL and triggered FasL-dependent pathway, which also involves caspase-8.	Reactive Oxygen Species	39-42	caspase 8	Homo sapiens	164-173
22434375-0	2012	Amplification activation loop between caspase-8 and -9 dominates artemisinin-induced apoptosis of ASTC-a-1 cells.	artemisinin	65-76	caspase 8	Homo sapiens	38-54
22311471-6	2012	The treatment with 2-DCB and PA resulted in the loss of mitochondrial membrane potential, and Fas, caspase-8 and caspase-3 activation.	Palmitic Acid	29-31	caspase 8	Homo sapiens	99-108
22434375-1	2012	Although caspases have been demonstrated to be involved in artemisinin (ARTE)-induced apoptosis, their exact functions are not well understood.	artemisinin	59-70	caspase 8	Homo sapiens	9-17
22434375-1	2012	Although caspases have been demonstrated to be involved in artemisinin (ARTE)-induced apoptosis, their exact functions are not well understood.	artemisinin	72-76	caspase 8	Homo sapiens	9-17
22401948-5	2012	Our results also indicated that MTT could activate apoptosis related factors such as caspase-8, caspase-3 or accelerate the leakage of cell contents after the appearance of MTT formazan crystals.	monooxyethylene trimethylolpropane tristearate	32-35	caspase 8	Homo sapiens	85-94
22434375-3	2012	ARTE treatment induces a rapid generation of reactive oxygen species (ROS), and ROS-dependent apoptosis as well as the activation of caspase-8, -9 and -3 via time- and dose-dependent fashion.	artemisinin	0-4	caspase 8	Homo sapiens	133-153
22434375-7	2012	Collectively, our data firstly demonstrate that ARTE triggers a ROS-mediated positive feedback amplification activation loop between caspase-8 and -9 independent of mitochondria, which dominantly mediated the ARTE-induced apoptosis via a caspase-3-independent apoptotic pathway in ASTC-a-1 cells.	Reactive Oxygen Species	64-67	caspase 8	Homo sapiens	133-149
22434375-8	2012	Our findings imply a potential to develop new derivatives from artemisinin to effectively initiate the amplification activation loop of caspases.	artemisinin	63-74	caspase 8	Homo sapiens	136-144
22493319-7	2012	The DNA-demethylating drug 5-Aza-2-deoxycytidine (5-azadC) induced rapid nuclear accumulation of FOXO3, ATM-dependent CREB phosphorylation, and caspase-8 expression in a FOXO3-dependent manner.	Decitabine	27-48	caspase 8	Homo sapiens	144-153
22493319-7	2012	The DNA-demethylating drug 5-Aza-2-deoxycytidine (5-azadC) induced rapid nuclear accumulation of FOXO3, ATM-dependent CREB phosphorylation, and caspase-8 expression in a FOXO3-dependent manner.	Decitabine	50-57	caspase 8	Homo sapiens	144-153
22493319-8	2012	This indicates that 5-azadC activates the FOXO3-ATM-CREB signaling pathway, which contributes to caspase-8 expression.	Decitabine	20-27	caspase 8	Homo sapiens	97-106
22426808-11	2012	The docking data suggested that C-K forms hydrogen bonds with Lys253, Thr904 and Gly362 in caspase 8, and with Thr62, Ser63 and Arg207 in caspase 9.	Hydrogen	42-50	caspase 8	Homo sapiens	91-100
22707267-3	2012	METHODS AND RESULTS: DHA induces apoptosis as detected by Annexin V-FITC/PI assay as well as induces cleavage of caspase-8 and -9, endoplasmic reticulum stress (ERS), and elevated levels of death receptor-5 (DR5) protein expression as detected by western blot assays.	Docosahexaenoic Acids	21-24	caspase 8	Homo sapiens	113-129
22707267-4	2012	Chemical inhibitors of caspase-8 and -9 and small interfering RNAs (siRNAs) show DHA to induce ERS/CHOP/DR5-mediated caspase-8 and -9 dependent apoptosis.	Docosahexaenoic Acids	81-84	caspase 8	Homo sapiens	23-39
22707267-4	2012	Chemical inhibitors of caspase-8 and -9 and small interfering RNAs (siRNAs) show DHA to induce ERS/CHOP/DR5-mediated caspase-8 and -9 dependent apoptosis.	Docosahexaenoic Acids	81-84	caspase 8	Homo sapiens	117-133
22707267-7	2012	CONCLUSION: Data, for the first time, demonstrate that DHA induces apoptosis in TNBC cells via activation of ERS/CHOP/DR5-mediated caspase-8 and -9 dependent pro-apoptotic events, and that different forms of vitamin E exhibit distinct effects on DHA-induced apoptosis; namely, inhibition by alphaT and enhancement by gammaT3.	Docosahexaenoic Acids	55-58	caspase 8	Homo sapiens	131-147
22395735-7	2012	Moreover, pretreatment with z-IETD-FMK             (caspase-8 inhibitor) or stable expression of dominant negative caspase-8 genes             blocked DHA/sulindac sulfide cotreatment-induced apoptosis.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	28-38	caspase 8	Homo sapiens	52-61
22395735-7	2012	Moreover, pretreatment with z-IETD-FMK             (caspase-8 inhibitor) or stable expression of dominant negative caspase-8 genes             blocked DHA/sulindac sulfide cotreatment-induced apoptosis.	Docosahexaenoic Acids	151-154	caspase 8	Homo sapiens	52-61
22395735-7	2012	Moreover, pretreatment with z-IETD-FMK             (caspase-8 inhibitor) or stable expression of dominant negative caspase-8 genes             blocked DHA/sulindac sulfide cotreatment-induced apoptosis.	Docosahexaenoic Acids	151-154	caspase 8	Homo sapiens	115-124
22395735-7	2012	Moreover, pretreatment with z-IETD-FMK             (caspase-8 inhibitor) or stable expression of dominant negative caspase-8 genes             blocked DHA/sulindac sulfide cotreatment-induced apoptosis.	sulindac sulfide	155-171	caspase 8	Homo sapiens	52-61
22395735-7	2012	Moreover, pretreatment with z-IETD-FMK             (caspase-8 inhibitor) or stable expression of dominant negative caspase-8 genes             blocked DHA/sulindac sulfide cotreatment-induced apoptosis.	sulindac sulfide	155-171	caspase 8	Homo sapiens	115-124
22673830-12	2012	The cleavage of caspase-8 in the LNCaP cells treated with volatile oil demonstrated that apoptosis occurred through an extrinsic pathway.	Oils	67-70	caspase 8	Homo sapiens	16-25
22739154-7	2012	Bortezomib and Ara-C also synergistically induced activation of caspase-9, caspase-8 and caspase-3.	Bortezomib	0-10	caspase 8	Homo sapiens	75-84
22739154-7	2012	Bortezomib and Ara-C also synergistically induced activation of caspase-9, caspase-8 and caspase-3.	Cytarabine	15-20	caspase 8	Homo sapiens	75-84
22739161-6	2012	The positive cell number of activated caspase 3, caspase 8, caspase 9 and the levels of activated caspase 3, caspase 9, p-JNK, P38 increased after Jurkat cells were treated with GA. ROS, CaMKII, caspase 3, caspase 9, MAPKK, JNK1/2 and P38 inhibitors had some significant effect on GA-induced apoptosis.	gambogic acid	178-180	caspase 8	Homo sapiens	49-58
22449440-10	2012	Interestingly, pretreatment with caspase-8 inhibitor significantly reduced the FRAP-induced activation of caspase-3 but not that of caspase-9, whereas the caspase-3 inhibitor, z-DEVD-fmk, markedly attenuated the FRAP-induced activation of caspase-8.	benzoylcarbonyl-aspartyl-glutamyl-valyl-aspartyl-fluoromethyl ketone	176-186	caspase 8	Homo sapiens	239-248
22739161-8	2012	It is concluded that GA induced apoptosis of Jurkat cells by activated caspases through activating of ROS-CaMKII-MAPKK-JNK/P38 pathway.	gambogic acid	21-23	caspase 8	Homo sapiens	71-79
22739161-8	2012	It is concluded that GA induced apoptosis of Jurkat cells by activated caspases through activating of ROS-CaMKII-MAPKK-JNK/P38 pathway.	ros	102-105	caspase 8	Homo sapiens	71-79
22182451-3	2012	SNX-2112 induced the degradation of multiple Hsp90 client proteins, activated both the mitochondrial-mediated and death receptor-mediated apoptotic pathways, downregulated Bcl-2 and Bcl-xL, upregulated Bid, cleaved caspase-9, caspase-7, caspase-3 and PARP, and activated caspase-8.	SNX 2112	0-8	caspase 8	Homo sapiens	271-280
22609785-7	2012	PCAC treatment decreased the expression of pro-caspase 8, 9, and 3, the main regulators of apoptotic cell death, in MDA-MB-231 cells, accompanied by the activation of caspase 8, 9, and 3.	pcac	0-4	caspase 8	Homo sapiens	47-56
22465181-7	2012	These results suggest that YC-1 may potentiate the apoptotic effect of licochalcone A on ovarian carcinoma cell lines by increasing the activation of the caspase-8- and Bid-dependent pathway and the mitochondria-mediated apoptotic pathway, leading to caspase activation.	licochalcone A	71-85	caspase 8	Homo sapiens	154-172
22491426-9	2012	Taken together, DON-induced rRNA cleavage is likely to be closely linked to apoptosis activation and appears to involve the sequential activation of PKR/Hck  p38 p53 caspase 8/9 caspase 3.	deoxynivalenol	16-19	caspase 8	Homo sapiens	166-175
22572929-0	2012	FG020326 sensitized multidrug resistant cancer cells to docetaxel-mediated apoptosis via enhancement of caspases activation.	Docetaxel	56-65	caspase 8	Homo sapiens	104-112
22572929-3	2012	Functional P-gp can confer resistance to activate caspase-8 and -3 dependent apoptosis induced by a range of different stimuli, including tumor necrosis and chemotherapeutic drugs such as docetaxel and vincristine.	Docetaxel	188-197	caspase 8	Homo sapiens	50-66
22572929-3	2012	Functional P-gp can confer resistance to activate caspase-8 and -3 dependent apoptosis induced by a range of different stimuli, including tumor necrosis and chemotherapeutic drugs such as docetaxel and vincristine.	Vincristine	202-213	caspase 8	Homo sapiens	50-66
22572929-6	2012	Therefore, the enhancement of caspase-8, -9 and -3 activation induced by docetaxel may be one of the key mechanisms of the reversal of P-gp mediated docetaxel resistance by FG020326.	Docetaxel	73-82	caspase 8	Homo sapiens	30-50
22572929-6	2012	Therefore, the enhancement of caspase-8, -9 and -3 activation induced by docetaxel may be one of the key mechanisms of the reversal of P-gp mediated docetaxel resistance by FG020326.	Docetaxel	149-158	caspase 8	Homo sapiens	30-50
22342732-5	2012	DHA-induced apoptosis was associated with mitochondrial membrane depolarization, release of cytochrome c, activation of caspases, and DNA fragmentation.	artenimol	0-3	caspase 8	Homo sapiens	120-128
22342732-7	2012	Attenuation of apoptosis in cells pretreated with Z-VAD-FMK suggested the involvement of caspase cascade.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	50-59	caspase 8	Homo sapiens	89-96
21901386-0	2012	Smac-mimetic compound SM-164 induces radiosensitization in breast cancer cells through activation of caspases and induction of apoptosis.	SM 164	22-28	caspase 8	Homo sapiens	101-109
21901386-7	2012	Consistently, blockage of caspase activation, through siRNA knockdown or treatment with a pan-caspase inhibitor z-VAD-fmk, inhibited apoptosis and abrogated SM-164 radiosensitization.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	112-121	caspase 8	Homo sapiens	26-33
21901386-7	2012	Consistently, blockage of caspase activation, through siRNA knockdown or treatment with a pan-caspase inhibitor z-VAD-fmk, inhibited apoptosis and abrogated SM-164 radiosensitization.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	112-121	caspase 8	Homo sapiens	94-101
21901386-7	2012	Consistently, blockage of caspase activation, through siRNA knockdown or treatment with a pan-caspase inhibitor z-VAD-fmk, inhibited apoptosis and abrogated SM-164 radiosensitization.	SM 164	157-163	caspase 8	Homo sapiens	26-33
21901386-7	2012	Consistently, blockage of caspase activation, through siRNA knockdown or treatment with a pan-caspase inhibitor z-VAD-fmk, inhibited apoptosis and abrogated SM-164 radiosensitization.	SM 164	157-163	caspase 8	Homo sapiens	94-101
22354875-10	2012	Dasatinib, an inhibitor of multi-tyrosine kinases including SFK, also inhibited SFK activity and induced reduction of Lyn protein levels, caspase-8 activation and apoptosis in NCI-H28 cells but not in other cell lines.	Dasatinib	0-9	caspase 8	Homo sapiens	138-147
22328720-8	2012	Cisplatin in combination with death receptor ligands enhanced caspase-8 and caspase-3 activation and reduced X-linked inhibitor-of-apoptosis protein (XIAP) levels in these cells.	Cisplatin	0-9	caspase 8	Homo sapiens	62-71
22154545-0	2012	Vorinostat/SAHA-induced apoptosis in malignant mesothelioma is FLIP/caspase 8-dependent and HR23B-independent.	Vorinostat	0-10	caspase 8	Homo sapiens	68-77
22154545-0	2012	Vorinostat/SAHA-induced apoptosis in malignant mesothelioma is FLIP/caspase 8-dependent and HR23B-independent.	Vorinostat	11-15	caspase 8	Homo sapiens	68-77
22362782-3	2012	Here, we demonstrate an autophagy-dependent mechanism of caspase-8 activation and initiation of the apoptotic cascade in response to SKI-I, a pan-sphingosine kinase inhibitor, and bortezomib, a proteasome inhibitor.	Bortezomib	180-190	caspase 8	Homo sapiens	57-66
22408249-5	2012	Subsequent FRET-based single cell time-lapse imaging at conditions where transcription dependent prosurvival signaling was blocked confirmed this hypothesis: caspase-8 activity was delayed by hours in the presence of proteasome inhibitors epoxomicin or bortezomib.	epoxomicin	239-249	caspase 8	Homo sapiens	158-167
22408249-5	2012	Subsequent FRET-based single cell time-lapse imaging at conditions where transcription dependent prosurvival signaling was blocked confirmed this hypothesis: caspase-8 activity was delayed by hours in the presence of proteasome inhibitors epoxomicin or bortezomib.	Bortezomib	253-263	caspase 8	Homo sapiens	158-167
22392915-6	2012	RESULTS: In the human MM cell line RPMI8226, treatment with PPP and LBH589 in combination resulted in a five-fold increase of apoptosis, and an additive effect on the cleavage of the active forms of caspase-8 was observed as compared with the single drug treatments.	Panobinostat	68-74	caspase 8	Homo sapiens	199-208
22450442-5	2012	Pycnidione also markedly reduced the expression of survivin and activated caspase-8 and -3, increased reactive oxygen species (ROS) generation, caused the collapse of the mitochondrial membrane potential (MMP), and enhanced PAI-1 production, thus triggering apoptosis in the A549 cells.	pycnidione	0-10	caspase 8	Homo sapiens	74-90
22446330-3	2012	We showed that treatment with CD437 led to cell cycle arrest and induced apoptosis through both the extrinsic- and intrinsic pathways (caspase 8, -9 and PARP cleavage) in both cell lines.	CD 437	30-35	caspase 8	Homo sapiens	135-148
22187010-4	2012	Bafilomycin A1, an inhibitor of ER function, effectively blocked poly(I:C)-induced activation of caspase-8, -9, and -3, MnSOD and glutathione peroxidase 1 and reduced poly(I:C)-induced SK-N-AS apoptosis.	bafilomycin	0-11	caspase 8	Homo sapiens	97-118
22187010-4	2012	Bafilomycin A1, an inhibitor of ER function, effectively blocked poly(I:C)-induced activation of caspase-8, -9, and -3, MnSOD and glutathione peroxidase 1 and reduced poly(I:C)-induced SK-N-AS apoptosis.	Poly I-C	65-74	caspase 8	Homo sapiens	97-118
22198116-3	2012	Interestingly, it was seen that HL60/VINC cells were more susceptible to undergo caspase-3/caspase-8-dependent apoptosis induced by the studied anthraquinone compounds compared with HL60 and HL60/DOX cells.	Anthraquinones	144-157	caspase 8	Homo sapiens	91-100
22187010-4	2012	Bafilomycin A1, an inhibitor of ER function, effectively blocked poly(I:C)-induced activation of caspase-8, -9, and -3, MnSOD and glutathione peroxidase 1 and reduced poly(I:C)-induced SK-N-AS apoptosis.	Poly I-C	65-73	caspase 8	Homo sapiens	97-118
22198116-0	2012	Anthraquinone antitumour agents, doxorubicin, pirarubicin and benzoperimidine BP1, trigger caspase-3/caspase-8-dependent apoptosis of leukaemia sensitive HL60 and resistant HL60/VINC and HL60/DOX cells.	Anthraquinones	0-13	caspase 8	Homo sapiens	101-110
22198116-0	2012	Anthraquinone antitumour agents, doxorubicin, pirarubicin and benzoperimidine BP1, trigger caspase-3/caspase-8-dependent apoptosis of leukaemia sensitive HL60 and resistant HL60/VINC and HL60/DOX cells.	Doxorubicin	33-44	caspase 8	Homo sapiens	101-110
22198116-0	2012	Anthraquinone antitumour agents, doxorubicin, pirarubicin and benzoperimidine BP1, trigger caspase-3/caspase-8-dependent apoptosis of leukaemia sensitive HL60 and resistant HL60/VINC and HL60/DOX cells.	pirarubicin	46-57	caspase 8	Homo sapiens	101-110
22311672-4	2012	Furthermore, RA/IFN-alpha combination also induces apoptosis by triggering both caspases-8 and -9 resulting in Bax and Bak activation.	bakuchiol	119-122	caspase 8	Homo sapiens	80-97
22159898-9	2012	Ziram induced increases in active caspases 3, 3/7, 8, and 9 and pan-caspase in a dose-dependent manner, and a caspase-3 inhibitor, Z-DEVD-FMK, partially but significantly inhibited the apoptosis.	benzoylcarbonyl-aspartyl-glutamyl-valyl-aspartyl-fluoromethyl ketone	131-141	caspase 8	Homo sapiens	34-41
22159898-10	2012	Moreover, a general caspase inhibitor, Z-VAD-FMK, significantly and almost completely blocked the apoptosis.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	39-48	caspase 8	Homo sapiens	20-27
22159898-12	2012	These findings indicate that ziram can induce apoptosis in human T cells, and the apoptosis is mediated by both the caspase-cascade and the mitochondria/cytochrome-c pathways.	Ziram	29-34	caspase 8	Homo sapiens	116-123
22159898-9	2012	Ziram induced increases in active caspases 3, 3/7, 8, and 9 and pan-caspase in a dose-dependent manner, and a caspase-3 inhibitor, Z-DEVD-FMK, partially but significantly inhibited the apoptosis.	Ziram	0-5	caspase 8	Homo sapiens	34-41
21120579-8	2012	The results suggest that hirsutenone may enhance the apoptotic effect of TRAIL on ovarian carcinoma cell lines by increasing the activation of the caspase-8- and Bid-dependent pathways and the mitochondria-mediated apoptotic pathway, leading to caspase activation.	hirsutenone	25-36	caspase 8	Homo sapiens	147-165
22200726-3	2012	SVB treatment induced expression of death receptor-related             proteins, such as death receptor 4, which further triggered activation of caspase-8             and cleavage of Bid.	SVB	0-3	caspase 8	Homo sapiens	145-154
22246103-9	2012	Taken together, our studies indicate that alpinetin inhibited             the proliferation of pancreatic cancer cells possibly through the regulation of             the Bcl-2 family and XIAP expression, release of cytochrome c and the activation             of caspases.	alpinetin	42-51	caspase 8	Homo sapiens	262-270
21779797-0	2012	Arsenic trioxide induces human pulmonary fibroblast cell death via the regulation of Bcl-2 family and caspase-8.	Arsenic Trioxide	0-16	caspase 8	Homo sapiens	102-111
21779797-10	2012	In conclusion, HPF cells were resistant to ATO and higher doses of ATO induced the growth inhibition and death in HPF cells via the regulation of Bcl-2 family and caspase-8.	Arsenic Trioxide	67-70	caspase 8	Homo sapiens	163-172
22543149-5	2012	RESULTS: Within the dose range of 5-15 mol/L, schisandrin B dose-dependently inhibited FAS and FADD expressions and caspase-8 activation.	schizandrin B	46-59	caspase 8	Homo sapiens	116-125
22147197-5	2012	Costunolide induced apoptosis through the extrinsic pathway, including the activation of Fas, caspase-8, caspase-3, and degradation of PARP.	costunolide	0-11	caspase 8	Homo sapiens	94-103
22198289-5	2012	On the other hand, caspase 8 in HUVEC was activated by DS, but not by H(2)O(2) and/or  O(2) (-).	ds	55-57	caspase 8	Homo sapiens	19-28
22543149-6	2012	CONCLUSION: Schisandrin B can partially inhibit H(2)O(2)-induced L02 cell apoptosis possibly by affecting the FAS-FADD-caspase-8 pathway.	schizandrin B	12-25	caspase 8	Homo sapiens	119-128
22543149-6	2012	CONCLUSION: Schisandrin B can partially inhibit H(2)O(2)-induced L02 cell apoptosis possibly by affecting the FAS-FADD-caspase-8 pathway.	Hydrogen Peroxide	48-56	caspase 8	Homo sapiens	119-128
21888623-0	2012	PEG-liposomal oxaliplatin induces apoptosis in human colorectal cancer cells via Fas/FasL and caspase-8.	Polyethylene Glycols	0-3	caspase 8	Homo sapiens	94-103
22245431-5	2012	GA also activated the protein expressions of fatty acid synthase ligand and caspase-8.	Gallic Acid	0-2	caspase 8	Homo sapiens	76-85
22262760-4	2012	Low doses of ACY-1215 combined with bortezomib triggered synergistic anti-MM activity, resulting in protracted endoplasmic reticulum stress and apoptosis via activation of caspase-3, caspase-8, and caspase-9 and poly (ADP) ribosome polymerase.	ricolinostat	13-21	caspase 8	Homo sapiens	183-192
22262760-4	2012	Low doses of ACY-1215 combined with bortezomib triggered synergistic anti-MM activity, resulting in protracted endoplasmic reticulum stress and apoptosis via activation of caspase-3, caspase-8, and caspase-9 and poly (ADP) ribosome polymerase.	Bortezomib	36-46	caspase 8	Homo sapiens	183-192
22313388-5	2012	In concert with the caspase-8 activation by EGCG, an enhanced expression in functional Fas/CD95 was identified.	epigallocatechin gallate	44-48	caspase 8	Homo sapiens	20-29
21785459-0	2012	DJ-1 inhibits TRAIL-induced apoptosis by blocking pro-caspase-8 recruitment to FADD.	fadd	79-83	caspase 8	Homo sapiens	54-63
22300659-6	2012	Counter screening, where the ability of these chosen flavonols to inhibit caspase 8 binding to itself was assessed, demonstrated that myricetin, morin and quercetin inhibited GST-E6 and His-caspase 8 binding in a specific manner.	Flavonols	53-62	caspase 8	Homo sapiens	74-83
22300659-6	2012	Counter screening, where the ability of these chosen flavonols to inhibit caspase 8 binding to itself was assessed, demonstrated that myricetin, morin and quercetin inhibited GST-E6 and His-caspase 8 binding in a specific manner.	Flavonols	53-62	caspase 8	Homo sapiens	190-199
22300659-6	2012	Counter screening, where the ability of these chosen flavonols to inhibit caspase 8 binding to itself was assessed, demonstrated that myricetin, morin and quercetin inhibited GST-E6 and His-caspase 8 binding in a specific manner.	myricetin	134-143	caspase 8	Homo sapiens	74-83
22300659-6	2012	Counter screening, where the ability of these chosen flavonols to inhibit caspase 8 binding to itself was assessed, demonstrated that myricetin, morin and quercetin inhibited GST-E6 and His-caspase 8 binding in a specific manner.	myricetin	134-143	caspase 8	Homo sapiens	190-199
22300659-6	2012	Counter screening, where the ability of these chosen flavonols to inhibit caspase 8 binding to itself was assessed, demonstrated that myricetin, morin and quercetin inhibited GST-E6 and His-caspase 8 binding in a specific manner.	Quercetin	155-164	caspase 8	Homo sapiens	74-83
22300659-6	2012	Counter screening, where the ability of these chosen flavonols to inhibit caspase 8 binding to itself was assessed, demonstrated that myricetin, morin and quercetin inhibited GST-E6 and His-caspase 8 binding in a specific manner.	Quercetin	155-164	caspase 8	Homo sapiens	190-199
21888623-0	2012	PEG-liposomal oxaliplatin induces apoptosis in human colorectal cancer cells via Fas/FasL and caspase-8.	Oxaliplatin	14-25	caspase 8	Homo sapiens	94-103
21888623-9	2012	These findings indicate that PEG-liposomal L-OHP enhances the anticancer potency of the chemotherapeutic agent; moreover, Fas/FasL and caspase-8 signalling pathways play a key role in mediating PEG-liposomal L-OHP-induced apoptosis.	Polyethylene Glycols	29-32	caspase 8	Homo sapiens	135-144
21888623-9	2012	These findings indicate that PEG-liposomal L-OHP enhances the anticancer potency of the chemotherapeutic agent; moreover, Fas/FasL and caspase-8 signalling pathways play a key role in mediating PEG-liposomal L-OHP-induced apoptosis.	Oxaliplatin	43-48	caspase 8	Homo sapiens	135-144
21888623-9	2012	These findings indicate that PEG-liposomal L-OHP enhances the anticancer potency of the chemotherapeutic agent; moreover, Fas/FasL and caspase-8 signalling pathways play a key role in mediating PEG-liposomal L-OHP-induced apoptosis.	Polyethylene Glycols	194-197	caspase 8	Homo sapiens	135-144
22179765-7	2012	The changes in the expression of             caspase-8, capsase-9, Bax and bcl-2 after VI-16 treatment suggested that the mitochondrial             pathway was involved in the apoptosis induced by VI-16.	vi-16	87-92	caspase 8	Homo sapiens	45-65
22134754-7	2012	Belinostat induced the expression of p21 and             p27, acetylation of p53 and G2/M arrest associated with Bcl2 and Bcl-Xl downmodulation             and significant reduction of survivin, IAPs and Akt/pAkt and increased caspase-8             and -9 expression/activity.	belinostat	0-10	caspase 8	Homo sapiens	227-255
22365665-4	2012	In the absence of IAPs, rapid and full generation of active IL-1beta by the NLRP3-caspase-1 inflammasome, or by caspase-8, required the kinase RIP3 and reactive oxygen species production.	Reactive Oxygen Species	152-175	caspase 8	Homo sapiens	112-121
24031135-3	2012	Inhibition of caspase-8 by pretreatment with Z-IETD-FMK, a membrane permeable selective caspase-8 inhibitor reduced mitochondrial cyt c release, the amount of PSox not only within but also on the surface of Jurkat cells, caspase-3 activation, and apoptotic cell number after treatment with anti-Fas antibody.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	45-55	caspase 8	Homo sapiens	14-23
24031135-3	2012	Inhibition of caspase-8 by pretreatment with Z-IETD-FMK, a membrane permeable selective caspase-8 inhibitor reduced mitochondrial cyt c release, the amount of PSox not only within but also on the surface of Jurkat cells, caspase-3 activation, and apoptotic cell number after treatment with anti-Fas antibody.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	45-55	caspase 8	Homo sapiens	88-97
21964635-0	2012	Fisetin induces apoptosis in human cervical cancer HeLa cells through ERK1/2-mediated activation of caspase-8-/caspase-3-dependent pathway.	fisetin	0-7	caspase 8	Homo sapiens	100-109
22266324-0	2012	Diosgenin induces apoptosis in IGF-1-stimulated human thyrocytes through two caspase-dependent pathways.	Diosgenin	0-9	caspase 8	Homo sapiens	77-84
22266324-5	2012	We found that diosgenin induced apoptosis in human thyrocytes pretreated with IGF-1 in a dose-dependent manner through the activation of caspase cascades.	Diosgenin	14-23	caspase 8	Homo sapiens	137-144
22266324-6	2012	Moreover, diosgenin inhibited FLIP and activated caspase-8 in the FAS-related apoptotic pathway.	ammonium ferrous sulfate	66-69	caspase 8	Homo sapiens	49-58
22266324-8	2012	These results indicate that diosgenin induces apoptosis in IGF-1-stimulated primary human thyrocytes through two caspase-dependent pathways.	Diosgenin	28-37	caspase 8	Homo sapiens	113-120
22002103-4	2012	Additionally, nucleoside derivative-induced apoptosis was inhibited by the selective inhibitors of caspase-2, -3, -8, and -9 and also by si-RNAs against caspase-2, -3, -8, and -9; however, inhibition of caspase-2 and -3 was more effective at preventing apoptosis than inhibition of caspase-8 and -9.	Nucleosides	14-24	caspase 8	Homo sapiens	282-298
21964635-5	2012	Moreover, treatment of HeLa cells with fisetin induced a sustained activation of the phosphorylation of ERK1/2, and inhibition of ERK1/2 by PD98059 (MEK1/2 inhibitor) or transfection with the mutant ERK1/2 expression vector significantly abolished the fisetin-induced apoptosis through the activation of caspase-8/-3 pathway.	fisetin	39-46	caspase 8	Homo sapiens	304-313
22155658-5	2012	BEHP was able to induce apoptosis involving caspases pathway, besides regulating mitochondrial enzymes.	Diethylhexyl Phthalate	0-4	caspase 8	Homo sapiens	44-52
22585859-6	2012	In the death-inducing signaling complex, the C-terminal zinc finger (Znf) domain of the A20 ubiquitin ligase mediates receptor-interacting protein 1 polyubiquitination through lysine-63-linked polyubiquitin chains, which bind to the caspase-8 protease domain and inhibit caspase-8 dimerization, cleavage, and the initiation of TRAIL-induced apoptosis in glioblastoma-derived cell lines and tumor-initiating cells.	Lysine	176-182	caspase 8	Homo sapiens	233-242
22585859-6	2012	In the death-inducing signaling complex, the C-terminal zinc finger (Znf) domain of the A20 ubiquitin ligase mediates receptor-interacting protein 1 polyubiquitination through lysine-63-linked polyubiquitin chains, which bind to the caspase-8 protease domain and inhibit caspase-8 dimerization, cleavage, and the initiation of TRAIL-induced apoptosis in glioblastoma-derived cell lines and tumor-initiating cells.	Lysine	176-182	caspase 8	Homo sapiens	271-280
22019693-6	2012	Additionally, cinobufacini also activated Fas-mediated apoptosis pathway obviously as evident by an increase in Fas expression, and caspase-8 and caspase-10 activation.	ammonium ferrous sulfate	42-45	caspase 8	Homo sapiens	132-141
21975943-8	2012	In examining this possibility, it was found that caspase-8 activation caused by deoxycholate was blocked by zinc.	Deoxycholic Acid	80-92	caspase 8	Homo sapiens	49-58
21975943-9	2012	Collectively, the results suggest that zinc can inhibit deoxycholate-induced apoptotic cell death mediated by caspases.	Deoxycholic Acid	56-68	caspase 8	Homo sapiens	110-118
21697648-0	2012	Cadmium-induced apoptosis and necrosis in human osteoblasts: role of caspases and mitogen-activated protein kinases pathways.	Cadmium	0-7	caspase 8	Homo sapiens	69-77
21697648-6	2012	Addition of caspase-8 and -3 inhibitors (Z-IETD-FMK and Z-DQMD-FMK) partially blocked these effects.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	41-51	caspase 8	Homo sapiens	12-28
21697648-6	2012	Addition of caspase-8 and -3 inhibitors (Z-IETD-FMK and Z-DQMD-FMK) partially blocked these effects.	Z-D(OMe)QMD(OMe)-fmk	56-66	caspase 8	Homo sapiens	12-28
21697648-11	2012	In conclusion, at least 2 pathways appear activated by cadmium in osteoblasts: a direct induction of caspase-8 followed by activation of caspase-3 and an indirect induction by phosphorylation of ERK1/2, p38, and JNK MAPK triggering activation of caspase-8 and -3.	Cadmium	55-62	caspase 8	Homo sapiens	101-110
21697648-11	2012	In conclusion, at least 2 pathways appear activated by cadmium in osteoblasts: a direct induction of caspase-8 followed by activation of caspase-3 and an indirect induction by phosphorylation of ERK1/2, p38, and JNK MAPK triggering activation of caspase-8 and -3.	Cadmium	55-62	caspase 8	Homo sapiens	246-262
21835222-7	2012	Because z-IEDT-fmk, an inhibitor of caspase-8, prevented both the cleavage of the focal adhesion-kinase FAK and cell detachment, we suggest that activation of caspase-8 can be responsible for both the decrement of FAK and the consequent cell detachment.	Z-IEDT-fmk	8-18	caspase 8	Homo sapiens	36-45
21835222-7	2012	Because z-IEDT-fmk, an inhibitor of caspase-8, prevented both the cleavage of the focal adhesion-kinase FAK and cell detachment, we suggest that activation of caspase-8 can be responsible for both the decrement of FAK and the consequent cell detachment.	Z-IEDT-fmk	8-18	caspase 8	Homo sapiens	159-168
22298457-8	2012	Dehydrocorydaline significantly inhibited MCF-7 cell proliferation in a dose- dependent manner, which could be reversed by a caspase-8 inhibitor, Z-IETD-FMK.	dehydrocorydalin	0-17	caspase 8	Homo sapiens	125-134
22298457-8	2012	Dehydrocorydaline significantly inhibited MCF-7 cell proliferation in a dose- dependent manner, which could be reversed by a caspase-8 inhibitor, Z-IETD-FMK.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	146-156	caspase 8	Homo sapiens	125-134
22298457-12	2012	These results showed that dehydrocorydaline inhibits MCF-7 cell proliferation by inducing apoptosis mediated by regulating Bax/Bcl-2, activating caspases as well as cleaving PARP.	dehydrocorydalin	26-43	caspase 8	Homo sapiens	145-153
21928090-5	2012	Active cucurbitacins induced caspase-8 activation only after subsequent TRAIL addition and caspase activation was required for apoptosis suggesting amplified proximal signaling from TRAIL death receptors.	Cucurbitacins	7-20	caspase 8	Homo sapiens	29-38
22994712-7	2012	In addition, terpinen-4-ol also induced apoptosis via an extrinsic pathway by caspase-8 activation resulting in the cleavage of cytosolic Bid.	terpinenol-4	13-26	caspase 8	Homo sapiens	78-87
22297752-0	2012	The effect of isolancifolide on the apoptosis in HL-60 cells through caspase-8-dependent and -independent pathways.	isolancifolide	14-28	caspase 8	Homo sapiens	69-78
22297752-5	2012	During exposure to isolancifolide, the pro-forms or full length of caspases-8, -3, and Bid were decreased, as assessed by Western blotting, while the levels of cleaved forms of caspases-8, -3, and PARP were increased.	isolancifolide	19-33	caspase 8	Homo sapiens	67-81
22297752-5	2012	During exposure to isolancifolide, the pro-forms or full length of caspases-8, -3, and Bid were decreased, as assessed by Western blotting, while the levels of cleaved forms of caspases-8, -3, and PARP were increased.	isolancifolide	19-33	caspase 8	Homo sapiens	177-191
22297752-7	2012	The caspase specific inhibitors, z-IETD-fmk and z-LEHD-fmk, blocked the accumulation of sub-G1 cells and the release of cytochrome c, but not that of Smac/DIABLO.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	33-43	caspase 8	Homo sapiens	4-11
22297752-7	2012	The caspase specific inhibitors, z-IETD-fmk and z-LEHD-fmk, blocked the accumulation of sub-G1 cells and the release of cytochrome c, but not that of Smac/DIABLO.	benzyloxycarbonyl-leucyl-glutamyl-histidyl-aspartic acid fluoromethyl ketone	48-58	caspase 8	Homo sapiens	4-11
22297752-8	2012	These results indicate that isolancifolide induces apoptosis of HL-60 cells through both death receptor and mitochondria pathways, in caspase-8-dependent and -independent manners, suggesting that isolancifolide may be useful in anticancer strategies.	isolancifolide	28-42	caspase 8	Homo sapiens	134-143
21800052-8	2012	These results suggest that radicicol may potentiate the apoptotic effect of TRAIL on ovarian carcinoma cell lines by increasing the activation of the caspase-8- and Bid-dependent pathway and the mitochondria-mediated apoptotic pathway, leading to caspase activation.	monorden	27-36	caspase 8	Homo sapiens	150-168
22508042-5	2012	Additionally, we detect that Src-mediated caspase-8 phosphorylation stimulates Src phosphorylation at Tyr-416 via the linkage of Src SH2 domain with phosph-Tyr-380 site of caspase-8.	Tyrosine	102-105	caspase 8	Homo sapiens	42-51
22508042-5	2012	Additionally, we detect that Src-mediated caspase-8 phosphorylation stimulates Src phosphorylation at Tyr-416 via the linkage of Src SH2 domain with phosph-Tyr-380 site of caspase-8.	Tyrosine	102-105	caspase 8	Homo sapiens	172-181
22508042-5	2012	Additionally, we detect that Src-mediated caspase-8 phosphorylation stimulates Src phosphorylation at Tyr-416 via the linkage of Src SH2 domain with phosph-Tyr-380 site of caspase-8.	Tyrosine	156-159	caspase 8	Homo sapiens	42-51
22508042-5	2012	Additionally, we detect that Src-mediated caspase-8 phosphorylation stimulates Src phosphorylation at Tyr-416 via the linkage of Src SH2 domain with phosph-Tyr-380 site of caspase-8.	Tyrosine	156-159	caspase 8	Homo sapiens	172-181
22508042-8	2012	Together, a simple model is that the peripherization of caspase-8 is well-poised to facilitate Src-mediated caspase-8 phosphrylation at Tyr-380, then binding of phospho-Tyr380 of caspase-8 to Src SH2 domain may maintain Src in an active conformation to induce EMT phenotype, a key step toward cancer metastasis.	Tyrosine	136-139	caspase 8	Homo sapiens	56-65
22508042-8	2012	Together, a simple model is that the peripherization of caspase-8 is well-poised to facilitate Src-mediated caspase-8 phosphrylation at Tyr-380, then binding of phospho-Tyr380 of caspase-8 to Src SH2 domain may maintain Src in an active conformation to induce EMT phenotype, a key step toward cancer metastasis.	Tyrosine	136-139	caspase 8	Homo sapiens	108-117
22508042-8	2012	Together, a simple model is that the peripherization of caspase-8 is well-poised to facilitate Src-mediated caspase-8 phosphrylation at Tyr-380, then binding of phospho-Tyr380 of caspase-8 to Src SH2 domain may maintain Src in an active conformation to induce EMT phenotype, a key step toward cancer metastasis.	Tyrosine	136-139	caspase 8	Homo sapiens	108-117
22606010-5	2012	Well-known initiator caspase-activating complexes include (1) DISC (Death Inducing Signaling Complex), which activates caspases-8 and 10; (2) Apoptosome, which activates caspase-9; and (3) PIDDosome, which activates caspase-2.	piddosome	189-198	caspase 8	Homo sapiens	119-136
22287961-6	2012	In genetically modified caspase-8-deficient Jurkat cells, the apoptotic effects are only slightly reduced, whereas, in FADD-negative Jurkat cells, the TBT effect is significantly diminished.	tributyltin	151-154	caspase 8	Homo sapiens	24-33
21959933-2	2012	Fas-induced apoptosis requires recruitment and activation of the initiator caspase, caspase-8 (in humans also caspase-10), within the death-inducing signalling complex.	ammonium ferrous sulfate	0-3	caspase 8	Homo sapiens	75-82
21959933-2	2012	Fas-induced apoptosis requires recruitment and activation of the initiator caspase, caspase-8 (in humans also caspase-10), within the death-inducing signalling complex.	ammonium ferrous sulfate	0-3	caspase 8	Homo sapiens	84-93
22759954-10	2012	Inhibition of NKCC1 activity with bumetanide accelerated AVD, early apoptosis, as well as activation of caspase-3 and caspase-8.	Bumetanide	34-44	caspase 8	Homo sapiens	118-127
22922291-5	2012	In addition, caspase-8 activity was evaluated by the incubation with a caspase-8 fluorogenic substrate, Ac-IEPD-AMC using a spectrofluorometer.	ac-iepd-amc	104-115	caspase 8	Homo sapiens	13-22
23109891-0	2012	Ethyl gallate induces apoptosis of HL-60 cells by promoting the expression of caspases-8, -9, -3, apoptosis-inducing factor and endonuclease G.	ethyl gallate	0-13	caspase 8	Homo sapiens	78-96
22550391-8	2012	Western blot and quantitative analysis showed that both p53 and caspase-8 increased after cell exposure to cadmium chloride.	Cadmium Chloride	107-123	caspase 8	Homo sapiens	64-73
22550391-10	2012	CONCLUSIONS: Cadmium chloride induced cytotoxicity and apoptosis in human lens epithelial cells and the mechanism of apoptosis involve an increased expression of p53 and caspase-8.	Cadmium Chloride	13-29	caspase 8	Homo sapiens	170-179
22843554-0	2012	Association between CASP8 and CASP10 polymorphisms and toxicity outcomes with platinum-based chemotherapy in Chinese patients with non-small cell lung cancer.	Platinum	78-86	caspase 8	Homo sapiens	20-25
21993665-0	2012	Acacetin induces apoptosis in human T cell leukemia Jurkat cells via             activation of a caspase cascade.	acacetin	0-8	caspase 8	Homo sapiens	97-104
21993665-6	2012	Acacetin-induced apoptosis             was blocked by a broad-spectrum caspase inhibitor, a caspase-3 inhibitor and a             caspase-8 inhibitor, but not by a caspase-9 inhibitor.	acacetin	0-8	caspase 8	Homo sapiens	71-78
21993665-6	2012	Acacetin-induced apoptosis             was blocked by a broad-spectrum caspase inhibitor, a caspase-3 inhibitor and a             caspase-8 inhibitor, but not by a caspase-9 inhibitor.	acacetin	0-8	caspase 8	Homo sapiens	130-139
22843554-2	2012	In this study, we aimed to comprehensively assess single nucleotide polymorphisms (SNPs) of the caspase-8 (CASP8) and caspase-10 (CASP10) genes in relation to toxicity outcomes with first-line platinum-based chemotherapy in patients with advanced non-small cell lung cancer (NSCLC).	Platinum	193-201	caspase 8	Homo sapiens	96-105
22843554-9	2012	Our results provide novel evidence that polymorphisms in CASP8 and CASP10 may modulate toxicity outcomes in patients with advanced NSCLC treated with platinum-based chemotherapy.	Platinum	150-158	caspase 8	Homo sapiens	57-62
22843554-2	2012	In this study, we aimed to comprehensively assess single nucleotide polymorphisms (SNPs) of the caspase-8 (CASP8) and caspase-10 (CASP10) genes in relation to toxicity outcomes with first-line platinum-based chemotherapy in patients with advanced non-small cell lung cancer (NSCLC).	Platinum	193-201	caspase 8	Homo sapiens	107-112
22843554-3	2012	We genotyped 13 tag SNPs of CASP8 and CASP10 in 663 patients with advanced NSCLC treated with platinum-based chemotherapy regimens.	Platinum	94-102	caspase 8	Homo sapiens	28-33
22010212-7	2011	In the subgroup of primary ALL cells, with low expression of caspase-8, methotrexate (MTX) upregulated the expression of caspase-8 mediated by the transcription factor p53, suggesting epigenetic silencing of caspase-8.	Methotrexate	72-84	caspase 8	Homo sapiens	61-70
24139412-0	2012	Hydroxyurea potentiates the caspase-independent killing of B-cell lines by rituximab and GA101.	Hydroxyurea	0-11	caspase 8	Homo sapiens	28-35
24139412-6	2012	Hydroxyurea specifically enhanced the direct caspase-independent killing pathway of both of these antibodies as exemplified by the resistance to broad spectrum caspase inhibitors, lack of internucleosomal DNA laddering, and lack of activation of caspases 3, 8, and 9.	Hydroxyurea	0-11	caspase 8	Homo sapiens	45-52
24139412-6	2012	Hydroxyurea specifically enhanced the direct caspase-independent killing pathway of both of these antibodies as exemplified by the resistance to broad spectrum caspase inhibitors, lack of internucleosomal DNA laddering, and lack of activation of caspases 3, 8, and 9.	Hydroxyurea	0-11	caspase 8	Homo sapiens	160-167
24139412-9	2012	Arresting antibody-sensitive cells in this stage of the cell cycle by means other than hydroxurea also sensitized the cells to caspase-independent antibody-mediated death, suggesting that the potentiating effect of hydroxyurea may be mediated via its effects upon the cell cycle.	Hydroxyurea	215-226	caspase 8	Homo sapiens	127-134
22431999-9	2012	In vitro studies demonstrated that MVs up-regulated in cisplatin-treated human tubular epithelial cells anti-apoptotic genes, such as Bcl-xL, Bcl2 and BIRC8 and down-regulated genes that have a central role in the execution-phase of cell apoptosis such as Casp1, Casp8 and LTA.	Cisplatin	55-64	caspase 8	Homo sapiens	263-268
21944661-4	2011	The proliferation inhibitory effect of SKLB703 was associated with its apoptosis-inducing effect by activating caspase-3 and caspase-9 rather than caspase 8.	sklb703	39-46	caspase 8	Homo sapiens	147-156
22010212-7	2011	In the subgroup of primary ALL cells, with low expression of caspase-8, methotrexate (MTX) upregulated the expression of caspase-8 mediated by the transcription factor p53, suggesting epigenetic silencing of caspase-8.	Methotrexate	86-89	caspase 8	Homo sapiens	61-70
22010212-7	2011	In the subgroup of primary ALL cells, with low expression of caspase-8, methotrexate (MTX) upregulated the expression of caspase-8 mediated by the transcription factor p53, suggesting epigenetic silencing of caspase-8.	Methotrexate	86-89	caspase 8	Homo sapiens	121-130
22010212-7	2011	In the subgroup of primary ALL cells, with low expression of caspase-8, methotrexate (MTX) upregulated the expression of caspase-8 mediated by the transcription factor p53, suggesting epigenetic silencing of caspase-8.	Methotrexate	86-89	caspase 8	Homo sapiens	121-130
22814014-6	2012	RESULTS: Exposure to VPA at concentrations above 5 mM resulted in an increase in DNA fragmentation, modulated expression of genes and proteins associated with apoptosis and activated caspases cascade.	Valproic Acid	21-24	caspase 8	Homo sapiens	183-191
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.	Guanosine Triphosphate	9-12	caspase 8	Homo sapiens	118-127
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	caspase 8	Homo sapiens	118-127
23152837-4	2012	Besides, some apoptosis related events were observed after treatment with dicycloplatin, including increase of reactive oxygen species (ROS), collapse of mitochondrial membrane potential (Deltapsim), release of cytochrome c from the mitochondria to the cytosol, upregulation of p53, which were accompanied by activation of caspase-9, caspase-3, caspase-8, and poly (ADP-ribose) polymerase cleavage in a concentration-dependent manner.	diammine(1,1-cyclobutanedicarboxylate)platinum(II)	74-87	caspase 8	Homo sapiens	345-354
23152837-5	2012	The role of apoptosis in dicycloplatin-mediated cell death was further confirmed by the concomitant treatment with caspase-8 or caspase-9 inhibitors, which inhibited apoptosis and PARP cleavage.	diammine(1,1-cyclobutanedicarboxylate)platinum(II)	25-38	caspase 8	Homo sapiens	115-124
22558117-6	2012	Mechanistic studies show that LBW242-induced apoptosis in ovarian cancer cells is associated with activation of caspase-8.	LBW242	30-36	caspase 8	Homo sapiens	112-121
22160723-7	2011	These cells exhibited a high yield of ROS-induced DNA single- and double-strand breaks and activation of the ATR-Chk1-ATM-Chk2-p53 pathway that led to Fas and caspase-8, -3, and -7 activation, whereas macrophages and DCs derived from them were protected.	Reactive Oxygen Species	38-41	caspase 8	Homo sapiens	159-180
22185222-8	2011	Caspase-8 and -3 activities were determined by using IETD-AFC and DEVD-AFC substrates and the fluorescence intensity was measured.	DEVD	66-70	caspase 8	Homo sapiens	0-16
22010212-8	2011	RNA interference in patient-derived B- and T-ALL cells revealed that effective cell death induction by most routine drug combinations involving MTX depended on the presence of caspase-8.	Methotrexate	144-147	caspase 8	Homo sapiens	176-185
22010212-7	2011	In the subgroup of primary ALL cells, with low expression of caspase-8, methotrexate (MTX) upregulated the expression of caspase-8 mediated by the transcription factor p53, suggesting epigenetic silencing of caspase-8.	Methotrexate	72-84	caspase 8	Homo sapiens	121-130
22010212-7	2011	In the subgroup of primary ALL cells, with low expression of caspase-8, methotrexate (MTX) upregulated the expression of caspase-8 mediated by the transcription factor p53, suggesting epigenetic silencing of caspase-8.	Methotrexate	72-84	caspase 8	Homo sapiens	121-130
21926110-7	2011	Haplotype analysis indicated that the FAS polymorphisms -670 A &gt; G (rs1800682) and -1377 G &gt; A (rs2234767) were both associated with OSCC in the Mixed Ancestry population (P = 0.006 and P = 0.004, respectively), as well as the CASP8 (-652 6Ndel:302His) haplotype (P = 0.0013).	ammonium ferrous sulfate	38-41	caspase 8	Homo sapiens	233-238
22170098-8	2011	MaviP35 potently inhibited human caspases 2 and 3, DCP-1, DRICE and CED-3 in vitro, but (in contrast to AcP35) only weakly suppressed the proteolytic activity of the initiator human caspases 8, 9 and 10.	mavip35	0-7	caspase 8	Homo sapiens	182-202
21951963-8	2011	The apoptosis induced by celastrol could be suppressed by Z-IETD-FMK and Z-LEHD-FMK, the respective caspase-8 and caspase-9 inhibitor.	celastrol	25-34	caspase 8	Homo sapiens	100-109
21945308-10	2011	Pretreatment with caspase inhibitors neutralized the pro-apoptotic activity of costunolide.	costunolide	79-90	caspase 8	Homo sapiens	18-25
21945308-12	2011	Additionally, the antioxidant N-acetyl-L-cysteine (NAC) significantly attenuated the costunolide-induced production of ROS, activation of caspases, down-regulation of Bcl-2, and apoptosis in platinum-resistant ovarian cancer cells.	costunolide	85-96	caspase 8	Homo sapiens	138-146
21854868-0	2011	Fas/FasL-dependent and -independent activation of caspase-8 in doxorubicin-treated human breast cancer MCF-7 cells: ADAM10 down-regulation activates Fas/FasL signaling pathway.	Doxorubicin	63-74	caspase 8	Homo sapiens	50-59
21854868-3	2011	Doxorubicin-induced caspase-8 activation was found to be mediated through Akt/ERK inactivation and FasL-independent Fas pathway in MCF-7 cells, while caspase-8 activation in MCF-7/Dox cells depended exclusively on FasL-stimulated Fas pathway.	Doxorubicin	0-11	caspase 8	Homo sapiens	20-29
21854868-3	2011	Doxorubicin-induced caspase-8 activation was found to be mediated through Akt/ERK inactivation and FasL-independent Fas pathway in MCF-7 cells, while caspase-8 activation in MCF-7/Dox cells depended exclusively on FasL-stimulated Fas pathway.	Doxorubicin	0-3	caspase 8	Homo sapiens	20-29
21854868-4	2011	Suppression of caspase-8 activation restored the viability of doxorubicin-treated MCF-7 cells and MCF-7/Dox cells.	Doxorubicin	62-73	caspase 8	Homo sapiens	15-24
21854868-4	2011	Suppression of caspase-8 activation restored the viability of doxorubicin-treated MCF-7 cells and MCF-7/Dox cells.	Doxorubicin	104-107	caspase 8	Homo sapiens	15-24
21854868-10	2011	Taken together, our data indicate that Akt/ERK-mediated caspase-8 activation and Fas/FasL-mediated caspase-8 activation mostly elucidate doxorubicin-induced death in MCF-7 cells and MCF-7/Dox cells, respectively.	Doxorubicin	137-148	caspase 8	Homo sapiens	56-65
21854868-10	2011	Taken together, our data indicate that Akt/ERK-mediated caspase-8 activation and Fas/FasL-mediated caspase-8 activation mostly elucidate doxorubicin-induced death in MCF-7 cells and MCF-7/Dox cells, respectively.	Doxorubicin	137-148	caspase 8	Homo sapiens	99-108
22019170-12	2011	CONCLUSIONS: Data suggest that paclitaxel induces nuclear translocation and activation of PKC-delta, which in turn causes Golgi-Cdk1 activation, leading to Golgi associated DR5 up-regulation, and caspase-8 and 3 activation.	Paclitaxel	31-41	caspase 8	Homo sapiens	196-211
21452372-4	2011	Escin sodium activated the initiator caspase-8, -9, and the effector caspase-3, degraded poly (ADP-ribose) polymerase (PARP) and attenuated the expression of Bcl-2.	escin sodium	0-12	caspase 8	Homo sapiens	37-50
22101335-4	2011	Knockdown experiments and knockout cells excluded a role of caspase-8 in curcumin-induced caspase-3 activation.	Curcumin	73-81	caspase 8	Homo sapiens	60-69
22019170-7	2011	Data revealed that paclitaxel induced an increase of Cdk1 activity and DR5 expression on the Golgi complex that was associated with increased cleavage of caspase-8, a DR5 downstream factor, and caspase-3 into catalytically active fragments.	Paclitaxel	19-29	caspase 8	Homo sapiens	154-163
22241962-7	2011	In support of this notion, inhibition of tumor necrosis factor alpha (TNFalpha) by the TNFalpha blocking antibody Enbrel reduces BV6- and gemcitabine-induced activation of caspase 8 and 3, loss of mitochondrial membrane potential, and apoptosis.	gemcitabine	138-149	caspase 8	Homo sapiens	172-187
21951963-8	2011	The apoptosis induced by celastrol could be suppressed by Z-IETD-FMK and Z-LEHD-FMK, the respective caspase-8 and caspase-9 inhibitor.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	58-68	caspase 8	Homo sapiens	100-109
21951963-8	2011	The apoptosis induced by celastrol could be suppressed by Z-IETD-FMK and Z-LEHD-FMK, the respective caspase-8 and caspase-9 inhibitor.	benzyloxycarbonyl-leucyl-glutamyl-histidyl-aspartic acid fluoromethyl ketone	73-83	caspase 8	Homo sapiens	100-109
21941003-5	2011	The toxic saturated free fatty acid palmitate induces an increase in DR5 mRNA and protein expression in Huh-7 human hepatoma cells leading to DR5 localization into lipid rafts, cell surface receptor clustering with subsequent recruitment of the initiator caspase-8, and ultimately cellular demise.	saturated	10-19	caspase 8	Homo sapiens	255-264
21941003-5	2011	The toxic saturated free fatty acid palmitate induces an increase in DR5 mRNA and protein expression in Huh-7 human hepatoma cells leading to DR5 localization into lipid rafts, cell surface receptor clustering with subsequent recruitment of the initiator caspase-8, and ultimately cellular demise.	free fatty acid palmitate	20-45	caspase 8	Homo sapiens	255-264
21941003-8	2011	Likewise, knockdown of DR5 or caspase-8 expression by shRNA technology attenuated palmitate-induced Bax activation and apoptosis in Huh-7 cells, without altering induction of ER stress markers.	Palmitates	82-91	caspase 8	Homo sapiens	30-39
21519949-5	2011	After cyanide treatment, all caspases increased their activities in homozygous and highly expanded heterozygous cells, caspase 8 and 9 increased also in those cells carrying low-size mutations, remarking their key role as "caspase initiators" in HD.	Cyanides	6-13	caspase 8	Homo sapiens	119-128
21807743-9	2011	NAC, caspase inhibitors, and p38MAPK inhibitor attenuated the UCB-induced apoptosis.	ucb	62-65	caspase 8	Homo sapiens	5-12
21881674-8	2011	About 30% of the apoptosis was blocked with BAPTA-AM alone; while a complete inhibition of such apoptosis was achieved with a combination of the caspase-9 inhibitor Z-LEHD-FMK and caspase-8 inhibitor Z-IETD-FMK, thus quantifying each role of the mitochondrial and ER pathways.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	200-210	caspase 8	Homo sapiens	180-189
22126780-8	2011	Caspase 8 activity in Raji cells was significantly enhanced by honokiol (P&lt;0.05).	honokiol	63-71	caspase 8	Homo sapiens	0-9
22126780-10	2011	CONCLUSION: Honokiol can induce apoptosis in Raji cells possibly in relation to enhancement of caspase 8 activity and Bad gene expression.	honokiol	12-20	caspase 8	Homo sapiens	95-104
21903588-6	2011	Although pretreatment with a caspase-8 inhibitor (Z-IETD-FMK) reduced Cholix-induced cytochrome c release and activation of caspases-3, -7, and -9, cytotoxicity was not decreased.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	50-60	caspase 8	Homo sapiens	29-38
22037414-9	2011	A CYLD substitution mutation at Asp 215 that cannot be cleaved by caspase 8 switches cell survival to necrotic cell death in response to TNF.	Aspartic Acid	32-35	caspase 8	Homo sapiens	66-75
21903588-6	2011	Although pretreatment with a caspase-8 inhibitor (Z-IETD-FMK) reduced Cholix-induced cytochrome c release and activation of caspases-3, -7, and -9, cytotoxicity was not decreased.	cholix	70-76	caspase 8	Homo sapiens	29-38
21903588-7	2011	Pretreatment with Z-YVAD-FMK, which inhibits caspase-1, -4, and -5, suppressed not only cytochrome c release, activation of caspase-3, -7, -8, or -9, and PARP cleavage, but also cytotoxicity, indicating that caspase-1, -4, and -5 activation is initiated at an early stage of Cholix-induced apoptosis and promotes caspase-8 activation.	benzyloxycarbonyltyrosyl-valyl-alanyl-aspartic acid fluoromethyl ketone	18-28	caspase 8	Homo sapiens	313-322
21864512-1	2011	Marizomib (NPI-0052) is a naturally derived irreversible proteasome inhibitor that potently induces apoptosis via a caspase-8 and ROS-dependent mechanism in leukemia cells.	marizomib	0-9	caspase 8	Homo sapiens	116-125
22014088-6	2011	Magnolol pretreatment increased the cleavage of caspase-8 and poly-(-ADP-ribose) polymerase (PARP), increased the expression of p21, a cell cycle inhibitor, and decreased the expression of proteins involved in the G2/M phase of cell cycle in skin samples from SKH-1 mice.Treatment of A431 cells with magnolol decreased cell viability and cell proliferation in a concentration dependent manner.	magnolol	0-8	caspase 8	Homo sapiens	48-57
21779837-6	2011	Caspase-8 and -10 were activated demonstrating the involvement of the extrinsic apoptotic pathway in silibinin-treated SW480 and SW620 cells.	Silybin	101-110	caspase 8	Homo sapiens	0-17
21892202-17	2011	Oridonin increased the levels of caspase-3 and caspase-8, and decreased the expression of pro-caspase 3 and pro-caspase 9, which were blocked by NAC.	oridonin	0-8	caspase 8	Homo sapiens	47-56
21843497-7	2011	Adoptive transfer of CD4(+) T cells from donors subjected to DS increased corneal epithelial apoptosis via activation of caspase-8 in recipients, similar to that in the donor mice.	ds	61-63	caspase 8	Homo sapiens	121-130
21786165-6	2011	The apoptosis induced by celastrol was indicated by the activation of caspase-8, bid cleavage, caspase-9 activation, caspase-3 activation, PARP cleavage and through the down regulation of anti-apoptototic proteins.	celastrol	25-34	caspase 8	Homo sapiens	70-79
21771726-9	2011	Thus, efficient restoration of caspase-8 expression in SCLC cells is achieved when a combination of DNMT and HDAC inhibitors is used, suggesting a combination of decitabine and VPA or CI-994 as a potential treatment for sensitization of SCLC cells lacking caspase-8 to TRAIL.	Decitabine	162-172	caspase 8	Homo sapiens	256-265
22108623-0	2011	2-Hydroxy-3-methylanthraquinone from Hedyotis diffusa WILLD induces apoptosis via alteration of Fas/FasL and activation of caspase-8 in human leukemic THP-1 cells.	2-hydroxy-3-methylanthraquinone	0-31	caspase 8	Homo sapiens	123-132
22108623-9	2011	Moreover, treatment of THP-1 cells with 2-hydroxy-3-methylanthraquinone from H. diffusa resulted in activation of caspase-8.	2-hydroxy-3-methylanthraquinone	40-71	caspase 8	Homo sapiens	114-123
21771726-4	2011	We found that combination of the DNMT inhibitor decitabine with an inhibitor of histone deacetylase (HDAC) significantly increased caspase-8 expression in SCLC cells at the RNA and protein levels.	Decitabine	48-58	caspase 8	Homo sapiens	131-140
21771726-9	2011	Thus, efficient restoration of caspase-8 expression in SCLC cells is achieved when a combination of DNMT and HDAC inhibitors is used, suggesting a combination of decitabine and VPA or CI-994 as a potential treatment for sensitization of SCLC cells lacking caspase-8 to TRAIL.	Valproic Acid	177-180	caspase 8	Homo sapiens	31-40
21771726-5	2011	Among all studied HDAC inhibitors, valproic acid (VPA) and CI-994 showed prolonged effects on histone acetylation, while combination with decitabine produced the most prominent effects on caspase-8 re-expression.	Decitabine	138-148	caspase 8	Homo sapiens	188-197
21771726-9	2011	Thus, efficient restoration of caspase-8 expression in SCLC cells is achieved when a combination of DNMT and HDAC inhibitors is used, suggesting a combination of decitabine and VPA or CI-994 as a potential treatment for sensitization of SCLC cells lacking caspase-8 to TRAIL.	tacedinaline	184-190	caspase 8	Homo sapiens	31-40
21771726-9	2011	Thus, efficient restoration of caspase-8 expression in SCLC cells is achieved when a combination of DNMT and HDAC inhibitors is used, suggesting a combination of decitabine and VPA or CI-994 as a potential treatment for sensitization of SCLC cells lacking caspase-8 to TRAIL.	Decitabine	162-172	caspase 8	Homo sapiens	31-40
21771726-9	2011	Thus, efficient restoration of caspase-8 expression in SCLC cells is achieved when a combination of DNMT and HDAC inhibitors is used, suggesting a combination of decitabine and VPA or CI-994 as a potential treatment for sensitization of SCLC cells lacking caspase-8 to TRAIL.	tacedinaline	184-190	caspase 8	Homo sapiens	256-265
21779875-5	2011	As for the known immunogenic compounds, CRT exposure was inhibited by the antioxidant GSH, the pan-caspase zVAD-FMK, and caspase-8 IETD-FMK inhibitor.	isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	131-139	caspase 8	Homo sapiens	121-130
21333751-0	2011	Fe3O4 nanoparticles with daunorubicin induce apoptosis through caspase 8-PARP pathway and inhibit K562 leukemia cell-induced tumor growth in vivo.	ferryl iron	0-5	caspase 8	Homo sapiens	63-72
21333751-3	2011	Fe(3)O(4) NPs increased the ability of DNR to induce apoptosis in both adriamycin-sensitive and adriamycin-resistant K562 cells through the caspase 8-poly(ADP-ribose) polymerase pathway.	fe(3)o	0-6	caspase 8	Homo sapiens	140-149
21951288-6	2011	Likewise, caspase 3 and caspase 8 activities were induced in the presence of the EA extract and I3-O-R after 48 h of incubation.	ea	81-83	caspase 8	Homo sapiens	24-33
21951288-6	2011	Likewise, caspase 3 and caspase 8 activities were induced in the presence of the EA extract and I3-O-R after 48 h of incubation.	isorhamnetin 3-O-rutinoside	96-102	caspase 8	Homo sapiens	24-33
21656672-0	2011	Dicaffeoylquinic acids in Yerba mate (Ilex paraguariensis St. Hilaire) inhibit NF-kappaB nucleus translocation in macrophages and induce apoptosis by activating caspases-8 and -3 in human colon cancer cells.	caffeoylquinic acid	0-22	caspase 8	Homo sapiens	161-178
21333751-3	2011	Fe(3)O(4) NPs increased the ability of DNR to induce apoptosis in both adriamycin-sensitive and adriamycin-resistant K562 cells through the caspase 8-poly(ADP-ribose) polymerase pathway.	Doxorubicin	96-106	caspase 8	Homo sapiens	140-149
21333751-0	2011	Fe3O4 nanoparticles with daunorubicin induce apoptosis through caspase 8-PARP pathway and inhibit K562 leukemia cell-induced tumor growth in vivo.	Daunorubicin	25-37	caspase 8	Homo sapiens	63-72
21774540-6	2011	Four water-soluble cleavable aldehyde polymers (CAP1, CAP2, CAP3, and CAP4) ranging in types of linker groups, length of the linker groups, have been prepared and characterized, each demonstrating the ability to selectively enrich and sequence primary-amine peptides from a complex human proteome containing blocked (dimethylated amine) and unblocked (primary amine) peptides.	Aldehydes	29-37	caspase 8	Homo sapiens	70-74
21725606-0	2011	Induction of apoptosis by ethanol extract of Prunus mume in U937 human leukemia cells through activation of caspases.	Ethanol	26-33	caspase 8	Homo sapiens	108-116
21992775-8	2011	LCA kills BE(2)-m17 and SK-n-MCIXC cell lines by triggering not only the intrinsic (mitochondrial) apoptotic cell death pathway driven by mitochondrial outer membrane permeabilization and initiator caspase-9 activation, but also the extrinsic (death receptor) pathway of apoptosis involving activation of the initiator caspase-8.	Lithocholic Acid	0-3	caspase 8	Homo sapiens	319-328
22357491-8	2011	CONCLUSION: CASP8-652 6N DD genotype may play a role in CWP development and interact with SNPs of FAS-1377, FAS-670 and FASL-844.	ammonium ferrous sulfate	98-101	caspase 8	Homo sapiens	12-17
22357491-8	2011	CONCLUSION: CASP8-652 6N DD genotype may play a role in CWP development and interact with SNPs of FAS-1377, FAS-670 and FASL-844.	ammonium ferrous sulfate	108-111	caspase 8	Homo sapiens	12-17
21877710-8	2011	Cumulatively, these investigations show that the naringenin derivative N101-43 induces apoptosis via up-regulation of Fas/FasL expression, activation of caspase cascades, and inhibition of PI3K/Akt survival signaling pathways in NCI-H460 and A549 cells.	naringenin	49-59	caspase 8	Homo sapiens	153-160
21785112-5	2011	NGA could increase the expression of the apoptosis-related proteins FasL, caspase-3, caspase-8, caspase-9, and Bax and decrease the expression of anti-apoptotic protein Bcl-2 accompanied by the mitochondrial transmembrane damage.	neo-gambogic acid	0-3	caspase 8	Homo sapiens	85-94
21868525-8	2011	In addition, GA also activated the death receptor-dependent pathway by enhancing the protein expressions of fatty acid synthase (FAS), FAS ligand (FASL), caspase-8 and BCL-2 interacting domain (BID).	Gallic Acid	13-15	caspase 8	Homo sapiens	154-163
21667042-7	2011	In GS9450-treated patients, during treatment and follow-up, percentages of activated caspase-3+ and caspase-8 expression tended to decrease, in contrast to placebo-treated patients.	gs9450	3-9	caspase 8	Homo sapiens	100-109
21868525-10	2011	The results showed that GA-mediated apoptosis of HL-60 cells mainly depended on up-regulation of the mRNA of caspase-8, caspase-9, caspase-3, AIF and Endo G.	Gallic Acid	24-26	caspase 8	Homo sapiens	109-118
21616659-8	2011	MMC and curcumin together synergistically enhanced apoptosis in MCF-7 cells and the apoptosis most likely resulted from both the activation of caspases and modulation of bcl-2/bax expression.	Mitomycin	0-3	caspase 8	Homo sapiens	143-151
21616659-8	2011	MMC and curcumin together synergistically enhanced apoptosis in MCF-7 cells and the apoptosis most likely resulted from both the activation of caspases and modulation of bcl-2/bax expression.	Curcumin	8-16	caspase 8	Homo sapiens	143-151
21697465-3	2011	Poly(I   C), a synthetic analogue of viral dsRNA, rapidly triggers caspase 8 activation and apoptosis in HeLa cells.	Poly I-C	0-10	caspase 8	Homo sapiens	67-76
21843907-4	2011	The data suggests that the imidazo[1,2-a]pyridine-induced cell death in HT-29 and Caco-2 cells is mediated via pathway(s) that include the release of cytochrome c from the mitochondria to the cytosol and the activation of caspase 3 and caspase 8.	imidazo(1,2-a)pyridine	27-49	caspase 8	Homo sapiens	236-245
21620827-8	2011	In conclusion, we demonstrate herein that sclareol kills human tumor cells by inducing arrest at the G(1)-phase of the cell cycle followed by apoptosis that involves activation of caspases-8, -9 and -3 via a p53-independent mechanism.	sclareol	42-50	caspase 8	Homo sapiens	180-201
21697465-6	2011	Individually expressed HSV R1s counteracted caspase 8 activation by poly(I   C).	Poly I-C	68-78	caspase 8	Homo sapiens	44-53
21697465-10	2011	TRIF silencing reduced poly(I   C)-triggered caspase 8 activation in mock- and ICP6Delta-infected cells, confirming that TRIF is involved in poly(I   C)-induced apoptosis.	Poly I-C	23-34	caspase 8	Homo sapiens	45-54
21697465-10	2011	TRIF silencing reduced poly(I   C)-triggered caspase 8 activation in mock- and ICP6Delta-infected cells, confirming that TRIF is involved in poly(I   C)-induced apoptosis.	Poly I-C	141-152	caspase 8	Homo sapiens	45-54
21341336-0	2011	Corosolic acid triggers mitochondria and caspase-dependent apoptotic cell death in osteosarcoma MG-63 cells.	corosolic acid	0-14	caspase 8	Homo sapiens	41-48
21746806-3	2011	CEMB-induced cytotoxicity is accompanied by activation of downstream effector caspases (caspases 3 and 7) and by upstream initiator caspases involved in both the extrinsic (caspase 8) and intrinsic (caspase 9) apoptotic pathways.	cemb	0-4	caspase 8	Homo sapiens	173-182
21746806-4	2011	By using short interfering RNAs (siRNA), we show evidence that knockdown of caspase 8, DR4, Apaf-1, and Bid impairs CEMB-induced cell death.	cemb	116-120	caspase 8	Homo sapiens	76-85
21341336-4	2011	Corosolic acid treatment triggered the activation of caspase-8, 9 and 3.	corosolic acid	0-14	caspase 8	Homo sapiens	53-71
21341336-5	2011	The apoptosis was obviously inhibited by pretreatment with a general caspase inhibitor, z-VAD-FMK.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	88-97	caspase 8	Homo sapiens	69-76
21341336-7	2011	All these results indicated that corosolic acid-induced apoptosis was associated with the activation of caspases via a mitochondrial pathway.	corosolic acid	33-47	caspase 8	Homo sapiens	104-112
21536373-8	2011	Furthermore, combination of DOXO+alpha-TOS induced increased levels of Fas and Bax protein expression and cleavage of caspase-8 and caspase-9, suggesting that combination treatment induced Fas/caspase-8 and Bax mediated mitochondria dependent apoptosis.	Doxorubicin	28-32	caspase 8	Homo sapiens	118-127
21984149-9	2011	The combination of IDA with rapamycin enhanced the expressions of Caspase 3, PARP, Caspase 8 and Caspase 9.	Sirolimus	28-37	caspase 8	Homo sapiens	83-92
21536373-8	2011	Furthermore, combination of DOXO+alpha-TOS induced increased levels of Fas and Bax protein expression and cleavage of caspase-8 and caspase-9, suggesting that combination treatment induced Fas/caspase-8 and Bax mediated mitochondria dependent apoptosis.	Doxorubicin	28-32	caspase 8	Homo sapiens	193-202
21536373-8	2011	Furthermore, combination of DOXO+alpha-TOS induced increased levels of Fas and Bax protein expression and cleavage of caspase-8 and caspase-9, suggesting that combination treatment induced Fas/caspase-8 and Bax mediated mitochondria dependent apoptosis.	alpha-Tocopherol	33-42	caspase 8	Homo sapiens	118-127
21536373-8	2011	Furthermore, combination of DOXO+alpha-TOS induced increased levels of Fas and Bax protein expression and cleavage of caspase-8 and caspase-9, suggesting that combination treatment induced Fas/caspase-8 and Bax mediated mitochondria dependent apoptosis.	alpha-Tocopherol	33-42	caspase 8	Homo sapiens	193-202
21347788-7	2011	Finally, we found that knocking down GRP78 causes resistance to curcumin treatment through the suppression of caspase-3 and caspase-8 expression levels.	Curcumin	64-72	caspase 8	Homo sapiens	124-133
21702500-6	2011	PEITC also induced caspase-8 and truncated BID.	phenethyl isothiocyanate	0-5	caspase 8	Homo sapiens	19-28
21072520-7	2011	The apoptotic effect induced by (S)-HDAC42 was through both intrinsic and extrinsic pathways, as evidenced by increased cleavage of caspase-3, caspase-8, and caspase-9 and release of cytochrome c from mitochondria.	HDAC-42	32-42	caspase 8	Homo sapiens	143-152
21910059-5	2011	In our study, we found that ursolic acid induced the appearance of Fas receptor and cleavage of caspase-8, -3 and PARP.	ursolic acid	28-40	caspase 8	Homo sapiens	96-109
22066458-6	2011	Furthermore, beta-sitosterul also induced HepG2 cells apoptosis, lost mitochondrial membrane potential, activated caspase-3, caspase-8 and caspase-9, up-regulate Bax, tBid protein, down-regulation Bcl-2 protein.	beta-sitosterul	13-28	caspase 8	Homo sapiens	125-134
21566207-6	2011	The broad-spectrum caspase inhibitor Z-VAD-fmk and the caspase-9- and caspase-8-specific inhibitors significantly attenuated apoptosis.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	37-46	caspase 8	Homo sapiens	19-26
21466843-7	2011	Celastrol-induced apoptosis was characterized by cleavage of caspase-9, caspase-8, caspase-3, and PARP protein, increased Fas and FasL expression, and a reduction in the mitochondrial membrane potential.	celastrol	0-9	caspase 8	Homo sapiens	72-81
21801448-11	2011	Our data suggest the importance of caspase-8-mediated positive feedback amplification in the p53/p73-dependent apoptosis induced by etoposide in HNSCC cells.	Etoposide	132-141	caspase 8	Homo sapiens	35-44
21801448-0	2011	Essential role of caspase-8 in p53/p73-dependent apoptosis induced by etoposide in head and neck carcinoma cells.	Etoposide	70-79	caspase 8	Homo sapiens	18-27
21801448-3	2011	We recently reported that the reconstitution of procaspase-8 is sufficient for sensitizing cisplatin- but not etoposide-induced apoptosis, in chemoresistant and caspase-8 deficient HOC313 head and neck squamous cell carcinoma (HNSCC) cells.	Cisplatin	91-100	caspase 8	Homo sapiens	51-60
21801448-4	2011	RESULTS: We show that p53/p73-dependent caspase-8 activation is required for sensitizing etoposide-induced apoptosis by utilizing HOC313 cells carrying a temperature-sensitive p53G285K mutant.	Etoposide	89-98	caspase 8	Homo sapiens	40-49
21801448-6	2011	In addition to p53 restoration, caspase-8 reconstitution was needed for sensitization to etoposide-induced apoptosis, mitochondria depolarization, and cleavage of the procaspases-3, and -9.	Etoposide	89-98	caspase 8	Homo sapiens	32-41
21801448-9	2011	Finally, the caspase-9 inhibitor Ac-LEHD-CHO or caspase-9 siRNA blocked etoposide-induced caspase-8 activation, Bid cleavage, and apoptosis in both cell lines, indicating that p53/p73-dependent caspase-8 activation lies downstream of mitochondria.	Etoposide	72-81	caspase 8	Homo sapiens	90-99
21801448-9	2011	Finally, the caspase-9 inhibitor Ac-LEHD-CHO or caspase-9 siRNA blocked etoposide-induced caspase-8 activation, Bid cleavage, and apoptosis in both cell lines, indicating that p53/p73-dependent caspase-8 activation lies downstream of mitochondria.	Etoposide	72-81	caspase 8	Homo sapiens	194-203
21801448-10	2011	CONCLUSIONS: we conclude that p53 and p73 can act as upstream regulators of caspase-8, and that caspase-8 is an essential mediator of the p53/p73-dependent apoptosis induced by etoposide in HNSCC cells.	Etoposide	177-186	caspase 8	Homo sapiens	96-105
21468663-4	2011	In this study, we showed that etoposide treatment activated caspase-8 and caspase-3, leading to cleavages of p53, Bid and PARP, which subsequently induced apoptosis.	Etoposide	30-39	caspase 8	Homo sapiens	60-69
21519916-4	2011	Concomitantly, the co-treatment of cryptotanshinone and TNF-alpha elicited apoptosis, manifested by enhanced the number of terminal deoxynucleotide transferase-mediated dUTP-nick-end labeling (TUNEL)-positive cells, the sub-G1 cell populations, and the activation of caspase-8 and -3, in comparison with the treatment with either drug alone.	cryptotanshinone	35-51	caspase 8	Homo sapiens	267-283
21519916-5	2011	The treatment with cryptotanshinone further suppressed TNF-alpha-mediated expression of c-FLIP(L), Bcl-x(L), but the increased level of tBid (a caspase-8 substrate).	cryptotanshinone	19-35	caspase 8	Homo sapiens	144-153
21801359-8	2011	The caspase-3 inhibitor zDEVD-fmk and the caspase-8 inhibitor zIETD-fmk blocked the apoptosis of A549 cells induced by co-treatment with AFMC and TRAIL.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	62-71	caspase 8	Homo sapiens	42-51
21801359-8	2011	The caspase-3 inhibitor zDEVD-fmk and the caspase-8 inhibitor zIETD-fmk blocked the apoptosis of A549 cells induced by co-treatment with AFMC and TRAIL.	afmc	137-141	caspase 8	Homo sapiens	42-51
21519916-5	2011	The treatment with cryptotanshinone further suppressed TNF-alpha-mediated expression of c-FLIP(L), Bcl-x(L), but the increased level of tBid (a caspase-8 substrate).	tBID	136-140	caspase 8	Homo sapiens	144-153
21519916-10	2011	Overall, our findings suggest that cryptotanshinone can sensitize TNF-alpha-induced apoptosis in human myeloid leukemia KBM-5 cells, which appears through ROS-dependent activation of caspase-8 and p38.	cryptotanshinone	35-51	caspase 8	Homo sapiens	183-192
21519916-10	2011	Overall, our findings suggest that cryptotanshinone can sensitize TNF-alpha-induced apoptosis in human myeloid leukemia KBM-5 cells, which appears through ROS-dependent activation of caspase-8 and p38.	Reactive Oxygen Species	155-158	caspase 8	Homo sapiens	183-192
21424253-0	2011	Camalexin induces apoptosis in T-leukemia Jurkat cells by increased concentration of reactive oxygen species and activation of caspase-8 and caspase-9.	camalexin	0-9	caspase 8	Homo sapiens	127-136
21646299-5	2011	Significant TLR3-mediated apoptosis was induced by polyinosinic-polycytidylic acid, a dsRNA analog, via caspase-8-dependent mechanisms.	Poly I-C	51-82	caspase 8	Homo sapiens	104-113
21514013-3	2011	LJJ-10-induced apoptosis was associated with enhancing ROS generation, DNA damage, and an increase of the protein levels of Fas, FasL, FADD, caspase-8, cytochrome c, Apaf-1, AIF, Endo G, caspase-9 and caspase-3 in U-2 OS cells.	ljj-10	0-6	caspase 8	Homo sapiens	141-150
21514013-4	2011	LJJ-10-triggered growth inhibition was significantly attenuated by N-acetylcysteine, cyclosporine A, anti-FasL monoclonal antibody, and caspase-8, -9 and -3 specific inhibitors in U-2 OS cells.	ljj-10	0-6	caspase 8	Homo sapiens	136-156
21679466-13	2011	On the molecular level, cladribine induced PARP cleavage and activation of caspase-8 and caspase-3.	Cladribine	24-34	caspase 8	Homo sapiens	75-84
21138480-5	2011	Western blotting showed that 5-ALA-PDT activates both the caspase-8 and caspase-9 pathways, which differed from previous studies conducted in other cell types.	Aminolevulinic Acid	29-34	caspase 8	Homo sapiens	58-67
21138480-7	2011	The caspases activation was inhibited by JNK inhibitor SP600125.	pyrazolanthrone	55-63	caspase 8	Homo sapiens	4-12
21138480-10	2011	CONCLUSION: These results demonstrate significant involvement of caspase-8 and -9 and their upstream NF-kappaB-JNK pathways in ALA-PDT-induced apoptosis.	Alanine	127-130	caspase 8	Homo sapiens	65-81
21435100-0	2011	Hydroxycamptothecin-loaded Fe3O4 nanoparticles induce human lung cancer cell apoptosis through caspase-8 pathway activation and disrupt tight junctions.	hydroxycamptothecinum	0-19	caspase 8	Homo sapiens	95-104
21437721-0	2011	Synthetic glycosidated phospholipids induce apoptosis through activation of FADD, caspase-8 and the mitochondrial death pathway.	Phospholipids	23-36	caspase 8	Homo sapiens	82-91
21437721-5	2011	Apoptosis induced by Ino-C2-PAF and its glucosidated derivate, Glc-PAF, was dependent on the DISC components FADD and caspase-8.	c2-paf	25-31	caspase 8	Homo sapiens	118-127
21437721-5	2011	Apoptosis induced by Ino-C2-PAF and its glucosidated derivate, Glc-PAF, was dependent on the DISC components FADD and caspase-8.	Glc-PAF	63-70	caspase 8	Homo sapiens	118-127
21437721-7	2011	In addition, the overexpression of crmA, c-Flip or dominant negative FADD as well as treatment with the caspase-8 inhibitor z-IETD-fmk protected against Ino-C2-PAF-induced apoptosis.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	124-134	caspase 8	Homo sapiens	104-113
21535269-6	2011	Caspase-3 and caspase-8 activities were induced by both K3O-ir and R3O-ir flavonoids showing highest activity with compound concentration of 400 mug/ml.	Flavonoids	74-84	caspase 8	Homo sapiens	14-23
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	caspase 8	Homo sapiens	46-55
21435100-0	2011	Hydroxycamptothecin-loaded Fe3O4 nanoparticles induce human lung cancer cell apoptosis through caspase-8 pathway activation and disrupt tight junctions.	ferryl iron	27-32	caspase 8	Homo sapiens	95-104
21435100-3	2011	In the present study we investigate the hypothesis that the unique water dispersible oleic acid-Triton X-100-coated Fe3O4 nanoparticles loaded with HCPT disrupt epithelial cell-cell junctions and induce human lung cancer cell apoptosis through the caspase-8 pathway.	Water	67-72	caspase 8	Homo sapiens	248-257
21435100-3	2011	In the present study we investigate the hypothesis that the unique water dispersible oleic acid-Triton X-100-coated Fe3O4 nanoparticles loaded with HCPT disrupt epithelial cell-cell junctions and induce human lung cancer cell apoptosis through the caspase-8 pathway.	Oleic Acid	85-95	caspase 8	Homo sapiens	248-257
21435100-3	2011	In the present study we investigate the hypothesis that the unique water dispersible oleic acid-Triton X-100-coated Fe3O4 nanoparticles loaded with HCPT disrupt epithelial cell-cell junctions and induce human lung cancer cell apoptosis through the caspase-8 pathway.	Octoxynol	96-108	caspase 8	Homo sapiens	248-257
21435100-3	2011	In the present study we investigate the hypothesis that the unique water dispersible oleic acid-Triton X-100-coated Fe3O4 nanoparticles loaded with HCPT disrupt epithelial cell-cell junctions and induce human lung cancer cell apoptosis through the caspase-8 pathway.	ferryl iron	116-121	caspase 8	Homo sapiens	248-257
21435100-3	2011	In the present study we investigate the hypothesis that the unique water dispersible oleic acid-Triton X-100-coated Fe3O4 nanoparticles loaded with HCPT disrupt epithelial cell-cell junctions and induce human lung cancer cell apoptosis through the caspase-8 pathway.	10-hydroxycamptothecin	148-152	caspase 8	Homo sapiens	248-257
21435100-9	2011	Compared with void Fe3O4 nanoparticles or HCPT drug alone, HCPT drug-loaded nanoparticles evoked synergistic effects by increasing cell apoptosis with enhanced activation of the caspase-8 pathway.	10-hydroxycamptothecin	59-63	caspase 8	Homo sapiens	178-187
21419123-6	2011	Co-incubation with TNF-alpha+IL-1beta intensified the activation of NO/NOS, JNK1/2, caspase-8, caspase-9 and caspase-3 by UCB.	ucb	122-125	caspase 8	Homo sapiens	84-93
20013348-7	2011	Selected fluorinated taxanes, SB-T-12853 and SB-T-12854, at the death-inducing concentrations (30 nM for MDA-MB-435 and 300 nM for NCI/ADR-RES) were shown to activate significantly caspase-3, caspase-9, caspase-2 and also slightly caspase-8.	fluorinated taxanes	9-28	caspase 8	Homo sapiens	231-240
21473903-12	2011	Both FADD- and caspase-8-positive wild-type Jurkat clone A3, FADD-deficient Jurkat clone I2.1, and caspase-8-deficient Jurkat clone I9.2 exhibited similar susceptibilities to the cytotoxicity of DHURS, excluding an involvement of Fas/FasL system in triggering the apoptosis.	dhurs	195-200	caspase 8	Homo sapiens	15-24
21413021-8	2011	Sensitization by parthenolide to TRAIL stimulated in the three cell lines the extrinsic mechanism of apoptosis with the activation of both caspases 8 and 3, whereas mitochondria were not involved in the process.	parthenolide	17-29	caspase 8	Homo sapiens	139-155
21454451-7	2011	Plinabulin-induced apoptosis is mediated through activation of caspase-3, caspase-8, caspase-9, and poly(ADP-ribose) polymerase cleavage.	NPI 2358	0-10	caspase 8	Homo sapiens	74-83
21399877-0	2011	Proteasome inhibition by MG132 induces growth inhibition and death of human pulmonary fibroblast cells in a caspase-independent manner.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	caspase 8	Homo sapiens	108-115
21399877-5	2011	However, all the tested caspase inhibitors intensified HPF growth inhibition by MG132 and caspase-9 inhibitor also enhanced cell death and MMP ( Psim) loss.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	80-85	caspase 8	Homo sapiens	24-31
21399877-7	2011	In addition, each caspase inhibitor and siRNA differently affects ROS levels including O2 - regardless of cell growth inhibition and cell death levels.	ros	66-69	caspase 8	Homo sapiens	18-25
21399877-7	2011	In addition, each caspase inhibitor and siRNA differently affects ROS levels including O2 - regardless of cell growth inhibition and cell death levels.	Oxygen	87-89	caspase 8	Homo sapiens	18-25
21399877-8	2011	Caspase-8 and -9 inhibitors increased the number of GSH-depleted cells in MG132-treated HPF cells.	Glutathione	52-55	caspase 8	Homo sapiens	0-16
21399877-8	2011	Caspase-8 and -9 inhibitors increased the number of GSH-depleted cells in MG132-treated HPF cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	74-79	caspase 8	Homo sapiens	0-16
21399877-9	2011	In conclusion, MG132 induced growth inhibition and death in HPF cells in a caspase-independent manner.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	15-20	caspase 8	Homo sapiens	75-82
21569377-9	2011	In summary, suppression of microglial MMP-2 secretion by M.tb-infected monocyte-dependent networks paradoxically involves the pro-inflammatory mediators TNF-alpha, p38 MAP kinase and NFkappaB in addition to a novel caspase 8-dependent pathway.	Terbium	59-61	caspase 8	Homo sapiens	215-224
21367858-4	2011	Poly(I-C) induced the activation of both caspases 8 and 9, indicating that TLR3 triggered the signaling of both the extrinsic and intrinsic apoptotic pathways.	Poly I-C	0-8	caspase 8	Homo sapiens	41-57
21392513-6	2011	Monitoring of intracellular calcium ([Ca(2+)](i)) levels by flow cytometric analysis of Fluo-3-AM fluorescence indicated an increase in cytosolic calcium that correlated with the cleavage of caspases.	Calcium	28-35	caspase 8	Homo sapiens	191-199
21392513-6	2011	Monitoring of intracellular calcium ([Ca(2+)](i)) levels by flow cytometric analysis of Fluo-3-AM fluorescence indicated an increase in cytosolic calcium that correlated with the cleavage of caspases.	Fluo-3	88-97	caspase 8	Homo sapiens	191-199
21392513-6	2011	Monitoring of intracellular calcium ([Ca(2+)](i)) levels by flow cytometric analysis of Fluo-3-AM fluorescence indicated an increase in cytosolic calcium that correlated with the cleavage of caspases.	Calcium	146-153	caspase 8	Homo sapiens	191-199
21392513-8	2011	The data demonstrate that IKA induced apoptosis in HL-60 cells through genotoxicity and caspase activation which was in part correlated to an increase in intracellular calcium levels and activation of p38 MAP kinase.	ikarugamycin	26-29	caspase 8	Homo sapiens	88-95
21288283-7	2011	In addition, caspase activation during bufalin- and cinobufagin-induced apoptosis was further confirmed by caspase-3 inhibitor Z-DEVD-FMK, caspase-8 inhibitor Z-IETD-FMK, caspase-9 inhibitor Z-LEHD-FMK and caspase-10 inhibitor Z-AEVD-FMK.	bufalin	39-46	caspase 8	Homo sapiens	139-148
21573233-8	2011	Specific inhibition of p38 with SB203580 did not show any effect whereas inhibition of JNK phosphorylation with SP600125 notably reversed pM-induced cleavage of PARP, caspase-8 and -3, demonstrating a significant role of JNK in pM-induced cell death.	pyrazolanthrone	112-120	caspase 8	Homo sapiens	167-183
21288283-7	2011	In addition, caspase activation during bufalin- and cinobufagin-induced apoptosis was further confirmed by caspase-3 inhibitor Z-DEVD-FMK, caspase-8 inhibitor Z-IETD-FMK, caspase-9 inhibitor Z-LEHD-FMK and caspase-10 inhibitor Z-AEVD-FMK.	cinobufagin	52-63	caspase 8	Homo sapiens	139-148
21826987-6	2011	17DMAG and TNFalpha cotreated cells showed typical apoptotic morphologies and enhancing of activation of caspases.	17DMAG	0-6	caspase 8	Homo sapiens	105-113
21787711-10	2011	The activities of caspase-3, caspase-8 and caspase-9 were significantly increased in cells treated with tas41 compared with those in the control group.	tas41	104-109	caspase 8	Homo sapiens	29-38
21787711-12	2011	These findings demonstrate that tas41 can inhibit the proliferation of, and induce apoptosis in, Caco-2 cells by activating caspase-3, caspase-8 and caspase-9, downregulating the expressions of VEGF, upregulating the ratio of bax/bcl-2.	tas41	32-37	caspase 8	Homo sapiens	135-144
21234653-9	2011	Mechanistically, DHA activated caspase-3, caspase-8, and caspase-9; upregulated the expression of Bax, FAS, and cyclin D1; downregulated the expression of Bcl-2, Cdc25B, and cyclin B1; and inhibited the activity of NF-kB.	artenimol	17-20	caspase 8	Homo sapiens	42-51
21487429-0	2011	Drug-induced caspase 8 upregulation sensitises cisplatin-resistant ovarian carcinoma cells to rhTRAIL-induced apoptosis.	Cisplatin	47-56	caspase 8	Homo sapiens	13-22
21524306-14	2011	Moreover, maslinic acid produced belated caspase-8 activity, thus amplifying the initial mitochondrial apoptotic signaling.	maslinic acid	10-23	caspase 8	Homo sapiens	41-50
21487429-6	2011	Pre-exposure of particularly CP70 to cisplatin resulted in strongly elevated caspase 8 protein and mRNA levels.	Cisplatin	37-46	caspase 8	Homo sapiens	77-86
21487429-8	2011	Cisplatin-induced caspase 8 protein levels were essential for the rhTRAIL-sensitising effect as demonstrated using caspase 8 small-interfering RNA (siRNA) and caspase-8 overexpressing constructs.	Cisplatin	0-9	caspase 8	Homo sapiens	18-27
21487429-8	2011	Cisplatin-induced caspase 8 protein levels were essential for the rhTRAIL-sensitising effect as demonstrated using caspase 8 small-interfering RNA (siRNA) and caspase-8 overexpressing constructs.	Cisplatin	0-9	caspase 8	Homo sapiens	115-124
21487429-8	2011	Cisplatin-induced caspase 8 protein levels were essential for the rhTRAIL-sensitising effect as demonstrated using caspase 8 small-interfering RNA (siRNA) and caspase-8 overexpressing constructs.	Cisplatin	0-9	caspase 8	Homo sapiens	159-168
21308745-4	2011	Cyclosporin A or the caspase-8 inhibitor Z-IETD-FMK blocked AE-induced loss of mitochondrial membrane potential and prevented increases in reactive oxygen species and Ca(++).	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	41-51	caspase 8	Homo sapiens	21-30
21308745-4	2011	Cyclosporin A or the caspase-8 inhibitor Z-IETD-FMK blocked AE-induced loss of mitochondrial membrane potential and prevented increases in reactive oxygen species and Ca(++).	Reactive Oxygen Species	139-162	caspase 8	Homo sapiens	21-30
21418589-5	2011	The decrease in cellular O2-, which was accompanied by a brief accumulation of H2O2 and downregulation of phosphorylated Akt (p-Akt) and cellular FLICE-inhibitory protein, sensitized K562 leukemia cells and human promyelocytic leukemia (HL-60) cells to TRAIL-induced apoptosis.	Superoxides	25-27	caspase 8	Homo sapiens	146-151
21282353-0	2011	Radiosensitization of head and neck squamous cell carcinoma by a SMAC-mimetic compound, SM-164, requires activation of caspases.	smac	65-69	caspase 8	Homo sapiens	119-127
21282353-0	2011	Radiosensitization of head and neck squamous cell carcinoma by a SMAC-mimetic compound, SM-164, requires activation of caspases.	SM 164	88-94	caspase 8	Homo sapiens	119-127
21282353-3	2011	In this study, we characterized SM-164, a small second mitochondria-derived activator of caspase -mimetic compound that promotes degradation of cellular inhibitor of apoptosis-1(cIAP-1; also known as baculoviral IAP repeat-containing protein 2, BIRC2) and releases active caspases from the X-linked inhibitor of apoptosis inhibitory binding as a radiosensitizing agent in HNSCC cells.	SM 164	32-38	caspase 8	Homo sapiens	272-280
21282353-4	2011	We found that SM-164 at nanomolar concentrations induced radiosensitization in some HNSCC cell lines in a manner dependent on intrinsic sensitivity to caspase activation and apoptosis induction.	SM 164	14-20	caspase 8	Homo sapiens	151-158
21282353-5	2011	Blockage of caspase activation via short interfering RNA knockdown or a pan-caspase inhibitor, z-VAD-fmk, largely abrogated SM-164 radiosensitization.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	95-104	caspase 8	Homo sapiens	12-19
21282353-5	2011	Blockage of caspase activation via short interfering RNA knockdown or a pan-caspase inhibitor, z-VAD-fmk, largely abrogated SM-164 radiosensitization.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	95-104	caspase 8	Homo sapiens	76-83
21282353-9	2011	Thus, SM-164 is a potent radiosensitizer via a mechanism involving caspase activation and holds promise for future clinical development as a novel class of radiosensitizer for the treatment of a subset of head and neck cancer patients.	SM 164	6-12	caspase 8	Homo sapiens	67-74
21183680-3	2011	In addition, we showed that EGF induces caspase-8 ubiquitination and degradation through the proteasome pathway, and phosphorylation of Thr-263 is associated with caspase-8 stability.	Threonine	136-139	caspase 8	Homo sapiens	163-172
21130866-7	2011	The antioxidant polyethylene glycol-catalase abolished FasL induction and caspase-8 activation due to H(2)O(2).	Hydrogen Peroxide	102-110	caspase 8	Homo sapiens	74-83
21130866-8	2011	FasL up-regulation; activation of caspases-8, -2, -9, and -3; and chromatin condensation were decreased by the p53 inhibitor pifithrin-alpha, implicating p53 as an upstream factor in the activation of death receptor-mediated apoptosis by H(2)O(2).	pifithrin	125-140	caspase 8	Homo sapiens	34-60
21183680-4	2011	Finally, RSK2 blocks Fas-induced apoptosis through its phosphorylation of caspase-8.	ammonium ferrous sulfate	21-24	caspase 8	Homo sapiens	74-83
21183680-0	2011	Phosphorylation of caspase-8 (Thr-263) by ribosomal S6 kinase 2 (RSK2) mediates caspase-8 ubiquitination and stability.	Threonine	30-33	caspase 8	Homo sapiens	19-28
21282356-5	2011	Curcumin-mediated ER stress via inhibiting the activity of SERCA2 caused increasing expressions of CHOP and its transcription target death receptor 5 (TRAIL-R2), leading to a caspase-3 and caspase-8 cascade-dependent apoptosis in SW872 cells in vitro and in vivo.	Curcumin	0-8	caspase 8	Homo sapiens	189-198
21183680-0	2011	Phosphorylation of caspase-8 (Thr-263) by ribosomal S6 kinase 2 (RSK2) mediates caspase-8 ubiquitination and stability.	Threonine	30-33	caspase 8	Homo sapiens	80-89
21183680-2	2011	Here, we report that RSK2 phosphorylates caspase-8, and Thr-263 was identified as a novel caspase-8 phosphorylation site.	Threonine	56-59	caspase 8	Homo sapiens	90-99
21241278-5	2011	Siltuximab with melphalan enhanced activation of caspase-8, caspase-9, and the downstream effector caspase-3 compared with either of the single agents.	Melphalan	16-25	caspase 8	Homo sapiens	49-58
21113647-0	2011	Butylated hydroxyanisole inhibits the growth of HeLa cervical cancer cells via caspase-dependent apoptosis and GSH depletion.	Butylated Hydroxyanisole	0-24	caspase 8	Homo sapiens	79-86
21113647-7	2011	The number of glutathione (GSH)-depleted cells was increased in 150 muM BHA-treated cells, which was attenuated by caspase inhibitors.	Glutathione	14-25	caspase 8	Homo sapiens	115-122
21113647-7	2011	The number of glutathione (GSH)-depleted cells was increased in 150 muM BHA-treated cells, which was attenuated by caspase inhibitors.	Glutathione	27-30	caspase 8	Homo sapiens	115-122
21113647-7	2011	The number of glutathione (GSH)-depleted cells was increased in 150 muM BHA-treated cells, which was attenuated by caspase inhibitors.	Butylated Hydroxyanisole	72-75	caspase 8	Homo sapiens	115-122
21113647-8	2011	In conclusion, BHA inhibited the growth of HeLa cells via caspase-dependent apoptosis, which seemed to be related to increase in GSH depletion and O(2)( -) level.	Butylated Hydroxyanisole	15-18	caspase 8	Homo sapiens	58-65
21113647-8	2011	In conclusion, BHA inhibited the growth of HeLa cells via caspase-dependent apoptosis, which seemed to be related to increase in GSH depletion and O(2)( -) level.	Glutathione	129-132	caspase 8	Homo sapiens	58-65
21113647-8	2011	In conclusion, BHA inhibited the growth of HeLa cells via caspase-dependent apoptosis, which seemed to be related to increase in GSH depletion and O(2)( -) level.	o(2)	147-151	caspase 8	Homo sapiens	58-65
21052098-4	2011	We demonstrated that Ad-ING4 plus CDDP induced synergistic growth inhibition, enhanced apoptosis, and had an additive effect on upregulation of Fas, Bax, Bak, cleaved Bid, cleaved caspase-8, caspase-9, caspase-3 and cleaved PARP, and on downregulation of Bcl-2 and Bcl-X(L) in SMMC-7721 hepatocarcinoma cells.	Cisplatin	34-38	caspase 8	Homo sapiens	180-189
21072056-4	2011	In this study, we have identified a native complex containing caspase-8 and BID on the mitochondrial membrane, and showed that death receptor activation by Fas or tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) induced the cleavage of BID (tBID formation) within this complex.	tBID	256-260	caspase 8	Homo sapiens	62-71
21176918-7	2011	Additionally, induction of apoptosis by tetrandrine was associated with a very strong and prominent caspase-9, caspase-8, and caspase-3 activation as well as PARP cleavage.	tetrandrine	40-51	caspase 8	Homo sapiens	111-120
21191032-6	2011	Using activated caspase 3 and caspase 8 as indicators of apoptosis, flow cytometry, confocal microscopy, and Western blot analyses demonstrated that inflammation-induced MDSC treated with a Fas agonist contain lower levels of activated caspases, suggesting that inflammation enhances resistance to Fas-mediated apoptosis.	ammonium ferrous sulfate	190-193	caspase 8	Homo sapiens	30-39
21191032-6	2011	Using activated caspase 3 and caspase 8 as indicators of apoptosis, flow cytometry, confocal microscopy, and Western blot analyses demonstrated that inflammation-induced MDSC treated with a Fas agonist contain lower levels of activated caspases, suggesting that inflammation enhances resistance to Fas-mediated apoptosis.	ammonium ferrous sulfate	190-193	caspase 8	Homo sapiens	236-244
21225911-8	2011	Western blot analysis identified the effects of ABT-737 on survival and apoptosis-regulatory proteins PARP, caspase-8, and cytochrome-c.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	48-51	caspase 8	Homo sapiens	108-117
21206980-5	2011	Furthermore, the inhibitors of caspase-3, caspase-8 and caspase-9 reduced the accelerative effect of MG132 on TRAIL-mediated apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	101-106	caspase 8	Homo sapiens	42-51
20876774-9	2011	Mechanistic studies revealed that 5-FU-mediated suppression of c-FLIP results in increased TRAIL-induced recruitment and activation of caspase-8 at the death-inducing signalling complex (DISC), leading to caspase-3 activation and caspase-dependent cell death.	Fluorouracil	34-38	caspase 8	Homo sapiens	135-144
21338526-8	2011	Treatment of HCC827 cells with the ruthenium(II)-arene complex resulted in dose-dependent cell apoptosis as indicated by high cleaved Caspase-8,9 ratio.	ruthenium(ii)-arene	35-54	caspase 8	Homo sapiens	134-143
21338526-11	2011	Treatment of HCC827 cells with the ruthenium(II)-arene complex resulted in dose-dependent cell apoptosis as indicated by high cleaved Caspase-8,9 ratio.	ruthenium(ii)-arene	35-54	caspase 8	Homo sapiens	134-143
21157427-6	2011	Finally, we demonstrate that this acetylation/phosphorylation signalling network controls SRSF2 accumulation as well as caspase-8 pre-mRNA splicing in response to cisplatin and determines whether cells undergo apoptosis or G(2)/M cell cycle arrest.	Cisplatin	163-172	caspase 8	Homo sapiens	120-129
21107704-0	2011	Sequential caspase-2 and caspase-8 activation is essential for saikosaponin a-induced apoptosis of human colon carcinoma cell lines.	saikosaponin D	63-77	caspase 8	Homo sapiens	25-34
21107704-6	2011	Additionally, SSa-induced apoptosis was inhibited by both the selective caspase-2 inhibitor z-VDVAD-fmk and the selective caspase-8 inhibitor z-IETD-fmk and also by si-RNAs against caspase-2 and caspase-8.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	142-152	caspase 8	Homo sapiens	122-131
21107704-9	2011	Moreover, inhibition of caspase-2 activation by the pharmacological inhibitor z-VDVAD-fmk, or by knockdown of protein levels using a si-RNA, suppressed SSa-induced caspase-8 activation, Bid cleavage, and the conformational activation of Bax.	benzoylcarbonyl-valyl-aspartyl-valyl-alanyl-aspartyl-fluoromethyl ketone	78-89	caspase 8	Homo sapiens	164-173
21134410-6	2011	Celastrol caused activation of caspase-7, -8, and -9, PARP cleavage, caspase-8-mediated bid cleavage, and release of cytochrome c and AIF.	celastrol	0-9	caspase 8	Homo sapiens	69-78
21062083-5	2011	Mitosomal daunorubicin plus amlodipine were about 97 nm, selectively accumulated in mitochondria, induced the swelling and disruption of mitochondria, dissipated the mitochondrial membrane potential, released a large amount of cytochrome C by translocation, cleaved Bid, and initiated a cascade of caspase 8 and 3 reactions.	Daunorubicin	10-22	caspase 8	Homo sapiens	298-307
21062083-5	2011	Mitosomal daunorubicin plus amlodipine were about 97 nm, selectively accumulated in mitochondria, induced the swelling and disruption of mitochondria, dissipated the mitochondrial membrane potential, released a large amount of cytochrome C by translocation, cleaved Bid, and initiated a cascade of caspase 8 and 3 reactions.	Amlodipine	28-38	caspase 8	Homo sapiens	298-307
21082355-0	2011	Modulation of ROS/MAPK signaling pathways by okadaic acid leads to cell death via, mitochondrial mediated caspase-dependent mechanism.	Reactive Oxygen Species	14-17	caspase 8	Homo sapiens	106-113
21082355-0	2011	Modulation of ROS/MAPK signaling pathways by okadaic acid leads to cell death via, mitochondrial mediated caspase-dependent mechanism.	Okadaic Acid	45-57	caspase 8	Homo sapiens	106-113
21082355-9	2011	ROS scavenger-N-acetyl cysteine, mitochondrial stabilizer-cyclosporin-A, and broad spectrum caspase inhibitor Z-VAD-FMK inhibited the OA induced caspase-3 activation, DNA damage and cell death but caspase-8 inhibitor had no effect.	Reactive Oxygen Species	0-3	caspase 8	Homo sapiens	197-206
21082355-9	2011	ROS scavenger-N-acetyl cysteine, mitochondrial stabilizer-cyclosporin-A, and broad spectrum caspase inhibitor Z-VAD-FMK inhibited the OA induced caspase-3 activation, DNA damage and cell death but caspase-8 inhibitor had no effect.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	110-119	caspase 8	Homo sapiens	92-99
21082355-9	2011	ROS scavenger-N-acetyl cysteine, mitochondrial stabilizer-cyclosporin-A, and broad spectrum caspase inhibitor Z-VAD-FMK inhibited the OA induced caspase-3 activation, DNA damage and cell death but caspase-8 inhibitor had no effect.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	110-119	caspase 8	Homo sapiens	197-206
21054559-4	2011	Our findings show that the expression levels of the analysed genes did not differ between allergic patients and healthy controls, while higher expression levels of ETS2 and CASP8 were detected in the nickel-exposed workers.	Nickel	200-206	caspase 8	Homo sapiens	173-178
21054559-5	2011	Changes in ETS2 and CASP8 expression are likely to be related to nickel exposure rather than to allergy.	Nickel	65-71	caspase 8	Homo sapiens	20-25
20876774-9	2011	Mechanistic studies revealed that 5-FU-mediated suppression of c-FLIP results in increased TRAIL-induced recruitment and activation of caspase-8 at the death-inducing signalling complex (DISC), leading to caspase-3 activation and caspase-dependent cell death.	Fluorouracil	34-38	caspase 8	Homo sapiens	135-142
21229607-9	2011	Additionally, DIM induced increases in the levels of cleaved caspase-8, truncated Bid, Fas, and Fas ligand, and the caspase-8 inhibitor Z-IETD-FMK was shown to mitigate DIM-induced apoptosis and the cleavage of caspase-3, PARP, and Bid.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	136-146	caspase 8	Homo sapiens	116-125
21216935-6	2011	Cisplatin and fisetin as single agents activated caspases-8 and -3 and caspases-9 and -7, respectively, whereas combination treatment activated all 4 caspases.	Cisplatin	0-9	caspase 8	Homo sapiens	49-88
21152878-5	2011	Colorimetric assays indicated that pretreatment with a specific inhibitor of caspase-8 (Z-IETD-FMK) significantly reduced activities of caspase-8 and caspase-3 in examined HT29 cells.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	88-98	caspase 8	Homo sapiens	77-86
21216935-6	2011	Cisplatin and fisetin as single agents activated caspases-8 and -3 and caspases-9 and -7, respectively, whereas combination treatment activated all 4 caspases.	fisetin	14-21	caspase 8	Homo sapiens	49-88
21165570-5	2011	Quercetin triggered the extrinsic apoptosis pathway through activation of caspase-8 and induction of Bid cleavage, Bax conformation change and cytochrome c release.	Quercetin	0-9	caspase 8	Homo sapiens	74-83
21152878-5	2011	Colorimetric assays indicated that pretreatment with a specific inhibitor of caspase-8 (Z-IETD-FMK) significantly reduced activities of caspase-8 and caspase-3 in examined HT29 cells.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	88-98	caspase 8	Homo sapiens	136-145
21152878-6	2011	gamma-Humulene stimulated the death receptor 5 (DR5), DR4, Fas-associated protein with death domain (FADD), the cleavage of caspase-8 and cleavage caspase-3, but reduced the protein levels of cellular Fas-associated death-domain-like IL-1ss-converting enzyme inhibitory protein (c-FLIP) by Western blot analysis.	gamma-Humulene	0-14	caspase 8	Homo sapiens	124-133
21152878-7	2011	Consequently, gamma-humulene-triggered cell death was significantly attenuated by DR5 siRNA and the caspase-8 inhibitor.	gamma-Humulene	14-28	caspase 8	Homo sapiens	100-109
21152878-8	2011	Based on our results, we suggest that gamma-humulene induced apoptotic cell death in HT29 cells through a DR5-mediated caspase-8 and -3-dependent signaling pathway.	gamma-Humulene	38-52	caspase 8	Homo sapiens	119-135
21067863-4	2011	In addition, combined niflumic acid-ciglitazone treatment significantly induced ER stress responses, and suppression of CHOP expression significantly attenuated the combined niflumic acid-ciglitazone treatment-induced activation of caspase-8 and caspase-3, and the subsequent apoptotic cell death, indicating a role of ER stress in caspase-8 activation and apoptosis.	Niflumic Acid	174-187	caspase 8	Homo sapiens	232-241
21425578-6	2011	The activities of Caspase-3,-8 and -9 all markedly enhanced after treatment in SMMC-7721 cells, while in Hep3B cells, activities of Caspase-3 and -9 enhanced, but that of Caspase-8 unchanged.	smmc	79-83	caspase 8	Homo sapiens	171-180
20717871-0	2011	Glycyrol induces apoptosis in human Jurkat T cell lymphocytes via the Fas-FasL/caspase-8 pathway.	glycyrol	0-8	caspase 8	Homo sapiens	79-88
20717871-4	2011	Consequently, it was shown that caspase-8 and -9 were involved in the activation of apoptosis after glycyrol treatment.	glycyrol	100-108	caspase 8	Homo sapiens	32-48
21067863-0	2011	Combined treatment with the Cox-2 inhibitor niflumic acid and PPARgamma ligand ciglitazone induces ER stress/caspase-8-mediated apoptosis in human lung cancer cells.	Niflumic Acid	44-57	caspase 8	Homo sapiens	109-118
21067863-4	2011	In addition, combined niflumic acid-ciglitazone treatment significantly induced ER stress responses, and suppression of CHOP expression significantly attenuated the combined niflumic acid-ciglitazone treatment-induced activation of caspase-8 and caspase-3, and the subsequent apoptotic cell death, indicating a role of ER stress in caspase-8 activation and apoptosis.	Niflumic Acid	174-187	caspase 8	Homo sapiens	332-341
21067863-0	2011	Combined treatment with the Cox-2 inhibitor niflumic acid and PPARgamma ligand ciglitazone induces ER stress/caspase-8-mediated apoptosis in human lung cancer cells.	ciglitazone	79-90	caspase 8	Homo sapiens	109-118
21067863-4	2011	In addition, combined niflumic acid-ciglitazone treatment significantly induced ER stress responses, and suppression of CHOP expression significantly attenuated the combined niflumic acid-ciglitazone treatment-induced activation of caspase-8 and caspase-3, and the subsequent apoptotic cell death, indicating a role of ER stress in caspase-8 activation and apoptosis.	ciglitazone	188-199	caspase 8	Homo sapiens	232-241
21067863-4	2011	In addition, combined niflumic acid-ciglitazone treatment significantly induced ER stress responses, and suppression of CHOP expression significantly attenuated the combined niflumic acid-ciglitazone treatment-induced activation of caspase-8 and caspase-3, and the subsequent apoptotic cell death, indicating a role of ER stress in caspase-8 activation and apoptosis.	ciglitazone	188-199	caspase 8	Homo sapiens	332-341
21067863-6	2011	Taken together, these results suggest that sequential ER stress and caspase-8 activation are critical in combined niflumic acid-ciglitazone treatment-induced apoptosis in human lung cancer cells.	Niflumic Acid	114-127	caspase 8	Homo sapiens	68-77
21067863-6	2011	Taken together, these results suggest that sequential ER stress and caspase-8 activation are critical in combined niflumic acid-ciglitazone treatment-induced apoptosis in human lung cancer cells.	ciglitazone	128-139	caspase 8	Homo sapiens	68-77
21253389-6	2011	Octreotide significantly increased caspase-3, caspase-8 and caspase-2 activity.	Octreotide	0-10	caspase 8	Homo sapiens	46-55
21272366-12	2011	Caspase 8 protein expression was restored by MG-132 and IFN-gamma pretreatment, which also re-established sensitivity to rhTRAIL and agonistic DR4 antibody in SW948-TR.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	45-51	caspase 8	Homo sapiens	0-9
21245990-9	2011	LY294002 promoted oxaliplatin-induced Fas ligand (FasL) expression, Fas-associated death domain protein recruitment, caspase-8, Bid, and caspase-3 activation, and the short form of cellular caspase-8/FLICE-inhibitory protein (c-FLIP(S)) inhibition.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	0-8	caspase 8	Homo sapiens	117-126
21179037-9	2011	In NCI-H929 cells, PBOX-15-induced apoptosis was shown to be caspase-8 dependent, with independent activation of extrinsic and intrinsic apoptotic pathways.	PBOX-15	19-26	caspase 8	Homo sapiens	61-70
21127198-4	2011	As indicated by accumulation of the membrane phospholipid phosphatidylserine, DNA breaks, intracellular esterase activity, and activation of caspase-8, -9, and -3, we concluded that DBA potentiated TRAIL-induced apoptosis in colon cancer cells.	dibenzylidene acetone	182-185	caspase 8	Homo sapiens	141-162
21245990-9	2011	LY294002 promoted oxaliplatin-induced Fas ligand (FasL) expression, Fas-associated death domain protein recruitment, caspase-8, Bid, and caspase-3 activation, and the short form of cellular caspase-8/FLICE-inhibitory protein (c-FLIP(S)) inhibition.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	0-8	caspase 8	Homo sapiens	190-199
21368885-0	2011	Ion channel inhibitors block caspase activation by mechanisms other than restoring intracellular potassium concentration.	Potassium	97-106	caspase 8	Homo sapiens	29-36
21245990-9	2011	LY294002 promoted oxaliplatin-induced Fas ligand (FasL) expression, Fas-associated death domain protein recruitment, caspase-8, Bid, and caspase-3 activation, and the short form of cellular caspase-8/FLICE-inhibitory protein (c-FLIP(S)) inhibition.	Oxaliplatin	18-29	caspase 8	Homo sapiens	117-126
21368885-3	2011	We have studied the effect of staurosporine (STS), a well-established apoptosis inducer, on the membrane potential of HeLa cells to determine the nature of STS-activated ion conductances and their role in the activation of different caspases.	Staurosporine	30-43	caspase 8	Homo sapiens	233-241
21245990-9	2011	LY294002 promoted oxaliplatin-induced Fas ligand (FasL) expression, Fas-associated death domain protein recruitment, caspase-8, Bid, and caspase-3 activation, and the short form of cellular caspase-8/FLICE-inhibitory protein (c-FLIP(S)) inhibition.	Oxaliplatin	18-29	caspase 8	Homo sapiens	190-199
21245990-10	2011	In vivo, LY294002 inhibited oxaliplatin-induced activation of Akt and NFkappaB, and increased oxaliplatin-induced expression of FasL, inhibition of c-FLIP(S), and activation of caspase-8, Bid, and caspase-3.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	9-17	caspase 8	Homo sapiens	177-186
21245990-10	2011	In vivo, LY294002 inhibited oxaliplatin-induced activation of Akt and NFkappaB, and increased oxaliplatin-induced expression of FasL, inhibition of c-FLIP(S), and activation of caspase-8, Bid, and caspase-3.	Oxaliplatin	94-105	caspase 8	Homo sapiens	177-186
21113177-6	2011	Sal B (50 mumol/L) inhibited the increase in LC3-II, reduced the abundance of LC3 immunofluorescence and intensity of Caspase-8 fluorescence, and enhanced cellular viability and ATP levels in myocytes under GD 3 h, regardless of whether chloroquine was present.	salvianolic acid B	0-5	caspase 8	Homo sapiens	118-127
21214929-8	2011	RESULTS: Combination treatments of alpha-TEA plus DOXO or CDDP act cooperatively to induce apoptosis, caspase-8 and caspase-9 cleavage, p73, phospho-c-Ab1 and phospho-JNK protein expression, and increase expression of p53 downstream mediators; namely, death receptor-5, CD95/APO-1 (Fas), Bax and Noxa, as well as Yap nuclear translocation - plus reduce expression of Bcl-2.	2,5,7,8-tetramethyl-2R-(4R,8R,12-trimethyltridecyl)chroman-6-yloxy acetic acid	35-44	caspase 8	Homo sapiens	102-111
21214929-8	2011	RESULTS: Combination treatments of alpha-TEA plus DOXO or CDDP act cooperatively to induce apoptosis, caspase-8 and caspase-9 cleavage, p73, phospho-c-Ab1 and phospho-JNK protein expression, and increase expression of p53 downstream mediators; namely, death receptor-5, CD95/APO-1 (Fas), Bax and Noxa, as well as Yap nuclear translocation - plus reduce expression of Bcl-2.	Doxorubicin	50-54	caspase 8	Homo sapiens	102-111
21214929-8	2011	RESULTS: Combination treatments of alpha-TEA plus DOXO or CDDP act cooperatively to induce apoptosis, caspase-8 and caspase-9 cleavage, p73, phospho-c-Ab1 and phospho-JNK protein expression, and increase expression of p53 downstream mediators; namely, death receptor-5, CD95/APO-1 (Fas), Bax and Noxa, as well as Yap nuclear translocation - plus reduce expression of Bcl-2.	Cisplatin	58-62	caspase 8	Homo sapiens	102-111
20888374-4	2011	Treatment of caspase-specific inhibitors revealed that FR-induced apoptosis was caspase-8-dependent and inhibition of caspase-9 activity resulted in unexpected, marked enhancement of cell death.	1-((4,5-bis(4-methoxyphenyl)-2-thiazoyl)carbonyl)-4-methylpiperazine	55-57	caspase 8	Homo sapiens	80-89
21467650-10	2011	These results suggest that costunolide induces apoptosis in human endometriotic epithelial cells by inhibiting the prosurvival NFkappaB and Akt pathway, leading to the downregulation of anti-apoptotic protein Bcl-xL and XIAP and the activation of caspases.	costunolide	27-38	caspase 8	Homo sapiens	247-255
21114484-3	2011	PR-924-induced apoptosis in MM cells is associated with activation of caspase-3, caspase-8, caspase-9, BID, PARP and cytochrome-c release.	PR-924	0-6	caspase 8	Homo sapiens	81-90
21804216-2	2011	Recently, we have demonstrated that harmol, a beta-carboline alkaloid, induces apoptosis by caspase-8 activation independently from Fas/Fas ligand interaction in human non-small cell lung cancer (NSCLC) H596 cells.	harmol	36-42	caspase 8	Homo sapiens	92-101
21804216-2	2011	Recently, we have demonstrated that harmol, a beta-carboline alkaloid, induces apoptosis by caspase-8 activation independently from Fas/Fas ligand interaction in human non-small cell lung cancer (NSCLC) H596 cells.	beta-carboline alkaloid	46-69	caspase 8	Homo sapiens	92-101
21788697-2	2011	Therefore, the purpose of the present study was to investigate whether caspase-8, -9, and -3 activation and poly-(ADP-ribose)-polymerase (PARP) cleavage are involved in the mechanism by which GnRH-Ag induces apoptosis in human granulosa-luteal cells.	gnrh-ag	192-199	caspase 8	Homo sapiens	71-92
21037225-4	2011	Here, we show that cisplatin or a more potent platinum(IV) complex LA-12 used in 20-fold lower concentration enhanced killing effects of TRAIL in human colon and prostate cancer cell lines via stimulation of caspase activity and overall apoptosis.	Cisplatin	19-28	caspase 8	Homo sapiens	208-215
21037225-4	2011	Here, we show that cisplatin or a more potent platinum(IV) complex LA-12 used in 20-fold lower concentration enhanced killing effects of TRAIL in human colon and prostate cancer cell lines via stimulation of caspase activity and overall apoptosis.	Platinum	46-54	caspase 8	Homo sapiens	208-215
21166494-0	2011	Silibinin-induced apoptosis in MCF7 and T47D human breast carcinoma cells involves caspase-8 activation and mitochondrial pathway.	Silybin	0-9	caspase 8	Homo sapiens	83-92
21037225-4	2011	Here, we show that cisplatin or a more potent platinum(IV) complex LA-12 used in 20-fold lower concentration enhanced killing effects of TRAIL in human colon and prostate cancer cell lines via stimulation of caspase activity and overall apoptosis.	UNII-37WM0V5E17	67-72	caspase 8	Homo sapiens	208-215
21037225-6	2011	Small interfering RNA-mediated DR5 silencing rescued cells from sensitizing effects of platinum drugs on TRAIL-induced caspase-8 activation and apoptosis, showing the functional importance of DR5 in the effects observed.	Platinum	87-95	caspase 8	Homo sapiens	119-128
21691071-9	2011	When cells were pretreated with Z-IETD-fmk, a caspase 8 specific inhibitor, the activation of caspase 3 and caspase 9 were significantly delayed.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	32-42	caspase 8	Homo sapiens	46-55
21691071-11	2011	Our results suggest that, during H H(2)O(2)-induced apoptosis, caspase 3 is activated directly through caspase 8 and is not through the mitochondria-dependent caspase 9 activation.	Hydrogen Peroxide	35-43	caspase 8	Homo sapiens	103-112
21297918-8	2011	Further caspases activity was measured and it was found that gallic acid activated the caspase-3 but not caspase-8 indicating the involvement of intrinsic pathway of cell apoptosis.	Gallic Acid	61-72	caspase 8	Homo sapiens	8-16
20954801-8	2011	Caspase inhibitors partially altered ROS levels, but did not reduce GSH-depleted cell number, in GA-treated HPF cells.	Reactive Oxygen Species	37-40	caspase 8	Homo sapiens	0-7
21122037-10	2011	The diketopiperazine disulfides were found to induce apoptosis in HCT116 cells based on cell morphology, DNA fragmentation observed by agarose gel electrophoresis, Annexin-V/PI staining using a flow cytometer and cleavage of poly (ADP-ribose) polymerase (PARP), caspase-3, caspase-8, caspase-9 and Bcl-2 family proteins (Bcl-2, Bcl-xL and Bax) using Western blotting analysis.	diketopiperazine disulfides	4-31	caspase 8	Homo sapiens	273-282
20881210-7	2011	In HeLa cells, these events were inhibited specifically by zVAD-fmk and DEVD-cho (caspase inhibitors), blebbistatin, Y-27632 (ROCK inhibitor), and genistein, annexin V, and cytochalasin B (inhibitors of blebbing and engulfment).	aspartyl-glutamyl-valyl-aspartal	72-80	caspase 8	Homo sapiens	82-89
21128834-5	2011	Activation of caspase-3, caspase-8, and caspase-9 was observed within cisplatin-treated HEI-OC1 cells.	Cisplatin	70-79	caspase 8	Homo sapiens	25-34
20964705-8	2011	Melatonin treatment also resulted in a reduction in caspase-8 activity, tumor necrosis factor receptor-1 (TNF-R1) expression, and phosphorylated Janus kinase (JNK) expression, and increased expression of cellular FLICE-inhibitory protein (c-FLIP).	Melatonin	0-9	caspase 8	Homo sapiens	52-61
21997748-6	2011	We have developed several reference selection functions in SelCon and obtained improved QA results over existing QA methods in experiments using CASP7 and CASP8 data.	selcon	59-65	caspase 8	Homo sapiens	155-160
25214386-0	2011	Artemisinin induces caspase-8/9-mediated and Bax/Bak-independent apoptosis in human lung adenocarcinoma (ASTC-a-1) cells.	artemisinin	0-11	caspase 8	Homo sapiens	20-29
21755010-10	2011	Combined use of 6-OAP and bortezomib induced potentiated cytotoxicity with inactivation of ERK1/2 and activation of JNK1/2 and Casp-8/-3.	6-O-angeloylprenolin	16-21	caspase 8	Homo sapiens	127-133
21755010-10	2011	Combined use of 6-OAP and bortezomib induced potentiated cytotoxicity with inactivation of ERK1/2 and activation of JNK1/2 and Casp-8/-3.	Bortezomib	26-36	caspase 8	Homo sapiens	127-133
21343676-5	2011	Caspase-3, caspase-8, and caspase-9 were highly activated following combined X-ray irradiation and AsA treatment, but caspase-8 activity was not markedly increased after X-ray irradiation alone.	Ascorbic Acid	99-102	caspase 8	Homo sapiens	11-20
21343676-9	2011	With regard to the apoptosis-inducing factors, we hypothesized that Bax and caspase-8 were activated after combined X-ray irradiation and AsA treatment compared with either treatment alone.	Ascorbic Acid	138-141	caspase 8	Homo sapiens	76-85
21161819-7	2011	Proanthocyanidin-enriched and flavonol-enriched fractions of cranberry also increased caspase-8 and caspase-9 activity, suggesting that these compounds play a possible role in apoptosis induction.	proanthocyanidin	0-16	caspase 8	Homo sapiens	86-95
21161819-7	2011	Proanthocyanidin-enriched and flavonol-enriched fractions of cranberry also increased caspase-8 and caspase-9 activity, suggesting that these compounds play a possible role in apoptosis induction.	3-hydroxyflavone	30-38	caspase 8	Homo sapiens	86-95
20920557-0	2010	Irciniastatin A induces JNK activation that is involved in caspase-8-dependent apoptosis via the mitochondrial pathway.	psymberin	0-15	caspase 8	Homo sapiens	59-68
21251389-4	2011	Fas, FasL and caspase-8 mRNA expression was estimated by reverse transcription-polymerase chain reaction (RT-PCR) 48 hrs after DADS treatment.	diallyl disulfide	127-131	caspase 8	Homo sapiens	14-23
20868669-4	2010	Trichostatin A induced nuclear damage, decreased Bid and Bcl-2 protein levels, increased in Bax levels, induced cytochrome c release, activated caspase-8, -9 and -3, and increased tumor suppressor p53 levels.	trichostatin A	0-14	caspase 8	Homo sapiens	144-164
20868669-7	2010	The results suggest that 18beta-glycyrrhetinic acid may potentiate the apoptotic effects of trichostatin A against ovarian carcinoma cell lines by increasing the activation of the caspase-8-dependent pathway as well as the activation of the mitochondria-mediated cell death pathway, leading to activation of caspases.	18alpha-glycyrrhetinic acid	25-51	caspase 8	Homo sapiens	180-189
20868669-7	2010	The results suggest that 18beta-glycyrrhetinic acid may potentiate the apoptotic effects of trichostatin A against ovarian carcinoma cell lines by increasing the activation of the caspase-8-dependent pathway as well as the activation of the mitochondria-mediated cell death pathway, leading to activation of caspases.	18alpha-glycyrrhetinic acid	25-51	caspase 8	Homo sapiens	308-316
20868669-7	2010	The results suggest that 18beta-glycyrrhetinic acid may potentiate the apoptotic effects of trichostatin A against ovarian carcinoma cell lines by increasing the activation of the caspase-8-dependent pathway as well as the activation of the mitochondria-mediated cell death pathway, leading to activation of caspases.	trichostatin A	92-106	caspase 8	Homo sapiens	180-189
20868669-7	2010	The results suggest that 18beta-glycyrrhetinic acid may potentiate the apoptotic effects of trichostatin A against ovarian carcinoma cell lines by increasing the activation of the caspase-8-dependent pathway as well as the activation of the mitochondria-mediated cell death pathway, leading to activation of caspases.	trichostatin A	92-106	caspase 8	Homo sapiens	308-316
20833157-6	2010	We further demonstrated that knockdown of caspase-8 using its siRNA inhibited the mitochondrial translocation of tBid, the activations of caspase-9 and caspase-3, and subsequent DNA fragmentation by haplophytin-A.	tBID	113-117	caspase 8	Homo sapiens	42-51
20833157-8	2010	During haplophytin-A-induced apoptosis, caspase-8-stimulated tBid provide a link between the death receptor-mediated extrinsic pathway and the mitochondria- mediated intrinsic pathway.	tBID	61-65	caspase 8	Homo sapiens	40-49
21127496-8	2010	alpha-TOS (100 mumol/L) inhibited Akt activation and augmented the activity of caspase 3 and caspase 8 in breast cancer cells expressing erbB2.	alpha-Tocopherol	0-9	caspase 8	Homo sapiens	93-102
20805366-4	2010	The anti-MM activity of ONX-0912 is associated with activation of caspase-8, caspase-9, caspase-3, and poly(ADP) ribose polymerase, as well as inhibition of migration of MM cells and angiogenesis.	ONX 0912	24-32	caspase 8	Homo sapiens	66-75
20804743-3	2010	Our results clearly show that PTX augments TRAIL-mediated activation of caspase-8 and induces cleavage of Bid, although PTX alone cannot activate caspase-8.	Pentoxifylline	30-33	caspase 8	Homo sapiens	72-81
21119362-8	2010	Caspase 3 activity was greater in CK18- HeLa cells than in CK18+ HeLa cells at 8 and 18 hours after FasL treatment (P &lt; 0.05), an effect abrogated by the caspase 8 inhibitor IETD-fmk (P &lt; 0.05).	isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	177-185	caspase 8	Homo sapiens	157-166
20832390-6	2010	Knocking down DR5 using siRNA completely attenuated Chl-induced caspase-8 cleavage but partially inhibited apoptosis.	Chlorogenic Acid	52-55	caspase 8	Homo sapiens	64-73
20953137-7	2010	ATO treatment increased mRNA levels of interferon regulatory factor-1 and TRAIL, as well as protein levels of caspase 8 and cleaved caspase 3, indicating the involvement of the extrinsic apoptotic pathway in the mutated p53 myeloma cells.	Arsenic Trioxide	0-3	caspase 8	Homo sapiens	110-119
20953137-8	2010	ATO also activated caspases 3 and 9, indicating involvement of the intrinsic apoptotic pathway in the wild type p53 myeloma cells.	Arsenic Trioxide	0-3	caspase 8	Homo sapiens	19-27
21311676-3	2010	Melatonin treatment (0 to 3 mM) induced the fragmentation of poly(ADP-ribose) polymerase (PARP) and activation of caspase-3, caspase-8, and caspase-9.	Melatonin	0-9	caspase 8	Homo sapiens	125-134
20812379-8	2010	RMDE also enhanced caspase-8 activity, indicating the involvement of the death receptor pathway in RMDE-mediated SCC-25 cell apoptosis.	rmde	0-4	caspase 8	Homo sapiens	19-28
20937773-0	2010	Cdk1/cyclin B1 controls Fas-mediated apoptosis by regulating caspase-8 activity.	ammonium ferrous sulfate	24-27	caspase 8	Homo sapiens	61-70
20932751-3	2010	In addition, stimulation of HL-60 cells with CWJ-081 induced a series of intracellular events: (1) the activations of caspase-8, -9, and -3; (2) the cleavage of poly (ADP-ribose) polymerase-1 (PARP-1); (3) the loss of mitochondrial membrane potential (DeltaPsi(m)); (4) the release of cytochrome c; and (5) the modulation of Bcl-2 family proteins.	CWJ-081	45-52	caspase 8	Homo sapiens	118-139
21299121-7	2010	These effects of dioscorealide B might result in the activation of caspase-8, -9 and -7, which lead to apoptosis in MCF-7 cells.	dioscorealide B	17-32	caspase 8	Homo sapiens	67-87
20567954-6	2010	Our results showed that overexpression of PAK5 inhibited camptothecin-induced apoptosis by inhibiting the activity of caspase-8 in CRC cells.	Camptothecin	57-69	caspase 8	Homo sapiens	118-127
20674553-5	2010	Moreover, antofine potentiated tumor necrosis factor-alpha (TNF-alpha)-induced apoptosis, which was demonstrated by the increase of Annexin V-positive cell population and of the cleavage of poly (ADP-ribose) polymerase (PARP) and caspase-8.	antofine	10-18	caspase 8	Homo sapiens	230-239
20837473-4	2010	Intracellular esterase activity, sub-G(1) cell cycle arrest, and caspase-8, -9, and -3 activity assays revealed that gossypol potentiated TRAIL-induced apoptosis in human colon cancer cells.	Gossypol	117-125	caspase 8	Homo sapiens	65-86
20943386-7	2010	Ursolic acid also stimulated Bid cleavage, which indicates that the apoptotic action of caspase-8-mediated Bid cleavage leads to the activation of caspase-9.	ursolic acid	0-12	caspase 8	Homo sapiens	88-97
20958191-7	2010	Resveratrol almost completely suppressed cell proliferation, and induced RPE cell necrosis and caspase 3/7- and caspase 8-dependent apoptosis.	Resveratrol	0-11	caspase 8	Homo sapiens	95-121
20958191-8	2010	Curcumin inhibited RPE cell increase exclusively by inducing caspase 3/7-dependent but caspase 8-independent cell death and necrosis.	Curcumin	0-8	caspase 8	Homo sapiens	87-96
20878065-0	2010	Triptolide inactivates Akt and induces caspase-dependent death in cervical cancer cells via the mitochondrial pathway.	triptolide	0-10	caspase 8	Homo sapiens	39-46
20878065-3	2010	Exposure of cervical cancer cells to triptolide induced apoptosis, which was accompanied by loss of mitochondrial membrane potential, caspase processing (caspase-8, -9 and -3), and cleavage of the caspase substrate, poly(ADP-ribose) polymerase.	triptolide	37-47	caspase 8	Homo sapiens	134-141
20878065-3	2010	Exposure of cervical cancer cells to triptolide induced apoptosis, which was accompanied by loss of mitochondrial membrane potential, caspase processing (caspase-8, -9 and -3), and cleavage of the caspase substrate, poly(ADP-ribose) polymerase.	triptolide	37-47	caspase 8	Homo sapiens	154-174
20878065-4	2010	The cytotoxic effects of triptolide were significantly inhibited by the caspase inhibitor, z-VAD-fmk.	triptolide	25-35	caspase 8	Homo sapiens	72-79
20878065-4	2010	The cytotoxic effects of triptolide were significantly inhibited by the caspase inhibitor, z-VAD-fmk.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	91-100	caspase 8	Homo sapiens	72-79
20878065-8	2010	These findings show that triptolide induces caspase-dependent, mitochondria-mediated apoptosis in cervical cancer cells, in part, by negatively regulating Akt and Mcl-1.	triptolide	25-35	caspase 8	Homo sapiens	44-51
20878071-2	2010	This study was performed to elucidate whether mitochondria and caspases are involved in the modulation of apoptosis and cell cycle arrest by cantharidin in human bladder cancer cells.	Cantharidin	141-152	caspase 8	Homo sapiens	63-71
20974006-3	2010	RESULTS: In this study, we demonstrate that alpha-TEA induces the accumulation of cell surface membrane ceramide, leading to co-localization with Fas, DR5, and FADD, followed by activation of caspases-8 and -9 and apoptosis in human MDA-MB-231 breast cancer cells.	alpha-TEA	44-53	caspase 8	Homo sapiens	192-209
20696207-8	2010	Caspases were inhibited with zVAD-FMK and zDEVD-FMK; autophagy with 3-methyladenine, LY294002, and wortmannin.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	29-37	caspase 8	Homo sapiens	0-8
20696207-8	2010	Caspases were inhibited with zVAD-FMK and zDEVD-FMK; autophagy with 3-methyladenine, LY294002, and wortmannin.	benzoylcarbonyl-aspartyl-glutamyl-valyl-aspartyl-fluoromethyl ketone	42-51	caspase 8	Homo sapiens	0-8
20696207-8	2010	Caspases were inhibited with zVAD-FMK and zDEVD-FMK; autophagy with 3-methyladenine, LY294002, and wortmannin.	3-methyladenine	68-83	caspase 8	Homo sapiens	0-8
20696207-8	2010	Caspases were inhibited with zVAD-FMK and zDEVD-FMK; autophagy with 3-methyladenine, LY294002, and wortmannin.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	85-93	caspase 8	Homo sapiens	0-8
20696207-8	2010	Caspases were inhibited with zVAD-FMK and zDEVD-FMK; autophagy with 3-methyladenine, LY294002, and wortmannin.	Wortmannin	99-109	caspase 8	Homo sapiens	0-8
20665667-4	2010	Inhibition of PKCdelta using rottlerin or PKCdelta siRNA reverses the inhibitory effect of PKCdelta on caspase-8 activation leading to TRAIL-induced apoptosis.	rottlerin	29-38	caspase 8	Homo sapiens	103-112
20665667-8	2010	Together, these results strongly suggest that overexpression of PKCdelta inhibits caspase-8 activation leading to inhibition of TRAIL-induced apoptosis and its inhibition by rottlerin, siRNA, or cleavage by caspase-3 sensitizes cells to TRAIL-induced apoptosis.	rottlerin	174-183	caspase 8	Homo sapiens	82-91
20870287-4	2010	Br-cAMP-stimulated differentiation of isolated CT into multinucleated syncytia in culture is not blocked with three different low molecular weight inhibitors of caspase-8: broad caspase inhibitors zVAD-fmk and qVD-OPh and the caspase-8-specific inhibitor zIETD-fmk.	8-Bromo Cyclic Adenosine Monophosphate	0-7	caspase 8	Homo sapiens	226-235
20659543-10	2010	Caspase-8, caspase-3, Bax, P53 and P21 mRNAs as well as proteins were increased while Bcl-2 mRNA and protein were decreased significantly by 24 h of PE treatment.	pe	149-151	caspase 8	Homo sapiens	0-9
20877355-6	2010	Cotreatment with fenretinide and DR ligands resulted in synergistic death compared with either agent alone; caspase-8 and Bid were cleaved in a time-dependent manner.	Fenretinide	17-28	caspase 8	Homo sapiens	108-117
20974006-5	2010	Functional knockdown of ASMase with either the chemical inhibitor, desipramine, or siRNA markedly reduces alpha-TEA-induced cell surface membrane accumulation of ceramide and its co-localization with Fas, DR5, and FADD, cleavage of caspases-8 and -9 and apoptosis, suggesting an early and critical role for ASMase in alpha-TEA-induced apoptosis.	alpha-TEA	106-115	caspase 8	Homo sapiens	232-249
20674638-6	2010	Cotreatment with a caspase-8 inhibitor (Z-IETD-FMK) or a polyethylene glycol (Mr 2000) (PEG 2000) effectively prevented the activation of caspase-3 induced by DDAB.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	40-50	caspase 8	Homo sapiens	19-28
20735432-8	2010	Mechanistically, PDCD4 significantly increased cisplatin-induced cleavage of caspase-3 and caspase-8, but had only a slight impact on caspase-9 cleavage and the expression of Bax and Bcl-2 in vitro and in vivo.	Cisplatin	47-56	caspase 8	Homo sapiens	91-100
20674558-6	2010	DP increased the levels of reactive oxygen species (ROS) in HepG2 cells, and antioxidant N-acetylcysteine (NAC) completely blocked DP-induced ROS accumulation and the disruption of the balance between Bax and Bcl-2 proteins, and effectively blocked the decreased MMP and apoptosis, but had no effect on the activation of caspase-8 and the up-regulations of DR4 and DR5 induced by DP.	1-(3',4',5'-trimethoxyphenyl)-3-(3'',4''-dimethoxy-2'-hydroxyphenyl)propane	131-133	caspase 8	Homo sapiens	321-330
20674638-6	2010	Cotreatment with a caspase-8 inhibitor (Z-IETD-FMK) or a polyethylene glycol (Mr 2000) (PEG 2000) effectively prevented the activation of caspase-3 induced by DDAB.	didodecyldimethylammonium	159-163	caspase 8	Homo sapiens	19-28
20674638-7	2010	These results suggest that DDAB can trigger caspase-3-mediated apoptosis through the extrinsic caspase-8 pathway and cytotoxic pore formation in cell membrane.	didodecyldimethylammonium	27-31	caspase 8	Homo sapiens	95-104
20674558-6	2010	DP increased the levels of reactive oxygen species (ROS) in HepG2 cells, and antioxidant N-acetylcysteine (NAC) completely blocked DP-induced ROS accumulation and the disruption of the balance between Bax and Bcl-2 proteins, and effectively blocked the decreased MMP and apoptosis, but had no effect on the activation of caspase-8 and the up-regulations of DR4 and DR5 induced by DP.	1-(3',4',5'-trimethoxyphenyl)-3-(3'',4''-dimethoxy-2'-hydroxyphenyl)propane	0-2	caspase 8	Homo sapiens	321-330
20674558-6	2010	DP increased the levels of reactive oxygen species (ROS) in HepG2 cells, and antioxidant N-acetylcysteine (NAC) completely blocked DP-induced ROS accumulation and the disruption of the balance between Bax and Bcl-2 proteins, and effectively blocked the decreased MMP and apoptosis, but had no effect on the activation of caspase-8 and the up-regulations of DR4 and DR5 induced by DP.	Acetylcysteine	89-105	caspase 8	Homo sapiens	321-330
20674558-6	2010	DP increased the levels of reactive oxygen species (ROS) in HepG2 cells, and antioxidant N-acetylcysteine (NAC) completely blocked DP-induced ROS accumulation and the disruption of the balance between Bax and Bcl-2 proteins, and effectively blocked the decreased MMP and apoptosis, but had no effect on the activation of caspase-8 and the up-regulations of DR4 and DR5 induced by DP.	Acetylcysteine	107-110	caspase 8	Homo sapiens	321-330
20674558-6	2010	DP increased the levels of reactive oxygen species (ROS) in HepG2 cells, and antioxidant N-acetylcysteine (NAC) completely blocked DP-induced ROS accumulation and the disruption of the balance between Bax and Bcl-2 proteins, and effectively blocked the decreased MMP and apoptosis, but had no effect on the activation of caspase-8 and the up-regulations of DR4 and DR5 induced by DP.	1-(3',4',5'-trimethoxyphenyl)-3-(3'',4''-dimethoxy-2'-hydroxyphenyl)propane	131-133	caspase 8	Homo sapiens	321-330
20735432-9	2010	A specific caspase-8 inhibitor, Z-ITED-FMK, attenuated cisplatin-induced apoptosis in PDCD4-overexpressing ovarian cancer cells.	z-ited-fmk	32-42	caspase 8	Homo sapiens	11-20
20735432-9	2010	A specific caspase-8 inhibitor, Z-ITED-FMK, attenuated cisplatin-induced apoptosis in PDCD4-overexpressing ovarian cancer cells.	Cisplatin	55-64	caspase 8	Homo sapiens	11-20
21229646-6	2010	RESULTS: cell death rate induced by the tested compound was decreased with the caspase-3 inhibitor Ac-DEVD-CHO, and the inhibitors of caspase-2 (Z-VDVAD-FMK) and -4 (ZYVAD- FMK), but not with the caspase-9 inhibitor z-LEHD-FMK and caspase-8 inhibitor z-IETD-FMK.	acetyl-aspartyl-glutamyl-valyl-aspartal	99-110	caspase 8	Homo sapiens	231-240
20811662-4	2010	In vitro, nafamostat mesilate inhibited NF-kappaB activation of human pancreatic cancer cell line (Panc-1) by suppressing IkappaBalpha phosphorylation and induced caspase-8 mediated apoptosis.	nafamostat	10-29	caspase 8	Homo sapiens	163-172
20696234-7	2010	Furthermore, blocking the extracellular signal-regulated protein kinase and c-Jun N-terminal kinase pathways showed increased apoptosis and the activation of caspases in J-7-induced apoptosis.	j-7	170-173	caspase 8	Homo sapiens	158-166
20136500-6	2010	Since pan-caspase inhibitor z-VAD-fmk abolished the TNF-alpha-induced mitochondrial changes, z-DEVD-fmk, an inhibitor of caspase-3 had no effect, suggesting that TNF-alpha-induced mitochondrial changes or cytochrome c and Smac release requires caspase-8 but not caspase-3 activation.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	28-37	caspase 8	Homo sapiens	10-17
21364680-0	2010	Resistance to caspase-8 and -9 fragments in a malignant pleural mesothelioma cell line with acquired cisplatin-resistance.	Cisplatin	101-110	caspase 8	Homo sapiens	14-30
21364680-4	2010	Acquisition of cisplatin-resistance resulted in basal fragmentation of caspase-8 and -9 without a concomitant increase in proteolytic activity, and there was an increased basal caspase-3/7 activity.	Cisplatin	15-24	caspase 8	Homo sapiens	71-87
21364680-7	2010	We therefore concluded that in vitro acquisition of cisplatin-resistance rendered P31res1.2 cells resistant to caspase-8 and caspase-9 fragments and that cisplatin-induced, initiator-caspase independent caspase-3/7 activation was necessary to overcome this resistance.	Cisplatin	52-61	caspase 8	Homo sapiens	111-120
20553909-4	2010	TSA prevented TGF-beta1-induced apoptosis and the activation of caspase-8 and caspase-9 in RPTECs but did not inhibit the TGF-beta1-induced phosphorylation of Smad3 and p38 mitogen-activated protein kinase (MAPK).	trichostatin A	0-3	caspase 8	Homo sapiens	64-73
20675131-0	2010	Unnatural enantiomer of chaetocin shows strong apoptosis-inducing activity through caspase-8/caspase-3 activation.	chaetocin	24-33	caspase 8	Homo sapiens	83-92
20647931-5	2010	Western blot indicated that evodiamine treatment decreased the expression of procaspase-8, procaspase-9, and procaspase-3 in lovo cells, accompanied by the activation of caspase-8, caspase-9, and caspase-3.	evodiamine	28-38	caspase 8	Homo sapiens	80-89
20580860-4	2010	Kinetic studies of caspase-3 and caspase-8 inhibition were carried out with these urazole ring-containing irreversible peptidomimetics and a known irreversible caspase inhibitor, Z-VAD-fmk.	urazole	82-89	caspase 8	Homo sapiens	33-42
20580860-6	2010	Z-VAD-fmk and the peptidomimetic inhibitors inhibit caspase-3 and caspase-8 via a three-step kinetic mechanism.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	0-9	caspase 8	Homo sapiens	66-75
20580860-7	2010	Inhibition of both caspase-3 and caspase-8 by Z-VAD-fmk and of caspase-3 by the peptidomimetic inhibitors proceeds via two rapid equilibrium steps followed by a relatively fast inactivation step.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	46-55	caspase 8	Homo sapiens	33-42
20675131-4	2010	The unnatural enantiomer of chaetocin (ent-chaetocin) was more potent than chaetocin, and was found to induce apoptosis through the caspase-8/caspase-3 activation pathway.	chaetocin	28-37	caspase 8	Homo sapiens	132-141
20675131-4	2010	The unnatural enantiomer of chaetocin (ent-chaetocin) was more potent than chaetocin, and was found to induce apoptosis through the caspase-8/caspase-3 activation pathway.	Ent-Chaetocin	39-52	caspase 8	Homo sapiens	132-141
20675131-4	2010	The unnatural enantiomer of chaetocin (ent-chaetocin) was more potent than chaetocin, and was found to induce apoptosis through the caspase-8/caspase-3 activation pathway.	chaetocin	43-52	caspase 8	Homo sapiens	132-141
20449638-6	2010	In addition, our study showed that caspase 3 was activated by caspase 8, not caspase 9, in Smmc-7721 cells treated with VK(2).	smmc	91-95	caspase 8	Homo sapiens	62-71
20802973-0	2010	Caspase-8 and p38MAPK in DATS-induced apoptosis of human CNE2 cells.	diallyl trisulfide	25-29	caspase 8	Homo sapiens	0-9
20802973-3	2010	In this study, we investigated the function of p38 mitogen-activated protein kinase (MAPK) and caspase-8 in DATS-induced apoptosis of human CNE2 cells using MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide], flow cytometry assay, and Western blotting.	diallyl trisulfide	108-112	caspase 8	Homo sapiens	95-104
20802973-9	2010	The results indicated that DATS activates p38MAPK and caspase-8, but both inhibitors have an effect on P38MAPK and caspase-8 activity.	diallyl trisulfide	27-31	caspase 8	Homo sapiens	54-63
20802973-10	2010	In conclusion, our data indicate that p38MAPK and caspase-8 are involved in the process of DATS-induced apoptosis in human CNE2 cells and interact with each other.	diallyl trisulfide	91-95	caspase 8	Homo sapiens	50-59
20229524-9	2010	Isoangustone A increased apoptotic cells, the cleavage of PARP and caspases, and the levels of DR4 and Mcl-1S.	isoangustone	0-12	caspase 8	Homo sapiens	67-75
21687829-13	2010	In conclusion, these data demonstrated GrTP and EGCG induced apoptosis in intestinal epithelia mediated by caspase-8 through a FADD dependent pathway.	epigallocatechin gallate	48-52	caspase 8	Homo sapiens	107-116
20397191-7	2010	Moreover, treatment with z-DEVD-fmk (a specific caspase-3 inhibitor) and the overexpression of Bcl-2 prevented eupafolin-stimulated caspase-8 activation.	benzoylcarbonyl-aspartyl-glutamyl-valyl-aspartyl-fluoromethyl ketone	25-35	caspase 8	Homo sapiens	132-141
20397191-7	2010	Moreover, treatment with z-DEVD-fmk (a specific caspase-3 inhibitor) and the overexpression of Bcl-2 prevented eupafolin-stimulated caspase-8 activation.	eupafolin	111-120	caspase 8	Homo sapiens	132-141
20503248-10	2010	Furthermore, by using the TUNEL assay, evodiamine-induced apoptosis was observed at 48 h and extended to 72 h. Western blotting demonstrated that evodiamine treatment induced the activation of caspase-8, caspase-9, caspase-3, and the cleavage of poly ADP-ribose polymerase (PARP).	evodiamine	39-49	caspase 8	Homo sapiens	193-202
20663933-2	2010	Treatment of Jurkat T-lymphoma cells with DHA induced a breakdown of the mitochondrial transmembrane potential, release of cytochrome c, activation of caspases, and DNA fragmentation indicative of apoptosis induction.	artenimol	42-45	caspase 8	Homo sapiens	151-159
20878579-1	2010	OBJECTIVE: To investigate the effect of fragile histidine triad (FHIT) gene transfection on human colorectal cancer cell line SW480 through up-regulation of caspase-8 expression.	Histidine	48-57	caspase 8	Homo sapiens	157-166
20678472-5	2010	It activated multicaspases, and increased the activities of caspase-8 and caspase-9 in both MG-63 and SaOS-2 cells.	Magnesium	92-94	caspase 8	Homo sapiens	60-69
20812284-6	2010	Apoptosis in HeLa cells was also observed as PE extract caused DNA fragmentation and increased activity of caspase-3/7 and caspase-8, but not caspase-9, and up-regulation of the Fas protein indicating a death receptor-mediated mechanism of apoptosis.	pe	45-47	caspase 8	Homo sapiens	123-132
20727207-12	2010	The caspase-8 and -9 inhibitors Z-IETD-FMK and Z-LEHD-FMK induced a reduction in fucoidan-mediated apoptosis.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	32-42	caspase 8	Homo sapiens	4-20
20727207-12	2010	The caspase-8 and -9 inhibitors Z-IETD-FMK and Z-LEHD-FMK induced a reduction in fucoidan-mediated apoptosis.	benzyloxycarbonyl-leucyl-glutamyl-histidyl-aspartic acid fluoromethyl ketone	47-57	caspase 8	Homo sapiens	4-20
20503248-11	2010	These results suggested that evodiamine inhibited the growth of the ARO cells, arrested them at M phase, and induced apoptosis through caspases signaling.	evodiamine	29-39	caspase 8	Homo sapiens	135-143
20503248-10	2010	Furthermore, by using the TUNEL assay, evodiamine-induced apoptosis was observed at 48 h and extended to 72 h. Western blotting demonstrated that evodiamine treatment induced the activation of caspase-8, caspase-9, caspase-3, and the cleavage of poly ADP-ribose polymerase (PARP).	evodiamine	146-156	caspase 8	Homo sapiens	193-202
20512627-6	2010	Combined Dox + DMPS treatment-induced apoptosis was accompanied by the activation of caspase-8 and caspase-3 as well as PARP cleavage.	Doxorubicin	9-12	caspase 8	Homo sapiens	85-94
20195576-8	2010	The effects of the caspase inhibitor, z-VAD-FMK, on the timing of caspase activity are also investigated and are shown to dramatically slow the apoptotic process.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	38-47	caspase 8	Homo sapiens	19-26
20510339-3	2010	Fas-induced apoptosis can be restored in these cells by up-regulation of caspase 8 expression by means of transient transfection with a caspase 8-encoding plasmid.	ammonium ferrous sulfate	0-3	caspase 8	Homo sapiens	73-82
20510339-3	2010	Fas-induced apoptosis can be restored in these cells by up-regulation of caspase 8 expression by means of transient transfection with a caspase 8-encoding plasmid.	ammonium ferrous sulfate	0-3	caspase 8	Homo sapiens	136-145
20510339-4	2010	Furthermore, treatment of primary astrocytes with the demethylating agent 5-Aza-dC restores caspase 8 expression and increases the sensibility of neonatal astrocytes to the cytotoxic effect of Fas activation.	Decitabine	74-82	caspase 8	Homo sapiens	92-101
20512627-6	2010	Combined Dox + DMPS treatment-induced apoptosis was accompanied by the activation of caspase-8 and caspase-3 as well as PARP cleavage.	N,N-dimethylphytosphingosine	15-19	caspase 8	Homo sapiens	85-94
19940991-11	2010	CONCLUSION: The present findings demonstrate that Se-induced apoptosis in carcinoma cells is basically a caspase-dependent process involving complicated mechanisms.	Selenium	50-52	caspase 8	Homo sapiens	105-112
20421362-3	2010	From the cells surviving apoptogenic Fas stimulation, four candidate shRNA sequences were obtained that provided resistance to Fas-induced cell death, including two shRNAs for caspase-8, an shRNA for Bid, and an shRNA for Fas.	ammonium ferrous sulfate	127-130	caspase 8	Homo sapiens	176-185
20063052-6	2010	Taken together, the results of the present study indicate that intracellularly transported adenosine activates caspase-3 by neutralizing caspase-3 inhibition due to IAP as a result of decreased IAP2 expression and reduced IAP activity in response to increased DIABLO expression and perhaps DIABLO release from damaged mitochondria, in addition to caspase-8 activation.	Adenosine	91-100	caspase 8	Homo sapiens	347-356
21132068-3	2010	We show that prostate cancer DU145 cells expressing a high level of JNK1 become susceptible to apoptosis after treatment with HMG, in which caspase 8 is activated and cytochrome c is released to the cytosol.	Menotropins	126-129	caspase 8	Homo sapiens	140-149
19908232-7	2010	Chemosensitization by ursolic acid in cancer cells was dependent on the amplified activation of intrinsic pathway (caspase-8-BID-mitochondria-cytochrome c-caspase-3) by augmentation of BID cleavage and activation of Fas/FasL-caspase-8 pathway.	ursolic acid	22-34	caspase 8	Homo sapiens	115-124
20237495-7	2010	Furthermore, death ligand and diclofenac/HA-mediated apoptosis were blocked by the same caspase inhibitors, indicating related pathways.	Diclofenac	30-40	caspase 8	Homo sapiens	88-95
20237495-7	2010	Furthermore, death ligand and diclofenac/HA-mediated apoptosis were blocked by the same caspase inhibitors, indicating related pathways.	ha	41-43	caspase 8	Homo sapiens	88-95
20653475-6	2010	CONCLUSIONS: NAC prevents the increased expression levels of p53 and CASP8 induced by long-term maintained hypoxia.	Acetylcysteine	13-16	caspase 8	Homo sapiens	69-74
20686688-5	2010	CONCLUSION: Taken together, ER stress plays an important role in alpha-TEA induced apoptosis by enhancing DR5/caspase-8 pro-apoptotic signaling and suppressing anti-apoptotic factors c-FLIP and Bcl-2 via ER stress mediated JNK/CHOP/DR5/caspase-8 signaling.	2,5,7,8-tetramethyl-2R-(4R,8R,12-trimethyltridecyl)chroman-6-yloxy acetic acid	65-74	caspase 8	Homo sapiens	110-119
20686688-5	2010	CONCLUSION: Taken together, ER stress plays an important role in alpha-TEA induced apoptosis by enhancing DR5/caspase-8 pro-apoptotic signaling and suppressing anti-apoptotic factors c-FLIP and Bcl-2 via ER stress mediated JNK/CHOP/DR5/caspase-8 signaling.	2,5,7,8-tetramethyl-2R-(4R,8R,12-trimethyltridecyl)chroman-6-yloxy acetic acid	65-74	caspase 8	Homo sapiens	236-245
19908232-7	2010	Chemosensitization by ursolic acid in cancer cells was dependent on the amplified activation of intrinsic pathway (caspase-8-BID-mitochondria-cytochrome c-caspase-3) by augmentation of BID cleavage and activation of Fas/FasL-caspase-8 pathway.	ursolic acid	22-34	caspase 8	Homo sapiens	225-234
20351548-6	2010	We showed that C3N inhibited the proliferation of ECA109 cells moderately in a dose and time-dependent manner and induced apoptosis in the ECA109 cell line through a mitochondrial pathway by triggered cytochrome c release from the mitochondria, with caspase-2 functioning upstream of caspase-9 rather than association with Fas and caspase-8.	c3n	15-18	caspase 8	Homo sapiens	331-340
20351548-8	2010	These results suggest that C3N-induced apoptosis of ECA109 cells in vitro was dependent on caspase-2 or mitochondria or caspase-9 and independent of the Fas-FasL or caspase-8 pathway.	c3n	27-30	caspase 8	Homo sapiens	165-174
20352217-7	2010	Treatment with darbufelone also induced apoptosis by activating caspase-3 and caspase-8.	darbufelone	15-26	caspase 8	Homo sapiens	78-87
20683014-0	2010	Role of caspases and CD95/Fas in the apoptotic effects of a nucleotide analog PMEG in CCRF-CEM cells.	9-((2-phosphonylmethoxy)ethyl)guanine	78-82	caspase 8	Homo sapiens	8-16
20683014-3	2010	The objective of this study was to determine the requirements for caspase and CD95/Fas activation in PMEG-induced apoptosis.	9-((2-phosphonylmethoxy)ethyl)guanine	101-105	caspase 8	Homo sapiens	66-73
20683014-7	2010	CONCLUSION: PMEG-induced apoptosis is caspase- and CD95/Fas-independent.	9-((2-phosphonylmethoxy)ethyl)guanine	12-16	caspase 8	Homo sapiens	38-45
20394499-3	2010	In search of cancer therapeutics that can overcome TRAIL resistance, we show here that celecoxib and camptothecin can sensitize TRAIL-resistant HCC cell lines, HepG2 and Hep3B, to TRAIL-induced apoptosis through downregulation of cellular Fas-associated death domain-like interleukin-1beta-converting enzyme-inhibitory protein (c-FLIP) and cleavage of caspase-8 and caspase-3 in the HCC cells.	Celecoxib	87-96	caspase 8	Homo sapiens	352-361
20394499-3	2010	In search of cancer therapeutics that can overcome TRAIL resistance, we show here that celecoxib and camptothecin can sensitize TRAIL-resistant HCC cell lines, HepG2 and Hep3B, to TRAIL-induced apoptosis through downregulation of cellular Fas-associated death domain-like interleukin-1beta-converting enzyme-inhibitory protein (c-FLIP) and cleavage of caspase-8 and caspase-3 in the HCC cells.	Camptothecin	101-113	caspase 8	Homo sapiens	352-361
20472914-3	2010	The proportion of both viable and dead spermatozoa expressing activated caspases was detected by flow cytometry through the use of different specific carboxyfluorescein-labeled caspase inhibitors.	6-carboxyfluorescein	150-168	caspase 8	Homo sapiens	72-80
20202478-7	2010	Several distinctive features of sea bass caspase-8 were identified, which include two death effector domains, the caspase family domains p20 and p10, the caspase-8 active-site pentapeptide and potential aspartic acid cleavage sites.	Aspartic Acid	203-216	caspase 8	Homo sapiens	41-50
20202478-7	2010	Several distinctive features of sea bass caspase-8 were identified, which include two death effector domains, the caspase family domains p20 and p10, the caspase-8 active-site pentapeptide and potential aspartic acid cleavage sites.	Aspartic Acid	203-216	caspase 8	Homo sapiens	41-48
20202478-11	2010	piscicida (Phdp), known to induce selective apoptosis of macrophages and neutrophils, resulted in an increased expression of caspase-8 in the spleen, one of the main affected organs by Phdp infection.	phdp	11-15	caspase 8	Homo sapiens	125-134
20202478-11	2010	piscicida (Phdp), known to induce selective apoptosis of macrophages and neutrophils, resulted in an increased expression of caspase-8 in the spleen, one of the main affected organs by Phdp infection.	phdp	185-189	caspase 8	Homo sapiens	125-134
20362650-0	2010	Titanium dioxide nanoparticles cause apoptosis in BEAS-2B cells through the caspase 8/t-Bid-independent mitochondrial pathway.	titanium dioxide	0-16	caspase 8	Homo sapiens	76-85
20799830-0	2010	Single-cell analysis of dihydroartemisinin-induced apoptosis through reactive oxygen species-mediated caspase-8 activation and mitochondrial pathway in ASTC-a-1 cells using fluorescence imaging techniques.	artenimol	24-42	caspase 8	Homo sapiens	102-111
20799830-0	2010	Single-cell analysis of dihydroartemisinin-induced apoptosis through reactive oxygen species-mediated caspase-8 activation and mitochondrial pathway in ASTC-a-1 cells using fluorescence imaging techniques.	Reactive Oxygen Species	69-92	caspase 8	Homo sapiens	102-111
20799830-6	2010	Confocal imaging analysis in a single living cell and Western blot assay showed that DHA triggered ROS-dependent Bax translocation, mitochondrial membrane depolarization, alteration of mitochondrial morphology, cytochrome c release, caspase-9, caspase-8, and caspase-3 activation, indicating the coexistence of ROS-mediated mitochondrial and death receptor pathway.	artenimol	85-88	caspase 8	Homo sapiens	244-253
20799830-6	2010	Confocal imaging analysis in a single living cell and Western blot assay showed that DHA triggered ROS-dependent Bax translocation, mitochondrial membrane depolarization, alteration of mitochondrial morphology, cytochrome c release, caspase-9, caspase-8, and caspase-3 activation, indicating the coexistence of ROS-mediated mitochondrial and death receptor pathway.	Reactive Oxygen Species	99-102	caspase 8	Homo sapiens	244-253
20799830-7	2010	Collectively, our findings demonstrate for the first time that DHA induces cell apoptosis by triggering ROS-mediated caspase-8/Bid activation and the mitochondrial pathway, which provides some novel insights into the application of DHA as a potential anticancer drug and a new therapeutic strategy by targeting ROS signaling in lung adenocarcinoma therapy in the future.	artenimol	63-66	caspase 8	Homo sapiens	117-126
20799830-7	2010	Collectively, our findings demonstrate for the first time that DHA induces cell apoptosis by triggering ROS-mediated caspase-8/Bid activation and the mitochondrial pathway, which provides some novel insights into the application of DHA as a potential anticancer drug and a new therapeutic strategy by targeting ROS signaling in lung adenocarcinoma therapy in the future.	Reactive Oxygen Species	104-107	caspase 8	Homo sapiens	117-126
20799830-7	2010	Collectively, our findings demonstrate for the first time that DHA induces cell apoptosis by triggering ROS-mediated caspase-8/Bid activation and the mitochondrial pathway, which provides some novel insights into the application of DHA as a potential anticancer drug and a new therapeutic strategy by targeting ROS signaling in lung adenocarcinoma therapy in the future.	artenimol	232-235	caspase 8	Homo sapiens	117-126
20143425-3	2010	Here, we report that staurosporine (STS)-induced apoptosis induces caspase-8 and/or-2-dependent gamma-secretase activation.	Staurosporine	21-34	caspase 8	Homo sapiens	67-76
20143425-3	2010	Here, we report that staurosporine (STS)-induced apoptosis induces caspase-8 and/or-2-dependent gamma-secretase activation.	Staurosporine	36-39	caspase 8	Homo sapiens	67-76
20651361-9	2010	Curcumin-induced apoptosis was also stimulated through the FAS/caspase-8 (extrinsic) pathway and ER stress proteins, growth arrest- and DNA damage-inducible gene 153 (GADD153) and glucose-regulated protein 78 (GRP78) were activated in the NCI-H460 cells.	Curcumin	0-8	caspase 8	Homo sapiens	63-72
20404512-7	2010	Moreover, Avasimibe inhibited the growth of the cells by inducing cell cycle arrest and induced apoptosis as a result of caspase-8 and caspase-3 activation.	avasimibe	10-19	caspase 8	Homo sapiens	121-130
20651361-10	2010	Apoptotic cell death induced by curcumin was significantly reversed by pretreatment with ROS scavenger or caspase-8 inhibitor.	Curcumin	32-40	caspase 8	Homo sapiens	106-115
20428772-8	2010	The levels of caspase-3, -8 and -9 involved in apigenin-induced apoptosis indicating caspase-dependent pathway was induced by apigenin.	Apigenin	47-55	caspase 8	Homo sapiens	14-21
20019748-4	2010	Instead, poly I:C-induced activation of caspase-8 via TLR3 and its adapter TRIF was required for apoptosis.	Poly I-C	9-17	caspase 8	Homo sapiens	40-49
20019748-6	2010	Significantly, sensitisation towards poly I:C-dependent caspase-8 activation and apoptosis in melanoma cells was also achieved by the synthetic Smac mimetic/inhibitor of apoptosis protein (IAP) antagonist, LBW242, or by specific downregulation of cIAP1 by siRNA.	Poly I-C	37-45	caspase 8	Homo sapiens	56-65
20019748-6	2010	Significantly, sensitisation towards poly I:C-dependent caspase-8 activation and apoptosis in melanoma cells was also achieved by the synthetic Smac mimetic/inhibitor of apoptosis protein (IAP) antagonist, LBW242, or by specific downregulation of cIAP1 by siRNA.	smac	144-148	caspase 8	Homo sapiens	56-65
20019748-7	2010	Inactivation of caspase-8 by CrmA overexpression reduced poly I:C/LBW242-induced apoptosis.	Poly I	57-63	caspase 8	Homo sapiens	16-25
20019748-7	2010	Inactivation of caspase-8 by CrmA overexpression reduced poly I:C/LBW242-induced apoptosis.	LBW242	66-72	caspase 8	Homo sapiens	16-25
20471514-5	2010	When bortezomib was added, some proapoptotic genes (CARD9, TRAIL) were upregulated, and some antiapoptotic genes (BCL2, BCL3, FLICE) were downregulated.	Bortezomib	5-15	caspase 8	Homo sapiens	126-131
20154269-6	2010	Thus, increased activation of NF-kappaB can alter sensitivity to tamoxifen by modulating CASP8 activity, with consequent effects on BCL2 expression, mitochondrial function, and apoptosis.	Tamoxifen	65-74	caspase 8	Homo sapiens	89-94
19418023-6	2010	Our data showed that MMPT caused activation of caspase-3, caspase-6 and caspase-8, but not caspase-9.	mmpt	21-25	caspase 8	Homo sapiens	72-81
20515944-5	2010	Increased processing of caspase-8 often accompanied enhancement of TRAIL-induced apoptosis by bortezomib.	Bortezomib	94-104	caspase 8	Homo sapiens	24-33
19538462-5	2010	Accordingly, increased activation of Caspase-8 and Caspase-3 following nickel treatment was observed.	Nickel	71-77	caspase 8	Homo sapiens	37-46
19428234-10	2010	Moreover, tryptophan reduced the expression of the pro-inflammatory cytokines tumor necrosis factor-alpha, interleukin (IL)-6, interferon (IFN)-gamma, IL-12p40, IL-1beta and IL-17, as well as IL-8 and intracellular adhesion molecule-1, and resulted in increased expression of apoptosis initiators caspase-8 and Bax.	Tryptophan	10-20	caspase 8	Homo sapiens	297-306
20515944-7	2010	For some ESCC, bortezomib treatment resulted in a more efficient recruitment of caspase-8 and the Fas-associated death domain to the death-inducing signaling complex.	Bortezomib	15-25	caspase 8	Homo sapiens	80-89
20004081-8	2010	RESULTS: The caspase inhibitors inhibited butyrate- and propionate-induced neutrophil apoptosis treated or untreated with lipopolysaccharide or tumor necrosis factor-alpha, whereas GPR and MAPK inhibitors had no effect.	Butyrates	42-50	caspase 8	Homo sapiens	13-20
20004081-8	2010	RESULTS: The caspase inhibitors inhibited butyrate- and propionate-induced neutrophil apoptosis treated or untreated with lipopolysaccharide or tumor necrosis factor-alpha, whereas GPR and MAPK inhibitors had no effect.	Propionates	56-66	caspase 8	Homo sapiens	13-20
19900759-2	2010	In the gene expression assay using a DNA microalley, adenosine upregulated mRNAs for tumor necrosis factor (TNF), TNF receptor 1-associated death domain protein (TRADD), TNF related apoptosis-inducing ligand receptor 2 (TRAIL-R2), TRADD/receptor-interacting protein kinase 1 (RIPK1), Fas-associated death domain protein (FADD), and caspase-9, involving activation of caspase-8 and -9 followed by the effector caspase-3.	Adenosine	53-62	caspase 8	Homo sapiens	367-383
19900759-3	2010	The results of the present study suggest that adenosine induces HepG2 cell apoptosis by activating those caspases as a result from tuning apoptosis-mediator gene transcription.	Adenosine	46-55	caspase 8	Homo sapiens	105-113
20154224-5	2010	Time course experiments revealed that bleomycin induced apoptosis within 4 h. Caspase-8, the initiator caspase for the extrinsic pathway, was activated within 2 h and preceded activation of the effector caspases-3 and -6 (4 h).	Bleomycin	38-47	caspase 8	Homo sapiens	78-87
20404718-11	2010	Vpr induced sustained ERK activation in HK2 cells and incubation with U0126 reduced Vpr-induced caspase-8 activation, BID cleavage and apoptosis.	U 0126	70-75	caspase 8	Homo sapiens	96-105
20404718-13	2010	CONCLUSIONS: These studies delineate a novel pathway of Vpr-induced apoptosis in RTEC, which is mediated by sustained ERK activation, resulting in caspase 8-mediated cleavage of BID to tBID, thereby facilitating Bax-mediated mitochondrial injury and apoptosis.	tBID	185-189	caspase 8	Homo sapiens	147-156
20190189-3	2010	GCS-100 induced inhibition of proliferation, accumulation of cells in sub-G(1) and G(1) phases, and apoptosis with activation of both caspase-8 and -9 pathways.	GCS-100	0-7	caspase 8	Homo sapiens	134-150
20561413-5	2010	The results showed that the subtoxic concentration of bortezomib combined with 10 ng/ml of TRAIL enhanced apoptosis of HL-60 cells, as compared with TRAIL used alone; the expression of caspase-8 increased correspondingly.	Bortezomib	54-64	caspase 8	Homo sapiens	185-194
20561413-6	2010	It is concluded that subtoxic concentration of bortezomib can sensitize HL-60 cells to TRAIL and its mechanism may be related to upregulation of caspase-8 expression.	Bortezomib	47-57	caspase 8	Homo sapiens	145-154
20094800-4	2010	Flunarizine-induced DNA fragmentation was inhibited by the caspase-3 inhibitor z-DEVD-fmk, the caspase-8/caspase-10 inhibitor z-IETD-fmk, and the caspase-10 inhibitor z-AEVD-fmk, but was not reduced in caspase-8-deficient Jurkat cells, indicating the involvement of caspase-10 upstream of caspase-3 activation.	Flunarizine	0-11	caspase 8	Homo sapiens	95-104
20094800-4	2010	Flunarizine-induced DNA fragmentation was inhibited by the caspase-3 inhibitor z-DEVD-fmk, the caspase-8/caspase-10 inhibitor z-IETD-fmk, and the caspase-10 inhibitor z-AEVD-fmk, but was not reduced in caspase-8-deficient Jurkat cells, indicating the involvement of caspase-10 upstream of caspase-3 activation.	Flunarizine	0-11	caspase 8	Homo sapiens	202-211
19942342-6	2010	AE-induced loss of mitochondrial membrane potential (MMP) and increase in cellular Ca(++) content, reactive oxygen species (ROS) and apoptotic cell death were suppressed by the treatment of cyclosporin A (CsA) or caspase-8 inhibitor Z-IETD-FMK.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	233-243	caspase 8	Homo sapiens	213-222
20081872-6	2010	Immunohistochemical analysis revealed that (-)-gossypol enhanced caspase-3 and caspase-8 expression and decreased the expression of PCNA, Bcl-2 and CD31 in tumour tissues.	Gossypol	43-55	caspase 8	Homo sapiens	79-88
19942342-8	2010	In addition, suppression of caspase-8 with the specific inhibitor Z-IETD-FMK inhibited AE-induced the activation of Bax, the cleavage of Bid, the translocation of tBid to the mitochondria and the release of cytochrome c, apoptosis-inducing factor (AIF) and Endo G from the mitochondria and subsequent apoptosis.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	66-76	caspase 8	Homo sapiens	28-37
19942342-8	2010	In addition, suppression of caspase-8 with the specific inhibitor Z-IETD-FMK inhibited AE-induced the activation of Bax, the cleavage of Bid, the translocation of tBid to the mitochondria and the release of cytochrome c, apoptosis-inducing factor (AIF) and Endo G from the mitochondria and subsequent apoptosis.	tBID	163-167	caspase 8	Homo sapiens	28-37
20133021-5	2010	While apoptosis induction by the menthoxymalonyl hydrazone was characterized by an upfront increase in caspase-8 activity, all other hydrazones elicited a hike in caspase-9 activity.	menthoxymalonyl hydrazone	33-58	caspase 8	Homo sapiens	103-112
20356928-3	2010	Subsequent analyses suggested that the divergence of caspase-8 activation and Bid cleavage are critically controlled by kinase signalling: inhibiting protein kinase CK2 by using 5,6-dichloro-l-(beta-D-ribofuranosyl-1)-benzimidazole (DRB) or by overexpression of a dominant-negative CK2alpha catalytic subunit largely eliminated the lag time between caspase-8 activation and Bid cleavage.	5,6-dichloro-l-(beta-d-ribofuranosyl-1)-benzimidazole	178-231	caspase 8	Homo sapiens	53-62
20356928-3	2010	Subsequent analyses suggested that the divergence of caspase-8 activation and Bid cleavage are critically controlled by kinase signalling: inhibiting protein kinase CK2 by using 5,6-dichloro-l-(beta-D-ribofuranosyl-1)-benzimidazole (DRB) or by overexpression of a dominant-negative CK2alpha catalytic subunit largely eliminated the lag time between caspase-8 activation and Bid cleavage.	Dichlororibofuranosylbenzimidazole	233-236	caspase 8	Homo sapiens	53-62
20442297-0	2010	Bortezomib sensitizes human renal cell carcinomas to TRAIL apoptosis through increased activation of caspase-8 in the death-inducing signaling complex.	Bortezomib	0-10	caspase 8	Homo sapiens	101-110
20219915-4	2010	Employing viruses with mutations in UL36, the gene that encodes the viral inhibitor of caspase-8 activation (vICA), our data indicate that both caspase-dependent and -independent death pathways are activated in response to infection.	vica	109-113	caspase 8	Homo sapiens	87-96
20219915-8	2010	Early in differentiation, vICA-deficient virus-induced cell death was dependent on caspases and inhibited by the pan-caspase inhibitor z-VAD(OMe)-fluoromethyl ketone.	vica	26-30	caspase 8	Homo sapiens	83-91
20442297-8	2010	These data suggest that the molecular basis for bortezomib sensitization of RCC to TRAIL primarily involves early amplification of caspase-8 activity.	Bortezomib	48-58	caspase 8	Homo sapiens	131-140
20372860-7	2010	Z-VAD-FMK treatment inhibited, but did not abolish, LVEP-induced apoptosis, indicating that caspases other than caspase-3 participate in this pathway.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	0-9	caspase 8	Homo sapiens	92-100
20096282-7	2010	Combination of carboplatin and Akt inhibitor-induced cell viability loss was reduced by selective inhibitors of caspase-8, -9 and -3.	Carboplatin	15-26	caspase 8	Homo sapiens	112-132
20033885-5	2010	Recent work in breast carcinoma has implicated the histidine variant of CASP8 D302H (rs1045485) as a protective risk allele.	Histidine	51-60	caspase 8	Homo sapiens	72-77
20033885-10	2010	CONCLUSION: These results suggest that histidine variant of CASP8 D302H is a protective allele for aggressive PCa with potential utility for identification of patients at differential risk for this clinically significant phenotype.	Histidine	39-48	caspase 8	Homo sapiens	60-65
20096282-8	2010	The results suggest that Akt inhibitor may enhance a carboplatin toxicity against ovarian carcinoma cell lines by increasing activation of the caspase-8 and Bid pathway as well as activation of the mitochondria-mediated apoptotic pathway, leading to mitochondrial cytochrome c release and subsequent caspase-3 activation.	Carboplatin	53-64	caspase 8	Homo sapiens	143-152
20416058-0	2010	Doxorubicin and etoposide sensitize small cell lung carcinoma cells expressing caspase-8 to TRAIL.	Doxorubicin	0-11	caspase 8	Homo sapiens	79-88
20416058-4	2010	RESULTS: We demonstrated that doxorubicin and etoposide markedly sensitized SCLC cells expressing caspase-8 to apoptotic effects of TRAIL.	Etoposide	46-55	caspase 8	Homo sapiens	98-107
20421971-0	2010	Docosahexaenoic acid induces apoptosis in MCF-7 cells in vitro and in vivo via reactive oxygen species formation and caspase 8 activation.	Docosahexaenoic Acids	0-20	caspase 8	Homo sapiens	117-126
20416058-8	2010	CONCLUSIONS: Our results highlight significant applicability of doxorubicin and etoposide in sensitization of SCLC cells expressing caspase-8 to treatment with TRAIL.	Doxorubicin	64-75	caspase 8	Homo sapiens	132-141
20416058-0	2010	Doxorubicin and etoposide sensitize small cell lung carcinoma cells expressing caspase-8 to TRAIL.	Etoposide	16-25	caspase 8	Homo sapiens	79-88
20416058-8	2010	CONCLUSIONS: Our results highlight significant applicability of doxorubicin and etoposide in sensitization of SCLC cells expressing caspase-8 to treatment with TRAIL.	Etoposide	80-89	caspase 8	Homo sapiens	132-141
20421971-4	2010	Co-presence of antioxidants or selective inhibition or knockdown of caspase 8 each effectively abrogates the cytotoxic effect of DHA.	Docosahexaenoic Acids	129-132	caspase 8	Homo sapiens	68-77
20416058-4	2010	RESULTS: We demonstrated that doxorubicin and etoposide markedly sensitized SCLC cells expressing caspase-8 to apoptotic effects of TRAIL.	Doxorubicin	30-41	caspase 8	Homo sapiens	98-107
20348907-5	2010	We show that a deficiency in the adenomatous polyposis coli (APC) gene and subsequent activation of beta-catenin lead to the repression of cellular caspase-8 inhibitor c-FLIP (also known as CFLAR) expression through activation of c-Myc, and that all-trans-retinyl acetate (RAc) independently upregulates tumour necrosis factor-related apoptosis-inducing ligand (TRAIL) death receptors and suppresses decoy receptors.	retinol acetate	256-271	caspase 8	Homo sapiens	148-157
20110807-3	2010	Cucurbitacin E at high concentrations (1-10 mol/l) induced apoptosis of HL-60 cells and activation of caspase-3, caspase-8, and caspase-9.	cucurbitacin E	0-14	caspase 8	Homo sapiens	113-122
20154087-2	2010	As indicated by assays that measure plasma membrane integrity, phosphatidylserine exposure, mitochondrial activity, and activation of caspase-8, caspase-9, and caspase-3, celastrol potentiated the TRAIL-induced apoptosis in human breast cancer cells, and converted TRAIL-resistant cells to TRAIL-sensitive cells.	celastrol	171-180	caspase 8	Homo sapiens	134-143
20227390-5	2010	Pretreatment with rosiglitazone also suppressed radiation-induced H2AX phosphorylation in response to DNA damage and AKT activation for cell survival; on the contrary, rosiglitazone pretreatment enhanced radiation-induced caspase-8, -9, and -3 activation and PARP cleavage in HT-29 cells.	Rosiglitazone	168-181	caspase 8	Homo sapiens	222-243
20110807-4	2010	Jurkat leukemia cells with or without caspase-8 expression were nearly equally sensitive to cucurbitacin E-induced apoptosis.	cucurbitacin E	92-106	caspase 8	Homo sapiens	38-47
20045058-4	2010	The predicted amino acid sequence of abCaspase contained two domains of p20 and p10 which were conserved in the caspase family, including the cysteine active site pentapeptide "QSCRG" and the histidine active site signature "HTVYDCVVVIFLTHG".	Cysteine	142-150	caspase 8	Homo sapiens	112-119
19779494-3	2010	The SMS inhibition elicited by FasL (1) was abrogated by benzyloxycarbonyl valyl-alanyl-aspartyl-(O-methyl)-fluoromethylketone (zVAD-fmk), a broad-spectrum caspase inhibitor; (2) did not occur in caspase-8-deficient cells and (3) was not affected in caspase-9-deficient cells.	valyl-alanyl	75-87	caspase 8	Homo sapiens	196-205
19779494-3	2010	The SMS inhibition elicited by FasL (1) was abrogated by benzyloxycarbonyl valyl-alanyl-aspartyl-(O-methyl)-fluoromethylketone (zVAD-fmk), a broad-spectrum caspase inhibitor; (2) did not occur in caspase-8-deficient cells and (3) was not affected in caspase-9-deficient cells.	-(o-methyl)-fluoromethylketone	96-126	caspase 8	Homo sapiens	196-205
20198319-8	2010	Specific caspase inhibitor blocking studies reveal that the caspase-8/-3 cascade pathway plays a key role in apoptosis of LNCaP cells induced by Ppa-conjugate 2.1.	ppa	145-148	caspase 8	Homo sapiens	60-69
19728331-0	2010	Ursodeoxycholic acid switches oxaliplatin-induced necrosis to apoptosis by inhibiting reactive oxygen species production and activating p53-caspase 8 pathway in HepG2 hepatocellular carcinoma.	Ursodeoxycholic Acid	0-20	caspase 8	Homo sapiens	140-149
19728331-0	2010	Ursodeoxycholic acid switches oxaliplatin-induced necrosis to apoptosis by inhibiting reactive oxygen species production and activating p53-caspase 8 pathway in HepG2 hepatocellular carcinoma.	Oxaliplatin	30-41	caspase 8	Homo sapiens	140-149
19728331-10	2010	In conclusion, UDCA switches oxaliplatin-induced necrosis to apoptosis via inhibition of ROS production and activation of the p53-caspase 8 pathway in HepG2 cells.	Oxaliplatin	29-40	caspase 8	Homo sapiens	130-139
20146252-5	2010	Both extrinsic and intrinsic apoptotic pathways appear to be triggered by UA treatment, because inhibiting activation of both caspase-8 and -9 could prevent UA-induced apoptosis in PC-3 cells.	ursolic acid	74-76	caspase 8	Homo sapiens	126-142
20146252-5	2010	Both extrinsic and intrinsic apoptotic pathways appear to be triggered by UA treatment, because inhibiting activation of both caspase-8 and -9 could prevent UA-induced apoptosis in PC-3 cells.	ursolic acid	157-159	caspase 8	Homo sapiens	126-142
20146252-8	2010	Importantly, experimentally lowering FasL expression by siRNA significantly inhibited UA-induced caspase-8 activation and at least partly attenuated the consequent apoptosis, suggesting an involvement of FasL and its regulating pathway in the cell killing effect of UA.	ursolic acid	86-88	caspase 8	Homo sapiens	97-106
20146252-8	2010	Importantly, experimentally lowering FasL expression by siRNA significantly inhibited UA-induced caspase-8 activation and at least partly attenuated the consequent apoptosis, suggesting an involvement of FasL and its regulating pathway in the cell killing effect of UA.	ursolic acid	266-268	caspase 8	Homo sapiens	97-106
19784869-5	2010	Pretreatment of a caspase-8 inhibitor (Z-IETD-FMK), caspase-9 inhibitor (Z-LEHD-FMK) and caspase-3 inhibitor (Z-DEVE-FMK) significantly increased the viable of GBM 8401 cells implied that the participations of caspases.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	39-49	caspase 8	Homo sapiens	18-27
20204304-0	2010	Propyl gallate inhibits the growth of HeLa cells via caspase-dependent apoptosis as well as a G1 phase arrest of the cell cycle.	Propyl Gallate	0-14	caspase 8	Homo sapiens	53-60
20204304-4	2010	In addition, PG induced apoptosis, which was accompanied by the loss of mitochondrial membrane potential (MMP; DeltaPsim), activation of caspase-3 and caspase-8 and PARP cleavage.	Propyl Gallate	13-15	caspase 8	Homo sapiens	151-160
20204304-5	2010	All the tested caspase inhibitors (pan-caspase, caspase-3, -8 or -9 inhibitor) significantly rescued HeLa cells from PG-induced cell death.	Propyl Gallate	117-119	caspase 8	Homo sapiens	15-22
20204304-7	2010	In conclusion, PG inhibited the growth of HeLa cells via caspase-dependent apoptosis as well as a G1 phase arrest of the cell cycle.	Propyl Gallate	15-17	caspase 8	Homo sapiens	57-64
20138029-6	2010	The results indicate that the cytotoxic 5-methoxy-1,4-naphthoquinone activates caspases 8 and 3/7 and thus induces apoptosis independent of mitochondria.	1,4-Naphthalenedione, 5-methoxy-	40-68	caspase 8	Homo sapiens	79-95
20393600-8	2010	Acrolein caused activation of caspase-8, caspase-2, caspase-7, and the cross-talk pathway mediated by Bid cleavage.	Acrolein	0-8	caspase 8	Homo sapiens	30-39
20393600-10	2010	FasL upregulation and caspase-8 activation were decreased by p53 inhibitor pifithrin-alpha and antioxidant polyethylene glycol catalase.	pifithrin	75-90	caspase 8	Homo sapiens	22-31
20060030-0	2010	Indole-3-carbinol induces apoptosis through p53 and activation of caspase-8 pathway in lung cancer A549 cells.	indole-3-carbinol	0-17	caspase 8	Homo sapiens	66-75
20060030-8	2010	The inhibition of caspase-8 by z-IETD-FMK significantly decreased cleavage of procaspase-8,-3 and PARP in I3C-treated A549 cells.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	31-41	caspase 8	Homo sapiens	18-27
19813266-10	2010	Genistein triggered the receptor-mediated apoptotic pathway through upregulation of TNF-alpha, FasL, TRADD, and FADD and activation of caspase-8.	Genistein	0-9	caspase 8	Homo sapiens	135-144
20005942-7	2010	Besides Huh7 cell, OA or UA treatments concentration-dependently elevated caspase-3 and caspase-8 activities in other three cell lines (P&lt;0.05).	ursolic acid	25-27	caspase 8	Homo sapiens	88-97
20179203-6	2010	Detailed analysis of the underlying molecular mechanism revealed that bortezomib treatment induced mitochondrial accumulation of NOXA, which potentiated the release of mitochondrial second mitochondria-derived activator of caspase (SMAC) in response to CTL effector functions, including caspase-8 and granzyme B.	Bortezomib	70-80	caspase 8	Homo sapiens	287-296
19927299-5	2010	Increases in Fas/FasL protein expression, caspase-8 activation, the production of tBid and the loss of mitochondrial membrane potential were noted with K562 cells that were treated with a combination of U0126 and AA.	U 0126	203-208	caspase 8	Homo sapiens	42-51
19784869-5	2010	Pretreatment of a caspase-8 inhibitor (Z-IETD-FMK), caspase-9 inhibitor (Z-LEHD-FMK) and caspase-3 inhibitor (Z-DEVE-FMK) significantly increased the viable of GBM 8401 cells implied that the participations of caspases.	z-deve-fmk	110-120	caspase 8	Homo sapiens	210-218
20127023-7	2010	In addition to the cell cycle arrest, KBH-A42 also induced apoptosis in these cells, which was accompanied by the activation of caspases, including caspase-9, caspase-8 and caspase-3.	KBH A42	38-45	caspase 8	Homo sapiens	128-136
20128807-6	2010	SZ-685C had a direct apoptosis-inducing effect through both the extrinsic and intrinsic apoptotic pathways, as shown by activation of caspase-8 and 9 as well as effector caspase-3 and poly (ADP-ribose) polymerase.	SZ 685C	0-7	caspase 8	Homo sapiens	134-143
20127023-7	2010	In addition to the cell cycle arrest, KBH-A42 also induced apoptosis in these cells, which was accompanied by the activation of caspases, including caspase-9, caspase-8 and caspase-3.	KBH A42	38-45	caspase 8	Homo sapiens	159-168
20127023-8	2010	The pan-caspase inhibitor, Z-VAD-fmk, partially blocked the cell death induced by KBH-A42.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	27-36	caspase 8	Homo sapiens	8-15
20127023-8	2010	The pan-caspase inhibitor, Z-VAD-fmk, partially blocked the cell death induced by KBH-A42.	KBH A42	82-89	caspase 8	Homo sapiens	8-15
20127023-9	2010	These results indicate that KBH-A42 induces cell cycle arrest and apoptosis via the up-regulation of p21WAF1 and caspase activation, respectively, regardless of the presence of P-gp in the leukemia cells.	KBH A42	28-35	caspase 8	Homo sapiens	113-120
19751707-8	2010	The incubation of MOLT-3 cells with mahanine in the presence of caspase-8 inhibitor or FasL-neutralizing NOK-2 antibody resulted in the decrease of mahanine-induced cell death.	mahanine	36-44	caspase 8	Homo sapiens	64-73
19751707-8	2010	The incubation of MOLT-3 cells with mahanine in the presence of caspase-8 inhibitor or FasL-neutralizing NOK-2 antibody resulted in the decrease of mahanine-induced cell death.	mahanine	148-156	caspase 8	Homo sapiens	64-73
20025279-6	2010	Western blot data revealed that EEAP stimulated an increase in the level of protein expression of Fas, FasL, caspase-8, and tBid.	eeap	32-36	caspase 8	Homo sapiens	109-118
20132554-5	2010	Demethylation agent 5-aza-2"-deoxycytidine (5-aza-dc) selectively inhibits DNA methyltransferases, DNMT3a and DNMT3b, and restored CASP8 and maspin gene expression in breast cancer cells.	Decitabine	20-42	caspase 8	Homo sapiens	131-136
20132554-5	2010	Demethylation agent 5-aza-2"-deoxycytidine (5-aza-dc) selectively inhibits DNA methyltransferases, DNMT3a and DNMT3b, and restored CASP8 and maspin gene expression in breast cancer cells.	Decitabine	44-52	caspase 8	Homo sapiens	131-136
20132554-6	2010	5-aza-dc also reduced histone H3k9me2 occupancy on CASP8 promoter in SKBR3cells, but not in MCF-7 cells.	Decitabine	0-8	caspase 8	Homo sapiens	51-56
20132554-8	2010	CASP8 mRNA and protein level in MCF-7 cells were increased by the 5-aza-dc in combination with TSA.	Azacitidine	66-71	caspase 8	Homo sapiens	0-5
20132554-8	2010	CASP8 mRNA and protein level in MCF-7 cells were increased by the 5-aza-dc in combination with TSA.	trichostatin A	95-98	caspase 8	Homo sapiens	0-5
20132554-9	2010	Data from our study also demonstrated that treatment with 5-FU caused a significant increase in unmethylated CASP8 and in CASP8 mRNA in all 3 cancer lines.	Fluorouracil	58-62	caspase 8	Homo sapiens	109-114
20132554-9	2010	Data from our study also demonstrated that treatment with 5-FU caused a significant increase in unmethylated CASP8 and in CASP8 mRNA in all 3 cancer lines.	Fluorouracil	58-62	caspase 8	Homo sapiens	122-127
19969555-7	2010	Overexpression of either constitutively active myristylated-Akt (Myr-Akt) or Dn-caspase-8 partially blocked theaflavin-induced mitochondrial permeability transition and apoptosis of p53-mutated cells, whereas cotransfection of Myr-Akt and Dn-caspase-8 completely abolished theaflavin effect thereby negating the possibility of existence of third pathways.	theaflavin	273-283	caspase 8	Homo sapiens	80-89
20086182-6	2010	Furthermore, the number of the CASP8 -652 6N del (but not 302H) variant allele tended to correlate with increased levels of camptothecin-induced p53-mediated apoptosis in T lymphocytes from 170 cancer-free controls.	Camptothecin	124-136	caspase 8	Homo sapiens	31-36
19874821-5	2010	Caspase-8 activity induced by exposure to UV-B at 150 mJ/cm(2) was significantly reduced when the cells were incubated in 0.3 microM BDS-I or 0.05-1 mM quinidine.	Quinidine	152-161	caspase 8	Homo sapiens	0-9
19969555-0	2010	Theaflavins target Fas/caspase-8 and Akt/pBad pathways to induce apoptosis in p53-mutated human breast cancer cells.	theaflavin	0-11	caspase 8	Homo sapiens	23-32
19969555-4	2010	Further studies demonstrated theaflavin-induced Fas upregulation through the activation of c-jun N-terminal kinase, Fas-FADD interaction in a Fas ligand-independent manner, caspase-8 activation and t-Bid formation.	theaflavin	29-39	caspase 8	Homo sapiens	173-182
19969555-7	2010	Overexpression of either constitutively active myristylated-Akt (Myr-Akt) or Dn-caspase-8 partially blocked theaflavin-induced mitochondrial permeability transition and apoptosis of p53-mutated cells, whereas cotransfection of Myr-Akt and Dn-caspase-8 completely abolished theaflavin effect thereby negating the possibility of existence of third pathways.	theaflavin	108-118	caspase 8	Homo sapiens	80-89
19969555-7	2010	Overexpression of either constitutively active myristylated-Akt (Myr-Akt) or Dn-caspase-8 partially blocked theaflavin-induced mitochondrial permeability transition and apoptosis of p53-mutated cells, whereas cotransfection of Myr-Akt and Dn-caspase-8 completely abolished theaflavin effect thereby negating the possibility of existence of third pathways.	theaflavin	108-118	caspase 8	Homo sapiens	242-251
20080300-8	2010	Specific caspase 8 inhibitions with specific peptide inhibitors or antisense oligonucleotides or silencing with siRNA substantiate potential differentiation-related roles, unrelated to initiation of intercellular fusion, for both procaspase 8 and activated caspase 8.	Oligonucleotides	77-93	caspase 8	Homo sapiens	9-18
19142583-8	2010	Activation of caspase 8 and lack of cleavage of caspase 9, caspase 3 and PARP suggest the possibility of BPSQ triggering extrinsic pathway for induction of apoptosis, which is discussed.	bpsq	105-109	caspase 8	Homo sapiens	14-23
19966593-7	2010	In the presence of Cu, DSF caused activation of the extrinsic pathway of apoptosis as measured by caspase-8 cleavage.	Copper	19-21	caspase 8	Homo sapiens	98-107
19966593-8	2010	The addition of Z-IETD-FMK, a selective caspase-8 inhibitor, was protective against DSF-Cu-induced apoptosis.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	16-26	caspase 8	Homo sapiens	40-49
19966593-8	2010	The addition of Z-IETD-FMK, a selective caspase-8 inhibitor, was protective against DSF-Cu-induced apoptosis.	dsf-cu	84-90	caspase 8	Homo sapiens	40-49
19949310-7	2010	Jurkat cells without expression of caspase-8 were not sensitive to CDODO-Me-12, but were somewhat responsive to CDODO-Me-11.	methyl 2-cyano-3,11-dioxooleana-1,12-dien-30-oate	112-123	caspase 8	Homo sapiens	35-44
20522977-4	2010	In addition, the activations of caspase-8, -9, and -3 were significantly increased 36 h after donepezil treatment.	Donepezil	94-103	caspase 8	Homo sapiens	32-53
20823585-3	2010	In addition, IPA induced the activations of caspase-8, -9, -3, and cleavage of poly(ADP ribose) polymerase (PARP-1) in HeLa cells.	ipa	13-16	caspase 8	Homo sapiens	44-53
20823585-4	2010	Pretreatment with a specific caspase-8, -9, or -3 inhibitor neutralized the pro-apoptotic activity of IPA in HeLa cells.	ipa	102-105	caspase 8	Homo sapiens	29-38
19949310-4	2010	CDODO-Me-12 was 10-fold more effective than CDODO-Me-11 in inducing apoptosis which was correlated with the activation of caspase-8 and caspase-9.	methyl 2-cyano-3,12-dioxooleana-1, 12-dien-30-oate	0-11	caspase 8	Homo sapiens	122-131
19965674-5	2010	Furthermore, studies using biochemical inhibitors of caspase-8 versus caspase-9 demonstrate that NPI-0052 plus lenalidomide-triggered apoptosis is primarily dependent on caspase-8 signaling.	Lenalidomide	111-123	caspase 8	Homo sapiens	53-62
19965674-5	2010	Furthermore, studies using biochemical inhibitors of caspase-8 versus caspase-9 demonstrate that NPI-0052 plus lenalidomide-triggered apoptosis is primarily dependent on caspase-8 signaling.	Lenalidomide	111-123	caspase 8	Homo sapiens	170-179
20005201-0	2010	Nitric oxide and thioredoxin type 1 modulate the activity of caspase 8 in HepG2 cells.	Nitric Oxide	0-12	caspase 8	Homo sapiens	61-70
20005201-1	2010	Herein, we report that nitric oxide (NO) and the thioredoxin/thioredoxin reductase system affect the activity of caspase 8 in HepG2 cells.	Nitric Oxide	23-35	caspase 8	Homo sapiens	113-122
20005201-3	2010	The latter process was inhibited in thioredoxin reductase-deficient HepG2 cells, in which, however, lipoic acid markedly reactivated caspase 8.	Thioctic Acid	100-111	caspase 8	Homo sapiens	133-142
19894226-11	2010	(-)-Epigallocatechin and EGCG also induced caspase-8 activity.	gallocatechol	0-20	caspase 8	Homo sapiens	43-52
19894226-11	2010	(-)-Epigallocatechin and EGCG also induced caspase-8 activity.	epigallocatechin gallate	25-29	caspase 8	Homo sapiens	43-52
19949310-4	2010	CDODO-Me-12 was 10-fold more effective than CDODO-Me-11 in inducing apoptosis which was correlated with the activation of caspase-8 and caspase-9.	methyl 2-cyano-3,11-dioxooleana-1,12-dien-30-oate	44-55	caspase 8	Homo sapiens	122-131
20847396-5	2010	Caspase-8, acting upstream of caspase-3, was found to mediate the synaptotoxic actions of Abeta in an ifenprodil-reversible fashion.	ifenprodil	102-112	caspase 8	Homo sapiens	0-9
20145726-0	2010	PCI-24781, a Novel Hydroxamic Acid HDAC Inhibitor, Exerts Cytotoxicity and Histone Alterations via Caspase-8 and FADD in Leukemia Cells.	abexinostat	0-9	caspase 8	Homo sapiens	99-108
20145726-2	2010	In the present study, we show that apoptosis induction and histone alterations by PCI-24781, a novel hydroxamic acid-based HDAC inhibitor, require caspase-8 and the adaptor molecule, Fas-associated death domain (FADD), in acute leukemia cells.	abexinostat	82-91	caspase 8	Homo sapiens	147-156
19918833-1	2010	The synthesis, enzymatic evaluation, and molecular modeling studies of new fluorogenic tetrapeptide-based substrates selective for caspase 8, having the general structure Ac-IETD-AXX, are described.	ac-ietd-axx	171-182	caspase 8	Homo sapiens	131-140
19918833-3	2010	They were subsequently coupled with the caspase-8-selective tetrapeptide Ac-IETD-OH under newly developed synthetic conditions to give the desired substrates in good yields and in high enantiomeric purity.	ac-ietd-oh	73-83	caspase 8	Homo sapiens	40-49
19918833-6	2010	Molecular modeling studies based on the X-ray crystal structures of both human caspases 3 and 8 revealed that there is sufficient room within both active sites to accommodate substrates with moderately bulky substituents in the 3- and 4-positions of the fluorogenic coumarins and quinolin-2(1H)-ones.	Coumarins	266-275	caspase 8	Homo sapiens	79-87
19918833-6	2010	Molecular modeling studies based on the X-ray crystal structures of both human caspases 3 and 8 revealed that there is sufficient room within both active sites to accommodate substrates with moderately bulky substituents in the 3- and 4-positions of the fluorogenic coumarins and quinolin-2(1H)-ones.	quinolin-2	280-290	caspase 8	Homo sapiens	79-87
19918833-6	2010	Molecular modeling studies based on the X-ray crystal structures of both human caspases 3 and 8 revealed that there is sufficient room within both active sites to accommodate substrates with moderately bulky substituents in the 3- and 4-positions of the fluorogenic coumarins and quinolin-2(1H)-ones.	Hydrogen	291-293	caspase 8	Homo sapiens	79-87
20001229-4	2010	Among them, DMPH had the highest antileukemic activity and induced apoptosis via caspase-8, caspase-3, and caspase-9 activation.	N,N-dimethylphytosphingosine	12-16	caspase 8	Homo sapiens	81-90
20053768-3	2010	Previously, the small-molecule 4-(4-chloro-2-methylphenoxy)-N-hydroxybutanamide (that we propose be named droxinostat) was identified as a chemical sensitizer to death receptor stimuli, decreasing the expression of the caspase-8 inhibitor FLIP.	4-(4-chloro-2-methylphenoxy)-N-hydroxybutanamide	31-79	caspase 8	Homo sapiens	219-228
20053768-3	2010	Previously, the small-molecule 4-(4-chloro-2-methylphenoxy)-N-hydroxybutanamide (that we propose be named droxinostat) was identified as a chemical sensitizer to death receptor stimuli, decreasing the expression of the caspase-8 inhibitor FLIP.	4-(4-chloro-2-methylphenoxy)-N-hydroxybutanamide	106-117	caspase 8	Homo sapiens	219-228
20358476-6	2010	Caspase-3, caspase-8, and caspase-9 were activated, and cytochrome c and apoptosis-inducing factor (AIF) were released from mitochondria following curcumin treatment.	Curcumin	147-155	caspase 8	Homo sapiens	11-20
19833726-7	2009	Furthermore, E64D and leupeptin, which are able to function as inhibitors of autophagic degradation, reversed the effect of caspase-8 inhibitors in the M2-macrophage polarization, indicating a role of autophagy in this mechanism.	leupeptin	22-31	caspase 8	Homo sapiens	124-133
20661831-7	2010	Caspase-8 inhibition abrogated Bid cleavage and strongly reduced caspase-9 activation, suggesting that the cross-talk mechanism mediated by caspase-8-dependent Bid cleavage can contribute to the activation of the intrinsic apoptotic pathway by curcumin + carnosic acid.	salvin	255-268	caspase 8	Homo sapiens	0-9
20661831-7	2010	Caspase-8 inhibition abrogated Bid cleavage and strongly reduced caspase-9 activation, suggesting that the cross-talk mechanism mediated by caspase-8-dependent Bid cleavage can contribute to the activation of the intrinsic apoptotic pathway by curcumin + carnosic acid.	salvin	255-268	caspase 8	Homo sapiens	140-149
20110767-7	2010	Chitosan 1130 and chitosan oligosaccharide induced apoptotic cell death which was mediated by activation of the effector caspases 3/7.	chitosan 1130	0-13	caspase 8	Homo sapiens	121-129
20110767-7	2010	Chitosan 1130 and chitosan oligosaccharide induced apoptotic cell death which was mediated by activation of the effector caspases 3/7.	D-Glucosaminide	18-42	caspase 8	Homo sapiens	121-129
20046832-5	2009	In the lipid rafts, Fas interacts with Fas-associated death domain (FADD) and Caspase-8 to form death-inducing signaling complex (DISC) and thus mediates cell apoptosis.	ammonium ferrous sulfate	20-23	caspase 8	Homo sapiens	78-87
19852930-0	2009	Association of caspase-8 mutation with chemoresistance to cisplatin in HOC313 head and neck squamous cell carcinoma cells.	Cisplatin	58-67	caspase 8	Homo sapiens	15-24
19852930-5	2009	Reconstitution of caspase-8 by stable transfection of wild-type caspase-8 sensitized the cells to cisplatin-, but not etoposide-induced apoptosis.	Cisplatin	98-107	caspase 8	Homo sapiens	18-27
19852930-5	2009	Reconstitution of caspase-8 by stable transfection of wild-type caspase-8 sensitized the cells to cisplatin-, but not etoposide-induced apoptosis.	Cisplatin	98-107	caspase 8	Homo sapiens	64-73
19852930-6	2009	Consistent with this, cisplatin, but not etoposide, induced TNF-alpha and TRAIL mRNA in caspase-8 reconstituted HOC313 cells, accompanied by activation of the reconstituted caspase-8 and its downstream caspase-3.	Cisplatin	22-31	caspase 8	Homo sapiens	88-97
19852930-6	2009	Consistent with this, cisplatin, but not etoposide, induced TNF-alpha and TRAIL mRNA in caspase-8 reconstituted HOC313 cells, accompanied by activation of the reconstituted caspase-8 and its downstream caspase-3.	Cisplatin	22-31	caspase 8	Homo sapiens	173-182
19852930-7	2009	These results indicate that the loss of caspase-8 plays an important role in acquisition of chemoresistance to cisplatin in HOC313 cells.	Cisplatin	111-120	caspase 8	Homo sapiens	40-49
20661831-5	2010	Early stage of curcumin/carnosic acid-induced apoptosis was associated with cleavage (activation) of caspase-8, caspase-9, and caspase-3 and the proapoptotic protein Bid, but not with oxidative stress or altered levels of other Bcl-2 family proteins (Bcl-2, Bcl-xl, Mcl-1, Bax, and Bak).	Curcumin	15-23	caspase 8	Homo sapiens	101-110
20661831-5	2010	Early stage of curcumin/carnosic acid-induced apoptosis was associated with cleavage (activation) of caspase-8, caspase-9, and caspase-3 and the proapoptotic protein Bid, but not with oxidative stress or altered levels of other Bcl-2 family proteins (Bcl-2, Bcl-xl, Mcl-1, Bax, and Bak).	salvin	24-37	caspase 8	Homo sapiens	101-110
20661831-7	2010	Caspase-8 inhibition abrogated Bid cleavage and strongly reduced caspase-9 activation, suggesting that the cross-talk mechanism mediated by caspase-8-dependent Bid cleavage can contribute to the activation of the intrinsic apoptotic pathway by curcumin + carnosic acid.	Curcumin	244-252	caspase 8	Homo sapiens	0-9
20661831-7	2010	Caspase-8 inhibition abrogated Bid cleavage and strongly reduced caspase-9 activation, suggesting that the cross-talk mechanism mediated by caspase-8-dependent Bid cleavage can contribute to the activation of the intrinsic apoptotic pathway by curcumin + carnosic acid.	Curcumin	244-252	caspase 8	Homo sapiens	140-149
20368033-2	2010	METHODS: Immunohistochemical technique with SP method was used to detect the expressions of caspase-8, RIP and NF-kappaBp65 in 30 OLP cases and 15 normal oral mucosa specimens.	TFF2 protein, human	44-46	caspase 8	Homo sapiens	92-101
19748591-3	2009	In addition, both extrinsic (caspase-8) and intrinsic pathway (caspase-9) could be implicated in the N-Nitrosamines-induced apoptosis.	n-nitrosamines	101-115	caspase 8	Homo sapiens	29-38
19777442-12	2009	The caspase-8 inhibitor IETD-FMK and the mitochondrial membrane permeabilization inhibitor bongkrekic acid (BK), partially prevented cell death by TNF + CHX.	isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	24-32	caspase 8	Homo sapiens	4-13
19928967-4	2009	The combinatory use of AE and 5-fluorouracil (5-Fu) achieved significantly more cell death in A431 and SCC25 cells than only the use of AE or 5-Fu, likely via regulation of caspase-8, -9, and -3 expressions.	Fluorouracil	30-44	caspase 8	Homo sapiens	173-194
19928967-4	2009	The combinatory use of AE and 5-fluorouracil (5-Fu) achieved significantly more cell death in A431 and SCC25 cells than only the use of AE or 5-Fu, likely via regulation of caspase-8, -9, and -3 expressions.	Fluorouracil	46-50	caspase 8	Homo sapiens	173-194
19797069-5	2009	Although caspase 8 and caspase 3 were activated by TcdA in OVCAR3 ovarian carcinoma and T84 colonic cancer cells, pancaspase and caspase 8, 3, and 9 inhibitors did not block TcdA-induced cell death.	tcda	51-55	caspase 8	Homo sapiens	9-18
20193270-1	2009	OBJECTIVE: To explore the potential mechanism of trichloroethylene (TCE)-induced apoptosis in normal human epidermis keratinocyte (NHEK) by assaying the Caspase activities, mitochondrial membrane potential (DeltaPsim) and apoptosis in vitro.	Trichloroethylene	68-71	caspase 8	Homo sapiens	153-160
20037825-13	2009	The activity of caspase-3 rather than caspase-8 was substantially enhanced in the EGCG group.	epigallocatechin gallate	82-86	caspase 8	Homo sapiens	38-47
19927172-5	2009	RESULTS: Treatment with Abeta(31-35) (25 micromol/L) for 24 h induced significant increases in the activities of caspase-3 and caspase-8 in the cortical neurons.	UNII-042A8N37WH	24-29	caspase 8	Homo sapiens	127-136
19906200-4	2009	Fas-induced apoptosis was dependent on the caspase-8 activation, since the overexpression of c-FLIP(long), a natural inhibitor of caspase-8 activation, blocked apoptosis induced by Fas.	ammonium ferrous sulfate	0-3	caspase 8	Homo sapiens	43-52
19906200-4	2009	Fas-induced apoptosis was dependent on the caspase-8 activation, since the overexpression of c-FLIP(long), a natural inhibitor of caspase-8 activation, blocked apoptosis induced by Fas.	ammonium ferrous sulfate	0-3	caspase 8	Homo sapiens	130-139
19906200-4	2009	Fas-induced apoptosis was dependent on the caspase-8 activation, since the overexpression of c-FLIP(long), a natural inhibitor of caspase-8 activation, blocked apoptosis induced by Fas.	ammonium ferrous sulfate	181-184	caspase 8	Homo sapiens	43-52
19906200-4	2009	Fas-induced apoptosis was dependent on the caspase-8 activation, since the overexpression of c-FLIP(long), a natural inhibitor of caspase-8 activation, blocked apoptosis induced by Fas.	ammonium ferrous sulfate	181-184	caspase 8	Homo sapiens	130-139
20030923-10	2009	GA could decrease the mitochondrial membrane potential and increase the activated caspase 3, caspase 8, caspase 9 positive cell levels by 2.19%, -1.95%, 34.01% in 24 hr and 60.4%, 71.3%, 77.7% in 48 hr respectively.	gambogic acid	0-2	caspase 8	Homo sapiens	93-102
20193325-4	2009	The effect of bortezomib and adriamycin on the expression levels of caspase-3, caspase-8 and PARP were measured by Nestern blot.	Bortezomib	14-24	caspase 8	Homo sapiens	79-88
20193325-4	2009	The effect of bortezomib and adriamycin on the expression levels of caspase-3, caspase-8 and PARP were measured by Nestern blot.	Doxorubicin	29-39	caspase 8	Homo sapiens	79-88
20193325-8	2009	After the Jurkat cells were treated with bortezomib, apparent shear bands of caspase-8, caspase-3 and PARP proteins were observed.	Bortezomib	41-51	caspase 8	Homo sapiens	77-86
20193270-4	2009	NHEK was pretreated with inhibitor of Caspase-3 or 9 to verify the activation of Caspases by TCE treatment.	Trichloroethylene	93-96	caspase 8	Homo sapiens	81-89
19728097-8	2009	The DG, CA1, CA3 and MA showed an increment of caspase-8 activity, which was reversed by PEG sTNFRI, except in the MA.	Polyethylene Glycols	89-92	caspase 8	Homo sapiens	47-56
19710364-5	2009	Mib1 was found to bind to cellular Fas-associated death domain (FADD)-like IL-1b converting enzyme (FLICE)-like inhibitory proteins (cFLIP-L and cFLIP-S), whereas only cFLIP-s can inhibit Mib1-induced cell death.	ammonium ferrous sulfate	35-38	caspase 8	Homo sapiens	100-105
19819288-10	2009	All of the caspase inhibitors (caspase-3, -8, -9 and pan-caspase inhibitor) markedly rescued the Calu-6 cells from FCCP-induced cell death.	Carbonyl Cyanide p-Trifluoromethoxyphenylhydrazone	115-119	caspase 8	Homo sapiens	11-18
19561399-0	2009	Alpha-tocopheryl succinate potentiates the paclitaxel-induced apoptosis through enforced caspase 8 activation in human H460 lung cancer cells.	alpha-Tocopherol	0-26	caspase 8	Homo sapiens	89-98
19446953-2	2009	Here we show that 4HPR induces apoptosis through increased level of ROS and activation of caspase-8, 9 and 3, and inhibits growth of several MM cell lines in a dose-dependent manner.	Fenretinide	18-22	caspase 8	Homo sapiens	90-108
19457606-0	2009	Corosolic acid induces apoptosis through mitochondrial pathway and caspase activation in human cervix adenocarcinoma HeLa cells.	corosolic acid	0-14	caspase 8	Homo sapiens	67-74
19457606-5	2009	Moreover, CRA treatment triggered the activation of caspase-8, -9 and -3 in HeLa cells.	corosolic acid	10-13	caspase 8	Homo sapiens	52-72
19506904-8	2009	Suppression of caspase-8 resulted in reduced FR901228-activated caspase-9 and -3/7.	romidepsin	45-53	caspase 8	Homo sapiens	15-24
19415457-0	2009	Human beta-galactoside alpha-2,3-sialyltransferase (ST3Gal III) attenuated Taxol-induced apoptosis in ovarian cancer cells by downregulating caspase-8 activity.	Paclitaxel	75-80	caspase 8	Homo sapiens	141-150
19415457-2	2009	In this report, we found that Taxol treatment resulted in caspase-8-dependent apoptosis in SKOV3 human ovarian cancer cells.	Paclitaxel	30-35	caspase 8	Homo sapiens	58-67
19415457-5	2009	Furthermore, ST3Gal III overexpression inhibited Taxol-triggered caspase-8 activation, indicating that ST3Gal III upregulation produces cellular resistance to Taxol and hence reduces the efficacy of Taxol therapy.	Paclitaxel	49-54	caspase 8	Homo sapiens	65-74
19415457-5	2009	Furthermore, ST3Gal III overexpression inhibited Taxol-triggered caspase-8 activation, indicating that ST3Gal III upregulation produces cellular resistance to Taxol and hence reduces the efficacy of Taxol therapy.	Paclitaxel	159-164	caspase 8	Homo sapiens	65-74
19415457-5	2009	Furthermore, ST3Gal III overexpression inhibited Taxol-triggered caspase-8 activation, indicating that ST3Gal III upregulation produces cellular resistance to Taxol and hence reduces the efficacy of Taxol therapy.	Paclitaxel	159-164	caspase 8	Homo sapiens	65-74
19887560-8	2009	LD(50) treatment of medulloblastoma cells with perifosine led to the cleavage of caspase 9, caspase 7, caspase 3, and poly-ADP ribosylation protein, although caspase 8 was not detectable.	perifosine	47-57	caspase 8	Homo sapiens	158-167
19826055-8	2009	Pharmacologic inhibition and small interfering RNA knockdown of caspase-8 significantly inhibited PBOX-15-induced apoptosis.	PBOX-15	98-105	caspase 8	Homo sapiens	64-73
19473188-0	2009	Sulphasalazine accelerates apoptosis in neutrophils exposed to immune complex: Role of caspase pathway.	Sulfasalazine	0-14	caspase 8	Homo sapiens	87-94
19473188-13	2009	Treatment of neutrophils with 20 micromol/L of the caspase 8 or 9 inhibitors Z-IETD-fmk or Z-LEHD-fmk, respectively, demonstrated that the SSZ-induced pro-apoptotic effect was mediated by a caspase 8- but not caspase 9-dependent pathway.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	77-87	caspase 8	Homo sapiens	51-60
19473188-13	2009	Treatment of neutrophils with 20 micromol/L of the caspase 8 or 9 inhibitors Z-IETD-fmk or Z-LEHD-fmk, respectively, demonstrated that the SSZ-induced pro-apoptotic effect was mediated by a caspase 8- but not caspase 9-dependent pathway.	benzyloxycarbonyl-leucyl-glutamyl-histidyl-aspartic acid fluoromethyl ketone	91-101	caspase 8	Homo sapiens	51-60
19473188-13	2009	Treatment of neutrophils with 20 micromol/L of the caspase 8 or 9 inhibitors Z-IETD-fmk or Z-LEHD-fmk, respectively, demonstrated that the SSZ-induced pro-apoptotic effect was mediated by a caspase 8- but not caspase 9-dependent pathway.	Sulfasalazine	139-142	caspase 8	Homo sapiens	51-60
19473188-13	2009	Treatment of neutrophils with 20 micromol/L of the caspase 8 or 9 inhibitors Z-IETD-fmk or Z-LEHD-fmk, respectively, demonstrated that the SSZ-induced pro-apoptotic effect was mediated by a caspase 8- but not caspase 9-dependent pathway.	Sulfasalazine	139-142	caspase 8	Homo sapiens	190-199
19523746-2	2009	Specifically, treatment with the selective caspase 3 inhibitor DEVD-fmk or the selective caspase 8 inhibitor IETD-fmk in growth media (GM), prior to culture in differentiation media (DM), inhibited differentiation.	isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	109-117	caspase 8	Homo sapiens	89-98
19713356-5	2009	Expression of a Bid mutant in which caspase-8 cleavage site was mutated (D59A) reactivated oxaliplatin-induced apoptosis in Bid-deficient cells but failed to reactivate death receptor-induced apoptosis, suggesting that caspase-8-mediated Bid cleavage did not contribute to oxaliplatin-induced apoptosis.	Oxaliplatin	91-102	caspase 8	Homo sapiens	36-45
19695221-8	2009	Western blotting revealed that combination therapy downregulated angiogenic factors and also induced extrinsic pathway of apoptosis with activation of caspase-8 for Bid cleavage to tBid.	tBID	181-185	caspase 8	Homo sapiens	151-160
19561399-0	2009	Alpha-tocopheryl succinate potentiates the paclitaxel-induced apoptosis through enforced caspase 8 activation in human H460 lung cancer cells.	Paclitaxel	43-53	caspase 8	Homo sapiens	89-98
19561399-5	2009	Pretreatment with z-VAD-FMK (a pan-caspase inhibitor) or z-IETD-FMK (a caspase-8 inhibitor) blocked TOS/paclitaxel cotreatment-induced PARP cleavage and apoptosis, suggesting that TOS potentiates the paclitaxel-induced apoptosis through enforced caspase 8 activation in H460 cells.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	18-27	caspase 8	Homo sapiens	71-80
19561399-5	2009	Pretreatment with z-VAD-FMK (a pan-caspase inhibitor) or z-IETD-FMK (a caspase-8 inhibitor) blocked TOS/paclitaxel cotreatment-induced PARP cleavage and apoptosis, suggesting that TOS potentiates the paclitaxel-induced apoptosis through enforced caspase 8 activation in H460 cells.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	18-27	caspase 8	Homo sapiens	246-255
19561399-5	2009	Pretreatment with z-VAD-FMK (a pan-caspase inhibitor) or z-IETD-FMK (a caspase-8 inhibitor) blocked TOS/paclitaxel cotreatment-induced PARP cleavage and apoptosis, suggesting that TOS potentiates the paclitaxel-induced apoptosis through enforced caspase 8 activation in H460 cells.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	57-67	caspase 8	Homo sapiens	71-80
19561399-5	2009	Pretreatment with z-VAD-FMK (a pan-caspase inhibitor) or z-IETD-FMK (a caspase-8 inhibitor) blocked TOS/paclitaxel cotreatment-induced PARP cleavage and apoptosis, suggesting that TOS potentiates the paclitaxel-induced apoptosis through enforced caspase 8 activation in H460 cells.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	57-67	caspase 8	Homo sapiens	246-255
19561399-5	2009	Pretreatment with z-VAD-FMK (a pan-caspase inhibitor) or z-IETD-FMK (a caspase-8 inhibitor) blocked TOS/paclitaxel cotreatment-induced PARP cleavage and apoptosis, suggesting that TOS potentiates the paclitaxel-induced apoptosis through enforced caspase 8 activation in H460 cells.	tos	100-103	caspase 8	Homo sapiens	71-80
19561399-5	2009	Pretreatment with z-VAD-FMK (a pan-caspase inhibitor) or z-IETD-FMK (a caspase-8 inhibitor) blocked TOS/paclitaxel cotreatment-induced PARP cleavage and apoptosis, suggesting that TOS potentiates the paclitaxel-induced apoptosis through enforced caspase 8 activation in H460 cells.	tos	100-103	caspase 8	Homo sapiens	246-255
19561399-5	2009	Pretreatment with z-VAD-FMK (a pan-caspase inhibitor) or z-IETD-FMK (a caspase-8 inhibitor) blocked TOS/paclitaxel cotreatment-induced PARP cleavage and apoptosis, suggesting that TOS potentiates the paclitaxel-induced apoptosis through enforced caspase 8 activation in H460 cells.	Paclitaxel	104-114	caspase 8	Homo sapiens	71-80
19561399-5	2009	Pretreatment with z-VAD-FMK (a pan-caspase inhibitor) or z-IETD-FMK (a caspase-8 inhibitor) blocked TOS/paclitaxel cotreatment-induced PARP cleavage and apoptosis, suggesting that TOS potentiates the paclitaxel-induced apoptosis through enforced caspase 8 activation in H460 cells.	Paclitaxel	104-114	caspase 8	Homo sapiens	246-255
19561399-5	2009	Pretreatment with z-VAD-FMK (a pan-caspase inhibitor) or z-IETD-FMK (a caspase-8 inhibitor) blocked TOS/paclitaxel cotreatment-induced PARP cleavage and apoptosis, suggesting that TOS potentiates the paclitaxel-induced apoptosis through enforced caspase 8 activation in H460 cells.	tos	180-183	caspase 8	Homo sapiens	71-80
19561399-5	2009	Pretreatment with z-VAD-FMK (a pan-caspase inhibitor) or z-IETD-FMK (a caspase-8 inhibitor) blocked TOS/paclitaxel cotreatment-induced PARP cleavage and apoptosis, suggesting that TOS potentiates the paclitaxel-induced apoptosis through enforced caspase 8 activation in H460 cells.	Paclitaxel	200-210	caspase 8	Homo sapiens	71-80
19646526-3	2009	Here we show that cytosolic 2-cysPrx suppresses the TNF-alpha-induced apoptosis of human cervical cancer cells in a caspase-8-dependent manner.	2-cysprx	28-36	caspase 8	Homo sapiens	116-125
19646526-9	2009	Thus, this study illustrates that intracellular reactive oxygen species regulated by cytosolic 2-cysPrx is involved in the TNF-alpha-induced apoptotic cell death via controlling caspase activation.	Reactive Oxygen Species	48-71	caspase 8	Homo sapiens	178-185
19646526-9	2009	Thus, this study illustrates that intracellular reactive oxygen species regulated by cytosolic 2-cysPrx is involved in the TNF-alpha-induced apoptotic cell death via controlling caspase activation.	2-cysprx	95-103	caspase 8	Homo sapiens	178-185
19668227-0	2009	Paclitaxel promotes a caspase 8-mediated apoptosis through death effector domain association with microtubules.	Paclitaxel	0-10	caspase 8	Homo sapiens	22-31
19616521-7	2009	Moreover, the apoptosis induced by suillin was suppressed by both caspase-8 and -9 inhibitors.	suillin	35-42	caspase 8	Homo sapiens	66-82
19668227-3	2009	Paclitaxel, a microtubule-stabilizing agent, induces a caspase-dependent apoptosis, although the precise mechanism(s) remain unclear.	Paclitaxel	0-10	caspase 8	Homo sapiens	55-62
19668227-4	2009	Here, we used genetic approaches to evaluate the role of caspase 8 in paclitaxel-mediated apoptosis.	Paclitaxel	70-80	caspase 8	Homo sapiens	57-66
19668227-5	2009	We observed that caspase 8-expressing cells are more sensitive to paclitaxel than caspase 8-deficient cells.	Paclitaxel	66-76	caspase 8	Homo sapiens	17-26
19668227-6	2009	Mechanistically, caspase 8 was found associated with microtubules, and this interaction increased after paclitaxel treatment.	Paclitaxel	104-114	caspase 8	Homo sapiens	17-26
19668227-9	2009	Microtubule association, and paclitaxel sensitivity, depends on a critical lysine (K156) within a microtubule-binding motif (KLD) in DED-b of caspase 8.	Paclitaxel	29-39	caspase 8	Homo sapiens	142-151
19668227-9	2009	Microtubule association, and paclitaxel sensitivity, depends on a critical lysine (K156) within a microtubule-binding motif (KLD) in DED-b of caspase 8.	Lysine	75-81	caspase 8	Homo sapiens	142-151
19668227-9	2009	Microtubule association, and paclitaxel sensitivity, depends on a critical lysine (K156) within a microtubule-binding motif (KLD) in DED-b of caspase 8.	3-(2-Chloro-6-fluorophenyl)-5-methylisoxazole-4-carbonyl chloride	83-87	caspase 8	Homo sapiens	142-151
19846952-5	2009	Real-time PCR showed that berberine stimulated gene expression of caspase-8, -9 and -3, apoptosis-inducing factor and endonuclease G.	Berberine	26-35	caspase 8	Homo sapiens	66-86
19846952-0	2009	Berberine induced apoptosis via promoting the expression of caspase-8, -9 and -3, apoptosis-inducing factor and endonuclease G in SCC-4 human tongue squamous carcinoma cancer cells.	Berberine	0-9	caspase 8	Homo sapiens	60-80
19398149-5	2009	Combined treatment with Myricetin and TRAIL augmented the activation of initiator caspases-8/-9 and effector caspases-3/-7.	myricetin	24-33	caspase 8	Homo sapiens	82-122
19450542-7	2009	Deficiencies in CL inhibit the formation of tBid and prevent apoptosis by removing an essential activation platform for the autoprocessing of caspase-8.	tBID	44-48	caspase 8	Homo sapiens	142-151
19857055-5	2009	Western blot analysis revealed that piceatannol increased the protein levels of cleaved caspase-8, -9, -7, and -3 and cleaved poly(ADP-ribose) polymerase (PARP).	3,3',4,5'-tetrahydroxystilbene	36-47	caspase 8	Homo sapiens	88-113
19052865-5	2009	We hypothesize that apoptosis induced by treatment of Hep G2 and BEL-7402 cells with PA-MSHA is mediated by the mannose residues of PA-MSHA and is propagated through the extrinsic apoptosis pathway directly through caspase-8.	pa-msha	85-92	caspase 8	Homo sapiens	215-224
19052865-5	2009	We hypothesize that apoptosis induced by treatment of Hep G2 and BEL-7402 cells with PA-MSHA is mediated by the mannose residues of PA-MSHA and is propagated through the extrinsic apoptosis pathway directly through caspase-8.	Mannose	112-119	caspase 8	Homo sapiens	215-224
19857055-8	2009	Caspase-8 and -9 inhibitors mitigated piceatannol-induced apoptosis.	3,3',4,5'-tetrahydroxystilbene	38-49	caspase 8	Homo sapiens	0-16
19857055-9	2009	The caspase-8 inhibitor suppressed the piceatannol-induced cleavage of Bid, caspase-3, and PARP.	3,3',4,5'-tetrahydroxystilbene	39-50	caspase 8	Homo sapiens	4-13
19555659-0	2009	Titanium dioxide nanoparticles induce apoptosis through the JNK/p38-caspase-8-Bid pathway in phytohemagglutinin-stimulated human lymphocytes.	titanium dioxide	0-16	caspase 8	Homo sapiens	68-77
19464267-6	2009	DMNB potentiated TRAIL-induced cytotoxicity and apoptosis through inhibition of DNA-PK/Akt pathway and activation of caspase-8, -9 and -3 in K562 cells.	4,5-dimethoxy-2-nitrobenzaldehyde	0-4	caspase 8	Homo sapiens	117-137
19754176-9	2009	Caspase-8-specific inhibitor, z-ITED-fmk, canceled the cytotoxicity of fucoidan, activation of caspase-7, -8, and -9, and a series of changes in Bax, Bid, and cytochrome c.	z-ited-fmk	30-40	caspase 8	Homo sapiens	0-9
19628709-7	2009	NF-kappaB up-regulates Fas and predisposes to Fas-induced cell death, which is caspase-8 mediated and can be prevented by CFLAR overexpression.	ammonium ferrous sulfate	23-26	caspase 8	Homo sapiens	79-88
19628709-7	2009	NF-kappaB up-regulates Fas and predisposes to Fas-induced cell death, which is caspase-8 mediated and can be prevented by CFLAR overexpression.	ammonium ferrous sulfate	46-49	caspase 8	Homo sapiens	79-88
19706414-3	2009	In vitro cleavage assays demonstrate that OPN is cleaved at Asp-135 and Asp-157 by caspase-8.	Aspartic Acid	60-63	caspase 8	Homo sapiens	83-92
19706414-3	2009	In vitro cleavage assays demonstrate that OPN is cleaved at Asp-135 and Asp-157 by caspase-8.	Aspartic Acid	72-75	caspase 8	Homo sapiens	83-92
19555659-5	2009	We also observed that inhibition of caspase-8 by z-IETD-fmk suppressed the caspase-8/Bid activation, caspase-3-mediated PARP cleavage, and apoptosis.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	49-59	caspase 8	Homo sapiens	36-45
19555659-5	2009	We also observed that inhibition of caspase-8 by z-IETD-fmk suppressed the caspase-8/Bid activation, caspase-3-mediated PARP cleavage, and apoptosis.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	49-59	caspase 8	Homo sapiens	75-84
19597472-4	2009	HDACI, for example, valproic acid (VA), suberoylanilide hydroxamic acid (SAHA) and MS-275, cooperate with IFN-gamma to upregulate caspase-8 in cancer cells lacking caspase-8, thereby restoring sensitivity to TRAIL-induced apoptosis.	Valproic Acid	20-33	caspase 8	Homo sapiens	130-139
19597472-4	2009	HDACI, for example, valproic acid (VA), suberoylanilide hydroxamic acid (SAHA) and MS-275, cooperate with IFN-gamma to upregulate caspase-8 in cancer cells lacking caspase-8, thereby restoring sensitivity to TRAIL-induced apoptosis.	Valproic Acid	35-37	caspase 8	Homo sapiens	130-139
19597472-4	2009	HDACI, for example, valproic acid (VA), suberoylanilide hydroxamic acid (SAHA) and MS-275, cooperate with IFN-gamma to upregulate caspase-8 in cancer cells lacking caspase-8, thereby restoring sensitivity to TRAIL-induced apoptosis.	Vorinostat	40-71	caspase 8	Homo sapiens	130-139
19597472-4	2009	HDACI, for example, valproic acid (VA), suberoylanilide hydroxamic acid (SAHA) and MS-275, cooperate with IFN-gamma to upregulate caspase-8 in cancer cells lacking caspase-8, thereby restoring sensitivity to TRAIL-induced apoptosis.	Vorinostat	73-77	caspase 8	Homo sapiens	130-139
19555659-7	2009	In addition, the selective p38 inhibitor SB203580 and selective JNK inhibitor SP600125 suppressed nano-TiO(2)-induced apoptosis and caspase-8 activation to moderate and significant extents, respectively.	SB 203580	41-49	caspase 8	Homo sapiens	132-141
19555659-7	2009	In addition, the selective p38 inhibitor SB203580 and selective JNK inhibitor SP600125 suppressed nano-TiO(2)-induced apoptosis and caspase-8 activation to moderate and significant extents, respectively.	pyrazolanthrone	78-86	caspase 8	Homo sapiens	132-141
19555659-7	2009	In addition, the selective p38 inhibitor SB203580 and selective JNK inhibitor SP600125 suppressed nano-TiO(2)-induced apoptosis and caspase-8 activation to moderate and significant extents, respectively.	titanium dioxide	103-109	caspase 8	Homo sapiens	132-141
19555659-9	2009	Our results suggest that nano-TiO(2)-induced apoptosis is mediated by the p38/JNK pathway and the caspase-8-dependent Bid pathway in human lymphocytes.	titanium dioxide	30-36	caspase 8	Homo sapiens	98-107
18624760-8	2009	Caspase-8 inhibitor effectively suppressed acitretin-induced apoptosis whereas caspase-9 inhibitor did not.	Acitretin	43-52	caspase 8	Homo sapiens	0-9
19608730-5	2009	Cyclosporine was shown to upregulate the expression of TGF-beta in the colonic tissue, enhance the expression of p-Smad2 and cFLIP in epithelial cells, and inhibit caspase-8 activity but not caspase-1 or -9.	Cyclosporine	0-12	caspase 8	Homo sapiens	164-173
19434396-5	2009	Treatment with pan-caspase inhibitor, caspase-3 inhibitor, caspase-8 inhibitor or caspase-9 inhibitor significantly prevented apoptosis in PG-treated HeLa cells at 24 h. The intracellular ROS levels including O (2) (*-) were increased or decreased in PG-treated HeLa cells depending on the incubation times (1 or 24 h).	Propyl Gallate	139-141	caspase 8	Homo sapiens	59-68
19387079-6	2009	Vorinostat increased p53 expression and activated caspases -8, -9 and -3, whereas caspase inhibition abrogated vorinostat-induced apoptosis.	Vorinostat	0-10	caspase 8	Homo sapiens	50-72
19665028-6	2009	A wholly similar inhibition of human CASP3 and CASP8 by SERPINA3-3 (uniprotkb:Q3ZEJ6) was also observed with k(ass) of 1.5x10(5) and 2.7x10(6) M(-1)s(-1), respectively and form SDS-stable complexes with both caspases.	Sodium Dodecyl Sulfate	177-180	caspase 8	Homo sapiens	47-52
19665028-7	2009	By site-directed mutagenesis of bovSERPINA3-3, we identified Asp(371) as the potential P1 residue for caspases.	Aspartic Acid	61-64	caspase 8	Homo sapiens	102-110
19590527-0	2009	The cytotoxic macrolide FD-891 induces caspase-8-dependent mitochondrial release of cytochrome c and subsequent apoptosis in human leukemia Jurkat cells.	Macrolides	14-23	caspase 8	Homo sapiens	39-48
19590527-0	2009	The cytotoxic macrolide FD-891 induces caspase-8-dependent mitochondrial release of cytochrome c and subsequent apoptosis in human leukemia Jurkat cells.	FD 891	24-30	caspase 8	Homo sapiens	39-48
19625063-8	2009	Chemotherapy with doxorubicin or cisplatin (Ben Venue Laboratories, Bedford, Ohio) decreased the expression of the anti-apoptotic protein cFLIP(S) and increased caspase-8 cleavage, reversing TRAIL resistance in T24 cells.	Doxorubicin	18-29	caspase 8	Homo sapiens	161-170
19625063-8	2009	Chemotherapy with doxorubicin or cisplatin (Ben Venue Laboratories, Bedford, Ohio) decreased the expression of the anti-apoptotic protein cFLIP(S) and increased caspase-8 cleavage, reversing TRAIL resistance in T24 cells.	Cisplatin	33-42	caspase 8	Homo sapiens	161-170
19737941-4	2009	Western blotting showed suberoylanilide hydroxamic acid increased Fas, Fas ligand, DR4, and DR5 protein expression and activated caspase-8 and caspase-9.	Vorinostat	24-55	caspase 8	Homo sapiens	129-138
19549763-3	2009	Treatment of cells with the caspase-3-specific inhibitor N-benzyloxycarbonyl-Asp-Glu-Val-Asp-fluoromethyl ketone or caspase-3-specific small interacting RNA (siRNA) prevented the etoposide-induced activation of caspase-8 and inhibited apoptosis.	Z-Asp-Glu-Val-Asp-FMK	57-112	caspase 8	Homo sapiens	211-220
19549763-3	2009	Treatment of cells with the caspase-3-specific inhibitor N-benzyloxycarbonyl-Asp-Glu-Val-Asp-fluoromethyl ketone or caspase-3-specific small interacting RNA (siRNA) prevented the etoposide-induced activation of caspase-8 and inhibited apoptosis.	Etoposide	179-188	caspase 8	Homo sapiens	211-220
19549763-5	2009	Furthermore, the etoposide-induced processing of caspase-2 required the expression of caspase-8, and the etoposide-mediated processing of caspase-8 required the expression of caspase-2, indicating that these two caspases activate each other after etoposide treatment.	Etoposide	17-26	caspase 8	Homo sapiens	86-95
19549763-5	2009	Furthermore, the etoposide-induced processing of caspase-2 required the expression of caspase-8, and the etoposide-mediated processing of caspase-8 required the expression of caspase-2, indicating that these two caspases activate each other after etoposide treatment.	Etoposide	105-114	caspase 8	Homo sapiens	138-147
19737941-5	2009	The apoptosis was almost completely inhibited by caspase-8 inhibitor Z-IETD-FMK and attenuated by caspase-9 inhibitor Z-LEHD-FMK.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	69-79	caspase 8	Homo sapiens	49-58
19549763-5	2009	Furthermore, the etoposide-induced processing of caspase-2 required the expression of caspase-8, and the etoposide-mediated processing of caspase-8 required the expression of caspase-2, indicating that these two caspases activate each other after etoposide treatment.	Etoposide	105-114	caspase 8	Homo sapiens	138-147
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	caspase 8	Homo sapiens	62-70
19549763-6	2009	We also observed that etoposide-mediated apoptosis was decreased by treating the cells with the caspase-6-specific inhibitor benzyloxycarbonyl-Val-Glu(OMe)-Ile-Asp-(OMe)-fluoromethyl ketone and that caspase-6 was activated by a caspase-8-dependent mechanism.	Etoposide	22-31	caspase 8	Homo sapiens	228-237
19549763-6	2009	We also observed that etoposide-mediated apoptosis was decreased by treating the cells with the caspase-6-specific inhibitor benzyloxycarbonyl-Val-Glu(OMe)-Ile-Asp-(OMe)-fluoromethyl ketone and that caspase-6 was activated by a caspase-8-dependent mechanism.	benzyloxycarbonyl-val-glu	125-150	caspase 8	Homo sapiens	228-237
19549763-7	2009	Finally, we show that rottlerin blocks etoposide-induced apoptosis by inhibiting the PKCdelta-mediated activation of caspase-3 and by degrading caspase-2, which prevents caspase-8 activation.	rottlerin	22-31	caspase 8	Homo sapiens	170-179
19549763-7	2009	Finally, we show that rottlerin blocks etoposide-induced apoptosis by inhibiting the PKCdelta-mediated activation of caspase-3 and by degrading caspase-2, which prevents caspase-8 activation.	Etoposide	39-48	caspase 8	Homo sapiens	170-179
19545618-5	2009	Moreover, when PBMC were treated with high p,p"-DDE concentration (80 microg/ml) several apoptotic biochemical events were triggered, such as activation of caspase-8, Bid, caspase-9 and caspase-3, as well as degradation of PARP and ubiquitination.	Dichlorodiphenyl Dichloroethylene	43-51	caspase 8	Homo sapiens	156-165
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	caspase 8	Homo sapiens	101-110
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	caspase 8	Homo sapiens	62-69
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	caspase 8	Homo sapiens	251-260
19626005-4	2009	Here we show that loss of XIAP (X-chromosome linked inhibitor of apoptosis protein) function by gene targeting or treatment with a second mitochondria-derived activator of caspases (SMAC, also called DIABLO; direct IAP-binding protein with low pI) mimetic drug in mice rendered hepatocytes and beta-cells independent of BID for FAS-induced apoptosis.	ammonium ferrous sulfate	328-331	caspase 8	Homo sapiens	172-180
19481559-0	2009	N,N-dimethyl phytosphingosine induces caspase-8-dependent cytochrome c release and apoptosis through ROS generation in human leukemia cells.	N,N-dimethylphytosphingosine	0-29	caspase 8	Homo sapiens	38-47
19465019-6	2009	Recruitment of FADD and caspase-8 to the TRAIL-dependent DISC was diminished in a concentration-dependent manner in cells exposed to PAO.	oxophenylarsine	133-136	caspase 8	Homo sapiens	24-33
19481559-0	2009	N,N-dimethyl phytosphingosine induces caspase-8-dependent cytochrome c release and apoptosis through ROS generation in human leukemia cells.	Reactive Oxygen Species	101-104	caspase 8	Homo sapiens	38-47
19481559-6	2009	We also observed that DMPS activated the caspase-8-Bid-Bax pathway and that the inhibition of caspase-8 by z-IETD-fmk or small interfering RNA suppressed the cleavage of Bid, cytochrome c release, caspase-3 activation, and apoptotic cell death.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	107-117	caspase 8	Homo sapiens	94-103
19481559-6	2009	We also observed that DMPS activated the caspase-8-Bid-Bax pathway and that the inhibition of caspase-8 by z-IETD-fmk or small interfering RNA suppressed the cleavage of Bid, cytochrome c release, caspase-3 activation, and apoptotic cell death.	N,N-dimethylphytosphingosine	22-26	caspase 8	Homo sapiens	41-50
19481559-7	2009	In addition, cells subjected to DMPS exhibited significantly increased reactive oxygen species (ROS) generation, and ROS scavengers, such as quercetin and Tiron, but not N-acetylcysteine (NAC), inhibited DMPS-induced activations of caspase-8, -3 and subsequent apoptotic cell death, indicating the role of ROS in caspase-8-mediated apoptosis.	N,N-dimethylphytosphingosine	32-36	caspase 8	Homo sapiens	232-241
19481559-6	2009	We also observed that DMPS activated the caspase-8-Bid-Bax pathway and that the inhibition of caspase-8 by z-IETD-fmk or small interfering RNA suppressed the cleavage of Bid, cytochrome c release, caspase-3 activation, and apoptotic cell death.	N,N-dimethylphytosphingosine	22-26	caspase 8	Homo sapiens	94-103
19481559-7	2009	In addition, cells subjected to DMPS exhibited significantly increased reactive oxygen species (ROS) generation, and ROS scavengers, such as quercetin and Tiron, but not N-acetylcysteine (NAC), inhibited DMPS-induced activations of caspase-8, -3 and subsequent apoptotic cell death, indicating the role of ROS in caspase-8-mediated apoptosis.	N,N-dimethylphytosphingosine	32-36	caspase 8	Homo sapiens	313-322
19661327-7	2009	CWC-8 treatment also caused a time-dependent increase in Fas/CD95, FADD, cytosolic cytochrome c, caspase-8/-9/-3 active form, Apaf-1, AIF, Bax protein levels, and decrease in Bcl-2 protein level.	cwc-8	0-5	caspase 8	Homo sapiens	97-106
19481559-7	2009	In addition, cells subjected to DMPS exhibited significantly increased reactive oxygen species (ROS) generation, and ROS scavengers, such as quercetin and Tiron, but not N-acetylcysteine (NAC), inhibited DMPS-induced activations of caspase-8, -3 and subsequent apoptotic cell death, indicating the role of ROS in caspase-8-mediated apoptosis.	Reactive Oxygen Species	117-120	caspase 8	Homo sapiens	232-241
19481559-7	2009	In addition, cells subjected to DMPS exhibited significantly increased reactive oxygen species (ROS) generation, and ROS scavengers, such as quercetin and Tiron, but not N-acetylcysteine (NAC), inhibited DMPS-induced activations of caspase-8, -3 and subsequent apoptotic cell death, indicating the role of ROS in caspase-8-mediated apoptosis.	Reactive Oxygen Species	117-120	caspase 8	Homo sapiens	313-322
19481559-7	2009	In addition, cells subjected to DMPS exhibited significantly increased reactive oxygen species (ROS) generation, and ROS scavengers, such as quercetin and Tiron, but not N-acetylcysteine (NAC), inhibited DMPS-induced activations of caspase-8, -3 and subsequent apoptotic cell death, indicating the role of ROS in caspase-8-mediated apoptosis.	Quercetin	141-150	caspase 8	Homo sapiens	232-241
19481559-7	2009	In addition, cells subjected to DMPS exhibited significantly increased reactive oxygen species (ROS) generation, and ROS scavengers, such as quercetin and Tiron, but not N-acetylcysteine (NAC), inhibited DMPS-induced activations of caspase-8, -3 and subsequent apoptotic cell death, indicating the role of ROS in caspase-8-mediated apoptosis.	Quercetin	141-150	caspase 8	Homo sapiens	313-322
19481559-7	2009	In addition, cells subjected to DMPS exhibited significantly increased reactive oxygen species (ROS) generation, and ROS scavengers, such as quercetin and Tiron, but not N-acetylcysteine (NAC), inhibited DMPS-induced activations of caspase-8, -3 and subsequent apoptotic cell death, indicating the role of ROS in caspase-8-mediated apoptosis.	1,2-Dihydroxybenzene-3,5-Disulfonic Acid Disodium Salt	155-160	caspase 8	Homo sapiens	232-241
19481559-7	2009	In addition, cells subjected to DMPS exhibited significantly increased reactive oxygen species (ROS) generation, and ROS scavengers, such as quercetin and Tiron, but not N-acetylcysteine (NAC), inhibited DMPS-induced activations of caspase-8, -3 and subsequent apoptotic cell death, indicating the role of ROS in caspase-8-mediated apoptosis.	1,2-Dihydroxybenzene-3,5-Disulfonic Acid Disodium Salt	155-160	caspase 8	Homo sapiens	313-322
19481559-7	2009	In addition, cells subjected to DMPS exhibited significantly increased reactive oxygen species (ROS) generation, and ROS scavengers, such as quercetin and Tiron, but not N-acetylcysteine (NAC), inhibited DMPS-induced activations of caspase-8, -3 and subsequent apoptotic cell death, indicating the role of ROS in caspase-8-mediated apoptosis.	Reactive Oxygen Species	117-120	caspase 8	Homo sapiens	232-241
19481559-7	2009	In addition, cells subjected to DMPS exhibited significantly increased reactive oxygen species (ROS) generation, and ROS scavengers, such as quercetin and Tiron, but not N-acetylcysteine (NAC), inhibited DMPS-induced activations of caspase-8, -3 and subsequent apoptotic cell death, indicating the role of ROS in caspase-8-mediated apoptosis.	Reactive Oxygen Species	117-120	caspase 8	Homo sapiens	313-322
19481559-8	2009	Taken together, these results indicate that caspase-8 acts upstream of caspase-3, and that the caspase-8-mediated mitochondrial pathway is important in DMPS-induced apoptosis.	N,N-dimethylphytosphingosine	152-156	caspase 8	Homo sapiens	95-104
19481559-9	2009	Our results also suggest that ROS are critical regulators of caspase-8-mediated apoptosis in DMPS-treated leukemia cells.	Reactive Oxygen Species	30-33	caspase 8	Homo sapiens	61-70
19481559-9	2009	Our results also suggest that ROS are critical regulators of caspase-8-mediated apoptosis in DMPS-treated leukemia cells.	N,N-dimethylphytosphingosine	93-97	caspase 8	Homo sapiens	61-70
19661327-8	2009	CWC-8 also promoted caspase-8/-9 and -3 activities; however, pretreatment of cells with pan-caspase, caspase-8/-9 and -3 inhibitors led to reduced cell growth inhibition action.	cwc-8	0-5	caspase 8	Homo sapiens	20-39
19661327-8	2009	CWC-8 also promoted caspase-8/-9 and -3 activities; however, pretreatment of cells with pan-caspase, caspase-8/-9 and -3 inhibitors led to reduced cell growth inhibition action.	cwc-8	0-5	caspase 8	Homo sapiens	101-120
19661300-10	2009	Both SB-T-1216 and paclitaxel activated caspase-3, caspase-9, caspase-2 and caspase-8 in sensitive as well as resistant cells.	CHEMBL204644	5-14	caspase 8	Homo sapiens	76-85
19661300-10	2009	Both SB-T-1216 and paclitaxel activated caspase-3, caspase-9, caspase-2 and caspase-8 in sensitive as well as resistant cells.	Paclitaxel	19-29	caspase 8	Homo sapiens	76-85
19381674-3	2009	We demonstrate that gal-1 induced proteolytic cleavage of the death agonist Bid, a member of the Bcl-2/Bcl-xL family and a substrate of activated caspase-8, was inhibited by caspase-8 inhibitor II (Z-IETD-FMK).	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	198-208	caspase 8	Homo sapiens	146-155
19723075-9	2009	Erufosine was found to cause cell shrinkage, chromatin condensation, and caspase-8 and -3 activation.	erucylphospho-N,N,N-trimethylpropylammonium	0-9	caspase 8	Homo sapiens	73-89
19423619-7	2009	The presence of z-IETD-fmk, a caspase-8 inhibitor, markedly reversed tBid formation and caspase activation and partially reversed the dissipation of platelet DeltaPsim stimulated by resveratrol.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	16-26	caspase 8	Homo sapiens	30-39
19423619-7	2009	The presence of z-IETD-fmk, a caspase-8 inhibitor, markedly reversed tBid formation and caspase activation and partially reversed the dissipation of platelet DeltaPsim stimulated by resveratrol.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	16-26	caspase 8	Homo sapiens	30-37
19423619-7	2009	The presence of z-IETD-fmk, a caspase-8 inhibitor, markedly reversed tBid formation and caspase activation and partially reversed the dissipation of platelet DeltaPsim stimulated by resveratrol.	tBID	69-73	caspase 8	Homo sapiens	30-39
19423619-7	2009	The presence of z-IETD-fmk, a caspase-8 inhibitor, markedly reversed tBid formation and caspase activation and partially reversed the dissipation of platelet DeltaPsim stimulated by resveratrol.	Resveratrol	182-193	caspase 8	Homo sapiens	30-39
19423619-7	2009	The presence of z-IETD-fmk, a caspase-8 inhibitor, markedly reversed tBid formation and caspase activation and partially reversed the dissipation of platelet DeltaPsim stimulated by resveratrol.	Resveratrol	182-193	caspase 8	Homo sapiens	30-37
19723056-9	2009	Interestingly, inhibition of caspase-8 resulted in remarkable reduction of genistein-induced apoptosis.	Genistein	75-84	caspase 8	Homo sapiens	29-38
19563533-7	2009	Continuous refreshing of the simvastatin-containing medium abrogated the mitochondrial amplification loop via caspase 8.	Simvastatin	29-40	caspase 8	Homo sapiens	110-119
19563533-8	2009	Moreover, conditional medium, supplemented with mevalonic acid in order to nullify a possible contamination by statins, significantly triggered caspase 8 activity.	Mevalonic Acid	48-62	caspase 8	Homo sapiens	144-153
19381674-3	2009	We demonstrate that gal-1 induced proteolytic cleavage of the death agonist Bid, a member of the Bcl-2/Bcl-xL family and a substrate of activated caspase-8, was inhibited by caspase-8 inhibitor II (Z-IETD-FMK).	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	198-208	caspase 8	Homo sapiens	174-183
19578756-5	2009	Both RT4 (grade I; wild-type p53) and T24 (grade III; mutant p53) cell types proved to be vulnerable to cisplatin apoptotic activity, albeit in a grade-dependent and drug dose-specific manner, as demonstrated by the proteolytic processing profiles of Caspase-8, Caspase-9, Caspase-3, and the Caspase repertoire characteristic substrates PARP and Lamin A/C, as well.	Cisplatin	104-113	caspase 8	Homo sapiens	251-260
19755441-8	2009	Caspase inhibitors prevented the quercetin-induced loss of cell viability.	Quercetin	33-42	caspase 8	Homo sapiens	0-7
19578756-5	2009	Both RT4 (grade I; wild-type p53) and T24 (grade III; mutant p53) cell types proved to be vulnerable to cisplatin apoptotic activity, albeit in a grade-dependent and drug dose-specific manner, as demonstrated by the proteolytic processing profiles of Caspase-8, Caspase-9, Caspase-3, and the Caspase repertoire characteristic substrates PARP and Lamin A/C, as well.	Cisplatin	104-113	caspase 8	Homo sapiens	251-258
19551546-8	2009	Our data indicate that sanazole can enhance the hyperthermia induced-apoptosis through the Fas-caspase-8- and [Ca(2+)](i)-dependent apoptotic pathways.	AK 2123	23-31	caspase 8	Homo sapiens	95-104
19111365-7	2009	All of the tested caspase inhibitors, especially pan-caspase inhibitor (Z-VAD), markedly rescued Calu-6 cells from AMA-induced Calu-6 cell death.	z-vad	72-77	caspase 8	Homo sapiens	18-25
19111365-7	2009	All of the tested caspase inhibitors, especially pan-caspase inhibitor (Z-VAD), markedly rescued Calu-6 cells from AMA-induced Calu-6 cell death.	z-vad	72-77	caspase 8	Homo sapiens	53-60
19446247-3	2009	Thiosulfinates activated the initiator caspase-8, and -9, and the effector caspase-3.	thiosulfinates	0-14	caspase 8	Homo sapiens	39-56
19446247-4	2009	In the present study, thiosulfinates were found to stimulate Bid cleavage, indicating that the apoptotic action of caspase-8-mediated Bid cleavage leads to the activation of caspase-9.	thiosulfinates	22-36	caspase 8	Homo sapiens	115-124
19446247-7	2009	These results indicate that thiosulfinates from A. tuberosum L. inhibited cell proliferation and activated both the caspase-dependent and caspase-independent apoptotic pathways in HT-29 cells.	thiosulfinates	28-42	caspase 8	Homo sapiens	116-123
19446247-7	2009	These results indicate that thiosulfinates from A. tuberosum L. inhibited cell proliferation and activated both the caspase-dependent and caspase-independent apoptotic pathways in HT-29 cells.	thiosulfinates	28-42	caspase 8	Homo sapiens	138-145
19409917-8	2009	Ovatodiolide treatment also induced apoptosis, as indicated by caspase activation, DNA fragmentation, and poly (ADP-ribose) polymerase (PARP) cleavage.	ovatodiolide	0-12	caspase 8	Homo sapiens	63-70
19409917-10	2009	The action of ovatodiolide was correlated with a rapid and sustained increase in ROS production and down-regulation of FLICE inhibitory protein (FLIP), which is an endogenous caspase-8 inhibitor and is sensitive to intracellular redox status.	ovatodiolide	14-26	caspase 8	Homo sapiens	175-184
19409917-11	2009	Pretreatment of Ca9-22 cells with N-acetylcysteine, a thiol antioxidant, abolished all of ovatodiolide-induced effects, including ROS generation, down-regulation of FLIP, caspase activation, apoptosis as well as cell cycle arrest.	Acetylcysteine	34-50	caspase 8	Homo sapiens	171-178
19409917-11	2009	Pretreatment of Ca9-22 cells with N-acetylcysteine, a thiol antioxidant, abolished all of ovatodiolide-induced effects, including ROS generation, down-regulation of FLIP, caspase activation, apoptosis as well as cell cycle arrest.	ovatodiolide	90-102	caspase 8	Homo sapiens	171-178
19220423-7	2009	Those effects were accompanied by increased activation of caspases in cells treated by MK886 + TNF-alpha.	MK-886	87-92	caspase 8	Homo sapiens	58-66
19406930-4	2009	The TRAIL cytotoxicity by Prx I knockdown was dependent on activation of caspase-8/3 cascades, which was ablated by addition of inhibitors for p38 MAPK, ROS or Nox, suggesting the association with Nox-driven redox signaling.	Reactive Oxygen Species	153-156	caspase 8	Homo sapiens	73-82
19406930-4	2009	The TRAIL cytotoxicity by Prx I knockdown was dependent on activation of caspase-8/3 cascades, which was ablated by addition of inhibitors for p38 MAPK, ROS or Nox, suggesting the association with Nox-driven redox signaling.	nox	197-200	caspase 8	Homo sapiens	73-82
19350268-2	2009	METHODS: The extent of promoter methylation in the DR4, DR5, DcR1, DcR2, and CASP8 genes was quantified using bisulfite modification and methylation-specific polymerase chain reaction.	hydrogen sulfite	110-119	caspase 8	Homo sapiens	77-82
19260109-0	2009	Detection of CpG island hypermethylation of caspase-8 in neuroblastoma using an oligonucleotide array.	Oligonucleotides	80-95	caspase 8	Homo sapiens	44-53
19329756-9	2009	Furthermore, this caspase 8 activation was dependent on ceramide generation by acidic sphingomyelinase.	Ceramides	56-64	caspase 8	Homo sapiens	18-27
19372210-0	2009	S-Adenosylmethionine and methylthioadenosine inhibit cellular FLICE inhibitory protein expression and induce apoptosis in colon cancer cells.	S-Adenosylmethionine	0-20	caspase 8	Homo sapiens	62-67
19372210-0	2009	S-Adenosylmethionine and methylthioadenosine inhibit cellular FLICE inhibitory protein expression and induce apoptosis in colon cancer cells.	5'-methylthioadenosine	25-44	caspase 8	Homo sapiens	62-67
19496190-7	2009	Additionally, ethanol-treated cells displayed enhanced susceptibility to Fas-mediated apoptosis that was blocked by GSH depletion as a result of diminished caspase-8 activity.	Ethanol	14-21	caspase 8	Homo sapiens	156-165
19496190-7	2009	Additionally, ethanol-treated cells displayed enhanced susceptibility to Fas-mediated apoptosis that was blocked by GSH depletion as a result of diminished caspase-8 activity.	ammonium ferrous sulfate	73-76	caspase 8	Homo sapiens	156-165
19496190-7	2009	Additionally, ethanol-treated cells displayed enhanced susceptibility to Fas-mediated apoptosis that was blocked by GSH depletion as a result of diminished caspase-8 activity.	Glutathione	116-119	caspase 8	Homo sapiens	156-165
19096828-10	2009	TUNEL assay performed in LE cells treated with 1 mM of UA showed significant incorporation of dNTPs in the nucleus after 24 h. In the presence of the caspase inhibitors, we observed the significant decrease in the activity of caspases-8 and -3 in 0.5 and 1 mM UA-treated LE cells.	uranyl acetate	55-57	caspase 8	Homo sapiens	150-157
19216720-10	2009	CONCLUSIONS: The present paper highlights that staurosporine engages the intrinsic mitochondrial apoptotic pathway via caspase-8 or caspase-9 signalling cascades and via caspase-independent cell death, as well as through p53 activity.	Staurosporine	47-60	caspase 8	Homo sapiens	119-128
19096828-10	2009	TUNEL assay performed in LE cells treated with 1 mM of UA showed significant incorporation of dNTPs in the nucleus after 24 h. In the presence of the caspase inhibitors, we observed the significant decrease in the activity of caspases-8 and -3 in 0.5 and 1 mM UA-treated LE cells.	uranyl acetate	55-57	caspase 8	Homo sapiens	226-243
19096828-10	2009	TUNEL assay performed in LE cells treated with 1 mM of UA showed significant incorporation of dNTPs in the nucleus after 24 h. In the presence of the caspase inhibitors, we observed the significant decrease in the activity of caspases-8 and -3 in 0.5 and 1 mM UA-treated LE cells.	Parathion	94-99	caspase 8	Homo sapiens	150-157
19096828-10	2009	TUNEL assay performed in LE cells treated with 1 mM of UA showed significant incorporation of dNTPs in the nucleus after 24 h. In the presence of the caspase inhibitors, we observed the significant decrease in the activity of caspases-8 and -3 in 0.5 and 1 mM UA-treated LE cells.	Parathion	94-99	caspase 8	Homo sapiens	226-243
19096828-10	2009	TUNEL assay performed in LE cells treated with 1 mM of UA showed significant incorporation of dNTPs in the nucleus after 24 h. In the presence of the caspase inhibitors, we observed the significant decrease in the activity of caspases-8 and -3 in 0.5 and 1 mM UA-treated LE cells.	uranyl acetate	260-262	caspase 8	Homo sapiens	150-157
19096828-10	2009	TUNEL assay performed in LE cells treated with 1 mM of UA showed significant incorporation of dNTPs in the nucleus after 24 h. In the presence of the caspase inhibitors, we observed the significant decrease in the activity of caspases-8 and -3 in 0.5 and 1 mM UA-treated LE cells.	uranyl acetate	260-262	caspase 8	Homo sapiens	226-243
19346183-7	2009	This aside, sanguinarine also increased the activity of caspase-8.	sanguinarine	12-24	caspase 8	Homo sapiens	56-65
18973184-9	2009	Taken together, the results suggest that PPAC induces apoptosis through the death receptor-mediated apoptotic pathway where the activation of caspase-8 leads to the direct cleavage of execution caspases without the involvement of the mitochondria.	polyporenic acid C	41-45	caspase 8	Homo sapiens	142-151
19590723-0	2009	TRAIL-induced cell death and caspase-8 activation are inhibited by cisplatin but not carboplatin.	Cisplatin	67-76	caspase 8	Homo sapiens	29-38
19590723-3	2009	However it has been recently reported that cisplatin may inhibit tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced cell death through inactivation of caspases.	Cisplatin	43-52	caspase 8	Homo sapiens	172-180
19590723-8	2009	Whereas cisplatin inhibited caspase-8-mediated Bid cleavage, carboplatin had no effect on caspase-8 activity.	Cisplatin	8-17	caspase 8	Homo sapiens	28-37
19548908-11	2009	TPEN-mediated caspase-3 activation requires functional caspase-8, but is independent of H(2)O(2) generation.	N,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamine	0-4	caspase 8	Homo sapiens	55-64
18973184-0	2009	Polyporenic acid C induces caspase-8-mediated apoptosis in human lung cancer A549 cells.	polyporenic acid C	0-18	caspase 8	Homo sapiens	27-36
19135778-6	2009	Apoptosis caused by honokiol was also concomitant with the cleavage of caspases (caspase-3, -8, and -9) and Bid along with the suppressive expression of Bcl-2, but it was independent on the expression of Bax and p53.	honokiol	20-28	caspase 8	Homo sapiens	71-79
19831310-3	2009	In this report, after cell infection with BTV, the activation of caspase 8 was detected, proving the extrinsic receptor binding apoptotic pathway.	CHEMBL3972792	42-45	caspase 8	Homo sapiens	65-74
18805546-9	2009	The induction of apoptosis by either plaunotol or GGOH was dependent on the activation of both caspase-8 and caspase-9 pathways.	plaunotol	37-46	caspase 8	Homo sapiens	95-104
19414751-6	2009	Our results reveal that GalXM activates the extrinsic and intrinsic apoptotic pathways through the cleavage and recruitment of caspase-8.	galactoxylomannan	24-29	caspase 8	Homo sapiens	127-136
18805546-9	2009	The induction of apoptosis by either plaunotol or GGOH was dependent on the activation of both caspase-8 and caspase-9 pathways.	ggoh	50-54	caspase 8	Homo sapiens	95-104
19360334-5	2009	Our studies show that knockdown of STAT3 expression by siRNA reduced expression of Bcl-xL and survivin in MDA-MB-231 cells, and also led to Fas mediated intrinsic apoptotic pathway by activating caspases -8, -9, -3 and PARP1 cleavage.	ammonium ferrous sulfate	140-143	caspase 8	Homo sapiens	195-214
19264955-9	2009	Additionally, fisetin caused an increase in the protein levels of cleaved caspase-8, Fas ligand, death receptor 5, and TNF-related apoptosis-inducing ligand, and the caspase-8 inhibitor Z-IETD-FMK suppressed fisetin-induced apoptosis and the activation of caspase-3.	fisetin	14-21	caspase 8	Homo sapiens	74-83
19264955-9	2009	Additionally, fisetin caused an increase in the protein levels of cleaved caspase-8, Fas ligand, death receptor 5, and TNF-related apoptosis-inducing ligand, and the caspase-8 inhibitor Z-IETD-FMK suppressed fisetin-induced apoptosis and the activation of caspase-3.	fisetin	14-21	caspase 8	Homo sapiens	166-175
19264955-9	2009	Additionally, fisetin caused an increase in the protein levels of cleaved caspase-8, Fas ligand, death receptor 5, and TNF-related apoptosis-inducing ligand, and the caspase-8 inhibitor Z-IETD-FMK suppressed fisetin-induced apoptosis and the activation of caspase-3.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	186-196	caspase 8	Homo sapiens	166-175
19360361-5	2009	In addition, z-IETD-fmk, a selective caspase-8 inhibitor, suppressed the nimesulide- and radiation-induced cleavage activation of caspase-9, caspase-3, caspase-8, and Bid, and suppressed the concomitant apoptosis, indicating that the nimesulide-induced increase in radiosensitivity was initiated by caspase-8.	nimesulide	73-83	caspase 8	Homo sapiens	152-161
19360361-5	2009	In addition, z-IETD-fmk, a selective caspase-8 inhibitor, suppressed the nimesulide- and radiation-induced cleavage activation of caspase-9, caspase-3, caspase-8, and Bid, and suppressed the concomitant apoptosis, indicating that the nimesulide-induced increase in radiosensitivity was initiated by caspase-8.	nimesulide	234-244	caspase 8	Homo sapiens	37-46
19429276-4	2009	(2) Reduction of mitochondrial membrane potential and activation of caspase-8, caspase-9, and caspase-3 were observed, indicating that apoptotic signal by HL-n should pass through mitochondria and these caspases.	hl-n	155-159	caspase 8	Homo sapiens	68-77
19429276-4	2009	(2) Reduction of mitochondrial membrane potential and activation of caspase-8, caspase-9, and caspase-3 were observed, indicating that apoptotic signal by HL-n should pass through mitochondria and these caspases.	hl-n	155-159	caspase 8	Homo sapiens	203-211
19360361-0	2009	Nimesulide, a selective COX-2 inhibitor, acts synergistically with ionizing radiation against A549 human lung cancer cells through the activation of caspase-8 and caspase-3.	nimesulide	0-10	caspase 8	Homo sapiens	149-158
19360361-3	2009	The combined nimesulide-radiation treatment increased apoptosis, induced the cleavage of caspase-3, caspase-9, and poly(ADP-ribose) polymerase (PARP), activated caspase-8, and induced cleavage of Bid.	nimesulide	13-23	caspase 8	Homo sapiens	161-170
19360361-4	2009	A pan-caspase inhibitor, z-VAD-fmk, suppressed this increase in apoptosis and also suppressed the cleavage of caspase-8, caspase-3, and PARP, suggesting a caspase-dependent mechanism.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	25-34	caspase 8	Homo sapiens	6-13
19360361-4	2009	A pan-caspase inhibitor, z-VAD-fmk, suppressed this increase in apoptosis and also suppressed the cleavage of caspase-8, caspase-3, and PARP, suggesting a caspase-dependent mechanism.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	25-34	caspase 8	Homo sapiens	110-119
19360361-4	2009	A pan-caspase inhibitor, z-VAD-fmk, suppressed this increase in apoptosis and also suppressed the cleavage of caspase-8, caspase-3, and PARP, suggesting a caspase-dependent mechanism.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	25-34	caspase 8	Homo sapiens	110-117
19589263-6	2009	This effect could be blocked with the caspase inhibitors, z-VAD-fmk (pan-caspase inhibitor), z-DEVD-fmk (caspase-3 inhibitor) and z-LEHD-fmk (caspase-9 inhibitor), but not with z-IETD-fmk (caspase-8 inhibitor).	benzoylcarbonyl-aspartyl-glutamyl-valyl-aspartyl-fluoromethyl ketone	93-103	caspase 8	Homo sapiens	189-198
19360361-5	2009	In addition, z-IETD-fmk, a selective caspase-8 inhibitor, suppressed the nimesulide- and radiation-induced cleavage activation of caspase-9, caspase-3, caspase-8, and Bid, and suppressed the concomitant apoptosis, indicating that the nimesulide-induced increase in radiosensitivity was initiated by caspase-8.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	13-23	caspase 8	Homo sapiens	37-46
19360361-5	2009	In addition, z-IETD-fmk, a selective caspase-8 inhibitor, suppressed the nimesulide- and radiation-induced cleavage activation of caspase-9, caspase-3, caspase-8, and Bid, and suppressed the concomitant apoptosis, indicating that the nimesulide-induced increase in radiosensitivity was initiated by caspase-8.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	13-23	caspase 8	Homo sapiens	152-161
19360361-5	2009	In addition, z-IETD-fmk, a selective caspase-8 inhibitor, suppressed the nimesulide- and radiation-induced cleavage activation of caspase-9, caspase-3, caspase-8, and Bid, and suppressed the concomitant apoptosis, indicating that the nimesulide-induced increase in radiosensitivity was initiated by caspase-8.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	13-23	caspase 8	Homo sapiens	152-161
19360361-5	2009	In addition, z-IETD-fmk, a selective caspase-8 inhibitor, suppressed the nimesulide- and radiation-induced cleavage activation of caspase-9, caspase-3, caspase-8, and Bid, and suppressed the concomitant apoptosis, indicating that the nimesulide-induced increase in radiosensitivity was initiated by caspase-8.	nimesulide	73-83	caspase 8	Homo sapiens	37-46
19360361-5	2009	In addition, z-IETD-fmk, a selective caspase-8 inhibitor, suppressed the nimesulide- and radiation-induced cleavage activation of caspase-9, caspase-3, caspase-8, and Bid, and suppressed the concomitant apoptosis, indicating that the nimesulide-induced increase in radiosensitivity was initiated by caspase-8.	nimesulide	73-83	caspase 8	Homo sapiens	152-161
19589263-6	2009	This effect could be blocked with the caspase inhibitors, z-VAD-fmk (pan-caspase inhibitor), z-DEVD-fmk (caspase-3 inhibitor) and z-LEHD-fmk (caspase-9 inhibitor), but not with z-IETD-fmk (caspase-8 inhibitor).	benzyloxycarbonyl-leucyl-glutamyl-histidyl-aspartic acid fluoromethyl ketone	130-140	caspase 8	Homo sapiens	189-198
19589263-6	2009	This effect could be blocked with the caspase inhibitors, z-VAD-fmk (pan-caspase inhibitor), z-DEVD-fmk (caspase-3 inhibitor) and z-LEHD-fmk (caspase-9 inhibitor), but not with z-IETD-fmk (caspase-8 inhibitor).	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	177-187	caspase 8	Homo sapiens	38-45
19233849-9	2009	However, the fact that cleavage of Bid to tBid is mediated by executioner caspases suggests that a self-amplifying feed forward loop involving caspases, Bid, and mitochondria may help determine irreversible commitment to apoptosis.	tBID	42-46	caspase 8	Homo sapiens	74-82
19188482-5	2009	Tunicamycin induced apoptosis independently of the mitochondrial pathway but caused lysosomal destabilization followed by lysosomal membrane permeabilization (LMP), cathepsin B relocation from lysosomes to the cytosol, and caspase-8 and -3 activation.	Tunicamycin	0-11	caspase 8	Homo sapiens	223-239
19203346-6	2009	These results were accompanied by down-regulation of c-FLIP {cellular FLICE [FADD (Fas-associated death domain)-like interleukin 1beta-converting enzyme]-inhibitory protein} in imatinib-resistant K562 variants compared with K562 cells.	Imatinib Mesylate	177-185	caspase 8	Homo sapiens	70-75
19379505-16	2009	Apoptotic cell death induced by metallic nickel particles in JB6 cells is through a caspase-8/AIF mediated cytochrome c-independent pathway.	Nickel	41-47	caspase 8	Homo sapiens	84-93
19097688-0	2009	Andrographolide enhances 5-fluorouracil-induced apoptosis via caspase-8-dependent mitochondrial pathway involving p53 participation in hepatocellular carcinoma (SMMC-7721) cells.	andrographolide	0-15	caspase 8	Homo sapiens	62-71
19097688-0	2009	Andrographolide enhances 5-fluorouracil-induced apoptosis via caspase-8-dependent mitochondrial pathway involving p53 participation in hepatocellular carcinoma (SMMC-7721) cells.	Fluorouracil	25-39	caspase 8	Homo sapiens	62-71
19097688-8	2009	Surprisingly, the addition of ANDRO to 5-FU induces synergistic apoptosis, which could be corroborated to the increased caspase-8, p53 activity and the significant changes of Bax conformation in these cells, resulting in increased losses of mitochondrial membrane potential, increased release of cytochrome c, and activation of caspase-9 and caspase-3.	andrographolide	30-35	caspase 8	Homo sapiens	120-129
19097688-8	2009	Surprisingly, the addition of ANDRO to 5-FU induces synergistic apoptosis, which could be corroborated to the increased caspase-8, p53 activity and the significant changes of Bax conformation in these cells, resulting in increased losses of mitochondrial membrane potential, increased release of cytochrome c, and activation of caspase-9 and caspase-3.	Fluorouracil	39-43	caspase 8	Homo sapiens	120-129
19097688-9	2009	Suppression of caspase-8 with the specific inhibitor z-IETD-fmk abrogates largely ANDRO/5-FU biological activity by preventing mitochondrial membrane potential disappearance, caspase-3,9 activation and subsequent apoptosis.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	53-63	caspase 8	Homo sapiens	15-24
19097688-9	2009	Suppression of caspase-8 with the specific inhibitor z-IETD-fmk abrogates largely ANDRO/5-FU biological activity by preventing mitochondrial membrane potential disappearance, caspase-3,9 activation and subsequent apoptosis.	Fluorouracil	88-92	caspase 8	Homo sapiens	15-24
19379505-0	2009	Metallic nickel nano- and fine particles induce JB6 cell apoptosis through a caspase-8/AIF mediated cytochrome c-independent pathway.	Nickel	9-15	caspase 8	Homo sapiens	77-86
19351839-4	2009	Pretreatment of several melanoma lines just before gamma-irradiation with the inhibitor of ATM kinase KU-55933 suppressed p53 and nuclear factor-kappaB (NF-kappaB) activation but notably increased radiation-induced DR5 surface expression, down-regulated cFLIP (caspase-8 inhibitor) levels, and substantially enhanced exogenous TRAIL-induced apoptosis.	2-morpholin-4-yl-6-thianthren-1-yl-pyran-4-one	102-110	caspase 8	Homo sapiens	261-270
19414399-8	2009	EGCG promoted caspase-8, -9 and -3 activities in a time-dependent manner.	epigallocatechin gallate	0-4	caspase 8	Homo sapiens	14-34
19214542-7	2009	Reexpression of caspase-8 by 5-Aza-2"-deoxycytidine was not sufficient to restore TRAIL sensitivity in SCGs cells, suggesting that additional factors cause TRAIL resistance in SCGs.	Decitabine	29-51	caspase 8	Homo sapiens	16-25
19426671-4	2009	The combined treatment of ovarian cancer SKOV3 cells with TSA and TRAIL significantly activated caspase-8 and truncated Bid, resulting in the cytosolic accumulation of cytochrome c as well as the activation of caspase-9 and -3.	trichostatin A	58-61	caspase 8	Homo sapiens	96-105
19167455-3	2009	Involvement of the caspase and the metalloprotease families was confirmed by the observation that their respective broad spectrum inhibitors, Z-VAD-fmk and GM6001, each suppressed HD-induced microvesication.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	142-151	caspase 8	Homo sapiens	19-26
19167455-3	2009	Involvement of the caspase and the metalloprotease families was confirmed by the observation that their respective broad spectrum inhibitors, Z-VAD-fmk and GM6001, each suppressed HD-induced microvesication.	N-(2(R)-2-(hydroxamidocarbonylmethyl)-4-methylpentanoyl)-L-tryptophan methylamide	156-162	caspase 8	Homo sapiens	19-26
20103947-3	2009	Oligonucleotides coding for four shRNAs against caspase-8 were cloned into mammalian expression vector Pgenesil-1 containing U6 promoter, which were then introduced into Hepa1-6 cells using liposome-mediated transfection.	Oligonucleotides	0-16	caspase 8	Homo sapiens	48-57
19276256-10	2009	Furthermore, the combination of lexatumumab and cisplatin significantly enhanced caspase-8 activity, Bid cleavage, up-regulation of Bax, cytochrome c release, and caspase-9, caspase-6, and caspase-3 activities.	Cisplatin	48-57	caspase 8	Homo sapiens	81-90
19287965-0	2009	Induction of apoptosis in human leukemia U937 cells by anthocyanins through down-regulation of Bcl-2 and activation of caspases.	Anthocyanins	55-67	caspase 8	Homo sapiens	119-127
19287965-9	2009	Taken together, these results show that Bcl-2 and caspases are key regulators of apoptosis in response to anthocyanins in human leukemia U937 cells.	Anthocyanins	106-118	caspase 8	Homo sapiens	50-58
19493480-0	2009	[Changes of caspase-8 and caspase-9 activity during apoptosis of keratinocytes induced by trichloroethylene].	Trichloroethylene	90-107	caspase 8	Homo sapiens	12-21
19493480-1	2009	OBJECTIVE: To observe the change of caspase-8, caspase-9 activity and apoptosis rates in the process of trichloroethylene-induced damage in keratinocytes, and explore the tentative mechanism of apoptosis.	Trichloroethylene	104-121	caspase 8	Homo sapiens	36-45
19240112-4	2009	When cells are exposed to Fas-related signals, the ubiquitously expressed p21-activated kinase 2 (Pak2) can be activated via cleavage by caspases to release a constitutively active C-terminal fragment, which mediates cell death.	ammonium ferrous sulfate	26-29	caspase 8	Homo sapiens	137-145
19331667-0	2009	Fenretinide-induced caspase-8 activation and apoptosis in an established model of metastatic neuroblastoma.	Fenretinide	0-11	caspase 8	Homo sapiens	20-29
19276256-14	2009	CONCLUSIONS: Cisplatin sensitizes solid cancer cells to lexatumumab-induced apoptosis by potentiation of the extrinsic and intrinsic apoptotic pathways that lead to amplification of caspase activation, particularly caspase-8, suggesting the combination treatment of solid cancers with cisplatin and lexatumumab might overcome their resistance.	Cisplatin	13-22	caspase 8	Homo sapiens	215-224
19166881-4	2009	Our results showed that the expression of human CASP10 and CASP8 triggers certain apoptotic markers such as a massive production of reactive oxygen species (ROS), chromatin condensation and phosphatidylserine externalization, finally leading to cell death.	Reactive Oxygen Species	132-155	caspase 8	Homo sapiens	59-64
19278658-1	2009	Caspases are proteases with an active-site cysteine and aspartate specificity in their substrates.	Cysteine	43-51	caspase 8	Homo sapiens	0-8
19278658-1	2009	Caspases are proteases with an active-site cysteine and aspartate specificity in their substrates.	Aspartic Acid	56-65	caspase 8	Homo sapiens	0-8
19100720-5	2009	Bortezomib treatment did not significantly alter plasma membrane amount of DR4 and DR5 but increased Apo2L/TRAIL-induced caspase-8 and caspase-3 activation.	Bortezomib	0-10	caspase 8	Homo sapiens	121-130
19166881-4	2009	Our results showed that the expression of human CASP10 and CASP8 triggers certain apoptotic markers such as a massive production of reactive oxygen species (ROS), chromatin condensation and phosphatidylserine externalization, finally leading to cell death.	Reactive Oxygen Species	157-160	caspase 8	Homo sapiens	59-64
19275578-5	2009	While bortezomib induces several caspases, NPI-0052 activates predominantly caspase-8-dependent pathway.	Bortezomib	6-16	caspase 8	Homo sapiens	33-41
19223550-3	2009	We provide evidence that LY30-induced increase in intracellular H(2)O(2) up-regulates the expression of TRAIL receptors (DR4 and DR5) in SHEP-1 cells by activating mitogen-activated protein kinases, resulting in a significant amplification of TRAIL-mediated caspase-8 processing and activity, cytosolic translocation of cytochrome c, and cell death.	LY 303511	25-29	caspase 8	Homo sapiens	258-267
19223550-3	2009	We provide evidence that LY30-induced increase in intracellular H(2)O(2) up-regulates the expression of TRAIL receptors (DR4 and DR5) in SHEP-1 cells by activating mitogen-activated protein kinases, resulting in a significant amplification of TRAIL-mediated caspase-8 processing and activity, cytosolic translocation of cytochrome c, and cell death.	Hydrogen Peroxide	64-72	caspase 8	Homo sapiens	258-267
18708158-4	2009	Roscovitine reduced amounts of the caspase inhibitor XIAP, and API-2 increased amounts of the BH3-only protein Bim.	Roscovitine	0-11	caspase 8	Homo sapiens	35-42
21783950-0	2009	Ardipusilloside I induces apoptosis in human glioblastoma cells through a caspase-8-independent FasL/Fas-signaling pathway.	ardipusilloside I	0-17	caspase 8	Homo sapiens	74-83
21783950-7	2009	Additionally, we observed a significant decreased apoptosis after the trigger effection of FasL was abolished by the neutralization antibody anti-FasL antibody and an unchanged apoptosis level when the activation of caspase-8 was interrupted by specific inhibitor z-IETD-fmk, which suggested that a casepase-8 independent FasL/Fas-signaling-mediated death receptor pathway is involved.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	264-274	caspase 8	Homo sapiens	216-225
19579625-5	2009	Expressions of caspase-8, -3 and PARP after phosphatidylcholine stimulation were examined by immunoblotting.	Phosphatidylcholines	44-63	caspase 8	Homo sapiens	15-28
19579625-11	2009	Phosphatidylcholine was assumed to reduce hepatic carcinogenesis by apoptosis induction via the death ligands (Fas and/or TNF-alpha) pathway followed by caspase-8 and -3 inductions.	Phosphatidylcholines	0-19	caspase 8	Homo sapiens	153-169
21475816-4	2009	WEEH induced the expression of death receptor-related proteins such as Fas, tumor necrosis factor-related apoptosis-inducing ligand, death receptor (DR) 4 and DR5, which further triggered caspase-8 activation and truncated Bid cleavage.	weeh	0-4	caspase 8	Homo sapiens	188-197
19276187-0	2009	Activation of p38 mitogen-activated protein kinase is required for death receptor-independent caspase-8 activation and cell death in response to sphingosine.	Sphingosine	145-156	caspase 8	Homo sapiens	94-103
19212680-8	2009	Treatment of SH-SY5Y cells with EGCG activated caspase-8, indicating induction of the receptor-mediated pathway of apoptosis.	epigallocatechin gallate	32-36	caspase 8	Homo sapiens	47-56
19112105-0	2009	Caspase-8 mediates mitochondrial release of pro-apoptotic proteins in a manner independent of its proteolytic activity in apoptosis induced by the protein synthesis inhibitor acetoxycycloheximide in human leukemia Jurkat cells.	acetoxycycloheximide	175-195	caspase 8	Homo sapiens	0-9
19276187-3	2009	In this study, we show that sphingosine induces death receptor-independent caspase-8 activation and apoptotic cell death via p38 mitogen-activated protein kinase (MAPK) activation and that suppression of the MAPK/extracellular signal-regulated kinase (ERK) kinase/ERK pathway by protein phosphatase 2A (PP2A) is required for p38 MAPK activation.	Sphingosine	28-39	caspase 8	Homo sapiens	75-84
19276187-5	2009	Inhibition of p38 MAPK led to the marked suppression of death receptor-independent caspase-8 activation and subsequent cell death induced by sphingosine.	Sphingosine	141-152	caspase 8	Homo sapiens	83-92
19276187-9	2009	Our findings clearly imply that activation of p38 MAPK promotes death receptor-independent activation of caspase-8 and apoptotic cell death pathways, thus providing a novel cellular mechanism for the anticancer activity of sphingolipid metabolites.	Sphingolipids	223-235	caspase 8	Homo sapiens	105-114
19252748-7	2009	Furthermore, SD treatment significantly (P &lt; .05) increased the activity and expression of caspase-3 through activation of upstream caspase-8 in A431 cells rather than the activation of caspase 9.	sarcophine-diol	13-15	caspase 8	Homo sapiens	135-144
19112105-6	2009	Consistent with this notion, caspase-8-deficient Jurkat cells reconstituted with catalytically inactive caspase-8 became sensitive to Ac-CHX and exhibited apoptosis, caspase activation, the liberation of pro-apoptotic proteins into the cytosol, and Bak conformational change as efficiently as wild-type Jurkat cells.	acetoxycycloheximide	134-140	caspase 8	Homo sapiens	29-38
19112105-6	2009	Consistent with this notion, caspase-8-deficient Jurkat cells reconstituted with catalytically inactive caspase-8 became sensitive to Ac-CHX and exhibited apoptosis, caspase activation, the liberation of pro-apoptotic proteins into the cytosol, and Bak conformational change as efficiently as wild-type Jurkat cells.	acetoxycycloheximide	134-140	caspase 8	Homo sapiens	104-113
19112105-6	2009	Consistent with this notion, caspase-8-deficient Jurkat cells reconstituted with catalytically inactive caspase-8 became sensitive to Ac-CHX and exhibited apoptosis, caspase activation, the liberation of pro-apoptotic proteins into the cytosol, and Bak conformational change as efficiently as wild-type Jurkat cells.	bakuchiol	249-252	caspase 8	Homo sapiens	29-38
19112105-6	2009	Consistent with this notion, caspase-8-deficient Jurkat cells reconstituted with catalytically inactive caspase-8 became sensitive to Ac-CHX and exhibited apoptosis, caspase activation, the liberation of pro-apoptotic proteins into the cytosol, and Bak conformational change as efficiently as wild-type Jurkat cells.	bakuchiol	249-252	caspase 8	Homo sapiens	104-113
19112105-7	2009	Unlike caspase-3, -6, -7, and -9, a small but significant portion of caspase-8 was found to localize in mitochondria before and after exposure to Ac-CHX.	acetoxycycloheximide	146-152	caspase 8	Homo sapiens	69-78
19014919-7	2009	N-acetyl-l-cysteine pre-treatment rescued cells from MSt-2-induced ROS formation, mitochondrial membrane potential (Delta psi(m)) loss, Fas expression, caspase-8 and -3 activation and DNA fragmentation.	Acetylcysteine	0-19	caspase 8	Homo sapiens	152-168
19239902-5	2009	FAS triggers apoptosis through FADD-mediated recruitment and activation of caspase-8.	ammonium ferrous sulfate	0-3	caspase 8	Homo sapiens	75-84
19235152-5	2009	Pretreatment of a pan-caspase inhibitor (benzyloxycarbonyl)-Val-Ala-Asp-(fluoromethyl) ketone (z-VAD-fmk) significantly increases the viability of 1-treated HeLa cells implied that the participation of caspase; Western-blot analysis showed the activation of initiator caspase-8 and caspase-9, and executor caspase-3.	benzyloxycarbonyl)-val-ala-asp-(fluoromethyl) ketone	41-93	caspase 8	Homo sapiens	268-277
19084044-12	2009	Our experiments with caspase inhibitors Ac-DEVD-CHO, Z-IETD-FMK and Z-VAD-FMK inhibited capsase-3, 8 cleavages but did not prevent OA-induced apoptosis and DNA fragmentation.	acetyl-aspartyl-glutamyl-valyl-aspartal	40-51	caspase 8	Homo sapiens	21-28
19084044-12	2009	Our experiments with caspase inhibitors Ac-DEVD-CHO, Z-IETD-FMK and Z-VAD-FMK inhibited capsase-3, 8 cleavages but did not prevent OA-induced apoptosis and DNA fragmentation.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	53-63	caspase 8	Homo sapiens	21-28
19084044-12	2009	Our experiments with caspase inhibitors Ac-DEVD-CHO, Z-IETD-FMK and Z-VAD-FMK inhibited capsase-3, 8 cleavages but did not prevent OA-induced apoptosis and DNA fragmentation.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	68-77	caspase 8	Homo sapiens	21-28
19550122-10	2009	After mDRA-6 exposure, the proenzymes of Caspase-8, -9 and -3 were reduced and their active cleavage products were increased along with the increase of exposure time, the cleavage products of PARP were also increased, Bid was degraded to tBid, and an abundance of Cyto c was released from mitochondria, but the proenzyme of Caspase-10 showed no change and no cleavage products of Caspase-10 were detectable.	mdra-6	6-12	caspase 8	Homo sapiens	41-61
19550122-10	2009	After mDRA-6 exposure, the proenzymes of Caspase-8, -9 and -3 were reduced and their active cleavage products were increased along with the increase of exposure time, the cleavage products of PARP were also increased, Bid was degraded to tBid, and an abundance of Cyto c was released from mitochondria, but the proenzyme of Caspase-10 showed no change and no cleavage products of Caspase-10 were detectable.	tBID	238-242	caspase 8	Homo sapiens	41-61
19235152-5	2009	Pretreatment of a pan-caspase inhibitor (benzyloxycarbonyl)-Val-Ala-Asp-(fluoromethyl) ketone (z-VAD-fmk) significantly increases the viability of 1-treated HeLa cells implied that the participation of caspase; Western-blot analysis showed the activation of initiator caspase-8 and caspase-9, and executor caspase-3.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	95-104	caspase 8	Homo sapiens	268-277
19006686-5	2009	This study reports novel evidence, which demonstrates that chronic extrinsic cervical spinal cord compression leads to Fas-mediated apoptosis of neurons and oligodendrocytes which is associated with activation of caspase-8, -9 and -3 and progressive neurological deficits.	ammonium ferrous sulfate	119-122	caspase 8	Homo sapiens	213-233
19036482-7	2009	Subsequent gene expression analysis demonstrated that arginine increased the expression of caspase 8, which was validated at the protein level.	Arginine	54-62	caspase 8	Homo sapiens	91-100
19036482-8	2009	CONCLUSIONS: These results suggest that that inhibition of AGS cell growth by arginine is mediated through caspase 8 activation of apoptosis.	Arginine	78-86	caspase 8	Homo sapiens	107-116
19148843-4	2009	Canthaxanthin-induced apoptosis in this cell line was found to be accompanied by increased caspase-3 and caspase-8 activities, indicating its progression via caspase cascade.	Canthaxanthin	0-13	caspase 8	Homo sapiens	105-114
18956207-4	2009	Caspases-8, -9 and -3 activities were increased in irradiated hepatocytes and downregulation of apoptosis by IkappaB antisense oligonucleotides was mediated by suppression of caspases-9 and -3 activation but not of caspase-8 activation, suggesting that radiation-induced sensitization of hepatocytes to TNF-alpha-mediated apoptosis additionally requires changes upstream of caspase-8 activation.	Oligonucleotides	127-143	caspase 8	Homo sapiens	0-21
18956207-4	2009	Caspases-8, -9 and -3 activities were increased in irradiated hepatocytes and downregulation of apoptosis by IkappaB antisense oligonucleotides was mediated by suppression of caspases-9 and -3 activation but not of caspase-8 activation, suggesting that radiation-induced sensitization of hepatocytes to TNF-alpha-mediated apoptosis additionally requires changes upstream of caspase-8 activation.	Oligonucleotides	127-143	caspase 8	Homo sapiens	215-224
18956207-4	2009	Caspases-8, -9 and -3 activities were increased in irradiated hepatocytes and downregulation of apoptosis by IkappaB antisense oligonucleotides was mediated by suppression of caspases-9 and -3 activation but not of caspase-8 activation, suggesting that radiation-induced sensitization of hepatocytes to TNF-alpha-mediated apoptosis additionally requires changes upstream of caspase-8 activation.	Oligonucleotides	127-143	caspase 8	Homo sapiens	374-383
19148492-5	2009	17-AAG was a potent inducer of apoptosis, involving effective depletion of GSH and mitochondrial membrane (MM) depolarization, strong activation of caspase-8 and -9 and release of AIF from mitochondria to the cytosol.	tanespimycin	0-6	caspase 8	Homo sapiens	148-164
18973749-0	2009	Equol induces apoptosis through cytochrome c-mediated caspases cascade in human breast cancer MDA-MB-453 cells.	Equol	0-5	caspase 8	Homo sapiens	54-62
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	caspase 8	Homo sapiens	54-63
19017654-6	2009	Inhibition of caspase-9 reduced GCDCA-induced activation of caspase-6, whereas inhibition of caspase-6 reduced activation of caspase-8 placing caspase-6 between caspase-9 and caspase-8.	Glycochenodeoxycholic Acid	32-37	caspase 8	Homo sapiens	175-184
19000662-0	2009	Pyrogallol inhibits the growth of lung cancer Calu-6 cells via caspase-dependent apoptosis.	Pyrogallol	0-10	caspase 8	Homo sapiens	63-70
19000662-4	2009	The induction of apoptosis by PG was accompanied by the loss of mitochondrial membrane potential (DeltaPsi(m)), cytochrome c release from mitochondria and activation of caspase-3 and caspase-8.	Pyrogallol	30-32	caspase 8	Homo sapiens	183-192
19000662-5	2009	All tested caspase inhibitors, especially the pan-caspase inhibitor (Z-VAD), markedly rescued Calu-6 cells from PG-induced cell death.	z-vad	69-74	caspase 8	Homo sapiens	11-18
19000662-5	2009	All tested caspase inhibitors, especially the pan-caspase inhibitor (Z-VAD), markedly rescued Calu-6 cells from PG-induced cell death.	Pyrogallol	112-114	caspase 8	Homo sapiens	11-18
19000662-8	2009	In conclusion, PG inhibits the growth of Calu-6 cells via caspase-dependent apoptosis.	Pyrogallol	15-17	caspase 8	Homo sapiens	58-65
19159448-7	2009	In addition, up-regulation of caspase-3 and caspase-8 after SAH was decreased by atorvastatin treatment both in mRNA and in protein levels.	Atorvastatin	81-93	caspase 8	Homo sapiens	44-53
20077182-0	2009	Titanium dioxide (TiO2) nanoparticles induce JB6 cell apoptosis through activation of the caspase-8/Bid and mitochondrial pathways.	titanium dioxide	0-16	caspase 8	Homo sapiens	90-99
19160091-2	2009	We tried to determine the methylation status and its impact on the expression of two tumor related genes Casp-8 and Rb1 in 103 bladder tumor tissues and 48 control paraffin-embedded tissues by using MSP-PCR and SQRT-PCR.	Paraffin	164-172	caspase 8	Homo sapiens	105-111
19940360-0	2009	Fas-induced apoptosis of renal cell carcinoma is mediated by apoptosis signal-regulating kinase 1 via mitochondrial damage-dependent caspase-8 activation.	ammonium ferrous sulfate	0-3	caspase 8	Homo sapiens	133-142
19082486-4	2009	Doxorubicin induced dose-dependent G2/M and/or G1/S cell cycle arrest, followed by grade- and dose-dependent reduction in the amount of the cytosolic trimeric form of FasL, activation of Caspase-8, Caspase-9, Caspase-3, cleavage of PARP, Lamin A/C, Bcl-XL/S and interestingly Hsp90, and finally cell death.	Doxorubicin	0-11	caspase 8	Homo sapiens	187-196
18766198-8	2009	Our in vitro work shows that Hcy-mediated EPC toxicity is due to apoptosis involving caspase-8, cytochrome c release, and caspase-3 activation.	Homocysteine	29-32	caspase 8	Homo sapiens	85-94
19710936-5	2009	In both cell lines, apoptosis was abolished by caspase-9 inhibitor Z-LEHD-fmk but was weakly inhibited by caspase-8 inhibitor Z-IETD-fmk, indicating that caspase-9 activation was involved in TJ-41 induced apoptosis.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	126-136	caspase 8	Homo sapiens	106-115
19055367-9	2009	Caspase-8 inhibitor (Z-IETD) or wide-ranging caspase inhibitor (Z-VAD) significantly suppressed the bufotalin-induced apoptosis, while the anti-Fas neutralization antibody had no effect.	z-ietd	21-27	caspase 8	Homo sapiens	0-9
19055367-9	2009	Caspase-8 inhibitor (Z-IETD) or wide-ranging caspase inhibitor (Z-VAD) significantly suppressed the bufotalin-induced apoptosis, while the anti-Fas neutralization antibody had no effect.	bufotalin	100-109	caspase 8	Homo sapiens	0-9
18774638-7	2009	The growth-inhibitory action of mesalazine and butyrate was accompanied by a significant increase in caspase-3 activity, cleavage of PARP and caspase-8, while decreasing the expression of Xiap and Survivin simultaneously.	Mesalamine	32-42	caspase 8	Homo sapiens	142-151
18774638-7	2009	The growth-inhibitory action of mesalazine and butyrate was accompanied by a significant increase in caspase-3 activity, cleavage of PARP and caspase-8, while decreasing the expression of Xiap and Survivin simultaneously.	Butyrates	47-55	caspase 8	Homo sapiens	142-151
18987254-8	2009	Inhibition of caspases by z-VAD-fmk as well as overexpression of Fas-associated death domain-like interleukin-1beta-converting enzyme (FLICE)-like inhibitory proteins FLIP(L) and FLIP(S) to inhibit receptor-mediated apoptosis did not block PV-IgG-induced effects, indicating that apoptosis was not required.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	26-35	caspase 8	Homo sapiens	14-22
19122287-0	2009	3-Oxoolean-12-en-27-oic acid isolated from Aceriphyllum rossii induces caspase-8-dependent apoptosis in human promyelocytic leukemia HL-60 cells.	3-oxoolean-12-en-27-oic acid	0-28	caspase 8	Homo sapiens	71-80
19122287-4	2009	In addition, z-IETD-fmk (a caspase-8 inhibitor) and z-DEVD-fmk (a caspase-3 inhibitor) also completely neutralized the apoptotic effect of 3-OA in HL-60 cells.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	13-23	caspase 8	Homo sapiens	27-36
19122287-7	2009	Taken together, these results suggest that 3-oxoolean-12-en-27-oic acid induces apoptosis by activating caspase-8 via FasL-stimulated death receptor signaling.	3-oxoolean-12-en-27-oic acid	43-71	caspase 8	Homo sapiens	104-113
19082499-3	2009	In this report, using MIA PaCa-2 cells as in vitro model, we demonstrate EGCG-induced cell death involves activation of caspase-8 and disappearance of intact 21 kDa Bid protein.	epigallocatechin gallate	73-77	caspase 8	Homo sapiens	120-129
19082499-4	2009	Furthermore, exogenous expression of dominant negative caspase-8 or dominant negative FADD significantly abrogates apoptosis inducing ability of EGCG in MIA PaCa-2 cells.	epigallocatechin gallate	145-149	caspase 8	Homo sapiens	55-64
20077182-0	2009	Titanium dioxide (TiO2) nanoparticles induce JB6 cell apoptosis through activation of the caspase-8/Bid and mitochondrial pathways.	titanium dioxide	18-22	caspase 8	Homo sapiens	90-99
20077182-7	2009	Western-blot analysis showed an activation of caspase-8, Bid, BAX, and caspase-3 and a decrease of Bcl-2 in JB6 cells treated with TiO(2) particles.	titanium dioxide	131-137	caspase 8	Homo sapiens	46-55
19544974-2	2009	Here we showed that mitochondrial apoptosis signaling pathway played a vital role in apoptosis induced by sodium selenite based on the following findings: 1) cytochrome c release, activation of caspase 9, mitochondrial targeting, and oligermerization of Bax; 2) caspase 9, but not caspase 8, inhibitor could attenuate apoptosis; 3) downregulation of Bax and Bad by siRNA could delay sodium selenite-induced apoptosis.	Sodium Selenite	106-121	caspase 8	Homo sapiens	281-290
19239323-7	2009	However, blockade of morphine-induced cell death by beta-arrestin2 seems to be dependent on the inhibition of caspase-8, as inhibition of beta-arrestin2 and morphine treatment significantly enhanced the levels of cleaved caspase-8.	Morphine	21-29	caspase 8	Homo sapiens	110-119
19239323-7	2009	However, blockade of morphine-induced cell death by beta-arrestin2 seems to be dependent on the inhibition of caspase-8, as inhibition of beta-arrestin2 and morphine treatment significantly enhanced the levels of cleaved caspase-8.	Morphine	21-29	caspase 8	Homo sapiens	221-230
19239323-7	2009	However, blockade of morphine-induced cell death by beta-arrestin2 seems to be dependent on the inhibition of caspase-8, as inhibition of beta-arrestin2 and morphine treatment significantly enhanced the levels of cleaved caspase-8.	Morphine	157-165	caspase 8	Homo sapiens	110-119
19239323-7	2009	However, blockade of morphine-induced cell death by beta-arrestin2 seems to be dependent on the inhibition of caspase-8, as inhibition of beta-arrestin2 and morphine treatment significantly enhanced the levels of cleaved caspase-8.	Morphine	157-165	caspase 8	Homo sapiens	221-230
19239323-8	2009	These studies show for the first time that beta-arrestin2 blocks morphine-induced cell death through anti-apoptotic Akt and pro-apoptotic caspase-8 pathways.	Morphine	65-73	caspase 8	Homo sapiens	138-147
18974049-2	2008	Previously, we identified caspase 8 as an effector of migration, promoting motility in a manner dependent upon phosphorylation on Tyr-380 by Src family kinases and its subsequent association with Src homology 2 domain-containing proteins.	Tyrosine	130-133	caspase 8	Homo sapiens	26-35
19352436-5	2009	Silencing of Fas/CD95 by RNA interference, transfection with a FADD dominant-negative mutant that blocks Fas/CD95 signaling, and specific inhibition of caspase-8 prevented the apoptotic response triggered by edelfosine, hence demonstrating the functional role of DISC in drug-induced apoptosis.	edelfosine	208-218	caspase 8	Homo sapiens	152-161
19768687-5	2009	Moreover, the newly developed atomic structural refinement algorithm was tested in CASP8 and found to improve the hydrogen-bonding networks and the overall TM-score, which is mainly due to its ability of removing steric clashes so that the models can be generated from cluster centroids.	Hydrogen	114-122	caspase 8	Homo sapiens	83-88
19134456-7	2009	Puerarin significantly enhanced the gene expressions in endometriotic stromal cells, including BAD, BAX, CASP8, CASP9, TNFRSF6, CDKN1B, CDKN2A, IFNA1 and IFNB1, and reduced the gene expressions of FOS, CHEK2, SRC, ITGB5, MMP9, PDGFA and NFKBIA.	puerarin	0-8	caspase 8	Homo sapiens	105-110
18974049-6	2008	Interaction between caspase 8 and p85alpha promotes Rab5 GTP loading, alters endosomal trafficking, and results in the accumulation of Rab5-positive endosomes at the edge of the cell.	Guanosine Triphosphate	57-60	caspase 8	Homo sapiens	20-29
18974049-7	2008	Conversely, caspase 8-dependent GTP loading of Rab5 is overcome by increased expression of p85alpha in a Rab-GAP-dependent manner.	Guanosine Triphosphate	32-35	caspase 8	Homo sapiens	12-21
19091943-7	2008	We further used this approach to identify genes involved in the response of cancer cells to tumoricidal agents and found 4 genes required for the response of CML cells to imatinib treatment: PTPN1, NF1, SMARCB1, and SMARCE1, and 5 regulators of the response to FAS activation, FAS, FADD, CASP8, ARID1A and CBX1.	Imatinib Mesylate	171-179	caspase 8	Homo sapiens	288-293
18980244-6	2008	Furthermore, treatment with quercetin significantly decreased the protein levels of c-FLIP, an inhibitor of caspase-8, through proteasome-mediated degradation.	Quercetin	28-37	caspase 8	Homo sapiens	108-117
19084933-8	2008	The general caspase inhibitor (VAD-fmk) completely abolished metformin-induced PARP cleavage and apoptosis in ASPC-1 BxPc-3 and PANC-1, the caspase-8 specific inhibitor (IETD-fmk) and the caspase-9 specific inhibitor (LEHD-fmk) only partially abrogated metformin-induced apoptosis and PARP cleavage in BxPc-3 and PANC-1 cells.	VAD-fmk	31-38	caspase 8	Homo sapiens	140-149
19084933-8	2008	The general caspase inhibitor (VAD-fmk) completely abolished metformin-induced PARP cleavage and apoptosis in ASPC-1 BxPc-3 and PANC-1, the caspase-8 specific inhibitor (IETD-fmk) and the caspase-9 specific inhibitor (LEHD-fmk) only partially abrogated metformin-induced apoptosis and PARP cleavage in BxPc-3 and PANC-1 cells.	Metformin	61-70	caspase 8	Homo sapiens	140-149
19084933-8	2008	The general caspase inhibitor (VAD-fmk) completely abolished metformin-induced PARP cleavage and apoptosis in ASPC-1 BxPc-3 and PANC-1, the caspase-8 specific inhibitor (IETD-fmk) and the caspase-9 specific inhibitor (LEHD-fmk) only partially abrogated metformin-induced apoptosis and PARP cleavage in BxPc-3 and PANC-1 cells.	isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	170-178	caspase 8	Homo sapiens	140-149
19084933-12	2008	Hence, both caspase-8 and -9-initiated apoptotic signaling pathways contribute to metformin-induced apoptosis in pancreatic cell lines.	Metformin	82-91	caspase 8	Homo sapiens	12-28
19020753-7	2008	Treatment with anti-myeloma drugs (melphalan, dexamethasone, bortezomib and immunomodulatory compounds) induced apoptosis earlier in D1 transfectants compared with RPMI8226 and mock control via the activation of both caspase-8 and -9.	Melphalan	35-44	caspase 8	Homo sapiens	217-233
18845126-5	2008	The caspase-8 inhibitor (z-IETD-fmk), which failed to influence pFPhe-induced caspase-9 activation, completely blocked caspase-8 activation and PLCgamma-1 degradation with a marked reduction in caspase-3 activation and PARP degradation, indicating pFPhe-induced caspase-8 activation as a downstream event of mitochondria-dependent activation of caspase-9.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	25-35	caspase 8	Homo sapiens	4-13
18845126-5	2008	The caspase-8 inhibitor (z-IETD-fmk), which failed to influence pFPhe-induced caspase-9 activation, completely blocked caspase-8 activation and PLCgamma-1 degradation with a marked reduction in caspase-3 activation and PARP degradation, indicating pFPhe-induced caspase-8 activation as a downstream event of mitochondria-dependent activation of caspase-9.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	25-35	caspase 8	Homo sapiens	119-128
18845126-5	2008	The caspase-8 inhibitor (z-IETD-fmk), which failed to influence pFPhe-induced caspase-9 activation, completely blocked caspase-8 activation and PLCgamma-1 degradation with a marked reduction in caspase-3 activation and PARP degradation, indicating pFPhe-induced caspase-8 activation as a downstream event of mitochondria-dependent activation of caspase-9.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	25-35	caspase 8	Homo sapiens	119-128
18835311-0	2008	Activation of cAMP signaling enhances Fas-mediated apoptosis and activation-induced cell death through potentiation of caspase 8 activation.	Cyclic AMP	14-18	caspase 8	Homo sapiens	119-128
18835311-5	2008	Accordingly, cAMP was found to enhance the cleavage of caspase 8 at death-inducing signaling complex and lead to augmentation of the processing of Fas effector proteins.	Cyclic AMP	13-17	caspase 8	Homo sapiens	55-64
19037992-13	2008	These results suggest that bufalin and cinobufagin suppress cell proliferation and cause apoptosis in prostate cancer cells via a sequence of apoptotic modulators, including Bax, cytochrome c, and caspases.	bufalin	27-34	caspase 8	Homo sapiens	197-205
19037992-13	2008	These results suggest that bufalin and cinobufagin suppress cell proliferation and cause apoptosis in prostate cancer cells via a sequence of apoptotic modulators, including Bax, cytochrome c, and caspases.	cinobufagin	39-50	caspase 8	Homo sapiens	197-205
18848968-7	2008	DHCL promoted apoptosis with increased activation of caspases 8, 9, 7, 3, enhanced PARP cleavage, decreased Bcl-xL expression and increased levels of Bax, Bak, Bok, Bik, Bmf, and t-Bid.	dehydrocostus lactone	0-4	caspase 8	Homo sapiens	53-61
19020753-7	2008	Treatment with anti-myeloma drugs (melphalan, dexamethasone, bortezomib and immunomodulatory compounds) induced apoptosis earlier in D1 transfectants compared with RPMI8226 and mock control via the activation of both caspase-8 and -9.	Dexamethasone	46-59	caspase 8	Homo sapiens	217-233
19020753-7	2008	Treatment with anti-myeloma drugs (melphalan, dexamethasone, bortezomib and immunomodulatory compounds) induced apoptosis earlier in D1 transfectants compared with RPMI8226 and mock control via the activation of both caspase-8 and -9.	Bortezomib	61-71	caspase 8	Homo sapiens	217-233
19020760-10	2008	Treatment of hepatoma cells with 2-methoxyestradiol or lactic acid resulted in up-regulation of caspase-8, -9 and -3.	2-Methoxyestradiol	33-51	caspase 8	Homo sapiens	96-116
19020760-10	2008	Treatment of hepatoma cells with 2-methoxyestradiol or lactic acid resulted in up-regulation of caspase-8, -9 and -3.	Lactic Acid	55-66	caspase 8	Homo sapiens	96-116
19010914-6	2008	Perifosine and TRAIL synergized to activate caspase-8 and induce apoptosis, which was blocked by a caspase-8-selective inhibitor.	perifosine	0-10	caspase 8	Homo sapiens	44-53
18667267-3	2008	Furanodiene induced apoptosis of HL60 cells, characterized by DNA fragmentation, cleavage of poly (ADP-ribose) polymerase (PARP), caspase-3, caspase-8 and caspase-9.	furanodiene	0-11	caspase 8	Homo sapiens	141-150
18667267-4	2008	In the Bcl-2 family proteins, Bid protein (a substrate of caspase-8) was activated by furanodiene, but Bcl-2, Bax and Bcl-xL proteins were not influenced by furanodiene stimulation.	furanodiene	86-97	caspase 8	Homo sapiens	58-67
19099630-9	2008	The expression of caspase 8 and caspase 3 protein enhanced and reached the peak after treating with PUVA for 8 hours.	puva	100-104	caspase 8	Homo sapiens	18-27
19099630-11	2008	The possible mechanism is supposed to be up-regulating Fas, down-regulating FasL levels and then activating the levels of caspase 8 and caspase 3.	ammonium ferrous sulfate	55-58	caspase 8	Homo sapiens	122-131
19001025-12	2008	Isoproterenol and aldosterone upregulate Fas ligand expression, and Fas ligand and caspase-8 are required for isoproterenol and aldosterone to induce apoptosis.	Isoproterenol	110-123	caspase 8	Homo sapiens	83-92
19010914-6	2008	Perifosine and TRAIL synergized to activate caspase-8 and induce apoptosis, which was blocked by a caspase-8-selective inhibitor.	perifosine	0-10	caspase 8	Homo sapiens	99-108
19189638-0	2008	Role of caspases in 5-FU and selenium-induced growth inhibition of colorectal cancer cells.	Fluorouracil	20-24	caspase 8	Homo sapiens	8-16
18780184-7	2008	Initiator caspase-8, with Pro in the P5-anchoring position and no loop-4, had only 20% activity on tested pentapeptides relative to DEVD.	Proline	26-29	caspase 8	Homo sapiens	10-19
19189638-6	2008	Conversely, RKO cells expressing wildtype p53, proteolytically activated caspase-8, -9, -7 and -3 and unmethylated caspase-8 were more responsive to 5-FU and selenous acid-induced apoptosis.	Fluorouracil	149-153	caspase 8	Homo sapiens	73-97
19189638-0	2008	Role of caspases in 5-FU and selenium-induced growth inhibition of colorectal cancer cells.	Selenium	29-37	caspase 8	Homo sapiens	8-16
19189638-6	2008	Conversely, RKO cells expressing wildtype p53, proteolytically activated caspase-8, -9, -7 and -3 and unmethylated caspase-8 were more responsive to 5-FU and selenous acid-induced apoptosis.	Fluorouracil	149-153	caspase 8	Homo sapiens	73-82
18708163-5	2008	In contrast, the caspase inhibitors, p53-siRNA, and Noxa-siRNA suppressed H(2)O(2)-induced cell death.	Hydrogen Peroxide	74-82	caspase 8	Homo sapiens	17-24
19189638-6	2008	Conversely, RKO cells expressing wildtype p53, proteolytically activated caspase-8, -9, -7 and -3 and unmethylated caspase-8 were more responsive to 5-FU and selenous acid-induced apoptosis.	Selenious Acid	158-171	caspase 8	Homo sapiens	73-97
19189638-6	2008	Conversely, RKO cells expressing wildtype p53, proteolytically activated caspase-8, -9, -7 and -3 and unmethylated caspase-8 were more responsive to 5-FU and selenous acid-induced apoptosis.	Selenious Acid	158-171	caspase 8	Homo sapiens	73-82
18948750-0	2008	Ceramide promotes apoptosis in chronic myelogenous leukemia-derived K562 cells by a mechanism involving caspase-8 and JNK.	Ceramides	0-8	caspase 8	Homo sapiens	104-113
18948750-3	2008	C6-ceramide induces cleavage of Caspase-8 and Caspase-9, but only Caspase-8 is required for apoptosis.	N-caproylsphingosine	0-11	caspase 8	Homo sapiens	32-41
19210862-4	2008	Caspase-8 activity was evaluated by spectrophotometric detection of cleavage from p-nitroanilide-labeled IETD, a substrate of caspase-8.	p-nitroanilide	82-96	caspase 8	Homo sapiens	0-9
19210862-4	2008	Caspase-8 activity was evaluated by spectrophotometric detection of cleavage from p-nitroanilide-labeled IETD, a substrate of caspase-8.	p-nitroanilide	82-96	caspase 8	Homo sapiens	126-135
19210862-4	2008	Caspase-8 activity was evaluated by spectrophotometric detection of cleavage from p-nitroanilide-labeled IETD, a substrate of caspase-8.	IETD	105-109	caspase 8	Homo sapiens	0-9
19210862-4	2008	Caspase-8 activity was evaluated by spectrophotometric detection of cleavage from p-nitroanilide-labeled IETD, a substrate of caspase-8.	IETD	105-109	caspase 8	Homo sapiens	126-135
18710416-3	2008	In this study, we demonstrate that miltefosine-induced apoptosis is accompanied by elevated Fas, Fas-associated death domain (FADD) expression, caspase-8 activity and the increased distribution of Fas and FADD towards lipid raft microdomain to form death inducing signaling complex.	miltefosine	35-46	caspase 8	Homo sapiens	144-153
18709644-7	2008	Ebselen also induced the formation of DISC involving Fas, Fas-associated death domain (FADD) and active caspase 8 to transduce apoptotic signals in situations where NF-kappaB function was inhibited.	ebselen	0-7	caspase 8	Homo sapiens	104-113
19001439-11	2008	However, we also show that the combined treatment of TRAIL and kaempferol induces cleavage (activation) of caspase-8, thereby exerting a proapoptotic effect independent of survivin known not to inhibit caspase-8 activation.	kaempferol	63-73	caspase 8	Homo sapiens	107-116
19012662-8	2008	Melatonin treatment also resulted in increased caspase-8 activity, although no significant change was observed in Fas-L expression.	Melatonin	0-9	caspase 8	Homo sapiens	47-56
19001439-11	2008	However, we also show that the combined treatment of TRAIL and kaempferol induces cleavage (activation) of caspase-8, thereby exerting a proapoptotic effect independent of survivin known not to inhibit caspase-8 activation.	kaempferol	63-73	caspase 8	Homo sapiens	202-211
18787411-11	2008	Thus sorafenib and vorinostat promote ceramide-dependent CD95 activation followed by induction of multiple downstream survival regulatory signals: ceramide-CD95-PERK-FADD-pro-caspase 8 (death); ceramide-CD95-PERK-eIF2alpha- downward arrowc-FLIP-s (death); ceramide-CD95-PERK-ATG5-autophagy (survival).	Vorinostat	19-29	caspase 8	Homo sapiens	175-184
18922907-5	2008	The proapoptotic effects of this treatment combination were abrogated by a caspase-8 inhibitor, led to increased association of Fas and FADD before the onset of cell death, and were significantly reduced in cells transfected with a dominant-negative FADD construct or small interfering RNA targeting Fas.	ammonium ferrous sulfate	128-131	caspase 8	Homo sapiens	75-84
18922907-6	2008	These data suggest that bortezomib and IFN-alpha act through the extrinsic pathway of apoptosis via FADD-induced caspase-8 activation to initiate cell death.	Bortezomib	24-34	caspase 8	Homo sapiens	113-122
18726190-4	2008	In SW480 cells, lupulone triggered cell death through a cross-talk between TRAIL-DR4/DR5 and the mitochondrial (intrinsic) pathways involving caspase-8 activation and Bid protein cleavage.	lupulon	16-24	caspase 8	Homo sapiens	142-151
18726190-6	2008	In the metastatic SW620 cells, lupulone restored the sensibility of these cells to TRAIL ligand and activated the extrinsic apoptotic pathway via DR4/DR5 death receptors and the involvement of the caspase-8/caspase-3 cascade.	lupulon	31-39	caspase 8	Homo sapiens	197-206
18787411-3	2008	Low doses of sorafenib and vorinostat, but not the individual agents, caused an acidic sphingomyelinase and fumonisin B1-dependent increase in CD95 surface levels and CD95 association with caspase 8.	Sorafenib	13-22	caspase 8	Homo sapiens	189-198
18787411-3	2008	Low doses of sorafenib and vorinostat, but not the individual agents, caused an acidic sphingomyelinase and fumonisin B1-dependent increase in CD95 surface levels and CD95 association with caspase 8.	Vorinostat	27-37	caspase 8	Homo sapiens	189-198
18696228-9	2008	These results showed that TCDD influences BHV-1 induced apoptosis through members of Bcl-2 family and up-regulating activation of caspases.	Polychlorinated Dibenzodioxins	26-30	caspase 8	Homo sapiens	130-138
18787411-11	2008	Thus sorafenib and vorinostat promote ceramide-dependent CD95 activation followed by induction of multiple downstream survival regulatory signals: ceramide-CD95-PERK-FADD-pro-caspase 8 (death); ceramide-CD95-PERK-eIF2alpha- downward arrowc-FLIP-s (death); ceramide-CD95-PERK-ATG5-autophagy (survival).	Ceramides	147-155	caspase 8	Homo sapiens	175-184
18787411-11	2008	Thus sorafenib and vorinostat promote ceramide-dependent CD95 activation followed by induction of multiple downstream survival regulatory signals: ceramide-CD95-PERK-FADD-pro-caspase 8 (death); ceramide-CD95-PERK-eIF2alpha- downward arrowc-FLIP-s (death); ceramide-CD95-PERK-ATG5-autophagy (survival).	Sorafenib	5-14	caspase 8	Homo sapiens	175-184
18787411-11	2008	Thus sorafenib and vorinostat promote ceramide-dependent CD95 activation followed by induction of multiple downstream survival regulatory signals: ceramide-CD95-PERK-FADD-pro-caspase 8 (death); ceramide-CD95-PERK-eIF2alpha- downward arrowc-FLIP-s (death); ceramide-CD95-PERK-ATG5-autophagy (survival).	Ceramides	147-155	caspase 8	Homo sapiens	175-184
18787411-11	2008	Thus sorafenib and vorinostat promote ceramide-dependent CD95 activation followed by induction of multiple downstream survival regulatory signals: ceramide-CD95-PERK-FADD-pro-caspase 8 (death); ceramide-CD95-PERK-eIF2alpha- downward arrowc-FLIP-s (death); ceramide-CD95-PERK-ATG5-autophagy (survival).	Ceramides	147-155	caspase 8	Homo sapiens	175-184
18603276-7	2008	The caspase-8 inhibitor z-IETD-fmk failed to influence 17alpha-E(2)-mediated caspase-9 activation, but it markedly reduced caspase-3 activation and PARP degradation with the suppression of apoptosis, indicating the contribution of caspase-8; not as an upstream event of the mitochondrial cytochrome c release, but to caspase-3 activation.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	24-34	caspase 8	Homo sapiens	4-13
18615109-2	2008	We have shown that death of these precursors involved the Fas-dependent activation of caspase-8.	ammonium ferrous sulfate	58-61	caspase 8	Homo sapiens	86-95
18603835-10	2008	Silencing of cFLIP promoted cleavage of procaspase-8, and the cell death caused by cFLIP siRNA was completely blocked by a caspase-8 inhibitor (Z-IETD-FMK), indicating that cFLIP regulates apoptosis in KGN cells by inhibiting cleavage of procaspase-8.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	144-154	caspase 8	Homo sapiens	43-52
18770054-5	2008	Considering that the minocyicline decreases Citocrome discharge, reducing executors caspases expression proceeding from intrinsic pathway, is justified its effectiveness in TgALS, but could not be explained if apoptosis in SALS was developed primarily on FAS pathway.	minocyicline	21-33	caspase 8	Homo sapiens	84-92
18806879-7	2008	Pretreatment with a general caspase inhibitor (Z-VAD-FMK), a caspase-8 inhibitor (Z-IETD-FMK), and a caspase-9 inhibitor (Z-LEHD-FMK) reversed MMC-induced cellular damage.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	82-92	caspase 8	Homo sapiens	61-70
18806879-10	2008	CONCLUSIONS: These results indicate that mitomycin-induced cellular apoptosis in corneal endothelial cells may be mediated through caspase-8, caspase-9, and the mitochondrial regulated pathways as well as through upregulation of p53-dependent and p21-dependent signal transduction pathways.	Mitomycin	41-50	caspase 8	Homo sapiens	131-140
18485587-5	2008	In addition, inhibitors of caspase-8 or -9 partially protected HeLa cells from 2"-nitroflavone-induced cell death.	2'-nitroflavone	79-94	caspase 8	Homo sapiens	27-42
18642387-11	2008	We show that after caspase-8 activation, when centromeres shift to a peripheral localization, the spatial distribution of PML-NBs does not change while that of centromeres did.	pml-nbs	122-129	caspase 8	Homo sapiens	19-28
18765530-7	2008	Sorafenib and vorinostat treatment increased surface levels of CD95 and CD95 association with caspase-8.	Sorafenib	0-9	caspase 8	Homo sapiens	94-103
18765530-7	2008	Sorafenib and vorinostat treatment increased surface levels of CD95 and CD95 association with caspase-8.	Vorinostat	14-24	caspase 8	Homo sapiens	94-103
18757413-3	2008	CDDO-Me induced caspase-3, caspase-8, and caspase-9 activation; poly(ADP-ribose) polymerase cleavage; internucleosomal DNA fragmentation; and loss of 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide reduction in PC3 and DU145 cells.	bardoxolone methyl	0-7	caspase 8	Homo sapiens	27-36
18757413-4	2008	However, caspase-3 and caspase-8 inhibition by Z-DEVD-fmk and Z-IETD-fmk, respectively, or general caspase inhibition by BOC-D-fmk or Z-VAD-fmk did not rescue loss of cell viability induced by CDDO-Me, suggesting the activation of additional caspase-independent mechanisms.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	62-72	caspase 8	Homo sapiens	23-32
18807138-11	2008	However, cell viability was unaffected by addition of the caspase-8 inhibitor z-IETD-fmk.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	78-88	caspase 8	Homo sapiens	58-67
18728974-7	2008	The authors conclude that IFNgamma can sensitize SH-SY5Y cells to Adriamycin-, TNFalpha-, and TRAIL-induced apoptosis and this may be realized by the upregulation of caspase 8.	Doxorubicin	66-76	caspase 8	Homo sapiens	166-175
18524889-4	2008	Erlotinib induces apoptosis associated with the activation of caspases in a dose- and time-dependent manner.	Erlotinib Hydrochloride	0-9	caspase 8	Homo sapiens	62-70
18524889-5	2008	Erlotinib did not alter the expression of apoptotic receptors FAS and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), although it induced caspase-8 activation and BID cleavage.	Erlotinib Hydrochloride	0-9	caspase 8	Homo sapiens	155-164
18790785-9	2008	MSA induced a sequential activation of caspase-9 and then caspase-8.	methylselenic acid	0-3	caspase 8	Homo sapiens	58-67
19175174-1	2008	OBJECTIVE: To explore the effects of p,p"-DDE and beta-BHC on the apoptosis of Sertoli cells in vitro via activation of Caspase.	Dichlorodiphenyl Dichloroethylene	37-45	caspase 8	Homo sapiens	120-127
18622903-8	2008	Tanshinone IIA-induced catalytic activation of caspases was confirmed by cleavage of caspase-8 and caspase-3.	tanshinone	0-14	caspase 8	Homo sapiens	47-55
18622903-8	2008	Tanshinone IIA-induced catalytic activation of caspases was confirmed by cleavage of caspase-8 and caspase-3.	tanshinone	0-14	caspase 8	Homo sapiens	85-94
18622903-9	2008	These findings suggest that tanshinone IIA induces apoptosis in Colo-205 cells through both mitochondrial-mediated intrinsic and Fas-mediated extrinsic caspase cell-death pathways.	tanshinone	28-42	caspase 8	Homo sapiens	152-159
18622903-9	2008	These findings suggest that tanshinone IIA induces apoptosis in Colo-205 cells through both mitochondrial-mediated intrinsic and Fas-mediated extrinsic caspase cell-death pathways.	ammonium ferrous sulfate	129-132	caspase 8	Homo sapiens	152-159
18766267-10	2008	Simvastatin promotes detachment and EMP release by inhibiting prenylation, presumably via a caspase 8-dependent mechanism.	Simvastatin	0-11	caspase 8	Homo sapiens	92-101
19175174-1	2008	OBJECTIVE: To explore the effects of p,p"-DDE and beta-BHC on the apoptosis of Sertoli cells in vitro via activation of Caspase.	beta-hexachlorocyclohexane	50-58	caspase 8	Homo sapiens	120-127
19175174-10	2008	The expressions of Caspase-3, Caspase-8 and Caspase-9 were upregulated as the concentrations of p,p"-DDE, beta-BHC and their mixture were increased.	Dichlorodiphenyl Dichloroethylene	96-104	caspase 8	Homo sapiens	30-39
19175174-10	2008	The expressions of Caspase-3, Caspase-8 and Caspase-9 were upregulated as the concentrations of p,p"-DDE, beta-BHC and their mixture were increased.	beta-hexachlorocyclohexane	106-114	caspase 8	Homo sapiens	30-39
19175174-11	2008	CONCLUSION: p,p"-DDE, beta-BHC and their mixture could induce the apoptosis of Sertoli cells in vitro which was associated with activation of Caspase-3 mediated by cleavage of Caspase-8 and Caspase-9.	Dichlorodiphenyl Dichloroethylene	12-20	caspase 8	Homo sapiens	176-185
19175174-11	2008	CONCLUSION: p,p"-DDE, beta-BHC and their mixture could induce the apoptosis of Sertoli cells in vitro which was associated with activation of Caspase-3 mediated by cleavage of Caspase-8 and Caspase-9.	beta-hexachlorocyclohexane	22-30	caspase 8	Homo sapiens	176-185
18356818-12	2008	The pan-caspase inhibitor Z-VAD-FMK and caspase-8 inhibitor Z-IETD-FMK, but not the caspase-9 inhibitor Z-IEHD-FMK, protected tumor cells from MV-CEA/GA-induced PARP activation, indicating that apoptosis in combination-treated cells occurs mainly via the extrinsic caspase pathway.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	60-70	caspase 8	Homo sapiens	40-49
18618576-8	2008	In addition, 3-indole stimulated caspases-3, -9, and to a lesser extent caspase-8 activities in cancer cells, suggesting that the intrinsic mitochondria pathway was the potential mechanism involved in 3-indole-induced apoptosis.	1,1,3-tris(3-indolyl)cyclohexane	13-21	caspase 8	Homo sapiens	72-81
18676836-5	2008	The MUC1 cytoplasmic domain (MUC1-CD) binds directly to the caspase-8 p18 fragment upstream to the catalytic Cys(360) site.	Cysteine	109-112	caspase 8	Homo sapiens	60-69
18636160-8	2008	We hypothesize that 5-aza-2 deoxycytidine aza-dCR, decitabine may render TRAIL-resistant prostate cancer cells sensitive to caspase-8-mediated apoptosis and may, therefore, be therapeutically efficient.	5-aza-2 deoxycytidine aza-dcr	20-49	caspase 8	Homo sapiens	124-133
18636160-8	2008	We hypothesize that 5-aza-2 deoxycytidine aza-dCR, decitabine may render TRAIL-resistant prostate cancer cells sensitive to caspase-8-mediated apoptosis and may, therefore, be therapeutically efficient.	Decitabine	51-61	caspase 8	Homo sapiens	124-133
18636160-10	2008	Here, we provide evidence that treatment with sub-optimal concentrations of decitabine are additive to TRAIL effects in well-differentiated PCa cells whereas the same treatment shows synergistic effects in poorly-differentiated PCa cells through increased caspase-8 expression, down-modulation of Akt activation and through the expression of certain anti-apoptotic molecules including FLIP, PED/PEA-15, survivin and c-IAP-1.	Decitabine	76-86	caspase 8	Homo sapiens	256-265
18636160-11	2008	Our findings demonstrate that decitabine at relatively low concentrations restores caspase-8 expression and sensitises resistant PCa cells to TRAIL-induced apoptosis leading to important implications in novel therapeutic strategies targeting defective apoptosis pathways in advanced prostate tumors.	Decitabine	30-40	caspase 8	Homo sapiens	83-92
18508926-0	2008	DNA-ligase IV and DNA-protein kinase play a critical role in deficient caspases activation in apoptosis-resistant cancer cells by using doxorubicin.	Doxorubicin	136-147	caspase 8	Homo sapiens	71-79
18508926-5	2008	Inhibition of NHEJ by knocking out DNA-PK or DNA-ligase IV restored caspases activation and apoptosis sensitivity after doxorubicin treatment.	Doxorubicin	120-131	caspase 8	Homo sapiens	68-76
18508926-6	2008	In addition, inhibition of caspases activation prevented doxorubicin-induced apoptosis but could not prevent doxorubicin-induced DNA damage, indicating that induction of DNA damage is independent of caspases activation.	Doxorubicin	57-68	caspase 8	Homo sapiens	27-35
18508926-8	2008	We conclude that DNA damage left unrepaired by DNA-ligase IV or DNA-PK might be the initiator for caspases activation by doxorubicin in cancer cells.	Doxorubicin	121-132	caspase 8	Homo sapiens	98-106
18508926-9	2008	Failure in caspases activation using doxorubicin depends on loss of DNA damage and is due to higher rates of NHEJ-DNA-DBS-repair.	Doxorubicin	37-48	caspase 8	Homo sapiens	11-19
18650325-3	2008	Caspases were critically required, because the death was completely blocked by caspase inhibitor BAF [boc-aspartyl(OMe)-fluoromethylketone] and overexpression of dominant-negative mutants of caspase-9, -3, and -7 significantly blocked the death.	butyloxycarbonyl-O-methyl-aspartyl-fluoromethyl ketone	97-100	caspase 8	Homo sapiens	0-8
18650325-3	2008	Caspases were critically required, because the death was completely blocked by caspase inhibitor BAF [boc-aspartyl(OMe)-fluoromethylketone] and overexpression of dominant-negative mutants of caspase-9, -3, and -7 significantly blocked the death.	butyloxycarbonyl-O-methyl-aspartyl-fluoromethyl ketone	102-138	caspase 8	Homo sapiens	0-8
18544567-12	2008	Mesalazine-mediated increased caspase-3 activity, the expression of PTEN, cleavage of PARP and caspase-8 as well as reduced levels of survivin and Xiap were completely abolished in the PPARgamma mutant cell lines.	Mesalamine	0-10	caspase 8	Homo sapiens	95-104
18618576-8	2008	In addition, 3-indole stimulated caspases-3, -9, and to a lesser extent caspase-8 activities in cancer cells, suggesting that the intrinsic mitochondria pathway was the potential mechanism involved in 3-indole-induced apoptosis.	1,1,3-tris(3-indolyl)cyclohexane	201-209	caspase 8	Homo sapiens	72-81
18584328-3	2008	Peroxynitrite triggered endothelial cell apoptosis through caspases-8, -9 and -3 activation implying both mitochondrial and death receptor apoptotic pathways.	Peroxynitrous Acid	0-13	caspase 8	Homo sapiens	59-80
18676836-8	2008	The functional significance of these interactions is supported by the demonstration that MUC1 competes with caspase-8 for binding to FADD and blocks recruitment of caspase-8 to the death-inducing signaling complex.	fadd	133-137	caspase 8	Homo sapiens	108-117
18636153-6	2008	In addition, SAHA up-regulated the death receptor DR5, inducing the activation of caspase-8 with the consequent cleavage of Bid.	Vorinostat	13-17	caspase 8	Homo sapiens	82-91
18522940-4	2008	Caspase-8 on average was activated 45-600 min after TRAIL/cycloheximide addition.	Cycloheximide	58-71	caspase 8	Homo sapiens	0-9
18304628-0	2008	Resistance of acute myeloid leukemic cells to the triterpenoid CDDO-Imidazolide is associated with low caspase-8 and FADD levels.	triterpenoid TP-222	50-62	caspase 8	Homo sapiens	103-112
18304628-0	2008	Resistance of acute myeloid leukemic cells to the triterpenoid CDDO-Imidazolide is associated with low caspase-8 and FADD levels.	1-(2-cyano-3,12-dioxooleana-1,9-dien-28-oyl) imidazole	63-79	caspase 8	Homo sapiens	103-112
18304628-3	2008	Biochemical studies showed that CDDO-Im: induced a rapid and marked GSH depletion and antioxidants (GSH or NAC) completely inhibited its pro-apoptotic effect; sequentially activated caspase-8, -9 and -3; caspase inhibitors partially protected AML blasts from CDDO-Im-induced apoptosis; resistance of AML blasts to CDDO-Im-induced apoptosis correlated with low caspase-8/FADD and high Bcl-X(L) expression in leukemic blasts.	1-(2-cyano-3,12-dioxooleana-1,9-dien-28-oyl) imidazole	32-39	caspase 8	Homo sapiens	182-202
18304628-3	2008	Biochemical studies showed that CDDO-Im: induced a rapid and marked GSH depletion and antioxidants (GSH or NAC) completely inhibited its pro-apoptotic effect; sequentially activated caspase-8, -9 and -3; caspase inhibitors partially protected AML blasts from CDDO-Im-induced apoptosis; resistance of AML blasts to CDDO-Im-induced apoptosis correlated with low caspase-8/FADD and high Bcl-X(L) expression in leukemic blasts.	1-(2-cyano-3,12-dioxooleana-1,9-dien-28-oyl) imidazole	32-39	caspase 8	Homo sapiens	182-189
18304628-3	2008	Biochemical studies showed that CDDO-Im: induced a rapid and marked GSH depletion and antioxidants (GSH or NAC) completely inhibited its pro-apoptotic effect; sequentially activated caspase-8, -9 and -3; caspase inhibitors partially protected AML blasts from CDDO-Im-induced apoptosis; resistance of AML blasts to CDDO-Im-induced apoptosis correlated with low caspase-8/FADD and high Bcl-X(L) expression in leukemic blasts.	1-(2-cyano-3,12-dioxooleana-1,9-dien-28-oyl) imidazole	32-39	caspase 8	Homo sapiens	182-191
18304628-3	2008	Biochemical studies showed that CDDO-Im: induced a rapid and marked GSH depletion and antioxidants (GSH or NAC) completely inhibited its pro-apoptotic effect; sequentially activated caspase-8, -9 and -3; caspase inhibitors partially protected AML blasts from CDDO-Im-induced apoptosis; resistance of AML blasts to CDDO-Im-induced apoptosis correlated with low caspase-8/FADD and high Bcl-X(L) expression in leukemic blasts.	Glutathione	100-103	caspase 8	Homo sapiens	182-202
18304628-3	2008	Biochemical studies showed that CDDO-Im: induced a rapid and marked GSH depletion and antioxidants (GSH or NAC) completely inhibited its pro-apoptotic effect; sequentially activated caspase-8, -9 and -3; caspase inhibitors partially protected AML blasts from CDDO-Im-induced apoptosis; resistance of AML blasts to CDDO-Im-induced apoptosis correlated with low caspase-8/FADD and high Bcl-X(L) expression in leukemic blasts.	Glutathione	100-103	caspase 8	Homo sapiens	182-189
18304628-3	2008	Biochemical studies showed that CDDO-Im: induced a rapid and marked GSH depletion and antioxidants (GSH or NAC) completely inhibited its pro-apoptotic effect; sequentially activated caspase-8, -9 and -3; caspase inhibitors partially protected AML blasts from CDDO-Im-induced apoptosis; resistance of AML blasts to CDDO-Im-induced apoptosis correlated with low caspase-8/FADD and high Bcl-X(L) expression in leukemic blasts.	Glutathione	100-103	caspase 8	Homo sapiens	182-191
18304628-3	2008	Biochemical studies showed that CDDO-Im: induced a rapid and marked GSH depletion and antioxidants (GSH or NAC) completely inhibited its pro-apoptotic effect; sequentially activated caspase-8, -9 and -3; caspase inhibitors partially protected AML blasts from CDDO-Im-induced apoptosis; resistance of AML blasts to CDDO-Im-induced apoptosis correlated with low caspase-8/FADD and high Bcl-X(L) expression in leukemic blasts.	1-(2-cyano-3,12-dioxooleana-1,9-dien-28-oyl) imidazole	259-266	caspase 8	Homo sapiens	182-189
18304628-3	2008	Biochemical studies showed that CDDO-Im: induced a rapid and marked GSH depletion and antioxidants (GSH or NAC) completely inhibited its pro-apoptotic effect; sequentially activated caspase-8, -9 and -3; caspase inhibitors partially protected AML blasts from CDDO-Im-induced apoptosis; resistance of AML blasts to CDDO-Im-induced apoptosis correlated with low caspase-8/FADD and high Bcl-X(L) expression in leukemic blasts.	1-(2-cyano-3,12-dioxooleana-1,9-dien-28-oyl) imidazole	259-266	caspase 8	Homo sapiens	182-189
18514188-6	2008	We found that genistein induces caspase 8 dependent apoptotic pathway in NEO cells.	Genistein	14-23	caspase 8	Homo sapiens	32-41
18593930-6	2008	Our data indicate that pyrimethamine, when used at a clinically relevant concentration, induced apoptosis in metastatic melanoma cells via the activation of the cathepsin B and the caspase cascade (i.e., caspase-8 and caspase-9) and subsequent mitochondrial depolarization.	Pyrimethamine	23-36	caspase 8	Homo sapiens	204-213
18356818-12	2008	The pan-caspase inhibitor Z-VAD-FMK and caspase-8 inhibitor Z-IETD-FMK, but not the caspase-9 inhibitor Z-IEHD-FMK, protected tumor cells from MV-CEA/GA-induced PARP activation, indicating that apoptosis in combination-treated cells occurs mainly via the extrinsic caspase pathway.	geldanamycin	150-152	caspase 8	Homo sapiens	40-49
18398841-0	2008	A celecoxib derivative inhibits focal adhesion signaling and induces caspase-8-dependent apoptosis in human acute myeloid leukemia cells.	Celecoxib	2-11	caspase 8	Homo sapiens	69-78
17868340-4	2008	This process was accompanied by an increase of caspase activation, which could be blocked by caspase-8 inhibitor IETD.	IETD	113-117	caspase 8	Homo sapiens	93-102
18570872-5	2008	When deubiquitinated by AEG40730 treatment, RIP1 binds caspase-8 and induces apoptosis.	AEG 40730	24-32	caspase 8	Homo sapiens	55-64
18448526-9	2008	Fas immunoprecipitation detected FADD (Fas-associated death domain protein) and caspase 8, suggesting a Fas-dependent formation of the death-inducing signaling complex.	ammonium ferrous sulfate	0-3	caspase 8	Homo sapiens	80-89
18402771-0	2008	Essential roles of caspases and their upstream regulators in rotenone-induced apoptosis.	Rotenone	61-69	caspase 8	Homo sapiens	19-27
18402771-1	2008	In the present study, we examined whether caspases and their upstream regulators are involved in rotenone-induced cytotoxicity.	Rotenone	97-105	caspase 8	Homo sapiens	42-50
18402771-7	2008	In conclusion, our results demonstrate significant involvement of caspases and their upstream regulators in rotenone-induced cytotoxicity.	Rotenone	108-116	caspase 8	Homo sapiens	66-74
18460448-4	2008	DIM-C-pPhBr and DIM-C-pPhF not only induced CHOP but also activated death receptor 5 (CHOP dependent), cleavage of caspase 8 and poly (ADP ribose) polymerase (PARP) that is consistent with activation of the extrinsic pathway of apoptosis.	dim-c-pphbr	0-11	caspase 8	Homo sapiens	115-157
18342014-0	2008	Retinoic acid induces caspase-8 transcription via phospho-CREB and increases apoptotic responses to death stimuli in neuroblastoma cells.	Tretinoin	0-13	caspase 8	Homo sapiens	22-31
18342014-3	2008	Here we show that four different retinoic acid (RA) derivatives also increase caspase-8 protein expression in neuroblastoma, medulloblastoma and small cell lung carcinoma cell lines.	Tretinoin	33-46	caspase 8	Homo sapiens	78-87
18342014-3	2008	Here we show that four different retinoic acid (RA) derivatives also increase caspase-8 protein expression in neuroblastoma, medulloblastoma and small cell lung carcinoma cell lines.	Tretinoin	48-50	caspase 8	Homo sapiens	78-87
18458681-5	2008	Roscovitine facilitated TRAIL death-inducing signaling complex formation and the activation of caspase-8.	Roscovitine	0-11	caspase 8	Homo sapiens	95-104
18460448-4	2008	DIM-C-pPhBr and DIM-C-pPhF not only induced CHOP but also activated death receptor 5 (CHOP dependent), cleavage of caspase 8 and poly (ADP ribose) polymerase (PARP) that is consistent with activation of the extrinsic pathway of apoptosis.	dim-c-pphf	16-26	caspase 8	Homo sapiens	115-157
18705520-6	2008	Immunohistochemistry staining showed that Caspase 3 and Caspase 8 were both strong positive expression in SACC-2 cells of salidroside groups, and poor positive expression in SACC-2 cells of control group, the difference was significant (P&lt;0.01).	rhodioloside	122-133	caspase 8	Homo sapiens	56-65
18058803-4	2008	AMR-Me induced DNA fragmentation and PARP degradation which were preceded by changing Bax/Bcl-2 ratios, cytochrome c release, and subsequent induction of pro-caspase-9 and -7 processing in breast carcinoma MCF-7 cells, but it did not act on Fas/Fas ligand pathways and the activation of caspase-8, suggesting AMR-Me triggered the mitochondrial apoptotic pathway.	methyl 25-hydroxy-3-oxoolean-12-en-28-oate	0-6	caspase 8	Homo sapiens	287-296
18497995-6	2008	CdA treatment of Jurkat T leukemia cells resulted in the activation of caspase-3, -8, and -9, while inhibition of these caspases prevented the CdA-induced loss of Delta Psi m, as well as DNA fragmentation.	Cladribine	143-146	caspase 8	Homo sapiens	120-128
18266928-7	2008	The rescue was total when the caspase 8 inhibitor z-IETD-FMK was added in combination with SB216763.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	50-60	caspase 8	Homo sapiens	30-39
18354056-0	2008	Dependence of reactive oxygen species and FLICE inhibitory protein on lipofectamine-induced apoptosis in human lung epithelial cells.	Lipofectamine	70-83	caspase 8	Homo sapiens	42-47
18628592-6	2008	Treatment with N-acetyl-L-cysteine also inhibited expression of apoptotic proteins such as Bax and Smac and abrogated caspase-8 activation.	Acetylcysteine	15-34	caspase 8	Homo sapiens	118-127
18566240-7	2008	Furthermore, suppression of caspase-8 activity with Z-IETD-FMK partially inhibited release of cytochrome c and Bid cleavage induced by AMAD, whereas exposure to Z-LETD-FMK, a caspase-9 inhibitor, had no effect.	z-letd-fmk	161-171	caspase 8	Homo sapiens	28-37
18435487-8	2008	To confirm the geraniin-relevant signaling pathway, using immunoblot analysis we found that geraniin-induced apoptosis was associated with the up-regulation of Fas ligand expression, the activation of caspase-8, the cleavage of Bid, and the induction of cytochrome c release from mitochondria to the cytosol.	Geraniin	92-100	caspase 8	Homo sapiens	201-210
18566239-8	2008	We show that As2O3 decreases AKT protein via caspase-mediated degradation, abrogated by caspase-6, caspase-8, caspase-9, and caspase-3 inhibitors but not proteosome inhibitors.	Arsenic Trioxide	13-18	caspase 8	Homo sapiens	99-108
18358694-7	2008	Moreover, chelerythrine, but not dihydrochelerythrine, elevated the activity of caspase-8.	chelerythrine	10-23	caspase 8	Homo sapiens	80-89
18566240-0	2008	Emodin azide methyl anthraquinone derivative triggers mitochondrial-dependent cell apoptosis involving in caspase-8-mediated Bid cleavage.	azide methyl anthraquinone	7-33	caspase 8	Homo sapiens	106-115
18566240-7	2008	Furthermore, suppression of caspase-8 activity with Z-IETD-FMK partially inhibited release of cytochrome c and Bid cleavage induced by AMAD, whereas exposure to Z-LETD-FMK, a caspase-9 inhibitor, had no effect.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	52-62	caspase 8	Homo sapiens	28-37
18446845-8	2008	Further results indicate that caspase-3, caspase-8 and caspase-9 are all activated by ESS, together with cleavage of downstream caspase-3 target proteins.	ESS	86-89	caspase 8	Homo sapiens	41-50
18396304-3	2008	The results indicated that zinc supplementation significantly inhibited ethanol-induced HepG2 cell apoptosis (measured by cytochrome c release from mitochondria and caspase-3 activation) by attenuation of reactive oxygen species (ROS) production, increase in the cellular level of GSH, inhibition of ethanol-induced sFasR and FasL overexpression and caspase-8 activation.	Ethanol	72-79	caspase 8	Homo sapiens	350-359
18485876-2	2008	Cycloheximide promotes caspase-8 activation by eliminating endogenous caspase-8 inhibitor, c-FLIP, while Smac mimetic does so by triggering autodegradation of cIAP1 and cIAP2 (cIAP1/2), leading to the release of receptor interacting protein kinase (RIPK1) from the activated TNF receptor complex to form a caspase-8-activating complex consisting of RIPK1, FADD, and caspase-8.	Cycloheximide	0-13	caspase 8	Homo sapiens	23-32
18485876-2	2008	Cycloheximide promotes caspase-8 activation by eliminating endogenous caspase-8 inhibitor, c-FLIP, while Smac mimetic does so by triggering autodegradation of cIAP1 and cIAP2 (cIAP1/2), leading to the release of receptor interacting protein kinase (RIPK1) from the activated TNF receptor complex to form a caspase-8-activating complex consisting of RIPK1, FADD, and caspase-8.	Cycloheximide	0-13	caspase 8	Homo sapiens	70-79
18485876-2	2008	Cycloheximide promotes caspase-8 activation by eliminating endogenous caspase-8 inhibitor, c-FLIP, while Smac mimetic does so by triggering autodegradation of cIAP1 and cIAP2 (cIAP1/2), leading to the release of receptor interacting protein kinase (RIPK1) from the activated TNF receptor complex to form a caspase-8-activating complex consisting of RIPK1, FADD, and caspase-8.	Cycloheximide	0-13	caspase 8	Homo sapiens	70-79
18485876-2	2008	Cycloheximide promotes caspase-8 activation by eliminating endogenous caspase-8 inhibitor, c-FLIP, while Smac mimetic does so by triggering autodegradation of cIAP1 and cIAP2 (cIAP1/2), leading to the release of receptor interacting protein kinase (RIPK1) from the activated TNF receptor complex to form a caspase-8-activating complex consisting of RIPK1, FADD, and caspase-8.	Cycloheximide	0-13	caspase 8	Homo sapiens	70-79
18549619-4	2008	The expression level of DR5 on surface of HL-60 cells and caspase-8 activity in HL-60 cells of rsTRAIL group and Ara-C + rsTRAIL tandem group was determined by flow cytometry.	rstrail	95-102	caspase 8	Homo sapiens	58-67
18549619-6	2008	The apoptosis rate of HL-60 cells in Ara-C + rsTRAIL tandem given group was higher than that in Ara-C + rsTRAIL simultaneously given group, the expression level of DR5 on surface of HL-60 cells and intracellular activity of caspase-8 in Ara-C + rsTRAIL tandem given group were higher than those in rsTRAIL group.	Cytarabine	37-42	caspase 8	Homo sapiens	224-233
18549619-6	2008	The apoptosis rate of HL-60 cells in Ara-C + rsTRAIL tandem given group was higher than that in Ara-C + rsTRAIL simultaneously given group, the expression level of DR5 on surface of HL-60 cells and intracellular activity of caspase-8 in Ara-C + rsTRAIL tandem given group were higher than those in rsTRAIL group.	rstrail	45-52	caspase 8	Homo sapiens	224-233
18549619-12	2008	The mechanism may correlate with up-regulation of the expression level of DR5 and/or caspase-8 in HL-60 cells by Ara-C.	Cytarabine	113-118	caspase 8	Homo sapiens	85-94
18509533-4	2008	Fe-SP treatment led to the activation of markers of the extrinsic (Caspase-8) and intrinsic (Caspase-9) pathway of apoptosis as well as of executioner Caspase-3 while PARP-1 was deactivated.	3-N-(2-fluoroethyl)spiperone	0-5	caspase 8	Homo sapiens	67-76
18375387-4	2008	Lansoprazole also inhibits indomethacin-induced Fas-mediated mucosal cell death by down-regulating Fas or FasL expression and inhibiting caspase-8 activation.	Lansoprazole	0-12	caspase 8	Homo sapiens	137-146
18375387-4	2008	Lansoprazole also inhibits indomethacin-induced Fas-mediated mucosal cell death by down-regulating Fas or FasL expression and inhibiting caspase-8 activation.	Indomethacin	27-39	caspase 8	Homo sapiens	137-146
18375387-4	2008	Lansoprazole also inhibits indomethacin-induced Fas-mediated mucosal cell death by down-regulating Fas or FasL expression and inhibiting caspase-8 activation.	ammonium ferrous sulfate	48-51	caspase 8	Homo sapiens	137-146
18359480-3	2008	Co-treatment with ATO plus quercetin caused mitochondrial transmembrane potential dissipation, stimulated the mitochondrial apoptotic pathway, as indicated by cytochrome c and Omi/Htra2 release, XIAP and Bcl-X(L) down-regulation, and Bax activation, and caused caspase-8/Bid activation.	Arsenic Trioxide	18-21	caspase 8	Homo sapiens	261-270
18359480-3	2008	Co-treatment with ATO plus quercetin caused mitochondrial transmembrane potential dissipation, stimulated the mitochondrial apoptotic pathway, as indicated by cytochrome c and Omi/Htra2 release, XIAP and Bcl-X(L) down-regulation, and Bax activation, and caused caspase-8/Bid activation.	Quercetin	27-36	caspase 8	Homo sapiens	261-270
18214855-7	2008	Z-IETD-fmk and Z-VDVAD-fmk were used to block the activation of caspase-8 and caspase-2, respectively; however, the progression of apoptosis were not affected, suggesting that caspase-8 and caspase-2 were not involved in this experimental model.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	0-10	caspase 8	Homo sapiens	64-73
18214855-7	2008	Z-IETD-fmk and Z-VDVAD-fmk were used to block the activation of caspase-8 and caspase-2, respectively; however, the progression of apoptosis were not affected, suggesting that caspase-8 and caspase-2 were not involved in this experimental model.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	0-10	caspase 8	Homo sapiens	176-185
18214855-7	2008	Z-IETD-fmk and Z-VDVAD-fmk were used to block the activation of caspase-8 and caspase-2, respectively; however, the progression of apoptosis were not affected, suggesting that caspase-8 and caspase-2 were not involved in this experimental model.	benzoylcarbonyl-valyl-aspartyl-valyl-alanyl-aspartyl-fluoromethyl ketone	15-26	caspase 8	Homo sapiens	64-73
18396304-4	2008	These results indicate that zinc can inhibit ethanol-induced hepatocyte apoptosis by several independent mechanisms, among others by an indirect antioxidative effect and probably by inhibition of caspase-8 and caspase-9 activation.	Ethanol	45-52	caspase 8	Homo sapiens	196-205
18451540-5	2008	The activation of caspase-8 and -9 and degradation of poly-(ADP-ribose) polymerase (PARP) was time-dependently detected by incubation with costunolide.	costunolide	139-150	caspase 8	Homo sapiens	18-34
18216014-0	2008	Identification of a critical tyrosine residue in caspase 8 that promotes cell migration.	Tyrosine	29-37	caspase 8	Homo sapiens	49-58
18216014-2	2008	Here, we show that tyrosine 380 in the linker loop of human caspase 8 is a critical switch determining caspase 8 function.	Tyrosine	19-27	caspase 8	Homo sapiens	60-69
18216014-2	2008	Here, we show that tyrosine 380 in the linker loop of human caspase 8 is a critical switch determining caspase 8 function.	Tyrosine	19-27	caspase 8	Homo sapiens	103-112
18216014-5	2008	Instead, we find that integrin-mediated adhesion promotes caspase 8 phosphorylation on tyrosine 380.	Tyrosine	87-95	caspase 8	Homo sapiens	58-67
18451540-6	2008	Pretreatment of cells with caspase-3, -8 and broad spectrum caspase inhibitors significantly blocked costunolide-induced apoptosis, but caspase-9 inhibitor failed to block apoptosis.	costunolide	101-112	caspase 8	Homo sapiens	27-34
18451540-8	2008	Costunolide-induced repression of telomerase was prevented by pretreatment of cells with caspase-3, -8 and broad spectrum caspase inhibitors, but caspase-9 inhibitor was no effect.	costunolide	0-11	caspase 8	Homo sapiens	89-96
18451172-4	2008	In contrast, the addition of low-dose TRAIL to nocodazole was associated with maximally increased caspase-3, caspase-8, and caspase-9 activation, which efficiently abrogated the mitotic delay and markedly increased cell death.	Nocodazole	47-57	caspase 8	Homo sapiens	109-118
18359761-8	2008	Pretreatment of cells with caspase inhibitor (Z-VAD-FMK) blocked fisetin-induced activation of caspases.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	46-55	caspase 8	Homo sapiens	95-103
18359761-8	2008	Pretreatment of cells with caspase inhibitor (Z-VAD-FMK) blocked fisetin-induced activation of caspases.	fisetin	65-72	caspase 8	Homo sapiens	95-103
18522899-8	2008	Immunoblotting revealed increased Fas and caspase-8 expression by suramin treatment.	Suramin	66-73	caspase 8	Homo sapiens	42-51
18376857-5	2008	The Fas death receptor pathway was also activated following indioside D treatment, and triggered the activation of caspase-8 and cleavage of Bid, which also acted through the mitochondrial apoptosis pathway.	indioside D	60-71	caspase 8	Homo sapiens	115-124
18221384-6	2008	When HA14-1 was added to bortezomib in vitro, we observed a synergistic anti-proliferative effect and enhancement of apoptosis and caspase activation, including activation of caspase-8, in LCLs.	Bortezomib	25-35	caspase 8	Homo sapiens	175-184
18288482-4	2008	Gal-1 stimulated DNA-fragmentation could be efficiently inhibited by caspase-8 inhibitor II (Z-IETD-FMK) and a neutralizing Fas mAb.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	93-103	caspase 8	Homo sapiens	69-78
17979179-6	2008	Finally, we show that apoptotic cell death induced by TPEN involved mitochondrial injury and caspase 3 and caspase 8 activation.	N,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamine	54-58	caspase 8	Homo sapiens	107-116
18068200-6	2008	The 7kCh-induced caspase-8 activity was blocked partially by pre-treatment with z-VAD-fmk and z-IETD-fmk, a caspase-8 inhibitor.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	80-89	caspase 8	Homo sapiens	17-26
18413764-4	2008	ABT-737 was shown to enhance TRAIL-induced apoptosis as shown by DNA fragmentation, activation of caspase-8 and Bid, and cleavage of caspase-3 and poly(ADP-ribose) polymerase.	ABT-737	0-7	caspase 8	Homo sapiens	98-107
18289527-3	2008	Nevertheless, we have surprisingly found that CHX, as well as its structural analogue acetoxycycloheximide (Ac-CHX), prevents TNF-alpha-mediated activation of NF-kappaB and caspase-8 in human lung carcinoma A549 cells.	Cycloheximide	46-49	caspase 8	Homo sapiens	173-182
18289527-3	2008	Nevertheless, we have surprisingly found that CHX, as well as its structural analogue acetoxycycloheximide (Ac-CHX), prevents TNF-alpha-mediated activation of NF-kappaB and caspase-8 in human lung carcinoma A549 cells.	acetoxycycloheximide	86-106	caspase 8	Homo sapiens	173-182
18289527-3	2008	Nevertheless, we have surprisingly found that CHX, as well as its structural analogue acetoxycycloheximide (Ac-CHX), prevents TNF-alpha-mediated activation of NF-kappaB and caspase-8 in human lung carcinoma A549 cells.	ac-chx	108-114	caspase 8	Homo sapiens	173-182
18222463-2	2008	The MES behavior of a set of four CAPs (synthesized at 85 degrees C by a precipitation method) of increasing CM and therefore of increasing MES (CAP4 &gt; CAP3 &gt; CAP2 &gt; CAP1) was quantified.	2-(N-morpholino)ethanesulfonic acid	4-7	caspase 8	Homo sapiens	145-149
18222463-2	2008	The MES behavior of a set of four CAPs (synthesized at 85 degrees C by a precipitation method) of increasing CM and therefore of increasing MES (CAP4 &gt; CAP3 &gt; CAP2 &gt; CAP1) was quantified.	2-(N-morpholino)ethanesulfonic acid	140-143	caspase 8	Homo sapiens	145-149
18297401-3	2008	Although vinorelbine induces DNA fragmentation that is inhibited by specific peptide inhibitors for caspases-9 and -3 in Jurkat cells, caspase-8 deficiency retards vinorelbine-induced apoptosis.	Vinorelbine	164-175	caspase 8	Homo sapiens	135-144
18297401-4	2008	Activation of caspase-8 is also observed in vinorelbine-treated cells, and the activity is diminished when the caspase-3 activity is blocked by a specific peptide inhibitor, Ac-DNLC-CHO.	Vinorelbine	44-55	caspase 8	Homo sapiens	14-23
18297401-4	2008	Activation of caspase-8 is also observed in vinorelbine-treated cells, and the activity is diminished when the caspase-3 activity is blocked by a specific peptide inhibitor, Ac-DNLC-CHO.	ac-dnlc-cho	174-185	caspase 8	Homo sapiens	14-23
18297401-6	2008	These results suggest that vinorelbine-induced apoptosis is enhanced by the activation of caspase-8 via caspase-9-mediated activation of caspase-3, but not through a Fas-triggered signal.	Vinorelbine	27-38	caspase 8	Homo sapiens	90-99
18297401-9	2008	A downstream substrate for caspase-8, Bid, is also cleaved in vinorelbine-treated cells, but the Bid truncation is also observed in caspase-8-deficient Jurkat cells.	Vinorelbine	62-73	caspase 8	Homo sapiens	27-36
18360714-4	2008	The apoptosis induced by thiosulfinates is associated with the activation of initiator caspase-8, and -9, and the effector caspase-3.	thiosulfinates	25-39	caspase 8	Homo sapiens	87-104
18360714-5	2008	Thiosulfinates stimulated Bid cleavage, indicating that the apoptotic action of caspase-8-mediated Bid cleavage leads to the activation of caspase-9.	thiosulfinates	0-14	caspase 8	Homo sapiens	80-89
18068200-6	2008	The 7kCh-induced caspase-8 activity was blocked partially by pre-treatment with z-VAD-fmk and z-IETD-fmk, a caspase-8 inhibitor.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	80-89	caspase 8	Homo sapiens	108-117
18068200-6	2008	The 7kCh-induced caspase-8 activity was blocked partially by pre-treatment with z-VAD-fmk and z-IETD-fmk, a caspase-8 inhibitor.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	94-104	caspase 8	Homo sapiens	17-26
18068200-6	2008	The 7kCh-induced caspase-8 activity was blocked partially by pre-treatment with z-VAD-fmk and z-IETD-fmk, a caspase-8 inhibitor.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	94-104	caspase 8	Homo sapiens	108-117
18068200-7	2008	However, pre-treatment with z-ATAD-fmk, a caspase-12 inhibitor, followed by 7kCh exposure lead to significantly increased caspase-8 activity.	z-atad-fmk	28-38	caspase 8	Homo sapiens	122-131
18187175-0	2008	Desferrioxamine (DFX) induces apoptosis through the p38-caspase8-Bid-Bax pathway in PHA-stimulated human lymphocytes.	Deferoxamine	17-20	caspase 8	Homo sapiens	56-64
17689285-4	2008	In OSCC cells treated with EGFR inhibitors, Fas-mediated apoptosis was accompanied by caspase-8 activation but not Bid cleavage.	ammonium ferrous sulfate	44-47	caspase 8	Homo sapiens	86-95
18187175-3	2008	DFX treatment activated caspase-9, caspase-3, and caspase-8.	Deferoxamine	0-3	caspase 8	Homo sapiens	50-59
18187175-0	2008	Desferrioxamine (DFX) induces apoptosis through the p38-caspase8-Bid-Bax pathway in PHA-stimulated human lymphocytes.	Deferoxamine	0-15	caspase 8	Homo sapiens	56-64
18187175-5	2008	DFX treatment also enhanced caspase-8 activity, Bid cleavage, and the conformational activation of Bax.	Deferoxamine	0-3	caspase 8	Homo sapiens	28-37
18187175-8	2008	In addition, the selective p38 inhibitor SB203580 suppressed DFX-induced apoptosis and caspase-8 activation, whereas the JNK inhibitor, SP600125, and the ERK inhibitor, PD98059, had no effect.	SB 203580	41-49	caspase 8	Homo sapiens	87-96
18325696-8	2008	Thus, our results demonstrated that rapid cytochrome c release in CEM T-leukemia cells exposed to sanguinarine or chelerythrine was not accompanied by changes in Bax, Bcl-2 and Bcl-X((L/S)) proteins in the mitochondrial fraction, and preceded activation of the initiator caspase-8.	chelerythrine	114-127	caspase 8	Homo sapiens	271-280
18325696-2	2008	In this study, we found that sanguinarine and chelerythrine induce apoptosis in human CEM T-leukemia cells, and that is accompanied by an early increase in cytosolic cytochrome c that precedes caspases-8, -9 and -3 processing.	sanguinarine	29-41	caspase 8	Homo sapiens	193-214
18325696-2	2008	In this study, we found that sanguinarine and chelerythrine induce apoptosis in human CEM T-leukemia cells, and that is accompanied by an early increase in cytosolic cytochrome c that precedes caspases-8, -9 and -3 processing.	chelerythrine	46-59	caspase 8	Homo sapiens	193-214
18187175-9	2008	Our results suggest that DFX-induced apoptosis is mediated by the p38 pathway and a caspase-8-dependent Bid-Bax pathway in human lymphocytes.	Deferoxamine	25-28	caspase 8	Homo sapiens	84-93
18426650-0	2008	[Relation of apoptosis of K562 cells induced by naringenin in vitro to enzyme activity changes of caspase-3 and caspase-8 and expression of FAS/FASL proteins].	naringenin	48-58	caspase 8	Homo sapiens	112-121
18241849-5	2008	Furthermore, anisomycin-treated cells also showed caspase-8 activation, mitochondrial membrane potential collapse, Bid activation, caspase-3 cleavage and cytochrome c release into the cytosol.	Anisomycin	13-23	caspase 8	Homo sapiens	50-59
17891182-5	2008	Expression of CEA and/or a chimeric protein consisting of the NCAM extracellular domain attached to the CEA-GPI anchor correlates with an early inactivation of caspase-9 and activation of the PI3-K/Akt survival pathway, and at later times, inactivation of caspase-8.	Glycosylphosphatidylinositols	108-111	caspase 8	Homo sapiens	256-265
18242119-11	2008	In addition, nocodazole-induced apoptosis involves the apical caspase-8 and -9 and the effector caspase-3.	Nocodazole	13-23	caspase 8	Homo sapiens	62-78
18082672-8	2008	In addition, the combination 5-FU plus scFv23/TNF induced apoptosis and this synergistic effect was dependent on activation of caspase-8 and caspase-3.	Fluorouracil	29-33	caspase 8	Homo sapiens	127-136
18167055-4	2008	Furthermore, apoptosis in the Tca-8113 cells was accompanied by the activation of protease caspase-8, -9, -3 and low expression of Bcl-2 protein.	Trichloroacetic Acid	30-33	caspase 8	Homo sapiens	91-108
18276737-0	2008	Caspase-8 has an essential role in resveratrol-induced apoptosis of rheumatoid fibroblast-like synoviocytes.	Resveratrol	35-46	caspase 8	Homo sapiens	0-9
18276737-5	2008	RESULTS: We show that activation of caspase-8 is essential for triggering resveratrol-induced apoptotic signalling via the involvement of the mitochondrial pathway in RA FLS.	Resveratrol	74-85	caspase 8	Homo sapiens	36-45
18276737-8	2008	Analysis of upstream signalling events affected by resveratrol revealed that the activated caspase-8 triggered mitochondrial apoptotic events by inducing Bid cleavage without any alteration in the levels of Bax, Bcl-xL or Bcl2.	Resveratrol	51-62	caspase 8	Homo sapiens	91-100
18276737-9	2008	The caspase-8 inhibitor or over-expression of crmA abrogated cell death induced by resveratrol and prevented processing of the downstream cascade.	Resveratrol	83-94	caspase 8	Homo sapiens	4-13
18276737-10	2008	CONCLUSION: The results suggest that resveratrol causes activation of caspase-8, which in turn results in modulation of mitochondrial apoptotic machinery to promote apoptosis of RA FLS.	Resveratrol	37-48	caspase 8	Homo sapiens	70-79
18086677-2	2008	Here we report a novel mechanism regulating neutrophil survival dynamically through the tyrosine phosphorylation or dephosphorylation of caspase-8.	Tyrosine	88-96	caspase 8	Homo sapiens	137-146
18086677-3	2008	Caspase-8 is tyrosine-phosphorylated in freshly isolated neutrophils but spontaneously dephosphorylates in culture, in association with the progression of constitutive apoptosis.	Tyrosine	13-21	caspase 8	Homo sapiens	0-9
18086677-4	2008	Phosphorylation of caspase-8 on Tyr-310 facilitates its interaction with the Src-homology domain 2 containing tyrosine phosphatase-1 (SHP-1) and enables SHP-1 to dephosphorylate caspase-8, permitting apoptosis to proceed.	Tyrosine	32-35	caspase 8	Homo sapiens	19-28
18086677-4	2008	Phosphorylation of caspase-8 on Tyr-310 facilitates its interaction with the Src-homology domain 2 containing tyrosine phosphatase-1 (SHP-1) and enables SHP-1 to dephosphorylate caspase-8, permitting apoptosis to proceed.	Tyrosine	32-35	caspase 8	Homo sapiens	178-187
18086677-5	2008	The non-receptor tyrosine kinase, Lyn, can phosphorylate caspase-8 on Tyr-397 and Tyr-465, rendering it resistant to activational cleavage and inhibiting apoptosis.	Tyrosine	70-73	caspase 8	Homo sapiens	57-66
18292936-8	2008	Western blot analysis of apoptosis-related proteins demonstrated that treatment with MZ-5-156 (10(-6) M) for 48 h significantly increased the protein levels of Fas, phospho-p53 (Ser46), p53AIP1 (p53-regulated Apoptosis-Inducing Protein 1), and caspase-8, -9, and -3, and decreased the protein level of Bcl-2.	mz-5	85-89	caspase 8	Homo sapiens	244-265
18196534-10	2008	Investigations of alpha-TEA-triggered apoptosis showed dual signaling from Fas with essential roles for both FADD and Daxx with FADD initiating the classical pathway mediated by caspase-8 activation and Daxx initiating an alternate pathway involving activation of JNK, c-Jun, and increased levels of Fas and FasL.	alpha-TEA	18-27	caspase 8	Homo sapiens	178-187
18181022-7	2008	In addition, ardipusilloside III exposure resulted in time-dependent BAD dephosphorylation and cleavage as well as activation of caspase-8 and caspase-3.	ardipusilloside III	13-32	caspase 8	Homo sapiens	129-138
18036820-0	2008	A novel sesquiterpenoid dimer parviflorene F induces apoptosis by up-regulating the expression of TRAIL-R2 and a caspase-dependent mechanism.	sesquiterpenoid	8-23	caspase 8	Homo sapiens	113-120
18036820-0	2008	A novel sesquiterpenoid dimer parviflorene F induces apoptosis by up-regulating the expression of TRAIL-R2 and a caspase-dependent mechanism.	parviflorene F	30-44	caspase 8	Homo sapiens	113-120
17997382-6	2008	After longer periods of ATP depletion-recovery, we observed a significant increase in TNF-alpha protein levels (P&lt;0.001) and caspase-8 activation (P&lt;0.001), both of which were decreased (P&lt;0.001) by treatment with MnTmPyP.	Adenosine Triphosphate	24-27	caspase 8	Homo sapiens	128-137
17999062-0	2008	Dup-697, a specific COX-2 inhibitor, suppresses growth and induces apoptosis on K562 leukemia cells by cell-cycle arrest and caspase-8 activation.	DuP 697	0-7	caspase 8	Homo sapiens	125-134
17999062-4	2008	It arrested G1-S phase transmit on cell cycle and its apoptosis activity was partially abrogated by pretreating K562 cells with Z-IETD-fmk, a specific inhibitor of caspase-8.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	128-138	caspase 8	Homo sapiens	164-173
18181022-8	2008	Therefore, both the intrinsic pathway of apoptosis, mediated by BAD dephosphorylation and cleavage, and the extrinisic pathway of apoptosis, mediated by caspase-8 and caspase-3 activation, were involved in ardipusilloside III-induced apoptosis.	ardipusilloside III	206-225	caspase 8	Homo sapiens	153-162
18245485-2	2008	We report in this study that apoptosis was induced by the ER stress inducer thapsigargin or tunicamycin via a caspase-8-mediated pathway in the melanoma cell line Me1007, although the MEK/ERK pathway was activated in this cell line.	Thapsigargin	76-88	caspase 8	Homo sapiens	110-119
17453339-10	2008	We also found that inhibition of cFLIP(L) expression in T47D cells decreased Fas-mediated caspase-8 activation and activation of effector caspases.	ammonium ferrous sulfate	77-80	caspase 8	Homo sapiens	90-99
17453339-11	2008	We propose that in T47D p43 cFLIP(L) in the Fas-DISC may promote caspase-8 activation.	ammonium ferrous sulfate	44-47	caspase 8	Homo sapiens	65-74
18245485-2	2008	We report in this study that apoptosis was induced by the ER stress inducer thapsigargin or tunicamycin via a caspase-8-mediated pathway in the melanoma cell line Me1007, although the MEK/ERK pathway was activated in this cell line.	Tunicamycin	92-103	caspase 8	Homo sapiens	110-119
18202789-0	2008	Protective effects of resveratrol on UVB-irradiated HaCaT cells through attenuation of the caspase pathway.	Resveratrol	22-33	caspase 8	Homo sapiens	91-98
18202802-0	2008	Induction of apoptosis by pectenotoxin-2 is mediated with the induction of DR4/DR5, Egr-1 and NAG-1, activation of caspases and modulation of the Bcl-2 family in p53-deficient Hep3B hepatocellular carcinoma cells.	pectenotoxin 2	26-40	caspase 8	Homo sapiens	115-123
17637740-2	2008	We found that the cytotoxic drugs methotrexate (MTX) and 5-fluorouracil (5-FU) were both able to sensitize resistant tumor cells for induction of apoptosis by p53-mediated upregulation of caspase-8.	Fluorouracil	73-77	caspase 8	Homo sapiens	188-197
18202802-8	2008	PTX-2 activated caspases (caspase-3, -8 and -9) and the blockade of caspase-3 activity by the caspase-3 inhibitor prevented the PTX-2-induced apoptosis in Hep3B cells.	pectenotoxin 2	0-5	caspase 8	Homo sapiens	16-24
17637740-3	2008	Increase in caspase-8 messenger RNA and protein expression disabled tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced proliferation and restored sensitivity toward TRAIL-induced apoptosis which was inhibited by transfection of p53 decoy oligonucleotides, p53 shRNA and caspase-8 shRNA.	Oligonucleotides	259-275	caspase 8	Homo sapiens	12-21
17637740-2	2008	We found that the cytotoxic drugs methotrexate (MTX) and 5-fluorouracil (5-FU) were both able to sensitize resistant tumor cells for induction of apoptosis by p53-mediated upregulation of caspase-8.	Methotrexate	34-46	caspase 8	Homo sapiens	188-197
17955373-8	2008	In cell lines deficient in either CD95 (Fas, APO-1) signalling, FADD or caspase-8, MC was still able to potently induce cell death and PARP cleavage.	Methylcholanthrene	83-85	caspase 8	Homo sapiens	72-81
17637740-2	2008	We found that the cytotoxic drugs methotrexate (MTX) and 5-fluorouracil (5-FU) were both able to sensitize resistant tumor cells for induction of apoptosis by p53-mediated upregulation of caspase-8.	Methotrexate	48-51	caspase 8	Homo sapiens	188-197
17637740-2	2008	We found that the cytotoxic drugs methotrexate (MTX) and 5-fluorouracil (5-FU) were both able to sensitize resistant tumor cells for induction of apoptosis by p53-mediated upregulation of caspase-8.	Fluorouracil	57-71	caspase 8	Homo sapiens	188-197
18250974-3	2008	Fas engagement drives the formation of a complex termed DISC (death-inducing signaling complex), which contains the adaptor molecule Fas-associated protein, two members of the caspase family caspase-8 and -10, and a pseudo-caspase termed c-FLIP.	ammonium ferrous sulfate	0-3	caspase 8	Homo sapiens	176-183
18250974-3	2008	Fas engagement drives the formation of a complex termed DISC (death-inducing signaling complex), which contains the adaptor molecule Fas-associated protein, two members of the caspase family caspase-8 and -10, and a pseudo-caspase termed c-FLIP.	ammonium ferrous sulfate	0-3	caspase 8	Homo sapiens	191-208
18173754-6	2008	The increase of apoptosis by the combination of ATO and SB203580 was accompanied by the activation of caspase-9 and caspase-8 suggesting that both extrinsic and intrinsic apoptotic pathways are involved.	Arsenic Trioxide	48-51	caspase 8	Homo sapiens	116-125
18173754-6	2008	The increase of apoptosis by the combination of ATO and SB203580 was accompanied by the activation of caspase-9 and caspase-8 suggesting that both extrinsic and intrinsic apoptotic pathways are involved.	SB 203580	56-64	caspase 8	Homo sapiens	116-125
18667818-9	2008	Moreover, the quenching of ROS generation by N-acetyl-L-cysteine administration, a scavenger of ROS, reversed the sanguinarine-induced apoptosis effects via inhibition of ROS production, MMP collapse, tBid expression and the subsequent activation of caspases.	Reactive Oxygen Species	27-30	caspase 8	Homo sapiens	250-258
18199714-6	2008	Both lovastatin and simvastatin induced activation of caspase-8, caspase-3, and, to a lesser extent, caspase-9.	Lovastatin	5-15	caspase 8	Homo sapiens	54-63
18199714-6	2008	Both lovastatin and simvastatin induced activation of caspase-8, caspase-3, and, to a lesser extent, caspase-9.	Simvastatin	20-31	caspase 8	Homo sapiens	54-63
18667818-9	2008	Moreover, the quenching of ROS generation by N-acetyl-L-cysteine administration, a scavenger of ROS, reversed the sanguinarine-induced apoptosis effects via inhibition of ROS production, MMP collapse, tBid expression and the subsequent activation of caspases.	Acetylcysteine	45-64	caspase 8	Homo sapiens	250-258
18667818-8	2008	Sanguinarine also promoted the activation of caspase-8 and truncation of Bid (tBid).	sanguinarine	0-12	caspase 8	Homo sapiens	45-54
18667818-9	2008	Moreover, the quenching of ROS generation by N-acetyl-L-cysteine administration, a scavenger of ROS, reversed the sanguinarine-induced apoptosis effects via inhibition of ROS production, MMP collapse, tBid expression and the subsequent activation of caspases.	sanguinarine	114-126	caspase 8	Homo sapiens	250-258
18667818-11	2008	CONCLUSION: Our data imply that sanguinarine-induced ROS are key mediators of MMP collapse, which leads to the release of cytochrome c followed by caspase activation, culminating in apoptosis.	sanguinarine	32-44	caspase 8	Homo sapiens	147-154
18667818-11	2008	CONCLUSION: Our data imply that sanguinarine-induced ROS are key mediators of MMP collapse, which leads to the release of cytochrome c followed by caspase activation, culminating in apoptosis.	Reactive Oxygen Species	53-56	caspase 8	Homo sapiens	147-154
18089778-5	2007	Stimulation of motility with epidermal growth factor induced the phosphorylation of caspase-8 on tyrosine-380 and the interaction of caspase-8 with the p85 alpha subunit of phosphatidylinositol 3-kinase.	Tyrosine	97-105	caspase 8	Homo sapiens	84-93
18161513-0	2008	Sulfur mustard induces apoptosis in cultured normal human airway epithelial cells: evidence of a dominant caspase-8-mediated pathway and differential cellular responses.	Mustard Gas	0-14	caspase 8	Homo sapiens	106-115
18336733-7	2008	However, some differences in the apoptosis mechanisms between the two forms of the drug seem to exist because PMN treatment with the specific caspase 8 inhibitor (Z-IETD-FMK) only blocks OM-HCl mediated apoptosis.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	163-173	caspase 8	Homo sapiens	142-151
18336733-7	2008	However, some differences in the apoptosis mechanisms between the two forms of the drug seem to exist because PMN treatment with the specific caspase 8 inhibitor (Z-IETD-FMK) only blocks OM-HCl mediated apoptosis.	om-hcl	187-193	caspase 8	Homo sapiens	142-151
18336733-8	2008	We observed cleavage of caspase 8 only in the cells incubated with OM-HCl while the executioner caspase 3 was activated with both forms of the drug.	om-hcl	67-73	caspase 8	Homo sapiens	24-33
18662573-3	2008	BID is activated downstream of death receptors by caspase-8 cleavage and N-myristoylation to target mitochondria where it activates BAX, BAK, and the downstream apoptotic pathway.	bakuchiol	137-140	caspase 8	Homo sapiens	50-59
17694514-8	2007	Inhibition of caspase-9 specifically reduced v-Myc-stimulated apoptosis, whereas inhibition of caspase-8 and -3/7 reduced apoptosis both in v-myc-expressing and parental ETO-treated U-937 cells.	Etoposide	170-173	caspase 8	Homo sapiens	95-111
18089778-6	2007	Tyrosine-380 was required for the restoration of cell motility and cell adhesion in caspase-8-null cells, demonstrating the importance of the caspase-8-p85 interaction for these nonapoptotic functions.	Tyrosine	0-8	caspase 8	Homo sapiens	84-93
18089778-6	2007	Tyrosine-380 was required for the restoration of cell motility and cell adhesion in caspase-8-null cells, demonstrating the importance of the caspase-8-p85 interaction for these nonapoptotic functions.	Tyrosine	0-8	caspase 8	Homo sapiens	142-151
18089778-7	2007	These results suggest that caspase-8 phosphorylation converts it from a proapoptotic factor to a cell motility factor that, through tyrosine-380, interacts with p85, an established cell migration component.	Tyrosine	132-140	caspase 8	Homo sapiens	27-36
17879163-3	2007	Here we report that an altered matrix, consisting of a mutated, nonfunctional high-affinity heparin-binding domain and the V region of fibronectin (V+H-), induced anoikis in human SCC cells; this response was blocked by inhibitors of caspase-8 and caspase-3.	Heparin	92-99	caspase 8	Homo sapiens	234-243
18056196-14	2007	The pan-caspase inhibitor Z-VAD-FMK and the caspase-8 inhibitor Z-IETD-FMK, but not the caspase-9 inhibitor Z-IEHD-FMK, protected glioma cells from MV-CEA/RT-induced cleavage of poly(ADP-ribose) polymerase (PARP), indicating that the apoptotic death in combination-treated cells is mostly mediated via the extrinsic caspase pathway.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	64-74	caspase 8	Homo sapiens	44-53
17922191-0	2007	Molecular mechanism of Mitomycin C-dependent caspase-8 regulation: implications for apoptosis and synergism with interferon-alpha signalling.	Mitomycin	23-34	caspase 8	Homo sapiens	45-54
17922191-5	2007	However, strong caspase-8 promoter induction was found after Mitomycin C (MMC) treatment and this correlated with an increase in endogenous caspase-8 mRNA expression.	Mitomycin	61-72	caspase 8	Homo sapiens	16-25
17922191-5	2007	However, strong caspase-8 promoter induction was found after Mitomycin C (MMC) treatment and this correlated with an increase in endogenous caspase-8 mRNA expression.	Mitomycin	61-72	caspase 8	Homo sapiens	140-149
17922191-5	2007	However, strong caspase-8 promoter induction was found after Mitomycin C (MMC) treatment and this correlated with an increase in endogenous caspase-8 mRNA expression.	Mitomycin	74-77	caspase 8	Homo sapiens	16-25
17922191-5	2007	However, strong caspase-8 promoter induction was found after Mitomycin C (MMC) treatment and this correlated with an increase in endogenous caspase-8 mRNA expression.	Mitomycin	74-77	caspase 8	Homo sapiens	140-149
17922191-8	2007	MMC treatment resulted in higher caspase-8 enzymatic activity and apoptosis and could be synergistically enhanced by co-stimulation with interferon-alpha (IFNalpha) via independent transcriptional mechanisms.	Mitomycin	0-3	caspase 8	Homo sapiens	33-42
17973862-9	2007	In CH-11-resistant cells, cellular Fas-associated death domain-like interleukin-1b-converting enzyme inhibitory protein (c-FLIP) proteins were recruited to the DISC, resulting in inhibition of caspase 8 and caspase 10 cleavage.	4-dimethylamino-3',4'-dimethoxychalcone	3-8	caspase 8	Homo sapiens	193-202
17973862-9	2007	In CH-11-resistant cells, cellular Fas-associated death domain-like interleukin-1b-converting enzyme inhibitory protein (c-FLIP) proteins were recruited to the DISC, resulting in inhibition of caspase 8 and caspase 10 cleavage.	ammonium ferrous sulfate	35-38	caspase 8	Homo sapiens	193-202
17922852-8	2007	Furthermore, the combination of doxorubicin and lexatumumab significantly enhanced caspase 8 activity, Bid cleavage, Bcl-xL decrease, release of cytochrome c, and caspase 9 and caspase 3 activity, and induced synergistic apoptosis.	Doxorubicin	32-43	caspase 8	Homo sapiens	83-92
17922852-9	2007	The activation of caspases and apoptosis induced with lexatumumab and doxorubicin was blocked by the human recombinant DR5:Fc chimeric protein.	Doxorubicin	70-81	caspase 8	Homo sapiens	18-26
18082045-3	2007	This study aimed to explore the effect of the demethylation agent 5-azacytidine on caspase-8 expression and whether 5-azacytidine can increase the sensitivity of chemotherapy drug doxorubicin to NB cells.	Azacitidine	66-79	caspase 8	Homo sapiens	83-92
17375293-3	2007	Proteolysis of the N-terminus (encompassing H1 and H2) of Bid by caspase 8 in apoptosis yields activated "tBid" (truncated Bid), which translocates to the mitochondria and induces the efflux of cytochrome c.	tBID	106-110	caspase 8	Homo sapiens	65-74
18158826-5	2007	In addition, phloretin induced cleavage of caspase-8, -9, -7, and -3 and poly(ADP-ribose) polymerase.	Phloretin	13-22	caspase 8	Homo sapiens	43-68
18158826-7	2007	The present results indicate that phloretin inhibits HT-29 cell growth by inducing apoptosis, which may be mediated through changes in mitochondrial membrane permeability and activation of the caspase pathways.	Phloretin	34-43	caspase 8	Homo sapiens	193-200
17913816-10	2007	Further, NSm protein expression inhibited the staurosporine-induced activation of caspase-8 and -9, demonstrating that other viral proteins were dispensable for NSm"s function in inhibiting apoptosis.	Staurosporine	46-59	caspase 8	Homo sapiens	82-98
17855501-11	2007	These studies demonstrated that the PI-3K inhibitors, wortmannin and LY294002, antagonize the ability of CSF-1 to inhibit DC differentiation and to promote caspase activation.	Wortmannin	54-64	caspase 8	Homo sapiens	156-163
17855501-11	2007	These studies demonstrated that the PI-3K inhibitors, wortmannin and LY294002, antagonize the ability of CSF-1 to inhibit DC differentiation and to promote caspase activation.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	69-77	caspase 8	Homo sapiens	156-163
18065490-6	2007	Pharmacologic or genetic inhibition of caspase-8 reduced flavopiridol toxicity, but abolished killing by vorinostat and cell death caused by the vorinostat/flavopiridol regimen.	alvocidib	57-69	caspase 8	Homo sapiens	39-48
18065490-6	2007	Pharmacologic or genetic inhibition of caspase-8 reduced flavopiridol toxicity, but abolished killing by vorinostat and cell death caused by the vorinostat/flavopiridol regimen.	Vorinostat	105-115	caspase 8	Homo sapiens	39-48
18065490-6	2007	Pharmacologic or genetic inhibition of caspase-8 reduced flavopiridol toxicity, but abolished killing by vorinostat and cell death caused by the vorinostat/flavopiridol regimen.	Vorinostat	145-155	caspase 8	Homo sapiens	39-48
18065490-6	2007	Pharmacologic or genetic inhibition of caspase-8 reduced flavopiridol toxicity, but abolished killing by vorinostat and cell death caused by the vorinostat/flavopiridol regimen.	alvocidib	156-168	caspase 8	Homo sapiens	39-48
18082045-7	2007	Caspase-8 mRNA expression in SH-SY5Y cells was detectable 3 days after 5-azacytidine treatment, and increased significantly 5 days after 5-azacytidine treatment (P &lt; 0.05).	Azacitidine	71-84	caspase 8	Homo sapiens	0-9
18082045-7	2007	Caspase-8 mRNA expression in SH-SY5Y cells was detectable 3 days after 5-azacytidine treatment, and increased significantly 5 days after 5-azacytidine treatment (P &lt; 0.05).	Azacitidine	137-150	caspase 8	Homo sapiens	0-9
18082045-9	2007	Caspase-8 inhibitor pretreatment resulted in an increased survival rate of SH-SY5Y cells (92.95 +/- 3.48%, 78.39 +/- 4.28 %, 62.31 +/- 6.50% and 49.92 +/- 5.77%) compared with the 5-azacytidine+doxorubicin treatment group.	Azacitidine	180-193	caspase 8	Homo sapiens	0-9
18082045-9	2007	Caspase-8 inhibitor pretreatment resulted in an increased survival rate of SH-SY5Y cells (92.95 +/- 3.48%, 78.39 +/- 4.28 %, 62.31 +/- 6.50% and 49.92 +/- 5.77%) compared with the 5-azacytidine+doxorubicin treatment group.	Doxorubicin	194-205	caspase 8	Homo sapiens	0-9
18082045-10	2007	CONCLUSIONS: 5-azacytidine may enhance anti-tumor efficacy of doxorubicin to NB cell lines, possibly through an up-regulation of caspase-8 mRNA expression.	Azacitidine	13-26	caspase 8	Homo sapiens	129-138
18082045-10	2007	CONCLUSIONS: 5-azacytidine may enhance anti-tumor efficacy of doxorubicin to NB cell lines, possibly through an up-regulation of caspase-8 mRNA expression.	Doxorubicin	62-73	caspase 8	Homo sapiens	129-138
17904098-0	2007	Hypoxia/reoxygenation induces apoptosis through a ROS-mediated caspase-8/Bid/Bax pathway in human lymphocytes.	Reactive Oxygen Species	50-53	caspase 8	Homo sapiens	63-72
17928124-0	2007	Interaction between caspase-8 activation and endoplasmic reticulum stress in glycochenodeoxycholic acid-induced apoptotic HepG2 cells.	Glycochenodeoxycholic Acid	77-103	caspase 8	Homo sapiens	20-29
17928124-7	2007	Immunofluorescence microscopic analysis showed that treatment with GCDCA increased the cleavage of BAP31, an integral membrane protein of ER, and pretreatment with Z-IETD-FMK suppressed the increase of caspase-8 and BAP31 cleavage.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	164-174	caspase 8	Homo sapiens	202-211
17904098-6	2007	Furthermore, suppression of caspase-8 activity with z-IETD-fmk prevented Bid cleavage and Bax activation during apoptosis.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	52-62	caspase 8	Homo sapiens	28-37
17904098-7	2007	N-acetylcysteine (NAC), a well-known ROS scavenger, suppressed caspase-8 activation and the subsequent cleavage of caspase-9 and caspase-3, indicating the role of ROS in caspase-8-mediated apoptosis.	Acetylcysteine	0-16	caspase 8	Homo sapiens	63-72
17904098-7	2007	N-acetylcysteine (NAC), a well-known ROS scavenger, suppressed caspase-8 activation and the subsequent cleavage of caspase-9 and caspase-3, indicating the role of ROS in caspase-8-mediated apoptosis.	Acetylcysteine	0-16	caspase 8	Homo sapiens	170-179
17904098-7	2007	N-acetylcysteine (NAC), a well-known ROS scavenger, suppressed caspase-8 activation and the subsequent cleavage of caspase-9 and caspase-3, indicating the role of ROS in caspase-8-mediated apoptosis.	Acetylcysteine	18-21	caspase 8	Homo sapiens	63-72
17904098-7	2007	N-acetylcysteine (NAC), a well-known ROS scavenger, suppressed caspase-8 activation and the subsequent cleavage of caspase-9 and caspase-3, indicating the role of ROS in caspase-8-mediated apoptosis.	Acetylcysteine	18-21	caspase 8	Homo sapiens	170-179
17727829-6	2007	N-Acetyl-l-cysteine (NAC) pretreatment resulted in the increase in glutathione concentration, reduction of intracellular ROS, complete inhibition of DNA fragmentation, mitochondrial membrane potential (MMP) collapse, Fas externalization and caspase-8 activation.	Acetylcysteine	0-19	caspase 8	Homo sapiens	241-250
17904098-7	2007	N-acetylcysteine (NAC), a well-known ROS scavenger, suppressed caspase-8 activation and the subsequent cleavage of caspase-9 and caspase-3, indicating the role of ROS in caspase-8-mediated apoptosis.	Reactive Oxygen Species	163-166	caspase 8	Homo sapiens	170-179
17727829-8	2007	Pretreatment with an intracellular Ca2+ chelator, BAPTA-AM reduced MS5-induced DNA fragmentation and caspase-8 activation while it has marginal effects on MMP collapse.	1,2-bis(2-aminophenoxy)ethane N,N,N',N'-tetraacetic acid acetoxymethyl ester	50-58	caspase 8	Homo sapiens	101-110
17904098-8	2007	Overall, our results indicate that H/R induces apoptosis via a mitochondrial pathway involving caspase-8/Bid/Bax activation in human lymphocytes.	r	37-38	caspase 8	Homo sapiens	95-104
17727829-9	2007	Taken together our present data showed that a rapid increase in intracellular ROS by MS5 triggers apoptosis via the Fas/caspase-8-mediated mitochondrial pathway suggesting that the presence of diketone makes the compound more potent to induce apoptosis.	Reactive Oxygen Species	78-81	caspase 8	Homo sapiens	120-129
17904098-9	2007	Our results also suggest that ROS are critical regulators of caspase-8-mediated apoptosis in H/R-treated human lymphocytes.	Reactive Oxygen Species	30-33	caspase 8	Homo sapiens	61-70
17986867-5	2007	The BPDE-induced apoptosis in H460 cells correlated with up-regulation of pro-apoptotic protein Bak, downregulation of anti-apoptotic Bcl-2 family members Bcl-2 and Bcl-xL, release of cytochrome c from mitochondria to the cytosol without a change in mitochondrial membrane potential or mitochondrial morphology (electron microscopy), and cleavage of caspase-8, -9, and -3.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	4-8	caspase 8	Homo sapiens	350-371
17727829-9	2007	Taken together our present data showed that a rapid increase in intracellular ROS by MS5 triggers apoptosis via the Fas/caspase-8-mediated mitochondrial pathway suggesting that the presence of diketone makes the compound more potent to induce apoptosis.	1,4-diselenophene-1,4-diketone	193-201	caspase 8	Homo sapiens	120-129
17986867-8	2007	The BPDE-induced apoptosis was partially but statistically significantly attenuated in the presence of specific inhibitors of caspase-9 (z-LEHDfmk) and caspase-8 (z-IETDfmk).	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	4-8	caspase 8	Homo sapiens	152-161
17893514-8	2007	In view of these results and taking into consideration that K562 cells are Fas-null, we suggested that caspase-8 is activated in a Fas-independent manner downstream of caspase-9.	ammonium ferrous sulfate	75-78	caspase 8	Homo sapiens	103-112
17893514-8	2007	In view of these results and taking into consideration that K562 cells are Fas-null, we suggested that caspase-8 is activated in a Fas-independent manner downstream of caspase-9.	ammonium ferrous sulfate	131-134	caspase 8	Homo sapiens	103-112
17673311-7	2007	P38-MAPK-specific inhibitors attenuate the As(2)O(3) plus TNFalpha-provoked activation of caspase-8/Bid, Bax translocation, cytochrome c release, and apoptosis induction.	Arsenic Trioxide	43-52	caspase 8	Homo sapiens	90-99
17974980-7	2007	Inhibition of JNK, caspase-4, or caspase-8 activation diminished edelfosine-induced apoptosis.	edelfosine	65-75	caspase 8	Homo sapiens	33-42
17974980-8	2007	Edelfosine treatment led to the generation of the p20 caspase-8 cleavage fragment of BAP31, directing proapoptotic signals between the ER and the mitochondria.	edelfosine	0-10	caspase 8	Homo sapiens	54-63
17565448-0	2007	Nitric oxide upregulation of caspase-8 mRNA expression in lung endothelial cells: role of JAK2/STAT-1 signaling.	Nitric Oxide	0-12	caspase 8	Homo sapiens	29-38
17619073-7	2007	Similar to function way of SM, cDDP causes cancer cell apoptosis though caspase-8/caspase-3 and Bax/cytochrome c pathways, but the resistance to cDDP is correlated with Bcl-2 and Bcl-xL overexpression.	beta-solamarine	27-29	caspase 8	Homo sapiens	72-81
17619073-7	2007	Similar to function way of SM, cDDP causes cancer cell apoptosis though caspase-8/caspase-3 and Bax/cytochrome c pathways, but the resistance to cDDP is correlated with Bcl-2 and Bcl-xL overexpression.	Cisplatin	31-35	caspase 8	Homo sapiens	72-81
17907002-6	2007	Furthermore, pre-treatment with the ROS scavenger N-acetylcysteine (NAC) and the caspase-8 inhibitor z-IETD-fmk was found to effectively prevent UVB-induced apoptosis, suggesting that UVB-induced HaCaT cell apoptosis was partially due to generation of ROS and activation of the caspase-8 pathway.	Reactive Oxygen Species	36-39	caspase 8	Homo sapiens	278-287
17907002-6	2007	Furthermore, pre-treatment with the ROS scavenger N-acetylcysteine (NAC) and the caspase-8 inhibitor z-IETD-fmk was found to effectively prevent UVB-induced apoptosis, suggesting that UVB-induced HaCaT cell apoptosis was partially due to generation of ROS and activation of the caspase-8 pathway.	Acetylcysteine	50-66	caspase 8	Homo sapiens	278-287
17907002-6	2007	Furthermore, pre-treatment with the ROS scavenger N-acetylcysteine (NAC) and the caspase-8 inhibitor z-IETD-fmk was found to effectively prevent UVB-induced apoptosis, suggesting that UVB-induced HaCaT cell apoptosis was partially due to generation of ROS and activation of the caspase-8 pathway.	Acetylcysteine	68-71	caspase 8	Homo sapiens	278-287
17907002-6	2007	Furthermore, pre-treatment with the ROS scavenger N-acetylcysteine (NAC) and the caspase-8 inhibitor z-IETD-fmk was found to effectively prevent UVB-induced apoptosis, suggesting that UVB-induced HaCaT cell apoptosis was partially due to generation of ROS and activation of the caspase-8 pathway.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	101-111	caspase 8	Homo sapiens	81-90
17907002-6	2007	Furthermore, pre-treatment with the ROS scavenger N-acetylcysteine (NAC) and the caspase-8 inhibitor z-IETD-fmk was found to effectively prevent UVB-induced apoptosis, suggesting that UVB-induced HaCaT cell apoptosis was partially due to generation of ROS and activation of the caspase-8 pathway.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	101-111	caspase 8	Homo sapiens	278-287
17907002-6	2007	Furthermore, pre-treatment with the ROS scavenger N-acetylcysteine (NAC) and the caspase-8 inhibitor z-IETD-fmk was found to effectively prevent UVB-induced apoptosis, suggesting that UVB-induced HaCaT cell apoptosis was partially due to generation of ROS and activation of the caspase-8 pathway.	Reactive Oxygen Species	252-255	caspase 8	Homo sapiens	81-90
17565448-1	2007	We recently reported that nitric oxide (NO) modulates expression of multiple genes associated with apoptotic pathways, including expression of caspase-8.	Nitric Oxide	26-38	caspase 8	Homo sapiens	143-152
17565448-10	2007	These studies demonstrate that a NO-dependent increase in caspase-8 mRNA levels is associated with phosphorylation of STAT-1 at Ser-727 and STAT1 binding to the caspase-8 promoter in cultured PAEC.	Serine	128-131	caspase 8	Homo sapiens	58-67
18025281-7	2007	SAHA also activated the extrinsic apoptosis pathway, including increased Fas and Fas ligand (FasL) expression, activation of caspase-8, and cleavage of Bid.	Vorinostat	0-4	caspase 8	Homo sapiens	125-134
17673978-4	2007	Treatment of SW620 cells with 50 microM berberine resulted in activation of the caspase 3 and caspase 8, cleavage of poly ADP-ribose polymerase (PARP) and the release of cytochrome c; whereas, the expression of BID and anti-apoptosis factor c-IAP1, Bcl-2, and Bcl-(XL) were decreased markedly.	Berberine	40-49	caspase 8	Homo sapiens	94-103
17765201-3	2007	Furthermore, SB-induced apoptosis on HepG2 cells was mediated by activation of caspase-8 and -9, mitochondrial membrane potential (Deltapsim) collapse and the leakage of cytochrome c.	saxifragifolin B	13-15	caspase 8	Homo sapiens	79-95
17914284-6	2007	Finally, we present a mitochondria-priming model to explain how c-Myc-Bak interaction amplifies the TRAIL-induced caspase 8-Bid pathway to induce full-blown apoptosis.	bakuchiol	70-73	caspase 8	Homo sapiens	114-123
17698840-4	2007	In contrast, TRAIL caused increased binding between Mcl-1 and Bak that was diminished by treatment with the caspase 8 inhibitor N-(N(alpha)-acetylisoleucylglutamylthreonyl) aspartic acid (O-methyl ester)-fluoromethyl ketone (IETD(OMe)-fmk) or the c-Jun N-terminal kinase inhibitor SP600125.	n-(n(alpha)-acetylisoleucylglutamylthreonyl) aspartic acid	128-186	caspase 8	Homo sapiens	108-117
17698840-4	2007	In contrast, TRAIL caused increased binding between Mcl-1 and Bak that was diminished by treatment with the caspase 8 inhibitor N-(N(alpha)-acetylisoleucylglutamylthreonyl) aspartic acid (O-methyl ester)-fluoromethyl ketone (IETD(OMe)-fmk) or the c-Jun N-terminal kinase inhibitor SP600125.	o-methyl ester)-fluoromethyl ketone	188-223	caspase 8	Homo sapiens	108-117
17698840-4	2007	In contrast, TRAIL caused increased binding between Mcl-1 and Bak that was diminished by treatment with the caspase 8 inhibitor N-(N(alpha)-acetylisoleucylglutamylthreonyl) aspartic acid (O-methyl ester)-fluoromethyl ketone (IETD(OMe)-fmk) or the c-Jun N-terminal kinase inhibitor SP600125.	IETD(OMe)-fmk	225-238	caspase 8	Homo sapiens	108-117
17698840-4	2007	In contrast, TRAIL caused increased binding between Mcl-1 and Bak that was diminished by treatment with the caspase 8 inhibitor N-(N(alpha)-acetylisoleucylglutamylthreonyl) aspartic acid (O-methyl ester)-fluoromethyl ketone (IETD(OMe)-fmk) or the c-Jun N-terminal kinase inhibitor SP600125.	pyrazolanthrone	281-289	caspase 8	Homo sapiens	108-117
18253090-4	2007	In the current work, we determined the modulatory effects of CDDO-Me on the levels of c-FLIP, a major inhibitor of death receptor-mediated caspase-8 activation, and its impact on CDDO-Me-induced apoptosis and enhancement of TRAIL-induced apoptosis in human lung cancer cells.	bardoxolone methyl	61-68	caspase 8	Homo sapiens	139-148
17909059-4	2007	Sorafenib/TRAIL-induced cell death was accompanied by mitochondrial injury and release of cytochrome c, Smac, and AIF into the cytosol and caspase-9, caspase-3, caspase-7, and caspase-8 activation.	Sorafenib	0-9	caspase 8	Homo sapiens	176-185
17897295-6	2007	Biochemical studies showed that: (i) Bortezomib activated caspase-8 and caspase-3 and decreased cellular FLICE [Fas-associated death domain (FADD)-like interleukin-1beta-converting enzyme]-inhibitory protein (c-FLIP) levels in AML blasts; (ii) high c-FLIP levels in AML blasts were associated with low Bortezomib sensitivity.	Bortezomib	37-47	caspase 8	Homo sapiens	58-67
17897295-6	2007	Biochemical studies showed that: (i) Bortezomib activated caspase-8 and caspase-3 and decreased cellular FLICE [Fas-associated death domain (FADD)-like interleukin-1beta-converting enzyme]-inhibitory protein (c-FLIP) levels in AML blasts; (ii) high c-FLIP levels in AML blasts were associated with low Bortezomib sensitivity.	Bortezomib	37-47	caspase 8	Homo sapiens	105-110
17493842-0	2007	Caspase-8 dependent osteosarcoma cell apoptosis induced by proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	80-85	caspase 8	Homo sapiens	0-9
17493842-8	2007	This suggests that the apoptosis induced by MG132 in MG63 cells is caspase-8 dependent, p27 and bcl-2 family related.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	44-49	caspase 8	Homo sapiens	67-76
17909059-7	2007	Similarly, inhibition of the receptor-mediated apoptotic cascade with a caspase-8 dominant-negative mutant significantly blocked sorafenib/TRAIL-induced lethality but not Mcl-1 down-regulation or Bak/Bax conformational change, indicating that TRAIL-mediated receptor pathway activation is required for maximal lethality.	Sorafenib	129-138	caspase 8	Homo sapiens	72-81
17894646-3	2007	It protects human neuroblastoma cells (SH-SY5Y) from hydrogen peroxide (H2O2)-induced apoptosis by preventing caspase-3 activation via either caspase-8 or caspase-9.	Hydrogen Peroxide	53-70	caspase 8	Homo sapiens	142-151
17644308-3	2007	In this study, we show that RIP3 is cleaved at Asp328 by caspase-8 under apoptotic stimuli, which is blocked by pan-caspase inhibitor Z-VAD-FMK.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	134-143	caspase 8	Homo sapiens	57-66
17585337-0	2007	p38 MAPK and MSK1 mediate caspase-8 activation in manganese-induced mitochondria-dependent cell death.	Manganese	50-59	caspase 8	Homo sapiens	26-35
17585337-4	2007	We show here that Mn(2+)-induced cell death in human B cells is associated with caspase-8-dependent mitochondrial activation leading to caspase-3 activity and apoptosis.	Manganese(2+)	18-24	caspase 8	Homo sapiens	80-89
17585337-5	2007	We used specific caspase-8 interfering shRNAs to reduce caspase-8 expression, and this also reduced Mn(2+)-induced caspase-3 activation and apoptosis.	Manganese(2+)	100-106	caspase 8	Homo sapiens	17-26
17585337-5	2007	We used specific caspase-8 interfering shRNAs to reduce caspase-8 expression, and this also reduced Mn(2+)-induced caspase-3 activation and apoptosis.	Manganese(2+)	100-106	caspase 8	Homo sapiens	56-65
17585337-6	2007	Mn(2+)-triggered caspase-8 activation is associated with a specific pathway, which is independent of Fas-associated death domain protein, and dependent on the sequential activation of p38-mitogen-activated protein kinase (p38 MAPK) and mitogen- and stress-response kinase 1 (MSK1).	Manganese(2+)	0-6	caspase 8	Homo sapiens	17-26
17585337-7	2007	Inhibition of p38 activity using either pharmacological inhibitors or dominant-negative mutant forms of p38 blocked Mn(2+)-mediated phosphorylation of MSK1 and blocked subsequent caspase-8 activation.	Manganese(2+)	116-122	caspase 8	Homo sapiens	179-188
17585337-9	2007	These findings suggest a novel model for the regulation of caspase-8 during Mn(2+)-induced apoptosis based on the sequential activation of p38 MAPK, MSK1, caspase-8 and mitochondria, respectively.	Manganese(2+)	76-82	caspase 8	Homo sapiens	59-68
17585337-9	2007	These findings suggest a novel model for the regulation of caspase-8 during Mn(2+)-induced apoptosis based on the sequential activation of p38 MAPK, MSK1, caspase-8 and mitochondria, respectively.	Manganese(2+)	76-82	caspase 8	Homo sapiens	155-164
17585340-5	2007	Preincubation of cells with LY30 significantly amplified TRAIL signaling as evidenced by enhanced DNA fragmentation, caspases 2, 3, 8, and 9 activation, and reduction in the tumor colony formation.	ly30	28-32	caspase 8	Homo sapiens	117-125
17894646-3	2007	It protects human neuroblastoma cells (SH-SY5Y) from hydrogen peroxide (H2O2)-induced apoptosis by preventing caspase-3 activation via either caspase-8 or caspase-9.	Hydrogen Peroxide	72-76	caspase 8	Homo sapiens	142-151
17697742-9	2007	VPA induced apoptosis via the extrinsic pathway involving engagement of the caspase-8-dependent cascade.	Valproic Acid	0-3	caspase 8	Homo sapiens	76-85
17656415-8	2007	In addition, 10 nM DHT was able to induce the cleavage of caspases 8, 9 and 3 and cause DNA laddering, and these effects were reversed either by casodex or OHFlut.	Dihydrotestosterone	19-22	caspase 8	Homo sapiens	58-77
17656415-8	2007	In addition, 10 nM DHT was able to induce the cleavage of caspases 8, 9 and 3 and cause DNA laddering, and these effects were reversed either by casodex or OHFlut.	bicalutamide	145-152	caspase 8	Homo sapiens	58-77
17656415-8	2007	In addition, 10 nM DHT was able to induce the cleavage of caspases 8, 9 and 3 and cause DNA laddering, and these effects were reversed either by casodex or OHFlut.	ohflut	156-162	caspase 8	Homo sapiens	58-77
17659258-0	2007	Bile acid-induced TGR5-dependent c-Jun-N terminal kinase activation leads to enhanced caspase 8 activation in hepatocytes.	Bile Acids and Salts	0-9	caspase 8	Homo sapiens	86-95
17397922-2	2007	Treatment of K562 cells with IQDMA resulted in G2/M phase cell cycle arrest, presumably involving the concomitant up-regulation of p21 and apoptosis through up-regulation of FasL and sequential activation of caspase-8 and caspase-3.	N'-(11H-indolo(3,2-c)quinolin-6-yl)-N,N-dimethylethane-1,2-diamine	29-34	caspase 8	Homo sapiens	208-217
17397922-5	2007	Further investigation showed that SP600125 reduced the activation of FasL, caspase-3, caspase-8, and led to a marked decline of p21.	pyrazolanthrone	34-42	caspase 8	Homo sapiens	86-95
17452973-5	2007	IRF-1-induced apoptosis involves caspase-8 since apoptosis is significantly decreased by the caspase-8-specific inhibitor IETD, c-FLIP expression and in caspase-8-deficient cancer cells.	IETD	122-126	caspase 8	Homo sapiens	33-42
17452973-5	2007	IRF-1-induced apoptosis involves caspase-8 since apoptosis is significantly decreased by the caspase-8-specific inhibitor IETD, c-FLIP expression and in caspase-8-deficient cancer cells.	IETD	122-126	caspase 8	Homo sapiens	93-102
17452973-5	2007	IRF-1-induced apoptosis involves caspase-8 since apoptosis is significantly decreased by the caspase-8-specific inhibitor IETD, c-FLIP expression and in caspase-8-deficient cancer cells.	IETD	122-126	caspase 8	Homo sapiens	93-102
17659258-8	2007	In conclusion, bile acids activate TGR5, which leads to JNK activation and reduced complex formation of JNK with caspase 8, thus facilitating caspase 8 recruitment to DISC.	Bile Acids and Salts	15-25	caspase 8	Homo sapiens	142-151
17786311-3	2007	Bortezomib efficiently up-regulated p21(waf1/cip1) and p27(kip1) expression, and induced apoptosis accompanied by the expression of cleaved-PARP, DR4 and activated caspase-8 in EFT cells.	Bortezomib	0-10	caspase 8	Homo sapiens	164-173
17636462-8	2007	Resveratrol enhanced the apoptosis-inducing potential of TRAIL, and these effects were inhibited by either dominant negative FADD or caspase-8 siRNA.	Resveratrol	0-11	caspase 8	Homo sapiens	133-142
17659258-5	2007	TGR5 inhibition attenuated bile acid-induced caspase 8 activation, which resulted from reduced bile acid-induced caspase 8 recruited to a death-inducing signaling complex (DISC).	Bile Acids and Salts	27-36	caspase 8	Homo sapiens	45-54
17659258-5	2007	TGR5 inhibition attenuated bile acid-induced caspase 8 activation, which resulted from reduced bile acid-induced caspase 8 recruited to a death-inducing signaling complex (DISC).	Bile Acids and Salts	27-36	caspase 8	Homo sapiens	113-122
17659258-5	2007	TGR5 inhibition attenuated bile acid-induced caspase 8 activation, which resulted from reduced bile acid-induced caspase 8 recruited to a death-inducing signaling complex (DISC).	Bile Acids and Salts	95-104	caspase 8	Homo sapiens	45-54
17659258-5	2007	TGR5 inhibition attenuated bile acid-induced caspase 8 activation, which resulted from reduced bile acid-induced caspase 8 recruited to a death-inducing signaling complex (DISC).	Bile Acids and Salts	95-104	caspase 8	Homo sapiens	113-122
17659258-7	2007	JNK formed complexes with caspase 8, which were reduced following bile acid treatment, but this reduction was prevented when TGR5 or JNK was inhibited.	Bile Acids and Salts	66-75	caspase 8	Homo sapiens	26-35
17659258-8	2007	In conclusion, bile acids activate TGR5, which leads to JNK activation and reduced complex formation of JNK with caspase 8, thus facilitating caspase 8 recruitment to DISC.	Bile Acids and Salts	15-25	caspase 8	Homo sapiens	113-122
17609291-9	2007	Inhibition of IDO-mediated TEC death by a caspase-8-specific inhibitor (Z-IETD-FMK), as well as the absence of an IDO effect in Fas-deficient and FasL-deficient TEC, supports a Fas/FasL-dependent, caspase-8-mediated mechanism for IDO-enhanced TEC death.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	72-82	caspase 8	Homo sapiens	42-51
17970047-7	2007	Selenium, on the other hand, increased the expression of FADD, a key adaptor molecule responsible for recruitment of caspase-8 to the Fas oligomer.	Selenium	0-8	caspase 8	Homo sapiens	117-126
17520191-1	2007	Bid, a member of the pro-apoptotic Bcl-2 protein family, is activated through caspase-8-mediated cleavage into a truncated form (p15 tBid) during TNF-alpha(tumor necrosis factor alpha)-induced apoptosis.	tBID	133-137	caspase 8	Homo sapiens	78-87
17970047-8	2007	The significance of the above changes was confirmed by the detection of considerably more caspase-8 in both the Fas or FADD immunoprecipitate obtained from cells treated with the doxorubicin/selenium combination.	ammonium ferrous sulfate	112-115	caspase 8	Homo sapiens	90-99
17970047-8	2007	The significance of the above changes was confirmed by the detection of considerably more caspase-8 in both the Fas or FADD immunoprecipitate obtained from cells treated with the doxorubicin/selenium combination.	Doxorubicin	179-190	caspase 8	Homo sapiens	90-99
17970047-8	2007	The significance of the above changes was confirmed by the detection of considerably more caspase-8 in both the Fas or FADD immunoprecipitate obtained from cells treated with the doxorubicin/selenium combination.	Selenium	191-199	caspase 8	Homo sapiens	90-99
17887940-0	2007	Effect of methanolic extract from silkworm droppings on proliferation and caspase activity in HT-29 human colon cancer cells.	methanolic	10-20	caspase 8	Homo sapiens	74-81
17943553-6	2007	Caspase-8, -9, -3 and pan-caspase inhibitors partially reversed silymarin-induced apoptosis of CH11-treated cells.	Silymarin	64-73	caspase 8	Homo sapiens	0-17
17943553-6	2007	Caspase-8, -9, -3 and pan-caspase inhibitors partially reversed silymarin-induced apoptosis of CH11-treated cells.	4-dimethylamino-3',4'-dimethoxychalcone	95-99	caspase 8	Homo sapiens	0-17
17404499-4	2007	The mechanism of Zvad-induced cell death was proposed to require caspase-8 inhibition.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	17-21	caspase 8	Homo sapiens	65-74
17887940-8	2007	Interestingly, caspase-9 and -3, but not caspase-8, were activated in response to SDME treatment.	sdme	82-86	caspase 8	Homo sapiens	41-50
17578896-10	2007	Collectively, our data argue that BBR3610 promotes cell killing via a caspase 8-dependent mechanism, which can be enhanced by ERBB1/PI3K inhibitors that promote additional BBR3610-dependent cell killing via activation of BAX and caspase 9.	BBR3610	34-41	caspase 8	Homo sapiens	70-79
17658284-5	2007	The reversible aldehyde form of inhibitors for human caspase-8 and -9, Ac-LEHD-CHO and Ac-IETD-CHO, are equally efficient in inhibiting Chinese hamster caspase-8.	Aldehydes	15-23	caspase 8	Homo sapiens	53-69
17578896-10	2007	Collectively, our data argue that BBR3610 promotes cell killing via a caspase 8-dependent mechanism, which can be enhanced by ERBB1/PI3K inhibitors that promote additional BBR3610-dependent cell killing via activation of BAX and caspase 9.	BBR3610	172-179	caspase 8	Homo sapiens	70-79
17578896-6	2007	Small molecule or molecular inhibition of caspase 8 function abolished the toxicity of BBR3610 and of BBR3610 + ERBB1 inhibitor treatments, whereas inhibition of caspase 9 suppressed the ability of ERBB1 inhibitors to enhance BBR3610 lethality.	BBR3610	87-94	caspase 8	Homo sapiens	42-51
17578896-6	2007	Small molecule or molecular inhibition of caspase 8 function abolished the toxicity of BBR3610 and of BBR3610 + ERBB1 inhibitor treatments, whereas inhibition of caspase 9 suppressed the ability of ERBB1 inhibitors to enhance BBR3610 lethality.	BBR3610	102-109	caspase 8	Homo sapiens	42-51
17585882-6	2007	Colorimetric assays of cells treated for 36 h with EGCG demonstrated a reduction in activities of caspases 3 (50%) and 9 (70%) but not caspase 8, indicating initiation of apoptosis.	epigallocatechin gallate	51-55	caspase 8	Homo sapiens	135-144
17578896-6	2007	Small molecule or molecular inhibition of caspase 8 function abolished the toxicity of BBR3610 and of BBR3610 + ERBB1 inhibitor treatments, whereas inhibition of caspase 9 suppressed the ability of ERBB1 inhibitors to enhance BBR3610 lethality.	BBR3610	102-109	caspase 8	Homo sapiens	42-51
17898872-1	2007	Our study has shown that the Amaryllidaceae isocarbostyril narciclasine induces marked apoptosis-mediated cytotoxic effects in human cancer cells but not in normal fibroblasts by triggering the activation of the initiator caspases of the death receptor pathway (caspase-8 and caspase-10) at least in human MCF-7 breast and PC-3 prostate carcinoma cells.	amaryllidaceae isocarbostyril narciclasine	29-71	caspase 8	Homo sapiens	222-230
17898872-1	2007	Our study has shown that the Amaryllidaceae isocarbostyril narciclasine induces marked apoptosis-mediated cytotoxic effects in human cancer cells but not in normal fibroblasts by triggering the activation of the initiator caspases of the death receptor pathway (caspase-8 and caspase-10) at least in human MCF-7 breast and PC-3 prostate carcinoma cells.	amaryllidaceae isocarbostyril narciclasine	29-71	caspase 8	Homo sapiens	262-271
17898872-3	2007	Caspase-8 was found to interact with Fas and DR4 receptors on narciclasine treatment.	ammonium ferrous sulfate	37-40	caspase 8	Homo sapiens	0-9
17898872-3	2007	Caspase-8 was found to interact with Fas and DR4 receptors on narciclasine treatment.	narciclasine	62-74	caspase 8	Homo sapiens	0-9
17898872-4	2007	However, narciclasine-induced downstream apoptotic pathways in MCF-7 cells diverged from those in PC-3 cells, where caspase-8 directly activated effector caspases such as caspase-3 in the absence of any further release of mitochondrial proapoptotic effectors.	narciclasine	9-21	caspase 8	Homo sapiens	116-125
17898872-4	2007	However, narciclasine-induced downstream apoptotic pathways in MCF-7 cells diverged from those in PC-3 cells, where caspase-8 directly activated effector caspases such as caspase-3 in the absence of any further release of mitochondrial proapoptotic effectors.	narciclasine	9-21	caspase 8	Homo sapiens	154-162
17846503-4	2007	Maximum caspase 7 activity was observed with 100 microM acacetin for 24 h. Caspase 8 and 9 activation cascades mediated the activation of caspase 7.	acacetin	56-64	caspase 8	Homo sapiens	75-84
17846503-7	2007	Pretreatment of cells with N-acetylcysteine (NAC) reduced ROS generation and cell growth inhibition, and pretreatment with NAC or a caspase 8 inhibitor (Z-IETD-FMK) inhibited the acacetin-induced loss of mitochondrial membrane potential and release of cytochrome c and AIF.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	153-163	caspase 8	Homo sapiens	132-141
17846503-7	2007	Pretreatment of cells with N-acetylcysteine (NAC) reduced ROS generation and cell growth inhibition, and pretreatment with NAC or a caspase 8 inhibitor (Z-IETD-FMK) inhibited the acacetin-induced loss of mitochondrial membrane potential and release of cytochrome c and AIF.	acacetin	179-187	caspase 8	Homo sapiens	132-141
17718901-6	2007	The ability of resveratrol to sensitize TRAIL-resistant LNCaP cells was inhibited by dominant negative FADD, caspase-8 siRNA or N-acetyl cysteine.	Resveratrol	15-26	caspase 8	Homo sapiens	109-118
17666435-5	2007	We previously reported that ceramide induced caspase-2 and caspase-8 activation, Bid cleavage, mitochondrial damage, and apoptosis.	Ceramides	28-36	caspase 8	Homo sapiens	59-68
17666435-8	2007	These results indicate a role for GSK-3beta in ceramide-induced apoptosis, in which GSK-3beta acts downstream of PP2A and the PI 3-kinase-Akt pathway, and upstream of caspase-2 and caspase-8.	Ceramides	47-55	caspase 8	Homo sapiens	181-190
17666813-0	2007	Saucernetin-7 isolated from Saururus chinensis induces caspase-dependent apoptosis in human promyelocytic leukemia HL-60 cells.	saucernetin-7	0-13	caspase 8	Homo sapiens	55-62
17666813-3	2007	z-VAD-fmk (a broad-caspase inhibitor) almost completely suppressed saucernetin-7-induced DNA ladder formation, thereby implicating the caspase cascade in the apoptotic process.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	0-9	caspase 8	Homo sapiens	19-26
17554377-5	2007	This internalization was closely relevant to intracellular glutathione (GSH) depletion in Jurkat cells downstream of Fas-associated death domain protein (FADD) and caspase 8.	Glutathione	59-70	caspase 8	Homo sapiens	164-173
17666813-3	2007	z-VAD-fmk (a broad-caspase inhibitor) almost completely suppressed saucernetin-7-induced DNA ladder formation, thereby implicating the caspase cascade in the apoptotic process.	saucernetin-7	67-80	caspase 8	Homo sapiens	19-26
17666813-5	2007	Taken together, the present study demonstrates that saucernetin-7 is a potent inducer of apoptosis and that its activity is facilitated by caspase-8 activation, Bid cleavage, Bax translocation to mitochondria, release of cytochrome c into cytoplasm, and subsequently caspase-3 activation, which offers a potential mechanism for the apoptosis-inducing activity of saucernetin-7.	saucernetin-7	52-65	caspase 8	Homo sapiens	139-148
17627812-2	2007	In this study, IFN-gamma mediated up-regulation of caspase-8 in human MB cells was found to result in chemosensitization to cisplatin, doxorubicin and etoposide, and sensitisation to radiation.	Cisplatin	124-133	caspase 8	Homo sapiens	51-60
17652735-12	2007	Caspase-8, caspase-3, and broad caspase inhibitors, but not caspase-9 inhibitor, inhibited MMC-induced cell death in nonpretreated and IFN-pretreated cells.	Mitomycin	91-94	caspase 8	Homo sapiens	0-9
17652735-12	2007	Caspase-8, caspase-3, and broad caspase inhibitors, but not caspase-9 inhibitor, inhibited MMC-induced cell death in nonpretreated and IFN-pretreated cells.	Mitomycin	91-94	caspase 8	Homo sapiens	11-18
17554377-8	2007	Overall, our results indicate that CD95(APO-1) induces the FADD- and caspase 8-dependent internalization of Na(+),K(+)-ATPase through intracellular GSH loss, and the subsequent generation of H(2)O(2)-mediated serine phosphorylation of Na(+),K(+)-ATPase alpha1 subunit.	Serine	209-215	caspase 8	Homo sapiens	69-78
17690453-2	2007	We have reported that tryptophol induces apoptosis in U937 cells via activation of caspase-8 followed by caspase-3.	tryptophol	22-32	caspase 8	Homo sapiens	83-92
17561974-0	2007	Cell cycle dependency of caspase activation in Fas-induced apoptosis in leukemia cells.	ammonium ferrous sulfate	47-50	caspase 8	Homo sapiens	25-32
17561974-2	2007	In the present study we have investigated the relationship between cell cycle progression and the activation of caspases (caspase-3 and caspase-8) in Fas (CD95)-mediated apoptosis in asynchronously growing leukemia cells.	ammonium ferrous sulfate	150-153	caspase 8	Homo sapiens	112-120
17561974-2	2007	In the present study we have investigated the relationship between cell cycle progression and the activation of caspases (caspase-3 and caspase-8) in Fas (CD95)-mediated apoptosis in asynchronously growing leukemia cells.	ammonium ferrous sulfate	150-153	caspase 8	Homo sapiens	136-145
17627812-2	2007	In this study, IFN-gamma mediated up-regulation of caspase-8 in human MB cells was found to result in chemosensitization to cisplatin, doxorubicin and etoposide, and sensitisation to radiation.	Doxorubicin	135-146	caspase 8	Homo sapiens	51-60
17627812-2	2007	In this study, IFN-gamma mediated up-regulation of caspase-8 in human MB cells was found to result in chemosensitization to cisplatin, doxorubicin and etoposide, and sensitisation to radiation.	Etoposide	151-160	caspase 8	Homo sapiens	51-60
17627812-4	2007	IFN-gamma mediated chemosensitization and radiosensitization effects were reduced by treatment with the caspase-8 specific inhibitor z-IETD-fmk.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	133-143	caspase 8	Homo sapiens	104-113
17554377-5	2007	This internalization was closely relevant to intracellular glutathione (GSH) depletion in Jurkat cells downstream of Fas-associated death domain protein (FADD) and caspase 8.	Glutathione	72-75	caspase 8	Homo sapiens	164-173
17554377-8	2007	Overall, our results indicate that CD95(APO-1) induces the FADD- and caspase 8-dependent internalization of Na(+),K(+)-ATPase through intracellular GSH loss, and the subsequent generation of H(2)O(2)-mediated serine phosphorylation of Na(+),K(+)-ATPase alpha1 subunit.	Glutathione	148-151	caspase 8	Homo sapiens	69-78
17554377-8	2007	Overall, our results indicate that CD95(APO-1) induces the FADD- and caspase 8-dependent internalization of Na(+),K(+)-ATPase through intracellular GSH loss, and the subsequent generation of H(2)O(2)-mediated serine phosphorylation of Na(+),K(+)-ATPase alpha1 subunit.	Hydrogen Peroxide	191-199	caspase 8	Homo sapiens	69-78
17559898-0	2007	Cytotoxicity of diacetoxyscirpenol is associated with apoptosis by activation of caspase-8 and interruption of cell cycle progression by down-regulation of cdk4 and cyclin B1 in human Jurkat T cells.	diacetoxyscirpenol	16-34	caspase 8	Homo sapiens	81-90
17559898-2	2007	Exposure to DAS (0.01-0.15 microM) caused apoptotic DNA fragmentation along with caspase-8 activation, Bid cleavage, mitochondrial cytochrome c release, activation of caspase-9 and caspase-3, and PARP degradation, without any alteration in the levels of Fas or FasL.	diacetoxyscirpenol	12-15	caspase 8	Homo sapiens	81-90
17559898-6	2007	The DAS-mediated apoptosis and activation of caspase-8, -9, and -3 were abrogated by either pan-caspase inhibitor (z-VAD-fmk) or caspase-8 inhibitor (z-IETD-fmk).	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	115-124	caspase 8	Homo sapiens	45-66
17559898-6	2007	The DAS-mediated apoptosis and activation of caspase-8, -9, and -3 were abrogated by either pan-caspase inhibitor (z-VAD-fmk) or caspase-8 inhibitor (z-IETD-fmk).	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	115-124	caspase 8	Homo sapiens	45-54
17559898-6	2007	The DAS-mediated apoptosis and activation of caspase-8, -9, and -3 were abrogated by either pan-caspase inhibitor (z-VAD-fmk) or caspase-8 inhibitor (z-IETD-fmk).	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	150-160	caspase 8	Homo sapiens	45-66
17559898-6	2007	The DAS-mediated apoptosis and activation of caspase-8, -9, and -3 were abrogated by either pan-caspase inhibitor (z-VAD-fmk) or caspase-8 inhibitor (z-IETD-fmk).	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	150-160	caspase 8	Homo sapiens	45-54
17559898-9	2007	These results demonstrate that the T-cell toxicity of DAS is attributable to not only apoptosis initiated by caspase-8 activation and subsequent mitochondrion-dependent or -independent activation of caspase cascades, which can be regulated by Bcl-xL, but also interruption of cell cycle progression caused by down-regulation of cdk4 and cyclin B1 proteins.	diacetoxyscirpenol	54-57	caspase 8	Homo sapiens	109-118
17021654-6	2007	Both mitomycin C and cisplatin induced apoptosis in C-33A cells via caspase-8 and -3 processing in a Fas/FasL-dependent manner and also suppressed IL-18 expression, while they down-regulated IkappaB expression and up-regulated p65 expression.	Mitomycin	5-16	caspase 8	Homo sapiens	68-84
17021654-6	2007	Both mitomycin C and cisplatin induced apoptosis in C-33A cells via caspase-8 and -3 processing in a Fas/FasL-dependent manner and also suppressed IL-18 expression, while they down-regulated IkappaB expression and up-regulated p65 expression.	Cisplatin	21-30	caspase 8	Homo sapiens	68-84
17021654-7	2007	These results suggest that both mitomycin C and cisplatin induce apoptosis, not only via the caspase-8 and -3 dependent Fas/FasL pathway, but also via the regulation of NF-kappaB activity and IL-18 expression in HPV-negative cervical cancer C-33A cells.	Mitomycin	32-43	caspase 8	Homo sapiens	93-109
17021654-7	2007	These results suggest that both mitomycin C and cisplatin induce apoptosis, not only via the caspase-8 and -3 dependent Fas/FasL pathway, but also via the regulation of NF-kappaB activity and IL-18 expression in HPV-negative cervical cancer C-33A cells.	Cisplatin	48-57	caspase 8	Homo sapiens	93-109
17396262-6	2007	In addition, it has been confirmed that the caspase-3 specific inhibitor, Z-DEVD-FMK, blocks the activation of caspase-8 in MNB-treated HL-60 cells.	benzoylcarbonyl-aspartyl-glutamyl-valyl-aspartyl-fluoromethyl ketone	74-84	caspase 8	Homo sapiens	111-120
17431216-3	2007	Real-time monitoring of initiator caspase activity showed that caspase-9 (66% of cells) and caspase-8 (15% of cells) were activated within 30 min of menadione administration, but no activation of caspase-2, -10, or -12 was detected.	Vitamin K 3	149-158	caspase 8	Homo sapiens	92-101
17431216-7	2007	In contrast, caspase-8 but not caspase-9 activation was blocked by the destruction of lysosomes (preincubation with Gly-Phe beta-naphthylamide, a cathepsin C substrate), loss of lysosomal acidity (bafilomycin A1), or inhibition of cathepsin L or D. Using pepstatin A-BODIPY FL conjugate, we confirmed translocation of cathepsin D out of lysosomes in response to menadione.	glycylphenylalanine 2-naphthylamide	116-142	caspase 8	Homo sapiens	13-22
17620439-5	2007	Enhancement of rhTRAIL-induced apoptosis by bortezomib was caspase dependent, implicating extrinsic as well as intrinsic apoptosis activation, as shown by increased processing of caspase-8 as well as caspase-9, and could be abrogated completely by overexpression of caspase-8 inhibitor cytokine response modifier A (CrmA), and partially by overexpression of Bcl-2.	Bortezomib	44-54	caspase 8	Homo sapiens	266-275
17431216-7	2007	In contrast, caspase-8 but not caspase-9 activation was blocked by the destruction of lysosomes (preincubation with Gly-Phe beta-naphthylamide, a cathepsin C substrate), loss of lysosomal acidity (bafilomycin A1), or inhibition of cathepsin L or D. Using pepstatin A-BODIPY FL conjugate, we confirmed translocation of cathepsin D out of lysosomes in response to menadione.	bafilomycin A1	197-211	caspase 8	Homo sapiens	13-22
17431216-7	2007	In contrast, caspase-8 but not caspase-9 activation was blocked by the destruction of lysosomes (preincubation with Gly-Phe beta-naphthylamide, a cathepsin C substrate), loss of lysosomal acidity (bafilomycin A1), or inhibition of cathepsin L or D. Using pepstatin A-BODIPY FL conjugate, we confirmed translocation of cathepsin D out of lysosomes in response to menadione.	pepstatin a-bodipy fl	255-276	caspase 8	Homo sapiens	13-22
17431216-7	2007	In contrast, caspase-8 but not caspase-9 activation was blocked by the destruction of lysosomes (preincubation with Gly-Phe beta-naphthylamide, a cathepsin C substrate), loss of lysosomal acidity (bafilomycin A1), or inhibition of cathepsin L or D. Using pepstatin A-BODIPY FL conjugate, we confirmed translocation of cathepsin D out of lysosomes in response to menadione.	Vitamin K 3	362-371	caspase 8	Homo sapiens	13-22
17431216-8	2007	We conclude that the oxidative stressor menadione induces two independent apoptotic pathways within pancreatic acinar cells: the classical mitochondrial calcium-dependent pathway that is initiated rapidly in the majority of cells, and a slower, caspase-8-mediated pathway that depends on the lysosomal activities of cathepsins and is used when the caspase-9 pathway is disabled.	Vitamin K 3	40-49	caspase 8	Homo sapiens	245-254
17356134-0	2007	NPI-0052, a novel proteasome inhibitor, induces caspase-8 and ROS-dependent apoptosis alone and in combination with HDAC inhibitors in leukemia cells.	marizomib	0-8	caspase 8	Homo sapiens	48-57
17356134-6	2007	NPI-0052-induced apoptosis was further probed using caspase-8 inhibitors, which were more protective than caspase-9 inhibitors.	marizomib	0-8	caspase 8	Homo sapiens	52-61
17549401-6	2007	Activation of caspase 8 accompanied by the release of cytochrome c and cleavage of PARP was also observed and indicative of Fas-mediated apoptosis.	ammonium ferrous sulfate	124-127	caspase 8	Homo sapiens	14-23
17574045-11	2007	Our data indicate that the mitochondria-dependent feedback loop of the caspase activation cascade and the generation of ROS are both essential in mediating profound cytotoxicity and apoptosis of MPM cells treated with CDDP and sFasL.	Cisplatin	218-222	caspase 8	Homo sapiens	71-78
17604333-9	2007	Silencing of either caspase-8 or death receptor 5 attenuated perifosine-induced apoptosis.	perifosine	61-71	caspase 8	Homo sapiens	20-29
17585225-8	2007	At low concentrations (3-6 mm) of lidocaine, caspase 3 was activated and release of cytochrome c was detected, whereas at higher concentrations (10 mm), no caspase activation was found.	Lidocaine	34-43	caspase 8	Homo sapiens	45-52
17585225-10	2007	Lidocaine also induced apoptotic caspase activation in neuroblastoma cells.	Lidocaine	0-9	caspase 8	Homo sapiens	33-40
17347868-5	2007	Conversely, the pancaspase inhibitor Q-VD-OPH inhibits lysosomal rupture, but only at early time points, suggesting that immediate lysosomal rupture involves caspases.	quinoline-val-asp(OMe)-CH2-OPH	37-45	caspase 8	Homo sapiens	158-166
17351739-3	2007	In HepG2 cells SAHA induced the extrinsic apoptotic pathway, increasing the expression of both FasL and FasL receptor and causing the activation of caspase-8.	Vorinostat	15-19	caspase 8	Homo sapiens	148-157
17476277-4	2007	This adhesion-dependent inhibition of mitoxantrone-induced apoptosis correlated with decreased activation of caspases-8 and 9, and cleavage of caspase 3 and PARP.	Mitoxantrone	38-50	caspase 8	Homo sapiens	109-125
17620439-6	2007	Enhanced surface expression of TRAIL-R2, but also TRAIL-R1, was associated with bortezomib treatment, which is likely to contribute to the increased processing of caspase-8 in the combination treatment.	Bortezomib	80-90	caspase 8	Homo sapiens	163-172
17475222-7	2007	The apoptosis induced by guggulsterone was also indicated by the activation of caspase-8, bid cleavage, cytochrome c release, caspase-9 activation, caspase-3 activation, and PARP cleavage.	pregna-4,17-diene-3,16-dione	25-38	caspase 8	Homo sapiens	79-88
17594508-13	2007	Furthermore, Ac-DNLD-CHO may be an attractive lead compound to generate novel effective non-peptidic pharmaceuticals for caspase-mediated apoptosis diseases, such as neurodegenerative disorders and viral infection diseases.	Ac-DNLD-CHO	13-24	caspase 8	Homo sapiens	121-128
17475221-9	2007	Furthermore, 2-Phenyl-4-quinolone induced the Mcl-1 cleavage, the phosphorylation of Bcl-2 and Bcl-xL (12-h treatment), and the caspase activation including caspase-8, -2 and -3 (24-h treatment).	2-phenyl-4-oxohydroquinoline	13-33	caspase 8	Homo sapiens	157-177
17493934-6	2007	Lonafarnib activated caspase-8 and its downstream caspases, whereas the caspase-8-specific inhibitor benzyloxycarbonyl-Ile-Glu(methoxy)-Thr-Asp(methoxy)-fluoromethyl ketone or small interfering RNA abrogated lonafarnib-induced apoptosis, indicating that lonafarnib induces caspase-8-dependent apoptosis.	lonafarnib	0-10	caspase 8	Homo sapiens	21-30
17493934-6	2007	Lonafarnib activated caspase-8 and its downstream caspases, whereas the caspase-8-specific inhibitor benzyloxycarbonyl-Ile-Glu(methoxy)-Thr-Asp(methoxy)-fluoromethyl ketone or small interfering RNA abrogated lonafarnib-induced apoptosis, indicating that lonafarnib induces caspase-8-dependent apoptosis.	lonafarnib	0-10	caspase 8	Homo sapiens	50-58
17493934-6	2007	Lonafarnib activated caspase-8 and its downstream caspases, whereas the caspase-8-specific inhibitor benzyloxycarbonyl-Ile-Glu(methoxy)-Thr-Asp(methoxy)-fluoromethyl ketone or small interfering RNA abrogated lonafarnib-induced apoptosis, indicating that lonafarnib induces caspase-8-dependent apoptosis.	benzyloxycarbonyl-ile-glu(methoxy)-thr-asp(methoxy)-fluoromethyl ketone	101-172	caspase 8	Homo sapiens	72-81
17493934-6	2007	Lonafarnib activated caspase-8 and its downstream caspases, whereas the caspase-8-specific inhibitor benzyloxycarbonyl-Ile-Glu(methoxy)-Thr-Asp(methoxy)-fluoromethyl ketone or small interfering RNA abrogated lonafarnib-induced apoptosis, indicating that lonafarnib induces caspase-8-dependent apoptosis.	benzyloxycarbonyl-ile-glu(methoxy)-thr-asp(methoxy)-fluoromethyl ketone	101-172	caspase 8	Homo sapiens	72-81
17493934-6	2007	Lonafarnib activated caspase-8 and its downstream caspases, whereas the caspase-8-specific inhibitor benzyloxycarbonyl-Ile-Glu(methoxy)-Thr-Asp(methoxy)-fluoromethyl ketone or small interfering RNA abrogated lonafarnib-induced apoptosis, indicating that lonafarnib induces caspase-8-dependent apoptosis.	lonafarnib	208-218	caspase 8	Homo sapiens	72-81
17493934-6	2007	Lonafarnib activated caspase-8 and its downstream caspases, whereas the caspase-8-specific inhibitor benzyloxycarbonyl-Ile-Glu(methoxy)-Thr-Asp(methoxy)-fluoromethyl ketone or small interfering RNA abrogated lonafarnib-induced apoptosis, indicating that lonafarnib induces caspase-8-dependent apoptosis.	lonafarnib	208-218	caspase 8	Homo sapiens	72-81
17493934-6	2007	Lonafarnib activated caspase-8 and its downstream caspases, whereas the caspase-8-specific inhibitor benzyloxycarbonyl-Ile-Glu(methoxy)-Thr-Asp(methoxy)-fluoromethyl ketone or small interfering RNA abrogated lonafarnib-induced apoptosis, indicating that lonafarnib induces caspase-8-dependent apoptosis.	lonafarnib	254-264	caspase 8	Homo sapiens	72-81
17493934-6	2007	Lonafarnib activated caspase-8 and its downstream caspases, whereas the caspase-8-specific inhibitor benzyloxycarbonyl-Ile-Glu(methoxy)-Thr-Asp(methoxy)-fluoromethyl ketone or small interfering RNA abrogated lonafarnib-induced apoptosis, indicating that lonafarnib induces caspase-8-dependent apoptosis.	lonafarnib	254-264	caspase 8	Homo sapiens	72-81
17594508-6	2007	In contrast, a well-known caspase-3 inhibitor, Ac-DEVD-CHO, inhibits all these caspases with similar Kiapp values.	acetyl-aspartyl-glutamyl-valyl-aspartal	47-58	caspase 8	Homo sapiens	79-87
17284528-7	2007	Enzastaurin induced dose-dependent apoptosis at 48 hours mediated via induction of caspase-3, caspase-8, caspase-9, and PARP cleavage.	enzastaurin	0-11	caspase 8	Homo sapiens	94-103
17291719-6	2007	However, inhibition of caspases with zVAD-fmk resulted in strong inhibition of all these signalling pathways in Colo357-BclxL, but enhanced NFkappaB and JNK signalling in PancTuI cells.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	37-45	caspase 8	Homo sapiens	23-31
17301064-0	2007	Apoptogenic activity of auraptene of Zanthoxylum schinifolium toward human acute leukemia Jurkat T cells is associated with ER stress-mediated caspase-8 activation that stimulates mitochondria-dependent or -independent caspase cascade.	aurapten	24-33	caspase 8	Homo sapiens	143-152
17505004-8	2007	Docetaxel mainly induced caspase-8 activation, whereas the addition of celecoxib and ZD1839 augmented the caspase-8 activation and enhanced caspase-9 activation.	Docetaxel	0-9	caspase 8	Homo sapiens	25-34
17567462-2	2007	The antioxidant glutathione (GSH) regulates cell death pathways by modulating the redox state of specific thiol residues of target proteins including transcription factors, stress kinases and caspases, which participate in tumor necrosis factor (TNF)-induced apoptosis.	Glutathione	16-27	caspase 8	Homo sapiens	192-200
17567462-2	2007	The antioxidant glutathione (GSH) regulates cell death pathways by modulating the redox state of specific thiol residues of target proteins including transcription factors, stress kinases and caspases, which participate in tumor necrosis factor (TNF)-induced apoptosis.	Glutathione	29-32	caspase 8	Homo sapiens	192-200
17567462-2	2007	The antioxidant glutathione (GSH) regulates cell death pathways by modulating the redox state of specific thiol residues of target proteins including transcription factors, stress kinases and caspases, which participate in tumor necrosis factor (TNF)-induced apoptosis.	Sulfhydryl Compounds	106-111	caspase 8	Homo sapiens	192-200
17567462-5	2007	Cytosol GSH regulates TNF hepatocyte apoptosis by modulating caspase 8 activation or NF-kappaB-dependent gene expression.	Glutathione	8-11	caspase 8	Homo sapiens	61-70
17939408-9	2007	Manumycin induced cytochrome C release from the mitochondria into the cytosol after 6 h treatment, and activated caspase-9, caspase-8, and caspase-3 after a 16h treatment.	manumycin	0-9	caspase 8	Homo sapiens	124-133
17303086-5	2007	Furthermore, overexpression of c-FLIP short in HuH-7 cells inhibited adenosine-induced caspase-8 activity.	Adenosine	69-78	caspase 8	Homo sapiens	87-96
17303086-6	2007	Taken together, these results suggest that intracellularly transported adenosine, perhaps converted AMP as the ensuing event, activates caspase-8 and the downstream effector caspase caspase-3 by neutralizing caspase-8 inhibition due to c-FLIP as a consequence of decreased c-FLIP expression, leading to apoptosis.	Adenosine	71-80	caspase 8	Homo sapiens	136-145
17410536-5	2007	Simultaneously, FUT-175 up-regulated the expression of tumor necrosis factor receptor-1 (TNFR1), which in turn activated the proapoptotic caspase-8 and Bid pathways and induced apoptosis in pancreatic cancer cells.	fut	16-19	caspase 8	Homo sapiens	138-147
17410536-6	2007	FUT-175-induced activation of Fas-associated death domain (FADD) and caspase-8 was suppressed by RNA interference-mediated inhibition of TNFR1 expression.	fut	0-3	caspase 8	Homo sapiens	69-78
17517333-6	2007	Multiple sequence alignments and functional substrate assays of recombinant protein suggest that AeDredd is an orthologue of Drosophila Dredd and human caspase-8, both central effectors of the death receptor-mediated apoptotic pathway.	aedredd	97-104	caspase 8	Homo sapiens	152-161
17517333-7	2007	AeDredd exhibits substrate specificity most similar to human caspase-8.	aedredd	0-7	caspase 8	Homo sapiens	61-70
17303086-6	2007	Taken together, these results suggest that intracellularly transported adenosine, perhaps converted AMP as the ensuing event, activates caspase-8 and the downstream effector caspase caspase-3 by neutralizing caspase-8 inhibition due to c-FLIP as a consequence of decreased c-FLIP expression, leading to apoptosis.	Adenosine	71-80	caspase 8	Homo sapiens	208-217
17303086-6	2007	Taken together, these results suggest that intracellularly transported adenosine, perhaps converted AMP as the ensuing event, activates caspase-8 and the downstream effector caspase caspase-3 by neutralizing caspase-8 inhibition due to c-FLIP as a consequence of decreased c-FLIP expression, leading to apoptosis.	Adenosine Monophosphate	100-103	caspase 8	Homo sapiens	136-145
17303086-6	2007	Taken together, these results suggest that intracellularly transported adenosine, perhaps converted AMP as the ensuing event, activates caspase-8 and the downstream effector caspase caspase-3 by neutralizing caspase-8 inhibition due to c-FLIP as a consequence of decreased c-FLIP expression, leading to apoptosis.	Adenosine Monophosphate	100-103	caspase 8	Homo sapiens	208-217
17505004-8	2007	Docetaxel mainly induced caspase-8 activation, whereas the addition of celecoxib and ZD1839 augmented the caspase-8 activation and enhanced caspase-9 activation.	Celecoxib	71-80	caspase 8	Homo sapiens	106-115
17505004-8	2007	Docetaxel mainly induced caspase-8 activation, whereas the addition of celecoxib and ZD1839 augmented the caspase-8 activation and enhanced caspase-9 activation.	Gefitinib	85-91	caspase 8	Homo sapiens	106-115
17510429-3	2007	In the present study, we show that PS-341 induced caspase-8-dependent apoptosis, cooperated with TRAIL to induce apoptosis, and up-regulated death receptor 5 (DR5) expression in human non-small cell lung cancer (NSCLC) cells.	Bortezomib	35-41	caspase 8	Homo sapiens	50-59
17440103-6	2007	In addition, we show that pretreatment of PEL cells with carbobenzoxy-Val-Ala-Asp-fluoromethylketone, a universal inhibitor of caspases, abrogates caspase and PARP activation and prevents cell death induced by sanguinarine.	carbobenzoxy-val-ala-asp-fluoromethylketone	57-100	caspase 8	Homo sapiens	127-135
17293177-12	2007	Tam-induced apoptosis was caspase-dependent and completely abrogated by either caspase-8 or -9 inhibitors.	Tamoxifen	0-3	caspase 8	Homo sapiens	79-94
17293177-15	2007	We here describe a novel mechanism of tamoxifen-induced apoptosis in chondrocytes, involving the activation of caspases and the FasL/Fas pathway, which diminishes the potential for bone growth.	Tamoxifen	38-47	caspase 8	Homo sapiens	111-119
17452997-0	2007	Bcl-2 cleavages at two adjacent sites by different caspases promote cisplatin-induced apoptosis.	Cisplatin	68-77	caspase 8	Homo sapiens	51-59
17452997-7	2007	These results indicate that Bcl-2 can be cleaved into two close fragments by different caspases during cisplatin-induced apoptosis, both of which contribute to the acceleration of apoptotic process.	Cisplatin	103-112	caspase 8	Homo sapiens	87-95
17487744-5	2007	In KG1a cells, bexarotene downregulated FLIP(Long) and activated caspase-8, thereby allowing for TRAIL-triggered apoptosis.	Bexarotene	15-25	caspase 8	Homo sapiens	65-74
17390070-6	2007	Functional screening of these selected cell lines using TNF-alpha, doxorubicin and radiation induced cell injury showed that a lack of functional caspase-8 resulted in resistance to TNF-alpha-induced apoptosis.	Doxorubicin	67-78	caspase 8	Homo sapiens	146-155
17593629-6	2007	RESULTS: Caveolin-1 and -2 were up-regulated 1 h after exposure to bleomycin and preceding the occurrence of caspase-8, and of caspase-3 and caspase-9 cleavage products.	Bleomycin	67-76	caspase 8	Homo sapiens	109-118
17426447-0	2007	Caspase-8 preferentially senses the apoptosis-inducing action of NG-18, a Gambogic acid derivative, in human leukemia HL-60 cells.	ng-18	65-70	caspase 8	Homo sapiens	0-9
17426447-0	2007	Caspase-8 preferentially senses the apoptosis-inducing action of NG-18, a Gambogic acid derivative, in human leukemia HL-60 cells.	gambogic acid	74-87	caspase 8	Homo sapiens	0-9
17426447-7	2007	The specific inhibition of caspase-8 activity using Z-IETD-FMK significantly blocked NG-18-induced apoptosis.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	52-62	caspase 8	Homo sapiens	27-36
17426447-7	2007	The specific inhibition of caspase-8 activity using Z-IETD-FMK significantly blocked NG-18-induced apoptosis.	ng-18	85-90	caspase 8	Homo sapiens	27-36
17426447-9	2007	Altogether, our data demonstrated that NG-18-induced apoptosis was dependent on caspases and caspase-8 acted as a key executor in the event.	ng-18	39-44	caspase 8	Homo sapiens	93-102
17437844-12	2007	The combination of doxorubicin and HGS-ETR1 significantly activated the caspase cascade, including caspase-8, 9, 6 and 3, which are the downstream molecules of death receptors.	Doxorubicin	19-30	caspase 8	Homo sapiens	99-120
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	caspase 8	Homo sapiens	190-199
17440103-6	2007	In addition, we show that pretreatment of PEL cells with carbobenzoxy-Val-Ala-Asp-fluoromethylketone, a universal inhibitor of caspases, abrogates caspase and PARP activation and prevents cell death induced by sanguinarine.	sanguinarine	210-222	caspase 8	Homo sapiens	127-135
17016430-7	2007	Mechanistic studies show that ABT-737-induced apoptosis is associated with activation of caspase-8, caspase-9 and caspase-3, followed by poly(ADP-ribose) polymerase cleavage.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	30-33	caspase 8	Homo sapiens	89-98
17391872-6	2007	Caspase-2 inhibitor (VDVAD-CHO/fmk) and caspase-8 inhibitor (IETD-CHO/fmk) completely blocked the T-2 toxin-induced process of procaspase-3, while caspase-9 inhibitor (LEHD-CHO/fmk) did so less effectively.	IETD-CHO	61-69	caspase 8	Homo sapiens	40-49
17391872-6	2007	Caspase-2 inhibitor (VDVAD-CHO/fmk) and caspase-8 inhibitor (IETD-CHO/fmk) completely blocked the T-2 toxin-induced process of procaspase-3, while caspase-9 inhibitor (LEHD-CHO/fmk) did so less effectively.	FMK	70-73	caspase 8	Homo sapiens	40-49
17391872-6	2007	Caspase-2 inhibitor (VDVAD-CHO/fmk) and caspase-8 inhibitor (IETD-CHO/fmk) completely blocked the T-2 toxin-induced process of procaspase-3, while caspase-9 inhibitor (LEHD-CHO/fmk) did so less effectively.	Ac-Ala-Ala-Val-Ala-Leu-Leu-Pro-Ala-Val-Leu-Leu-Ala-Leu-Leu-Ala-Pro-Leu-Glu-His-Asp-Cho	168-176	caspase 8	Homo sapiens	40-49
17391872-6	2007	Caspase-2 inhibitor (VDVAD-CHO/fmk) and caspase-8 inhibitor (IETD-CHO/fmk) completely blocked the T-2 toxin-induced process of procaspase-3, while caspase-9 inhibitor (LEHD-CHO/fmk) did so less effectively.	FMK	70-73	caspase 8	Homo sapiens	40-49
17260186-2	2007	Here, we demonstrate that addition of sclareol to cultures of human colon cancer HCT116 cells results in inhibition of DNA synthesis, arrest of cells at the G(1) phase of the cell cycle, activation of caspases-8, -9, PARP degradation, and DNA fragmentation, events characteristic of induction of apoptosis.	sclareol	38-46	caspase 8	Homo sapiens	201-215
17376296-9	2007	The AZ4 treated cells were then led to apoptosis after 48 h. This was associated with the activation of apoptotic enzyme caspase 3 and mediated by caspase 8, but not caspase 9 at various concentrations of AZ4 after being cultured for 48 h and 30 h, respectively.	az4	4-7	caspase 8	Homo sapiens	147-156
17376296-9	2007	The AZ4 treated cells were then led to apoptosis after 48 h. This was associated with the activation of apoptotic enzyme caspase 3 and mediated by caspase 8, but not caspase 9 at various concentrations of AZ4 after being cultured for 48 h and 30 h, respectively.	az4	205-208	caspase 8	Homo sapiens	147-156
17393415-6	2007	Apoptosis induced by Fas in FLS was detected with TUNEL staining and Western blotting of caspase 8 and poly(ADP-ribose) polymerase.	ammonium ferrous sulfate	21-24	caspase 8	Homo sapiens	89-98
17321792-4	2007	Caspase 3 was found to be activated by these fatty acids: caspase 8 was activated by 16:0 and only moderately by t18:1.	Fatty Acids	45-56	caspase 8	Homo sapiens	58-67
17321792-5	2007	Activation of caspase 3 by these fatty acids was fully inhibited by a caspase 8 inhibitor.	Fatty Acids	33-44	caspase 8	Homo sapiens	70-79
17436592-3	2007	In this study, the induction of apoptosis-related proteins and the activities of caspases in a DLD-1 cell line under medication with TAC-101 were investigated.	TAC 101	133-140	caspase 8	Homo sapiens	81-89
17326044-4	2007	Honokiol-induced activation of caspases was evaluated by Western blot and FACS analysis.	honokiol	0-8	caspase 8	Homo sapiens	31-39
17409683-3	2007	Since treatment of Gb3(+) cells with SAL caused an increase in externalization of phosphatidylserine via activation of P-glycoprotein, and apoptotic volume decrease via activation of G-protein activated K(+) channel-1, SAL may function as an inducer of early apoptotic signal; however, neither caspase-8 and -3 activation nor DNA fragmentation was observed.	sal	37-40	caspase 8	Homo sapiens	294-310
17332362-3	2007	Both betaTAC and N-betaTAC trigger the collapse of mitochondrial potential (DeltaPsi(m)) and modulate reactive oxygen species levels, following activation of intrinsic caspase-8 and caspase-9.	betatac	5-12	caspase 8	Homo sapiens	168-177
17332362-3	2007	Both betaTAC and N-betaTAC trigger the collapse of mitochondrial potential (DeltaPsi(m)) and modulate reactive oxygen species levels, following activation of intrinsic caspase-8 and caspase-9.	n-betatac	17-26	caspase 8	Homo sapiens	168-177
17185040-5	2007	JWH-015 induced cross-talk between extrinsic and intrinsic pathways of apoptosis involving caspase-8, caspase-9, and caspase-3 as well as loss of mitochondrial membrane potential.	JHW 015	0-7	caspase 8	Homo sapiens	91-100
17321467-0	2007	Nonylphenol induces apoptosis of Jurkat cells by a caspase-8 dependent mechanism.	nonylphenol	0-11	caspase 8	Homo sapiens	51-60
17321467-8	2007	The results demonstrated that nonylphenol inhibited the proliferation and induced loss of mitochondrial membrane potential, caspase-8 activation, internucleosomal DNA fragmentation.	nonylphenol	30-41	caspase 8	Homo sapiens	124-133
17321467-9	2007	Furthermore, a caspase-8 inhibitor, IETD-fmk, blocked loss of mitochondrial membrane potential and apoptosis.	isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	36-44	caspase 8	Homo sapiens	15-24
17321467-10	2007	These findings suggested that nonylphenol induced apoptosis of Jurkat cells by caspase-8 dependent mechanisms.	nonylphenol	30-41	caspase 8	Homo sapiens	79-88
17432717-9	2007	Expression of the death receptors DR5 and DR4 in two cell lines (A172 and U251) upregulated significantly when they were used in combination hTRAIL/TMZ treatment (p &lt; 0.05 compared with baseline control), leading to activation of caspase-8 and caspase-3 (p &lt; 0.05 compared with baseline control) and confirming an extrinsic apoptotic pathway.	Temozolomide	148-151	caspase 8	Homo sapiens	233-242
17448756-6	2007	Polyunsaturated fatty acids induced significant activation of upstream caspases 8 and 9 as well as caspase 3.	Fatty Acids, Unsaturated	0-27	caspase 8	Homo sapiens	71-87
17384534-7	2007	ABT-510 treatment of primary human brain MvEC propagated as a monolayer resulted in induction of apoptosis in a dose- and time-dependent manner through a caspase-8-dependent mechanism.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	0-3	caspase 8	Homo sapiens	154-163
17436592-8	2007	A 3-fold increase in caspase-3 activity and a 1.5-fold increase in caspase-8 activity were observed in cells treated with TAC-101 in comparison to the control cells (p&lt;0.01).	TAC 101	122-129	caspase 8	Homo sapiens	67-76
17273730-0	2007	Photosensitizer effect of curcumin on UVB-irradiated HaCaT cells through activation of caspase pathways.	Curcumin	26-34	caspase 8	Homo sapiens	87-94
17183590-6	2007	Activation of caspase-3, caspase-8, and caspase-9 was detected after treatment with cisplatin, and the cleavage of poly-(ADP)-ribose polymerase (PARP) was observed within cisplatin-treated HEI-OC1 cells.	Cisplatin	84-93	caspase 8	Homo sapiens	25-34
17183590-7	2007	JWH-015 inhibited the activation of caspase-3, caspase-8, and caspase-9; cleavage of PARP; and release of cytochrome c.	JHW 015	0-7	caspase 8	Homo sapiens	47-56
17339367-4	2007	Activation of apoptosis by sulforaphane in MDA-MB-231 cells seemed to be initiated through induction of Fas ligand, which resulted in activation of caspase-8, caspase-3, and poly(ADP-ribose) polymerase, whereas apoptosis in the other breast cancer cell lines was initiated by decreased Bcl-2 expression, release of cytochrome c into the cytosol, activation of caspase-9 and caspase-3, but not caspase-8, and poly(ADP-ribose) polymerase cleavage.	sulforaphane	27-39	caspase 8	Homo sapiens	148-157
17339367-4	2007	Activation of apoptosis by sulforaphane in MDA-MB-231 cells seemed to be initiated through induction of Fas ligand, which resulted in activation of caspase-8, caspase-3, and poly(ADP-ribose) polymerase, whereas apoptosis in the other breast cancer cell lines was initiated by decreased Bcl-2 expression, release of cytochrome c into the cytosol, activation of caspase-9 and caspase-3, but not caspase-8, and poly(ADP-ribose) polymerase cleavage.	sulforaphane	27-39	caspase 8	Homo sapiens	393-402
17273750-6	2007	Activation of caspases 3, 7, 8 and 9 was observed in HSG cells after cimetidine treatment, thus confirming that the apoptosis was induced by the activated caspases.	Cimetidine	69-79	caspase 8	Homo sapiens	14-22
17273730-6	2007	Furthermore, combination of UVB irradiation with curcumin synergistically induces apoptotic cell death in HaCaT cells through activation of caspase-8, and -3 as well as caspase-9 activation followed by release of cytochrome c.	Curcumin	49-57	caspase 8	Homo sapiens	140-157
17277134-5	2007	Ectopic overexpression of FLIP (the physiological inhibitor of the death receptor pathway) or application of zIETD-fmk (specific inhibitor of caspase-8, the initiator-caspase of the death receptor pathway) both specifically reduced rituximab-induced apoptosis in Ramos B cells.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	109-118	caspase 8	Homo sapiens	142-151
17379655-5	2007	Moreover, the sensitizing effect of Z-LLF-CHO on TRAIL-induced loss of cell viability is prevented by the selective caspase-8 inhibitor, Z-IETD-FMK.	N-benzyloxycarbonyl-leucyl-leucyl-phenylalaninal	36-45	caspase 8	Homo sapiens	116-125
17379655-5	2007	Moreover, the sensitizing effect of Z-LLF-CHO on TRAIL-induced loss of cell viability is prevented by the selective caspase-8 inhibitor, Z-IETD-FMK.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	137-147	caspase 8	Homo sapiens	116-125
17277134-2	2007	In this study, we demonstrate that rituximab sensitizes lymphoma B cells to Fas-induced apoptosis in a caspase-8-dependent manner.	ammonium ferrous sulfate	76-79	caspase 8	Homo sapiens	103-112
17131308-11	2007	Inhibition of caspase8 or caspase10 but not caspase9 significantly decreases DC-induced apoptosis in both cell lines.	Doxycycline	77-79	caspase 8	Homo sapiens	14-22
17277134-10	2007	Further analysis revealed that, upon stimulation with rituximab, Fas, caspase-8, and FADD were found in sucrose-gradient raft fractions together with CD20.	Sucrose	104-111	caspase 8	Homo sapiens	70-79
17277134-11	2007	In conclusion, in this study, we present evidence for the involvement of the death receptor pathway in rituximab-induced apoptosis of Ramos B cells with concomitant sensitization of these cells to Fas-mediated apoptosis via Fas multimerization and recruitment of caspase-8 and FADD to the DISC.	ammonium ferrous sulfate	197-200	caspase 8	Homo sapiens	263-272
17222828-0	2007	GSH-dependent regulation of Fas-mediated caspase-8 activation by acrolein.	Glutathione	0-3	caspase 8	Homo sapiens	41-50
17222828-1	2007	Activation of the cysteine protease caspase-8 by the death receptor Fas (CD95/APO-1) in B lymphoblastoid SKW6.4 cells or Jurkat T cells is associated with GSH depletion.	Glutathione	155-158	caspase 8	Homo sapiens	36-45
17222828-2	2007	Conversely, GSH depletion by the aldehyde acrolein (3-30 microM) was associated with inhibition of Fas-induced caspase-8 activation, although GSH depletion by buthionine sulfoximine (BSO) did not affect caspase-8 activation.	Glutathione	12-15	caspase 8	Homo sapiens	111-120
17222828-2	2007	Conversely, GSH depletion by the aldehyde acrolein (3-30 microM) was associated with inhibition of Fas-induced caspase-8 activation, although GSH depletion by buthionine sulfoximine (BSO) did not affect caspase-8 activation.	Glutathione	12-15	caspase 8	Homo sapiens	203-212
17222828-2	2007	Conversely, GSH depletion by the aldehyde acrolein (3-30 microM) was associated with inhibition of Fas-induced caspase-8 activation, although GSH depletion by buthionine sulfoximine (BSO) did not affect caspase-8 activation.	aldehyde acrolein	33-50	caspase 8	Homo sapiens	111-120
17222828-2	2007	Conversely, GSH depletion by the aldehyde acrolein (3-30 microM) was associated with inhibition of Fas-induced caspase-8 activation, although GSH depletion by buthionine sulfoximine (BSO) did not affect caspase-8 activation.	ammonium ferrous sulfate	99-102	caspase 8	Homo sapiens	111-120
17222828-3	2007	In contrast to BSO, acrolein caused a loss of caspase-8 cysteine content in association with direct alkylation of caspase-8.	Acrolein	20-28	caspase 8	Homo sapiens	46-55
17222828-3	2007	In contrast to BSO, acrolein caused a loss of caspase-8 cysteine content in association with direct alkylation of caspase-8.	Acrolein	20-28	caspase 8	Homo sapiens	114-123
17222828-3	2007	In contrast to BSO, acrolein caused a loss of caspase-8 cysteine content in association with direct alkylation of caspase-8.	Cysteine	56-64	caspase 8	Homo sapiens	46-55
17222828-4	2007	Our findings indicate that inhibition of caspase-8 by thiol-reactive agents such as acrolein is not due to GSH depletion but caused by direct protein thiol modifications.	Sulfhydryl Compounds	54-59	caspase 8	Homo sapiens	41-50
17222828-4	2007	Our findings indicate that inhibition of caspase-8 by thiol-reactive agents such as acrolein is not due to GSH depletion but caused by direct protein thiol modifications.	Acrolein	84-92	caspase 8	Homo sapiens	41-50
17222828-4	2007	Our findings indicate that inhibition of caspase-8 by thiol-reactive agents such as acrolein is not due to GSH depletion but caused by direct protein thiol modifications.	Sulfhydryl Compounds	150-155	caspase 8	Homo sapiens	41-50
17032924-6	2007	Mechanistic studies show that LBW242-induced apoptosis in MM cells is associated with activation of caspase-8, caspase-9, and caspase-3, followed by PARP cleavage.	LBW242	30-36	caspase 8	Homo sapiens	100-109
17191114-8	2007	Similarly, the pre-incubation of macrophages with PtdIns(3,5)BP prevented microparticle-induced upregulation of caspase 8, which is a major target molecule of ceramide action in the apoptosis pathway.	phosphatidylinositol 3,5-diphosphate	50-63	caspase 8	Homo sapiens	112-121
17191114-8	2007	Similarly, the pre-incubation of macrophages with PtdIns(3,5)BP prevented microparticle-induced upregulation of caspase 8, which is a major target molecule of ceramide action in the apoptosis pathway.	Ceramides	159-167	caspase 8	Homo sapiens	112-121
17191116-5	2007	Pretreatment with z-VAD-FMK (a pan-caspase inhibitor), z-IETD-FMK (a caspase-8 inhibitor) or z-LEHD-FMK (a caspase-9 inhibitor) blocked TOS and exisulind cotreatment-induced PARP cleavage and apoptosis.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	18-27	caspase 8	Homo sapiens	35-42
17191116-5	2007	Pretreatment with z-VAD-FMK (a pan-caspase inhibitor), z-IETD-FMK (a caspase-8 inhibitor) or z-LEHD-FMK (a caspase-9 inhibitor) blocked TOS and exisulind cotreatment-induced PARP cleavage and apoptosis.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	55-65	caspase 8	Homo sapiens	69-78
17191116-6	2007	Furthermore, TOS/exisulind cotreatment induced JNK phosphorylation, while pretreatment with SP600151 (a JNK inhibitor) partially blocked cotreatment-induced caspase-dependent PARP cleavage and apoptosis.	sp600151	92-100	caspase 8	Homo sapiens	157-164
17262884-0	2007	Involvement of MAPK, Bcl-2 family, cytochrome c, and caspases in induction of apoptosis by 1,6-O,O-diacetylbritannilactone in human leukemia cells.	O, O-diacetylbritannilactone	91-122	caspase 8	Homo sapiens	53-61
17284845-4	2007	Tryptophol induced apoptosis involving caspase-8 and -3 activation, followed by cleavage of poly (ADP-ribose) polymerase (PARP), as shown by measurement of enzyme activity and immunoblot analysis.	tryptophol	0-10	caspase 8	Homo sapiens	39-55
17284845-6	2007	These results indicate that tryptophol isolated from black soybean vinegar inhibited the proliferation of U937 cells by inducing apoptosis via a pathway involving caspase-8 followed by caspase-3, without affecting normal lymphocytes.	tryptophol	28-38	caspase 8	Homo sapiens	163-172
17105846-7	2007	Asoprisnil treatment significantly (P &lt; 0.05) increased TRAIL, DR4, and DR5 contents in cultured leiomyoma cells in a dose-dependent manner with a cleavage of caspase-8, -7, and -3, and decreased X-linked chromosome-linked inhibitor of apoptosis protein contents.	asoprisnil	0-10	caspase 8	Homo sapiens	162-183
17064874-5	2007	THDB also caused a marked increase in apoptosis, as characterized by DNA fragmentation (DNA ladder and sub G1 formation), and poly (ADP-ribose) polymerase (PARP) cleavage, which was associated with activation of caspase-3, caspase-8 and caspase-9.	(Z)-2-(6-(thieanisyl-2-yl)hexa-3-en-1,5-diynyl)benzenamine	0-4	caspase 8	Homo sapiens	223-232
17308071-9	2007	Activation of caspase-8 and Bid seemed to be a late event, and docetaxel was able to induce apoptosis in cells deficient in caspase-8 and Bid.	Docetaxel	63-72	caspase 8	Homo sapiens	124-133
17666167-0	2007	Impaired kinetics of Bax-GFP and Smac/DIABLO-GFP in caspase-8- and bid-silenced and Bcl-2 overexpressed breast cancer MCF-7 cells exposed to camptothecin.	Camptothecin	141-153	caspase 8	Homo sapiens	52-61
17164759-6	2007	Consequently, in combination with gemcitabine 4-PB shows an overadditive effect on induction of apoptosis in BxPc3 and T3M-4 cells (up to 4.5-fold compared to single drug treatment) with accompanied activation of Caspase 8, BH3 interacting domain death agonist (Bid) and poly (ADP-ribose) polymerase family, member 1 (PARP) cleavage.	gemcitabine 4-pb	34-50	caspase 8	Homo sapiens	213-222
17164759-6	2007	Consequently, in combination with gemcitabine 4-PB shows an overadditive effect on induction of apoptosis in BxPc3 and T3M-4 cells (up to 4.5-fold compared to single drug treatment) with accompanied activation of Caspase 8, BH3 interacting domain death agonist (Bid) and poly (ADP-ribose) polymerase family, member 1 (PARP) cleavage.	BH 3	224-227	caspase 8	Homo sapiens	213-222
17189826-6	2007	Without CO(2) peroxynitrite also induced the oxidation of hemoglobin and glutathione, the accumulation of lactate, a decrease in ATP, the clustering of band 3, the externalization of phosphatidylserine, and the activation of caspases 8 and 3 (biomarkers of apoptosis).	co(2) peroxynitrite	8-27	caspase 8	Homo sapiens	225-241
17404012-7	2007	Western blotting has revealed that DMNQ S-64 effectively activates the expression of caspase 8, 9, and 3, cleaves poly (ADP-ribose) polymerase, and increases the ratio of Bax/Bcl-2.	2,3-dimethoxy-1,4-naphthoquinone	35-39	caspase 8	Homo sapiens	85-104
17159907-4	2007	We now demonstrate that these SDS-stable forms of CD95 correspond to very high molecular weight DISC complexes (hiDISC) and are the sites of caspase-8 activation.	Sodium Dodecyl Sulfate	30-33	caspase 8	Homo sapiens	141-150
17159907-8	2007	Our data demonstrate that SDS-stable forms of CD95 are the sites of apoptosis initiation and represent an important early step in apoptosis signaling through CD95 before activation of caspases.	Sodium Dodecyl Sulfate	26-29	caspase 8	Homo sapiens	184-192
17213957-6	2007	When cells were pretreated with Z-IETD-fmk (caspase-8 specific inhibitor) the process of Bid activation was completely inhibited, but the apoptosis was only partially affected.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	32-42	caspase 8	Homo sapiens	44-53
17129359-4	2007	Furthermore, ZER-induced apoptosis in NB4 cells was initiated by the expression of Fas (CD95)/Fas Ligand (CD95L), concomitant with the activation of caspase-8.	zerumbone	13-16	caspase 8	Homo sapiens	149-158
17031493-6	2007	Vitamin C impedes the elevation of reactive oxygen species (ROS) levels induced by TRAIL and impairs caspase-8 activation.	Ascorbic Acid	0-9	caspase 8	Homo sapiens	101-110
17031493-7	2007	We found that the removal of hydrogen peroxide by extracellular catalase during TRAIL-induced apoptosis also impairs caspase-8 activation.	Hydrogen Peroxide	29-46	caspase 8	Homo sapiens	117-126
17031493-8	2007	These data suggest that hydrogen peroxide is produced during TRAIL-receptor ligation, and that the increase of intracellular ROS regulates the activation of caspase-8 during apoptosis.	Hydrogen Peroxide	24-41	caspase 8	Homo sapiens	157-166
17031493-8	2007	These data suggest that hydrogen peroxide is produced during TRAIL-receptor ligation, and that the increase of intracellular ROS regulates the activation of caspase-8 during apoptosis.	Reactive Oxygen Species	125-128	caspase 8	Homo sapiens	157-166
17762183-8	2007	These results show that the alkaline sondition (pH=8.0) induces cell apoptosis by activating caspase-8, which cleaves Bid to tBid, tBid translocation to mitochondria, and then activating the caspase-3 in the ASTC-a-1 cells.	tBID	125-129	caspase 8	Homo sapiens	93-102
17595512-7	2007	However, none of the sensitizers overcame resistance mediated by ectopic expression of the viral caspase 8 inhibitor, crm-A.	crm-a	118-123	caspase 8	Homo sapiens	97-106
17762183-8	2007	These results show that the alkaline sondition (pH=8.0) induces cell apoptosis by activating caspase-8, which cleaves Bid to tBid, tBid translocation to mitochondria, and then activating the caspase-3 in the ASTC-a-1 cells.	tBID	131-135	caspase 8	Homo sapiens	93-102
17143539-6	2007	The caspase-8 inhibitor Z-IETD-FMK and a blocking antibody to TNF-alpha both inhibited the contact-independent bystander effect in LN18 cells.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	24-34	caspase 8	Homo sapiens	4-13
16844342-4	2007	In addition, caspase-8 or caspase-9 inhibition with z-IETD-fmk or z-LEHD-fmk, respectively, largely prevented OA-induced apoptosis.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	52-62	caspase 8	Homo sapiens	13-22
16844342-4	2007	In addition, caspase-8 or caspase-9 inhibition with z-IETD-fmk or z-LEHD-fmk, respectively, largely prevented OA-induced apoptosis.	benzyloxycarbonyl-leucyl-glutamyl-histidyl-aspartic acid fluoromethyl ketone	66-76	caspase 8	Homo sapiens	13-22
18204303-5	2007	The effect of sodium butyrate was analyzed in the induction of caspase activities, formation of caspase active forms and mRNA levels in human breast cancer cell line MRK-nu-1.	Butyric Acid	14-29	caspase 8	Homo sapiens	63-70
17182797-0	2007	Activation of caspase-8 contributes to 3,3"-Diindolylmethane-induced apoptosis in colon cancer cells.	3,3'-diindolylmethane	39-60	caspase 8	Homo sapiens	14-23
17182797-9	2007	The caspase-8 inhibitor Z-IETD-FMK attenuated the DIM-induced apoptosis, indicating that increased activation of this enzyme contributed to the increase in p53-independent apoptosis that was observed in colon cancer cells.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	24-34	caspase 8	Homo sapiens	4-13
16888780-5	2007	In the presence of cycloheximide, the selected SCCHN sublines become susceptible to CH-11 Ab, and showed cleavage of caspase-8, suggesting that apoptosis resistance was mediated by an inhibitory protein(s) acting upstream of caspase-8.	Cycloheximide	19-32	caspase 8	Homo sapiens	117-126
16888780-5	2007	In the presence of cycloheximide, the selected SCCHN sublines become susceptible to CH-11 Ab, and showed cleavage of caspase-8, suggesting that apoptosis resistance was mediated by an inhibitory protein(s) acting upstream of caspase-8.	Cycloheximide	19-32	caspase 8	Homo sapiens	225-234
18204303-5	2007	The effect of sodium butyrate was analyzed in the induction of caspase activities, formation of caspase active forms and mRNA levels in human breast cancer cell line MRK-nu-1.	Butyric Acid	14-29	caspase 8	Homo sapiens	96-103
18204303-8	2007	Inhibitors of caspase-8 and caspase-10 reduced caspase-3 activity and subsequent DNA fragmentation induced by sodium butyrate.	Butyric Acid	110-125	caspase 8	Homo sapiens	14-23
17052983-6	2006	SDS-PAGE of isolated complexes showed near complete loss of the p10 subunit from initiator caspases 1 and 8 but not from the executioner caspase-6.	Sodium Dodecyl Sulfate	0-3	caspase 8	Homo sapiens	91-107
17143495-0	2007	Etodolac, a selective cyclooxygenase-2 inhibitor, induces apoptosis by activating caspases in human malignant rhabdoid tumor cells (FRTK-1).	Etodolac	0-8	caspase 8	Homo sapiens	82-90
17143495-4	2007	Etodolac induced apoptosis of FRTK-1 cells through activation of caspase-8, -9 and -3.	Etodolac	0-8	caspase 8	Homo sapiens	65-85
17143495-5	2007	Moreover, several caspase inhibitors completely or partially inhibited etodolac-induced apoptosis.	Etodolac	71-79	caspase 8	Homo sapiens	18-25
17143496-4	2007	Enhanced apoptosis in response to the combination treatment was associated with caspase-8 activation-mediated Bax and Bak activation and mitochondrial dysfunction.	bakuchiol	118-121	caspase 8	Homo sapiens	80-89
17143496-9	2007	These results indicate that phytosphingosine sensitizes cancer cells to TRAIL through the synergistic up-regulation of DR4 and DR5 in an NF-kappaB-dependent fashion resulting in caspase-8 activation and subsequent mitochondrial dysfunction.	phytosphingosine	28-44	caspase 8	Homo sapiens	178-187
17007887-9	2006	The experiments using inhibitors of caspases (Z-VAD-FMK, Z-DEVD-FMK and Z-IETD-FMK) confirmed that caspase-3 was involved in the apoptosis.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	46-55	caspase 8	Homo sapiens	36-44
17007887-9	2006	The experiments using inhibitors of caspases (Z-VAD-FMK, Z-DEVD-FMK and Z-IETD-FMK) confirmed that caspase-3 was involved in the apoptosis.	benzoylcarbonyl-aspartyl-glutamyl-valyl-aspartyl-fluoromethyl ketone	57-67	caspase 8	Homo sapiens	36-44
17007887-9	2006	The experiments using inhibitors of caspases (Z-VAD-FMK, Z-DEVD-FMK and Z-IETD-FMK) confirmed that caspase-3 was involved in the apoptosis.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	72-82	caspase 8	Homo sapiens	36-44
17112418-0	2006	Involvement of mitochondria and caspase pathways in N-demethyl-clarithromycin-induced apoptosis in human cervical cancer HeLa cell.	n-demethyl-clarithromycin	52-77	caspase 8	Homo sapiens	32-39
17112418-9	2006	The pan-caspase inhibitor (z-VAD-fmk), caspase-3 inhibitor (z-DEVD-fmk) and the caspase-9 inhibitor (z-LEHD-fmk) partially enhanced cell viability induced by N-demethyl-clarithromycin, but the caspase-8 inhibitor (z-IETD-fmk) had almost no effect.	benzyloxycarbonyl-leucyl-glutamyl-histidyl-aspartic acid fluoromethyl ketone	101-111	caspase 8	Homo sapiens	193-202
17112418-9	2006	The pan-caspase inhibitor (z-VAD-fmk), caspase-3 inhibitor (z-DEVD-fmk) and the caspase-9 inhibitor (z-LEHD-fmk) partially enhanced cell viability induced by N-demethyl-clarithromycin, but the caspase-8 inhibitor (z-IETD-fmk) had almost no effect.	n-demethyl-clarithromycin	158-183	caspase 8	Homo sapiens	193-202
17142968-4	2006	The apoptosis induced by H427 was inhibited efficiently with NAC and caspase-8 inhibitor but less efficiently with alpha-tocopherol and caspase-9 inhibitor.	Boc-L-3,3-Diphenylalanine	25-29	caspase 8	Homo sapiens	69-78
17122150-0	2006	Activation of caspase-8 and caspase-12 pathways by 7-ketocholesterol in human retinal pigment epithelial cells.	7-ketocholesterol	51-68	caspase 8	Homo sapiens	14-23
17145888-6	2006	Treatment with As(2)O(3) plus BSO, but not with As(2)O(3) alone, increased the levels of death receptor (DR) 5 protein and caspase-8 cleavage.	Arsenic Trioxide	15-24	caspase 8	Homo sapiens	123-132
17054427-0	2006	The c-Jun-N-terminal-Kinase inhibitor SP600125 enhances the butyrate derivative D1-induced apoptosis via caspase 8 activation in Kasumi 1 t(8;21) acute myeloid leukaemia cells.	pyrazolanthrone	38-46	caspase 8	Homo sapiens	105-114
17054427-0	2006	The c-Jun-N-terminal-Kinase inhibitor SP600125 enhances the butyrate derivative D1-induced apoptosis via caspase 8 activation in Kasumi 1 t(8;21) acute myeloid leukaemia cells.	Butyrates	60-68	caspase 8	Homo sapiens	105-114
17054427-4	2006	These experiments showed that SP600125 activated caspase 8 and confirmed that D1 activated the intrinsic pathway of apoptosis, as caspase 8 was not affected while Bcl-2 was down-regulated following D1 administration.	pyrazolanthrone	30-38	caspase 8	Homo sapiens	49-58
16988947-8	2006	Activation of caspase-8 cleaved Bid to truncated Bid (tBid) in cells treated with EGC and EGCG.	tBID	54-58	caspase 8	Homo sapiens	14-23
16988947-8	2006	Activation of caspase-8 cleaved Bid to truncated Bid (tBid) in cells treated with EGC and EGCG.	gallocatechol	82-85	caspase 8	Homo sapiens	14-23
16988947-8	2006	Activation of caspase-8 cleaved Bid to truncated Bid (tBid) in cells treated with EGC and EGCG.	epigallocatechin gallate	90-94	caspase 8	Homo sapiens	14-23
16988947-9	2006	EGC and EGCG induced apoptosis with caspase-8 activation and mitochondria-mediated pathway, whereas APG and GST caused apoptosis via an increase in intracellular free [Ca(2+)] with calpain activation and mitochondria-mediated pathway.	gallocatechol	0-3	caspase 8	Homo sapiens	36-45
16988947-9	2006	EGC and EGCG induced apoptosis with caspase-8 activation and mitochondria-mediated pathway, whereas APG and GST caused apoptosis via an increase in intracellular free [Ca(2+)] with calpain activation and mitochondria-mediated pathway.	epigallocatechin gallate	8-12	caspase 8	Homo sapiens	36-45
16988947-11	2006	Thus, plant-derived flavonoids cause cell death with activation of proteolytic activities of calpain and caspases in SH-SY5Y cells, and therefore serve as potential therapeutic agents for controlling the growth of neuroblastoma.	Flavonoids	20-30	caspase 8	Homo sapiens	105-113
17054996-6	2006	5-FU induced apoptosis primarily via a caspase-8-dependent pathway, and ADM and GEM via caspase-9.	Fluorouracil	0-4	caspase 8	Homo sapiens	39-48
17054996-7	2006	PD98059 enhanced the activity of caspase-8 and inhibited the activation of caspase-9.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	0-7	caspase 8	Homo sapiens	33-42
17169807-0	2006	Induction of apoptosis by d-limonene is mediated by a caspase-dependent mitochondrial death pathway in human leukemia cells.	Limonene	26-36	caspase 8	Homo sapiens	54-61
17067356-7	2006	Moreover, it was determined that the activation of caspase-3 could be blocked by the presence of a specific caspase-8 inhibitor, again linking death receptor-associated proteases to downstream effector caspase activity in alcohol-related death.	Alcohols	222-229	caspase 8	Homo sapiens	108-117
17172403-5	2006	Significant activation of caspase-8, caspase-9, and caspase-3 was observed only in cells treated with cisplatin/Apo2L/TRAIL combination and not in those exposed to either agent alone.	Cisplatin	102-111	caspase 8	Homo sapiens	26-35
17172403-7	2006	This observation strongly suggested that caspase-8 activation in cells treated with the cisplatin/Apo2L/TRAIL combination was secondary to the mitochondria-mediated amplification feedback loop and activation of the executioner caspase-3 was dependent on the recruitment of the intrinsic pathway characteristic of the type II cell.	Cisplatin	88-97	caspase 8	Homo sapiens	41-50
17172403-9	2006	Cisplatin sensitizes esophageal cancer cells to Apo2L/TRAIL cytotoxicity by potentiation of the mitochondria-dependent death signaling pathway that leads to amplification of caspase activation, particularly caspase-8, by the feedback loop to efficiently induce apoptosis.	Cisplatin	0-9	caspase 8	Homo sapiens	174-181
17172403-9	2006	Cisplatin sensitizes esophageal cancer cells to Apo2L/TRAIL cytotoxicity by potentiation of the mitochondria-dependent death signaling pathway that leads to amplification of caspase activation, particularly caspase-8, by the feedback loop to efficiently induce apoptosis.	Cisplatin	0-9	caspase 8	Homo sapiens	207-216
17027645-0	2006	Low dose cadmium poisoning results in sustained ERK phosphorylation and caspase activation.	Cadmium	9-16	caspase 8	Homo sapiens	72-79
17121904-5	2006	RESULTS: In this study, we showed that the combination of rapamycin and 17-AAG synergistically inhibited proliferation, induced apoptosis and cell cycle arrest, induced cleavage of poly(ADP-ribose) polymerase and caspase-8/caspase-9, and dysregulated signaling in the phosphatidylinositol 3-kinase/AKT/mTOR and cyclin D1/retinoblastoma pathways.	Sirolimus	58-67	caspase 8	Homo sapiens	213-222
17121904-5	2006	RESULTS: In this study, we showed that the combination of rapamycin and 17-AAG synergistically inhibited proliferation, induced apoptosis and cell cycle arrest, induced cleavage of poly(ADP-ribose) polymerase and caspase-8/caspase-9, and dysregulated signaling in the phosphatidylinositol 3-kinase/AKT/mTOR and cyclin D1/retinoblastoma pathways.	tanespimycin	72-78	caspase 8	Homo sapiens	213-222
17013758-6	2006	When apoptosis is induced by doxorubicin or TNF-alpha in an intact cell model, cleavage of caspases-8 and -9, but not caspase-2, was markedly enhanced by caspase-3.	Doxorubicin	29-40	caspase 8	Homo sapiens	91-108
17031492-5	2006	The dominant negative form of FADD containing DD could abolish these RTN3 generated events in the caspase-8 cascade.	Fumigant 93	32-34	caspase 8	Homo sapiens	98-107
17002685-0	2006	Cyclodextrin-induced apoptosis in human keratinocytes is caspase-8 dependent and accompanied by mitochondrial cytochrome c release.	Cyclodextrins	0-12	caspase 8	Homo sapiens	57-66
16774937-7	2006	On the other hand, together with TUNEL (terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling) assay, activations of caspase-8 and caspase-3 by TSA and ProI were noticed, suggesting the involvement of apoptotic process in chemosensitization of 267B1/K-ras cells.	deoxyuridine triphosphate	87-91	caspase 8	Homo sapiens	133-142
17002685-7	2006	We found that beta-CD and MbetaCD induce apoptosis via the activator caspase-8, which subsequently activates the effector caspases-3/-7.	betadex	14-21	caspase 8	Homo sapiens	69-78
17002685-7	2006	We found that beta-CD and MbetaCD induce apoptosis via the activator caspase-8, which subsequently activates the effector caspases-3/-7.	mbetacd	26-33	caspase 8	Homo sapiens	69-78
17016659-0	2006	Combination of 5-FU and IFNalpha enhances IFN signaling pathway and caspase-8 activity, resulting in marked apoptosis in hepatoma cell lines.	Fluorouracil	15-19	caspase 8	Homo sapiens	68-77
16877374-9	2006	Down-regulation of the B-cell lymphoma/leukaemia-2 (Bcl-2) expression with the activation of caspase-3, caspase-8 and caspase-9 was observed in ECSC after beta-HIVS treatment.	beta-hydroxyisovalerylshikonin	155-164	caspase 8	Homo sapiens	104-113
17016659-7	2006	Caspase-3, -9, and especially caspase-8 activity was higher with IFN alpha plus 5-FU than IFN or 5-FU alone.	Fluorouracil	80-84	caspase 8	Homo sapiens	30-39
17016659-7	2006	Caspase-3, -9, and especially caspase-8 activity was higher with IFN alpha plus 5-FU than IFN or 5-FU alone.	Fluorouracil	97-101	caspase 8	Homo sapiens	30-39
17016659-10	2006	In conclusion, caspase-8 is the most important factor that controls IFN and 5-FU-induced apoptosis in hepatoma cell lines.	Fluorouracil	76-80	caspase 8	Homo sapiens	15-24
16908599-5	2006	15d-PGJ(2)-induced inhibition of NF-kappaB function is rapidly followed by down-regulation of NF-kappaB-dependent antiapoptotic proteins cIAPs 1/2, Bcl-X(L), and cellular FLICE-inhibitory protein, leading to caspase activation and induction of apoptosis in breast cancer cells resistant to treatment with paclitaxel and doxorubicin.	15d-pgj	0-7	caspase 8	Homo sapiens	171-176
17177841-8	2006	The expression of Fas protein was induced, and caspase-8, caspase-3, and poly ADP-ribose polymerase (PARP) proteins were cleaved after ursolic acid treatment.	ursolic acid	135-147	caspase 8	Homo sapiens	47-56
17062895-5	2006	The underlying mechanism of zVAD-fmk-mediated sensitization to necrotic cell death involves the inhibition of caspase-8-mediated proteolysis of RIP1 and disturbance of the ANT-CypD interaction.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	28-36	caspase 8	Homo sapiens	110-119
17077022-10	2006	Inhibitor of caspase 8 inhibited the apoptosis of Jurkat cells induced with mDRA-6 while Inhibitor of caspase 9 showed less effect.	mdra-6	76-82	caspase 8	Homo sapiens	13-22
16949071-4	2006	Treatment of HL-60 cells with betuletol 3-methyl ether was associated with apoptosis induction which was prevented by a non-specific caspase inhibitor (z-VAD-fmk) and also by a specific inhibitor of caspase-8 (z-IETD-fmk) indicating activation of the extrinsic apoptotic pathway.	betuletol 3-methyl ether	30-54	caspase 8	Homo sapiens	199-208
16949071-4	2006	Treatment of HL-60 cells with betuletol 3-methyl ether was associated with apoptosis induction which was prevented by a non-specific caspase inhibitor (z-VAD-fmk) and also by a specific inhibitor of caspase-8 (z-IETD-fmk) indicating activation of the extrinsic apoptotic pathway.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	210-220	caspase 8	Homo sapiens	199-208
17088943-8	2006	Moreover, the signal transduction initiated by ethanol-induced protein kinases phosphorylation lead to increased expression of the transcription factors with subsequent expression of genes associated with the Fas apoptotic pathway (Fas receptor, Fas ligand, FADD and caspase 8).	Ethanol	47-54	caspase 8	Homo sapiens	267-276
16860949-4	2006	An extensive inhibitor for caspases, abolished the NGEN-induced apoptosis.	naringenin	51-55	caspase 8	Homo sapiens	27-35
16860318-9	2006	Pharmacological studies indicated that signaling for LPS-mediated SGLT-1 glucose uptake depends on caspase-8 and -9 activation, but occurs independently of caspase-3.	Glucose	73-80	caspase 8	Homo sapiens	99-115
16442262-4	2006	To show conventional chemotherapy drugs can trigger the caspase cascade, including caspase-8, -9, -3 and DNA fragmentation factor, Jurkat T leukemia cells were treated with cisplatin or etoposide in a dose-dependent and a time-dependent manner.	Cisplatin	173-182	caspase 8	Homo sapiens	83-129
16797629-7	2006	GTP treatment of SAOS-2 cells also resulted in significant activation of caspases as was evident by increased levels of cleaved caspase-3 and caspase-8 in these cells.	Guanosine Triphosphate	0-3	caspase 8	Homo sapiens	73-81
16797629-7	2006	GTP treatment of SAOS-2 cells also resulted in significant activation of caspases as was evident by increased levels of cleaved caspase-3 and caspase-8 in these cells.	Guanosine Triphosphate	0-3	caspase 8	Homo sapiens	142-151
16797629-9	2006	Taken together, these results indicate that GTP is a candidate therapeutic for osteosarcoma that mediates its antiproliferative and apoptotic effects via activation of caspases and inhibition of NF-kappaB.	Guanosine Triphosphate	44-47	caspase 8	Homo sapiens	168-176
16619034-4	2006	Importantly, apoptosis measured by flow cytometry was partially inhibited by Z-IETD-FMK, a specific inhibitor of caspase-8.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	77-87	caspase 8	Homo sapiens	113-122
16697418-6	2006	Interestingly, treatment of IHOK and HN4 cells with SB203580 and PD98059 abolished cytochrome c release, as well as the activation of caspase-3 and caspase-8.	SB 203580	52-60	caspase 8	Homo sapiens	148-157
16697418-6	2006	Interestingly, treatment of IHOK and HN4 cells with SB203580 and PD98059 abolished cytochrome c release, as well as the activation of caspase-3 and caspase-8.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	65-72	caspase 8	Homo sapiens	148-157
16850165-6	2006	alpha-TEA induced prolonged activation of c-Jun N-terminal kinase (JNK) and its substrate c-Jun; Bax conformational change; and cleavage of Bid and caspases-8, -9 and -3.	alpha-TEA	0-9	caspase 8	Homo sapiens	148-169
16927016-8	2006	Treatment of cells with butyrate resulted in both increased caspase-8 and -9 activity and reduced expression of XIAP and survivin.	Butyrates	24-32	caspase 8	Homo sapiens	60-76
16517139-4	2006	In addition, gamma-T3 stimulated a rise in caspase-8 and caspase-9 activities.	gamma-t3	13-21	caspase 8	Homo sapiens	43-52
16517139-5	2006	We also found that gamma-T3-induced apoptotic cell death was accompanied by up-regulation of Bax and a rise in the fragments of Bid and caspase-8.	gamma-t3	19-27	caspase 8	Homo sapiens	136-145
16872704-9	2006	The use of the specific caspase-8 inhibitor Z-IETD-FMK dramatically reduced apoptosis, demonstrating that caspase-8 is the upstream initiator caspase during SK-N-BE cells anoikis.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	44-54	caspase 8	Homo sapiens	24-33
16872704-9	2006	The use of the specific caspase-8 inhibitor Z-IETD-FMK dramatically reduced apoptosis, demonstrating that caspase-8 is the upstream initiator caspase during SK-N-BE cells anoikis.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	44-54	caspase 8	Homo sapiens	106-115
16872704-9	2006	The use of the specific caspase-8 inhibitor Z-IETD-FMK dramatically reduced apoptosis, demonstrating that caspase-8 is the upstream initiator caspase during SK-N-BE cells anoikis.	sk-n	157-161	caspase 8	Homo sapiens	24-33
16872704-9	2006	The use of the specific caspase-8 inhibitor Z-IETD-FMK dramatically reduced apoptosis, demonstrating that caspase-8 is the upstream initiator caspase during SK-N-BE cells anoikis.	sk-n	157-161	caspase 8	Homo sapiens	106-115
16970398-6	2006	High-resolution crystal structures of caspase-3 and caspase-8 in complex with aza-peptide Michael acceptor inhibitors demonstrate the nucleophilic attack on C2 and provide insight into the selectivity and potency of the inhibitors with respect to the P1" moiety.	Azathioprine	78-81	caspase 8	Homo sapiens	52-61
16951345-4	2006	z-FA-FMK inhibits the processing of caspase-8 and caspase-3 to their respective subunits in resting T cells stimulated through the Ag receptor, but has no effect on the activation of these caspases during Fas-induced apoptosis in proliferating T cells.	MDL 201053	0-8	caspase 8	Homo sapiens	36-45
16316721-3	2006	In the absence of an intact p53 and without changing Bax level, at nM range triptolide induced apoptosis with concomitant DNA fragmentation, S phase cell cycle arrest, mitochondrial cytochrome c release and the activation of caspases.	triptolide	76-86	caspase 8	Homo sapiens	225-233
16316721-4	2006	Besides, both caspases 8 and 9 were activated and the simultaneous inhibition of both was required to completely block triptolide"s apoptotic effect.	triptolide	119-129	caspase 8	Homo sapiens	14-30
16316721-5	2006	Importantly, triptolide induced the appearance of a truncated 23kD Bcl-2 which was inhibited by the general caspase inhibitor Z-VAD-FMK.	triptolide	13-23	caspase 8	Homo sapiens	108-115
16316721-5	2006	Importantly, triptolide induced the appearance of a truncated 23kD Bcl-2 which was inhibited by the general caspase inhibitor Z-VAD-FMK.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	126-135	caspase 8	Homo sapiens	108-115
16316721-6	2006	In the MCF-7 cells that possessed the wild type p53 but lacked caspases 3, triptolide induced cell death with an increase in p53 but Bcl-2 remained unaltered.	triptolide	75-85	caspase 8	Homo sapiens	63-71
16316721-10	2006	Our data suggest that in the absence of an intact p53 and without altering Bax level triptolide induces apoptosis activates a positive amplification loop involving caspase-mediated Bcl-2 cleavage/activation, mitochondrial cytochrome c release and further activation of caspases.	triptolide	85-95	caspase 8	Homo sapiens	164-171
16316721-10	2006	Our data suggest that in the absence of an intact p53 and without altering Bax level triptolide induces apoptosis activates a positive amplification loop involving caspase-mediated Bcl-2 cleavage/activation, mitochondrial cytochrome c release and further activation of caspases.	triptolide	85-95	caspase 8	Homo sapiens	269-277
16946501-3	2006	Caspase 8 inhibitor z-IETD, but neither caspase 1 inhibitor Ac-YVAD nor caspase 10 inhibitor z-AEVD, effectively blocked oridonin-induced cell death as well as DNA fragmentation.	z-ietd	20-26	caspase 8	Homo sapiens	0-9
16946501-3	2006	Caspase 8 inhibitor z-IETD, but neither caspase 1 inhibitor Ac-YVAD nor caspase 10 inhibitor z-AEVD, effectively blocked oridonin-induced cell death as well as DNA fragmentation.	oridonin	121-129	caspase 8	Homo sapiens	0-9
16946501-6	2006	However, inhibition of ERK by PD98059 reversed oridonin-induced cell death as well as the activation of caspase 8, indicating that ERK-mediated control occured upstream of caspase 8.	oridonin	47-55	caspase 8	Homo sapiens	172-181
16571651-5	2006	The apoptosis induced by co-treatment with SFN and TRAIL was markedly blocked by a dominant negative form of the TRAIL receptor or caspase inhibitors.	sulforaphane	43-46	caspase 8	Homo sapiens	131-138
16442262-4	2006	To show conventional chemotherapy drugs can trigger the caspase cascade, including caspase-8, -9, -3 and DNA fragmentation factor, Jurkat T leukemia cells were treated with cisplatin or etoposide in a dose-dependent and a time-dependent manner.	Etoposide	186-195	caspase 8	Homo sapiens	83-129
16754784-4	2006	From a mechanistic standpoint, cannabidiol exposure resulted in activation of caspase-8, caspase-9, and caspase-3, cleavage of poly(ADP-ribose) polymerase, and a decrease in full-length Bid, suggesting possible cross-talk between the intrinsic and extrinsic apoptotic pathways.	Cannabidiol	31-42	caspase 8	Homo sapiens	78-87
16951203-0	2006	Flavopiridol induces cellular FLICE-inhibitory protein degradation by the proteasome and promotes TRAIL-induced early signaling and apoptosis in breast tumor cells.	alvocidib	0-12	caspase 8	Homo sapiens	30-35
16951203-6	2006	Down-regulation of cellular FLICE-inhibitory proteins (c-FLIP; c-FLIP(L) and c-FLIP(S)) is observed on flavopiridol treatment.	alvocidib	103-115	caspase 8	Homo sapiens	28-33
16865278-9	2006	Subsequently, activation of caspase-8 and caspase-3 was observed following the treatment with NS-398 and IFN-beta.	N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide	94-100	caspase 8	Homo sapiens	28-37
16741989-8	2006	In the type I H9 and SKW6.4 cells and type II Jurkat cells, the caspase-8 inhibitor Z-Ile-Glu(OMe)-Thr-Asp(OMe)-CH2F (IETD) prevented the cell killing.	z-ile-glu	84-93	caspase 8	Homo sapiens	64-73
16741989-8	2006	In the type I H9 and SKW6.4 cells and type II Jurkat cells, the caspase-8 inhibitor Z-Ile-Glu(OMe)-Thr-Asp(OMe)-CH2F (IETD) prevented the cell killing.	Threonine	99-102	caspase 8	Homo sapiens	64-73
16741989-8	2006	In the type I H9 and SKW6.4 cells and type II Jurkat cells, the caspase-8 inhibitor Z-Ile-Glu(OMe)-Thr-Asp(OMe)-CH2F (IETD) prevented the cell killing.	Aspartic Acid	103-106	caspase 8	Homo sapiens	64-73
16741989-8	2006	In the type I H9 and SKW6.4 cells and type II Jurkat cells, the caspase-8 inhibitor Z-Ile-Glu(OMe)-Thr-Asp(OMe)-CH2F (IETD) prevented the cell killing.	IETD	118-122	caspase 8	Homo sapiens	64-73
16607283-6	2006	Inhibition of caspase-8 by dominant-negative caspase-8 or by the relatively specific caspase-8 inhibitior zIETD.fmk inhibited the increase in apoptosis provided by 5-dAzaC and IFN-gamma, indicating that caspase-8 is a key mediator of this sensitization effect.	5-dazac	164-171	caspase 8	Homo sapiens	14-23
16607283-0	2006	5-Aza-2"-deoxycytidine and IFN-gamma cooperate to sensitize for TRAIL-induced apoptosis by upregulating caspase-8.	Decitabine	0-22	caspase 8	Homo sapiens	104-113
16607283-7	2006	Thus, by demonstrating that 5-dAzaC and IFN-gamma at relatively low individual concentrations cooperate to restore caspase-8 expression and sensitize resistant neuroblastoma and medulloblastoma cells to TRAIL-induced apoptosis, our findings have important implications for novel strategies targeting defective apoptosis pathways in neuroectodermal tumors.	5-dazac	28-35	caspase 8	Homo sapiens	115-124
16607283-3	2006	Here, we provide for the first time evidence that combined treatment with suboptimal concentrations of the demethylating agent 5-Aza-2"-deoxycytidine (5-dAzaC) and interferon-gamma (IFN-gamma) cooperated to upregulate caspase-8 expression in neuroblastoma and medulloblastoma cells lacking caspase-8.	Decitabine	127-149	caspase 8	Homo sapiens	218-227
16607283-3	2006	Here, we provide for the first time evidence that combined treatment with suboptimal concentrations of the demethylating agent 5-Aza-2"-deoxycytidine (5-dAzaC) and interferon-gamma (IFN-gamma) cooperated to upregulate caspase-8 expression in neuroblastoma and medulloblastoma cells lacking caspase-8.	Decitabine	127-149	caspase 8	Homo sapiens	290-299
16843824-10	2006	The interdependence of caspases 8, 9, 2, and 3 in the cascade provides evidence for the presence of an extensive feedback amplification loop in beta-carotene-induced apoptosis in Molt 4 cells.	beta Carotene	144-157	caspase 8	Homo sapiens	23-46
16607283-3	2006	Here, we provide for the first time evidence that combined treatment with suboptimal concentrations of the demethylating agent 5-Aza-2"-deoxycytidine (5-dAzaC) and interferon-gamma (IFN-gamma) cooperated to upregulate caspase-8 expression in neuroblastoma and medulloblastoma cells lacking caspase-8.	5-dazac	151-158	caspase 8	Homo sapiens	218-227
16607283-3	2006	Here, we provide for the first time evidence that combined treatment with suboptimal concentrations of the demethylating agent 5-Aza-2"-deoxycytidine (5-dAzaC) and interferon-gamma (IFN-gamma) cooperated to upregulate caspase-8 expression in neuroblastoma and medulloblastoma cells lacking caspase-8.	5-dazac	151-158	caspase 8	Homo sapiens	290-299
16607283-4	2006	Consequently, activation of caspase-8 and downstream caspases upon addition of TNF-related apoptosis-inducing ligand (TRAIL) was restored by pretreatment with 5-dAzaC and IFN-gamma.	5-dazac	159-166	caspase 8	Homo sapiens	28-37
16607283-4	2006	Consequently, activation of caspase-8 and downstream caspases upon addition of TNF-related apoptosis-inducing ligand (TRAIL) was restored by pretreatment with 5-dAzaC and IFN-gamma.	5-dazac	159-166	caspase 8	Homo sapiens	53-61
16886176-5	2006	The DNA methylation status of putative caspase-8 and STAT-1 regulatory elements were determined by bisulfite-modified sequencing analysis.	hydrogen sulfite	99-108	caspase 8	Homo sapiens	39-48
16806159-5	2006	Several targets of caspases and Bcl-2 family of proteins were detected and the data demonstrated that bromovulone III induced the activation of caspase-8, -9 and -3, and Bid cleavage in which the caspase-8 activation occurred the first.	bromovulone	102-113	caspase 8	Homo sapiens	19-27
16806159-5	2006	Several targets of caspases and Bcl-2 family of proteins were detected and the data demonstrated that bromovulone III induced the activation of caspase-8, -9 and -3, and Bid cleavage in which the caspase-8 activation occurred the first.	bromovulone	102-113	caspase 8	Homo sapiens	144-164
16806159-5	2006	Several targets of caspases and Bcl-2 family of proteins were detected and the data demonstrated that bromovulone III induced the activation of caspase-8, -9 and -3, and Bid cleavage in which the caspase-8 activation occurred the first.	bromovulone	102-113	caspase 8	Homo sapiens	144-153
16806159-10	2006	Although it has been suggested that Fas-mediated signaling may contribute to the caspase-8 activation induced by DNA-damaging agents; however, bromovulone III did not induce any DNA breakage, suggesting that bromovulone III-induced Fas/caspase-8-dependent signaling is not through the direct target on DNA damage.	ammonium ferrous sulfate	36-39	caspase 8	Homo sapiens	81-90
16806159-10	2006	Although it has been suggested that Fas-mediated signaling may contribute to the caspase-8 activation induced by DNA-damaging agents; however, bromovulone III did not induce any DNA breakage, suggesting that bromovulone III-induced Fas/caspase-8-dependent signaling is not through the direct target on DNA damage.	bromovulone III	208-223	caspase 8	Homo sapiens	81-90
16806159-10	2006	Although it has been suggested that Fas-mediated signaling may contribute to the caspase-8 activation induced by DNA-damaging agents; however, bromovulone III did not induce any DNA breakage, suggesting that bromovulone III-induced Fas/caspase-8-dependent signaling is not through the direct target on DNA damage.	bromovulone III	208-223	caspase 8	Homo sapiens	236-245
16550602-6	2006	The sensitization of these cells by SAHA was accompanied by activation of caspase 8, caspase 9 and caspase 3 and was concomitant with Bid and PARP cleavage.	Vorinostat	36-40	caspase 8	Homo sapiens	74-83
16766531-6	2006	Of interest, BAY 11-7085-induced PPAR-gamma1 dephosphorylation was followed by PARP and caspase-8 cleavage as well as by PPAR-gamma1 protein degradation.	BAY 11-7085	13-24	caspase 8	Homo sapiens	88-97
16869889-4	2006	Pretreatment with the p38 kinase-inhibitor SB203580 decreased hA-induced apoptosis and caspase-3 activation by approximately 30%; as did combined SB203580 and JNK inhibitor I, by about 70%; and the combination of SB203580, the JNK inhibitor I and a caspase-8 inhibitor, by 100%.	SB 203580	43-51	caspase 8	Homo sapiens	249-258
16988766-8	2006	RESULTS: Eupatilin significantly reduced bile acid-mediated hepatocyte apoptosis by attenuating bile acid-induced caspase 8 cleavage.	Bile Acids and Salts	41-50	caspase 8	Homo sapiens	114-123
16988766-8	2006	RESULTS: Eupatilin significantly reduced bile acid-mediated hepatocyte apoptosis by attenuating bile acid-induced caspase 8 cleavage.	Bile Acids and Salts	96-105	caspase 8	Homo sapiens	114-123
16988766-10	2006	In particular, the eupatilin-mediated inhibition of bile acid-induced c-Jun N-terminal kinase activation was found to be responsible for attenuating caspase 8 cleavage.	eupatilin	19-28	caspase 8	Homo sapiens	149-158
16988766-10	2006	In particular, the eupatilin-mediated inhibition of bile acid-induced c-Jun N-terminal kinase activation was found to be responsible for attenuating caspase 8 cleavage.	Bile Acids and Salts	52-61	caspase 8	Homo sapiens	149-158
17203870-13	2006	PIN &amp; prostate cancer lesions were found to strongly express of FADD &amp; CASPASE-8 proteins.	Adenosine Monophosphate	5-8	caspase 8	Homo sapiens	79-88
16140459-4	2006	Both the (Bu(2)Sn)(2)TPPS and the (Bu(3)Sn)(4)TPPS compounds activate caspase-8 and caspase-9 leading to caspase-3 activation.	(bu(2)sn)	9-18	caspase 8	Homo sapiens	70-79
16140459-4	2006	Both the (Bu(2)Sn)(2)TPPS and the (Bu(3)Sn)(4)TPPS compounds activate caspase-8 and caspase-9 leading to caspase-3 activation.	2)tpps	19-25	caspase 8	Homo sapiens	70-79
16140459-4	2006	Both the (Bu(2)Sn)(2)TPPS and the (Bu(3)Sn)(4)TPPS compounds activate caspase-8 and caspase-9 leading to caspase-3 activation.	(bu(3)sn)	34-43	caspase 8	Homo sapiens	70-79
17203870-13	2006	PIN &amp; prostate cancer lesions were found to strongly express of FADD &amp; CASPASE-8 proteins.	Adenosine Monophosphate	74-77	caspase 8	Homo sapiens	79-88
16714221-7	2006	The apoptotic inhibition of fraxetin is associated with inhibition of TNF-alpha and IL-1beta-mediated Fas expression and enhancement of FLIP expression, resulting in a decrease of caspase-8 and caspase-3 activation.	fraxetin	28-36	caspase 8	Homo sapiens	180-189
16603484-4	2006	Treatment with caspase-3, -8, and -9 inhibitors inhibited annexin V staining, as well as caspase-3 activity, pointing to an important role of these caspases in crambene-induced acinar cell apoptosis.	1-cyano-2-hydroxy-3-butene	160-168	caspase 8	Homo sapiens	148-156
16699949-5	2006	MG-132 treatment increases binding of DR5 to the adaptor protein FADD, and causes caspase-8 activation and cleavage of pro-apoptotic BID.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	caspase 8	Homo sapiens	82-91
16624285-6	2006	Inhibition of ceramide synthesis de novo also prevented caspase activation and apoptosis.	Ceramides	14-22	caspase 8	Homo sapiens	56-63
16826547-3	2006	In full-length BID, the putative hydrophobic binding surface of its BH3 motif is substantially occluded by intramolecular contacts, many of which are removed on BID"s transformation to tBID by cleavage with caspase 8, required for tBID"s pro-apoptotic action on mitochondria, thereby releasing cytochrome c.	BH 3	68-71	caspase 8	Homo sapiens	207-216
16826547-3	2006	In full-length BID, the putative hydrophobic binding surface of its BH3 motif is substantially occluded by intramolecular contacts, many of which are removed on BID"s transformation to tBID by cleavage with caspase 8, required for tBID"s pro-apoptotic action on mitochondria, thereby releasing cytochrome c.	tBID	185-189	caspase 8	Homo sapiens	207-216
16826547-3	2006	In full-length BID, the putative hydrophobic binding surface of its BH3 motif is substantially occluded by intramolecular contacts, many of which are removed on BID"s transformation to tBID by cleavage with caspase 8, required for tBID"s pro-apoptotic action on mitochondria, thereby releasing cytochrome c.	tBID	231-235	caspase 8	Homo sapiens	207-216
16891471-7	2006	In the case of other clones, expression of procaspase-8 protein was lost and this was associated with a novel Leu(22)--&gt;Phe(22) point mutation in CASP-8 gene.	Leucine	110-113	caspase 8	Homo sapiens	149-155
16733806-0	2006	Bortezomib induces in HepG2 cells IkappaBalpha degradation mediated by caspase-8.	Bortezomib	0-10	caspase 8	Homo sapiens	71-80
16733806-2	2006	The effect already appeared at 4 h of treatment and preceded the onset of apoptosis which was observed at 24 h. Our results demonstrate that bortezomib-induced IkappaBalpha degradation occurred in conjunction with the activation of caspase-8; moreover, the decrease in IkappaBalpha level was prevented in a dose-dependent manner by the addition of z-IETD, a specific inhibitor of caspase-8.	Bortezomib	141-151	caspase 8	Homo sapiens	232-241
16733806-2	2006	The effect already appeared at 4 h of treatment and preceded the onset of apoptosis which was observed at 24 h. Our results demonstrate that bortezomib-induced IkappaBalpha degradation occurred in conjunction with the activation of caspase-8; moreover, the decrease in IkappaBalpha level was prevented in a dose-dependent manner by the addition of z-IETD, a specific inhibitor of caspase-8.	Bortezomib	141-151	caspase 8	Homo sapiens	380-389
16733806-6	2006	In addition, the activation of caspase-8 can exert, at least in the first phase of treatment with bortezomib, a protective effect in both HepG2 and Chang liver cells, favouring the activation of the survival factor NF-kappaB.	Bortezomib	98-108	caspase 8	Homo sapiens	31-40
16891469-7	2006	DR5/Fc chimera protein, zVAD-fmk pancaspase inhibitor, and caspase-8 inhibitor efficiently blocked the activation of these apoptotic signal mediators and the induction of apoptotic cell death enhanced by cotreatment with 15d-PGJ(2) and TRAIL.	15d-pgj	221-228	caspase 8	Homo sapiens	59-68
16891471-7	2006	In the case of other clones, expression of procaspase-8 protein was lost and this was associated with a novel Leu(22)--&gt;Phe(22) point mutation in CASP-8 gene.	Phenylalanine	123-126	caspase 8	Homo sapiens	149-155
16647044-0	2006	Carbon monoxide protects hepatocytes from TNF-alpha/Actinomycin D by inhibition of the caspase-8-mediated apoptotic pathway.	Carbon Monoxide	0-15	caspase 8	Homo sapiens	87-96
16636047-6	2006	In U937 cells exposed to TPA, these proteolytic events can be inhibited by expression of a caspase-8 dominant negative mutant or the cowpox virus CrmA caspase inhibitor.	Tetradecanoylphorbol Acetate	25-28	caspase 8	Homo sapiens	91-100
16647044-0	2006	Carbon monoxide protects hepatocytes from TNF-alpha/Actinomycin D by inhibition of the caspase-8-mediated apoptotic pathway.	Dactinomycin	52-65	caspase 8	Homo sapiens	87-96
16009487-3	2006	In T24 cells, cisplatin induce apoptosis and the activation of caspase-8, -9 and -3 and poly(ADP-ribose) polymerase cleavage.	Cisplatin	14-23	caspase 8	Homo sapiens	63-83
16478887-6	2006	Plasminogen treatment also markedly reduced internucleosomal DNA fragmentation and reduced levels of active caspase 3, caspase 8, and caspase 9 induced by TNFalpha or by cycloheximide.	Cycloheximide	170-183	caspase 8	Homo sapiens	119-128
16754997-5	2006	The caspases, caspase-9 and -3, but not caspase-8, were found to be activated in response to RPAE treatment, and the caspase-3 inhibitor, Ac-DEVD-CHO, and the caspase-9 inhibitor, z-LEHD-FMK, but not the caspase-8 inhibitor, z-IETD-FMK, attenuated RPAE-induced DNA fragmentation and PARP cleavage.	benzyloxycarbonyl-leucyl-glutamyl-histidyl-aspartic acid fluoromethyl ketone	180-190	caspase 8	Homo sapiens	4-12
16754997-5	2006	The caspases, caspase-9 and -3, but not caspase-8, were found to be activated in response to RPAE treatment, and the caspase-3 inhibitor, Ac-DEVD-CHO, and the caspase-9 inhibitor, z-LEHD-FMK, but not the caspase-8 inhibitor, z-IETD-FMK, attenuated RPAE-induced DNA fragmentation and PARP cleavage.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	225-235	caspase 8	Homo sapiens	4-12
16754997-5	2006	The caspases, caspase-9 and -3, but not caspase-8, were found to be activated in response to RPAE treatment, and the caspase-3 inhibitor, Ac-DEVD-CHO, and the caspase-9 inhibitor, z-LEHD-FMK, but not the caspase-8 inhibitor, z-IETD-FMK, attenuated RPAE-induced DNA fragmentation and PARP cleavage.	acetyl-aspartyl-glutamyl-valyl-aspartal	138-149	caspase 8	Homo sapiens	4-12
16755000-0	2006	Silibinin prevents UV-induced HaCaT cell apoptosis partly through inhibition of caspase-8 pathway.	Silybin	0-9	caspase 8	Homo sapiens	80-89
16755000-6	2006	The caspase-8 inhibitor z-IETD-fmk at 10 microM increased the ratio of UV-irradiated HaCaT cell viability, suggesting that UV-induced HaCaT cell apoptosis was partially due to activation of the caspase-8 pathway.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	24-34	caspase 8	Homo sapiens	4-13
16755000-6	2006	The caspase-8 inhibitor z-IETD-fmk at 10 microM increased the ratio of UV-irradiated HaCaT cell viability, suggesting that UV-induced HaCaT cell apoptosis was partially due to activation of the caspase-8 pathway.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	24-34	caspase 8	Homo sapiens	194-203
16019139-8	2006	Our results indicated that MMC induced apoptosis in SiHa/pRSV-luc and SiHa cells via caspase-8 and -3 processing, in a Fas/FasL-dependent manner.	Mitomycin	27-30	caspase 8	Homo sapiens	85-101
16755000-9	2006	Consequently, the protective effect of silibinin against UV irradiation in HaCaT cells is exerted by inactivation of caspase-8 after direct down-regulation of FADD expression, resulting in blockage of UV-induced apoptosis.	Silybin	39-48	caspase 8	Homo sapiens	117-126
16019139-11	2006	These results suggest that MMC induces apoptosis, not only through caspase-8 and -3 dependent Fas/FasL pathway, but also via the regulation of NF-kappaB activity and IL-18 expression.	Mitomycin	27-30	caspase 8	Homo sapiens	67-83
16685442-0	2006	Combination treatment with arsenic trioxide and sulindac augments their apoptotic potential in lung cancer cells through activation of caspase cascade and mitochondrial dysfunction.	Arsenic Trioxide	27-43	caspase 8	Homo sapiens	135-142
16684125-13	2006	The apoptosis induced by amlodipine is through caspase 8 and then the 3/7 signalling pathway.	Amlodipine	25-35	caspase 8	Homo sapiens	47-56
16685442-0	2006	Combination treatment with arsenic trioxide and sulindac augments their apoptotic potential in lung cancer cells through activation of caspase cascade and mitochondrial dysfunction.	Sulindac	48-56	caspase 8	Homo sapiens	135-142
16685448-6	2006	We also demonstrate that treatment with sulindac sulfide, but not sulindac, results in a very early robust activation of both caspase-8 and -9.	sulindac sulfide	40-56	caspase 8	Homo sapiens	126-142
16440323-4	2006	Apoptotic enhancement by hyperthermia was primarily mediated by caspase-8 activation, as the specific inhibitor, Z-IETD, blocked cell death, whereas direct engagement of the intrinsic apoptotic pathway (with doxorubicin) was not affected.	z-ietd	113-119	caspase 8	Homo sapiens	64-73
16685448-6	2006	We also demonstrate that treatment with sulindac sulfide, but not sulindac, results in a very early robust activation of both caspase-8 and -9.	Sulindac	40-48	caspase 8	Homo sapiens	126-142
16685448-7	2006	Furthermore, we show that the apoptotic effects of sulindac sulfide can be reverted by both the caspase-8 and -9 inhibitors.	sulindac sulfide	51-67	caspase 8	Homo sapiens	96-112
16845445-8	2006	And the phosphorothioate antisense oligodeoxynucleotides to fas-associated death domain protein (FADD) could block the expression of FADD, which is an upstream factor of caspase-8 in the Fas/FasL pathway.	Parathion	8-24	caspase 8	Homo sapiens	170-179
16845445-8	2006	And the phosphorothioate antisense oligodeoxynucleotides to fas-associated death domain protein (FADD) could block the expression of FADD, which is an upstream factor of caspase-8 in the Fas/FasL pathway.	Oligodeoxyribonucleotides	35-56	caspase 8	Homo sapiens	170-179
16684533-0	2006	Caspase-8 acts as a key upstream executor of mitochondria during justicidin A-induced apoptosis in human hepatoma cells.	justicidins	65-77	caspase 8	Homo sapiens	0-9
16684533-3	2006	In this study, justicidin A activated caspase-8 to increase tBid, disrupted mitochondrial membrane potential (Delta psi(m)), and caused the release of cytochrome c and Smac/DIABLO in Hep 3B and Hep G2 cells.	justicidins	15-27	caspase 8	Homo sapiens	38-47
16684533-3	2006	In this study, justicidin A activated caspase-8 to increase tBid, disrupted mitochondrial membrane potential (Delta psi(m)), and caused the release of cytochrome c and Smac/DIABLO in Hep 3B and Hep G2 cells.	tBID	60-64	caspase 8	Homo sapiens	38-47
16684533-5	2006	Caspase-8 inhibitor (Z-IETD) attenuated the justicidin A-induced disruption of Delta psi(m).	z-ietd	21-27	caspase 8	Homo sapiens	0-9
16684533-5	2006	Caspase-8 inhibitor (Z-IETD) attenuated the justicidin A-induced disruption of Delta psi(m).	justicidins	44-56	caspase 8	Homo sapiens	0-9
16684533-7	2006	These results indicate that justicidin A-induced apoptosis in these cells proceeds via caspase-8 and is followed by mitochondrial disruption.	justicidins	28-40	caspase 8	Homo sapiens	87-96
16631160-4	2006	Platycodin D-induced apoptosis in HaCaT cells was confirmed by DNA fragmentation, caspase-3 activation, and caspase-8 activation.	platycodin D	0-12	caspase 8	Homo sapiens	108-117
16772874-0	2006	Coordinated expression of caspase 8, 3 and 7 mRNA in temporal cortex of Alzheimer disease: relationship to formic acid extractable abeta42 levels.	formic acid	107-118	caspase 8	Homo sapiens	26-44
16516327-4	2006	The activities of caspase 3 and 7 (marked as caspase 3/7), and caspase 8 were significantly activated by topotecan with amlodipine co-treated as the stealth liposomes.	Topotecan	105-114	caspase 8	Homo sapiens	63-72
16532269-1	2006	Pulse-treatment of U-937 human promonocytic cells with cadmium chloride followed by recovery caused caspase-9/caspase-3-dependent, caspase-8-independent apoptosis.	Cadmium Chloride	55-71	caspase 8	Homo sapiens	131-140
16646028-0	2006	Fas activation of a proinflammatory program in rheumatoid synoviocytes and its regulation by FLIP and caspase 8 signaling.	ammonium ferrous sulfate	0-3	caspase 8	Homo sapiens	102-111
16385419-6	2006	In both HeLa and PANC-1 cells, apoptosis induced by triptolide was associated with activation of both caspase-3 and caspase-8, and cleavage of poly(ADP-ribose) polymerase and Bid.	triptolide	52-62	caspase 8	Homo sapiens	116-125
16516327-4	2006	The activities of caspase 3 and 7 (marked as caspase 3/7), and caspase 8 were significantly activated by topotecan with amlodipine co-treated as the stealth liposomes.	Amlodipine	120-130	caspase 8	Homo sapiens	63-72
16516327-7	2006	In conclusion, apoptotic effect is associated with deletion of intracellular Ca2+ by amlodipine through activation of caspase 8 and then 3/7 activities.	Amlodipine	85-95	caspase 8	Homo sapiens	118-127
16619028-3	2006	Src activation triggers Caspase-8 phosphorylation on Tyr380 and impairs Fas-induced apoptosis.	ammonium ferrous sulfate	72-75	caspase 8	Homo sapiens	24-33
16619028-7	2006	These data provide the first evidence for a direct role of tyrosine phosphorylation in the control of caspases and reveal a new mechanism through which tyrosine kinases inhibit apoptosis and participate in tumor progression.	Tyrosine	59-67	caspase 8	Homo sapiens	102-110
16827126-5	2006	The effects of (-)-gossypol on the expression of apoptotic-regulated gene markers in both death receptor- and mitochondria-mediated apoptotic pathways, such as the Bcl-2 family and caspase, etc., were detected by RT-PCR and Western blot analysis.	Gossypol	15-27	caspase 8	Homo sapiens	181-188
16827126-11	2006	By using caspase inhibitors, (-)-gossypol caused apoptosis via the caspase-dependent pathways.	Gossypol	29-41	caspase 8	Homo sapiens	9-16
16827126-11	2006	By using caspase inhibitors, (-)-gossypol caused apoptosis via the caspase-dependent pathways.	Gossypol	29-41	caspase 8	Homo sapiens	67-74
16827126-12	2006	CONCLUSION: Our results indicated that the apoptotic processes caused by (-)-gossypol are mediated by the regulation of the Bcl-2 and caspase families in human prostate cancer cells.	Gossypol	73-85	caspase 8	Homo sapiens	134-141
16772874-6	2006	Further, there was a strong positive correlation of caspase-8 levels with formic acid extractable Abeta42 levels.	formic acid	74-85	caspase 8	Homo sapiens	52-61
16539849-11	2006	When HepG2 cells were treated with 3 mmol/L adenosine, mitochondrial membrane potential and the activity of caspase-8 or -9 remained unchanged.	Adenosine	44-53	caspase 8	Homo sapiens	108-123
16169029-4	2006	In the early stages, both rapid and transient ROS generation triggered apoptosis via Fas activation and subsequent caspase-8-dependent Bid cleavage, as well as by calpain-mediated mitochondrial Bax cleavage.	Reactive Oxygen Species	46-49	caspase 8	Homo sapiens	115-124
16618745-4	2006	Inhibition of caspase-8 expression using caspase-8 antisense or small interfering RNA (siRNA) oligonucleotides partially blocks radiation-induced apoptosis.	Oligonucleotides	94-110	caspase 8	Homo sapiens	14-23
16618745-4	2006	Inhibition of caspase-8 expression using caspase-8 antisense or small interfering RNA (siRNA) oligonucleotides partially blocks radiation-induced apoptosis.	Oligonucleotides	94-110	caspase 8	Homo sapiens	41-50
16618754-7	2006	Our results showed that the production of hydrogen peroxide derived from MnSOD dismutation activated caspase-8, which might down-regulate Bcl-2 expression and induce Bax translocation to mitochondria.	Hydrogen Peroxide	42-59	caspase 8	Homo sapiens	101-110
16242776-6	2006	Upregulation of c-FLIP(L) protein, an inhibitor of apoptosis induced by tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), correspond with inhibition of ATRA-induced (autocrine TRAIL-mediated) caspase-8 activation and apoptosis.	Tretinoin	167-171	caspase 8	Homo sapiens	207-216
16618756-5	2006	Exogenous expression of dominant-negative caspase-8 or dominant-negative FADD reverts the effect of 2-methoxyestradiol-mediated cell death.	2-Methoxyestradiol	100-118	caspase 8	Homo sapiens	42-51
16618756-6	2006	In parallel with this observation, Z-IETD-FMK, a cell permeable irreversible inhibitor of caspase-8, can render significant protection against 2-methoxyestradiol-induced apoptosis.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	35-45	caspase 8	Homo sapiens	90-99
16618756-6	2006	In parallel with this observation, Z-IETD-FMK, a cell permeable irreversible inhibitor of caspase-8, can render significant protection against 2-methoxyestradiol-induced apoptosis.	2-Methoxyestradiol	143-161	caspase 8	Homo sapiens	90-99
16730193-7	2006	Inhibition of caspase-8 activation in the presence of Z-IETD-FMK abolished the TNF-alpha-induced increases in mitochondrial Cyt C release, loss of delta psi(m) and apoptosis.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	54-64	caspase 8	Homo sapiens	14-23
16528474-0	2006	JNK and AP-1 mediate apoptosis induced by bortezomib in HepG2 cells via FasL/caspase-8 and mitochondria-dependent pathways.	Bortezomib	42-52	caspase 8	Homo sapiens	77-86
16528476-4	2006	The overexpression of Bcl-xL, an anti-apoptotic protein, completely inhibited the activation of the caspases and apoptosis, assuming that NAPS-induced apoptosis was initiated by the mitochondria.	N-acetylphytosphingosine	138-142	caspase 8	Homo sapiens	100-108
16332727-5	2006	The subsequent downstream effects of DIM/DIM-C-pPhtBu- and Tg-induced ER stress included CHOP-dependent induction of death receptor DR5 and subsequent cleavage of caspase 8, caspase 3, Bid and PARP.	Thapsigargin	59-61	caspase 8	Homo sapiens	163-172
16596338-0	2006	Mitochondria and calpains mediate caspase-dependent apoptosis induced by doxycycline in HeLa cells.	Doxycycline	73-84	caspase 8	Homo sapiens	34-41
16231322-4	2006	This study was undertaken to elucidate the effect of FHIT expression and the role of Bcl-2-caspase signaling in paclitaxel-induced apoptosis in lung cancer cells.	Paclitaxel	112-122	caspase 8	Homo sapiens	91-98
16231322-10	2006	When caspase activation was blocked by a pan-caspase inhibitor in FHIT-expressing cells, paclitaxel-induced apoptotic cell death was decreased similar to that in control vector-transfected cells.	Paclitaxel	89-99	caspase 8	Homo sapiens	5-12
16231322-10	2006	When caspase activation was blocked by a pan-caspase inhibitor in FHIT-expressing cells, paclitaxel-induced apoptotic cell death was decreased similar to that in control vector-transfected cells.	Paclitaxel	89-99	caspase 8	Homo sapiens	45-52
16438941-7	2006	Potentiation of camptothecin-induced apoptosis by TRAIL appears dependent on cooperation between extrinsic and intrinsic pathways, as documented by loss of the sensitization to apoptosis following reduction of caspase 8 after small interfering RNA transfection.	Camptothecin	16-28	caspase 8	Homo sapiens	210-219
16304056-3	2006	However, inhibition of endogenous c-FLIP expression by specific c-FLIP siRNA in Karpas 299 and SU-DHL1 cells treated with CH-11 resulted in FAS-mediated cell death associated with increased annexin V binding, apoptotic morphology, and cleavage of caspase-8.	4-dimethylamino-3',4'-dimethoxychalcone	122-127	caspase 8	Homo sapiens	247-256
16319070-0	2006	A peroxisome proliferator-activated receptor-gamma agonist, troglitazone, facilitates caspase-8 and -9 activities by increasing the enzymatic activity of protein-tyrosine phosphatase-1B on human glioma cells.	Troglitazone	60-72	caspase 8	Homo sapiens	86-102
16319070-4	2006	Here we proposed a novel mechanism of proapoptotic effect induced by a pharmacological peroxisome proliferator-activated receptor-gamma (PPARgamma) agonist, troglitazone, that facilitates caspase signaling in human glioma cells.	Troglitazone	157-169	caspase 8	Homo sapiens	188-195
16319070-10	2006	Knockdown of STAT3 by STAT3-small interfering RNA negated the inhibitory effect of PTP inhibitor on troglitazone, indicating that troglitazone uses a STAT3 inactivation mechanism that makes caspase-8/9 activities susceptible to cytotoxic agents in glioma cells and that PTP1B plays a critical role in the down-regulation of activated STAT3, as well as FLIP and Bcl-2.	Troglitazone	100-112	caspase 8	Homo sapiens	190-199
16319070-8	2006	When given with tumor necrosis factor-related apoptosis-inducing ligand or caspase-dependent chemotherapeutic agents, such as etoposide and paclitaxel, troglitazone exhibited a synergistic effect by facilitating caspase-8/9 activities.	Etoposide	126-135	caspase 8	Homo sapiens	212-221
16319070-10	2006	Knockdown of STAT3 by STAT3-small interfering RNA negated the inhibitory effect of PTP inhibitor on troglitazone, indicating that troglitazone uses a STAT3 inactivation mechanism that makes caspase-8/9 activities susceptible to cytotoxic agents in glioma cells and that PTP1B plays a critical role in the down-regulation of activated STAT3, as well as FLIP and Bcl-2.	Troglitazone	130-142	caspase 8	Homo sapiens	190-199
16319070-11	2006	When taken with caspase-dependent anti-neoplastic agents, troglitazone may be a promising drug for use against malignant gliomas because it facilitates the caspase cascade, thereby lowering thresholds for the apoptosis induction of glioma cells.	Troglitazone	58-70	caspase 8	Homo sapiens	16-23
16319070-8	2006	When given with tumor necrosis factor-related apoptosis-inducing ligand or caspase-dependent chemotherapeutic agents, such as etoposide and paclitaxel, troglitazone exhibited a synergistic effect by facilitating caspase-8/9 activities.	Troglitazone	152-164	caspase 8	Homo sapiens	212-221
16319070-11	2006	When taken with caspase-dependent anti-neoplastic agents, troglitazone may be a promising drug for use against malignant gliomas because it facilitates the caspase cascade, thereby lowering thresholds for the apoptosis induction of glioma cells.	Troglitazone	58-70	caspase 8	Homo sapiens	156-163
16397504-6	2006	Ceramide analogs also induced cell death in Jurkat mutants that are deficient in cell death signaling proteins, including FADD, caspase-8 and 10, and RIP.	Ceramides	0-8	caspase 8	Homo sapiens	128-137
16407197-2	2006	Caspase 8-mediated cleavage of the BH3-only protein Bid into a truncated protein (tBid) and subsequent translocation of tBid to mitochondria has been implicated in death receptor signaling.	tBID	82-86	caspase 8	Homo sapiens	0-9
16407197-2	2006	Caspase 8-mediated cleavage of the BH3-only protein Bid into a truncated protein (tBid) and subsequent translocation of tBid to mitochondria has been implicated in death receptor signaling.	tBID	120-124	caspase 8	Homo sapiens	0-9
16493077-6	2006	The caspase-8 inhibitor Z-IETD-FMK inhibited cell death associated with differentiation in a dose-dependent manner.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	24-34	caspase 8	Homo sapiens	4-13
16493077-10	2006	These data suggest that C5b-9 through PI3K signaling can rescue OLG from Fas-mediated apoptosis by regulating caspase-8 processing.	ammonium ferrous sulfate	73-76	caspase 8	Homo sapiens	110-119
16722146-8	2006	Further, in Ca922 and HSC6 but not in HOC313, caspase 8 inhibitor restored loss of viability induced either with LY294002 and TRAIL or even with etoposide alone.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	113-121	caspase 8	Homo sapiens	46-55
16722146-8	2006	Further, in Ca922 and HSC6 but not in HOC313, caspase 8 inhibitor restored loss of viability induced either with LY294002 and TRAIL or even with etoposide alone.	Etoposide	145-154	caspase 8	Homo sapiens	46-55
16465382-9	2006	TRAIL-induced, but not SAHA-induced, cell killing could be prevented by the caspase-8 inhibitor, z-IEDT-fmk.	Z-IEDT-fmk	97-107	caspase 8	Homo sapiens	76-85
16441517-6	2006	GD3-induced apoptosis occurred via caspase-8 activation, as GD3 caused cleavage of caspase-8 and inhibition of caspase-8 activation by zlETD-fmk minimized GD3-induced apoptosis.	zletd-fmk	135-144	caspase 8	Homo sapiens	35-44
16458195-8	2006	Studies using antioxidants and specific caspase inhibitors indicated that activation of caspase-8, but not caspase-9, mediates ROS-dependent caspase-3 activation and suggested that ROS from NADPH oxidase activate caspase-8.	Reactive Oxygen Species	127-130	caspase 8	Homo sapiens	88-97
16436312-6	2006	The anti-apoptosis exerted by BT involved the blocking of Cd-induced reactive oxygen species (ROS) generation, the abrogation of the Cd-induced Fas upregulation, the blocking of caspase-8-dependent Bid activation, and subsequent inhibition of mitochondrial pathway.	betulin	30-32	caspase 8	Homo sapiens	178-187
16458195-8	2006	Studies using antioxidants and specific caspase inhibitors indicated that activation of caspase-8, but not caspase-9, mediates ROS-dependent caspase-3 activation and suggested that ROS from NADPH oxidase activate caspase-8.	Reactive Oxygen Species	127-130	caspase 8	Homo sapiens	213-222
16458195-8	2006	Studies using antioxidants and specific caspase inhibitors indicated that activation of caspase-8, but not caspase-9, mediates ROS-dependent caspase-3 activation and suggested that ROS from NADPH oxidase activate caspase-8.	Reactive Oxygen Species	181-184	caspase 8	Homo sapiens	88-97
16458195-8	2006	Studies using antioxidants and specific caspase inhibitors indicated that activation of caspase-8, but not caspase-9, mediates ROS-dependent caspase-3 activation and suggested that ROS from NADPH oxidase activate caspase-8.	Reactive Oxygen Species	181-184	caspase 8	Homo sapiens	213-222
16253284-7	2006	That protection results in a significant reduction of caspase-3 activity induced by staurosporine which by its turn seems to result from a protection observed in the membrane receptor pathway (caspase-8) together with a protection observed in the mitochondrial pathway (caspase-9).	Staurosporine	84-97	caspase 8	Homo sapiens	193-202
16434995-0	2006	TRAIL sensitisation by arsenic trioxide is caspase-8 dependent and involves modulation of death receptor components and Akt.	Arsenic Trioxide	23-39	caspase 8	Homo sapiens	43-52
16434995-3	2006	The combination of ATO and TRAIL synergistically enhanced cleavage of caspase-8, which was blocked by the caspase inhibitor IETD.fmk as well as in cells deficient for caspase-8, suggesting a requirement for the death-inducing signalling complex.	Arsenic Trioxide	19-22	caspase 8	Homo sapiens	70-79
16434995-3	2006	The combination of ATO and TRAIL synergistically enhanced cleavage of caspase-8, which was blocked by the caspase inhibitor IETD.fmk as well as in cells deficient for caspase-8, suggesting a requirement for the death-inducing signalling complex.	Arsenic Trioxide	19-22	caspase 8	Homo sapiens	167-176
16434995-3	2006	The combination of ATO and TRAIL synergistically enhanced cleavage of caspase-8, which was blocked by the caspase inhibitor IETD.fmk as well as in cells deficient for caspase-8, suggesting a requirement for the death-inducing signalling complex.	isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	124-132	caspase 8	Homo sapiens	70-79
16441437-0	2006	Cryptococcus neoformans capsular polysaccharide component galactoxylomannan induces apoptosis of human T-cells through activation of caspase-8.	Polysaccharides	33-47	caspase 8	Homo sapiens	133-142
16483679-6	2006	The combined treatment of TNF-alpha/DOX also resulted in a significant decrease of mRNA levels of anti-apoptotic genes, such as the cellular inhibitor of apoptosis-1 (c-IAP1), and the long isoform of B cell leukemia/lymphoma x gene (Bcl-xL), leading to efficient induction of caspase-8 cleavage and cell death.	Doxorubicin	36-39	caspase 8	Homo sapiens	276-285
16189662-7	2006	Moreover, berberine induced the activation of caspase-8 and -3, and caused the cleavage of poly ADP-ribose polymerase (PARP) and the cytochrome c release, whereas the expression of Bid and anti-apoptosis factor Bcl-XL were decreased markedly.	Berberine	10-19	caspase 8	Homo sapiens	46-62
16189662-10	2006	These results indicated that the potential of anti-hepatoma activity of berberine may be mediated through a caspases-mitochondria-dependent pathway.	Berberine	72-81	caspase 8	Homo sapiens	108-116
16357524-7	2006	Moreover, the caspase 8 inhibitor (Z-IETD-FMK) could efficiently block caspase 8 activation and resulted in inhibition of caspase 3 activation and cleavage.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	35-45	caspase 8	Homo sapiens	14-23
16357524-7	2006	Moreover, the caspase 8 inhibitor (Z-IETD-FMK) could efficiently block caspase 8 activation and resulted in inhibition of caspase 3 activation and cleavage.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	35-45	caspase 8	Homo sapiens	71-80
16082389-3	2006	Inhibition of Fas ligand- and TNF-related apoptosis-inducing ligand-induced apoptosis by muristerone A occurs at the level of caspase-8 activation and is neutralized by phosphatidylinositol-3-kinase/Akt, protein kinase C and mitogen-activated protein kinase inhibitors.	muristerone A	89-100	caspase 8	Homo sapiens	126-135
16330535-0	2006	Fas costimulation of naive CD4 T cells is controlled by NF-kappaB signaling and caspase activity.	ammonium ferrous sulfate	0-3	caspase 8	Homo sapiens	80-87
16443735-8	2006	Immunoreactivity for both caspase 8 and 10 correlated with the apoptotic index previously assessed by terminal deoxynucleotidyl transferase mediated dUTP nick end labelling (p = 0.02 and p = 0.04, respectively) and M30 (p &lt; 0.001 and p = 0.003, respectively) approaches.	deoxyuridine triphosphate	149-153	caspase 8	Homo sapiens	26-35
16492559-3	2006	Biochemical and crystallographic data suggest that p35-N circularization results from the trapping of a native chemical ligation intermediate in the p35/caspase complex, in which the N-terminal Cys2 of p35 attacks the Asp87-Cys360" thioester to form an equilibrium between Asp87-Cys2 and Asp87-Cys360".	Nitrogen	55-56	caspase 8	Homo sapiens	153-160
16330535-7	2006	Thus, Fas-mediated costimulation of naive CD4 T cells is driven by active caspases, and NF-kappaB acts as a dominant survival-supporting factor of Fas-costimulated cells containing high levels of activated caspase-8 and -3.	ammonium ferrous sulfate	6-9	caspase 8	Homo sapiens	74-82
16330535-7	2006	Thus, Fas-mediated costimulation of naive CD4 T cells is driven by active caspases, and NF-kappaB acts as a dominant survival-supporting factor of Fas-costimulated cells containing high levels of activated caspase-8 and -3.	ammonium ferrous sulfate	6-9	caspase 8	Homo sapiens	206-222
16393981-0	2006	Sodium salicylate promotes neutrophil apoptosis by stimulating caspase-dependent turnover of Mcl-1.	Sodium Salicylate	0-17	caspase 8	Homo sapiens	63-70
16676399-6	2006	An increased activation of caspase-3 and caspase-8 by 2-ME was observed, and inhibition of caspase-3 decreased the apoptotic effect.	2-Methoxyestradiol	54-58	caspase 8	Homo sapiens	41-50
16399228-4	2006	Alisol B acetate induced Bax up-regulation and nuclear translocation; it also induced the activation of initiator caspase-8 and caspase-9, and executor caspase-3, suggesting the involvement of both extrinsic and intrinsic apoptosis pathways.	alisol B monoacetate	0-16	caspase 8	Homo sapiens	114-123
16399228-5	2006	Taken together, it is suggested that alisol B acetate induces apoptosis in PC-3 cells via a mitochondria-mediated mechanism with activation of caspase-8, -9 and -3.	alisol B monoacetate	37-53	caspase 8	Homo sapiens	143-163
16393981-4	2006	Sodium salicylate resulted in rapid activation of caspase-3, -8, -9, and -10, and salicylate-accelerated Mcl-1 turnover was partly blocked by caspase inhibitors.	Sodium Salicylate	0-17	caspase 8	Homo sapiens	50-57
16393981-3	2006	Whereas constitutive and GM-CSF-modified Mcl-1 turnover is regulated by the proteasome, the accelerated sodium salicylate-induced Mcl-1 turnover is mediated largely via caspases.	Sodium Salicylate	104-121	caspase 8	Homo sapiens	169-177
16393981-4	2006	Sodium salicylate resulted in rapid activation of caspase-3, -8, -9, and -10, and salicylate-accelerated Mcl-1 turnover was partly blocked by caspase inhibitors.	Salicylates	7-17	caspase 8	Homo sapiens	50-57
16397262-6	2006	Western blot analysis revealed activation of caspase-8 and caspase-3 within the first 6 to 12 hours of treatment with doxazosin in both PC-3 and BPH-1 cells.	Doxazosin	118-127	caspase 8	Homo sapiens	45-54
16433890-9	2006	Furthermore, trimidox-induced apoptosis was prevented by a broad-spectrum caspase inhibitor, a caspase-3, and a caspase-9 inhibitor, but not by a caspase-8 inhibitor.	3,4,5-trihydroxybenzamidoxime	13-21	caspase 8	Homo sapiens	74-81
16242324-2	2006	In this study, we further investigated which caspases were activated by safrole oxide during the apoptosis.	safrole oxide	72-85	caspase 8	Homo sapiens	45-53
16242324-3	2006	The data showed that the activity of caspase-3, -8, and -9 was significantly enhanced by the compound, which suggested that safrole oxide might be used as a caspase promoter to initiate lung cancer cell apoptosis.	safrole oxide	124-137	caspase 8	Homo sapiens	37-44
16397262-7	2006	Doxazosin-induced apoptosis was blocked by specific caspase-8 inhibitors, supporting the functional involvement of caspase-8 in doxazosin-induced apoptosis.	Doxazosin	0-9	caspase 8	Homo sapiens	52-61
16397262-7	2006	Doxazosin-induced apoptosis was blocked by specific caspase-8 inhibitors, supporting the functional involvement of caspase-8 in doxazosin-induced apoptosis.	Doxazosin	0-9	caspase 8	Homo sapiens	115-124
16397262-7	2006	Doxazosin-induced apoptosis was blocked by specific caspase-8 inhibitors, supporting the functional involvement of caspase-8 in doxazosin-induced apoptosis.	Doxazosin	128-137	caspase 8	Homo sapiens	52-61
16397262-7	2006	Doxazosin-induced apoptosis was blocked by specific caspase-8 inhibitors, supporting the functional involvement of caspase-8 in doxazosin-induced apoptosis.	Doxazosin	128-137	caspase 8	Homo sapiens	115-124
16397262-9	2006	Doxazosin increased FADD recruitment and subsequent caspase-8 activation, implicating Fas-mediated apoptosis as the underlying mechanism of the effect of doxazosin in prostate cells.	Doxazosin	0-9	caspase 8	Homo sapiens	52-61
15965903-6	2006	DFMO decreased caspase-8 activity and procaspase-8 content, an apical caspase essential for TNF-induced apoptosis.	Eflornithine	0-4	caspase 8	Homo sapiens	15-24
16732410-6	2006	A significant increase of activated caspase-1 in donors, of caspase-8 in patients and caspase-9 in patients and donors after cryopreservation were found, whereas, the application of 14% glycerol resulted in higher amounts of activated caspase than did 7% glycerol.	Glycerol	186-194	caspase 8	Homo sapiens	60-69
16522534-9	2006	Caffeine at concentrations higher than 100 microM significantly increased cleaved caspase-9, caspase-3 and PARP expression in HUVECs at 24-h treatment compared with untreated cultures, whereas 30 microM caffeine significantly increased only caspase-3 expression at 24 h. Caffeine did not affect cleaved caspase-8 expression at 48 h. These results suggest that high concentrations of caffeine inhibit cell growth of HUVECs and induce apoptosis through the caspase-9 pathway.	Caffeine	0-8	caspase 8	Homo sapiens	303-312
16368960-9	2006	Glutamine or alanyl-glutamine significantly reduced TxA-induced apoptosis of T84 cells by 47% and inhibited activation of caspase 8.	Glutamine	0-9	caspase 8	Homo sapiens	122-131
16368960-9	2006	Glutamine or alanyl-glutamine significantly reduced TxA-induced apoptosis of T84 cells by 47% and inhibited activation of caspase 8.	alanylglutamine	13-29	caspase 8	Homo sapiens	122-131
16368960-12	2006	Glutamine and alanyl-glutamine inhibited the apoptosis of T84 cells by preventing caspase 8 activation and reduced TxA-induced intestinal secretion and disruption.	Glutamine	0-9	caspase 8	Homo sapiens	82-91
16368960-12	2006	Glutamine and alanyl-glutamine inhibited the apoptosis of T84 cells by preventing caspase 8 activation and reduced TxA-induced intestinal secretion and disruption.	alanylglutamine	14-30	caspase 8	Homo sapiens	82-91
17035713-7	2006	CAA but not acrolein inhibited the cysteine proteases caspase-3, caspase-8 and cathepsin B.	chloroacetaldehyde	0-3	caspase 8	Homo sapiens	65-74
16051289-7	2006	Meanwhile, immunoblotting analysis also showed that the co-administration of esculetin and Taxol could increase the expression of Bax and the cytosolic release of cytochrome C and enhance the expression of Fas and Fas ligand while the activation of caspase-8 and caspase-3 was also increased.	esculetin	77-86	caspase 8	Homo sapiens	249-258
16965246-6	2006	The DATS-induced DNA fragmentation was significantly attenuated in the presence of pan-caspase inhibitor zVAD-fmk and specific inhibitors of caspase-9 (zLEHD-fmk) and caspase-8 (zIETD-fmk).	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	178-187	caspase 8	Homo sapiens	167-176
16931898-5	2006	In addition, T and 5alpha-DHT induced proteolytic cleavage of caspase 8 and inhibited proliferation of DPC at 10(-5) M. High concentrations of T and 5alpha-DHT were needed to induce apoptotic effects in DPC.	Dihydrotestosterone	19-29	caspase 8	Homo sapiens	62-71
16931898-5	2006	In addition, T and 5alpha-DHT induced proteolytic cleavage of caspase 8 and inhibited proliferation of DPC at 10(-5) M. High concentrations of T and 5alpha-DHT were needed to induce apoptotic effects in DPC.	Dihydrotestosterone	149-159	caspase 8	Homo sapiens	62-71
16051289-7	2006	Meanwhile, immunoblotting analysis also showed that the co-administration of esculetin and Taxol could increase the expression of Bax and the cytosolic release of cytochrome C and enhance the expression of Fas and Fas ligand while the activation of caspase-8 and caspase-3 was also increased.	Paclitaxel	91-96	caspase 8	Homo sapiens	249-258
16246840-1	2005	Stimulation of cell surface Fas (CD95) results in recruitment of cytoplasmic proteins and activation of caspase-8, which in turn activates downstream effector caspases leading to programmed cell death.	ammonium ferrous sulfate	28-31	caspase 8	Homo sapiens	104-113
16208414-3	2005	We show that A3D8 induces activation of both initiator caspase-8 and -9 and effector caspase-3 and -7 but only inhibition of caspase-3/7 and caspase-8 reduces A3D8-induced apoptosis.	a3d8	13-17	caspase 8	Homo sapiens	55-71
16246840-0	2005	Nitric oxide negatively regulates Fas CD95-induced apoptosis through inhibition of ubiquitin-proteasome-mediated degradation of FLICE inhibitory protein.	Nitric Oxide	0-12	caspase 8	Homo sapiens	128-133
16246840-0	2005	Nitric oxide negatively regulates Fas CD95-induced apoptosis through inhibition of ubiquitin-proteasome-mediated degradation of FLICE inhibitory protein.	ammonium ferrous sulfate	34-37	caspase 8	Homo sapiens	128-133
16215673-5	2005	However, when Apo2L/TRAIL was combined with the Bcl-xL inhibitor, BH3I-2", it induced apoptosis synergistically through activation of Caspase-8 and the proapoptotic Bcl-2 family member Bid, resulting in the activation of effector Caspase-3 and proteolytic cleavage of Poly(ADP-ribose) polymerase, events that were blocked by the pan-caspase inhibitor zVAD-fmk.	BH3I-2'	66-72	caspase 8	Homo sapiens	134-143
16228292-5	2005	Cisplatin exerted same effects on cell viability and apoptosis in both cells, but released smaller amounts of cytochrome c while activated more caspase-8 in MCF-7/E6.	Cisplatin	0-9	caspase 8	Homo sapiens	144-153
16364918-1	2005	The death-inducing signaling complex (DISC) comprising Fas, Fas-associated death domain (FADD), and caspase-8/10 is assembled via homotypic associations between death domains (DDs) of Fas and FADD and between death effector domains (DEDs) of FADD and caspase-8/10.	fadd	89-93	caspase 8	Homo sapiens	251-260
16364918-1	2005	The death-inducing signaling complex (DISC) comprising Fas, Fas-associated death domain (FADD), and caspase-8/10 is assembled via homotypic associations between death domains (DDs) of Fas and FADD and between death effector domains (DEDs) of FADD and caspase-8/10.	ammonium ferrous sulfate	60-63	caspase 8	Homo sapiens	251-260
16364918-1	2005	The death-inducing signaling complex (DISC) comprising Fas, Fas-associated death domain (FADD), and caspase-8/10 is assembled via homotypic associations between death domains (DDs) of Fas and FADD and between death effector domains (DEDs) of FADD and caspase-8/10.	fadd	192-196	caspase 8	Homo sapiens	100-109
16364918-1	2005	The death-inducing signaling complex (DISC) comprising Fas, Fas-associated death domain (FADD), and caspase-8/10 is assembled via homotypic associations between death domains (DDs) of Fas and FADD and between death effector domains (DEDs) of FADD and caspase-8/10.	fadd	192-196	caspase 8	Homo sapiens	251-260
16364918-1	2005	The death-inducing signaling complex (DISC) comprising Fas, Fas-associated death domain (FADD), and caspase-8/10 is assembled via homotypic associations between death domains (DDs) of Fas and FADD and between death effector domains (DEDs) of FADD and caspase-8/10.	fadd	192-196	caspase 8	Homo sapiens	100-109
16364918-1	2005	The death-inducing signaling complex (DISC) comprising Fas, Fas-associated death domain (FADD), and caspase-8/10 is assembled via homotypic associations between death domains (DDs) of Fas and FADD and between death effector domains (DEDs) of FADD and caspase-8/10.	fadd	192-196	caspase 8	Homo sapiens	251-260
16361572-10	2005	Caspase-3 and caspase-8 activity also increased significantly in docetaxel-treated SKOV3 and HeyA8 cells but not in the taxane-resistant cells.	Docetaxel	65-74	caspase 8	Homo sapiens	14-23
16040627-7	2005	Collectively, our results indicate that alpha,beta-unsaturated aldehydes can inhibit constitutive neutrophil apoptosis by common mechanisms, involving changes in cellular GSH status resulting in reduced activation of initiator caspases as well as inactivation of caspase-3 by modification of its critical cysteine residue.	alpha,beta-unsaturated aldehydes	40-72	caspase 8	Homo sapiens	227-235
16040627-7	2005	Collectively, our results indicate that alpha,beta-unsaturated aldehydes can inhibit constitutive neutrophil apoptosis by common mechanisms, involving changes in cellular GSH status resulting in reduced activation of initiator caspases as well as inactivation of caspase-3 by modification of its critical cysteine residue.	Glutathione	171-174	caspase 8	Homo sapiens	227-235
16157660-3	2005	Here we show that pyrimethamine, used at a pharmacologically relevant concentration, induced per se apoptosis of activated lymphocytes via the activation of the caspase-8- and caspase-10-dependent cascade and subsequent mitochondrial depolarization.	Pyrimethamine	18-31	caspase 8	Homo sapiens	161-170
16208414-3	2005	We show that A3D8 induces activation of both initiator caspase-8 and -9 and effector caspase-3 and -7 but only inhibition of caspase-3/7 and caspase-8 reduces A3D8-induced apoptosis.	a3d8	13-17	caspase 8	Homo sapiens	55-64
16208414-4	2005	Moreover, A3D8 induces mitochondrial alterations (decrease in mitochondrial membrane potential DeltaPsi m and cytochrome c release), which are reduced by caspase-8 inhibitor, suggesting that caspase-8 is primarily involved in A3D8-induced apoptosis of NB4 cells.	a3d8	10-14	caspase 8	Homo sapiens	154-163
16208414-4	2005	Moreover, A3D8 induces mitochondrial alterations (decrease in mitochondrial membrane potential DeltaPsi m and cytochrome c release), which are reduced by caspase-8 inhibitor, suggesting that caspase-8 is primarily involved in A3D8-induced apoptosis of NB4 cells.	a3d8	10-14	caspase 8	Homo sapiens	191-200
16208414-4	2005	Moreover, A3D8 induces mitochondrial alterations (decrease in mitochondrial membrane potential DeltaPsi m and cytochrome c release), which are reduced by caspase-8 inhibitor, suggesting that caspase-8 is primarily involved in A3D8-induced apoptosis of NB4 cells.	a3d8	226-230	caspase 8	Homo sapiens	154-163
16208414-4	2005	Moreover, A3D8 induces mitochondrial alterations (decrease in mitochondrial membrane potential DeltaPsi m and cytochrome c release), which are reduced by caspase-8 inhibitor, suggesting that caspase-8 is primarily involved in A3D8-induced apoptosis of NB4 cells.	a3d8	226-230	caspase 8	Homo sapiens	191-200
16412349-15	2005	After treatment with VPA, the level of caspase 3 in U937 increased from (14.09 +/- 1.19)% to (32.30 +/- 2.47)%, and caspase 8 from (4.58 +/- 1.41)% to (86.47 +/- 3.26)% (P &lt; 0.01), but there was no significant change in caspase 9 [(13.25 +/- 3.11)% and (10.95 +/- 1.30)%].	Valproic Acid	21-24	caspase 8	Homo sapiens	116-125
16183855-0	2005	Apoptosis induced by a new member of saponin family is mediated through caspase-8-dependent cleavage of Bcl-2.	Saponins	37-44	caspase 8	Homo sapiens	72-81
16373712-5	2005	In the search of the molecular mechanisms involved in the sensitization activity of 3,3"-diindolylmethane, we found that combined treatment of 3,3"-diindolylmethane and TRAIL led to significant down-regulation of the cellular FLICE inhibitory protein expression (c-FLIP).	3,3'-diindolylmethane	84-105	caspase 8	Homo sapiens	226-231
16373712-5	2005	In the search of the molecular mechanisms involved in the sensitization activity of 3,3"-diindolylmethane, we found that combined treatment of 3,3"-diindolylmethane and TRAIL led to significant down-regulation of the cellular FLICE inhibitory protein expression (c-FLIP).	3,3'-diindolylmethane	143-164	caspase 8	Homo sapiens	226-231
16179347-0	2005	Fas-, caspase 8-, and caspase 3-dependent signaling regulates the activity of the aminophospholipid translocase and phosphatidylserine externalization in human erythrocytes.	aminophospholipid	82-99	caspase 8	Homo sapiens	6-15
16179347-5	2005	In support of our contention that caspases play a functional role in the mature red cell, the oxidatively stressed red cell recapitulated apoptotic events, including translocation of Fas into rafts, formation of a Fas-associated complex, and activation of caspases 8 and 3.	ammonium ferrous sulfate	183-186	caspase 8	Homo sapiens	34-42
16179347-5	2005	In support of our contention that caspases play a functional role in the mature red cell, the oxidatively stressed red cell recapitulated apoptotic events, including translocation of Fas into rafts, formation of a Fas-associated complex, and activation of caspases 8 and 3.	ammonium ferrous sulfate	214-217	caspase 8	Homo sapiens	34-42
16275996-8	2005	Guggulsterone treatment resulted in cleavage (activation) of caspase-9, caspase-8, and caspase-3, and guggulsterone-induced cell death was significantly attenuated in the presence of general caspase inhibitor as well as specific inhibitors of caspase-9 and caspase-8.	pregna-4,17-diene-3,16-dione	0-13	caspase 8	Homo sapiens	72-81
16289096-10	2005	In addition, caspase-8-deficient Jurkat T cells are resistant to Fas- and TNF-alpha-induced cell death.	ammonium ferrous sulfate	65-68	caspase 8	Homo sapiens	13-22
15906362-7	2005	These results indicate that TQ-induced apoptosis is associated with the activation of caspases 8, 9 and 3, with caspase-8 acting as an upstream activator.	thymoquinone	28-30	caspase 8	Homo sapiens	86-105
15906362-7	2005	These results indicate that TQ-induced apoptosis is associated with the activation of caspases 8, 9 and 3, with caspase-8 acting as an upstream activator.	thymoquinone	28-30	caspase 8	Homo sapiens	112-121
15906362-0	2005	Thymoquinone induces apoptosis through activation of caspase-8 and mitochondrial events in p53-null myeloblastic leukemia HL-60 cells.	thymoquinone	0-12	caspase 8	Homo sapiens	53-62
15906362-4	2005	The apoptosis induced by TQ was inhibited by a general caspase inhibitor, z-VAD-FMK; a caspase-3-specific inhibitor, z-DEVD-FMK; as well as a caspase-8-specific inhibitor, z-IETD-FMK.	thymoquinone	25-27	caspase 8	Homo sapiens	55-62
15906362-4	2005	The apoptosis induced by TQ was inhibited by a general caspase inhibitor, z-VAD-FMK; a caspase-3-specific inhibitor, z-DEVD-FMK; as well as a caspase-8-specific inhibitor, z-IETD-FMK.	thymoquinone	25-27	caspase 8	Homo sapiens	142-151
15906362-5	2005	Moreover, the caspase-8 inhibitor blocked the TQ-induced activation of caspase-3, PARP cleavage and the release of cytochrome c from mitochondria into the cytoplasm.	thymoquinone	46-48	caspase 8	Homo sapiens	14-23
16309197-5	2005	Western blot analysis indicated that the induction of apoptosis by GA and ursolic acid was accompanied with an activation of caspase-8 and a reduction in the anti-apoptotic proteins, Bcl-2 and Bcl-xL, although the pro-apoptotic proteins, Bax and Bak, remained unaffected.	Glycyrrhetinic Acid	67-69	caspase 8	Homo sapiens	125-134
16309197-5	2005	Western blot analysis indicated that the induction of apoptosis by GA and ursolic acid was accompanied with an activation of caspase-8 and a reduction in the anti-apoptotic proteins, Bcl-2 and Bcl-xL, although the pro-apoptotic proteins, Bax and Bak, remained unaffected.	ursolic acid	74-86	caspase 8	Homo sapiens	125-134
16275996-8	2005	Guggulsterone treatment resulted in cleavage (activation) of caspase-9, caspase-8, and caspase-3, and guggulsterone-induced cell death was significantly attenuated in the presence of general caspase inhibitor as well as specific inhibitors of caspase-9 and caspase-8.	pregna-4,17-diene-3,16-dione	0-13	caspase 8	Homo sapiens	257-266
16275996-8	2005	Guggulsterone treatment resulted in cleavage (activation) of caspase-9, caspase-8, and caspase-3, and guggulsterone-induced cell death was significantly attenuated in the presence of general caspase inhibitor as well as specific inhibitors of caspase-9 and caspase-8.	pregna-4,17-diene-3,16-dione	102-115	caspase 8	Homo sapiens	257-266
16151646-4	2005	There was minimal effect on MGd-induced apoptosis by the caspase inhibitor z-VAD-fmk, even though caspase-3 activity (as measured by DEVD-cleavage) was completely inhibited.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	75-84	caspase 8	Homo sapiens	57-64
16137654-5	2005	Of several analogs of HU44 that were made, the beta-Asp methyl ester (2) is an effective inhibitor against caspase-3 and caspase-8, and less effective against caspase-1.	beta-asp methyl ester	47-68	caspase 8	Homo sapiens	121-130
15982670-7	2005	The apoptotic inhibition of myricetin is associated with inhibition of TNF-alpha and IL-1beta-mediated Fas expression and enhancement of FLIP expression, resulting in a decrease of caspase-8 and caspase-3 activation.	myricetin	28-37	caspase 8	Homo sapiens	181-190
16320200-6	2005	A broad-spectrum inhibitor of caspases, Z-Asp-CH (2)-DCB, attenuated the cytotoxicity induced by these compounds, suggesting that JA, JB, JC and JD induced apoptosis through a caspase-dependent pathway.	benzyloxycarbonyl-Asp-CH2OC(O)-2,6-dichlorobenzene	40-56	caspase 8	Homo sapiens	30-38
16320200-6	2005	A broad-spectrum inhibitor of caspases, Z-Asp-CH (2)-DCB, attenuated the cytotoxicity induced by these compounds, suggesting that JA, JB, JC and JD induced apoptosis through a caspase-dependent pathway.	benzyloxycarbonyl-Asp-CH2OC(O)-2,6-dichlorobenzene	40-56	caspase 8	Homo sapiens	30-37
16007134-3	2005	Here, we address a potential role of death receptor signaling through the FADD/caspase-8 death-inducing signaling complex in As2O3-induced cell death.	Arsenic Trioxide	125-130	caspase 8	Homo sapiens	79-88
16007152-5	2005	The broad-specificity caspase inhibitor z-VAD-fmk completely blocked Mcl-1 cleavage induced by PDT, STS or UVC, providing evidence for Mcl-1 as a substrate for caspases.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	40-49	caspase 8	Homo sapiens	160-168
16151646-5	2005	However, MGd-induced apoptosis was reduced to baseline levels by the more potent caspase inhibitor Q-VD-OPh, demonstrating that MGd-induced apoptosis is indeed caspase-dependent.	quinoline-val-asp(OMe)-CH2-OPH	99-107	caspase 8	Homo sapiens	81-88
16151646-5	2005	However, MGd-induced apoptosis was reduced to baseline levels by the more potent caspase inhibitor Q-VD-OPh, demonstrating that MGd-induced apoptosis is indeed caspase-dependent.	quinoline-val-asp(OMe)-CH2-OPH	99-107	caspase 8	Homo sapiens	160-167
16151646-7	2005	Our results demonstrating differential sensitivity of drug-induced apoptosis to caspase inhibitors suggest that the term "caspase-independent apoptosis" cannot be solely defined as apoptosis that is not inhibited by z-VAD-fmk as has been utilized in some published studies.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	216-225	caspase 8	Homo sapiens	80-87
16086031-7	2005	Reactive oxygen species (ROS) were also detected within 1 h after AF treatment, and the antioxidant N-acetyl-L-cysteine (NAC) effectively protected the cells from apoptosis by inhibiting the phosphorylation of p38 MAPK and the activation of caspases.	Reactive Oxygen Species	0-23	caspase 8	Homo sapiens	241-249
16086031-7	2005	Reactive oxygen species (ROS) were also detected within 1 h after AF treatment, and the antioxidant N-acetyl-L-cysteine (NAC) effectively protected the cells from apoptosis by inhibiting the phosphorylation of p38 MAPK and the activation of caspases.	Acetylcysteine	100-119	caspase 8	Homo sapiens	241-249
16080161-9	2005	The methylation status of the caspase 8 gene was determined by bisulfate modification of genomic DNA, cloning, and sequencing.	hydrogen sulfate	63-72	caspase 8	Homo sapiens	30-39
16173963-7	2005	BAY 11-7082- and curcumin-induced cell death was associated with downregulation of Bcl-xL, cyclin D1, XIAP and c-FLIP, followed by caspase-8, poly(ADP-ribose) polymerase cleavage and activation.	3-(4-methylphenylsulfonyl)-2-propenenitrile	0-11	caspase 8	Homo sapiens	131-140
16173963-7	2005	BAY 11-7082- and curcumin-induced cell death was associated with downregulation of Bcl-xL, cyclin D1, XIAP and c-FLIP, followed by caspase-8, poly(ADP-ribose) polymerase cleavage and activation.	Curcumin	17-25	caspase 8	Homo sapiens	131-140
16197575-8	2005	In contrast, beta-epoxide induced a slight increase in caspase-8 activity but had no effect on mitochondrial membrane potential or cytochrome c release.	beta-epoxide	13-25	caspase 8	Homo sapiens	55-64
16186332-10	2005	CONCLUSIONS: Mitomycin-C induced the apoptosis of HTCFs through the activation of intrinsic and extrinsic caspase cascades with mitochondrial dysfunction.	Mitomycin	13-24	caspase 8	Homo sapiens	106-113
16096840-7	2005	Immediately or 24 h after severe exercise, (1) lymphocyte GSH level and MTP had diminished while active caspase-8, -9, and -3 contents and DNA fragmentation had risen; and (2) H2O2 induced- lymphocyte PS exposure and DNA fragmentation were enhanced.	Hydrogen Peroxide	176-180	caspase 8	Homo sapiens	104-125
16227396-4	2005	Sulindac sulfide activated both the caspase-8-dependent and mitochondrial apoptotic pathways.	sulindac sulfide	0-16	caspase 8	Homo sapiens	36-45
15919146-0	2005	Molecular mechanisms of econazole-induced toxicity on human colon cancer cells: G0/G1 cell cycle arrest and caspase 8-independent apoptotic signaling pathways.	Econazole	24-33	caspase 8	Homo sapiens	108-117
16227396-6	2005	Coadministration of sulindac sulfide and the small-molecule Bcl-2 inhibitor HA14-1 increased apoptosis induction and enhanced caspase-8 and caspase-9 cleavage, Bax redistribution, and cytochrome c and second mitochondria-derived activator of caspase release.	sulindac sulfide	20-36	caspase 8	Homo sapiens	126-135
16227396-7	2005	Given that sulindac sulfide activated caspase-8 and increased membrane death receptor (DR4 and DR5) protein levels, we evaluated its combination with the endogenous death receptor ligand tumor necrosis factor-related apoptosis-inducing ligand (TRAIL).	sulindac sulfide	11-27	caspase 8	Homo sapiens	38-47
16112422-3	2005	Gemcitabine treatment of Colo357 cells increased CD95 surface expression, raising the possibility of the involvement of CD95 in gemcitabine-mediated caspase-8 activation.	gemcitabine	0-11	caspase 8	Homo sapiens	149-158
16135376-0	2005	Collapse of mitochondrial membrane potential and caspases activation are early events in okadaic acid-treated Caco-2 cells.	Okadaic Acid	89-101	caspase 8	Homo sapiens	49-57
16112422-3	2005	Gemcitabine treatment of Colo357 cells increased CD95 surface expression, raising the possibility of the involvement of CD95 in gemcitabine-mediated caspase-8 activation.	gemcitabine	128-139	caspase 8	Homo sapiens	149-158
16112422-1	2005	This study investigates the role of caspase-8 and DN-FADD, an inhibitor of CD95-dependent caspase-8 activation, in gemcitabine-induced apoptosis of Colo357 pancreatic cancer cells.	gemcitabine	115-126	caspase 8	Homo sapiens	36-45
16112422-1	2005	This study investigates the role of caspase-8 and DN-FADD, an inhibitor of CD95-dependent caspase-8 activation, in gemcitabine-induced apoptosis of Colo357 pancreatic cancer cells.	gemcitabine	115-126	caspase 8	Homo sapiens	90-99
16166305-9	2005	Elevated DAG in turn activates the delta isoform of phospholipid-dependent serine/threonine protein kinase C, which then accelerates the cleavage of caspase-8.	Diglycerides	9-12	caspase 8	Homo sapiens	149-158
16112422-2	2005	Gemcitabine-mediated apoptosis was monitored by the kinetics of caspase-8 activation and cytochrome c release.	gemcitabine	0-11	caspase 8	Homo sapiens	64-73
16166312-7	2005	GCS-100-induced apoptosis is associated with activation of caspase-8 and caspase-3 followed by proteolytic cleavage of poly(ADP-ribose) polymerase enzyme.	GCS-100	0-7	caspase 8	Homo sapiens	59-68
16166305-9	2005	Elevated DAG in turn activates the delta isoform of phospholipid-dependent serine/threonine protein kinase C, which then accelerates the cleavage of caspase-8.	Phospholipids	52-64	caspase 8	Homo sapiens	149-158
15914674-9	2005	Downstream of the calpain activation simvastatin led to a translocation of Bax to mitochondria in a caspase 8-independent manner.	Simvastatin	37-48	caspase 8	Homo sapiens	100-109
16037944-8	2005	Compared with 5-FU pretreatment, caspase-8 was more efficiently recruited to the DISC in MG132 pretreated cells despite the presence of fewer death receptors and more cFLIP in the DISC.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	89-94	caspase 8	Homo sapiens	33-42
16210785-1	2005	We investigated the role of the caspase activation cascade in apoptosis induced by ionizing radiation or hydrogen peroxide (H(2)O(2)) in human leukemia HL60 cells.	Hydrogen Peroxide	105-122	caspase 8	Homo sapiens	32-39
16210785-4	2005	Activity assay of caspases revealed that caspase-3, -8 and -9 were activated 2 h after exposure to H(2)O(2), whereas in irradiated cells caspase-3 and -9 activation occurred 4 h after exposure but increased caspase-8 activation was not observed.	Water	99-104	caspase 8	Homo sapiens	18-26
16210785-7	2005	Moreover, treatment with the caspase-8 inhibitor Z-IETD-FMK increased cell survival and prevented accumulation of DNA fragments in H(2)O(2)-treated cells, but not in irradiated cells.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	49-59	caspase 8	Homo sapiens	29-38
16170023-3	2005	Glucose withdrawal or paclitaxel increase intracellular ceramide, down-regulate cellular FLICE inhibitory protein (cFLIP), and sensitize cells to TRAIL.	Paclitaxel	22-32	caspase 8	Homo sapiens	89-94
16044419-8	2005	Similarly upon treatment with cisplatin SiHa cells had more activation of caspases compared to that seen in HeLa cells under conditions of NF-kappaB inhibition by biological or chemical inhibitors.	Cisplatin	30-39	caspase 8	Homo sapiens	74-82
16103097-6	2005	Generation of ROS by CCCP was responsible for TRAIL-induced Bax and caspase activation because scavenging ROS completely abrogated apical caspase-8 activation and further downstream events leading to cell death.	Reactive Oxygen Species	14-17	caspase 8	Homo sapiens	138-147
15995977-9	2005	Expression of anti-apoptotic Bcl-2 was down regulated when the cells were treated with XN for 48--72 h. We conclude that induction of apoptosis by downregulation of Bcl-2 and activation of the caspase cascade may contribute to the chemopreventive or therapeutic potential of XN.	xanthohumol	87-89	caspase 8	Homo sapiens	193-200
15995977-9	2005	Expression of anti-apoptotic Bcl-2 was down regulated when the cells were treated with XN for 48--72 h. We conclude that induction of apoptosis by downregulation of Bcl-2 and activation of the caspase cascade may contribute to the chemopreventive or therapeutic potential of XN.	xanthohumol	275-277	caspase 8	Homo sapiens	193-200
16054126-10	2005	Taken together, these studies suggest that PEITC is an apoptotic inducer that acts on the mitochondria and the feedback amplification loop of caspase-8/Bid pathways in PLC/PRF/5 cells.	phenethyl isothiocyanate	43-48	caspase 8	Homo sapiens	142-151
16103097-6	2005	Generation of ROS by CCCP was responsible for TRAIL-induced Bax and caspase activation because scavenging ROS completely abrogated apical caspase-8 activation and further downstream events leading to cell death.	Reactive Oxygen Species	106-109	caspase 8	Homo sapiens	138-147
16010441-13	2005	We also found that etoposide bypassed Fas-FADD interaction in MML-1R by activating caspase-8 and caspase-3.	Etoposide	19-28	caspase 8	Homo sapiens	83-92
16133866-5	2005	The pan-caspase inhibitor Z-VAD-FMK and the caspase-8 inhibitor Z-IETD-FMK could inhibit K562 cell apoptosis.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	64-74	caspase 8	Homo sapiens	44-53
16133866-8	2005	The most striking anti-apoptotic effect though was obtained by the translational inhibitor cycloheximide, which abolished caspase 8 processing, blocked Bid cleavage and maintained the mitochondrial transmembrane potential.	Cycloheximide	91-104	caspase 8	Homo sapiens	122-131
15993097-4	2005	The HAoSMC death was inhibited by a neutralizing anti-TNF receptor 1 (TNFR1) antibody and by the caspase inhibitors of z-VAD and z-DEVD.	haosmc	4-10	caspase 8	Homo sapiens	97-104
15993097-4	2005	The HAoSMC death was inhibited by a neutralizing anti-TNF receptor 1 (TNFR1) antibody and by the caspase inhibitors of z-VAD and z-DEVD.	z-vad	119-124	caspase 8	Homo sapiens	97-104
15993097-4	2005	The HAoSMC death was inhibited by a neutralizing anti-TNF receptor 1 (TNFR1) antibody and by the caspase inhibitors of z-VAD and z-DEVD.	z-devd	129-135	caspase 8	Homo sapiens	97-104
15993097-6	2005	7-Ketocholesterol inhibited translocation of the nuclear factor kappaB (NF-kappaB) subunits of p65 and p50 from the cytosol into the nucleus, increase of NF-kappaB activity, and expression of caspase-8 homolog Fas ligand interleukin-1-converting enzyme inhibitory protein by TNF-alpha.	7-ketocholesterol	0-17	caspase 8	Homo sapiens	192-201
16014680-5	2005	Inhibition of the c-kit tyrosine kinase with imatinib mesylate (1.0-10 micromol/l) induced profound apoptosis in cultured mast cells as judged by typical apoptotic morphology, increased number of apoptotic nucleosomes, and activation of caspases 8 and 9.	Imatinib Mesylate	45-62	caspase 8	Homo sapiens	237-253
16061660-7	2005	SP600125 enhanced cleavage of caspase 3 and caspase 8, the most upstream caspase in the CD95 pathway.	pyrazolanthrone	0-8	caspase 8	Homo sapiens	44-53
16010437-5	2005	ATO activated the intrinsic (mitochondrial) pathway of apoptosis, which involved disrupting mitochondrial membrane potential, increased Bax/Bcl-2 ratio and caspase-9 activation, as well as the extrinsic (death receptor) pathway mediated by Fas and caspase-8 activation.	Arsenic Trioxide	0-3	caspase 8	Homo sapiens	248-257
16129047-0	2005	[Effect of curcumin on caspase 8- and caspase 9- induced apoptosis of lymphoma Raji cell].	Curcumin	11-19	caspase 8	Homo sapiens	23-32
15978942-8	2005	THC treatment of wild-type Jurkat cells caused cytochrome c release, and cleavage of caspase-8, -9, -2, -10, and Bid.	Dronabinol	0-3	caspase 8	Homo sapiens	85-94
16093436-4	2005	In addition, treatment of SKBR-3-LP cells with scFv23/TNF resulted in down-regulation of Akt phosphorylation and induced apoptosis through cleavage of caspase-8, caspase-3, and poly(ADP-ribose) polymerase.	skbr-3-lp	26-35	caspase 8	Homo sapiens	151-160
16129047-6	2005	The expressions of caspase 8 and caspase 9 in Raji cells after treatment with curcumin at 25 micromol/L (IC(50)) and for 24 hours were detected by Western blot.	Curcumin	78-86	caspase 8	Homo sapiens	19-28
16129047-10	2005	It is concluded that the expression of caspase 8 and caspase 9 plays an important role in the proliferation and apoptosis of Raji cells, so that curcumin showed inhibitive effect on Raji cells at various concentrations.	Curcumin	145-153	caspase 8	Homo sapiens	39-48
15802527-2	2005	Immunoblot analysis demonstrates that R-etodolac induces apoptosis characterized by caspase-8, -9, and -3 and PARP (poly-ADP [adenosine diphosphate]-ribose polymerase) cleavage and down-regulation of cyclin D1 expression.	Etodolac	38-48	caspase 8	Homo sapiens	84-105
15894295-5	2005	The apoptotic effect of LCY-2-CHO was diminished by the presence of zVEID-fmk (caspase-6 inhibitor), zIETD-fmk (caspase-8 inhibitor), and zVAD-fmk (non-selective caspase inhibitor), but was not altered by several antioxidants, and cathepsin inhibitor.	9-(2-chlorobenzyl)-9H-carbazole-3-carbaldehyde	24-33	caspase 8	Homo sapiens	112-121
15849201-7	2005	This process serves to feed forward Fas activation, with approximately 2% of full caspase 8 activation sufficient for maximal ASMase translocation, leading to death-inducing signaling complex formation within ceramide-rich platforms, and apoptosis.	Ceramides	209-217	caspase 8	Homo sapiens	82-91
15849201-11	2005	These studies thus define two distinct mechanisms for biologically relevant ASMase activation within rafts; a Fas-mediated mechanism dependent upon caspase 8 and FADD, and a UV-induced mechanism independent of caspase activation.	ammonium ferrous sulfate	110-113	caspase 8	Homo sapiens	148-157
15849201-12	2005	Consistent with this notion, genetic depletion or pharmacologic inhibition of caspase 8 or FADD, which render Jurkat cells incapable of sphingolipid signaling and apoptosis upon Fas ligation, did not impair these events upon UV-C stimulation.	Sphingolipids	136-148	caspase 8	Homo sapiens	78-87
15964311-7	2005	Treatment with 1 microM Cin resulted in an activation of caspase-8 and cleavage of Bid to its truncated form in a time-dependent pattern.	cinnamaldehyde	24-27	caspase 8	Homo sapiens	57-66
16024638-8	2005	Accordingly, it also abrogated CD437-induced up-regulation of DR4, activation of caspase-8 and caspase-3, and increased DNA fragmentation.	CD 437	31-36	caspase 8	Homo sapiens	81-90
16024639-5	2005	Tunicamycin and TRAIL cooperatively activated caspase-8, -10, -9, and -3 and Bid cleavage and this activation was also blocked in the presence of the DR5/Fc chimera.	Tunicamycin	0-11	caspase 8	Homo sapiens	46-72
15940365-2	2005	In the HS-5 hBMSC, TNF-alpha and H2O2 increased intracellular ROS levels and induced cell apoptosis through activation of caspases, JNK and NF-kappaB.	Hydrogen Peroxide	33-37	caspase 8	Homo sapiens	122-130
15922728-0	2005	CD437, a synthetic retinoid, induces apoptosis in human respiratory epithelial cells via caspase-independent mitochondrial and caspase-8-dependent pathways both up-regulated by JNK signaling pathway.	Retinoids	19-27	caspase 8	Homo sapiens	127-136
15922728-3	2005	Apoptosis was abolished by caspase-8 inhibitor z-IETD-fmk which preserved S-phase cells but was weakly inhibited by others selective caspase-inhibitors, indicating that caspase-8 activation was involved.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	47-57	caspase 8	Homo sapiens	27-36
15922728-3	2005	Apoptosis was abolished by caspase-8 inhibitor z-IETD-fmk which preserved S-phase cells but was weakly inhibited by others selective caspase-inhibitors, indicating that caspase-8 activation was involved.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	47-57	caspase 8	Homo sapiens	169-178
15922728-11	2005	In addition, using SP600125, JNK inhibitor, we demonstrated that CD437 activates the JNK-MAP kinase signaling pathway upstream to mitochondrial and caspase-8 pathways.	pyrazolanthrone	19-27	caspase 8	Homo sapiens	148-157
15922728-11	2005	In addition, using SP600125, JNK inhibitor, we demonstrated that CD437 activates the JNK-MAP kinase signaling pathway upstream to mitochondrial and caspase-8 pathways.	CD 437	65-70	caspase 8	Homo sapiens	148-157
15907983-12	2005	Paclitaxel showed anti-proliferate activity through the membrane death receptor (DR)-mediated apoptotic pathway involving activation of caspase-8 with a TRAIL-dependent fashion as well as the mitochondrial-mediated pathway involving down-regulation of bcl-2 by cytochrome c release.	Paclitaxel	0-10	caspase 8	Homo sapiens	136-145
15942663-4	2005	LY294002 increased Hep3B cell susceptibility to chemotherapy-induced apoptosis by enhancing the expression of DR4 and DR5 and the activation of caspase-8 and -3.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	0-8	caspase 8	Homo sapiens	144-160
16008108-5	2005	In contrast, treatment with 20 microM gamma-tocotrienol (cytotoxic dose) resulted in caspase-8 and -3 activation and apoptosis.	plastochromanol 8	38-55	caspase 8	Homo sapiens	85-101
15985761-6	2005	TRAIL (100 ng/ml) with LY 294002 (20 micromol/l) activated the extrinsic pathway, causing progressive cleavage of caspase-8 and caspase-3.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	23-32	caspase 8	Homo sapiens	114-123
15864316-6	2005	Cotreatment of these cells with the inhibitor of transcription actinomycin D resulted in a dramatic decrease in cell viability and induced activation of caspase-8.	Dactinomycin	63-76	caspase 8	Homo sapiens	153-162
15864316-8	2005	Inhibitors of caspase-8 or overexpression of FLIP completely blocked apoptosis induced by actinomycin D plus TRAIL cotreatment.	Dactinomycin	90-103	caspase 8	Homo sapiens	14-23
15924153-7	2005	Interestingly, cotreatment of Hank-1 with cycloheximide, a protein synthesis inhibitor, markedly sensitized cells to Fas-mediated apoptosis along with caspase 8 activation and c-FLIP(L) (cellular FLICE inhibitory protein long form) downregulation.	Cycloheximide	42-55	caspase 8	Homo sapiens	151-160
15924153-7	2005	Interestingly, cotreatment of Hank-1 with cycloheximide, a protein synthesis inhibitor, markedly sensitized cells to Fas-mediated apoptosis along with caspase 8 activation and c-FLIP(L) (cellular FLICE inhibitory protein long form) downregulation.	ammonium ferrous sulfate	117-120	caspase 8	Homo sapiens	151-160
15930312-7	2005	Analysis of the TRAIL pathway revealed that caspase-8 processing was enhanced in a p21-dependent fashion in cells exposed to TRAIL and bortezomib as compared with cells treated with TRAIL alone.	Bortezomib	135-145	caspase 8	Homo sapiens	44-53
15896464-5	2005	Ellipticine treatment increased the expression of Fas/APO-1 and its ligands, mFas ligand and sFas ligand, and subsequent activation of caspase-8.	ellipticine	0-11	caspase 8	Homo sapiens	135-144
15915027-11	2005	Sevoflurane-induced apoptosis was blocked by the general caspase inhibitor Z-VAD.fmk.	Sevoflurane	0-11	caspase 8	Homo sapiens	57-64
15915027-11	2005	Sevoflurane-induced apoptosis was blocked by the general caspase inhibitor Z-VAD.fmk.	z-vad	75-80	caspase 8	Homo sapiens	57-64
15930300-5	2005	Concomitant treatment with CDDO or CDDO-Im reverses the TRAIL-resistant phenotype, promoting robust caspase-8 processing and induction of TRAIL-mediated apoptosis in vitro.	2-cyano-3,12-dioxoolean-1,9-dien-28-oic acid	27-31	caspase 8	Homo sapiens	100-109
15930300-5	2005	Concomitant treatment with CDDO or CDDO-Im reverses the TRAIL-resistant phenotype, promoting robust caspase-8 processing and induction of TRAIL-mediated apoptosis in vitro.	1-(2-cyano-3,12-dioxooleana-1,9-dien-28-oyl) imidazole	35-42	caspase 8	Homo sapiens	100-109
15772077-4	2005	These events were inhibited by benzyloxycarbonyl-VAD-fluoromethyl ketone, a broad spectrum caspase inhibitor, indicating that caspases were functionally and actively involved.	benzyloxycarbonyl-vad-fluoromethyl ketone	31-72	caspase 8	Homo sapiens	126-134
16226733-5	2005	Activities of caspases-8, -9, and -3 were increased in resting CD4+ T cells treated with fluvastatin (10 microM).	Fluvastatin	89-100	caspase 8	Homo sapiens	14-36
15726400-0	2005	Apoptosis by gemcitabine in non-small cell lung cancer cell line KNS62 is induced downstream of caspase 8 and is profoundly blocked by Bcl-xL over-expression.	gemcitabine	13-24	caspase 8	Homo sapiens	96-105
15870947-4	2005	Cisplatin treatment induced the activation of caspase-8, -9 and -3 and the release of cytochrome c in apoptosis-sensitive Ma-46.	Cisplatin	0-9	caspase 8	Homo sapiens	46-66
16226733-6	2005	In strongly activated CD4+ T cells, fluvastatin inhibited the activation of caspase-8 induced by PMA/I and increased caspase-9 activity.	Fluvastatin	36-47	caspase 8	Homo sapiens	76-85
16226733-10	2005	In conclusion, fluvastatin induces apoptosis in resting T cells but not in strongly activated T cells, a difference that might be due to the interaction between caspase-8 and caspase-9.	Fluvastatin	15-26	caspase 8	Homo sapiens	161-170
15782141-7	2005	Inhibitors of these caspases suppressed MX3350-1-induced apoptosis.	mx3350-1	40-48	caspase 8	Homo sapiens	20-28
15897598-4	2005	In these models, both SAHA and m-carboxycinnamic acid bis-hydroxamide induced growth arrest and caspase-mediated apoptosis and increased p21 protein levels, retinoblastoma hypophosphorylation, BH3-interacting domain death agonist cleavage, Bax up-regulation, down-regulation of Bcl-2, A1, and Bcl-x(L) expression, and cleavage of poly(ADP-ribose) polymerase and caspase-8, -9, -3, -7, and -2.	Vorinostat	22-26	caspase 8	Homo sapiens	362-391
15677568-8	2005	These results extend the observation that Fas-dependent activation of caspase-8 accounts for apoptosis of early stage MDS erythroid cells and demonstrate for the first time that FADD is a valuable target to correct ineffective erythropoiesis in these syndromes.	ammonium ferrous sulfate	42-45	caspase 8	Homo sapiens	70-79
15677568-8	2005	These results extend the observation that Fas-dependent activation of caspase-8 accounts for apoptosis of early stage MDS erythroid cells and demonstrate for the first time that FADD is a valuable target to correct ineffective erythropoiesis in these syndromes.	fadd	178-182	caspase 8	Homo sapiens	70-79
15897598-4	2005	In these models, both SAHA and m-carboxycinnamic acid bis-hydroxamide induced growth arrest and caspase-mediated apoptosis and increased p21 protein levels, retinoblastoma hypophosphorylation, BH3-interacting domain death agonist cleavage, Bax up-regulation, down-regulation of Bcl-2, A1, and Bcl-x(L) expression, and cleavage of poly(ADP-ribose) polymerase and caspase-8, -9, -3, -7, and -2.	carboxycinnamic acid bishydroxamide	31-69	caspase 8	Homo sapiens	362-391
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	caspase 8	Homo sapiens	116-125
15782135-4	2005	We show here that, in contrast to other caspases such as caspase-9 and -3, caspase-8 can be sumoylated at lysine 156.	Lysine	106-112	caspase 8	Homo sapiens	75-84
16080463-6	2005	Caspase 8 and 9 activities were measured in cells overexpressing Bcl-xL or c-FLIP exposed to docetaxel and paclitaxel using fluorescent substrate cleavage assay.	Docetaxel	93-102	caspase 8	Homo sapiens	0-9
16080463-6	2005	Caspase 8 and 9 activities were measured in cells overexpressing Bcl-xL or c-FLIP exposed to docetaxel and paclitaxel using fluorescent substrate cleavage assay.	Paclitaxel	107-117	caspase 8	Homo sapiens	0-9
15863893-4	2005	We observed that codonoposide 1c caused activation of caspase-8, caspase-9, and caspase-3.	Codonoposide 1c	17-32	caspase 8	Homo sapiens	54-63
15863893-5	2005	A broad caspase inhibitor (z-VAD-fmk), caspase-8 inhibitor (z-IETD-fmk), and caspase-3 inhibitor (z-DEVD-fmk) almost completely suppressed codonoposide 1c-induced DNA fragmentation.	Codonoposide 1c	139-154	caspase 8	Homo sapiens	39-48
15863893-8	2005	Taken together, our data indicate that codonoposide 1c is a potent inducer of apoptosis and facilates its activity via Bid cleavage and translocation to mitochondria, Bax reduction in cytosol, release of cytochrome c and Smac/DIABLO into the cytosol, and subsequently caspase activation, providing a potential mechanism for the cytotoxic activity of codonoposide 1c.	Codonoposide 1c	39-54	caspase 8	Homo sapiens	268-275
15614529-2	2005	In contrast to a previous study, a rapid and dramatic decrease in levels of cellular FLICE (Fas-associated death domain-like IL-1beta-converting enzyme) inhibitory protein (cFLIP) following cycloheximide treatment was observed in all RCCs studied.	Cycloheximide	190-203	caspase 8	Homo sapiens	85-90
15614529-2	2005	In contrast to a previous study, a rapid and dramatic decrease in levels of cellular FLICE (Fas-associated death domain-like IL-1beta-converting enzyme) inhibitory protein (cFLIP) following cycloheximide treatment was observed in all RCCs studied.	Cycloheximide	190-203	caspase 8	Homo sapiens	92-151
15614529-5	2005	Therefore, cycloheximide treatment resulted in an increase in the pro-caspase-8 to cFLIP ratio, which correlated with sensitization to TRAIL-mediated apoptosis.	Cycloheximide	11-24	caspase 8	Homo sapiens	70-79
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	caspase 8	Homo sapiens	77-86
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	caspase 8	Homo sapiens	52-61
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	16-19	caspase 8	Homo sapiens	77-86
15809727-0	2005	Histone deacetylase inhibitors, N-butyric acid and trichostatin A, induce caspase-8- but not caspase-9-dependent apoptosis in human malignant glioma cells.	Fatty Acids	32-46	caspase 8	Homo sapiens	74-83
15875775-6	2005	Using immunocytochemistry staining and cellular caspase-3 activity assay, andrographolide-treated cells showed considerable caspase-3 activation and caspase-8 in PC-3 cells at 4 and 2 hours after treatment, respectively.	andrographolide	74-89	caspase 8	Homo sapiens	149-158
15809727-0	2005	Histone deacetylase inhibitors, N-butyric acid and trichostatin A, induce caspase-8- but not caspase-9-dependent apoptosis in human malignant glioma cells.	trichostatin A	51-65	caspase 8	Homo sapiens	74-83
15809727-10	2005	Taken together, the HDAC inhibitors, N-butyric acid and trichostatin A, induce caspase-8- but not caspase-9-dependent apoptosis with or without p21-mediated G1 arrest in human malignant glioma cells.	Fatty Acids	37-51	caspase 8	Homo sapiens	79-88
15809727-10	2005	Taken together, the HDAC inhibitors, N-butyric acid and trichostatin A, induce caspase-8- but not caspase-9-dependent apoptosis with or without p21-mediated G1 arrest in human malignant glioma cells.	trichostatin A	56-70	caspase 8	Homo sapiens	79-88
15515013-5	2005	Depsipeptide activated caspases-8 and -10, which in turn cleave caspases-3 and -7, leading to apoptotic cell death in both cell lines.	Depsipeptides	0-12	caspase 8	Homo sapiens	23-41
15812552-9	2005	Surprisingly, in GLC4-Adr indomethacin induced caspase-8 and caspase-9 activation as well as Bid cleavage, while both caspase-8 and caspase-9 specific inhibitors blocked indomethacin-induced apoptosis.	Indomethacin	26-38	caspase 8	Homo sapiens	47-56
15817572-6	2005	When nocodazole induced apoptosis was inhibited by the use of inhibitors of the two main apical caspases-8 and -9 in PBMC, the frequencies of micronucleated binucleates (MNCB) increased with inhibition of these caspases confirming that apoptosis can eliminate micronucleated cells.	Nocodazole	5-15	caspase 8	Homo sapiens	96-113
15817572-6	2005	When nocodazole induced apoptosis was inhibited by the use of inhibitors of the two main apical caspases-8 and -9 in PBMC, the frequencies of micronucleated binucleates (MNCB) increased with inhibition of these caspases confirming that apoptosis can eliminate micronucleated cells.	Nocodazole	5-15	caspase 8	Homo sapiens	96-104
15710602-3	2005	Inhibition of the upstream caspase 8 by IETD significantly rescued TNF effects on SK1, yet the caspase 7 inhibitor DEVD failed to have any effect, suggesting that the decline in SK1 occurs downstream of the initiator caspase but upstream of the effector caspase.	IETD	40-44	caspase 8	Homo sapiens	27-36
15863130-13	2005	Additionally, IFNgamma and cisplatin can increase sensitivity to anti-Fas in a subset of HPV-positive cervical cancer cell lines by upregulation of Fas and caspase-8 expression without major changes in p53 levels.	Cisplatin	27-36	caspase 8	Homo sapiens	156-165
15809765-0	2005	IFN-gamma enhances paclitaxel-induced apoptosis that is modulated by activation of caspases 8 and 3 with a concomitant down regulation of the AKT survival pathway in cultured human keratinocytes.	Paclitaxel	19-29	caspase 8	Homo sapiens	83-99
15809765-11	2005	The synergistic effect of these two agents on HaCaT cells relies on a pathway involving caspases 8 and 3, with activity increasing by 48 h. Collectively, our data indicate that i) paclitaxel-induced apoptosis is enhanced by IFN-gamma; ii) the down-regulation of PI3-K/AKT survival pathway may help potentiate the apoptotic effects of paclitaxel and iii) the apoptotic signaling pathways are initiated with the activation of caspases 8 and 3 activities.	Paclitaxel	180-190	caspase 8	Homo sapiens	88-104
15809765-11	2005	The synergistic effect of these two agents on HaCaT cells relies on a pathway involving caspases 8 and 3, with activity increasing by 48 h. Collectively, our data indicate that i) paclitaxel-induced apoptosis is enhanced by IFN-gamma; ii) the down-regulation of PI3-K/AKT survival pathway may help potentiate the apoptotic effects of paclitaxel and iii) the apoptotic signaling pathways are initiated with the activation of caspases 8 and 3 activities.	Paclitaxel	180-190	caspase 8	Homo sapiens	424-440
15812552-9	2005	Surprisingly, in GLC4-Adr indomethacin induced caspase-8 and caspase-9 activation as well as Bid cleavage, while both caspase-8 and caspase-9 specific inhibitors blocked indomethacin-induced apoptosis.	Indomethacin	170-182	caspase 8	Homo sapiens	118-127
15812552-10	2005	In GLC4-Adr, doxorubicin plus indomethacin resulted in elevated caspase activity and a 2.7-fold enhanced sensitivity to doxorubicin.	Doxorubicin	13-24	caspase 8	Homo sapiens	64-71
15812552-10	2005	In GLC4-Adr, doxorubicin plus indomethacin resulted in elevated caspase activity and a 2.7-fold enhanced sensitivity to doxorubicin.	Indomethacin	30-42	caspase 8	Homo sapiens	64-71
15749389-8	2005	Hydrogen peroxide (30 microM) exposure potentiated Be-induced caspase-8 activation, and was also attenuated by MnTBAP.	Hydrogen Peroxide	0-17	caspase 8	Homo sapiens	62-71
15899123-10	2005	CONCLUSION: Shikonin induces HeLa cell apoptosis through the ERK, p53 and caspase pathways.	shikonin	12-20	caspase 8	Homo sapiens	74-81
15572588-2	2005	In neutrophils, however, the broad-spectrum caspase inhibitor z-VAD-fmk enhances tumor necrosis factor-alpha (TNF alpha)-induced cell death, and this has been interpreted as evidence for caspase-dependent and -independent cell death pathways.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	62-71	caspase 8	Homo sapiens	44-51
15572588-2	2005	In neutrophils, however, the broad-spectrum caspase inhibitor z-VAD-fmk enhances tumor necrosis factor-alpha (TNF alpha)-induced cell death, and this has been interpreted as evidence for caspase-dependent and -independent cell death pathways.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	62-71	caspase 8	Homo sapiens	187-194
15572588-5	2005	Boc-D-fmk, a similar broad-spectrum caspase inhibitor, and z-IETD-fmk, a selective caspase-8 inhibitor, caused a concentration-dependent inhibition of only TNF alpha-stimulated apoptosis.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	59-69	caspase 8	Homo sapiens	83-92
15802789-6	2005	To study the molecular mechanisms behind the induction of apoptosis by EGCG, the activity of caspases in MKN-45 cells treated with EGCG was examined.	epigallocatechin gallate	71-75	caspase 8	Homo sapiens	93-101
15802789-6	2005	To study the molecular mechanisms behind the induction of apoptosis by EGCG, the activity of caspases in MKN-45 cells treated with EGCG was examined.	epigallocatechin gallate	131-135	caspase 8	Homo sapiens	93-101
15802789-7	2005	Activity levels of caspases-3, -8 and -9 were elevated in EGCG-treated cells, suggesting that these caspases are involved in the apoptosis induced by EGCG.	epigallocatechin gallate	58-62	caspase 8	Homo sapiens	19-27
15802789-7	2005	Activity levels of caspases-3, -8 and -9 were elevated in EGCG-treated cells, suggesting that these caspases are involved in the apoptosis induced by EGCG.	epigallocatechin gallate	150-154	caspase 8	Homo sapiens	19-27
15661812-0	2005	Antineoplastic cyclic astin analogues kill tumour cells via caspase-mediated induction of apoptosis.	cyclic astin	15-27	caspase 8	Homo sapiens	60-67
15661812-7	2005	We also observed that the cyclic astin induced apoptosis in a human papillary thyroid carcinoma cell line (NPA cell line) and that apoptotis was associated with activation of caspases.	cyclic astin	26-38	caspase 8	Homo sapiens	175-183
15661812-8	2005	The caspase family inhibitor, Z-Val-Asp-(OMe)-FMK, protected NPA cells from cyclic analogue astin-induced apoptosis.	z-val-asp-(ome)-fmk	30-49	caspase 8	Homo sapiens	4-11
15661812-8	2005	The caspase family inhibitor, Z-Val-Asp-(OMe)-FMK, protected NPA cells from cyclic analogue astin-induced apoptosis.	cyclic analogue astin	76-97	caspase 8	Homo sapiens	4-11
15661812-9	2005	To determine which caspase was specifically activated, we assayed caspase activity in astin-treated cells in the presence of specific caspase and 8, 9 or 3 inhibitors, i.e. Z-IETD-FMK, Z-LEHD-FMK Z-DEVD-FMK, which inhibit caspases 8, 9 and 3, respectively.	astin	86-91	caspase 8	Homo sapiens	19-26
15661812-9	2005	To determine which caspase was specifically activated, we assayed caspase activity in astin-treated cells in the presence of specific caspase and 8, 9 or 3 inhibitors, i.e. Z-IETD-FMK, Z-LEHD-FMK Z-DEVD-FMK, which inhibit caspases 8, 9 and 3, respectively.	astin	86-91	caspase 8	Homo sapiens	66-73
15661812-9	2005	To determine which caspase was specifically activated, we assayed caspase activity in astin-treated cells in the presence of specific caspase and 8, 9 or 3 inhibitors, i.e. Z-IETD-FMK, Z-LEHD-FMK Z-DEVD-FMK, which inhibit caspases 8, 9 and 3, respectively.	astin	86-91	caspase 8	Homo sapiens	66-73
15661812-9	2005	To determine which caspase was specifically activated, we assayed caspase activity in astin-treated cells in the presence of specific caspase and 8, 9 or 3 inhibitors, i.e. Z-IETD-FMK, Z-LEHD-FMK Z-DEVD-FMK, which inhibit caspases 8, 9 and 3, respectively.	astin	86-91	caspase 8	Homo sapiens	222-241
15788689-7	2005	The JNK inhibitor SP600125 substantially decreased the activation of caspases and apoptosis induced by MSeA combination with SN38 or etoposide and completely blocked these events induced by MSeA/paclitaxel.	Etoposide	133-142	caspase 8	Homo sapiens	69-77
15626723-5	2005	Asiatic acid treatment triggered the mitochondrial apoptotic pathway indicated by changing Bax/Bcl-2 ratios, cytochrome c release, and caspase-9 activation, but it did not act on Fas/Fas ligand pathways and the activation of caspase-8.	asiatic acid	0-12	caspase 8	Homo sapiens	225-234
15640164-8	2005	These findings reveal a new mechanistic link between Rb-E2F and the extrinsic (caspase 8-mediated) apoptotic pathway.	rb-e2f	53-59	caspase 8	Homo sapiens	79-88
15788689-7	2005	The JNK inhibitor SP600125 substantially decreased the activation of caspases and apoptosis induced by MSeA combination with SN38 or etoposide and completely blocked these events induced by MSeA/paclitaxel.	pyrazolanthrone	18-26	caspase 8	Homo sapiens	69-77
15788689-7	2005	The JNK inhibitor SP600125 substantially decreased the activation of caspases and apoptosis induced by MSeA combination with SN38 or etoposide and completely blocked these events induced by MSeA/paclitaxel.	methylselenic acid	103-107	caspase 8	Homo sapiens	69-77
15615731-6	2005	Finally, we show that the extensive caspase 8 cleavage seen during TRAIL-etoposide synergy is a consequence and not a cause of the apoptotic cascade activated downstream of Bid.	Etoposide	73-82	caspase 8	Homo sapiens	36-45
15637055-1	2005	Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) induces programmed cell death through the caspase activation cascade and translocation of cleaved Bid (tBid) by the apical caspase-8 to mitochondria to induce oligomerization of multidomain Bax and Bak.	tBID	167-171	caspase 8	Homo sapiens	187-196
15788689-7	2005	The JNK inhibitor SP600125 substantially decreased the activation of caspases and apoptosis induced by MSeA combination with SN38 or etoposide and completely blocked these events induced by MSeA/paclitaxel.	methylselenic acid	190-194	caspase 8	Homo sapiens	69-77
15788689-7	2005	The JNK inhibitor SP600125 substantially decreased the activation of caspases and apoptosis induced by MSeA combination with SN38 or etoposide and completely blocked these events induced by MSeA/paclitaxel.	Irinotecan	125-129	caspase 8	Homo sapiens	69-77
15788689-8	2005	The caspase-8 inhibitor zIETDfmk completely abolished apoptosis and caspase-9 and caspase-3 cleavage, whereas the caspase-9 inhibitor zLEHDfmk significantly decreased caspase-3 cleavage and apoptosis but had no effect on caspase-8 cleavage.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	24-32	caspase 8	Homo sapiens	4-13
15788689-8	2005	The caspase-8 inhibitor zIETDfmk completely abolished apoptosis and caspase-9 and caspase-3 cleavage, whereas the caspase-9 inhibitor zLEHDfmk significantly decreased caspase-3 cleavage and apoptosis but had no effect on caspase-8 cleavage.	benzyloxycarbonyl-leucyl-glutamyl-histidyl-aspartic acid fluoromethyl ketone	134-142	caspase 8	Homo sapiens	221-230
15777082-1	2005	The role of mitochondria and apical caspases in apoptosis induced by the benzene metabolite hydroquinone (HQ) remains to be elucidated.	Benzene	73-80	caspase 8	Homo sapiens	36-44
15843887-2	2005	Human cytomegalovirus (HCMV) encodes at least two proteins that directly interfere with the apoptotic signaling pathways, viral inhibitor of caspase-8-induced apoptosis vICA (pUL36), and mitochondria-localized inhibitor of apoptosis vMIA (pUL37 x 1).	vica	169-173	caspase 8	Homo sapiens	141-150
15843887-3	2005	vICA associates with pro-caspase-8 and appears to block its recruitment to the death-inducing signaling complex (DISC), a step preceding caspase-8 activation.	vica	0-4	caspase 8	Homo sapiens	25-34
15843887-3	2005	vICA associates with pro-caspase-8 and appears to block its recruitment to the death-inducing signaling complex (DISC), a step preceding caspase-8 activation.	vica	0-4	caspase 8	Homo sapiens	137-146
15579484-0	2005	Activation of the caspase-8/Bid and Bax pathways in aspirin-induced apoptosis in gastric cancer.	Aspirin	52-59	caspase 8	Homo sapiens	18-27
15579484-7	2005	We showed that aspirin activated caspase-8, caspase-9 and capase-3, cleaved and translocated Bid, induced a conformational change in and translocation of Bax and cytochrome c release.	Aspirin	15-22	caspase 8	Homo sapiens	33-42
15579484-8	2005	In addition, suppression of caspase-8 with the specific inhibitor z-IETD-fmk, as well as the pan-caspase inhibitor z-VAD-fmk, prevented Bid cleavage and subsequent apoptosis.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	66-76	caspase 8	Homo sapiens	28-37
15579484-10	2005	In conclusion, our results identify a role of caspase-8/Bid and activation of Bax as a novel mechanism for aspirin-induced apoptosis in gastric cancer.	Aspirin	107-114	caspase 8	Homo sapiens	46-55
15777082-7	2005	Although ZVAD-sensitive caspase-8 processing occurred in both cell types, pretreatment with either fas-receptor blocking ZB4 or fas-ligand NOK1 neutralizing antibodies did not inhibit HQ-induced apoptosis.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	9-13	caspase 8	Homo sapiens	24-33
15777082-8	2005	In conclusion, our results demonstrate that HQ induced apoptosis in Jurkat cells occurs via a ZVAD-inhibitable, caspase-dependent process, while in HL-60 cells, apoptosis occurs predominantly via caspase-independent mechanisms.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	94-98	caspase 8	Homo sapiens	112-119
15777082-1	2005	The role of mitochondria and apical caspases in apoptosis induced by the benzene metabolite hydroquinone (HQ) remains to be elucidated.	hydroquinone	92-104	caspase 8	Homo sapiens	36-44
15767547-7	2005	A general caspase inhibitor (Z-VAD-FMK) and a specific caspase-8 inhibitor II (Z-IETD-FMK) blocked boswellic acid acetate-induced apoptosis.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	79-89	caspase 8	Homo sapiens	55-64
15750764-4	2005	Fas pathway analysis showed that Fas-resistant apoptosis of Fas-positive myeloma cells parallels FLIP (FLICE/caspase-8-inhibitory protein) expression.	ammonium ferrous sulfate	0-3	caspase 8	Homo sapiens	103-108
15750764-4	2005	Fas pathway analysis showed that Fas-resistant apoptosis of Fas-positive myeloma cells parallels FLIP (FLICE/caspase-8-inhibitory protein) expression.	ammonium ferrous sulfate	33-36	caspase 8	Homo sapiens	103-108
15750764-7	2005	Further analysis showed that manumycin-induced apoptosis involved caspases activation and was prevented by the addition of caspases specific inhibitors.	manumycin	29-38	caspase 8	Homo sapiens	66-74
15750764-7	2005	Further analysis showed that manumycin-induced apoptosis involved caspases activation and was prevented by the addition of caspases specific inhibitors.	manumycin	29-38	caspase 8	Homo sapiens	123-131
15688188-10	2005	Moreover, rutin reduced RANK protein, whereas 17beta-oestradiol and quercetin promoted apoptosis by cleavage of caspase-8 and caspase-3.	Estradiol	46-63	caspase 8	Homo sapiens	112-121
15688188-10	2005	Moreover, rutin reduced RANK protein, whereas 17beta-oestradiol and quercetin promoted apoptosis by cleavage of caspase-8 and caspase-3.	Quercetin	68-77	caspase 8	Homo sapiens	112-121
15688188-12	2005	Thus, the anti-resorbing properties of flavonols are mainly mediated by ER proteins through the inhibition of RANK protein or the activation of caspases.	Flavonols	39-48	caspase 8	Homo sapiens	144-152
15576458-0	2005	Dexamethasone induces apoptosis in proliferative chondrocytes through activation of caspases and suppression of the Akt-phosphatidylinositol 3"-kinase signaling pathway.	Dexamethasone	0-13	caspase 8	Homo sapiens	84-92
15576458-5	2005	Apoptosis was associated with cleavage of poly-ADP-ribose polymerase (PARP) and alpha-fodrin and activation of caspases-8, -9, and -3 (Western), an effect that was counteracted when chondrocytes were cocultured with Dexa + IGF-I.	Dexamethasone	216-220	caspase 8	Homo sapiens	111-133
15576458-6	2005	Inhibitors for caspases-8, -9, and -3 (50 microm each) equally suppressed Dexa-induced apoptosis (P &lt; 0.01).	Dexamethasone	74-78	caspase 8	Homo sapiens	15-37
15576458-13	2005	We conclude that Dexa-induced apoptosis is caspase dependent with an early activation of caspase-8.	Dexamethasone	17-21	caspase 8	Homo sapiens	43-50
15576458-13	2005	We conclude that Dexa-induced apoptosis is caspase dependent with an early activation of caspase-8.	Dexamethasone	17-21	caspase 8	Homo sapiens	89-98
15767547-7	2005	A general caspase inhibitor (Z-VAD-FMK) and a specific caspase-8 inhibitor II (Z-IETD-FMK) blocked boswellic acid acetate-induced apoptosis.	boswellic acid acetate	99-121	caspase 8	Homo sapiens	55-64
15767547-9	2005	These data taken together suggest that boswellic acid acetate induces myeloid leukemia cell apoptosis through activation of caspase-8 by induced expression of DR4 and DR5, and that the activated caspase-8 either directly activates caspase-3 by cleavage or indirectly by cleaving Bid, which in turn decreases mitochondria membrane potential.	boswellic acid acetate	39-61	caspase 8	Homo sapiens	124-133
15611097-6	2005	Using an in vivo affinity labeling approach, we demonstrate that caspase-8 is activated in etoposide-treated cells in vivo in the absence of the receptor-induced death-inducing signaling complex formation.	Etoposide	91-100	caspase 8	Homo sapiens	65-74
15770551-2	2005	Indeed, we have found that an ent-kaurene diterpene, ent-11alpha-hydroxy-16-kauren-15-one (KD), induced apoptosis via caspase-8 activation in human promyelocytic leukemia HL-60 cells.	Diterpenes, Kaurane	30-41	caspase 8	Homo sapiens	118-127
15770551-2	2005	Indeed, we have found that an ent-kaurene diterpene, ent-11alpha-hydroxy-16-kauren-15-one (KD), induced apoptosis via caspase-8 activation in human promyelocytic leukemia HL-60 cells.	Diterpenes	42-51	caspase 8	Homo sapiens	118-127
15770551-2	2005	Indeed, we have found that an ent-kaurene diterpene, ent-11alpha-hydroxy-16-kauren-15-one (KD), induced apoptosis via caspase-8 activation in human promyelocytic leukemia HL-60 cells.	ent-11alpha-hydroxy-16-kauren-15-one	53-89	caspase 8	Homo sapiens	118-127
15770551-6	2005	Pretreatment with SB203580, a specific inhibitor of p38 (MAPK), attenuated induction of apoptosis by KD and inhibited activation of caspase-8.	SB 203580	18-26	caspase 8	Homo sapiens	132-141
15770551-7	2005	Cleavage of Bid, a typical substrate of caspase-8, was also inhibited by treatment with SB203580, suggesting that activation of p38 (MAPK) occurs upstream of caspase-8 during KD-induced apoptosis.	SB 203580	88-96	caspase 8	Homo sapiens	40-49
15770551-7	2005	Cleavage of Bid, a typical substrate of caspase-8, was also inhibited by treatment with SB203580, suggesting that activation of p38 (MAPK) occurs upstream of caspase-8 during KD-induced apoptosis.	SB 203580	88-96	caspase 8	Homo sapiens	158-167
15720974-7	2005	The BVDV NS3Delta50-induced apoptotic process was inhibited by caspase-8- and -9-specific peptide inhibitors (Z-IETD-FMK and Z-LEHD-FMK).	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	110-120	caspase 8	Homo sapiens	63-72
15720974-7	2005	The BVDV NS3Delta50-induced apoptotic process was inhibited by caspase-8- and -9-specific peptide inhibitors (Z-IETD-FMK and Z-LEHD-FMK).	benzyloxycarbonyl-leucyl-glutamyl-histidyl-aspartic acid fluoromethyl ketone	125-135	caspase 8	Homo sapiens	63-72
15608676-14	2005	Additionally, we show that Chk1 deficiency potentiates 5-FU efficacy through the preferential induction of the caspase-8 pathway and subsequent caspase-3 activation.	Fluorouracil	55-59	caspase 8	Homo sapiens	111-120
15528219-5	2005	Fluorescence-activated cell sorting analysis of Annexin V/propidium iodide (PI) stained cells revealed that alpha-santalol induces a strong apoptosis as early as 3 h post-treatment, which increases further in a concentration- and a time-dependent manner up to 12 h. Mechanistic studies showed an involvement of caspase-3 activation and poly(ADP-ribose) polymerase cleavage through activation of upstream caspase-8 and -9.	a-santalol	108-122	caspase 8	Homo sapiens	404-420
15528219-7	2005	Pre-treatment of cells with caspase-8 or -9 inhibitor, pan caspase inhibitor or cycloheximide totally blocked alpha-santalol-caused caspase-3 activity and cleavage, but only partially reversed apoptotic cell death.	a-santalol	110-124	caspase 8	Homo sapiens	28-43
15498850-4	2005	15d-PGJ(2)-induced apoptosis occurs through multiple caspase activation pathways involving caspase-8 and caspase-9, and is prevented by pretreatment with the pan-caspase inhibitor ZVAD (z-Val-Ala-Asp).	15d-pgj	0-7	caspase 8	Homo sapiens	53-60
15498850-4	2005	15d-PGJ(2)-induced apoptosis occurs through multiple caspase activation pathways involving caspase-8 and caspase-9, and is prevented by pretreatment with the pan-caspase inhibitor ZVAD (z-Val-Ala-Asp).	15d-pgj	0-7	caspase 8	Homo sapiens	91-100
15498850-4	2005	15d-PGJ(2)-induced apoptosis occurs through multiple caspase activation pathways involving caspase-8 and caspase-9, and is prevented by pretreatment with the pan-caspase inhibitor ZVAD (z-Val-Ala-Asp).	15d-pgj	0-7	caspase 8	Homo sapiens	91-98
15498850-4	2005	15d-PGJ(2)-induced apoptosis occurs through multiple caspase activation pathways involving caspase-8 and caspase-9, and is prevented by pretreatment with the pan-caspase inhibitor ZVAD (z-Val-Ala-Asp).	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	180-184	caspase 8	Homo sapiens	53-60
15498850-4	2005	15d-PGJ(2)-induced apoptosis occurs through multiple caspase activation pathways involving caspase-8 and caspase-9, and is prevented by pretreatment with the pan-caspase inhibitor ZVAD (z-Val-Ala-Asp).	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	180-184	caspase 8	Homo sapiens	91-100
15498850-4	2005	15d-PGJ(2)-induced apoptosis occurs through multiple caspase activation pathways involving caspase-8 and caspase-9, and is prevented by pretreatment with the pan-caspase inhibitor ZVAD (z-Val-Ala-Asp).	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	180-184	caspase 8	Homo sapiens	91-98
15498850-4	2005	15d-PGJ(2)-induced apoptosis occurs through multiple caspase activation pathways involving caspase-8 and caspase-9, and is prevented by pretreatment with the pan-caspase inhibitor ZVAD (z-Val-Ala-Asp).	z-val-ala-asp	186-199	caspase 8	Homo sapiens	53-60
15498850-4	2005	15d-PGJ(2)-induced apoptosis occurs through multiple caspase activation pathways involving caspase-8 and caspase-9, and is prevented by pretreatment with the pan-caspase inhibitor ZVAD (z-Val-Ala-Asp).	z-val-ala-asp	186-199	caspase 8	Homo sapiens	91-100
15498850-4	2005	15d-PGJ(2)-induced apoptosis occurs through multiple caspase activation pathways involving caspase-8 and caspase-9, and is prevented by pretreatment with the pan-caspase inhibitor ZVAD (z-Val-Ala-Asp).	z-val-ala-asp	186-199	caspase 8	Homo sapiens	91-98
15710431-7	2005	Immunoprecipition of Fas death-inducing signaling complex (DISC) and Western blot suggested that the actin depolymerization accelerated caspase-8 activation, while LPA inhibited the association and activation of caspase-8 at the DISC.	lysophosphatidic acid	164-167	caspase 8	Homo sapiens	212-221
15661236-11	2005	DISC staining proved that LPA inhibited Fas receptor aggregation and caspase-8 activation at the membrane, which further inhibited caspase-3 and 7 activation in the cytosol.	lysophosphatidic acid	26-29	caspase 8	Homo sapiens	69-78
15684474-0	2005	Dracorhodin perchlorate induces A375-S2 cell apoptosis via accumulation of p53 and activation of caspases.	dracorhodin	0-23	caspase 8	Homo sapiens	97-105
15684474-8	2005	Taken together, dracorhodin perchlorate induces apoptosis in A375-S2 cells via accumulation of p53, alters the Bax/Bcl-2 ratio, and activates caspases and p38/JNK MAPKs.	dracorhodin	16-39	caspase 8	Homo sapiens	142-150
15723652-6	2005	Enzymatic activity measurements of caspases revealed that caspase-3 and caspase-9 are activated in phytosphingosine-induced apoptosis, but there is little activation of caspase-8 suggesting that phytosphingosine influences mitochondrial functions.	phytosphingosine	195-211	caspase 8	Homo sapiens	35-43
15657078-2	2005	We show here that TNFR2-mediated apoptosis in PVC60 cells can be blocked by the broad-spectrum caspase inhibitor zVAD-fmk, the caspase-8 inhibitor zIETD-fmk and by CrmA, a viral inhibitor of caspase-1 and caspase-8.	crma	164-168	caspase 8	Homo sapiens	205-214
15607733-6	2005	These data suggest that amiloride sensitizes both tumor cells to TRAIL-induced apoptosis by promoting Akt dephosphorylation and caspase-8 activation via the intracellular acidification and that Na(+)/H(+) exchanger inhibitors may play an important role in the anti-cancer activity of TRAIL, especially, in TRAIL-resistant tumors with highly active and expressed Akt.	Amiloride	24-33	caspase 8	Homo sapiens	128-137
15607369-6	2005	RA treatment induced cleavage of caspase-8 and PARP in NB4.	Tretinoin	0-2	caspase 8	Homo sapiens	33-42
15713901-6	2005	Addition of irreversible caspase inhibitors (e.g., the pan-caspase inhibitor zVAD-fmk) to G3139-treated cells almost completely blocked cytotoxicity.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	77-85	caspase 8	Homo sapiens	25-32
15713901-6	2005	Addition of irreversible caspase inhibitors (e.g., the pan-caspase inhibitor zVAD-fmk) to G3139-treated cells almost completely blocked cytotoxicity.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	77-85	caspase 8	Homo sapiens	59-66
15713901-6	2005	Addition of irreversible caspase inhibitors (e.g., the pan-caspase inhibitor zVAD-fmk) to G3139-treated cells almost completely blocked cytotoxicity.	oblimersen	90-95	caspase 8	Homo sapiens	25-32
15713901-6	2005	Addition of irreversible caspase inhibitors (e.g., the pan-caspase inhibitor zVAD-fmk) to G3139-treated cells almost completely blocked cytotoxicity.	oblimersen	90-95	caspase 8	Homo sapiens	59-66
15639338-3	2005	The effects of CH-11 were associated with activation of caspase-8, -9, and -3, cleavage of poly(ADP-ribose)polymerase-PARP, and decreased mitochondrial membrane potential (MMP), but these parameters were not significantly changed after PUFA pretreatment.	4-dimethylamino-3',4'-dimethoxychalcone	15-20	caspase 8	Homo sapiens	56-77
15537572-3	2005	Our results suggest that failure to observe cytochrome c release may be due to the use of different buffers because after permeabilization by caspase-8 cleaved human Bid (tBid), cytochrome c dissociation from mitochondria was highly dependent on ionic strength and required 50-80 mm KCl, NaCl, or LiCl.	tBID	171-175	caspase 8	Homo sapiens	142-151
15537572-3	2005	Our results suggest that failure to observe cytochrome c release may be due to the use of different buffers because after permeabilization by caspase-8 cleaved human Bid (tBid), cytochrome c dissociation from mitochondria was highly dependent on ionic strength and required 50-80 mm KCl, NaCl, or LiCl.	Potassium Chloride	283-286	caspase 8	Homo sapiens	142-151
15537572-3	2005	Our results suggest that failure to observe cytochrome c release may be due to the use of different buffers because after permeabilization by caspase-8 cleaved human Bid (tBid), cytochrome c dissociation from mitochondria was highly dependent on ionic strength and required 50-80 mm KCl, NaCl, or LiCl.	Sodium Chloride	288-292	caspase 8	Homo sapiens	142-151
15537572-3	2005	Our results suggest that failure to observe cytochrome c release may be due to the use of different buffers because after permeabilization by caspase-8 cleaved human Bid (tBid), cytochrome c dissociation from mitochondria was highly dependent on ionic strength and required 50-80 mm KCl, NaCl, or LiCl.	Lithium Chloride	297-301	caspase 8	Homo sapiens	142-151
15540114-2	2005	Here, we show that treatment with the histone deacetylase (HDAC) inhibitor FR901228 renders Fas-resistant osteosarcoma cell lines sensitive to Fas-mediated apoptosis by downregulating expression of cellular FLIP (cellular FLICE-inhibitory protein), an inhibitor of Fas-mediated activation of caspase-8.	romidepsin	75-83	caspase 8	Homo sapiens	292-301
15592525-7	2005	In addition, expression of an NF-kappaB-activating domain-deletion mutant of FLASH or transfection of FLASH AS oligonucleotides abolished TNF-alpha and caspase-8, but not phorbol 12-myristate 13-acetate, -induced activation of NF-kappaB.	Oligonucleotides	111-127	caspase 8	Homo sapiens	152-161
15634909-4	2005	Importantly, our data indicate that the effect of wtp53 on the Fas-mediated pathway involves a degradation of short cellular FLICE inhibitory protein resulting in subsequent caspase 8 activation.	ammonium ferrous sulfate	63-66	caspase 8	Homo sapiens	125-130
15634909-4	2005	Importantly, our data indicate that the effect of wtp53 on the Fas-mediated pathway involves a degradation of short cellular FLICE inhibitory protein resulting in subsequent caspase 8 activation.	ammonium ferrous sulfate	63-66	caspase 8	Homo sapiens	174-183
15627477-3	2005	Indeed, we found that treatment of Jurkat cells with 3,4,5-THS, unlike treatment with resveratrol, induced activation of caspase-8 and apoptosis by a Fas-associated death domain (FADD) protein-dependent mechanism without involving the known death ligands CD95 ligand (CD95L), tumor necrosis factor alpha (TNFalpha) and TNF-related apoptosis-inducing ligand (TRAIL).	Resveratrol	53-62	caspase 8	Homo sapiens	121-130
15787279-5	2005	DDE46 enhanced the activity of the pro-apoptotic enzymes Caspase-3, Caspase-6, Caspase-8, and Caspase-9 leading to the apoptotic death of the leukemic cell line Jurkat.	dde46	0-5	caspase 8	Homo sapiens	79-88
15507514-3	2005	The present study supports that such a process triggered by finasteride is caspase dependent with a possible involvement of two effector caspases (caspase-3 and 6) and two initiator caspases (caspase-8 and 9).	Finasteride	60-71	caspase 8	Homo sapiens	192-207
15623796-9	2005	The demethylating agent 5-aza-2"-deoxycytidine restored caspase-8 expression and sensitivity to DR-mediated apoptosis.	Decitabine	24-46	caspase 8	Homo sapiens	56-65
15920677-5	2005	Clavulone II induced the disruption of mitochondrial membrane potential and activation of caspase-8, -9 and -3 in a time- and concentration-dependent manner.	clavulones	0-9	caspase 8	Homo sapiens	90-110
15920677-7	2005	Taken together, it is suggested that low concentrations of clavulone II induce the antiproliferative effect through the down-regulation of cyclin D1 expression and G1 arrest of the cell cycle, while that of high concentration induce the apoptotic cell death via the modulation of members of caspases and Bcl-2 family proteins in HL-60 cells.	clavulone II	59-71	caspase 8	Homo sapiens	291-299
16491956-0	2005	Irinotecan/5-fluorouracil combination induces alterations in mitochondrial membrane potential and caspases on colon cancer cell lines.	Irinotecan	0-10	caspase 8	Homo sapiens	98-106
15541481-4	2005	Triptolide induced apoptosis in MM cells through activation of the cystein protease caspase 8, 9 and 3, and subsequent cleavage of the DNA repair enzyme poly (ADP-ribose) polymerase.	triptolide	0-10	caspase 8	Homo sapiens	84-102
15796160-4	2005	Presence of the pan-caspase inhibitor, Z-VAD-fmk, did not prevent cell detachment, but it did prevent apoptosis of the detached cells indicating that the process of cell detachment, but not apoptosis, is independent of caspase activation.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	39-48	caspase 8	Homo sapiens	20-27
15796160-5	2005	He-CMG-induced apoptosis is associated with activation of the initiator caspases-8, and -9 and the effector caspase-3.	Helium	0-2	caspase 8	Homo sapiens	72-90
16201852-6	2005	A peptide inhibitor of caspase-8 completely blocked SFN-induced apoptosis and that for caspase-9 exerted a major protection; however, neither inhibitor attenuated SFN-induced G2/M arrest.	sulforaphane	52-55	caspase 8	Homo sapiens	23-32
16491956-0	2005	Irinotecan/5-fluorouracil combination induces alterations in mitochondrial membrane potential and caspases on colon cancer cell lines.	Fluorouracil	11-25	caspase 8	Homo sapiens	98-106
16491956-5	2005	In this study, we verified whether the collapse in mitochondrial membrane and the activation of caspases is responsible for increased apoptosis observed with CPT-11/5-FU treatment.	Irinotecan	158-164	caspase 8	Homo sapiens	96-104
16491956-5	2005	In this study, we verified whether the collapse in mitochondrial membrane and the activation of caspases is responsible for increased apoptosis observed with CPT-11/5-FU treatment.	Fluorouracil	165-169	caspase 8	Homo sapiens	96-104
16491956-12	2005	In spite of the differences among the cell lines, these results indicated that the increase in apoptosis in HT-29 cells observed with CPT-11 followed by 5-FU treatment could be explained by a disruption in mitochondria membrane potential that induced caspases activation.	Irinotecan	134-140	caspase 8	Homo sapiens	251-259
16491956-12	2005	In spite of the differences among the cell lines, these results indicated that the increase in apoptosis in HT-29 cells observed with CPT-11 followed by 5-FU treatment could be explained by a disruption in mitochondria membrane potential that induced caspases activation.	Fluorouracil	153-157	caspase 8	Homo sapiens	251-259
15516989-0	2004	Adenine deoxynucleotides fludarabine and cladribine induce apoptosis in a CD95/Fas receptor, FADD and caspase-8-independent manner by activation of the mitochondrial cell death pathway.	adenine deoxynucleotides	0-24	caspase 8	Homo sapiens	102-111
16416674-6	2005	Here, we report c-Abl dependent caspase-3 and caspase-8 activity in response to staurosporine.	Staurosporine	80-93	caspase 8	Homo sapiens	46-55
15386344-6	2004	Thus, activation of the Fas system is critical, which is in line with the finding that in sensitive cells, caspase-8 along with caspase-9 and -3 were activated by cDDP.	Cisplatin	163-167	caspase 8	Homo sapiens	107-116
15516989-0	2004	Adenine deoxynucleotides fludarabine and cladribine induce apoptosis in a CD95/Fas receptor, FADD and caspase-8-independent manner by activation of the mitochondrial cell death pathway.	fludarabine	25-36	caspase 8	Homo sapiens	102-111
15516989-0	2004	Adenine deoxynucleotides fludarabine and cladribine induce apoptosis in a CD95/Fas receptor, FADD and caspase-8-independent manner by activation of the mitochondrial cell death pathway.	Cladribine	41-51	caspase 8	Homo sapiens	102-111
15604295-0	2004	Caspase inhibitors, but not c-Jun NH2-terminal kinase inhibitor treatment, prevent cisplatin-induced hearing loss.	Cisplatin	83-92	caspase 8	Homo sapiens	0-7
15548389-9	2004	In addition, FK506 significantly reduced not only caspase-8 but also caspase-9 activation, to a similar extent as CsA, thus suggesting a protective effect at the mitochondrial level of this drug, as has already been reported for CsA.	Tacrolimus	13-18	caspase 8	Homo sapiens	50-59
15604261-4	2004	In these lines IFNalpha induced early activation of caspase-8, and DNA fragmentation was blocked by a caspase-8-selective inhibitor (IETDfmk), consistent with the involvement of death receptor(s) in cell death.	isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	133-140	caspase 8	Homo sapiens	102-111
15589827-5	2004	The increase of caspase-8, -9, -3 activities demonstrated that caspase was a key mediator of apoptotic pathways induced by lycorine.	lycorine	123-131	caspase 8	Homo sapiens	16-25
15452117-7	2004	Inhibitors of caspases-8, -6, or -3 partially inhibited taxol-induced apoptosis, whereas the caspase-10 inhibitor totally abrogated this process.	Paclitaxel	56-61	caspase 8	Homo sapiens	14-28
15286043-4	2004	Levels of activated caspases were assessed using fluorescein-labeled inhibitors of caspases (FLICA), Deltapsim using a lipophilic cationic dye, and DNA fragmentation by the terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) assay.	Fluorescein	49-60	caspase 8	Homo sapiens	20-28
15650242-5	2004	In addition, the apoptotic agent fenretinide (4HPR) and interferon-gamma (IFN-gamma) induce caspase-8 expression without modifying the methylation status of this gene.	Fenretinide	33-44	caspase 8	Homo sapiens	92-101
15650242-5	2004	In addition, the apoptotic agent fenretinide (4HPR) and interferon-gamma (IFN-gamma) induce caspase-8 expression without modifying the methylation status of this gene.	Fenretinide	46-50	caspase 8	Homo sapiens	92-101
15650242-9	2004	The retinoic acid analogue 4HPR, IFN-gamma, and the demethylating agent 5-aza-cytidine activate this promoter in NB cells that lack endogenous caspase-8, indicating that this element may regulate both constitutive and inducible CASP8 expression.	Tretinoin	4-17	caspase 8	Homo sapiens	143-152
15650242-9	2004	The retinoic acid analogue 4HPR, IFN-gamma, and the demethylating agent 5-aza-cytidine activate this promoter in NB cells that lack endogenous caspase-8, indicating that this element may regulate both constitutive and inducible CASP8 expression.	Tretinoin	4-17	caspase 8	Homo sapiens	228-233
15650242-9	2004	The retinoic acid analogue 4HPR, IFN-gamma, and the demethylating agent 5-aza-cytidine activate this promoter in NB cells that lack endogenous caspase-8, indicating that this element may regulate both constitutive and inducible CASP8 expression.	Azacitidine	72-86	caspase 8	Homo sapiens	143-152
15650242-9	2004	The retinoic acid analogue 4HPR, IFN-gamma, and the demethylating agent 5-aza-cytidine activate this promoter in NB cells that lack endogenous caspase-8, indicating that this element may regulate both constitutive and inducible CASP8 expression.	Azacitidine	72-86	caspase 8	Homo sapiens	228-233
15286043-4	2004	Levels of activated caspases were assessed using fluorescein-labeled inhibitors of caspases (FLICA), Deltapsim using a lipophilic cationic dye, and DNA fragmentation by the terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) assay.	deoxyuridine triphosphate	220-224	caspase 8	Homo sapiens	20-28
15297884-5	2004	LPA increased phosphatidylinositol 3-kinase (PI3K)-dependent Akt activation, cellular FLICE-inhibitory protein (cFLIP) expression, and Bad phosphorylation, resulting in inhibition of caspase-8 activation and Bad translocation to mitochondria.	lysophosphatidic acid	0-3	caspase 8	Homo sapiens	183-192
15547726-6	2004	IFN-gamma-mediated facilitation of apoptosis was inhibited by the pan-caspase inhibitor zVAD-fmk and the caspase-8 specific inhibitor zIEDT-fmk, indicating an important role of caspase-8 in mediating sensitation by IFN-gamma in neuroblastoma cells.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	88-96	caspase 8	Homo sapiens	177-186
15574786-2	2004	Here we show for the first time that SN38, the potent active metabolite of irinotecan, induces c-Jun NH(2)-terminal kinase activation, Fas up-regulation, and caspase 8-mediated apoptosis in multiple myeloma (MM) cells.	Irinotecan	75-85	caspase 8	Homo sapiens	158-167
15547726-6	2004	IFN-gamma-mediated facilitation of apoptosis was inhibited by the pan-caspase inhibitor zVAD-fmk and the caspase-8 specific inhibitor zIEDT-fmk, indicating an important role of caspase-8 in mediating sensitation by IFN-gamma in neuroblastoma cells.	ziedt-fmk	134-143	caspase 8	Homo sapiens	105-114
15547726-7	2004	In three of the cell lines [SK-N-BE(2), SK-N-DZ and IMR-32] caspase-8 expression was induced by IFN-gamma, but the cells were still resistant to TRAIL-mediated apoptosis.	sk-n-dz	40-47	caspase 8	Homo sapiens	60-69
15547726-6	2004	IFN-gamma-mediated facilitation of apoptosis was inhibited by the pan-caspase inhibitor zVAD-fmk and the caspase-8 specific inhibitor zIEDT-fmk, indicating an important role of caspase-8 in mediating sensitation by IFN-gamma in neuroblastoma cells.	ziedt-fmk	134-143	caspase 8	Homo sapiens	177-186
15547726-7	2004	In three of the cell lines [SK-N-BE(2), SK-N-DZ and IMR-32] caspase-8 expression was induced by IFN-gamma, but the cells were still resistant to TRAIL-mediated apoptosis.	sk-n-be	28-35	caspase 8	Homo sapiens	60-69
15507484-4	2004	Caspases 8 and 10 are the first caspases to be activated whereas caspase-8 inhibitor zIETD-fmk delays the activation of Bid, caspase-9 and caspase-3.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	85-94	caspase 8	Homo sapiens	65-74
15390286-0	2004	Interferon-gamma sensitizes osteosarcoma cells to Fas-induced apoptosis by up-regulating Fas receptors and caspase-8.	ammonium ferrous sulfate	50-53	caspase 8	Homo sapiens	107-116
15390286-8	2004	Addition to cultures of z-IETD-fmk, an inhibitor of caspase-8, significantly blocked this apoptosis.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	24-34	caspase 8	Homo sapiens	52-61
15390286-9	2004	CONCLUSIONS: IFN-gamma sensitizes osteosarcoma cells to Fas-induced apoptosis through up-regulation of Fas receptor and caspase-8.	ammonium ferrous sulfate	56-59	caspase 8	Homo sapiens	120-129
15572759-9	2004	RESULTS: Celecoxib treatment decreased cell survival, activated caspase cascades, and increased DNA fragmentation, all of which were abrogated when caspase 8 expression was silenced with caspase 8 siRNA.	Celecoxib	9-18	caspase 8	Homo sapiens	148-157
15572759-9	2004	RESULTS: Celecoxib treatment decreased cell survival, activated caspase cascades, and increased DNA fragmentation, all of which were abrogated when caspase 8 expression was silenced with caspase 8 siRNA.	Celecoxib	9-18	caspase 8	Homo sapiens	187-196
15572759-11	2004	Overexpression of a dominant negative Fas-associated death domain mutant, but not of BCL2, reduced the level of celecoxib-induced apoptosis, and silencing of DR5 expression by DR5 siRNA suppressed celecoxib-induced caspase 8 activation and apoptosis.	Celecoxib	112-121	caspase 8	Homo sapiens	215-224
15572759-11	2004	Overexpression of a dominant negative Fas-associated death domain mutant, but not of BCL2, reduced the level of celecoxib-induced apoptosis, and silencing of DR5 expression by DR5 siRNA suppressed celecoxib-induced caspase 8 activation and apoptosis.	Celecoxib	197-206	caspase 8	Homo sapiens	215-224
15566641-0	2004	[Enhancement of FG020326 on sensitivity of MCF-7/ADR cells to taxotere via enhancing activation of caspase-8 and caspase-3].	Docetaxel	62-70	caspase 8	Homo sapiens	99-108
15527805-5	2004	After combined TRAIL and ethanol treatment, a potentiation of caspase-8, -9, -3 activation, a proapoptotic Bid protein cleavage, a decrease of mitochondrial membrane potential, a complete poly(ADP)ribose polymerase cleavage, and disappearance of antiapoptotic Mcl-1 protein were demonstrated.	Ethanol	25-32	caspase 8	Homo sapiens	62-71
15566642-0	2004	[Inducement of FLICE inhibitory protein antisense oligonucleotides on apoptosis of human gastric cancer cell line BGC823].	Oligonucleotides	50-66	caspase 8	Homo sapiens	15-20
15566641-11	2004	Activities of caspase-3 and caspase-8 in MCF-7/ADR cells cultured with 10 micromol/L FG020326 and 0.1 micromol/L taxotere were increased in a time-dependent manner,and reached peak values at 48 h, which were significantly higher than those in cells cultured with taxotere alone.	Docetaxel	113-121	caspase 8	Homo sapiens	28-37
15566641-11	2004	Activities of caspase-3 and caspase-8 in MCF-7/ADR cells cultured with 10 micromol/L FG020326 and 0.1 micromol/L taxotere were increased in a time-dependent manner,and reached peak values at 48 h, which were significantly higher than those in cells cultured with taxotere alone.	Docetaxel	263-271	caspase 8	Homo sapiens	28-37
15566641-12	2004	CONCLUSION: FG020326 may reverse drug-resistance of MCF-7/ADR cells towards taxotere through enhancing activation of caspase-8 and caspase-3 induced by taxotere.	Docetaxel	152-160	caspase 8	Homo sapiens	117-126
15585135-7	2004	Our experiments showed that 5-FU engaged the mitochondrial apoptotic pathway involving cytosolic cytochrome c release and subsequent activation of caspase-9 and caspase-3 as well as the membrane death receptor (DR)-mediated apoptotic pathway involving activation of caspase-8 with an Apo-1/CD95 (Fas)-dependent fashion.	Fluorouracil	28-32	caspase 8	Homo sapiens	266-275
15514562-0	2004	Antitumor triptycene bisquinones induce a caspase-independent release of mitochondrial cytochrome c and a caspase-2-mediated activation of initiator caspase-8 and -9 in HL-60 cells by a mechanism which does not involve Fas signaling.	triptycene bisquinone	10-32	caspase 8	Homo sapiens	149-165
15450950-4	2004	A treatment of cadmium caused the caspase-8-dependent Bid cleavage, the release of cytochrome c (Cyt c), activation of caspase-9 and -3, and PARP cleavage.	Cadmium	15-22	caspase 8	Homo sapiens	34-43
15450951-3	2004	The MMC-induced cell death and decrease in the GSH contents in SCLC cells were inhibited by caspase inhibitors (z-DQMD.fmk, z-IETD.fmk and z-LEHD.fmk) and antioxidants (N-acetylcysteine, dithiothreitol and N-(2-mercaptopropionyl)glycine, melatonin, rutin and carboxy-PTIO).	Mitomycin	4-7	caspase 8	Homo sapiens	92-99
15450951-3	2004	The MMC-induced cell death and decrease in the GSH contents in SCLC cells were inhibited by caspase inhibitors (z-DQMD.fmk, z-IETD.fmk and z-LEHD.fmk) and antioxidants (N-acetylcysteine, dithiothreitol and N-(2-mercaptopropionyl)glycine, melatonin, rutin and carboxy-PTIO).	Glutathione	47-50	caspase 8	Homo sapiens	92-99
15450951-3	2004	The MMC-induced cell death and decrease in the GSH contents in SCLC cells were inhibited by caspase inhibitors (z-DQMD.fmk, z-IETD.fmk and z-LEHD.fmk) and antioxidants (N-acetylcysteine, dithiothreitol and N-(2-mercaptopropionyl)glycine, melatonin, rutin and carboxy-PTIO).	z-dqmd.fmk	112-122	caspase 8	Homo sapiens	92-99
15450951-3	2004	The MMC-induced cell death and decrease in the GSH contents in SCLC cells were inhibited by caspase inhibitors (z-DQMD.fmk, z-IETD.fmk and z-LEHD.fmk) and antioxidants (N-acetylcysteine, dithiothreitol and N-(2-mercaptopropionyl)glycine, melatonin, rutin and carboxy-PTIO).	Acetylcysteine	169-185	caspase 8	Homo sapiens	92-99
15450951-3	2004	The MMC-induced cell death and decrease in the GSH contents in SCLC cells were inhibited by caspase inhibitors (z-DQMD.fmk, z-IETD.fmk and z-LEHD.fmk) and antioxidants (N-acetylcysteine, dithiothreitol and N-(2-mercaptopropionyl)glycine, melatonin, rutin and carboxy-PTIO).	Dithiothreitol	187-201	caspase 8	Homo sapiens	92-99
15450951-3	2004	The MMC-induced cell death and decrease in the GSH contents in SCLC cells were inhibited by caspase inhibitors (z-DQMD.fmk, z-IETD.fmk and z-LEHD.fmk) and antioxidants (N-acetylcysteine, dithiothreitol and N-(2-mercaptopropionyl)glycine, melatonin, rutin and carboxy-PTIO).	Tiopronin	206-236	caspase 8	Homo sapiens	92-99
15450951-3	2004	The MMC-induced cell death and decrease in the GSH contents in SCLC cells were inhibited by caspase inhibitors (z-DQMD.fmk, z-IETD.fmk and z-LEHD.fmk) and antioxidants (N-acetylcysteine, dithiothreitol and N-(2-mercaptopropionyl)glycine, melatonin, rutin and carboxy-PTIO).	Melatonin	238-247	caspase 8	Homo sapiens	92-99
15450951-3	2004	The MMC-induced cell death and decrease in the GSH contents in SCLC cells were inhibited by caspase inhibitors (z-DQMD.fmk, z-IETD.fmk and z-LEHD.fmk) and antioxidants (N-acetylcysteine, dithiothreitol and N-(2-mercaptopropionyl)glycine, melatonin, rutin and carboxy-PTIO).	Rutin	249-254	caspase 8	Homo sapiens	92-99
15450951-3	2004	The MMC-induced cell death and decrease in the GSH contents in SCLC cells were inhibited by caspase inhibitors (z-DQMD.fmk, z-IETD.fmk and z-LEHD.fmk) and antioxidants (N-acetylcysteine, dithiothreitol and N-(2-mercaptopropionyl)glycine, melatonin, rutin and carboxy-PTIO).	1,3-dihydroxy-4,4,5,5-tetramethyl-2-(4-carboxyphenyl)tetrahydroimidazole	259-271	caspase 8	Homo sapiens	92-99
15520199-4	2004	CDDO-induced apoptosis was associated with the loss of mitochondrial inner transmembrane potential, caspases activation, the translocation of apoptosis-inducing factor to the nucleus, and DNA fragmentation in AML cells.	2-cyano-3,12-dioxoolean-1,9-dien-28-oic acid	0-4	caspase 8	Homo sapiens	100-108
15520199-5	2004	Apoptosis was equally evident in cells deficient in caspase-9 or caspase-8 after exposure to CDDO, suggesting caspase-independent cell death.	2-cyano-3,12-dioxoolean-1,9-dien-28-oic acid	93-97	caspase 8	Homo sapiens	65-74
15269006-7	2004	Treatment with BzATP activated caspase-9, and, in contrast to TNF-alpha, it had only a mild effect on caspase-8.	BzATP	15-20	caspase 8	Homo sapiens	102-111
15528887-6	2004	We also demonstrate that the process of apoptosis induced by butyrate and chemotherapeutic drugs involves the participation of caspases and induced activation of caspase-3, -8 and -9.	Butyrates	61-69	caspase 8	Homo sapiens	127-135
15509781-0	2004	Calcium binding of ARC mediates regulation of caspase 8 and cell death.	Calcium	0-7	caspase 8	Homo sapiens	46-55
15726829-4	2004	We demonstrated that ligation of CH-11 with its cognate receptor initiated execution of apoptotic program in interferon gamma-pretreated A549 cells as evidenced by activation of caspase and DNA fragmentation.	4-dimethylamino-3',4'-dimethoxychalcone	33-38	caspase 8	Homo sapiens	178-185
15726829-7	2004	A pan-caspase inhibitor, z-VAD, fully blocked cyt c release and oxidation of PtdSer in Fas-treated A549 cells.	z-vad	25-30	caspase 8	Homo sapiens	6-13
15726829-7	2004	A pan-caspase inhibitor, z-VAD, fully blocked cyt c release and oxidation of PtdSer in Fas-treated A549 cells.	ammonium ferrous sulfate	87-90	caspase 8	Homo sapiens	6-13
15475000-5	2004	In HepG2 cells, lithium repressed drug induction of CD95 expression and clustering at the cell surface as well as caspase-8 activation.	Lithium	16-23	caspase 8	Homo sapiens	114-123
15505232-3	2004	In human primary fibroblasts, HEMA induced a dose-dependent apoptosis that was confirmed by the activation of caspases-8, -9, and -3.	hydroxyethyl methacrylate	30-34	caspase 8	Homo sapiens	110-132
15509781-7	2004	In addition, binding and immunoprecipitation analyses revealed that the protein-protein interaction between ARC and caspase 8 was decreased by the increase of Ca(2+) concentration in vitro and by the treatment of HEK293 cells with thapsigargin in vivo.	Thapsigargin	231-243	caspase 8	Homo sapiens	116-125
15509781-8	2004	Caspase 8 activation was also required for the thapsigargin-induced cell death and suppressed by the ectopic expression of ARC.	Thapsigargin	47-59	caspase 8	Homo sapiens	0-9
15542777-8	2004	General and specific caspase inhibitors abrogated irofulven-induced apoptotic DNA fragmentation with the following order of potency: pan-caspase &gt; or = caspase-9 &gt; caspase-8/6 &gt; caspase-2 &gt; caspase-3/7 &gt; caspase-1/4.	irofulven	50-59	caspase 8	Homo sapiens	170-181
15509781-9	2004	These results suggest that calcium binding mediates regulation of caspase 8 and cell death by ARC.	Calcium	27-34	caspase 8	Homo sapiens	66-75
15492279-8	2004	After complete blockade of PTX-induced TP translation by TP antisense transfection, cleaved form of caspase-3 and poly(ADP-ribose) polymerase was increased, and this exaggeration of apoptosis also ran parallel with caspase-8 activation in a PTX dose-dependent manner.	Paclitaxel	27-30	caspase 8	Homo sapiens	215-224
15474362-2	2004	Several caspase inhibitors, such as the well-known peptidyl inhibitor carbobenzoxy-Val-Ala-Asp-fluoromethylketone (zVADfmk), can protect neurons from apoptotic death caused by mitochondrial toxins.	carbobenzoxy-val-ala-asp-fluoromethylketone	70-113	caspase 8	Homo sapiens	8-15
15474362-2	2004	Several caspase inhibitors, such as the well-known peptidyl inhibitor carbobenzoxy-Val-Ala-Asp-fluoromethylketone (zVADfmk), can protect neurons from apoptotic death caused by mitochondrial toxins.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	115-122	caspase 8	Homo sapiens	8-15
15474362-7	2004	Western blots performed on tissues from the midbrain following administration of MPTP or the striatum in 3NP-treated animals showed increases of the active forms of caspase-9 and caspase-8, as well as the caspase-8-mediated proapoptotic protein Bid, which were inhibited Q-VD-OPH treatment.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	81-85	caspase 8	Homo sapiens	179-188
15474362-7	2004	Western blots performed on tissues from the midbrain following administration of MPTP or the striatum in 3NP-treated animals showed increases of the active forms of caspase-9 and caspase-8, as well as the caspase-8-mediated proapoptotic protein Bid, which were inhibited Q-VD-OPH treatment.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	81-85	caspase 8	Homo sapiens	205-214
15474362-7	2004	Western blots performed on tissues from the midbrain following administration of MPTP or the striatum in 3NP-treated animals showed increases of the active forms of caspase-9 and caspase-8, as well as the caspase-8-mediated proapoptotic protein Bid, which were inhibited Q-VD-OPH treatment.	3-nitropropionic acid	105-108	caspase 8	Homo sapiens	179-188
15474362-7	2004	Western blots performed on tissues from the midbrain following administration of MPTP or the striatum in 3NP-treated animals showed increases of the active forms of caspase-9 and caspase-8, as well as the caspase-8-mediated proapoptotic protein Bid, which were inhibited Q-VD-OPH treatment.	3-nitropropionic acid	105-108	caspase 8	Homo sapiens	205-214
15451068-2	2004	We report that diclofenac, a NSAID, induces growth inhibition and apoptosis of HL-60 cells through modulation of mitochondrial functions regulated by reactive oxygen species (ROS), Akt, caspase-8, and Bid.	Diclofenac	15-25	caspase 8	Homo sapiens	186-195
15451068-4	2004	N-Acetyl-L-cysteine, an antioxidant, suppresses ROS generation, Akt inactivation, caspase-8 activation, and DNA fragmentation.	Acetylcysteine	0-19	caspase 8	Homo sapiens	82-91
15451068-7	2004	Ac-IETD-CHO, a caspase-8 inhibitor, suppresses Bid cleavage and DNA fragmentation.	Ac-IETD-CHO	0-11	caspase 8	Homo sapiens	15-24
15451068-9	2004	These results suggest the sequential mechanism of diclofenac-induced apoptosis of HL-60 cells: ROS generation suppresses Akt activity, thereby activating caspase-8, which stimulates Bid cleavage and induces cytochrome c release and the activation of caspase-9 and-3 in a CsA-insensitive mechanism.	Diclofenac	50-60	caspase 8	Homo sapiens	154-163
15451068-9	2004	These results suggest the sequential mechanism of diclofenac-induced apoptosis of HL-60 cells: ROS generation suppresses Akt activity, thereby activating caspase-8, which stimulates Bid cleavage and induces cytochrome c release and the activation of caspase-9 and-3 in a CsA-insensitive mechanism.	Reactive Oxygen Species	95-98	caspase 8	Homo sapiens	154-163
15326164-8	2004	Oxaliplatin-induced apoptosis, potentiated by kinase-defective c-Src mutants, was dependent on activation of caspase 8 and associated with Bid cleavage.	Oxaliplatin	0-11	caspase 8	Homo sapiens	109-118
15496290-5	2004	Caseamembrin C also induced the up-regulation of Fas ligand (FasL) expression, cleavage and activation of caspase-8 and caspase-9, Bid cleavage and activation of executor caspase-3.	CASEAMEMBRIN C	0-14	caspase 8	Homo sapiens	106-115
15496290-6	2004	However, z-IETD-FMK (Z-Ile-Glu-Thr-Asp-fluoromethyl ketone, a selective caspase-8 inhibitor) almost completely inhibited caseamembrin C-induced Bid cleavage without any modification of caspase-9 activation, indicating that the extrinsic pathway of FasL/caspase-8/Bid cascade only played a minor role in the apoptotic signaling.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	9-19	caspase 8	Homo sapiens	72-81
15496290-6	2004	However, z-IETD-FMK (Z-Ile-Glu-Thr-Asp-fluoromethyl ketone, a selective caspase-8 inhibitor) almost completely inhibited caseamembrin C-induced Bid cleavage without any modification of caspase-9 activation, indicating that the extrinsic pathway of FasL/caspase-8/Bid cascade only played a minor role in the apoptotic signaling.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	9-19	caspase 8	Homo sapiens	253-262
15496290-6	2004	However, z-IETD-FMK (Z-Ile-Glu-Thr-Asp-fluoromethyl ketone, a selective caspase-8 inhibitor) almost completely inhibited caseamembrin C-induced Bid cleavage without any modification of caspase-9 activation, indicating that the extrinsic pathway of FasL/caspase-8/Bid cascade only played a minor role in the apoptotic signaling.	z-ile	21-26	caspase 8	Homo sapiens	72-81
15496290-6	2004	However, z-IETD-FMK (Z-Ile-Glu-Thr-Asp-fluoromethyl ketone, a selective caspase-8 inhibitor) almost completely inhibited caseamembrin C-induced Bid cleavage without any modification of caspase-9 activation, indicating that the extrinsic pathway of FasL/caspase-8/Bid cascade only played a minor role in the apoptotic signaling.	z-ile	21-26	caspase 8	Homo sapiens	253-262
15496290-6	2004	However, z-IETD-FMK (Z-Ile-Glu-Thr-Asp-fluoromethyl ketone, a selective caspase-8 inhibitor) almost completely inhibited caseamembrin C-induced Bid cleavage without any modification of caspase-9 activation, indicating that the extrinsic pathway of FasL/caspase-8/Bid cascade only played a minor role in the apoptotic signaling.	asp-fluoromethyl ketone	35-58	caspase 8	Homo sapiens	72-81
15496290-6	2004	However, z-IETD-FMK (Z-Ile-Glu-Thr-Asp-fluoromethyl ketone, a selective caspase-8 inhibitor) almost completely inhibited caseamembrin C-induced Bid cleavage without any modification of caspase-9 activation, indicating that the extrinsic pathway of FasL/caspase-8/Bid cascade only played a minor role in the apoptotic signaling.	CASEAMEMBRIN C	121-135	caspase 8	Homo sapiens	72-81
15496290-6	2004	However, z-IETD-FMK (Z-Ile-Glu-Thr-Asp-fluoromethyl ketone, a selective caspase-8 inhibitor) almost completely inhibited caseamembrin C-induced Bid cleavage without any modification of caspase-9 activation, indicating that the extrinsic pathway of FasL/caspase-8/Bid cascade only played a minor role in the apoptotic signaling.	CASEAMEMBRIN C	121-135	caspase 8	Homo sapiens	253-262
15451068-9	2004	These results suggest the sequential mechanism of diclofenac-induced apoptosis of HL-60 cells: ROS generation suppresses Akt activity, thereby activating caspase-8, which stimulates Bid cleavage and induces cytochrome c release and the activation of caspase-9 and-3 in a CsA-insensitive mechanism.	Cyclosporine	271-274	caspase 8	Homo sapiens	154-163
15492284-8	2004	Moreover, application of the JNK-specific inhibitor SP600125 blocked CDDO-Me-induced increases in JNK activation, DR up-regulation, caspase-8 activation, and DNA fragmentation.	bardoxolone methyl	69-76	caspase 8	Homo sapiens	132-141
15492279-10	2004	These results indicate that PTX-induced TP up-regulation is associated with decreased caspase-8 activation.	Paclitaxel	28-31	caspase 8	Homo sapiens	86-95
15492284-4	2004	We found that CDDO-Me not only activated caspase-8 but also induced expression of DRs, particularly DR5, in a p53-independent mechanism.	bardoxolone methyl	14-21	caspase 8	Homo sapiens	41-50
15492284-7	2004	CDDO-Me rapidly activated c-Jun NH(2)-terminal kinase (JNK) before DR up-regulation and caspase-8 activation.	bardoxolone methyl	0-7	caspase 8	Homo sapiens	88-97
15492284-8	2004	Moreover, application of the JNK-specific inhibitor SP600125 blocked CDDO-Me-induced increases in JNK activation, DR up-regulation, caspase-8 activation, and DNA fragmentation.	pyrazolanthrone	52-60	caspase 8	Homo sapiens	132-141
15334061-7	2004	Knockdown of FLIP expression in MM cell lines, by a FLIPsiRNA, re-established the normal response to apoptosis induced by Fas or DR4/DR5, which was blocked by pretreatment with the caspase-8 inhibitor z-IETD-fmk.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	201-211	caspase 8	Homo sapiens	181-190
15205359-8	2004	Curcumin-induced activation of caspase 8 was blocked by Ku70 but not by Bcl-XL.	Curcumin	0-8	caspase 8	Homo sapiens	31-40
15292226-3	2004	Inhibition of p38 MAPK activity through the use of a specific inhibitor, SB202190, in combination with UVA treatment induced a rapid cleavage of caspase-9, caspase-8, and caspase-3, whereas UVA irradiation alone had no effect.	4-(4-fluorophenyl)-2-(4-hydroxyphenyl)-5-(4-pyridyl)imidazole	73-81	caspase 8	Homo sapiens	156-165
15345335-12	2004	Furthermore, upregulation of Fas appears to play a major role in the initiation of ZD1839-induced apoptosis, activation of caspase-8/caspase-3 cascade is involved in the execution phase of this death program.	Gefitinib	83-89	caspase 8	Homo sapiens	123-132
15205359-9	2004	However, caspase 8 activation by curcumin was accelerated in both AsBcl-XL and AsKu70 cells suggesting a possible feedback activation of caspase 8 by caspase 3.	Curcumin	33-41	caspase 8	Homo sapiens	9-18
15205359-9	2004	However, caspase 8 activation by curcumin was accelerated in both AsBcl-XL and AsKu70 cells suggesting a possible feedback activation of caspase 8 by caspase 3.	Curcumin	33-41	caspase 8	Homo sapiens	137-146
15554914-6	2004	Upregulation of Fas/FasL, in association with the activation of downstream caspase 8 activity, was observed following treatment with gossypol.	Gossypol	133-141	caspase 8	Homo sapiens	75-84
15375383-0	2004	Anandamide-induced cell death in primary neuronal cultures: role of calpain and caspase pathways.	anandamide	0-10	caspase 8	Homo sapiens	80-87
15375383-6	2004	Moreover, AEA caused cell death in caspase-3-deficient MCF-7 cell line and showed similar cytotoxic effects in caspase-9 dominant-negative, caspase-8 dominant-negative or mock-transfected SH-SY5Y neuroblastoma cells.	anandamide	10-13	caspase 8	Homo sapiens	140-149
19003264-5	2004	The use of chemical apoptosis inhibitors was utilised to investigate key components of hepatic apoptosis where caspases, predominantly caspase 8, were implicated in staurosporine (STS)-induced HepZ apoptosis.	Staurosporine	165-178	caspase 8	Homo sapiens	111-119
19003264-5	2004	The use of chemical apoptosis inhibitors was utilised to investigate key components of hepatic apoptosis where caspases, predominantly caspase 8, were implicated in staurosporine (STS)-induced HepZ apoptosis.	Staurosporine	165-178	caspase 8	Homo sapiens	135-144
19003264-5	2004	The use of chemical apoptosis inhibitors was utilised to investigate key components of hepatic apoptosis where caspases, predominantly caspase 8, were implicated in staurosporine (STS)-induced HepZ apoptosis.	Staurosporine	180-183	caspase 8	Homo sapiens	111-119
19003264-5	2004	The use of chemical apoptosis inhibitors was utilised to investigate key components of hepatic apoptosis where caspases, predominantly caspase 8, were implicated in staurosporine (STS)-induced HepZ apoptosis.	Staurosporine	180-183	caspase 8	Homo sapiens	135-144
15379865-3	2004	Cell death could be prevented by the general caspase inhibitor zVAD-fmk.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	63-71	caspase 8	Homo sapiens	45-52
15161936-0	2004	Kaurene diterpene induces apoptosis in human leukemia cells partly through a caspase-8-dependent pathway.	kaurene	0-7	caspase 8	Homo sapiens	77-86
15161936-0	2004	Kaurene diterpene induces apoptosis in human leukemia cells partly through a caspase-8-dependent pathway.	Diterpenes	8-17	caspase 8	Homo sapiens	77-86
15197489-6	2004	Upon paclitaxel treatment, caspase-2, caspase-3, and caspase-8 were activated in BCBL-1 cells.	Paclitaxel	5-15	caspase 8	Homo sapiens	53-62
15262979-0	2004	Sequential caspase-2 and caspase-8 activation upstream of mitochondria during ceramideand etoposide-induced apoptosis.	ceramideand	78-89	caspase 8	Homo sapiens	25-34
15262979-0	2004	Sequential caspase-2 and caspase-8 activation upstream of mitochondria during ceramideand etoposide-induced apoptosis.	Etoposide	90-99	caspase 8	Homo sapiens	25-34
15262979-4	2004	Here we report a potential regulatory role of caspase-2 on caspase-8 during ceramide-induced apoptosis.	Ceramides	76-84	caspase 8	Homo sapiens	59-68
15262979-6	2004	The expression of truncated Bid (tBid) and the reduction in mitochondrial transmembrane potential were blocked by caspase-2 or caspase-8, but not caspase-3, knockdown using an RNA interference technique.	tBID	33-37	caspase 8	Homo sapiens	127-136
15262979-7	2004	Ceramide-induced caspase-8 activation, mitochondrial damage, and apoptosis were blocked in caspase-2 short interfering RNA-expressing cells.	Ceramides	0-8	caspase 8	Homo sapiens	17-26
15262979-8	2004	Therefore, caspase-2 acts upstream of caspase-8 during ceramide-induced mitochondrial apoptosis.	Ceramides	55-63	caspase 8	Homo sapiens	38-47
15336528-5	2004	The recruitment of TRADD, FADD, and activation of caspase-8 and -3 in SM-treated A549 cells evidenced the activation of TNFRs signal transduction.	beta-solamarine	70-72	caspase 8	Homo sapiens	50-66
15336528-7	2004	Combinational treatment of SM and cisplatin synergistically enhanced caspase-8, -9, and -3 activities in A549 cells.	beta-solamarine	27-29	caspase 8	Homo sapiens	69-90
15336528-7	2004	Combinational treatment of SM and cisplatin synergistically enhanced caspase-8, -9, and -3 activities in A549 cells.	Cisplatin	34-43	caspase 8	Homo sapiens	69-90
15262979-9	2004	Similarly, sequential caspase-2 and caspase-8 activation upstream of mitochondria was also observed in etoposide-induced apoptosis.	Etoposide	103-112	caspase 8	Homo sapiens	36-45
15262979-10	2004	These data suggest sequential initiator caspase-2 and caspase-8 activation in the mitochondrial apoptotic pathway induced by ceramide or etoposide.	Ceramides	125-133	caspase 8	Homo sapiens	54-63
15262979-10	2004	These data suggest sequential initiator caspase-2 and caspase-8 activation in the mitochondrial apoptotic pathway induced by ceramide or etoposide.	Etoposide	137-146	caspase 8	Homo sapiens	54-63
15252032-4	2004	The late phase of the TRAIL-induced NF-kappaB is critically dependent on caspase 8 and can be blocked by pharmacological and genetic inhibitors of caspase 8 activation, such as benzyloxycarbonyl-VAD-fluoromethyl ketone, benzyloxycarbonyl-IETD-fluoromethyl ketone, and small interfering RNA targeting caspase 8 and FADD.	benzyloxycarbonyl-ietd-fluoromethyl ketone	220-262	caspase 8	Homo sapiens	73-82
15252032-4	2004	The late phase of the TRAIL-induced NF-kappaB is critically dependent on caspase 8 and can be blocked by pharmacological and genetic inhibitors of caspase 8 activation, such as benzyloxycarbonyl-VAD-fluoromethyl ketone, benzyloxycarbonyl-IETD-fluoromethyl ketone, and small interfering RNA targeting caspase 8 and FADD.	benzyloxycarbonyl-ietd-fluoromethyl ketone	220-262	caspase 8	Homo sapiens	147-156
15252032-4	2004	The late phase of the TRAIL-induced NF-kappaB is critically dependent on caspase 8 and can be blocked by pharmacological and genetic inhibitors of caspase 8 activation, such as benzyloxycarbonyl-VAD-fluoromethyl ketone, benzyloxycarbonyl-IETD-fluoromethyl ketone, and small interfering RNA targeting caspase 8 and FADD.	benzyloxycarbonyl-ietd-fluoromethyl ketone	220-262	caspase 8	Homo sapiens	147-156
15252032-6	2004	The late phase of TRAIL-induced NF-kappaB activation involves caspase mediated cleavage of IkappaBalpha between Asp(31) and Ser(32) residues to generate an N-terminal truncated fragment that is degraded by the proteasome via the N-end rule pathway.	Aspartic Acid	112-115	caspase 8	Homo sapiens	62-69
15252032-6	2004	The late phase of TRAIL-induced NF-kappaB activation involves caspase mediated cleavage of IkappaBalpha between Asp(31) and Ser(32) residues to generate an N-terminal truncated fragment that is degraded by the proteasome via the N-end rule pathway.	Serine	124-127	caspase 8	Homo sapiens	62-69
15481331-4	2004	Both time- and concentration-dependent effects on apoptosis were noted, which were effectively prevented by the caspase inhibitor z-VAD-fmk.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	130-139	caspase 8	Homo sapiens	112-119
15336257-5	2004	Among the compounds examined, a lignocresol derivative from bamboo (lig-8) exhibited the most potent neuroprotective activity against hydrogen peroxide (H(2)O(2))-induced apoptosis in human neuroblastoma cell line SH-SY5Y by preventing the caspase-3 activation via either caspase-8 or caspase-9.	lignocresol	32-43	caspase 8	Homo sapiens	272-281
15377153-9	2004	The caspase-3, -8, and -9 relative activities were all increased in the UVB group; however, arsenic significantly enhanced caspase-8 and -3 relative activities in UVB-irradiated keratinocytes (the UVB-As group).	Arsenic	92-99	caspase 8	Homo sapiens	123-139
15377153-11	2004	Our findings revealed that arsenic enhances UVB-induced keratinocyte apoptosis via suppression of Bcl-2 expression and stimulation of caspase-8 activity.	Arsenic	27-34	caspase 8	Homo sapiens	134-143
15258564-3	2004	Cisplatin significantly decreased FLIP protein level, induced cleavage of caspase-8 and caspase-3 and apoptosis in a concentration-dependent manner in cisplatin-sensitive but not -resistant cells.	Cisplatin	0-9	caspase 8	Homo sapiens	74-83
15258564-3	2004	Cisplatin significantly decreased FLIP protein level, induced cleavage of caspase-8 and caspase-3 and apoptosis in a concentration-dependent manner in cisplatin-sensitive but not -resistant cells.	Cisplatin	151-160	caspase 8	Homo sapiens	74-83
15258564-4	2004	While overexpression of FLIP-attenuated cisplatin-induced cleavage of caspase-8 and caspase-3 and apoptosis in chemosensitive cells, downregulation of FLIP in chemoresistant cells by siRNA increased apoptosis induced by cisplatin.	Cisplatin	40-49	caspase 8	Homo sapiens	70-79
15273737-5	2004	Inhibition of caspase-8 by z-IETD-fmk did not block the sensitizing effect of TNFalpha.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	27-37	caspase 8	Homo sapiens	14-23
15130948-4	2004	Violacein cytotoxicity in HL60 cells was preceded by activation of caspase 8, transcription of nuclear factor kappaB (NF-kappaB) target genes, and p38 mitogen-activated protein (MAP) kinase activation.	violacein	0-9	caspase 8	Homo sapiens	67-76
15131591-6	2004	Two separate signaling cascades, p53-mediated ROS-dependent and -independent pathways, both of which are initiated by caspase-8 activation, thus contribute to ceramide formation in TNF-alpha-induced apoptosis of human glioma cells.	Ceramides	159-167	caspase 8	Homo sapiens	118-127
15481331-5	2004	Accordingly, the role of caspases in aspirin-induced apoptosis was also evaluated.	Aspirin	37-44	caspase 8	Homo sapiens	25-33
15481331-8	2004	We conclude that physiologically relevant concentrations of aspirin induces apoptosis in human gastric cells through a caspase-mediated mechanism.	Aspirin	60-67	caspase 8	Homo sapiens	119-126
15289875-0	2004	Loss of caspase-8 activation pathway is a possible mechanism for CDDP resistance in human laryngeal squamous cell carcinoma, HEp-2 cells.	Cisplatin	65-69	caspase 8	Homo sapiens	8-17
15289875-6	2004	CDDP activated the caspase-8 pathway through TNFR superfamily receptors such as Fas, but not caspase-9 in HeLa cells.	Cisplatin	0-4	caspase 8	Homo sapiens	19-28
15289875-7	2004	On the other hand, the caspase-9 pathway was significantly activated in HEp-2 cells, although the activation of caspase-8 by CDDP was deficient.	Cisplatin	125-129	caspase 8	Homo sapiens	112-121
15289875-8	2004	This different response to CDDP in caspase-8 activation was not related with the expression level of either Fas or FasL in these cells.	Cisplatin	27-31	caspase 8	Homo sapiens	35-44
15289875-9	2004	We concluded from these results that loss of the caspase-8 activation pathway in HEp-2 cells was a possible mechanism for its resistance to CDDP-induced apoptosis.	Cisplatin	140-144	caspase 8	Homo sapiens	49-58
15289875-10	2004	The caspase-8 pathway might play an important role in CDDP-induced apoptosis in HPV-positive human squamous cell carcinomas.	Cisplatin	54-58	caspase 8	Homo sapiens	4-13
15205454-7	2004	Interestingly, a specific caspase-8 inhibitor, Z-IETD-fmk (where fmk is fluoromethyl ketone), blocked ETA-induced cleavage of D4-GDI, but a caspase-9 inhibitor (Z-LEHD-fmk) did not.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	47-57	caspase 8	Homo sapiens	26-35
15197583-8	2004	The protective effect of caspase-8 and -9 inhibitors on celecoxib-induced apoptosis suggests the importance of caspase-8 and -9 activation in this apoptotic pathway.	Celecoxib	56-65	caspase 8	Homo sapiens	25-41
15197583-8	2004	The protective effect of caspase-8 and -9 inhibitors on celecoxib-induced apoptosis suggests the importance of caspase-8 and -9 activation in this apoptotic pathway.	Celecoxib	56-65	caspase 8	Homo sapiens	111-127
15197583-11	2004	CONCLUSIONS: These data show that caspase-8 and -9 are involved in the apoptotic effect of celecoxib in cervical cancer cells.	Celecoxib	91-100	caspase 8	Homo sapiens	34-50
15224412-6	2004	Pan-caspase inhibitor (Z-VAD-FMK), caspase-3 inhibitor (Z-DEVD-FMK) or caspase-8 inhibitor (Z-IETD-FMK) effectively inhibited shikonin-induced cell death, while caspase-1 inhibitor (Ac-YVAD-CMK) and caspase-9 inhibitor (Z-LEHD-FMK) failed to affect cell death.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	92-102	caspase 8	Homo sapiens	71-80
15273325-9	2004	After deprotection and purification, the 5"-phosphorylated tetranucleotide was chemically coupled with m7GDP to yield the cap-4 structure.	tetranucleotide	59-74	caspase 8	Homo sapiens	122-127
15224412-6	2004	Pan-caspase inhibitor (Z-VAD-FMK), caspase-3 inhibitor (Z-DEVD-FMK) or caspase-8 inhibitor (Z-IETD-FMK) effectively inhibited shikonin-induced cell death, while caspase-1 inhibitor (Ac-YVAD-CMK) and caspase-9 inhibitor (Z-LEHD-FMK) failed to affect cell death.	shikonin	126-134	caspase 8	Homo sapiens	71-80
15454884-5	2004	Treatment of HUVECs with LLL-CHO, etoposide, or C2-ceramide induced DeltaPsim, activation of caspase-3, caspase-8, and caspase-9 and the appearance of hypodiploid DNA-positive cells.	lll-cho	25-32	caspase 8	Homo sapiens	104-113
15454884-5	2004	Treatment of HUVECs with LLL-CHO, etoposide, or C2-ceramide induced DeltaPsim, activation of caspase-3, caspase-8, and caspase-9 and the appearance of hypodiploid DNA-positive cells.	Etoposide	34-43	caspase 8	Homo sapiens	104-113
15454884-5	2004	Treatment of HUVECs with LLL-CHO, etoposide, or C2-ceramide induced DeltaPsim, activation of caspase-3, caspase-8, and caspase-9 and the appearance of hypodiploid DNA-positive cells.	N-acetylsphingosine	48-59	caspase 8	Homo sapiens	104-113
15205454-7	2004	Interestingly, a specific caspase-8 inhibitor, Z-IETD-fmk (where fmk is fluoromethyl ketone), blocked ETA-induced cleavage of D4-GDI, but a caspase-9 inhibitor (Z-LEHD-fmk) did not.	FMK	54-57	caspase 8	Homo sapiens	26-35
15205454-7	2004	Interestingly, a specific caspase-8 inhibitor, Z-IETD-fmk (where fmk is fluoromethyl ketone), blocked ETA-induced cleavage of D4-GDI, but a caspase-9 inhibitor (Z-LEHD-fmk) did not.	1,3-Difluoroacetone	72-91	caspase 8	Homo sapiens	26-35
15205454-7	2004	Interestingly, a specific caspase-8 inhibitor, Z-IETD-fmk (where fmk is fluoromethyl ketone), blocked ETA-induced cleavage of D4-GDI, but a caspase-9 inhibitor (Z-LEHD-fmk) did not.	benzyloxycarbonyl-leucyl-glutamyl-histidyl-aspartic acid fluoromethyl ketone	161-171	caspase 8	Homo sapiens	26-35
15205454-8	2004	Treatment of mast cells with caspase-3 inhibitor Z-DEVD-fmk or caspase-8 inhibitor Z-IETD-fmk reduced the generation of ssDNA induced by ETA, suggesting a role for caspase-8 and -3 in ETA-induced mast cell apoptosis.	benzoylcarbonyl-aspartyl-glutamyl-valyl-aspartyl-fluoromethyl ketone	49-59	caspase 8	Homo sapiens	164-180
15205454-8	2004	Treatment of mast cells with caspase-3 inhibitor Z-DEVD-fmk or caspase-8 inhibitor Z-IETD-fmk reduced the generation of ssDNA induced by ETA, suggesting a role for caspase-8 and -3 in ETA-induced mast cell apoptosis.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	83-93	caspase 8	Homo sapiens	63-72
15205454-8	2004	Treatment of mast cells with caspase-3 inhibitor Z-DEVD-fmk or caspase-8 inhibitor Z-IETD-fmk reduced the generation of ssDNA induced by ETA, suggesting a role for caspase-8 and -3 in ETA-induced mast cell apoptosis.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	83-93	caspase 8	Homo sapiens	164-180
15289496-2	2004	Here, we show that Fas activates NFkappaB via a pathway involving RIP, FADD, and caspase-8.	ammonium ferrous sulfate	19-22	caspase 8	Homo sapiens	81-90
15159409-5	2004	Fas-induced, caspase-8-independent exposure of the N terminus of Bak is blocked by staurosporine, a pan protein kinase inhibitor.	ammonium ferrous sulfate	0-3	caspase 8	Homo sapiens	13-22
15159409-5	2004	Fas-induced, caspase-8-independent exposure of the N terminus of Bak is blocked by staurosporine, a pan protein kinase inhibitor.	Staurosporine	83-96	caspase 8	Homo sapiens	13-22
15159409-6	2004	These results suggest that Fas stimulation not only activates caspase-8, but also a distinct signaling pathway involving protein kinase(s) to induce exposure of the N terminus of Bak.	ammonium ferrous sulfate	27-30	caspase 8	Homo sapiens	62-71
15301743-0	2004	Diosgenin induces apoptosis in HeLa cells via activation of caspase pathway.	Diosgenin	0-9	caspase 8	Homo sapiens	60-67
15276073-2	2004	Viability loss and decrease in GSH contents in small cell lung cancer (SCLC) cells treated with MG132 was attenuated by caspase inhibitors (z-IETD.fmk, z-LEHD.fmk and z-DQMD.fmk).	Glutathione	31-34	caspase 8	Homo sapiens	120-127
15276073-2	2004	Viability loss and decrease in GSH contents in small cell lung cancer (SCLC) cells treated with MG132 was attenuated by caspase inhibitors (z-IETD.fmk, z-LEHD.fmk and z-DQMD.fmk).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	96-101	caspase 8	Homo sapiens	120-127
15276073-2	2004	Viability loss and decrease in GSH contents in small cell lung cancer (SCLC) cells treated with MG132 was attenuated by caspase inhibitors (z-IETD.fmk, z-LEHD.fmk and z-DQMD.fmk).	z-ietd	140-146	caspase 8	Homo sapiens	120-127
15276073-7	2004	The results suggest that the toxicity of MG132 on SCLC cells is mediated by activation of caspase-8, -9 and -3.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	41-46	caspase 8	Homo sapiens	90-110
15219941-4	2004	Using a human colorectal cancer cell line COLO205, we first demonstrated that parthenolide acted through the cell death receptor pathway to activate caspase 8.	parthenolide	78-90	caspase 8	Homo sapiens	149-158
15219941-8	2004	Moreover, selective inhibition of caspase 8 activity by a synthetic caspase inhibitor (IETD-FMK) or overexpression of a viral protein (CrmA) suppressed the cleavage of Bid, conformational changes of Bax, cytochrome c release, and apoptosis.	isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	87-95	caspase 8	Homo sapiens	34-43
15219941-9	2004	Therefore, the proapoptotic Bcl-2 family members are important mediators relaying the cell death signaling elicited by parthenolide from caspase 8 to downstream effector caspases such as caspase 3, and eventually to cell death.	parthenolide	119-131	caspase 8	Homo sapiens	137-146
15301743-12	2004	CONCLUSION: Diosgenin induced HeLa cell apoptosis through caspase pathway.	Diosgenin	12-21	caspase 8	Homo sapiens	58-65
15301743-10	2004	Caspase family inhibitor (z-VAD-fmk), caspase-9 inhibitor (Ac-AAVALPAVLLALLAPLEHD-CHO), and caspase-3 inhibitor (z-DEVD-fmk) partially prevented diosgenin-induced apoptosis, but not caspase-8 inhibitor (z-IETD-fmk) and caspase-10 inhibitor (z-AEVD-fmk).	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	26-35	caspase 8	Homo sapiens	0-7
15301743-10	2004	Caspase family inhibitor (z-VAD-fmk), caspase-9 inhibitor (Ac-AAVALPAVLLALLAPLEHD-CHO), and caspase-3 inhibitor (z-DEVD-fmk) partially prevented diosgenin-induced apoptosis, but not caspase-8 inhibitor (z-IETD-fmk) and caspase-10 inhibitor (z-AEVD-fmk).	benzoylcarbonyl-aspartyl-glutamyl-valyl-aspartyl-fluoromethyl ketone	113-123	caspase 8	Homo sapiens	0-7
15197348-5	2004	The reduction in cell growth and enhancement in cell killing by the combination of GST-MDA-7 and radiation were blocked by an ROS scavenger, N-acetyl cysteine (NAC), a JNK1/2/3 inhibitor SP600125, a pan-caspase inhibitor (zVAD) and by an inhibitor of caspase 9 (LEHD), but not by an inhibitor of caspase 8 (IETD).	ros	126-129	caspase 8	Homo sapiens	296-305
15279653-5	2004	In order to elucidate the apoptosis signaling pathway, we examined the effect of various caspase inhibitors on the apoptosis induced by CH-11.	4-dimethylamino-3',4'-dimethoxychalcone	136-141	caspase 8	Homo sapiens	89-96
15279653-6	2004	Fas-mediated apoptosis of HSG cells was slightly inhibited by the caspase-9 inhibitor although it was mainly inhibited by that for caspase-8.	ammonium ferrous sulfate	0-3	caspase 8	Homo sapiens	131-140
15279653-7	2004	Based on this finding, we consider CH-11-induced apoptosis in HSG cells to be mainly mediated by the type I death signaling pathway that is caused by a caspase cascade initiated by the activation of caspase-8 at the death-inducing signaling complex (DISC).	4-dimethylamino-3',4'-dimethoxychalcone	35-40	caspase 8	Homo sapiens	152-159
15279653-7	2004	Based on this finding, we consider CH-11-induced apoptosis in HSG cells to be mainly mediated by the type I death signaling pathway that is caused by a caspase cascade initiated by the activation of caspase-8 at the death-inducing signaling complex (DISC).	4-dimethylamino-3',4'-dimethoxychalcone	35-40	caspase 8	Homo sapiens	199-208
15260130-6	2004	In addition, H2O2 significantly increased activities of all three caspases, caspase-3, caspase-8, and caspase-9, in comparison with non-H2O2 controls.	Hydrogen Peroxide	13-17	caspase 8	Homo sapiens	66-74
15254227-0	2004	Association of active caspase 8 with the mitochondrial membrane during apoptosis: potential roles in cleaving BAP31 and caspase 3 and mediating mitochondrion-endoplasmic reticulum cross talk in etoposide-induced cell death.	Etoposide	194-203	caspase 8	Homo sapiens	22-31
15254227-4	2004	In MDA-MB231 breast cancer cells treated with etoposide (VP16), active caspase 8 is detected only in the membrane fraction, which contains both mitochondria and endoplasmic reticulum (ER), as revealed by fractionation studies.	Etoposide	46-55	caspase 8	Homo sapiens	71-80
15370202-4	2004	Inhibition of PI3-kinase with specific inhibitor, LY294002, led to the induction of apoptosis that was caspase 8 dependent, but independent of Akt as LY294002 did not depress a high basal level of Akt activity found in CLL cells.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	50-58	caspase 8	Homo sapiens	103-112
15260130-6	2004	In addition, H2O2 significantly increased activities of all three caspases, caspase-3, caspase-8, and caspase-9, in comparison with non-H2O2 controls.	Hydrogen Peroxide	13-17	caspase 8	Homo sapiens	87-96
15276415-9	2004	The additions of inhibitors of caspase 3, caspase 8, and caspase 9 significantly reduced DMAs(V)-induced apoptosis.	N-myristoyl-alaninol	89-93	caspase 8	Homo sapiens	42-51
15517988-6	2004	Caspase-8 selections, as expected, yielded predominantly clones containing a Glu at P3.	Glutamic Acid	77-80	caspase 8	Homo sapiens	0-9
15148322-4	2004	Caspase 8 cleaves full-length Bid, resulting in truncated p15 tBid.	tBID	62-66	caspase 8	Homo sapiens	0-9
15117953-4	2004	Bid is not transcriptionally up-regulated in response to these stimuli but is activated by cleavage on aspartate residues 60 and/or 75, which are the targets of caspase-8 and granzyme B.	Aspartic Acid	103-112	caspase 8	Homo sapiens	161-170
15123718-1	2004	The proapoptotic Bcl-2 family protein Bid is cleaved by caspase-8 to release the C-terminal fragment tBid, which translocates to the outer mitochondrial membrane and induces massive cytochrome c release and cell death.	tBID	101-105	caspase 8	Homo sapiens	56-65
15207716-5	2004	We report here that disruption of lipid rafts by cholesterol-depleting compounds (methyl-beta-cyclodextrin, filipin III, cholesterol oxidase, and mevastatin) leads to a spontaneous clustering of Fas in the non-raft compartment of the plasma membrane, formation of Fas-FADD complexes, activation of caspase-8, and apoptosis.	Cholesterol	49-60	caspase 8	Homo sapiens	298-307
15207716-5	2004	We report here that disruption of lipid rafts by cholesterol-depleting compounds (methyl-beta-cyclodextrin, filipin III, cholesterol oxidase, and mevastatin) leads to a spontaneous clustering of Fas in the non-raft compartment of the plasma membrane, formation of Fas-FADD complexes, activation of caspase-8, and apoptosis.	methyl-beta-cyclodextrin	82-106	caspase 8	Homo sapiens	298-307
15207716-5	2004	We report here that disruption of lipid rafts by cholesterol-depleting compounds (methyl-beta-cyclodextrin, filipin III, cholesterol oxidase, and mevastatin) leads to a spontaneous clustering of Fas in the non-raft compartment of the plasma membrane, formation of Fas-FADD complexes, activation of caspase-8, and apoptosis.	mevastatin	146-156	caspase 8	Homo sapiens	298-307
15094781-6	2004	TRAIL-induced cell death could be further enhanced by cotreatment of IGR-N91-C8 and SH-EP cells with cycloheximide or subtoxic concentrations of chemotherapeutic drugs in a caspase-dependent manner.	Cycloheximide	101-114	caspase 8	Homo sapiens	173-180
15256749-5	2004	A general caspase inhibitor (z-VAD-fmk), caspase-8 inhibitor (z-IETD-fmk) and caspase-3 inhibitor (z-DEVD-fmk), almost completely suppressed the yomogin-induced DNA fragmentation.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	62-72	caspase 8	Homo sapiens	41-50
15192325-6	2004	A caspase-8 inhibitor, IETD-fmk, effectively suppressed poly (ADP-ribose) polymerase cleavage and cytochrome c release.	isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	23-31	caspase 8	Homo sapiens	2-11
15192325-7	2004	However, 4-O-methyl ascochlorin induced apoptosis in Jurkat cells deficient of caspase-8 or Fas-associated death domain protein.	4-O-methylascochlorin	9-31	caspase 8	Homo sapiens	79-88
15265368-13	2004	CONCLUSIONS: Activation and upregulation of caspase-3 or caspase-8 protein were responsible for Indomethacin-induced K562 cell apoptosis.	Indomethacin	96-108	caspase 8	Homo sapiens	57-66
15207741-10	2004	Furthermore, the levels of p21Cip1/WAF1, which inhibits the cleavage of caspase-8, was found to be highly induced in 1,25(OH)2D3-treated cells.	Calcitriol	117-128	caspase 8	Homo sapiens	72-81
15105837-9	2004	Thus, a potential mechanism for TRAIL sensitisation by 5-FU is the increased effectiveness of caspase-8 recruitment to and activation at the DISC facilitated by the downregulation of cFLIP and the consequent shift in the ratio of caspase-8 to cFLIP at the DISC.	Fluorouracil	55-59	caspase 8	Homo sapiens	94-103
15105837-9	2004	Thus, a potential mechanism for TRAIL sensitisation by 5-FU is the increased effectiveness of caspase-8 recruitment to and activation at the DISC facilitated by the downregulation of cFLIP and the consequent shift in the ratio of caspase-8 to cFLIP at the DISC.	Fluorouracil	55-59	caspase 8	Homo sapiens	230-239
15265368-6	2004	To reveal the activation of caspase-3 or caspase-8 in indomethacin-treated cells, Western blot detection was used.	Indomethacin	54-66	caspase 8	Homo sapiens	41-50
15252149-11	2004	In summary, selenite-induced p53 Ser15P appeared to be important for activating the caspase-mediated apoptosis involving both the caspase-8 and the caspase-9 pathways in the LNCaP cells.	Selenious Acid	12-20	caspase 8	Homo sapiens	130-139
15265368-9	2004	An increased expression of intracellular caspase-3 or caspase-8 was observed at higher doses of indomethacin (400 - 800 micromol/L).	Indomethacin	96-108	caspase 8	Homo sapiens	54-63
15116123-4	2004	VPA induced apoptosis in K562 cells led to decrease in Flip (FLICE/caspase-8 inhibitory protein) expression with Flip cleavage, which could not be observed in HL60 cells.	Valproic Acid	0-3	caspase 8	Homo sapiens	61-66
15073169-1	2004	Previously, we showed that sulforaphane (SFN), a naturally occurring cancer chemopreventive agent, effectively inhibits proliferation of PC-3 human prostate cancer cells by causing caspase-9- and caspase-8-mediated apoptosis.	sulforaphane	27-39	caspase 8	Homo sapiens	196-205
15163549-6	2004	Consistent with these data, the activities of caspase-3, caspase-9 and caspase-8 were elevated by simvastatin.	Simvastatin	98-109	caspase 8	Homo sapiens	71-80
15073169-1	2004	Previously, we showed that sulforaphane (SFN), a naturally occurring cancer chemopreventive agent, effectively inhibits proliferation of PC-3 human prostate cancer cells by causing caspase-9- and caspase-8-mediated apoptosis.	sulforaphane	41-44	caspase 8	Homo sapiens	196-205
15161627-5	2004	The appearance of diminished FRET was inhibited by a pan-caspase inhibitor z-VAD or D-&gt;A mutations in the LEVD sequence and was markedly increased by apoptosis-inducing agents, etoposide and camptothecin, or overexpression of a caspase 8-red fluorescent protein fusion protein.	Etoposide	180-189	caspase 8	Homo sapiens	231-240
15161627-5	2004	The appearance of diminished FRET was inhibited by a pan-caspase inhibitor z-VAD or D-&gt;A mutations in the LEVD sequence and was markedly increased by apoptosis-inducing agents, etoposide and camptothecin, or overexpression of a caspase 8-red fluorescent protein fusion protein.	z-vad	75-80	caspase 8	Homo sapiens	231-240
15161627-5	2004	The appearance of diminished FRET was inhibited by a pan-caspase inhibitor z-VAD or D-&gt;A mutations in the LEVD sequence and was markedly increased by apoptosis-inducing agents, etoposide and camptothecin, or overexpression of a caspase 8-red fluorescent protein fusion protein.	Camptothecin	194-206	caspase 8	Homo sapiens	231-240
15161627-9	2004	However, staurosporine induced cleavage of the probe in caspase 8-deficient cells by a mechanism that was inhibited by overexpression of bcl-x.	Staurosporine	9-22	caspase 8	Homo sapiens	56-65
15117910-10	2004	In addition, Hcy inhibited expression of the caspase-8 inhibitor FLICE-inhibitory protein (FLIP).	Homocysteine	13-16	caspase 8	Homo sapiens	45-54
15161627-5	2004	The appearance of diminished FRET was inhibited by a pan-caspase inhibitor z-VAD or D-&gt;A mutations in the LEVD sequence and was markedly increased by apoptosis-inducing agents, etoposide and camptothecin, or overexpression of a caspase 8-red fluorescent protein fusion protein.	d-&gt	84-89	caspase 8	Homo sapiens	231-240
15241888-5	2004	The pan-specific caspase inhibitor, ZVAD-fmk, abolished the PC-induced apoptosis,whereas the caspase-8 inhibitor IETD-fmk showed no effect, implying the involvement of the caspase 9 pathway.	isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	113-121	caspase 8	Homo sapiens	93-102
15008459-0	2004	Oridonin induced A375-S2 cell apoptosis via bax-regulated caspase pathway activation, dependent on the cytochrome c/caspase-9 apoptosome.	oridonin	0-8	caspase 8	Homo sapiens	58-65
15209353-4	2004	Here, we demonstrate that dehydrocostus lactone (DL), the major sesquiterpene lactone isolated from the roots of Saussurea lappa, inhibits NF-kappaB activation by preventing TNF-alpha-induced degradation and phosphorylation of its inhibitory protein I-kappaB alpha in human leukemia HL-60 cells and that DL renders HL-60 cells susceptible to TNF-alpha-induced apoptosis by enhancing caspase-8 and caspase-3 activities.	dehydrocostus lactone	26-47	caspase 8	Homo sapiens	383-392
15130763-11	2004	In conclusion, the tyrosine kinase p56/Lck is essential for apoptosis induction by Doxorubicin, Paclitaxel and 5-Fluorouracil regulating early steps of the mitochondrial apoptosis signaling cascade, including alteration of mitochondrial functions and caspase-activation.	Doxorubicin	83-94	caspase 8	Homo sapiens	251-258
15130763-11	2004	In conclusion, the tyrosine kinase p56/Lck is essential for apoptosis induction by Doxorubicin, Paclitaxel and 5-Fluorouracil regulating early steps of the mitochondrial apoptosis signaling cascade, including alteration of mitochondrial functions and caspase-activation.	Paclitaxel	96-106	caspase 8	Homo sapiens	251-258
15130763-11	2004	In conclusion, the tyrosine kinase p56/Lck is essential for apoptosis induction by Doxorubicin, Paclitaxel and 5-Fluorouracil regulating early steps of the mitochondrial apoptosis signaling cascade, including alteration of mitochondrial functions and caspase-activation.	Fluorouracil	111-125	caspase 8	Homo sapiens	251-258
14993214-8	2004	Electrophoretic mobility shift assay analysis demonstrated that IFN-gamma induces a complex between an oligonucleotide probe containing the ISRE motif and IRF-1 over a similar time scale to the induction of caspase-8 mRNA.	Oligonucleotides	103-118	caspase 8	Homo sapiens	207-216
14741615-0	2004	Effect of cobalt and chromium ions on bcl-2, bax, caspase-3, and caspase-8 expression in human U937 macrophages.	Chromium	21-29	caspase 8	Homo sapiens	65-74
14741615-2	2004	The purpose of this study was to analyze the effect of Co(2+) and Cr(3+) ions on the expression of bcl-2, bax, caspase-3 and caspase-8 to better understand the mechanisms leading to ion-induced apoptosis in macrophages.	Cobalt(2+)	55-61	caspase 8	Homo sapiens	125-134
14741615-7	2004	In conclusion, our results suggest that the modulation of the expression of proteins from the bcl-2 and the caspase families of proteins are implicated in the induction of macrophage apoptosis by Co(2+) and Cr(3+) ions.	Cobalt(2+)	196-202	caspase 8	Homo sapiens	108-115
15111130-0	2004	Protein kinase B inhibits apoptosis induced by actinomycin D in ECV304 cells through phosphorylation of caspase 8.	Dactinomycin	47-60	caspase 8	Homo sapiens	104-113
15258464-0	2004	2-MeOE2bisMATE induces caspase-dependent apoptosis in CAL51 breast cancer cells and overcomes resistance to TRAIL via cooperative activation of caspases.	2-methoxyestradiol-3,17-bis-O,O-sulfamate	0-14	caspase 8	Homo sapiens	23-30
15258464-0	2004	2-MeOE2bisMATE induces caspase-dependent apoptosis in CAL51 breast cancer cells and overcomes resistance to TRAIL via cooperative activation of caspases.	2-methoxyestradiol-3,17-bis-O,O-sulfamate	0-14	caspase 8	Homo sapiens	144-152
15258464-5	2004	We demonstrate that 2-MeOE2bisMATE-induced apoptosis of CAL51 breast cancer cells was associated with rapid activation of caspase 3 and 9, but not caspase 8 (as measured by BID cleavage) and was completely prevented by the caspase inhibitor zVADfmk.	2-methoxyestradiol-3,17-bis-O,O-sulfamate	20-34	caspase 8	Homo sapiens	147-156
15258464-5	2004	We demonstrate that 2-MeOE2bisMATE-induced apoptosis of CAL51 breast cancer cells was associated with rapid activation of caspase 3 and 9, but not caspase 8 (as measured by BID cleavage) and was completely prevented by the caspase inhibitor zVADfmk.	2-methoxyestradiol-3,17-bis-O,O-sulfamate	20-34	caspase 8	Homo sapiens	122-129
15258464-5	2004	We demonstrate that 2-MeOE2bisMATE-induced apoptosis of CAL51 breast cancer cells was associated with rapid activation of caspase 3 and 9, but not caspase 8 (as measured by BID cleavage) and was completely prevented by the caspase inhibitor zVADfmk.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	241-248	caspase 8	Homo sapiens	122-129
15258464-9	2004	Therefore, 2-MeOE2bisMATE-induced apoptosis is dependent on caspases and like 2-MeOE2, 2-MeOE2bisMATE can overcome resistance to TRAIL by stimulating activation of downstream caspases.	2-methoxyestradiol-3,17-bis-O,O-sulfamate	11-25	caspase 8	Homo sapiens	60-68
15258464-9	2004	Therefore, 2-MeOE2bisMATE-induced apoptosis is dependent on caspases and like 2-MeOE2, 2-MeOE2bisMATE can overcome resistance to TRAIL by stimulating activation of downstream caspases.	2-methoxyestradiol-3,17-bis-O,O-sulfamate	11-25	caspase 8	Homo sapiens	175-183
15258464-9	2004	Therefore, 2-MeOE2bisMATE-induced apoptosis is dependent on caspases and like 2-MeOE2, 2-MeOE2bisMATE can overcome resistance to TRAIL by stimulating activation of downstream caspases.	2-Methoxyestradiol	11-18	caspase 8	Homo sapiens	60-68
15258464-9	2004	Therefore, 2-MeOE2bisMATE-induced apoptosis is dependent on caspases and like 2-MeOE2, 2-MeOE2bisMATE can overcome resistance to TRAIL by stimulating activation of downstream caspases.	2-Methoxyestradiol	11-18	caspase 8	Homo sapiens	175-183
15258464-9	2004	Therefore, 2-MeOE2bisMATE-induced apoptosis is dependent on caspases and like 2-MeOE2, 2-MeOE2bisMATE can overcome resistance to TRAIL by stimulating activation of downstream caspases.	2-methoxyestradiol-3,17-bis-O,O-sulfamate	87-101	caspase 8	Homo sapiens	60-68
15258464-9	2004	Therefore, 2-MeOE2bisMATE-induced apoptosis is dependent on caspases and like 2-MeOE2, 2-MeOE2bisMATE can overcome resistance to TRAIL by stimulating activation of downstream caspases.	2-methoxyestradiol-3,17-bis-O,O-sulfamate	87-101	caspase 8	Homo sapiens	175-183
15209353-4	2004	Here, we demonstrate that dehydrocostus lactone (DL), the major sesquiterpene lactone isolated from the roots of Saussurea lappa, inhibits NF-kappaB activation by preventing TNF-alpha-induced degradation and phosphorylation of its inhibitory protein I-kappaB alpha in human leukemia HL-60 cells and that DL renders HL-60 cells susceptible to TNF-alpha-induced apoptosis by enhancing caspase-8 and caspase-3 activities.	dehydrocostus lactone	49-51	caspase 8	Homo sapiens	383-392
14990979-6	2004	Moreover, CDDO induced apoptosis in caspase-8 and FADD-deficient but not in Bcl-xL overexpressing Jurkat cells.	2-cyano-3,12-dioxoolean-1,9-dien-28-oic acid	10-14	caspase 8	Homo sapiens	36-45
14761933-2	2004	Whereas TNF-alpha-mediated apoptosis was almost absent in the presence of the caspase-8 inhibitor Z-Ac-Ala-Glu-Val-Asp-7-fluoromethyl ketone (Z-AEVD-FMK), the inhibitor had no effect on spontaneous apoptosis, suggesting that spontaneous apoptosis was independent of caspase-8.	z-ac-ala-glu-val-asp-7-fluoromethyl ketone	98-140	caspase 8	Homo sapiens	78-87
14761933-2	2004	Whereas TNF-alpha-mediated apoptosis was almost absent in the presence of the caspase-8 inhibitor Z-Ac-Ala-Glu-Val-Asp-7-fluoromethyl ketone (Z-AEVD-FMK), the inhibitor had no effect on spontaneous apoptosis, suggesting that spontaneous apoptosis was independent of caspase-8.	benzyloxycarbonyl-alanyl-glutamyl-valyl-aspartic acid fluoromethyl ketone	142-152	caspase 8	Homo sapiens	78-87
15141014-13	2004	Furthermore, the results of the present study point toward involvement of both caspase-8- and caspase-9-mediated pathways in apoptosis induction by PEITC.	phenethyl isothiocyanate	148-153	caspase 8	Homo sapiens	79-88
15124083-1	2004	We previously reported that ent-11alpha-hydroxy-16-kauren-15-one (KD) induces apoptosis through a caspase-dependent pathway and the induction of apoptosis is dependent on its enone group in human leukemia cells.	ent-11alpha-hydroxy-16-kauren-15-one	28-64	caspase 8	Homo sapiens	98-105
15981920-4	2004	Using the fluorochrome-labeled caspase inhibitor assay, it was found that both free DOX and P-(GFLG)-DOX activated caspases 3 and 9, but both forms of DOX did not have an effect on the activity of caspase 8, when compared to untreated cells.	Doxorubicin	84-87	caspase 8	Homo sapiens	31-38
15981920-4	2004	Using the fluorochrome-labeled caspase inhibitor assay, it was found that both free DOX and P-(GFLG)-DOX activated caspases 3 and 9, but both forms of DOX did not have an effect on the activity of caspase 8, when compared to untreated cells.	Doxorubicin	84-87	caspase 8	Homo sapiens	197-206
15981920-4	2004	Using the fluorochrome-labeled caspase inhibitor assay, it was found that both free DOX and P-(GFLG)-DOX activated caspases 3 and 9, but both forms of DOX did not have an effect on the activity of caspase 8, when compared to untreated cells.	p-(gflg)-dox	92-104	caspase 8	Homo sapiens	31-38
15981920-4	2004	Using the fluorochrome-labeled caspase inhibitor assay, it was found that both free DOX and P-(GFLG)-DOX activated caspases 3 and 9, but both forms of DOX did not have an effect on the activity of caspase 8, when compared to untreated cells.	Doxorubicin	101-104	caspase 8	Homo sapiens	197-206
15083198-6	2004	TRAIL-induced apoptosis and its augmentation by alpha-TOS were inhibited by the caspase-8 inhibitor Z-IETD-FMK and the pan-caspase inhibitor Z-VAD-FMK.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	100-110	caspase 8	Homo sapiens	80-89
15070698-5	2004	Importantly, CDDO-Im and bortezomib/proteasome inhibitor PS-341 trigger synergistic apoptosis in MM cells associated with loss of mitochondrial membrane potential, superoxide generation, release of mitochondrial proteins cytochrome c/second mitochondria-derived activator of caspases (cytochrome c/Smac), and activation of caspase-8, -9, and -3.	1-(2-cyano-3,12-dioxooleana-1,9-dien-28-oyl) imidazole	13-20	caspase 8	Homo sapiens	323-344
15070698-5	2004	Importantly, CDDO-Im and bortezomib/proteasome inhibitor PS-341 trigger synergistic apoptosis in MM cells associated with loss of mitochondrial membrane potential, superoxide generation, release of mitochondrial proteins cytochrome c/second mitochondria-derived activator of caspases (cytochrome c/Smac), and activation of caspase-8, -9, and -3.	Bortezomib	25-35	caspase 8	Homo sapiens	323-344
15070698-5	2004	Importantly, CDDO-Im and bortezomib/proteasome inhibitor PS-341 trigger synergistic apoptosis in MM cells associated with loss of mitochondrial membrane potential, superoxide generation, release of mitochondrial proteins cytochrome c/second mitochondria-derived activator of caspases (cytochrome c/Smac), and activation of caspase-8, -9, and -3.	Bortezomib	57-63	caspase 8	Homo sapiens	323-344
15013668-5	2004	We observed increased levels of several Fas-mediated apoptosis effectors (Fas, Fas ligand, FADD, FLICE), both in cell cultures at advanced passages and in skin cells of aged donors (above 45 years).	ammonium ferrous sulfate	40-43	caspase 8	Homo sapiens	97-102
15115612-6	2004	The activity of caspase-3, which is one of the major executioner caspases, was found to be inhibited by both Z-DEVD-MFK and Z-VAD-FMK.	z-devd-mfk	109-119	caspase 8	Homo sapiens	65-73
15115612-6	2004	The activity of caspase-3, which is one of the major executioner caspases, was found to be inhibited by both Z-DEVD-MFK and Z-VAD-FMK.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	124-133	caspase 8	Homo sapiens	65-73
15037574-9	2004	In ethanol-exposed corneal epithelium Tbeta(4) treatment inhibited caspase-2, -3, -8, and -9 activity, with caspase-8 showing the most significant inhibition.	Ethanol	3-10	caspase 8	Homo sapiens	108-117
14691451-6	2004	MG132 effectively cooperated with Apo2L/TRAIL to induce apoptosis in both Bax-proficient and -deficient cells that was coupled with caspases-8 and -3 activation and Bid cleavage.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	caspase 8	Homo sapiens	132-149
14987955-8	2004	It was confirmed that the activation of caspase 8, 9 and 3 and the cleavage of PARP by heyneanol A were completely blocked by adding Z-VAD-FMK, a caspase inhibitor.	heyneanol A	87-98	caspase 8	Homo sapiens	40-58
14987955-8	2004	It was confirmed that the activation of caspase 8, 9 and 3 and the cleavage of PARP by heyneanol A were completely blocked by adding Z-VAD-FMK, a caspase inhibitor.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	133-142	caspase 8	Homo sapiens	40-58
14563674-7	2004	For comparison, glutamine deprivation also caused apoptotic cell death but with slower temporal kinetics, stimulated caspases-2 and -3 but not caspases-8 or -9 activities, and led to considerable PARP cleavage.	Glutamine	16-25	caspase 8	Homo sapiens	143-159
15009062-5	2004	However, caspase-8 was processed and functional after treatment with staurosporine (STS).	Staurosporine	69-82	caspase 8	Homo sapiens	9-18
15009062-5	2004	However, caspase-8 was processed and functional after treatment with staurosporine (STS).	Staurosporine	84-87	caspase 8	Homo sapiens	9-18
14676829-0	2004	Essential role of caspases in epigallocatechin-3-gallate-mediated inhibition of nuclear factor kappa B and induction of apoptosis.	epigallocatechin gallate	30-56	caspase 8	Homo sapiens	18-26
14676829-4	2004	Here we show the essential role of caspases in EGCG-mediated inhibition of NF-kappa B and its subsequent apoptosis.	epigallocatechin gallate	47-51	caspase 8	Homo sapiens	35-43
14676829-6	2004	EGCG treatment of cells also resulted in significant activation of caspases, as shown by the dose- and time-dependent increase in DEVDase activity, and protein expression of caspase-3, -8 and -9.	epigallocatechin gallate	0-4	caspase 8	Homo sapiens	67-75
14676829-7	2004	EGCG-mediated caspase activation induces proteolytic cleavage of NF-kappa B/p65 subunit, leading to the loss of transactivation domains, and driving the cells towards apoptosis.	epigallocatechin gallate	0-4	caspase 8	Homo sapiens	14-21
14676829-8	2004	EGCG-mediated induction of apoptosis was significantly blocked by the caspase inhibitor N-benzyloxycarbonyl-Val-Ala-Asp(OMe)-fluoromethylketone (Z-VAD-FMK), and moderately blocked by the specific caspase-3 inhibitor Z-DEVD-FMK.	epigallocatechin gallate	0-4	caspase 8	Homo sapiens	70-77
14676829-8	2004	EGCG-mediated induction of apoptosis was significantly blocked by the caspase inhibitor N-benzyloxycarbonyl-Val-Ala-Asp(OMe)-fluoromethylketone (Z-VAD-FMK), and moderately blocked by the specific caspase-3 inhibitor Z-DEVD-FMK.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	88-143	caspase 8	Homo sapiens	70-77
14676829-8	2004	EGCG-mediated induction of apoptosis was significantly blocked by the caspase inhibitor N-benzyloxycarbonyl-Val-Ala-Asp(OMe)-fluoromethylketone (Z-VAD-FMK), and moderately blocked by the specific caspase-3 inhibitor Z-DEVD-FMK.	benzoylcarbonyl-aspartyl-glutamyl-valyl-aspartyl-fluoromethyl ketone	216-226	caspase 8	Homo sapiens	70-77
14676829-10	2004	Taken together, these studies for the first time demonstrate that EGCG-mediated activation of caspases is critical, at least in part, for inhibition of NF-kappa B and subsequent apoptosis.	epigallocatechin gallate	66-70	caspase 8	Homo sapiens	94-102
14750167-8	2004	Caspase-8 and Bid were cleaved in Colo357 cells exposed to gemcitabine, and there was no correlation with either Bcl-xL or with Bax expression.	gemcitabine	59-70	caspase 8	Homo sapiens	0-9
14726646-5	2004	ATO rapidly induced Apo2/TRAIL, activation of caspase 8, cleavage of BID, depolarization of mitochondrial membrane (MM) and release of AIF from mitochondria in a Bcl-2 independent fashion.	Arsenic Trioxide	0-3	caspase 8	Homo sapiens	46-55
31394674-9	2004	Apoptosis was partly inhibited by the addition of caspase inhibitors zVADfmk (general inhibitor) and zIETDfmk (selective caspase-8 inhibitor).	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	101-109	caspase 8	Homo sapiens	121-130
14977934-6	2004	Caspase-8, an initiator caspase in apoptosis, was found to be activated in these cells in response to BfLP stimulation.	bflp	102-106	caspase 8	Homo sapiens	0-9
15499173-0	2004	Proapoptotic effect of a dietary supplement: water soluble chitosan activates caspase-8 and modulating death receptor expression.	Water	45-50	caspase 8	Homo sapiens	78-117
14647422-8	2004	The role of the Fas-L/Fas signaling axis in IFNalpha-mediated apoptosis is demonstrated by the fact that addition of Fas-L neutralizing antibodies, just as caspase-8 inhibitor Z-IETD-FMK, effectively prevents IFNalpha-mediated apoptosis.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	176-186	caspase 8	Homo sapiens	156-165
14977852-11	2004	Moreover, we have identified a mechanism of cytotoxicity in dexamethasone-sensitive and -resistant myeloma cells induced by imexon that is caspase-8 dependent.	Dexamethasone	60-73	caspase 8	Homo sapiens	139-148
15163118-6	2004	After Fas triggering, the generation of the active sub-units of caspase-8 is significantly reduced in T1DM T-cells restimulated via TCR/CD3 and/or CD28.	ammonium ferrous sulfate	6-9	caspase 8	Homo sapiens	64-73
15028947-1	2004	AIM: We have previously reported that 15-deoxy-delta-prostaglandin J2 (15d-PGJ2), a potent ligand for peroxisome proliferator-activated receptor gamma (PPARgamma), induces caspase-mediated apoptosis in human pancreatic cancer cell lines.	15-deoxy-delta-prostaglandin j2	38-69	caspase 8	Homo sapiens	172-179
15028947-1	2004	AIM: We have previously reported that 15-deoxy-delta-prostaglandin J2 (15d-PGJ2), a potent ligand for peroxisome proliferator-activated receptor gamma (PPARgamma), induces caspase-mediated apoptosis in human pancreatic cancer cell lines.	15-deoxyprostaglandin J2	71-79	caspase 8	Homo sapiens	172-179
15028947-8	2004	SB202190, an inhibitor of p38, prevented 15d-PGJ2-induced activation of caspase-8, -9, and -3 and significantly decreased apoptosis.	4-(4-fluorophenyl)-2-(4-hydroxyphenyl)-5-(4-pyridyl)imidazole	0-8	caspase 8	Homo sapiens	72-93
15028947-8	2004	SB202190, an inhibitor of p38, prevented 15d-PGJ2-induced activation of caspase-8, -9, and -3 and significantly decreased apoptosis.	9-deoxy-delta-9-prostaglandin D2	45-49	caspase 8	Homo sapiens	72-93
14764700-7	2004	Fas immunoprecipitation reveals that caspase-3 is a component of the death-inducing signaling complex, suggesting that this cysteine protease is in close proximity to caspase-8.	ammonium ferrous sulfate	0-3	caspase 8	Homo sapiens	167-176
14871845-4	2004	Subsequent studies revealed that 2,3-DCPE could cause cleavage of caspase-8, caspase-3, caspase-9, and poly(ADP-ribose) polymerase and release of cytochrome c in cancer cells but not in normal human fibroblasts.	2-((3-(2,3-dichlorophenoxy)propyl)amino)ethanol	33-41	caspase 8	Homo sapiens	66-75
14719118-11	2004	Incubating cells with a caspase-8-specific inhibitor Ac-IETD-CHO prior to Ad-p53 infection inhibited caspase-8 activity and apoptosis.	Ac-IETD-CHO	53-64	caspase 8	Homo sapiens	101-110
14719107-4	2004	Furthermore, the apoptotic phenotypes totally disappeared with zVAD-fmk, a caspase inhibitor.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	63-71	caspase 8	Homo sapiens	75-82
15106734-5	2004	Increase of Fas/Apo-1 expression and caspase-8 and caspase-3 activation focused two typical steps in the pathway of the pro-apoptotic mechanism exhibited by polyamines, even if to a different extent: spermine &gt; spermidine &gt; putrescine.	Polyamines	157-167	caspase 8	Homo sapiens	37-46
14719107-8	2004	These results indicate that BLM-induced apoptosis in HL-60 cells results from the activation of a mitochondria-dependent caspase cascade which includes also the activation of the initiator caspase-8.	Bleomycin	28-31	caspase 8	Homo sapiens	189-198
14719118-11	2004	Incubating cells with a caspase-8-specific inhibitor Ac-IETD-CHO prior to Ad-p53 infection inhibited caspase-8 activity and apoptosis.	Ac-IETD-CHO	53-64	caspase 8	Homo sapiens	24-33
14707100-8	2004	Taken together, these data suggest that CO confers potent antiproliferative effects in CD3-activated T lymphocytes and that these antiproliferative effects in T lymphocytes are mediated by p21(Cip1)-dependent caspase activity, in particular caspase-8, independent of cGMP and mitogen-activated protein kinase signaling pathways.	Cyclic GMP	267-271	caspase 8	Homo sapiens	209-216
14761678-0	2004	A ginseng saponin metabolite-induced apoptosis in HepG2 cells involves a mitochondria-mediated pathway and its downstream caspase-8 activation and Bid cleavage.	Saponins	10-17	caspase 8	Homo sapiens	122-131
14761678-9	2004	The activation of caspase-8 was inhibited not only by zIETD-fmk but also by zVAD-fmk.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	54-63	caspase 8	Homo sapiens	18-27
14761678-9	2004	The activation of caspase-8 was inhibited not only by zIETD-fmk but also by zVAD-fmk.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	76-84	caspase 8	Homo sapiens	18-27
14672717-3	2004	Complestatin blocked TRAIL (TNF-related apoptosis-inducing ligand)-induced apoptosis and activation of caspase-3 and -8 at micromolar concentration levels without inhibiting the catalytic activities of these caspases.	complestatin	0-12	caspase 8	Homo sapiens	208-216
15015600-5	2004	Treatment of cells with L-OHP resulted in the activation of caspase-8, -9 and -3, in a mitochondrial membrane depolarisation, and in an increase of CD95 receptor and CD95 ligand levels.	Oxaliplatin	24-29	caspase 8	Homo sapiens	60-80
14514658-4	2004	SFN-induced apoptosis, and cleavage of procaspase-3 and PARP were blocked upon pre-treatment of cells with pan caspase inhibitor z-VADfmk, and specific inhibitors of caspase-9 (z-LEHDfmk) and caspase-8 (z-IETDfmk) suggesting involvement of both caspase-9 and caspase-8 pathways in SFN-induced cell death.	sulforaphane	0-3	caspase 8	Homo sapiens	192-201
12970672-4	2004	Culture with caspase 8 antisense oligonucleotides or peptide inhibitors reduced the fusion of cytotrophoblast with the syncytiotrophoblast, and resulted in multilayered cytotrophoblast.	Oligonucleotides	33-49	caspase 8	Homo sapiens	13-22
12970672-5	2004	Caspase 8 expression was suppressed by antisense oligonucleotides and caspase 8 activities were reduced by peptide inhibitors.	Oligonucleotides	49-65	caspase 8	Homo sapiens	0-9
15566959-8	2004	After 1 microM cisplatin treatment, Xrel3 had an anti-apoptotic effect, based on significantly lower levels of apoptotic proteins, including caspase-8, caspase-3 and p21.	Cisplatin	15-24	caspase 8	Homo sapiens	141-150
15566959-10	2004	After 5 microM cisplatin treatment, expression of HeLa Xrel3 had an apoptotic effect, based on significantly increased expression of the cell cycle inhibitor p21 and apoptotic proteins, including cleaved PARP, caspase-8, and caspase-3.	Cisplatin	15-24	caspase 8	Homo sapiens	210-219
13129434-5	2004	This apoptotic pathway induced by abrin is caspase 3-dependent but caspase 8-independent and involves mitochondrial membrane potential damage and reactive oxygen species production.	Reactive Oxygen Species	146-169	caspase 8	Homo sapiens	67-76
14514658-4	2004	SFN-induced apoptosis, and cleavage of procaspase-3 and PARP were blocked upon pre-treatment of cells with pan caspase inhibitor z-VADfmk, and specific inhibitors of caspase-9 (z-LEHDfmk) and caspase-8 (z-IETDfmk) suggesting involvement of both caspase-9 and caspase-8 pathways in SFN-induced cell death.	sulforaphane	0-3	caspase 8	Homo sapiens	259-268
14688367-11	2004	FLIP-caspase-8 balance seems tightly regulated in fibroblasts by extracellular factors that determine their susceptibility to Fas- or Fas-CHX-induced apoptosis.	ammonium ferrous sulfate	126-129	caspase 8	Homo sapiens	5-14
14720504-5	2004	Inhibitors of caspase-8 (z-IETD.fmk) and caspase-10 (z-AEVD.fmk) significantly reduced TNF-alpha/butyrate-induced apoptosis, based on nuclear morphology and terminal deoxynucleotide transferase-mediated dUTP-biotin nick-end labelling (TUNEL), although caspase inhibition was associated with a significant increase in cells demonstrating atypical nuclear condensation.	z-ietd	25-31	caspase 8	Homo sapiens	14-23
14720504-5	2004	Inhibitors of caspase-8 (z-IETD.fmk) and caspase-10 (z-AEVD.fmk) significantly reduced TNF-alpha/butyrate-induced apoptosis, based on nuclear morphology and terminal deoxynucleotide transferase-mediated dUTP-biotin nick-end labelling (TUNEL), although caspase inhibition was associated with a significant increase in cells demonstrating atypical nuclear condensation.	Butyrates	97-105	caspase 8	Homo sapiens	14-23
14720504-5	2004	Inhibitors of caspase-8 (z-IETD.fmk) and caspase-10 (z-AEVD.fmk) significantly reduced TNF-alpha/butyrate-induced apoptosis, based on nuclear morphology and terminal deoxynucleotide transferase-mediated dUTP-biotin nick-end labelling (TUNEL), although caspase inhibition was associated with a significant increase in cells demonstrating atypical nuclear condensation.	dutp-biotin	203-214	caspase 8	Homo sapiens	14-23
14720504-8	2004	Transmembrane resistance was also used a measure of the ability of caspase inhibitors to prevent TNF-alpha/butyrate-mediated damage to epithelial monolayers.	Butyrates	107-115	caspase 8	Homo sapiens	67-74
14720504-10	2004	In conclusion, synthetic caspase inhibitors can reduce the apoptotic response of CaCo-2 colonic epithelial cells to TNF-alpha/butyrate, improve the maintenance of viable cell numbers and block loss of transmembrane resistance.	Butyrates	126-134	caspase 8	Homo sapiens	25-32
14994280-0	2004	Generation of an oxidative stress precedes caspase activation during 7beta-hydroxycholesterol-induced apoptosis in U937 cells.	cholest-5-en-3 beta,7 alpha-diol	69-93	caspase 8	Homo sapiens	43-50
14688367-11	2004	FLIP-caspase-8 balance seems tightly regulated in fibroblasts by extracellular factors that determine their susceptibility to Fas- or Fas-CHX-induced apoptosis.	ammonium ferrous sulfate	134-137	caspase 8	Homo sapiens	5-14
14688367-11	2004	FLIP-caspase-8 balance seems tightly regulated in fibroblasts by extracellular factors that determine their susceptibility to Fas- or Fas-CHX-induced apoptosis.	Cycloheximide	138-141	caspase 8	Homo sapiens	5-14
14665704-8	2004	Using a XIAP inhibitor, phenoxodiol, we demonstrate that XIAP inactivation sensitizes trophoblast cells to Fas stimulation, as evidenced by the anti-Fas mAb-induced decrease in trophoblast cell viability and increase in caspase-8, caspase-9 and caspase-3 activation.	phenoxodiol	24-35	caspase 8	Homo sapiens	220-229
14689449-8	2004	Isolation of sphingolipid-rich plasma membrane microdomains (rafts) from the cells by sucrose density gradient ultracentrifugation revealed an enrichment of sphingomyelin, ceramide, and caspase 8.	Sphingolipids	13-25	caspase 8	Homo sapiens	186-195
14749474-5	2004	CDDO-Im treatment was associated with (a) depletion of glutathione, (b) increases in reactive oxygen species, (c) a reduction of the Fas-associated death domain (FADD)-like interleukin-1-converting enzyme (FLICE) inhibitory protein, (d) activation of caspase-8, and (e) a decrease of the mitochondrial transmembrane potential.	1-(2-cyano-3,12-dioxooleana-1,9-dien-28-oyl) imidazole	0-7	caspase 8	Homo sapiens	206-211
14749474-5	2004	CDDO-Im treatment was associated with (a) depletion of glutathione, (b) increases in reactive oxygen species, (c) a reduction of the Fas-associated death domain (FADD)-like interleukin-1-converting enzyme (FLICE) inhibitory protein, (d) activation of caspase-8, and (e) a decrease of the mitochondrial transmembrane potential.	1-(2-cyano-3,12-dioxooleana-1,9-dien-28-oyl) imidazole	0-7	caspase 8	Homo sapiens	251-260
14749474-7	2004	Inhibition of caspase-8 with z-IETD-fmk also abrogated CDDO-Im-induced decreases of the mitochondrial transmembrane potential and inhibited apoptosis.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	29-39	caspase 8	Homo sapiens	14-23
14749474-7	2004	Inhibition of caspase-8 with z-IETD-fmk also abrogated CDDO-Im-induced decreases of the mitochondrial transmembrane potential and inhibited apoptosis.	1-(2-cyano-3,12-dioxooleana-1,9-dien-28-oyl) imidazole	55-62	caspase 8	Homo sapiens	14-23
14749474-8	2004	These results demonstrate that CDDO-Im disrupts intracellular redox balance and thereby activates the extrinsic caspase-8-dependent apoptotic pathway.	1-(2-cyano-3,12-dioxooleana-1,9-dien-28-oyl) imidazole	31-38	caspase 8	Homo sapiens	112-121
14644092-6	2004	Subcellular fractionation studies revealed that the amount of mature caspase-8 but not pro-caspase at the membrane was increased following CD95-stimulation in the presence of DNP.	2,4-Dinitrophenol	175-178	caspase 8	Homo sapiens	69-78
14665704-8	2004	Using a XIAP inhibitor, phenoxodiol, we demonstrate that XIAP inactivation sensitizes trophoblast cells to Fas stimulation, as evidenced by the anti-Fas mAb-induced decrease in trophoblast cell viability and increase in caspase-8, caspase-9 and caspase-3 activation.	ammonium ferrous sulfate	107-110	caspase 8	Homo sapiens	220-229
15572302-8	2004	In contrast, an active role of calpains in addition to caspases was demonstrated in apoptosis induced by fisetin, apigenin, and 3,7-dihydroxyflavone.	fisetin	105-112	caspase 8	Homo sapiens	55-63
15572302-8	2004	In contrast, an active role of calpains in addition to caspases was demonstrated in apoptosis induced by fisetin, apigenin, and 3,7-dihydroxyflavone.	3,7-dihydroxyflavone	128-148	caspase 8	Homo sapiens	55-63
14522966-1	2003	We previously demonstrated that the phytosphingosine-induced apoptosis was accompanied by the concomitant induction of both the caspase-8-mediated and mitochondrial activation-mediated apoptosis pathways.	phytosphingosine	36-52	caspase 8	Homo sapiens	128-137
14695141-7	2003	EXPERIMENTAL DESIGN: We used immunohistochemistry to analyze the protein expression of the key initiator caspase-8 and caspase-9 in paraffin-embedded tumor samples from 77 well characterized MB patients and compared the expression levels of caspase-8 and caspase-9 with apoptosis indices, clinical variables, and survival outcomes.	Paraffin	132-140	caspase 8	Homo sapiens	105-114
14522966-3	2003	Phytosphingosine caused strong induction of caspase-8 activity and caspase-independent Bax translocation to the mitochondria.	phytosphingosine	0-16	caspase 8	Homo sapiens	44-53
14522966-5	2003	Activation of ERK1/2 by pretreatment with phorbol 12-myristate 13-acetate or forced expression of ERK1/2 attenuated phytosphingosine-induced caspase-8 activation.	Tetradecanoylphorbol Acetate	42-73	caspase 8	Homo sapiens	141-150
14522966-5	2003	Activation of ERK1/2 by pretreatment with phorbol 12-myristate 13-acetate or forced expression of ERK1/2 attenuated phytosphingosine-induced caspase-8 activation.	phytosphingosine	116-132	caspase 8	Homo sapiens	141-150
14522966-6	2003	However, Bax translocation and caspase-9 activation was unaffected, indicating that down-regulation of the ERK activity is specifically required for the phytosphingosine-induced caspase-8-dependent cell death pathway.	phytosphingosine	153-169	caspase 8	Homo sapiens	178-187
14522966-7	2003	On the other hand, treatment with SB203580, a p38 MAPK-specific inhibitor, or expression of a dominant negative form of p38 MAPK suppressed phytosphingosine-induced translocation of the proapoptotic protein, Bax, from the cytosol to mitochondria, cytochrome c release, and subsequent caspase-9 activation but did not affect caspase-8 activation, indicating that activation of p38 MAPK is involved in the mitochondrial activation-mediated cell death pathway.	SB 203580	34-42	caspase 8	Homo sapiens	324-333
14625033-0	2003	Decreased levels of CD95 and caspase-8 mRNA in multiple sclerosis patients with gadolinium-enhancing lesions on MRI.	Gadolinium	80-90	caspase 8	Homo sapiens	29-38
14645705-6	2003	Caspase 8 inhibition protects both CPT-11 pretreated wild-type and Bax-/- HCT116 cells from TRAIL-induced apoptosis, whereas caspase 9 inhibition only rescued the wild-type HCT116 cells from death induced by TRAIL.	Irinotecan	35-41	caspase 8	Homo sapiens	0-9
14644447-5	2003	Increases in caspase 8 and caspase 3 activity were also observed in human cells (K562) treated with 11-ala.	11-ala	100-106	caspase 8	Homo sapiens	13-22
14632785-7	2003	The caspase-8 specific inhibitor, Z-IETD, impaired caspase-8 activation and completely abrogated TRAIL-induced apoptosis.	z-ietd	34-40	caspase 8	Homo sapiens	4-13
14644418-4	2003	Cleavage of Bid, the caspase-8 substrate, was inhibited by the broad caspase inhibitor z-Val-Ala-Asp(OMe)-fluoromethylketone (zVAD-fmk), whereas cytochrome c release was not affected, suggesting that activation of caspase-8 and subsequent Bid cleavage occur downstream of cytochrome c release.	z-Val-Ala-Asp(Ome)-fluoromethylketone	87-124	caspase 8	Homo sapiens	21-30
14644418-4	2003	Cleavage of Bid, the caspase-8 substrate, was inhibited by the broad caspase inhibitor z-Val-Ala-Asp(OMe)-fluoromethylketone (zVAD-fmk), whereas cytochrome c release was not affected, suggesting that activation of caspase-8 and subsequent Bid cleavage occur downstream of cytochrome c release.	z-Val-Ala-Asp(Ome)-fluoromethylketone	87-124	caspase 8	Homo sapiens	214-223
14644418-4	2003	Cleavage of Bid, the caspase-8 substrate, was inhibited by the broad caspase inhibitor z-Val-Ala-Asp(OMe)-fluoromethylketone (zVAD-fmk), whereas cytochrome c release was not affected, suggesting that activation of caspase-8 and subsequent Bid cleavage occur downstream of cytochrome c release.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	126-134	caspase 8	Homo sapiens	21-30
14644418-4	2003	Cleavage of Bid, the caspase-8 substrate, was inhibited by the broad caspase inhibitor z-Val-Ala-Asp(OMe)-fluoromethylketone (zVAD-fmk), whereas cytochrome c release was not affected, suggesting that activation of caspase-8 and subsequent Bid cleavage occur downstream of cytochrome c release.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	126-134	caspase 8	Homo sapiens	214-223
15033719-8	2003	Interestingly, the apoptotic response to TRAIL was enhanced by co-treatment of SH-EP and IGR-N91-C8 cells with CHX or with sub-toxic concentration of doxorubicin (DOX) in a caspase-dependent manner, as cells could be protected from death by specific caspase-8 or pan-caspase inhibitors.	Doxorubicin	150-161	caspase 8	Homo sapiens	250-259
15033719-8	2003	Interestingly, the apoptotic response to TRAIL was enhanced by co-treatment of SH-EP and IGR-N91-C8 cells with CHX or with sub-toxic concentration of doxorubicin (DOX) in a caspase-dependent manner, as cells could be protected from death by specific caspase-8 or pan-caspase inhibitors.	Doxorubicin	163-166	caspase 8	Homo sapiens	250-259
15033719-9	2003	CHX or DOX was shown to enhance TRAIL-induced caspase-8 activation and loss of mitochondrial transmembrane potential.	Doxorubicin	7-10	caspase 8	Homo sapiens	46-55
15033719-11	2003	Moreover, DOX and CHX were able to sensitize NB cell lines to TRAIL-induced apoptosis in a caspase-8-dependent manner by engaging death receptor and mitochondrial signaling pathways.	Doxorubicin	10-13	caspase 8	Homo sapiens	91-100
14609740-7	2003	The hierarchy of caspase activation by diclofenac was investigated.	Diclofenac	39-49	caspase 8	Homo sapiens	17-24
14609740-9	2003	Inhibitors of MPT, prevented the downstream activation of the caspase cascade, thus showing that diclofenac opened the mitochondrial pore.	Diclofenac	97-107	caspase 8	Homo sapiens	62-69
14609740-10	2003	On the other hand, antioxidants were able to prevent caspase activation by diclofenac, revealing that oxidative stress at the mitochondrial level is in the root of MPT induction and caspase cascade activation.	Diclofenac	75-85	caspase 8	Homo sapiens	53-60
14609740-10	2003	On the other hand, antioxidants were able to prevent caspase activation by diclofenac, revealing that oxidative stress at the mitochondrial level is in the root of MPT induction and caspase cascade activation.	Diclofenac	75-85	caspase 8	Homo sapiens	182-189
14609740-13	2003	Caspases 8 and 9 are very likely the apical caspases in diclofenac-induced apoptosis.	Diclofenac	56-66	caspase 8	Homo sapiens	0-16
14609740-13	2003	Caspases 8 and 9 are very likely the apical caspases in diclofenac-induced apoptosis.	Diclofenac	56-66	caspase 8	Homo sapiens	44-52
14632785-7	2003	The caspase-8 specific inhibitor, Z-IETD, impaired caspase-8 activation and completely abrogated TRAIL-induced apoptosis.	z-ietd	34-40	caspase 8	Homo sapiens	51-60
14632785-10	2003	Interestingly, in some cell lines, TRAIL sensitivity and caspase-8 activity was enhanced or restored with the treatment of cycloheximide (CHX).	Cycloheximide	123-136	caspase 8	Homo sapiens	57-66
14632785-10	2003	Interestingly, in some cell lines, TRAIL sensitivity and caspase-8 activity was enhanced or restored with the treatment of cycloheximide (CHX).	Cycloheximide	138-141	caspase 8	Homo sapiens	57-66
14636829-8	2003	The cytoplasmic and nuclear events of bufadienolide-induced apoptosis were strongly inhibited in the presence of caspase 8, caspase 9, or caspase 3 inhibitors, as well as in the presence of the broad-spectrum caspase inhibitor Z-VAD-FMK.	bufadienolide	38-51	caspase 8	Homo sapiens	113-122
14662022-5	2003	Of the cell lines tested, SNU-216 showed the highest level of constitutively active Akt and the short form of FLICE inhibitory protein (FLIP(S)).	snu-216	26-33	caspase 8	Homo sapiens	110-115
14679006-4	2003	CT-32615 triggered apoptosis in MM cells via caspase-8, caspase-3, caspase-7, and poly (ADP-ribose) polymerase cleavage.	Carbon Tetrachloride	0-2	caspase 8	Homo sapiens	45-54
26680977-7	2003	When TRAIL was used alone, caspase8 was activated in the RPMI-8226 cell lines, but not in the ARH-77 and IM-9 cell lines.	rpmi	57-61	caspase 8	Homo sapiens	27-35
14645674-0	2003	Heterogeneous role of caspase-8 in fenretinide-induced apoptosis in epithelial ovarian carcinoma cell lines.	Fenretinide	35-46	caspase 8	Homo sapiens	22-31
14735224-5	2003	Testosterone-induced apoptosis was associated with the enhanced expression of Fas, FasL, and caspase-8.	Testosterone	0-12	caspase 8	Homo sapiens	93-102
14645674-4	2003	Transient transfection of cDNA-encoding cytokine response modifier A (CrmA), a caspase-8 inhibitor, diminished fenretinide-induced death in OV177 cells.	Fenretinide	111-122	caspase 8	Homo sapiens	79-88
14645674-6	2003	Further analysis demonstrated that inhibition of Fas ligand, tumor necrosis factor-alpha, or TRAIL signaling with blocking reagents did not affect fenretinide-induced apoptosis, raising the possibility that fenretinide activates caspase-8 in a death receptor-independent manner.	Fenretinide	207-218	caspase 8	Homo sapiens	229-238
14678771-5	2003	Caspase-8 and -6 were proteolytically activated during DeltaTau-1-triggered neuronal cell death, which was suppressed by IETD-fmk, caspase-8 inhibitor.	isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	121-129	caspase 8	Homo sapiens	0-16
14678771-5	2003	Caspase-8 and -6 were proteolytically activated during DeltaTau-1-triggered neuronal cell death, which was suppressed by IETD-fmk, caspase-8 inhibitor.	isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	121-129	caspase 8	Homo sapiens	131-140
14645674-9	2003	Similarly, fenretinide treatment increased ceramide levels equally in cells that do (OV177) and do not (OV202) rely on caspase-8 to initiate apoptosis.	Fenretinide	11-22	caspase 8	Homo sapiens	119-128
14645674-10	2003	These results indicate that synthetic retinoids can use caspase-8 as an initiating caspase, but they also indicate unexpected heterogeneity in caspase activation pathways among closely related cell lines.	Retinoids	38-47	caspase 8	Homo sapiens	56-65
12911332-1	2003	Cisplatin-selected cervix carcinoma HeLa cell lines induced less apoptosis, and weaker activation by cisplatin or Fas-activating antibody, of mitochondrial-associated caspase-9 and death receptor-mediated caspase-8 than did parental cells.	Cisplatin	0-9	caspase 8	Homo sapiens	205-214
14678771-7	2003	Cells deficient in caspase-8, but not caspase-3, became sensitized to DeltaTau-1-mediated toxicity upon reconstitution with caspase-8.	deltatau-1	70-80	caspase 8	Homo sapiens	19-28
14678771-7	2003	Cells deficient in caspase-8, but not caspase-3, became sensitized to DeltaTau-1-mediated toxicity upon reconstitution with caspase-8.	deltatau-1	70-80	caspase 8	Homo sapiens	124-133
12963734-4	2003	Inhibition of this pathway by the MEK inhibitors CI-1040 and PD098059 induced apoptosis through a unique pathway involving dephosphorylation and aggregation of Fas-associated death domain protein followed by death receptor-independent caspase-8 activation.	2-(2-chloro-4-iodophenylamino)-N-cyclopropylmethoxy-3,4-difluorobenzamide	49-56	caspase 8	Homo sapiens	235-244
12963734-4	2003	Inhibition of this pathway by the MEK inhibitors CI-1040 and PD098059 induced apoptosis through a unique pathway involving dephosphorylation and aggregation of Fas-associated death domain protein followed by death receptor-independent caspase-8 activation.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	61-69	caspase 8	Homo sapiens	235-244
12963734-5	2003	Jurkat cell variants lacking Fas-associated death domain protein or procaspase-8 were resistant to CI-1040-induced apoptosis, as were Jurkat or Molt3 cells treated with the O-methyl ester of the caspase-8 inhibitor N-(Nalpha-benzyloxycarbonylisoleucylglutamyl) aspartate fluoromethyl ketone.	2-(2-chloro-4-iodophenylamino)-N-cyclopropylmethoxy-3,4-difluorobenzamide	99-106	caspase 8	Homo sapiens	71-80
12911332-3	2003	Ac-IETD-CHO (acetyl-Ile-Glu-Thr-Asp-aldehyde), which has a certain preference for inhibiting caspase-8, or Fas-antagonistic antibody, significantly inhibited cisplatin-induced apoptosis in both parental and cisplatin-selected HeLa cell lines.	Ac-IETD-CHO	0-11	caspase 8	Homo sapiens	93-102
12911332-3	2003	Ac-IETD-CHO (acetyl-Ile-Glu-Thr-Asp-aldehyde), which has a certain preference for inhibiting caspase-8, or Fas-antagonistic antibody, significantly inhibited cisplatin-induced apoptosis in both parental and cisplatin-selected HeLa cell lines.	acetyl-ile	13-23	caspase 8	Homo sapiens	93-102
12911332-3	2003	Ac-IETD-CHO (acetyl-Ile-Glu-Thr-Asp-aldehyde), which has a certain preference for inhibiting caspase-8, or Fas-antagonistic antibody, significantly inhibited cisplatin-induced apoptosis in both parental and cisplatin-selected HeLa cell lines.	Glutamic Acid	24-27	caspase 8	Homo sapiens	93-102
12911332-3	2003	Ac-IETD-CHO (acetyl-Ile-Glu-Thr-Asp-aldehyde), which has a certain preference for inhibiting caspase-8, or Fas-antagonistic antibody, significantly inhibited cisplatin-induced apoptosis in both parental and cisplatin-selected HeLa cell lines.	Threonine	28-31	caspase 8	Homo sapiens	93-102
12911332-3	2003	Ac-IETD-CHO (acetyl-Ile-Glu-Thr-Asp-aldehyde), which has a certain preference for inhibiting caspase-8, or Fas-antagonistic antibody, significantly inhibited cisplatin-induced apoptosis in both parental and cisplatin-selected HeLa cell lines.	asp-aldehyde	32-44	caspase 8	Homo sapiens	93-102
12911332-3	2003	Ac-IETD-CHO (acetyl-Ile-Glu-Thr-Asp-aldehyde), which has a certain preference for inhibiting caspase-8, or Fas-antagonistic antibody, significantly inhibited cisplatin-induced apoptosis in both parental and cisplatin-selected HeLa cell lines.	Cisplatin	158-167	caspase 8	Homo sapiens	93-102
12911332-3	2003	Ac-IETD-CHO (acetyl-Ile-Glu-Thr-Asp-aldehyde), which has a certain preference for inhibiting caspase-8, or Fas-antagonistic antibody, significantly inhibited cisplatin-induced apoptosis in both parental and cisplatin-selected HeLa cell lines.	Cisplatin	207-216	caspase 8	Homo sapiens	93-102
14530215-0	2003	The CB1/VR1 agonist arvanil induces apoptosis through an FADD/caspase-8-dependent pathway.	arvanil	20-27	caspase 8	Homo sapiens	62-71
12920112-3	2003	Pre-treatment with 12-O-tetradecanoylphorbol-13-acetate (PMA) led to inhibition of TRAIL-induced apoptosis in HeLa cells, which was characterized by a reduction in phosphatidylserine (PS) externalization, decreased caspase-8 processing, and incomplete maturation and activation of caspase-3.	Tetradecanoylphorbol Acetate	19-55	caspase 8	Homo sapiens	215-224
12920112-3	2003	Pre-treatment with 12-O-tetradecanoylphorbol-13-acetate (PMA) led to inhibition of TRAIL-induced apoptosis in HeLa cells, which was characterized by a reduction in phosphatidylserine (PS) externalization, decreased caspase-8 processing, and incomplete maturation and activation of caspase-3.	Tetradecanoylphorbol Acetate	57-60	caspase 8	Homo sapiens	215-224
14981915-9	2003	Activations of caspases, particularly caspase-3, declined in the order of BHA/BHT &gt; BHA &gt; BMP &gt; BHT.	Butylated Hydroxyanisole	74-77	caspase 8	Homo sapiens	15-23
14981915-9	2003	Activations of caspases, particularly caspase-3, declined in the order of BHA/BHT &gt; BHA &gt; BMP &gt; BHT.	Butylated Hydroxytoluene	78-81	caspase 8	Homo sapiens	15-23
14981915-9	2003	Activations of caspases, particularly caspase-3, declined in the order of BHA/BHT &gt; BHA &gt; BMP &gt; BHT.	2-tert-butyl-4-methylphenol	96-99	caspase 8	Homo sapiens	15-23
14981915-9	2003	Activations of caspases, particularly caspase-3, declined in the order of BHA/BHT &gt; BHA &gt; BMP &gt; BHT.	Butylated Hydroxytoluene	105-108	caspase 8	Homo sapiens	15-23
14530215-14	2003	These results demonstrate that arvanil-induced apoptosis is essentially mediated through a mechanism that is typical of type II cells, and implicates the death-inducing signalling complex and the activation of caspase-8.	arvanil	31-38	caspase 8	Homo sapiens	210-219
14981925-9	2003	The CAPE- or CAO-induced apoptosis was also accompanied by a rapid loss of mitochondrial transmembrane potential and activation of caspase-3 and caspase-8, suggesting a mitochondrial-dependent mechanism.	caffeic acid phenethyl ester	4-8	caspase 8	Homo sapiens	145-154
14981925-9	2003	The CAPE- or CAO-induced apoptosis was also accompanied by a rapid loss of mitochondrial transmembrane potential and activation of caspase-3 and caspase-8, suggesting a mitochondrial-dependent mechanism.	cao	13-16	caspase 8	Homo sapiens	145-154
14981925-13	2003	In addition, we demonstrated that down-regulation of Mcl-1 gene expression and activation of caspase-8 are associated with CAPE-triggered cell apoptosis.	caffeic acid phenethyl ester	123-127	caspase 8	Homo sapiens	93-102
14530215-6	2003	Arvanil-induced apoptosis was initiated independently of any specific phase of the cell cycle, and it was inhibited by specific caspase-8 and -3 inhibitors and by the activation of protein kinase C. In addition, kinetic analysis by Western blots and fluorimetry showed that arvanil rapidly activates caspase-8, -7 and -3, and induces PARP cleavage.	arvanil	0-7	caspase 8	Homo sapiens	128-144
14530215-6	2003	Arvanil-induced apoptosis was initiated independently of any specific phase of the cell cycle, and it was inhibited by specific caspase-8 and -3 inhibitors and by the activation of protein kinase C. In addition, kinetic analysis by Western blots and fluorimetry showed that arvanil rapidly activates caspase-8, -7 and -3, and induces PARP cleavage.	arvanil	0-7	caspase 8	Homo sapiens	300-320
14576777-3	2003	Cathepsin D and cytochrome c were detected partially released to the cytosol after exposure to 0.1 muM staurosporine for 1 h. After 4 h, activation of caspase-9 and -3 was initiated and later caspase-8 activation and a decrease in full-length Bid were detected.	Staurosporine	103-116	caspase 8	Homo sapiens	192-201
14555232-8	2003	SBHA appeared to sensitize melanoma to TRAIL-induced apoptosis by up-regulation of pro-apoptotic proteins in the TRAIL-induced apoptotic pathway such as caspase-8, caspase-3, Bid, Bak, and Bax, and up-regulation of the BH3 domain only protein, Bim.	suberic bishydroxamate	0-4	caspase 8	Homo sapiens	153-162
14567999-4	2003	Interestingly, caspase-8 and cleavage of the proapoptotic member of the Bcl-2 family BID was also observed during apoptosis induced by myriadenolide, suggesting a role for the caspase-8/BID pathway.	myriadenolide	135-148	caspase 8	Homo sapiens	15-24
14567999-4	2003	Interestingly, caspase-8 and cleavage of the proapoptotic member of the Bcl-2 family BID was also observed during apoptosis induced by myriadenolide, suggesting a role for the caspase-8/BID pathway.	myriadenolide	135-148	caspase 8	Homo sapiens	176-185
14567999-6	2003	Furthermore, pretreatment of cells with the caspase-3 inhibitor DEVD-fmk completely blocked the activation of caspase-8, suggesting that the activation of the caspase-8/BID pathway is part of an amplification loop initiated by caspase-3.	devd-fmk	64-72	caspase 8	Homo sapiens	110-119
14567999-6	2003	Furthermore, pretreatment of cells with the caspase-3 inhibitor DEVD-fmk completely blocked the activation of caspase-8, suggesting that the activation of the caspase-8/BID pathway is part of an amplification loop initiated by caspase-3.	devd-fmk	64-72	caspase 8	Homo sapiens	159-168
12931220-9	2003	Accordingly, CDDO and CDDO-m induced concentration-dependent reductions in the levels of FLIP protein, an endogenous antagonist of caspase-8, without altering the levels of several other apoptosis-relevant proteins.	2-cyano-3,12-dioxoolean-1,9-dien-28-oic acid	13-17	caspase 8	Homo sapiens	131-140
12931220-9	2003	Accordingly, CDDO and CDDO-m induced concentration-dependent reductions in the levels of FLIP protein, an endogenous antagonist of caspase-8, without altering the levels of several other apoptosis-relevant proteins.	cddo-m	22-28	caspase 8	Homo sapiens	131-140
14617795-7	2003	Furthermore, TRAIL sensitization was associated with increased proteolytic procession of caspase-8 and its downstream target BID, and z-IETD-FMK, the inhibitor specific to active caspase-8 totally blocked LiCl-induced TRAIL sensitization.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	134-144	caspase 8	Homo sapiens	179-188
14617795-7	2003	Furthermore, TRAIL sensitization was associated with increased proteolytic procession of caspase-8 and its downstream target BID, and z-IETD-FMK, the inhibitor specific to active caspase-8 totally blocked LiCl-induced TRAIL sensitization.	Lithium Chloride	205-209	caspase 8	Homo sapiens	89-98
14617795-7	2003	Furthermore, TRAIL sensitization was associated with increased proteolytic procession of caspase-8 and its downstream target BID, and z-IETD-FMK, the inhibitor specific to active caspase-8 totally blocked LiCl-induced TRAIL sensitization.	Lithium Chloride	205-209	caspase 8	Homo sapiens	179-188
14567999-0	2003	Myriadenolide, a labdane diterpene isolated from Alomia myriadenia (asteraceae) induces depolarization of mitochondrial membranes and apoptosis associated with activation of caspases-8, -9, and -3 in Jurkat and THP-1 cells.	myriadenolide	0-13	caspase 8	Homo sapiens	174-196
14562039-5	2003	The lethal effects of MG-132/flavopiridol were not reduced in leukemic cells ectopically expressing Bcl-2, but were partially attenuated in cells ectopically expressing dominant-negative caspase-8 or CrmA.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	22-28	caspase 8	Homo sapiens	187-196
14562039-5	2003	The lethal effects of MG-132/flavopiridol were not reduced in leukemic cells ectopically expressing Bcl-2, but were partially attenuated in cells ectopically expressing dominant-negative caspase-8 or CrmA.	alvocidib	29-41	caspase 8	Homo sapiens	187-196
14534535-11	2003	These results reveal for the first time that P4 induces apoptosis in HOSE and OVCA cells via activation of a caspase-8-initiated Fas/FasL signaling pathway.	propiverine	45-47	caspase 8	Homo sapiens	109-118
14519653-5	2003	The remaining cell lines and primary cultures were resistant to TRAIL, but cisplatin, chemptothecin, and etoposide sensitized the resistant cell lines and primary cultures to TRAIL-induced apoptosis, which also occurred through the caspase-8-initiated caspase cascade.	Cisplatin	75-84	caspase 8	Homo sapiens	232-241
12969378-5	2003	Low alpha-toxin doses (3-30 ng ml-1) dose- and time-dependently induced apoptosis in both cell types, which was completely blocked by the caspase inhibitor zVAD-fmk.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	156-164	caspase 8	Homo sapiens	138-145
14508522-5	2003	Induction of apoptosis was accompanied by caspase-8 and caspase-9 activation, and could be blocked by treatment with the caspase inhibitor Z-VAD-FMK.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	139-148	caspase 8	Homo sapiens	42-51
13679856-6	2003	Western blotting analysis revealed that both TRAIL and glucose starvation induced Bid cleavage and FLIP degradation following caspase 8 activation in a time-dependent manner, and ARK5 overexpression clearly delayed Bid cleavage, FLIP degradation, and caspase 8 activation.	Glucose	55-62	caspase 8	Homo sapiens	126-135
13679856-6	2003	Western blotting analysis revealed that both TRAIL and glucose starvation induced Bid cleavage and FLIP degradation following caspase 8 activation in a time-dependent manner, and ARK5 overexpression clearly delayed Bid cleavage, FLIP degradation, and caspase 8 activation.	Glucose	55-62	caspase 8	Homo sapiens	251-260
12834589-6	2003	Caspase-8 activation is an upstream event in the apoptotic pathway triggered by the activation of cytokines receptors such as TNF-alpha receptor 1 (TNFR-1), and the presence of caspase-8 activation in fibroblast-like cells in the aseptic interface membranes of THAs suggests a possible TNF-alpha dependent apoptosis.	3,5-tetrahydroaldosterone sulfate	261-265	caspase 8	Homo sapiens	0-9
12834589-6	2003	Caspase-8 activation is an upstream event in the apoptotic pathway triggered by the activation of cytokines receptors such as TNF-alpha receptor 1 (TNFR-1), and the presence of caspase-8 activation in fibroblast-like cells in the aseptic interface membranes of THAs suggests a possible TNF-alpha dependent apoptosis.	3,5-tetrahydroaldosterone sulfate	261-265	caspase 8	Homo sapiens	177-186
12844494-5	2003	Moreover, NF-kappaB-dependent protection against Fas-mediated apoptosis was associated with decreased levels of caspase-8 activity and with the up-regulation of intracellular antiapoptotic proteins.	ammonium ferrous sulfate	49-52	caspase 8	Homo sapiens	112-121
12957653-8	2003	In conclusion, the mechanism of HOCl-oxLDL-induced apoptosis in monocytic U937 cells involves the two pathways of apical caspase activation: (i) death receptor-mediated caspase-8 and (ii) mitochondria-mediated caspase-9.	Hypochlorous Acid	32-36	caspase 8	Homo sapiens	169-178
12957657-8	2003	Further analysis suggested a redox-sensitive step early in Fas signaling at the level of initiator caspase (caspase-8) activation.	ammonium ferrous sulfate	59-62	caspase 8	Homo sapiens	108-117
14519653-5	2003	The remaining cell lines and primary cultures were resistant to TRAIL, but cisplatin, chemptothecin, and etoposide sensitized the resistant cell lines and primary cultures to TRAIL-induced apoptosis, which also occurred through the caspase-8-initiated caspase cascade.	Etoposide	105-114	caspase 8	Homo sapiens	232-241
14519653-9	2003	CONCLUSIONS: The results presented here indicate that cisplatin inhibits c-FLIP protein expression and phosphorylation to restore TRAIL-induced caspase-8-initiated apoptosis in melanoma cells, thus providing a new combined therapeutic strategy for melanomas.	Cisplatin	54-63	caspase 8	Homo sapiens	144-153
14522884-6	2003	Final studies revealed that the BH-P could activate caspase-8, caspase-3, and poly(ADP-ribose) polymerase and trigger the apoptosis of tumor cells.	bicyclo(2.2.1)hept-5-en-2-yl phenyl sulfoxide	32-36	caspase 8	Homo sapiens	52-61
12748063-0	2003	TNF-alpha-induced cell death in ethanol-exposed cells depends on p38 MAPK signaling but is independent of Bid and caspase-8.	Ethanol	32-39	caspase 8	Homo sapiens	114-123
12748063-7	2003	Specifically, ethanol-exposed cells display caspase-8- and Bid-independent cell killing during TNF-alpha treatment.	Ethanol	14-21	caspase 8	Homo sapiens	44-62
12811515-10	2003	Surprisingly, only topotecan, a topoisomerase I inhibitor, when used in combination with rTRAIL/Apo-2L led to significant apoptosis of DU-145 cells, as measured by caspase 8 activation, BID cleavage, and annexin V-FITC/PI staining.	Topotecan	19-28	caspase 8	Homo sapiens	164-173
12948852-0	2003	Induction of apoptosis in human hepatoblastoma cells by tetrandrine via caspase-dependent Bid cleavage and cytochrome c release.	tetrandrine	56-67	caspase 8	Homo sapiens	72-79
12948852-5	2003	Treatment of cells with tetrandrine caused the upregulation of p53, downregulation of Bcl-X(L), cleavage of Bid and Bax, and release of cytochrome c, which were accompanied by activation of caspases 9, 3 and 8.	tetrandrine	24-35	caspase 8	Homo sapiens	190-198
12948852-7	2003	A broad-spectrum caspase inhibitor and a caspase 8-specific inhibitor completely blocked tetrandrine-induced Bid processing, cytochrome c release, activation of caspase 3, and cell death.	tetrandrine	89-100	caspase 8	Homo sapiens	17-24
12948852-7	2003	A broad-spectrum caspase inhibitor and a caspase 8-specific inhibitor completely blocked tetrandrine-induced Bid processing, cytochrome c release, activation of caspase 3, and cell death.	tetrandrine	89-100	caspase 8	Homo sapiens	41-50
12962723-11	2003	Addition of the caspase inhibitor Z-VAD.fmk inhibited caspase 8 and 3 significantly but did not affect caspase 9.	z-vad	34-39	caspase 8	Homo sapiens	54-63
14500394-1	2003	The novel oleanane triterpenoid 2-cyano-3,12-dioxoolean-1,9-dien-28-oic acid (CDDO) induces apoptosis of human leukemia cells by activation of the extrinsic caspase-8 pathway.	oleanane	10-18	caspase 8	Homo sapiens	157-166
14500394-1	2003	The novel oleanane triterpenoid 2-cyano-3,12-dioxoolean-1,9-dien-28-oic acid (CDDO) induces apoptosis of human leukemia cells by activation of the extrinsic caspase-8 pathway.	triterpenoid TP-222	19-31	caspase 8	Homo sapiens	157-166
14500394-1	2003	The novel oleanane triterpenoid 2-cyano-3,12-dioxoolean-1,9-dien-28-oic acid (CDDO) induces apoptosis of human leukemia cells by activation of the extrinsic caspase-8 pathway.	2-cyano-3,12-dioxoolean-1,9-dien-28-oic acid	32-76	caspase 8	Homo sapiens	157-166
14500394-1	2003	The novel oleanane triterpenoid 2-cyano-3,12-dioxoolean-1,9-dien-28-oic acid (CDDO) induces apoptosis of human leukemia cells by activation of the extrinsic caspase-8 pathway.	2-cyano-3,12-dioxoolean-1,9-dien-28-oic acid	78-82	caspase 8	Homo sapiens	157-166
14500394-6	2003	The results also demonstrate that CDDO-induced: (a) stimulation of Jun NH(2)-terminal kinase; (b) activation of caspase-8; (c) loss of mitochondrial transmembrane potential; (d) release of cytochrome c; and (e) cleavage of caspase-3 are blocked by pretreatment with the antioxidant N-acetyl-L-cysteine and GSH but not with cysteine.	2-cyano-3,12-dioxoolean-1,9-dien-28-oic acid	34-38	caspase 8	Homo sapiens	112-121
12930371-9	2003	Analysis of Fas-induced activation of caspase-8 and -9 showed decreased activity of both caspases in HT, whereas activity of caspase-9 was increased and that of caspase-8 was decreased in GD.	ammonium ferrous sulfate	12-15	caspase 8	Homo sapiens	38-54
12930371-9	2003	Analysis of Fas-induced activation of caspase-8 and -9 showed decreased activity of both caspases in HT, whereas activity of caspase-9 was increased and that of caspase-8 was decreased in GD.	ammonium ferrous sulfate	12-15	caspase 8	Homo sapiens	89-97
12930371-9	2003	Analysis of Fas-induced activation of caspase-8 and -9 showed decreased activity of both caspases in HT, whereas activity of caspase-9 was increased and that of caspase-8 was decreased in GD.	ammonium ferrous sulfate	12-15	caspase 8	Homo sapiens	38-47
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	caspase 8	Homo sapiens	104-113
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	caspase 8	Homo sapiens	198-207
14500373-5	2003	Actinomycin D sensitized TRAIL-resistant cells through up-regulation of caspases (caspase-3, -9, and -8).	Dactinomycin	0-13	caspase 8	Homo sapiens	72-80
12938225-3	2003	Furthermore, following overexpression of a human Fas:FLICE construct, which directly induces caspase activation in a death-inducing signaling complex-independent manner, cells could not be protected through BCR stimulation.Co-incubation with cycloheximide partially reversed protection from apoptosis and increased Fas-stimulated initiator and effector caspase activation, suggesting new protein synthesis is necessary to induce protection upstream of caspase activation.	Cycloheximide	242-255	caspase 8	Homo sapiens	53-58
12938225-3	2003	Furthermore, following overexpression of a human Fas:FLICE construct, which directly induces caspase activation in a death-inducing signaling complex-independent manner, cells could not be protected through BCR stimulation.Co-incubation with cycloheximide partially reversed protection from apoptosis and increased Fas-stimulated initiator and effector caspase activation, suggesting new protein synthesis is necessary to induce protection upstream of caspase activation.	ammonium ferrous sulfate	49-52	caspase 8	Homo sapiens	53-58
12962723-11	2003	Addition of the caspase inhibitor Z-VAD.fmk inhibited caspase 8 and 3 significantly but did not affect caspase 9.	FMK	40-43	caspase 8	Homo sapiens	54-63
12888916-4	2003	The enhancement of Fas-induced apoptosis by pre-treatment with neuraminidase was inhibited by z-VAD-fmk, a broad caspase inhibitor, and Ac-LEHD-CHO, an inhibitor of caspase-9, but not by Ac-IETD-CHO an inhibitor of caspase-8 or 6, imipramine, an inhibitor of acidic sphingomyelinase, glutathione, an inhibitor of neutral sphingomyelinase and Fumonisin B1, an inhibitor of ceramide synthase.	ammonium ferrous sulfate	19-22	caspase 8	Homo sapiens	215-224
12883646-2	2003	We have recently demonstrated that anti-IgM and ionomycin trigger significant activation of caspase-3, -7 and -8 and for cleavage of the resident nuclear proteins poly(ADP-ribose) polymerase (PARP) and lamin B1 in Ramos-BL B cells, suggesting that these caspases may be localized to the nucleus as well as to the cytoplasm of Ramos-BL B cells.	Ionomycin	48-57	caspase 8	Homo sapiens	254-262
12874095-3	2003	Here we show that EPA protects endothelial cells from anoikis through upregulation of the cellular FLICE (Fas-associating protein with death domain-like interleukin-1-converting enzyme)-inhibitory protein (cFLIP), an endogenous inhibitor of caspase-8.	Eicosapentaenoic Acid	18-21	caspase 8	Homo sapiens	99-104
12874095-3	2003	Here we show that EPA protects endothelial cells from anoikis through upregulation of the cellular FLICE (Fas-associating protein with death domain-like interleukin-1-converting enzyme)-inhibitory protein (cFLIP), an endogenous inhibitor of caspase-8.	Eicosapentaenoic Acid	18-21	caspase 8	Homo sapiens	241-250
12865435-7	2003	Interestingly, we further found that caspases-8 and -10 are the initiator caspases in PMA-induced apoptosis and a ROCK-dependent enhancement of specific complex formation between the Fas-associated death domain (FADD) and pro-caspase-10 in pro-apoptotic cells.	Tetradecanoylphorbol Acetate	86-89	caspase 8	Homo sapiens	37-55
12865435-7	2003	Interestingly, we further found that caspases-8 and -10 are the initiator caspases in PMA-induced apoptosis and a ROCK-dependent enhancement of specific complex formation between the Fas-associated death domain (FADD) and pro-caspase-10 in pro-apoptotic cells.	Tetradecanoylphorbol Acetate	86-89	caspase 8	Homo sapiens	37-45
12865435-8	2003	In summary, these results revealed that, following PMA treatment, the upregulation of the RhoA/ROCK pathway contributes to a cellular context that switches-on myosin-mediated contraction, which provides a mechanism for triggering apoptotic induction mediated by caspase-8 and -10.	Tetradecanoylphorbol Acetate	51-54	caspase 8	Homo sapiens	262-279
12907654-10	2003	Activation of multiple caspases and PARP cleavage were also observed in the C4-2 tumors treated with doses resulting in effective tumor control at 42 days after Apo2L/TRAIL plus CPT-11 treatment.	Irinotecan	178-184	caspase 8	Homo sapiens	23-31
12917460-8	2003	In bronchiolar cells, cell death was inhibited by the caspase-8 (Z-IETD-fmk) and pan-caspase (Z-VAD-fmk) inhibitors and these inhibitors enhanced expression of CCL5 and increased the levels of the three secreted cytokines significantly.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	65-75	caspase 8	Homo sapiens	54-63
12917460-8	2003	In bronchiolar cells, cell death was inhibited by the caspase-8 (Z-IETD-fmk) and pan-caspase (Z-VAD-fmk) inhibitors and these inhibitors enhanced expression of CCL5 and increased the levels of the three secreted cytokines significantly.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	65-75	caspase 8	Homo sapiens	54-61
12919886-8	2003	CDDP down-regulated c-FLIP, tending to lower the activation threshold required for TRAIL-induced caspase-8 activation.	Cisplatin	0-4	caspase 8	Homo sapiens	97-106
12919886-9	2003	The CDDP-pretreated cells indeed demonstrated more increased TRAIL-mediated caspase-8 activation, loss of mitochondrial membrane potential (DeltaPsi(m)), and apoptosis than untreated cells.	Cisplatin	4-8	caspase 8	Homo sapiens	76-85
12919886-11	2003	Both the increased caspase activation and mitochondrial dysfunction induced by combination of CDDP and TRAIL would contribute to enhanced apoptotic cell death.	Cisplatin	94-98	caspase 8	Homo sapiens	19-26
12804643-0	2003	Differential recruitment of caspase 8 to cFlip confers sensitivity or resistance to Fas-mediated apoptosis in a subset of familial lymphoma patients.	ammonium ferrous sulfate	84-87	caspase 8	Homo sapiens	28-37
12804643-4	2003	Fas resistance in these cells was associated with reduced recruitment of the initiator caspase 8 compared to cFlip, an inhibitor of apoptosis, to the death-inducing signaling complex (DISC).	ammonium ferrous sulfate	0-3	caspase 8	Homo sapiens	87-96
14670183-0	2003	TRAIL activates a caspase 9/7-dependent pathway in caspase 8/10-defective SK-N-SH neuroblastoma cells with two functional end points: induction of apoptosis and PGE2 release.	Dinoprostone	161-165	caspase 8	Homo sapiens	51-60
14508070-6	2003	And the pan-caspase inhibitor z-Val-Ala-Asp (OMe) fluoromethyl-ketone (z-VAD-fmk) and Q-Val-Asp (OMe)-CH(2)-OPH (Q-VD (OMe)-OPH) prevented cell death induced by delta(12)-PGJ(2) showing participation of caspases in this process.	z-Val-Ala-Asp(Ome)-fluoromethylketone	30-69	caspase 8	Homo sapiens	12-19
14508070-6	2003	And the pan-caspase inhibitor z-Val-Ala-Asp (OMe) fluoromethyl-ketone (z-VAD-fmk) and Q-Val-Asp (OMe)-CH(2)-OPH (Q-VD (OMe)-OPH) prevented cell death induced by delta(12)-PGJ(2) showing participation of caspases in this process.	z-Val-Ala-Asp(Ome)-fluoromethylketone	30-69	caspase 8	Homo sapiens	203-211
14508070-6	2003	And the pan-caspase inhibitor z-Val-Ala-Asp (OMe) fluoromethyl-ketone (z-VAD-fmk) and Q-Val-Asp (OMe)-CH(2)-OPH (Q-VD (OMe)-OPH) prevented cell death induced by delta(12)-PGJ(2) showing participation of caspases in this process.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	71-80	caspase 8	Homo sapiens	12-19
14508070-6	2003	And the pan-caspase inhibitor z-Val-Ala-Asp (OMe) fluoromethyl-ketone (z-VAD-fmk) and Q-Val-Asp (OMe)-CH(2)-OPH (Q-VD (OMe)-OPH) prevented cell death induced by delta(12)-PGJ(2) showing participation of caspases in this process.	q-val-asp	86-95	caspase 8	Homo sapiens	203-211
14508070-6	2003	And the pan-caspase inhibitor z-Val-Ala-Asp (OMe) fluoromethyl-ketone (z-VAD-fmk) and Q-Val-Asp (OMe)-CH(2)-OPH (Q-VD (OMe)-OPH) prevented cell death induced by delta(12)-PGJ(2) showing participation of caspases in this process.	ch(2)-oph	102-111	caspase 8	Homo sapiens	12-19
14508070-6	2003	And the pan-caspase inhibitor z-Val-Ala-Asp (OMe) fluoromethyl-ketone (z-VAD-fmk) and Q-Val-Asp (OMe)-CH(2)-OPH (Q-VD (OMe)-OPH) prevented cell death induced by delta(12)-PGJ(2) showing participation of caspases in this process.	ch(2)-oph	102-111	caspase 8	Homo sapiens	203-211
14508070-10	2003	Taken together, our results suggest that delta(12)-PGJ(2)-induced apoptosis in HeLa cell utilized caspase cascade without Fas receptor-ligand interaction and accompanied with NF-kappaB inactivation.	delta(12)-prostaglandin J(2)	41-57	caspase 8	Homo sapiens	98-105
12902978-7	2003	Taken together, these findings indicate that PS-341 enhances TRAIL-induced apoptosis by increasing the cleavage of caspase 8, causing Bak-dependent release of mitochondrial proapoptotic proteins.	Bortezomib	45-51	caspase 8	Homo sapiens	115-124
12902978-7	2003	Taken together, these findings indicate that PS-341 enhances TRAIL-induced apoptosis by increasing the cleavage of caspase 8, causing Bak-dependent release of mitochondrial proapoptotic proteins.	bakuchiol	134-137	caspase 8	Homo sapiens	115-124
12689928-4	2003	UO126 modulated the levels of several intracellular proteins including B-cell lymphoma protein 2 (Bcl-2), myeloid cell leukemia-1 (Mcl-1) and caspase 8 homolog FLICE-inhibitory protein (cFLIP), and induced G2M cell-cycle arrest or apoptosis.	U 0126	0-5	caspase 8	Homo sapiens	142-151
12689928-4	2003	UO126 modulated the levels of several intracellular proteins including B-cell lymphoma protein 2 (Bcl-2), myeloid cell leukemia-1 (Mcl-1) and caspase 8 homolog FLICE-inhibitory protein (cFLIP), and induced G2M cell-cycle arrest or apoptosis.	U 0126	0-5	caspase 8	Homo sapiens	160-165
12937219-13	2003	The inhibitors of either caspase-3 or caspase-8 could prevent the Fas-induced apoptosis in HPMCs.	ammonium ferrous sulfate	66-69	caspase 8	Homo sapiens	38-47
12877678-0	2003	Chelerythrin activates caspase-8, downregulates FLIP long and short, and overcomes resistance to tumour necrosis factor-related apoptosis-inducing ligand in KG1a cells.	chelerythrin	0-12	caspase 8	Homo sapiens	23-32
12877678-4	2003	Chelerythrin by itself induced apoptosis in KG1a cells, and apoptosis was associated with activation of caspase-8.	chelerythrin	0-12	caspase 8	Homo sapiens	104-113
12877678-5	2003	While TRAIL alone failed to activate caspase-8 or induce apoptosis, the addition of TRAIL to chelerythrin-treated cells significantly enhanced cleavage of caspase-8 and apoptosis.	chelerythrin	93-105	caspase 8	Homo sapiens	155-164
12877678-7	2003	Downregulation of FLIP and induction of apoptosis were partially abrogated by pretreatment with the specific caspase-8 inhibitor, Z-IETD-FMK.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	130-140	caspase 8	Homo sapiens	109-118
12912965-3	2003	The combination of TRAIL and cisplatin synergistically enhanced apoptotic death, caspase-8 and caspase-3 activation, as well as poly(ADP-ribose) polymerase cleavage.	Cisplatin	29-38	caspase 8	Homo sapiens	81-90
12907654-13	2003	Our data indicate that the combined treatment of Apo2L/TRAIL and CPT-11 achieves tumor control in prostate cancer tumors through regulation of Bcl-2 family proteins and potent activation of caspases.	Irinotecan	65-71	caspase 8	Homo sapiens	190-198
12869656-7	2003	Both C2-ceramide and TNFalpha + CHX increased caspase 8- and 3-like activities in cytosolic extracts; however, treatment of cells with the broad-spectrum caspase inhibitor N-benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone protected NB16 cells from TNFalpha + CHX-induced cell death but did not prevent C2-ceramide cytotoxicity.	N-acetylsphingosine	5-16	caspase 8	Homo sapiens	46-55
12869656-7	2003	Both C2-ceramide and TNFalpha + CHX increased caspase 8- and 3-like activities in cytosolic extracts; however, treatment of cells with the broad-spectrum caspase inhibitor N-benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone protected NB16 cells from TNFalpha + CHX-induced cell death but did not prevent C2-ceramide cytotoxicity.	Cycloheximide	32-35	caspase 8	Homo sapiens	46-55
12869656-7	2003	Both C2-ceramide and TNFalpha + CHX increased caspase 8- and 3-like activities in cytosolic extracts; however, treatment of cells with the broad-spectrum caspase inhibitor N-benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone protected NB16 cells from TNFalpha + CHX-induced cell death but did not prevent C2-ceramide cytotoxicity.	Caspase Inhibitor VI	172-222	caspase 8	Homo sapiens	46-55
12881712-3	2003	FOXO3a was cleaved in vivo by caspases in leukemic Jurkat cells following engagement of Fas (CD95) receptor, staurosporine, and etoposide treatment, but not following engagement of CD99, a caspase-independent cell death inducer.	Staurosporine	109-122	caspase 8	Homo sapiens	30-38
12881712-5	2003	The expression of the death adapter FADD and caspase-8 was required for Fas-induced FOXO3a cleavage, but activation of survival pathways by overexpression of FLICE-inhibitory protein or phorbol myristate acetate treatment prevented it.	Tetradecanoylphorbol Acetate	186-211	caspase 8	Homo sapiens	45-54
12880425-5	2003	Generation of ROS and hyperpolarization of mitochondrial transmembrane potential (DeltaPsim) were early events, followed by increased Fas expression and activation of caspase-8, and then activation of caspase-3 and -9.	ros	14-17	caspase 8	Homo sapiens	167-176
12881712-3	2003	FOXO3a was cleaved in vivo by caspases in leukemic Jurkat cells following engagement of Fas (CD95) receptor, staurosporine, and etoposide treatment, but not following engagement of CD99, a caspase-independent cell death inducer.	Etoposide	128-137	caspase 8	Homo sapiens	30-38
12881712-5	2003	The expression of the death adapter FADD and caspase-8 was required for Fas-induced FOXO3a cleavage, but activation of survival pathways by overexpression of FLICE-inhibitory protein or phorbol myristate acetate treatment prevented it.	ammonium ferrous sulfate	72-75	caspase 8	Homo sapiens	45-54
12690107-5	2003	The proapoptotic effects of Ad-Bid were independent of p53 status and were augmented markedly by caspase-8 activators such as the DNA-damaging agent cisplatin.	Cisplatin	149-158	caspase 8	Homo sapiens	97-106
12649137-0	2003	Depsipeptide (FR901228) induces histone acetylation and inhibition of histone deacetylase in chronic lymphocytic leukemia cells concurrent with activation of caspase 8-mediated apoptosis and down-regulation of c-FLIP protein.	Depsipeptides	0-12	caspase 8	Homo sapiens	158-167
12649137-0	2003	Depsipeptide (FR901228) induces histone acetylation and inhibition of histone deacetylase in chronic lymphocytic leukemia cells concurrent with activation of caspase 8-mediated apoptosis and down-regulation of c-FLIP protein.	romidepsin	14-22	caspase 8	Homo sapiens	158-167
12649137-5	2003	Depsipeptide-induced apoptosis is caspase dependent, selectively involving the tumor necrosis factor (TNF) receptor (extrinsic pathway) initiating caspase 8 and effector caspase 3.	Depsipeptides	0-12	caspase 8	Homo sapiens	147-156
12721291-1	2003	Caspase-8 cleaves BID to tBID, which targets mitochondria and induces oligomerization of BAX and BAK within the outer membrane, resulting in release of cytochrome c from the organelle.	tBID	25-29	caspase 8	Homo sapiens	0-9
12841868-0	2003	Expression of short-form caspase 8 correlates with decreased sensitivity to Fas-mediated apoptosis in neuroblastoma cells.	ammonium ferrous sulfate	76-79	caspase 8	Homo sapiens	25-34
12623840-6	2003	Mechanistic studies indicated that the major effect of vitamin C was inhibition of the activation of caspase-8 with no effect on it enzymatic activity.	Ascorbic Acid	55-64	caspase 8	Homo sapiens	101-110
12841868-2	2003	Caspase 8, one of the initiator caspases, plays an important role in the Fas-Fas ligand pathway.	ammonium ferrous sulfate	73-76	caspase 8	Homo sapiens	0-9
12841868-2	2003	Caspase 8, one of the initiator caspases, plays an important role in the Fas-Fas ligand pathway.	ammonium ferrous sulfate	73-76	caspase 8	Homo sapiens	32-40
12841868-2	2003	Caspase 8, one of the initiator caspases, plays an important role in the Fas-Fas ligand pathway.	ammonium ferrous sulfate	77-80	caspase 8	Homo sapiens	0-9
12841868-2	2003	Caspase 8, one of the initiator caspases, plays an important role in the Fas-Fas ligand pathway.	ammonium ferrous sulfate	77-80	caspase 8	Homo sapiens	32-40
12841868-5	2003	Sensitivity to Fas-mediated cell death did not correlate with the expression of Fas in neuroblastoma cells, but was directly associated with the pattern of caspase 8 protein expression.	ammonium ferrous sulfate	15-18	caspase 8	Homo sapiens	156-165
12815459-7	2003	Furthermore, while induction of both caspase-3 and caspase-8 activities are observed in TNF-alpha and Casodex-treated cells, a novel cleavage product of procaspase-8 is seen in Casodex-treated cells.	bicalutamide	102-109	caspase 8	Homo sapiens	51-60
12815464-4	2003	Cisplatin-induced apoptosis was efficiently blocked by caspase-8 inhibitor zIETD-fmk in Tera cells, but only partially in Tera-CP cells.	Cisplatin	0-9	caspase 8	Homo sapiens	55-64
12841868-8	2003	More interestingly, a group of cell lines expressing a distinct short form of caspase 8 with splicing out of exon 3 consistently showed moderate sensitivity to Fas-mediated cell death.	ammonium ferrous sulfate	160-163	caspase 8	Homo sapiens	78-87
12815464-4	2003	Cisplatin-induced apoptosis was efficiently blocked by caspase-8 inhibitor zIETD-fmk in Tera cells, but only partially in Tera-CP cells.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	75-84	caspase 8	Homo sapiens	55-64
12837490-0	2003	Hyperforin a constituent of St John"s wort (Hypericum perforatum L.) extract induces apoptosis by triggering activation of caspases and with hypericin synergistically exerts cytotoxicity towards human malignant cell lines.	hyperforin a	0-12	caspase 8	Homo sapiens	123-131
12815464-5	2003	In addition, cisplatin induced FADD and caspase-8 recruitment to the CD95 receptor in Tera cells, which was not noticed in Tera-CP cells.	Cisplatin	13-22	caspase 8	Homo sapiens	40-49
12884866-3	2003	We previously reported that the prodomain-only isoforms of caspase-8 and -10 (PDCasp8/10), containing two DED motifs, could inhibit Fas-mediated apoptosis.	ammonium ferrous sulfate	132-135	caspase 8	Homo sapiens	59-76
12851490-0	2003	Arsenic trioxide selectively induces early and extensive apoptosis via the APO2/caspase-8 pathway engaging the mitochondrial pathway in myeloma cells with mutant p53.	Arsenic Trioxide	0-16	caspase 8	Homo sapiens	80-89
12851490-3	2003	In cells expressing mutated p53, ATO induced, G2/M arrest and activation caspase 8 and 3 and rapid and extensive apoptosis.	Arsenic Trioxide	33-36	caspase 8	Homo sapiens	73-88
12738800-8	2003	Fas was also increased after TBI vs. control and was associated with relative levels of caspase-8, supporting formation of a death complex.	ammonium ferrous sulfate	0-3	caspase 8	Homo sapiens	88-97
12837490-9	2003	In addition, the broad spectrum caspase inhibitor z-VAD-fmk inhibited both the appearance of PS exposure and the activation of caspases, illustrating the functional relevance of caspase activation during HP-induced apoptosis.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	50-59	caspase 8	Homo sapiens	32-39
12837490-9	2003	In addition, the broad spectrum caspase inhibitor z-VAD-fmk inhibited both the appearance of PS exposure and the activation of caspases, illustrating the functional relevance of caspase activation during HP-induced apoptosis.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	50-59	caspase 8	Homo sapiens	127-135
12837490-9	2003	In addition, the broad spectrum caspase inhibitor z-VAD-fmk inhibited both the appearance of PS exposure and the activation of caspases, illustrating the functional relevance of caspase activation during HP-induced apoptosis.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	50-59	caspase 8	Homo sapiens	127-134
12818572-7	2003	Z-IETD.fmk and Z-LEHD.fmk, selective inhibitors for caspases 8 and 9, respectively, abolished caspase 3 activation induced by Ad2/nchFasL or H/R.	z-ietd	0-6	caspase 8	Homo sapiens	52-68
12818572-7	2003	Z-IETD.fmk and Z-LEHD.fmk, selective inhibitors for caspases 8 and 9, respectively, abolished caspase 3 activation induced by Ad2/nchFasL or H/R.	z-lehd	15-21	caspase 8	Homo sapiens	52-68
12818572-7	2003	Z-IETD.fmk and Z-LEHD.fmk, selective inhibitors for caspases 8 and 9, respectively, abolished caspase 3 activation induced by Ad2/nchFasL or H/R.	FMK	7-10	caspase 8	Homo sapiens	52-68
12810637-6	2003	In contrast, death receptor and mitochondrial apoptosis signaling as well as caspase activity was enhanced by dexamethasone in lymphoid cells.	Dexamethasone	110-123	caspase 8	Homo sapiens	77-84
14532729-11	2003	PPAR-gamma agonist seems to enhance Fas-mediated apoptosis by affecting the way between caspase-8 and caspase-3.	ammonium ferrous sulfate	36-39	caspase 8	Homo sapiens	88-97
12929750-5	2003	Inhibition of caspase-8 by Lle-Glu (OMe)-Thr-Asp(OMe)-fluoromethyl ketone completely blocked caspase-3 cleavage and apoptosis in UVA-treated cells, suggesting that apoptosis was initiated by the Fas pathway.	Glutamic Acid	31-34	caspase 8	Homo sapiens	14-23
12929750-5	2003	Inhibition of caspase-8 by Lle-Glu (OMe)-Thr-Asp(OMe)-fluoromethyl ketone completely blocked caspase-3 cleavage and apoptosis in UVA-treated cells, suggesting that apoptosis was initiated by the Fas pathway.	Threonine	41-44	caspase 8	Homo sapiens	14-23
12929750-5	2003	Inhibition of caspase-8 by Lle-Glu (OMe)-Thr-Asp(OMe)-fluoromethyl ketone completely blocked caspase-3 cleavage and apoptosis in UVA-treated cells, suggesting that apoptosis was initiated by the Fas pathway.	asp(ome)	45-53	caspase 8	Homo sapiens	14-23
12929750-5	2003	Inhibition of caspase-8 by Lle-Glu (OMe)-Thr-Asp(OMe)-fluoromethyl ketone completely blocked caspase-3 cleavage and apoptosis in UVA-treated cells, suggesting that apoptosis was initiated by the Fas pathway.	1,3-Difluoroacetone	54-73	caspase 8	Homo sapiens	14-23
12929750-5	2003	Inhibition of caspase-8 by Lle-Glu (OMe)-Thr-Asp(OMe)-fluoromethyl ketone completely blocked caspase-3 cleavage and apoptosis in UVA-treated cells, suggesting that apoptosis was initiated by the Fas pathway.	ammonium ferrous sulfate	195-198	caspase 8	Homo sapiens	14-23
12929750-8	2003	These data support a mechanism for rapid, UVA-induced apoptosis in HL-60 cells involving initial formation of the Fas-FADD-caspase-8 death complex in an FasL-independent manner.	uva	42-45	caspase 8	Homo sapiens	123-132
12702723-9	2003	FADD and caspase-8 colocalized with Fas in Jurkat cells validating the presence of FAF1 in the authentic Fas-DISC.	ammonium ferrous sulfate	36-39	caspase 8	Homo sapiens	9-18
12702723-11	2003	In addition, the FAF1 deletion mutant lacking the N terminus where Fas, FADD, and caspase-8 interact protected Jurkat cells from Fas-induced apoptosis demonstrating dominant-negative phenotype.	ammonium ferrous sulfate	129-132	caspase 8	Homo sapiens	82-91
12810955-4	2003	We directed 21-nt siRNAs against caspase 8, which is a key enzyme in death receptor-mediated apoptosis.	21-nt	12-17	caspase 8	Homo sapiens	33-42
12810637-7	2003	To restore apoptosis sensitivity in dexamethasone-treated carcinomas, caspase-8 and caspase-9 were transfected.	Dexamethasone	36-49	caspase 8	Homo sapiens	70-79
12802283-5	2003	Either the addition of the specific caspase-8 inhibitor Z-IETD-fmk, or the overexpression of the antiapoptotic protein Bcl-2 significantly prevented BTS-induced apoptosis, suggesting the involvement of both caspase-8-regulated and mitochondria-dependent signalling pathways in this process.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	56-66	caspase 8	Homo sapiens	36-45
12802283-5	2003	Either the addition of the specific caspase-8 inhibitor Z-IETD-fmk, or the overexpression of the antiapoptotic protein Bcl-2 significantly prevented BTS-induced apoptosis, suggesting the involvement of both caspase-8-regulated and mitochondria-dependent signalling pathways in this process.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	56-66	caspase 8	Homo sapiens	207-216
12760867-4	2003	In the present study, we have asked whether the antiviral substances IFN and ribavirin could support CD95-mediated apoptosis by interfering with the activation of caspases, a family of proteases known for their essential role in apoptosis.	Ribavirin	77-86	caspase 8	Homo sapiens	163-171
12760867-12	2003	IFN and ribavirin also enhance CD95-mediated caspase activation, which might in part be responsible for the apoptosis-promoting effect of these antiviral compounds.	Ribavirin	8-17	caspase 8	Homo sapiens	45-52
12663669-4	2003	Cycloheximide but not LY294002 decreases expression of c-FLIP (cellular FLICE inhibitory protein), an inhibitor of caspase-8 activation.	Cycloheximide	0-13	caspase 8	Homo sapiens	115-124
12663669-5	2003	The caspase inhibitor zVADfmk completely blocks caspase activation, DNA degradation, and nuclear fragmentation in both cases but only prevents loss of DeltaPsi and cell death for cytokine plus cycloheximide treatment.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	22-29	caspase 8	Homo sapiens	4-11
12663669-5	2003	The caspase inhibitor zVADfmk completely blocks caspase activation, DNA degradation, and nuclear fragmentation in both cases but only prevents loss of DeltaPsi and cell death for cytokine plus cycloheximide treatment.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	22-29	caspase 8	Homo sapiens	48-55
12663669-5	2003	The caspase inhibitor zVADfmk completely blocks caspase activation, DNA degradation, and nuclear fragmentation in both cases but only prevents loss of DeltaPsi and cell death for cytokine plus cycloheximide treatment.	Cycloheximide	193-206	caspase 8	Homo sapiens	4-11
12663669-7	2003	The cathepsin B inhibitor CA-074-Me prevents loss of DeltaPsi, caspase activation, and cell death for EC treated with cytokine plus LY294002 but has no effect on EC treated with cytokine plus cycloheximide.	CA 074 methyl ester	26-35	caspase 8	Homo sapiens	63-70
12760867-10	2003	Furthermore, the positive effect on CD95-mediated caspase activation by IFN and ribavirin was confirmed by immunocytochemistry for activated caspase-3 and by immunoblot detection of activated caspase-3, caspase-7, and caspase-8.	Ribavirin	80-89	caspase 8	Homo sapiens	50-57
12760867-10	2003	Furthermore, the positive effect on CD95-mediated caspase activation by IFN and ribavirin was confirmed by immunocytochemistry for activated caspase-3 and by immunoblot detection of activated caspase-3, caspase-7, and caspase-8.	Ribavirin	80-89	caspase 8	Homo sapiens	218-227
12780785-6	2003	The ability of TRAIL and daunorubicin to induce super-additive apoptosis correlated with the ability of these agents to activate caspase 8 and to augment cellular levels of the truncated pro-apoptotic form of the BCL-2 family member BID.	Daunorubicin	25-37	caspase 8	Homo sapiens	129-138
12764618-4	2003	Using cleavage site-directed antibodies, specific intracellular detection for cleaved fragments of caspase-8 and -9 was accomplished during apoptosis induced by staurosporine and etoposide.	Staurosporine	161-174	caspase 8	Homo sapiens	99-115
12763222-12	2003	In contrast, simultaneous exposure of Lovo and WiDr cells to AG337 and inhibitors of caspases 8, 9 and 3 caused a decrease in the number of apoptotic cells compared with AG337 exposure alone.	nolatrexed	170-175	caspase 8	Homo sapiens	85-104
12763223-6	2003	Coincubation of TRAIL and doxorubicin led to the overexpression of TRAIL-R2 resulting in a synergistic effect of doxorubicin and TRAIL in TRAIL-sensitive cell lines and in the overcoming of TRAIL-resistance in all of the TRAIL-resistant cell lines, except HTB-91, which lacked caspase 8 expression.	Doxorubicin	26-37	caspase 8	Homo sapiens	277-286
12763223-6	2003	Coincubation of TRAIL and doxorubicin led to the overexpression of TRAIL-R2 resulting in a synergistic effect of doxorubicin and TRAIL in TRAIL-sensitive cell lines and in the overcoming of TRAIL-resistance in all of the TRAIL-resistant cell lines, except HTB-91, which lacked caspase 8 expression.	Doxorubicin	113-124	caspase 8	Homo sapiens	277-286
12764618-4	2003	Using cleavage site-directed antibodies, specific intracellular detection for cleaved fragments of caspase-8 and -9 was accomplished during apoptosis induced by staurosporine and etoposide.	Etoposide	179-188	caspase 8	Homo sapiens	99-115
12684647-5	2003	As2O3-treated cell lines also showed upregulation of CD95/CD95L expression and activation of caspases 8 and 3.	Arsenic Trioxide	0-5	caspase 8	Homo sapiens	93-109
12531793-0	2003	Arsenic trioxide-induced apoptosis in myeloma cells: p53-dependent G1 or G2/M cell cycle arrest, activation of caspase-8 or caspase-9, and synergy with APO2/TRAIL.	Arsenic Trioxide	0-16	caspase 8	Homo sapiens	111-120
12531793-6	2003	The use of caspase blocking peptides, fluorescence-tagged caspase-specific substrate peptides, and Western immunoblotting confirmed the involvement of primarily caspase-8 and -3 in ATO-induced apoptosis in myeloma cells with mutated p53 and primarily caspase-9 and -3 in cells expressing wt p53.	Arsenic Trioxide	181-184	caspase 8	Homo sapiens	161-177
12605597-0	2003	Nitric oxide donors inhibit formation of the Apaf-1/caspase-9 apoptosome and activation of caspases.	Nitric Oxide	0-12	caspase 8	Homo sapiens	91-99
12605597-2	2003	Nitric oxide (NO) or derived species can prevent programmed cell death in several cell types, reportedly through S-nitrosation and inactivation of active caspases.	Nitric Oxide	0-12	caspase 8	Homo sapiens	154-162
12605597-4	2003	Indeed, using Jurkat cells as a model system, we demonstrate that NO donors block Fas- and etoposide-induced caspase activation and apoptosis (downstream of mitochondrial membrane depolarization) and cytochrome c release.	ammonium ferrous sulfate	82-85	caspase 8	Homo sapiens	109-116
12605597-4	2003	Indeed, using Jurkat cells as a model system, we demonstrate that NO donors block Fas- and etoposide-induced caspase activation and apoptosis (downstream of mitochondrial membrane depolarization) and cytochrome c release.	Etoposide	91-100	caspase 8	Homo sapiens	109-116
12730681-5	2003	Our results further demonstrate that TG-induced apoptosis is coupled with DR5 upregulation and caspases 8 and 3 activation, as well as Bid cleavage in both Bax-proficient and -deficient cells, although caspase 3 activation was reduced in Bax-deficient cells.	Thapsigargin	37-39	caspase 8	Homo sapiens	95-111
12761581-9	2003	Exogenous addition of sphingosine also induced activation of Bax via a caspase-8-and Bid-independent mechanism.	Sphingosine	22-33	caspase 8	Homo sapiens	71-88
12771938-4	2003	The site in the apoptotic pathway acted on by U0126 appeared to be downstream of caspase-8 and Bid but upstream of caspase-3 in that the levels of proteolytic cleavage of caspase-8 and Bid by TRAIL were similar in cells with or without exposure to U0126.	U 0126	46-51	caspase 8	Homo sapiens	81-90
12771938-4	2003	The site in the apoptotic pathway acted on by U0126 appeared to be downstream of caspase-8 and Bid but upstream of caspase-3 in that the levels of proteolytic cleavage of caspase-8 and Bid by TRAIL were similar in cells with or without exposure to U0126.	U 0126	46-51	caspase 8	Homo sapiens	171-180
12771938-4	2003	The site in the apoptotic pathway acted on by U0126 appeared to be downstream of caspase-8 and Bid but upstream of caspase-3 in that the levels of proteolytic cleavage of caspase-8 and Bid by TRAIL were similar in cells with or without exposure to U0126.	U 0126	248-253	caspase 8	Homo sapiens	171-180
12522001-3	2003	Coadministration of tumor necrosis factor (TNF) soluble receptors, or ectopic expression of CrmA or dominant-negative caspase-8, abrogated potentiation of paclitaxel-induced mitochondrial injury and apoptosis by bryostatin 1, implicating the extrinsic apoptotic pathway in this process.	Paclitaxel	155-165	caspase 8	Homo sapiens	118-127
12773247-8	2003	TUDCA significantly inhibited the release of cytochrome C from mitochondria into cytosol, and the activity of caspase-9, 3 (t &gt; or = 13.00, P &lt; 0.01), especially at 12 h, caspase-3 activity decreased by 54.9% (t = 16.88, P &lt; 0.01) and 52.5%, however it had no obvious effect on the activity of caspase-8 (t = 1.94, P &gt; 0.05).	ursodoxicoltaurine	0-5	caspase 8	Homo sapiens	303-312
12773255-0	2003	[Role of caspase-8 and caspase-3 in hepatoma cells apoptosis induced by 5-fluorouracil].	Fluorouracil	72-86	caspase 8	Homo sapiens	9-18
12700660-5	2003	Taxol-induced cell death was inhibited by the use of synthetic, cell-permeable caspase-3- (zDEVD-fmk) or caspase-8-specific (zIETD-fmk) inhibitors.	Paclitaxel	0-5	caspase 8	Homo sapiens	105-114
12702572-10	2003	Blockade of Fas by Fas-fusion protein or inhibition of caspase 8 resulted in a partial inhibition of morphine-induced apoptosis.	Morphine	101-109	caspase 8	Homo sapiens	55-64
12700660-5	2003	Taxol-induced cell death was inhibited by the use of synthetic, cell-permeable caspase-3- (zDEVD-fmk) or caspase-8-specific (zIETD-fmk) inhibitors.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	125-134	caspase 8	Homo sapiens	105-114
12670894-5	2003	The caspase-8-specific inhibitor z-IETD-fmk, as well as pan-caspase inhibitor z-VAD-fmk, but not the calpain inhibitor E-64d, prevents Bid cleavage, Bax conformational change, and subsequent caspase-3 processing and apoptosis.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	33-43	caspase 8	Homo sapiens	4-13
12687014-5	2003	Stabilization of death receptors by TIMP-3 results in activation of caspase-8 and caspase-3, and subsequent apoptosis is blocked by specific caspase-8 inhibitor (Z-IETD-FMK) and by pan-caspase inhibitor (Z-DEVD-FMK).	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	162-172	caspase 8	Homo sapiens	68-77
12687014-5	2003	Stabilization of death receptors by TIMP-3 results in activation of caspase-8 and caspase-3, and subsequent apoptosis is blocked by specific caspase-8 inhibitor (Z-IETD-FMK) and by pan-caspase inhibitor (Z-DEVD-FMK).	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	162-172	caspase 8	Homo sapiens	141-150
12687014-5	2003	Stabilization of death receptors by TIMP-3 results in activation of caspase-8 and caspase-3, and subsequent apoptosis is blocked by specific caspase-8 inhibitor (Z-IETD-FMK) and by pan-caspase inhibitor (Z-DEVD-FMK).	benzoylcarbonyl-aspartyl-glutamyl-valyl-aspartyl-fluoromethyl ketone	204-214	caspase 8	Homo sapiens	68-77
12482325-0	2003	The anti-apoptotic effect of leukotriene D4 involves the prevention of caspase 8 activation and Bid cleavage.	Leukotriene D4	29-43	caspase 8	Homo sapiens	71-80
12482325-11	2003	This indicates that N -(2-cyclohexyloxy-4-nitrophenyl)methane sulphonamide-induced apoptosis is mediated by the activation of caspase 8, via generation of truncated Bid, and thereafter release of cytochrome c.	n -(2-cyclohexyloxy-4-nitrophenyl)methane sulphonamide	20-74	caspase 8	Homo sapiens	126-135
12670894-3	2003	Treating HCT116 cells with THG results in caspase-8 activation; Bid cleavage; Bax conformational change and mitochondrial translocation; the release of cytochrome c, Smac/Diablo, and Omi/HtrA2 into the cytosol; caspase-3 activation; and apoptosis.	Thapsigargin	27-30	caspase 8	Homo sapiens	42-51
12670894-6	2003	Caspase-8 processing is dependent on de novo protein synthesis; DR5 expression is strongly up-regulated by THG treatment.	Thapsigargin	107-110	caspase 8	Homo sapiens	0-9
12670900-4	2003	Both caspase-3 and caspase-8 activities were increased by anti-Fas antibody CH-11 only in cells at 32.5 degrees C with wild-type p53.	4-dimethylamino-3',4'-dimethoxychalcone	76-81	caspase 8	Homo sapiens	19-28
12692863-0	2003	5-Fluorouracil efficiently enhanced apoptosis induced by adenovirus-mediated transfer of caspase-8 in DLD-1 colon cancer cells.	Fluorouracil	0-14	caspase 8	Homo sapiens	89-98
12692863-9	2003	A potentiating effect of adenoviral treatment was also seen when 5-FU treatment was substituted by the overexpression of cyclin-dependent kinase inhibitors, p21(WAF1/CIP1) and p27(KIP1), suggesting that the cytostatic effect of 5-FU augmented apoptosis induced by caspase-8 gene transduction by inhibiting the dilution of gene products associated with cell division.	Fluorouracil	65-69	caspase 8	Homo sapiens	264-273
12669310-10	2003	Moreover, the general caspase inhibitor ZVAD blocked the cleavage and activation of most caspases tested except caspase-9.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	40-44	caspase 8	Homo sapiens	89-97
12645080-3	2003	Treatment of [(3)H]palmitate-labeled cells with staurosporine (to activate caspase 8 and induce apoptosis) or exogenous sphingomyelinase specifically increased the [(3)H]ceramide content of the Raft fraction.	Tritium	13-18	caspase 8	Homo sapiens	75-84
12645080-3	2003	Treatment of [(3)H]palmitate-labeled cells with staurosporine (to activate caspase 8 and induce apoptosis) or exogenous sphingomyelinase specifically increased the [(3)H]ceramide content of the Raft fraction.	Palmitates	19-28	caspase 8	Homo sapiens	75-84
12645080-3	2003	Treatment of [(3)H]palmitate-labeled cells with staurosporine (to activate caspase 8 and induce apoptosis) or exogenous sphingomyelinase specifically increased the [(3)H]ceramide content of the Raft fraction.	Staurosporine	48-61	caspase 8	Homo sapiens	75-84
12499380-1	2003	Evidence for caspase-8-ganglioside interaction in T cells.	Gangliosides	23-34	caspase 8	Homo sapiens	13-22
12649185-0	2003	Caspase-8 and apoptosis-inducing factor mediate a cytochrome c-independent pathway of apoptosis in human colon cancer cells induced by the dietary phytochemical chlorophyllin.	chlorophyllin	161-174	caspase 8	Homo sapiens	0-39
12551927-0	2003	Epoxycyclohexenone inhibits Fas-mediated apoptosis by blocking activation of pro-caspase-8 in the death-inducing signaling complex.	SCHEMBL8899778	0-18	caspase 8	Homo sapiens	81-90
12551927-0	2003	Epoxycyclohexenone inhibits Fas-mediated apoptosis by blocking activation of pro-caspase-8 in the death-inducing signaling complex.	ammonium ferrous sulfate	28-31	caspase 8	Homo sapiens	81-90
12551927-9	2003	ECH directly bound the large subunit of active caspase-8 that contains the active center cysteine and had a relatively higher affinity to pro-caspase-8.	Cysteine	89-97	caspase 8	Homo sapiens	47-56
12499380-5	2003	Scanning confocal microscopy showed that triggering through CD95/Fas induced a significant GM3-caspase-8 association, as revealed by nearly complete colocalization areas.	gm3	91-94	caspase 8	Homo sapiens	95-104
12499380-6	2003	Coimmunoprecipitation experiments demonstrated that GM3 and GM1 were immunoprecipitated by anti-caspase-8 only after triggering through CD95/Fas.	gm3	52-55	caspase 8	Homo sapiens	96-105
12499380-6	2003	Coimmunoprecipitation experiments demonstrated that GM3 and GM1 were immunoprecipitated by anti-caspase-8 only after triggering through CD95/Fas.	G(M1) Ganglioside	60-63	caspase 8	Homo sapiens	96-105
12499380-7	2003	This association was supported by the recruitment of caspase-8, as well as of CD95/Fas, to GEM upon CD95/Fas engagement, as revealed by the analysis of linear sucrose gradient fractions.	Sucrose	159-166	caspase 8	Homo sapiens	53-62
12393608-4	2003	Here, we found that inhibition of caspases by the general caspase inhibitor zVAD-fmk did not prevent TNF-alpha-induced PMN death.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	76-84	caspase 8	Homo sapiens	34-42
12393608-4	2003	Here, we found that inhibition of caspases by the general caspase inhibitor zVAD-fmk did not prevent TNF-alpha-induced PMN death.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	76-84	caspase 8	Homo sapiens	34-41
12639813-14	2003	CONCLUSION: Therapy with pentoxiphylline for 24 weeks is associated with a decline in the levels of caspase 1 and caspase 8.	Pentoxifylline	25-40	caspase 8	Homo sapiens	114-123
12700635-5	2003	Cotreatment of SCLC cells with the demethylating agent 5"-aza-2-deoxycytidine and IFNgamma partially restored Fas, TRAIL-R1 and caspase-8 expression and increased sensitivity to FasL and TRAIL-induced death.	Decitabine	55-77	caspase 8	Homo sapiens	128-137
12417974-4	2003	We have begun to systematically characterize hair cell death in an in vitro system by examining the activation of these specific caspases in degenerating hair cells after acutely damaging the whole avian basilar papilla with gentamicin.	Gentamicins	225-235	caspase 8	Homo sapiens	129-137
12417974-7	2003	Supplementation of z-VAD-fmk, a general caspase inhibitor, provided short-term protection against gentamicin-induced hair cell death.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	19-28	caspase 8	Homo sapiens	40-47
12417974-7	2003	Supplementation of z-VAD-fmk, a general caspase inhibitor, provided short-term protection against gentamicin-induced hair cell death.	Gentamicins	98-108	caspase 8	Homo sapiens	40-47
12417974-9	2003	At these time-points, specific fluorescent-labeled peptide substrates detected more active caspase-3, caspase-8, and caspase-9 in gentamicin-treated hair cells relative to controls.	Gentamicins	130-140	caspase 8	Homo sapiens	102-111
12417974-10	2003	Our data indicate that auditory hair cells degenerate as a result of gentamicin exposure in a caspase-dependent manner.	Gentamicins	69-79	caspase 8	Homo sapiens	94-101
12417974-11	2003	Specifically, the upstream caspases, caspase-8 and caspase-9, and the downstream caspase-3 are activated in aminoglycoside-damaged hair cells.	Aminoglycosides	108-122	caspase 8	Homo sapiens	27-35
12417974-11	2003	Specifically, the upstream caspases, caspase-8 and caspase-9, and the downstream caspase-3 are activated in aminoglycoside-damaged hair cells.	Aminoglycosides	108-122	caspase 8	Homo sapiens	37-46
12496285-3	2003	Fas agonistic antibody, CH-11, induced apoptosis in sensitive glioma cells through caspase-8 recruitment to the Fas-mediated death-inducing signaling complex (DISC) where caspase-8 was cleaved to initiate apoptosis through a systematic cleavage of downstream substrates.	4-dimethylamino-3',4'-dimethoxychalcone	24-29	caspase 8	Homo sapiens	83-92
12657720-0	2003	Z-FA-fmk inhibits effector caspases but not initiator caspases 8 and 10, and demonstrates that novel anticancer retinoid-related molecules induce apoptosis via the intrinsic pathway.	MDL 201053	0-8	caspase 8	Homo sapiens	27-35
12657720-0	2003	Z-FA-fmk inhibits effector caspases but not initiator caspases 8 and 10, and demonstrates that novel anticancer retinoid-related molecules induce apoptosis via the intrinsic pathway.	Retinoids	112-120	caspase 8	Homo sapiens	27-35
12657720-4	2003	Z-FA-fmk can inhibit caspase activity in vitro and selectively inhibits recombinant effector caspases 2, -3, -6, and -7.	MDL 201053	0-8	caspase 8	Homo sapiens	21-28
12657720-6	2003	These data correlate with the covalent binding of biotinylated Z-FA-fmk to the active large subunit of effector caspases.	MDL 201053	63-71	caspase 8	Homo sapiens	112-120
12657720-7	2003	This selective targeting of effector caspases is also observed in Jurkat cells and has been used to demonstrate that RRMs induce apoptosis through the mitochondrial pathway and activate caspase 8 in a Z-FA-fmk-sensitive manner.	MDL 201053	201-209	caspase 8	Homo sapiens	37-45
12657720-7	2003	This selective targeting of effector caspases is also observed in Jurkat cells and has been used to demonstrate that RRMs induce apoptosis through the mitochondrial pathway and activate caspase 8 in a Z-FA-fmk-sensitive manner.	MDL 201053	201-209	caspase 8	Homo sapiens	186-195
12657720-8	2003	Thus, Z-FA-fmk fails to inhibit Fas-mediated activation of caspase 8, but completely inhibits RRM-induced processing of caspase 8.	MDL 201053	6-14	caspase 8	Homo sapiens	120-129
12579296-0	2003	Beta-sitosterol, a plant sterol, induces apoptosis and activates key caspases in MDA-MB-231 human breast cancer cells.	gamma-sitosterol	0-15	caspase 8	Homo sapiens	69-77
12579296-0	2003	Beta-sitosterol, a plant sterol, induces apoptosis and activates key caspases in MDA-MB-231 human breast cancer cells.	Sterols	9-15	caspase 8	Homo sapiens	69-77
12579296-4	2003	The results of the present study indicate that beta-sitosterol supplementation at 16 microM for 3 days to MDA-MB-231 cells induces 39% and 80% increases in the activities of caspases 8 and 9, respectively, compared to cholesterol supplemented cells or controls.	gamma-sitosterol	47-62	caspase 8	Homo sapiens	174-190
12839663-0	2003	[The expression and activity of caspase-8 in the process of vitamin E succinate-induced apoptosis in human gastric carcinoma SGC-7901 cells].	alpha-Tocopherol	60-79	caspase 8	Homo sapiens	32-41
12839663-1	2003	OBJECTIVE: To investigate the role of caspase-8 in vitamin E succinate (VES)-induced apoptosis in human gastric carcinoma cells.	alpha-Tocopherol	51-70	caspase 8	Homo sapiens	38-47
12496285-3	2003	Fas agonistic antibody, CH-11, induced apoptosis in sensitive glioma cells through caspase-8 recruitment to the Fas-mediated death-inducing signaling complex (DISC) where caspase-8 was cleaved to initiate apoptosis through a systematic cleavage of downstream substrates.	4-dimethylamino-3',4'-dimethoxychalcone	24-29	caspase 8	Homo sapiens	171-180
12839663-1	2003	OBJECTIVE: To investigate the role of caspase-8 in vitamin E succinate (VES)-induced apoptosis in human gastric carcinoma cells.	alpha-Tocopherol	72-75	caspase 8	Homo sapiens	38-47
12496285-3	2003	Fas agonistic antibody, CH-11, induced apoptosis in sensitive glioma cells through caspase-8 recruitment to the Fas-mediated death-inducing signaling complex (DISC) where caspase-8 was cleaved to initiate apoptosis through a systematic cleavage of downstream substrates.	ammonium ferrous sulfate	0-3	caspase 8	Homo sapiens	83-92
12839663-2	2003	METHODS: The expression and activity of caspase-8 were measured by the Western Blot method with fluorescence and DAPI staining.	DAPI	113-117	caspase 8	Homo sapiens	40-49
12496285-3	2003	Fas agonistic antibody, CH-11, induced apoptosis in sensitive glioma cells through caspase-8 recruitment to the Fas-mediated death-inducing signaling complex (DISC) where caspase-8 was cleaved to initiate apoptosis through a systematic cleavage of downstream substrates.	ammonium ferrous sulfate	0-3	caspase 8	Homo sapiens	171-180
12496285-4	2003	In contrast, CH-11 stimulated cell growth in resistant glioma cells through recruitment of c-FLIP (cellular Fas-associated death domain (FADD)-like interleukin-1beta-converting enzyme (FLICE)-inhibitory protein) to the Fas-mediated DISC.	4-dimethylamino-3',4'-dimethoxychalcone	13-18	caspase 8	Homo sapiens	185-190
12496285-4	2003	In contrast, CH-11 stimulated cell growth in resistant glioma cells through recruitment of c-FLIP (cellular Fas-associated death domain (FADD)-like interleukin-1beta-converting enzyme (FLICE)-inhibitory protein) to the Fas-mediated DISC.	fadd	137-141	caspase 8	Homo sapiens	185-190
12496285-4	2003	In contrast, CH-11 stimulated cell growth in resistant glioma cells through recruitment of c-FLIP (cellular Fas-associated death domain (FADD)-like interleukin-1beta-converting enzyme (FLICE)-inhibitory protein) to the Fas-mediated DISC.	ammonium ferrous sulfate	108-111	caspase 8	Homo sapiens	185-190
12393500-4	2003	We here demonstrate molecular mechanisms whereby PS-341 mediates anti-MM activity by inducing p53 and MDM2 protein expression; inducing the phosphorylation (Ser15) of p53 protein; activating c-Jun NH(2)-terminal kinase (JNK), caspase-8, and caspase-3; and cleaving the DNA protein kinase catalytic subunit, ATM, and MDM2.	Bortezomib	49-55	caspase 8	Homo sapiens	226-235
12482880-0	2003	The mycotoxin penicillic acid inhibits Fas ligand-induced apoptosis by blocking self-processing of caspase-8 in death-inducing signaling complex.	Penicillic Acid	14-29	caspase 8	Homo sapiens	99-108
12482880-1	2003	Upon engagement with Fas ligand (FasL), Fas rapidly induces recruitment and self-processing of caspase-8 via the adaptor protein Fas-associated death domain (FADD), and activated caspase-8 cleaves downstream substrates such as caspase-3.	ammonium ferrous sulfate	21-24	caspase 8	Homo sapiens	95-104
12482880-1	2003	Upon engagement with Fas ligand (FasL), Fas rapidly induces recruitment and self-processing of caspase-8 via the adaptor protein Fas-associated death domain (FADD), and activated caspase-8 cleaves downstream substrates such as caspase-3.	ammonium ferrous sulfate	21-24	caspase 8	Homo sapiens	179-188
12482880-7	2003	Glutathione and cysteine neutralized an inhibitory effect of PCA on caspase-8, and PCA bound directly to the active center cysteine in the large subunit of caspase-8.	Glutathione	0-11	caspase 8	Homo sapiens	68-77
12482880-7	2003	Glutathione and cysteine neutralized an inhibitory effect of PCA on caspase-8, and PCA bound directly to the active center cysteine in the large subunit of caspase-8.	Glutathione	0-11	caspase 8	Homo sapiens	156-165
12482880-7	2003	Glutathione and cysteine neutralized an inhibitory effect of PCA on caspase-8, and PCA bound directly to the active center cysteine in the large subunit of caspase-8.	Cysteine	16-24	caspase 8	Homo sapiens	68-77
12482880-7	2003	Glutathione and cysteine neutralized an inhibitory effect of PCA on caspase-8, and PCA bound directly to the active center cysteine in the large subunit of caspase-8.	Cysteine	123-131	caspase 8	Homo sapiens	156-165
12454017-8	2003	In contrast, vanadate-elicited Fas aggregation and Fas-FADD association, as well as caspase-8 activation, were dependent on JNK activation but were minimally regulated by ROS generation.	Vanadates	13-21	caspase 8	Homo sapiens	84-93
12393527-8	2003	FADD-like interleukin 1 beta (IL-1beta)-converting enzyme (FLICE)-inhibitory protein (FLIP) has been reported to interact with FADD and/or caspase-8 at the death-inducing signaling complex (DISC) level following Fas stimulation and acts as a dominant-negative caspase-8.	ammonium ferrous sulfate	212-215	caspase 8	Homo sapiens	59-64
12393527-8	2003	FADD-like interleukin 1 beta (IL-1beta)-converting enzyme (FLICE)-inhibitory protein (FLIP) has been reported to interact with FADD and/or caspase-8 at the death-inducing signaling complex (DISC) level following Fas stimulation and acts as a dominant-negative caspase-8.	ammonium ferrous sulfate	212-215	caspase 8	Homo sapiens	139-148
12393527-8	2003	FADD-like interleukin 1 beta (IL-1beta)-converting enzyme (FLICE)-inhibitory protein (FLIP) has been reported to interact with FADD and/or caspase-8 at the death-inducing signaling complex (DISC) level following Fas stimulation and acts as a dominant-negative caspase-8.	ammonium ferrous sulfate	212-215	caspase 8	Homo sapiens	260-269
12454017-5	2003	In addition, vanadate induced FasL production, Fas (CD95) aggregation, and its association with the Fas-associated death domain (FADD), as well as the activation of caspase-8.	Vanadates	13-21	caspase 8	Homo sapiens	165-174
12454017-10	2003	On the other hand, dominant negative FADD and caspase-8 inhibitor completely eliminated vanadate-induced apoptosis.	Vanadates	88-96	caspase 8	Homo sapiens	46-55
12454017-11	2003	Thus, JNK signaling plays a major role in vanadate-mediated activation of the Fas-FADD-caspase-8 pathway that accounts for vanadate-induced apoptosis of CGPs.	Vanadates	42-50	caspase 8	Homo sapiens	87-96
12454017-11	2003	Thus, JNK signaling plays a major role in vanadate-mediated activation of the Fas-FADD-caspase-8 pathway that accounts for vanadate-induced apoptosis of CGPs.	Vanadates	123-131	caspase 8	Homo sapiens	87-96
12458208-6	2003	The crystal structure of the post-cleavage complex between p35 and caspase-8 shows that p35 forms a thioester bond with the active site cysteine of the caspase.	Cysteine	136-144	caspase 8	Homo sapiens	67-76
12566414-6	2003	A systematic examination of the downstream effectors of Fas signaling in IRF-4-transfected cells demonstrates an increased activation of caspase-8, as well as an increase in Fas receptor polarization.	ammonium ferrous sulfate	56-59	caspase 8	Homo sapiens	137-146
12629330-4	2003	We also investigated whether an inhibitor of caspase-8 (Z-IETD-FMK) does modulate IL-8 and MCP-1 secretion.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	56-66	caspase 8	Homo sapiens	45-54
12576460-6	2003	Caspase 8 was activated through a Fas-associated death domain protein (FADD)-dependent mechanism as demonstrated by inhibition of DT(388)-GMCSF-induced apoptosis on expression of a dominant negative FADD molecule.	dt(388)	130-137	caspase 8	Homo sapiens	0-9
12576463-0	2003	Phytosphingosine induces apoptotic cell death via caspase 8 activation and Bax translocation in human cancer cells.	phytosphingosine	0-16	caspase 8	Homo sapiens	50-59
12576463-3	2003	In this study, we report that phytosphingosine can potently induce apoptotic cell death in human cancer cells via caspase activation and caspase-independent cytochrome c release.	phytosphingosine	30-46	caspase 8	Homo sapiens	114-121
12576463-5	2003	Involvement of caspases was determined by immunoblot analysis and cell death detection assays after treatment with synthetic inhibitor z-Val-Ala-Asp-fluoromethyl ketone, z-DEVD-fmk, or z-IETD-fmk.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	135-168	caspase 8	Homo sapiens	15-23
12576463-5	2003	Involvement of caspases was determined by immunoblot analysis and cell death detection assays after treatment with synthetic inhibitor z-Val-Ala-Asp-fluoromethyl ketone, z-DEVD-fmk, or z-IETD-fmk.	benzoylcarbonyl-aspartyl-glutamyl-valyl-aspartyl-fluoromethyl ketone	170-180	caspase 8	Homo sapiens	15-23
12576463-5	2003	Involvement of caspases was determined by immunoblot analysis and cell death detection assays after treatment with synthetic inhibitor z-Val-Ala-Asp-fluoromethyl ketone, z-DEVD-fmk, or z-IETD-fmk.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	185-195	caspase 8	Homo sapiens	15-23
12576463-9	2003	We observed that phytosphingosine cause activation of caspase 8 in a DR-independent fashion.	phytosphingosine	17-33	caspase 8	Homo sapiens	54-63
12576463-15	2003	CONCLUSION: These findings indicate that phytosphingosine induces apoptotic cell death in human cancer cells by direct activation of caspase 8, and by mitochondrial translocation of Bax and subsequent release of cytochrome c into cytoplasm, providing a potential mechanism for the anticancer activity of phytosphingosine.	phytosphingosine	41-57	caspase 8	Homo sapiens	133-142
12527327-11	2003	These results suggested that CS-induced apoptosis of HL-60 cells might be caused by inhibiting Akt phosphorylation following cleavage of Bid through caspase-8 activation and subsequently via an Apaf complex-caspase cascade pathway.	cholesteryl succinate	29-31	caspase 8	Homo sapiens	149-158
12661987-7	2003	The apoptotic process was almost completely blocked in the presence of the general caspase inhibitor zVAD.fmk.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	101-105	caspase 8	Homo sapiens	83-90
12661987-7	2003	The apoptotic process was almost completely blocked in the presence of the general caspase inhibitor zVAD.fmk.	FMK	106-109	caspase 8	Homo sapiens	83-90
12661987-8	2003	In contrast, no or only minor effects were observed with the more specific caspase inhibitors DEVD.CHO, IETD.fmk, and DEVD.fmk.	aspartyl-glutamyl-valyl-aspartal	94-102	caspase 8	Homo sapiens	75-82
12661987-15	2003	The divalent calcium concentration, [Ca2+], appears to be involved in the activation of several caspases, resulting in DNA fragmentation, chromosomal condensation, and nuclear fragmentation.	Calcium	13-20	caspase 8	Homo sapiens	96-104
14607657-0	2003	Caspase-8 in apoptosis of hepatoma cell induced by 5-fluorouracil.	Fluorouracil	51-65	caspase 8	Homo sapiens	0-9
14607657-1	2003	OBJECTIVE: To explore the relationship between the changes in the activity of caspase-8 and apoptosis of HepG2 cells induced by 5-fluorouracil (5-Fu).	Fluorouracil	128-142	caspase 8	Homo sapiens	78-87
14607657-1	2003	OBJECTIVE: To explore the relationship between the changes in the activity of caspase-8 and apoptosis of HepG2 cells induced by 5-fluorouracil (5-Fu).	Fluorouracil	144-148	caspase 8	Homo sapiens	78-87
14607657-4	2003	The apoptotic rate of HepG2 cells induced by 5-Fu with or without the caspase-8 inhibitor IETD-FMK was measured by flow cytometry.	isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	90-98	caspase 8	Homo sapiens	70-79
14607657-5	2003	RESULTS: After the HepG2 cells were treated with 10(-2) mol/L 5-Fu, the caspase-8 activity increased gradually and reached the peak level (313.9+/-6.9) at 16 hours, then fell down.	Fluorouracil	62-66	caspase 8	Homo sapiens	72-81
14607657-7	2003	With the increasing concentration of 5-Fu, the caspase-8 activity was also increased; the activity in high concentration 5-Fu was significantly higher than that in low concentration 5-Fu (370.5+/-4.7 vs 313.7+/-6.9; 225.7+/-5.4 vs 183.3+/-4.8; 183.3+/-4.8 vs 124.0+/-6.2, P&lt;0.01).	Fluorouracil	37-41	caspase 8	Homo sapiens	47-56
14607657-7	2003	With the increasing concentration of 5-Fu, the caspase-8 activity was also increased; the activity in high concentration 5-Fu was significantly higher than that in low concentration 5-Fu (370.5+/-4.7 vs 313.7+/-6.9; 225.7+/-5.4 vs 183.3+/-4.8; 183.3+/-4.8 vs 124.0+/-6.2, P&lt;0.01).	Fluorouracil	121-125	caspase 8	Homo sapiens	47-56
14607657-7	2003	With the increasing concentration of 5-Fu, the caspase-8 activity was also increased; the activity in high concentration 5-Fu was significantly higher than that in low concentration 5-Fu (370.5+/-4.7 vs 313.7+/-6.9; 225.7+/-5.4 vs 183.3+/-4.8; 183.3+/-4.8 vs 124.0+/-6.2, P&lt;0.01).	Fluorouracil	121-125	caspase 8	Homo sapiens	47-56
14607657-8	2003	The caspase-8 activity was the highest at 1X10(-1) mol/L 5-Fu (370.5+/-4.7).	Fluorouracil	57-61	caspase 8	Homo sapiens	4-13
14607657-9	2003	The caspase-8 activity in low concentration 5-Fu was higher than in the blank control group and inhibitor group (124.0+/-6.2 vs 68.5+/-3.4; 124.0+/-6.2 vs 41.0+/-2.1, P&lt;0.01).	Fluorouracil	44-48	caspase 8	Homo sapiens	4-13
14607657-10	2003	IETD-FMK could block the activation of caspase-8 and reduce the apoptosis of HepG2 cells induced by 5-Fu.	isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	0-8	caspase 8	Homo sapiens	39-48
14607657-12	2003	CONCLUSIONS: 5-Fu can induce apoptosis of HepG2 cells via caspase-8 signal transduction pathway, which can be blocked by IETD-FMK.	Fluorouracil	13-17	caspase 8	Homo sapiens	58-67
14607657-12	2003	CONCLUSIONS: 5-Fu can induce apoptosis of HepG2 cells via caspase-8 signal transduction pathway, which can be blocked by IETD-FMK.	isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	121-129	caspase 8	Homo sapiens	58-67
14607657-13	2003	5-Fu promotes the increase of caspase-8 activity in a time- or concentration-dependent manner.	Fluorouracil	0-4	caspase 8	Homo sapiens	30-39
12527816-0	2003	Apoptosis induced by (E)-5-(2-bromovinyl)-2"-deoxyuridine in varicella zoster virus thymidine kinase-expressing cells is driven by activation of c-Jun/activator protein-1 and Fas ligand/caspase-8.	brivudine	21-57	caspase 8	Homo sapiens	186-195
12527816-11	2003	Transfection of dominant-negative Fas-associated death domain and inhibition of caspase-8 by N-benzyloxycarbonyl-IETD-fluoromethyl ketone strongly abrogated BVDU-induced apoptosis, indicating Fas/FasL to be crucially involved.	n-benzyloxycarbonyl-ietd-fluoromethyl ketone	93-137	caspase 8	Homo sapiens	80-89
12393559-9	2003	Caspase-8 inhibition counters cytochrome c release, caspase-9 and caspase-3 activation, and apoptosis, thus suggesting that caspase-8 inhibitor can directly inhibit caspase-9 and/or that DEX-induced caspase-8 activation is upstream to mitochondria and can regulate caspase-3 directly or through cytochrome c release and the consequent caspase-9/caspase-3 activation.	Dexamethasone	187-190	caspase 8	Homo sapiens	0-9
12393559-9	2003	Caspase-8 inhibition counters cytochrome c release, caspase-9 and caspase-3 activation, and apoptosis, thus suggesting that caspase-8 inhibitor can directly inhibit caspase-9 and/or that DEX-induced caspase-8 activation is upstream to mitochondria and can regulate caspase-3 directly or through cytochrome c release and the consequent caspase-9/caspase-3 activation.	Dexamethasone	187-190	caspase 8	Homo sapiens	199-208
12393559-0	2003	Dexamethasone-induced apoptosis of thymocytes: role of glucocorticoid receptor-associated Src kinase and caspase-8 activation.	Dexamethasone	0-13	caspase 8	Homo sapiens	105-114
12393559-10	2003	DEX-induced caspase-8 activation, like ceramide-induced caspase-8 activation, correlates with the formation of Fas-associated death domain protein (FADD)/caspase-8 complex.	Dexamethasone	0-3	caspase 8	Homo sapiens	12-21
12393559-10	2003	DEX-induced caspase-8 activation, like ceramide-induced caspase-8 activation, correlates with the formation of Fas-associated death domain protein (FADD)/caspase-8 complex.	Dexamethasone	0-3	caspase 8	Homo sapiens	56-65
12393559-10	2003	DEX-induced caspase-8 activation, like ceramide-induced caspase-8 activation, correlates with the formation of Fas-associated death domain protein (FADD)/caspase-8 complex.	Dexamethasone	0-3	caspase 8	Homo sapiens	56-65
12393559-10	2003	DEX-induced caspase-8 activation, like ceramide-induced caspase-8 activation, correlates with the formation of Fas-associated death domain protein (FADD)/caspase-8 complex.	Ceramides	39-47	caspase 8	Homo sapiens	12-21
12393559-10	2003	DEX-induced caspase-8 activation, like ceramide-induced caspase-8 activation, correlates with the formation of Fas-associated death domain protein (FADD)/caspase-8 complex.	Ceramides	39-47	caspase 8	Homo sapiens	56-65
12393559-10	2003	DEX-induced caspase-8 activation, like ceramide-induced caspase-8 activation, correlates with the formation of Fas-associated death domain protein (FADD)/caspase-8 complex.	Ceramides	39-47	caspase 8	Homo sapiens	56-65
12393559-11	2003	Caspase-8 activation is countered by the inhibition of macromolecular synthesis and of Src kinase, PI-PLC, and aSMase activation, suggesting it is downstream in the DEX-activated apoptotic pathway of thymocytes.	Dexamethasone	165-168	caspase 8	Homo sapiens	0-9
12407100-4	2003	Caspase 8 and 10 activation, bid cleavage, cytosolic cytochrome c, and caspase 3 activation by TRAIL were all increased by the bile acid glycochenodeoxycholate (GCDCA).	Bile Acids and Salts	127-136	caspase 8	Homo sapiens	0-9
12504792-5	2003	Since the pan-caspase inhibitor zVAD-fmk did not reduce lysosomal and mitochondrial destabilization, these events occur upstream of caspase activation.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	32-40	caspase 8	Homo sapiens	14-21
12504792-5	2003	Since the pan-caspase inhibitor zVAD-fmk did not reduce lysosomal and mitochondrial destabilization, these events occur upstream of caspase activation.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	32-40	caspase 8	Homo sapiens	132-139
12407100-4	2003	Caspase 8 and 10 activation, bid cleavage, cytosolic cytochrome c, and caspase 3 activation by TRAIL were all increased by the bile acid glycochenodeoxycholate (GCDCA).	Glycochenodeoxycholic Acid	137-159	caspase 8	Homo sapiens	0-9
12407100-4	2003	Caspase 8 and 10 activation, bid cleavage, cytosolic cytochrome c, and caspase 3 activation by TRAIL were all increased by the bile acid glycochenodeoxycholate (GCDCA).	Glycochenodeoxycholic Acid	161-166	caspase 8	Homo sapiens	0-9
12462380-7	2002	Moreover, neutralizing antibodies against the death receptor Fas and inhibitors of caspases, such as caspase-8 and -10, efficiently inhibited the EGC-triggered apoptosis.	gallocatechol	146-149	caspase 8	Homo sapiens	83-91
12543810-8	2003	In separate analysis of cells of early and late apoptotic stages, initiation of cisplatin-induced apoptosis appeared to be rather mediated by caspase-9 than by caspase-8.	Cisplatin	80-89	caspase 8	Homo sapiens	160-169
12605685-2	2003	Recently, we reported that the caspase-resistant BAP31 inhibited Fas-mediated apoptotic membrane fragmentation and the release of cytochrome c from mitochondria in KB epithelial cells (Nguyen M., Breckenridge G., Ducret A &amp; Shore G. (2000) Mol.	ammonium ferrous sulfate	65-68	caspase 8	Homo sapiens	31-38
12535213-7	2003	Pemphigus-sera-induced cell death is partially inhibited by pretreatment with anti-Fas ligand antibodies and by incubation with caspase-8 inhibitor Z-IETD-FMK.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	148-158	caspase 8	Homo sapiens	128-137
12770553-7	2003	Hence, Fas appears to be functional through a caspase-8-dependent pathway in a subpopulation of human foetal motoneurons.	ammonium ferrous sulfate	7-10	caspase 8	Homo sapiens	46-55
12655302-8	2003	Finally, we found that betaAP strongly activated caspase-8, and the cell-permeable, selective caspase-8 inhibitor z-IETD-FMK prevents both betaAP- and TRAIL-induced neurotoxicity.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	114-124	caspase 8	Homo sapiens	94-103
12645856-5	2003	Rifampicin, in a concentration-dependent manner, inhibited anti-CD95-induced apoptosis in both CD4+ and CD8+ T cells, which was associated with the inhibition of activation of both caspase-3 and caspase-8.	Rifampin	0-10	caspase 8	Homo sapiens	195-204
12488556-3	2003	Conversely, ectopic expression of CrmA or dominant-negative caspase-8 abrogated potentiation of ara-C-mediated apoptosis by bryostatin 1 but not by UCN-01.	Cytarabine	96-101	caspase 8	Homo sapiens	60-69
12488556-3	2003	Conversely, ectopic expression of CrmA or dominant-negative caspase-8 abrogated potentiation of ara-C-mediated apoptosis by bryostatin 1 but not by UCN-01.	bryostatin 1	124-136	caspase 8	Homo sapiens	60-69
14769541-4	2003	Although caspase-8 cleavage is an early event, reaching its maximum activation at 3 h, caspase-9 reaches its maximum activation only at 6 h. The addition of IETD-CHO, a caspase-8-specific inhibitor, completely prevents beta-Carotene-induced apoptosis, whereas only a partial prevention was observed in the presence of LEHD-CHO, a caspase-9-specific inhibitor.	IETD-CHO	157-165	caspase 8	Homo sapiens	9-18
14769541-4	2003	Although caspase-8 cleavage is an early event, reaching its maximum activation at 3 h, caspase-9 reaches its maximum activation only at 6 h. The addition of IETD-CHO, a caspase-8-specific inhibitor, completely prevents beta-Carotene-induced apoptosis, whereas only a partial prevention was observed in the presence of LEHD-CHO, a caspase-9-specific inhibitor.	IETD-CHO	157-165	caspase 8	Homo sapiens	169-178
14769541-4	2003	Although caspase-8 cleavage is an early event, reaching its maximum activation at 3 h, caspase-9 reaches its maximum activation only at 6 h. The addition of IETD-CHO, a caspase-8-specific inhibitor, completely prevents beta-Carotene-induced apoptosis, whereas only a partial prevention was observed in the presence of LEHD-CHO, a caspase-9-specific inhibitor.	beta Carotene	219-232	caspase 8	Homo sapiens	169-178
12633570-6	2002	Taken together, these findings suggest that IFN-gamma potentiates Fas- and TRAIL-mediated apoptosis by increasing caspase-8 expression via an IFN-gamma response element in A549 cells.	ammonium ferrous sulfate	66-69	caspase 8	Homo sapiens	114-123
12370493-0	2002	Intracellular superoxide induces apoptosis in VSMCs: role of mitochondrial membrane potential, cytochrome C and caspases.	Superoxides	14-24	caspase 8	Homo sapiens	112-120
12462380-7	2002	Moreover, neutralizing antibodies against the death receptor Fas and inhibitors of caspases, such as caspase-8 and -10, efficiently inhibited the EGC-triggered apoptosis.	gallocatechol	146-149	caspase 8	Homo sapiens	101-118
12437970-5	2002	Co-administration of the selective caspase-3 inhibitor z-DEVD-fmk or caspase-9 inhibitor z-LEHD-fmk significantly reduced C(2)-ceramide-induced cell death, while co-application of the caspase-8, inhibitor z-IETD-fmk, was without effect.	benzoylcarbonyl-aspartyl-glutamyl-valyl-aspartyl-fluoromethyl ketone	55-65	caspase 8	Homo sapiens	184-193
12657244-5	2002	DFO also caused release of cytochrome c from mitochondria and induced activation of caspase 3 and caspase 8.	Deferoxamine	0-3	caspase 8	Homo sapiens	98-107
12657244-6	2002	Interestingly, treatment of HL-60 cells with SB203580 greatly abolished cytochrome c release, and activation of caspase 3 and caspase 8.	SB 203580	45-53	caspase 8	Homo sapiens	126-135
12466493-8	2002	Second, both irreversible caspase inhibitors, z-DEVD-FMK and z-VAD-FMK, delayed MVV-induced cellular lysis as well as virus growth.	benzoylcarbonyl-aspartyl-glutamyl-valyl-aspartyl-fluoromethyl ketone	46-56	caspase 8	Homo sapiens	26-33
12466493-8	2002	Second, both irreversible caspase inhibitors, z-DEVD-FMK and z-VAD-FMK, delayed MVV-induced cellular lysis as well as virus growth.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	61-70	caspase 8	Homo sapiens	26-33
12466493-9	2002	Third, during SCPC in vitro infection by MVV, cells were positively stained with FITC-VAD-FMK, a probe that specifically stains cells containing active caspases.	fitc-vad-fmk	81-93	caspase 8	Homo sapiens	152-160
12507932-0	2002	Boswellic acids trigger apoptosis via a pathway dependent on caspase-8 activation but independent on Fas/Fas ligand interaction in colon cancer HT-29 cells.	boswellic acid	0-15	caspase 8	Homo sapiens	61-70
12507932-13	2002	The apoptosis induced by AK-BA was inhibited completely by caspase-3 or caspase-8 inhibitor and partially by caspase-9 inhibitor.	ak-ba	25-30	caspase 8	Homo sapiens	72-81
12415011-10	2002	Both forms of caspase-8-dependent cell death were also detected downstream of Fas in Jurkat T-cells, where Fas-dependent PS externalization and delayed ceramide production, which is similar to results shown here in A20 cells, have been reported.	ammonium ferrous sulfate	78-81	caspase 8	Homo sapiens	14-23
12415011-10	2002	Both forms of caspase-8-dependent cell death were also detected downstream of Fas in Jurkat T-cells, where Fas-dependent PS externalization and delayed ceramide production, which is similar to results shown here in A20 cells, have been reported.	Ceramides	152-160	caspase 8	Homo sapiens	14-23
12415011-13	2002	Thus, delayed elevation of ceramide is proposed to promote necrosis in those Fas-stimulated cells where caspase-8 activation was insufficient to trigger caspase-3-dependent apoptosis.	Ceramides	27-35	caspase 8	Homo sapiens	104-113
12439910-5	2002	After the cells were transiently transfected with Fas and FADD antisense oligonucleotides, respectively, caspase-8 activity was determined by flurometric method.	ammonium ferrous sulfate	50-53	caspase 8	Homo sapiens	105-114
12439910-10	2002	After SGC-7901 cells were transfected with Fas and FADD antisense oligonucleotides, caspase-8 activity was obviously decreased (P&lt;0.01), whereas Fas blocked more than FADD.	ammonium ferrous sulfate	43-46	caspase 8	Homo sapiens	84-93
12439910-10	2002	After SGC-7901 cells were transfected with Fas and FADD antisense oligonucleotides, caspase-8 activity was obviously decreased (P&lt;0.01), whereas Fas blocked more than FADD.	Oligonucleotides	66-82	caspase 8	Homo sapiens	84-93
12437970-6	2002	Immunoblot analysis of protein extracts from C(2)-ceramide-treated cortical neuronal cultures revealed upregulation of active caspase-9 and caspase-3 protein levels, whereas presence of active caspase-8 immunoreactivity was undetectable in this system.	A(2)C	45-49	caspase 8	Homo sapiens	193-202
12437970-6	2002	Immunoblot analysis of protein extracts from C(2)-ceramide-treated cortical neuronal cultures revealed upregulation of active caspase-9 and caspase-3 protein levels, whereas presence of active caspase-8 immunoreactivity was undetectable in this system.	Ceramides	50-58	caspase 8	Homo sapiens	193-202
12437970-5	2002	Co-administration of the selective caspase-3 inhibitor z-DEVD-fmk or caspase-9 inhibitor z-LEHD-fmk significantly reduced C(2)-ceramide-induced cell death, while co-application of the caspase-8, inhibitor z-IETD-fmk, was without effect.	A(2)C	122-126	caspase 8	Homo sapiens	184-193
12437970-5	2002	Co-administration of the selective caspase-3 inhibitor z-DEVD-fmk or caspase-9 inhibitor z-LEHD-fmk significantly reduced C(2)-ceramide-induced cell death, while co-application of the caspase-8, inhibitor z-IETD-fmk, was without effect.	Ceramides	127-135	caspase 8	Homo sapiens	184-193
12485870-0	2002	Prodigiosin induces caspase-9 and caspase-8 activation and cytochrome C release in Jurkat T cells.	Prodigiosin	0-11	caspase 8	Homo sapiens	34-43
12402161-6	2002	Furthermore, we have shown that inhibition of Fas mediated apoptosis is an early event in DU 145 cells, occurring upstream of Caspase 8 cleavage.	ammonium ferrous sulfate	46-49	caspase 8	Homo sapiens	126-135
12642685-4	2002	TRAIL and wortmannin together accelerated processing of caspase-8 on the DISC and apparently the release of caspase-8 from the DISC into the cytoplasm.	Wortmannin	10-20	caspase 8	Homo sapiens	56-65
12414664-7	2002	NSAIDs and 5-FU induced the mitochondrial release of cytochrome c as well as caspase-3 and -9 activation, and to a much lesser extent, caspase-8.	Fluorouracil	11-15	caspase 8	Homo sapiens	135-144
12642685-4	2002	TRAIL and wortmannin together accelerated processing of caspase-8 on the DISC and apparently the release of caspase-8 from the DISC into the cytoplasm.	Wortmannin	10-20	caspase 8	Homo sapiens	108-117
12385892-0	2002	Daunorubicin- and Ara-C-induced interphasic apoptosis of human type II leukemia cells is caspase-8-independent.	Daunorubicin	0-12	caspase 8	Homo sapiens	89-98
12404124-5	2002	We found that activation of both acid and neutral sphingomyelinases, triggered in the first minutes after U937 cell stimulation with TNF-alpha, is regulated in an inhibitory fashion by nitric oxide, working through generation of cyclic GMP and activation of protein kinase G. Using a range of inhibitors selective for either sphingomyelinase we found that the acid sphingomyelinase contributes to activation of the initiator caspase-8 and early DNA fragmentation and that inhibition of the acid enzyme by nitric oxide accounts for cyclic GMP-dependent early protection from apoptosis.	Nitric Oxide	185-197	caspase 8	Homo sapiens	425-434
12404126-7	2002	The ability of P-gp to inhibit caspase-8 activation was also ATP dependent.	Adenosine Triphosphate	61-64	caspase 8	Homo sapiens	31-40
12391322-6	2002	Further studies on these pathways showed that PS-341 decreases the levels of several antiapoptotic proteins and triggers a dual apoptotic pathway of mitochondrial cytochrome c release and caspase-9 activation, as well as activation of Jun kinase and a Fas/caspase-8-dependent apoptotic pathway [which is inhibited by a dominant negative (decoy) Fas construct].	Bortezomib	46-52	caspase 8	Homo sapiens	256-265
12270186-0	2002	Acyl dipeptides as reversible caspase inhibitors.	Dipeptides	5-15	caspase 8	Homo sapiens	30-37
12404126-8	2002	These studies demonstrate that P-gp inhibits Fas-induced caspase-8 activation but not formation of the DISC and that this activity of P-gp is dependent on ATP hydrolysis.	ammonium ferrous sulfate	45-48	caspase 8	Homo sapiens	57-66
12391190-7	2002	As expected, in activated PBL treated by anti-CD95 mAb, the pan-caspase inhibitor Cbz-Val-Ala-Asp(OMe)-fluoromethylketone and the caspase-8 inhibitor Cbz-Leu-Glu-Thr-Asp(OMe)-fluoromethylketone, but not the caspase-9 inhibitor Cbz-Leu-Glu-His-Asp(OMe)-fluoromethylketone, inhibit PS externalization and DeltaPsim disruption.	Cbz-Leu-Glu-Thr-Asp(OMe)-fluoromethylketone	150-193	caspase 8	Homo sapiens	130-139
12479703-8	2002	Caspase-8 and -9 were activated by gemcitabine treatment in this cell line, suggesting several mechanisms of action including death receptor pathway and mitochondrial damage.	gemcitabine	35-46	caspase 8	Homo sapiens	0-16
12161280-0	2002	Molecular mechanism of satratoxin-induced apoptosis in HL-60 cells: activation of caspase-8 and caspase-9 is involved in activation of caspase-3.	satratoxin	23-33	caspase 8	Homo sapiens	82-91
12161280-2	2002	Here we report that satratoxin G-treated human leukemia HL-60 cells underwent apoptosis through the action of caspase-3 which was activated by both caspase-8 and caspase-9.	satratoxin G	20-32	caspase 8	Homo sapiens	148-157
12161280-7	2002	Enzymic assay on IETD-AMC revealed that caspase-8 is strongly activated by exposure to satratoxin G while T-2 toxin (T-2) could not activate caspase-8 at an early stage of apoptosis.	IETD-AMC	17-25	caspase 8	Homo sapiens	40-49
12161280-7	2002	Enzymic assay on IETD-AMC revealed that caspase-8 is strongly activated by exposure to satratoxin G while T-2 toxin (T-2) could not activate caspase-8 at an early stage of apoptosis.	satratoxin G	87-99	caspase 8	Homo sapiens	40-49
12161280-9	2002	These findings indicate that satratoxin G-induced apoptosis involves activation of caspase-3 and DFF-40/CAD through both activation of caspase-8 and cytosolic accumulation of cytochrome c along with activation of caspase-9.	satratoxin	29-39	caspase 8	Homo sapiens	135-144
12351409-7	2002	CDDO induced rapid proteolytic processing of caspase-8, but not caspase-9, in CLL B cells, suggesting activation of a mitochondria-independent pathway.	2-cyano-3,12-dioxoolean-1,9-dien-28-oic acid	0-4	caspase 8	Homo sapiens	45-54
12351409-8	2002	CDDO-induced apoptosis of CLL B cells was blocked by cytokine response modifier A (CrmA), a suppressor of caspase-8, but not by X-linked inhibitor of apoptosis protein-baculovirus IAP repeat-3 (XIAP-BIR3), a fragment of XIAP, which selectively inhibits caspase-9.	2-cyano-3,12-dioxoolean-1,9-dien-28-oic acid	0-4	caspase 8	Homo sapiens	106-115
12351409-9	2002	Examination of CDDO effects on expression of several apoptosis-relevant genes demonstrated significant reductions in the levels of caspase-8 homolog Fas-ligand interleukin-1-converting enzyme (FLICE)-inhibitory protein (c-FLIP), an endogenous antagonist of caspase-8.	2-cyano-3,12-dioxoolean-1,9-dien-28-oic acid	15-19	caspase 8	Homo sapiens	131-140
12351409-9	2002	Examination of CDDO effects on expression of several apoptosis-relevant genes demonstrated significant reductions in the levels of caspase-8 homolog Fas-ligand interleukin-1-converting enzyme (FLICE)-inhibitory protein (c-FLIP), an endogenous antagonist of caspase-8.	2-cyano-3,12-dioxoolean-1,9-dien-28-oic acid	15-19	caspase 8	Homo sapiens	149-191
12351409-9	2002	Examination of CDDO effects on expression of several apoptosis-relevant genes demonstrated significant reductions in the levels of caspase-8 homolog Fas-ligand interleukin-1-converting enzyme (FLICE)-inhibitory protein (c-FLIP), an endogenous antagonist of caspase-8.	2-cyano-3,12-dioxoolean-1,9-dien-28-oic acid	15-19	caspase 8	Homo sapiens	193-198
12351409-9	2002	Examination of CDDO effects on expression of several apoptosis-relevant genes demonstrated significant reductions in the levels of caspase-8 homolog Fas-ligand interleukin-1-converting enzyme (FLICE)-inhibitory protein (c-FLIP), an endogenous antagonist of caspase-8.	2-cyano-3,12-dioxoolean-1,9-dien-28-oic acid	15-19	caspase 8	Homo sapiens	257-266
12145284-0	2002	Caspase-8-mediated BID cleavage and release of mitochondrial cytochrome c during Nomega-hydroxy-L-arginine-induced apoptosis in MDA-MB-468 cells.	N(omega)-hydroxyarginine	81-106	caspase 8	Homo sapiens	0-9
12203125-1	2002	Death induced by doxorubicin (dox) in neuroblastoma (NB) cells was originally thought to occur via the Fas pathway, however since studies suggest that caspase-8 expression is silenced in most high stage NB tumors, it is more probable that dox-induced death occurs via a different mechanism.	Doxorubicin	17-20	caspase 8	Homo sapiens	151-160
12239601-0	2002	Keto- and acetyl-keto-boswellic acids inhibit proliferation and induce apoptosis in Hep G2 cells via a caspase-8 dependent pathway.	keto- and acetyl-keto-boswellic acids	0-37	caspase 8	Homo sapiens	103-112
12357364-4	2002	Co-treatment of cells with the pan-caspase inhibitor Z-VAD-fmk attenuated some morphological and biochemical characteristics of apoptosis and delayed 2CdA-induced DeltaPsi(m) loss, but did not prevent cell death.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	53-62	caspase 8	Homo sapiens	35-42
12357364-4	2002	Co-treatment of cells with the pan-caspase inhibitor Z-VAD-fmk attenuated some morphological and biochemical characteristics of apoptosis and delayed 2CdA-induced DeltaPsi(m) loss, but did not prevent cell death.	2'-chloro-2'-deoxyadenosine	150-154	caspase 8	Homo sapiens	35-42
12203115-3	2002	We show that sulindac sulfide and SC-"236-induced apoptosis is coupled with upregulation of DR5, caspase 8 activation and Bid cleavage.	sulindac sulfide	13-29	caspase 8	Homo sapiens	97-106
12203115-3	2002	We show that sulindac sulfide and SC-"236-induced apoptosis is coupled with upregulation of DR5, caspase 8 activation and Bid cleavage.	4-(5-(4-chlorophenyl)-3-(trifluoromethyl)-1H-pyrazol-1-yl)benzenesulfonamide	34-41	caspase 8	Homo sapiens	97-106
12203125-1	2002	Death induced by doxorubicin (dox) in neuroblastoma (NB) cells was originally thought to occur via the Fas pathway, however since studies suggest that caspase-8 expression is silenced in most high stage NB tumors, it is more probable that dox-induced death occurs via a different mechanism.	Doxorubicin	30-33	caspase 8	Homo sapiens	151-160
12231544-3	2002	RESULTS: In K562 cells, coadministration of marginally toxic concentrations of STI571 (200 nM) and flavopiridol (150 nM) for 48 h resulted in a marked increase in mitochondrial damage (e.g., cytochrome c release), activation of caspase-3, caspase-8, and Bid, and apoptosis.	alvocidib	99-111	caspase 8	Homo sapiens	239-248
12203125-1	2002	Death induced by doxorubicin (dox) in neuroblastoma (NB) cells was originally thought to occur via the Fas pathway, however since studies suggest that caspase-8 expression is silenced in most high stage NB tumors, it is more probable that dox-induced death occurs via a different mechanism.	Doxorubicin	17-28	caspase 8	Homo sapiens	151-160
12181741-0	2002	Mitomycin C induces apoptosis and caspase-8 and -9 processing through a caspase-3 and Fas-independent pathway.	Mitomycin	0-11	caspase 8	Homo sapiens	34-50
12181741-0	2002	Mitomycin C induces apoptosis and caspase-8 and -9 processing through a caspase-3 and Fas-independent pathway.	ammonium ferrous sulfate	86-89	caspase 8	Homo sapiens	34-50
12181741-5	2002	MMC treatment led to pronounced caspase-8, -9, and -7 processing and early morphological features of apoptosis within 48 h. This could be inhibited by the broad-spectrum caspase inhibitor z-VAD.fmk and to a lesser extent by z-IETD.fmk and z-LEHD.fmk, which have a certain preference for inhibiting caspase-8 and -9, respectively.	Mitomycin	0-3	caspase 8	Homo sapiens	32-41
12181741-5	2002	MMC treatment led to pronounced caspase-8, -9, and -7 processing and early morphological features of apoptosis within 48 h. This could be inhibited by the broad-spectrum caspase inhibitor z-VAD.fmk and to a lesser extent by z-IETD.fmk and z-LEHD.fmk, which have a certain preference for inhibiting caspase-8 and -9, respectively.	Mitomycin	0-3	caspase 8	Homo sapiens	298-314
12181741-5	2002	MMC treatment led to pronounced caspase-8, -9, and -7 processing and early morphological features of apoptosis within 48 h. This could be inhibited by the broad-spectrum caspase inhibitor z-VAD.fmk and to a lesser extent by z-IETD.fmk and z-LEHD.fmk, which have a certain preference for inhibiting caspase-8 and -9, respectively.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	188-197	caspase 8	Homo sapiens	298-314
12181741-6	2002	MMC induced apoptosis in MCF-7 cells was not mediated by the death receptor pathway as demonstrated by experiments using the inhibiting anti-Fas antibody ZB4 and transfections with CrmA, a viral serpin inhibitor of caspase-8, and the dominant negative Fas-associated death domain (FADD-DN).	Mitomycin	0-3	caspase 8	Homo sapiens	215-224
12181741-6	2002	MMC induced apoptosis in MCF-7 cells was not mediated by the death receptor pathway as demonstrated by experiments using the inhibiting anti-Fas antibody ZB4 and transfections with CrmA, a viral serpin inhibitor of caspase-8, and the dominant negative Fas-associated death domain (FADD-DN).	crma	181-185	caspase 8	Homo sapiens	215-224
12181747-4	2002	In Jurkat cells, TPA strongly activated ERK and inhibited the IR-induced caspase-8/Bid cleavage and the loss of DeltaPsi(m).	Tetradecanoylphorbol Acetate	17-20	caspase 8	Homo sapiens	73-82
12181749-7	2002	Treatment with the caspase inhibitor benzyloxycarbonyl-Val-Ala-DL-Asp(OMe)-fluoromethylketone or overexpression of Bcl-2 prevent this shift and promote necrosis.	Z-Val-Ala-DL-Asp(OMe)-fluoromethylketone	37-93	caspase 8	Homo sapiens	19-26
12231544-3	2002	RESULTS: In K562 cells, coadministration of marginally toxic concentrations of STI571 (200 nM) and flavopiridol (150 nM) for 48 h resulted in a marked increase in mitochondrial damage (e.g., cytochrome c release), activation of caspase-3, caspase-8, and Bid, and apoptosis.	Imatinib Mesylate	79-85	caspase 8	Homo sapiens	239-248
12428923-7	2002	Experiments conducted with caspase inhibitors, bongkrekic acid, or DL-PDMP indicated that ceramide triggers mitochondrial collapse, followed by the activation of caspases-9, -8 and -3, and poly(ADP-ribose)polymerase cleavage.	Ceramides	90-98	caspase 8	Homo sapiens	27-34
12055196-2	2002	We here report a novel caspase-8 mutant with a naturally occurring deletion of leucine 62 (Delta Leu62casp-8).	Leucine	79-86	caspase 8	Homo sapiens	23-32
12055196-2	2002	We here report a novel caspase-8 mutant with a naturally occurring deletion of leucine 62 (Delta Leu62casp-8).	leu62casp	97-106	caspase 8	Homo sapiens	23-32
12165276-8	2002	Further investigation of CD95-mediated caspase activities revealed that supplementation of glutamine significantly decreased caspase-3 and caspase-8 activities in activated T cells.	Glutamine	91-100	caspase 8	Homo sapiens	139-148
12169276-6	2002	Rottlerin enhanced activation of caspase-8 and cleavage of Bid.	rottlerin	0-9	caspase 8	Homo sapiens	33-42
12154014-7	2002	We find that CK2 inhibits Apo2L/TRAIL-induced caspase-8-mediated cleavage of BID, thereby reducing the formation of tBID.	tBID	116-120	caspase 8	Homo sapiens	46-55
12212968-4	2002	The administration of agonistic anti-Fas antibody (CH-11) or cycloheximide alone did not induce apoptosis, whereas the co-administration of CH-11 with cycloheximide induced apoptosis in WI-38 cells, in which caspase-8 and -3, but not -9, were activated, and X chromosome-linked inhibitor of apoptosis (ILP) and FLICE-like inhibitor protein (FLIP(L)), but not bcl-xL and bcl-2, were remarkably down regulated.	4-dimethylamino-3',4'-dimethoxychalcone	140-145	caspase 8	Homo sapiens	208-224
12212968-4	2002	The administration of agonistic anti-Fas antibody (CH-11) or cycloheximide alone did not induce apoptosis, whereas the co-administration of CH-11 with cycloheximide induced apoptosis in WI-38 cells, in which caspase-8 and -3, but not -9, were activated, and X chromosome-linked inhibitor of apoptosis (ILP) and FLICE-like inhibitor protein (FLIP(L)), but not bcl-xL and bcl-2, were remarkably down regulated.	Cycloheximide	151-164	caspase 8	Homo sapiens	208-224
12138895-0	2002	Possible attenuation of fas-mediated signaling by dominant expression of caspase-8 aberrant isoform in adult T-cell leukemia cells.	ammonium ferrous sulfate	24-27	caspase 8	Homo sapiens	73-82
12432251-8	2002	In the Fas pathway, the anti-apoptotic activity of GAGE-7C maps downstream of caspase-8 activation and upstream of poly (ADP-ribose) polymerase (PARP) cleavage.	ammonium ferrous sulfate	7-10	caspase 8	Homo sapiens	78-87
12061801-6	2002	Western blot analysis showed that caspases 3, 7, 8, and 9 are activated by deprivation of Tyr/Phe.	Tyrosine	90-93	caspase 8	Homo sapiens	34-42
12061801-6	2002	Western blot analysis showed that caspases 3, 7, 8, and 9 are activated by deprivation of Tyr/Phe.	Phenylalanine	94-97	caspase 8	Homo sapiens	34-42
12061801-11	2002	These results indicate that activation of caspases, cleavage of Bid, and mitochondrial release of cytochrome c are required for apoptosis induced by Tyr/Phe deprivation.	Tyrosine	149-152	caspase 8	Homo sapiens	42-50
12061801-11	2002	These results indicate that activation of caspases, cleavage of Bid, and mitochondrial release of cytochrome c are required for apoptosis induced by Tyr/Phe deprivation.	Phenylalanine	153-156	caspase 8	Homo sapiens	42-50
12061815-7	2002	Consistent with this, ectopic expression of a mutant dominant-negative caspase 8 or CrmA resulted in a significant decrease in SB-/PMA-induced apoptosis, whereas Bcl-2 overexpression did not.	sb-/pma	127-134	caspase 8	Homo sapiens	71-80
12037669-2	2002	In this study, to explore the possibility that the mutations of the genes involved in the proximal pathway of Fas-mediated apoptosis (Fas, FADD, caspase 8 and caspase 10) are involved in cancer metastasis, we have analysed somatic mutation and deletion of these genes in 80 non-small cell lung cancers (NSCLCs) with (n=43) and without (n=37) metastasis to the regional lymph nodes.	ammonium ferrous sulfate	110-113	caspase 8	Homo sapiens	145-154
12097160-8	2002	Interestingly, a significant increase in the percentage of cells exhibiting caspase-8 and FLIP cleavage was observed upon Fas stimulation in interferon-gamma-treated U937 cells, in which the susceptibility to Fas is extremely enhanced.	ammonium ferrous sulfate	122-125	caspase 8	Homo sapiens	76-85
12097160-9	2002	In contrast, U937 cells treated with vitamin D(3) or all-trans retinoic acid showed Fas-resistance, and caspase-8 processing and FLIP cleavage were strongly inhibited.	Vitamin D	37-46	caspase 8	Homo sapiens	104-113
12097160-11	2002	Using this system, we found that Fas-susceptibility changes during U937 differentiation occur upstream of caspase-8 processing/activation.	ammonium ferrous sulfate	33-36	caspase 8	Homo sapiens	106-115
12193260-5	2002	Furthermore, imperatorin-induced apoptosis was significantly blocked by Z-VAD-FMK (a broad spectrum caspase inhibitor), Z-LEHD-FMK (a caspase-9 inhibitor) and Ac-DMQD-CHO (a caspase-3 inhibitor), but not by Z-IEDT-FMK (a caspase-8 inhibitor).	imperatorin	13-24	caspase 8	Homo sapiens	221-230
11992538-9	2002	Furthermore, Apo2L/TRAIL-induced apoptosis and its augmentation by chemotherapy was effectively inhibited by caspase-8 zIETD-fmk and caspase-3 zDEVD-fmk protease inhibitors and by the pan-caspase inhibitor zVAD-fmk.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	206-214	caspase 8	Homo sapiens	109-118
12215206-9	2002	Finally, after 16 h of treatment with MeHgCl, we observed activation of caspase-8, -9, and -3 along with increased expression of caspase-8 and -9.	methylmercuric chloride	38-44	caspase 8	Homo sapiens	72-93
12215206-9	2002	Finally, after 16 h of treatment with MeHgCl, we observed activation of caspase-8, -9, and -3 along with increased expression of caspase-8 and -9.	methylmercuric chloride	38-44	caspase 8	Homo sapiens	129-145
12010809-1	2002	Caspase-8 (Fas-associating protein with death domain-like interleukin-1beta- converting enzyme [FLICE]/MACH/Mch5) belongs to a family of cysteine proteases presumed to be the apex of the apoptotic signaling pathways.	ammonium ferrous sulfate	11-14	caspase 8	Homo sapiens	0-9
12010809-1	2002	Caspase-8 (Fas-associating protein with death domain-like interleukin-1beta- converting enzyme [FLICE]/MACH/Mch5) belongs to a family of cysteine proteases presumed to be the apex of the apoptotic signaling pathways.	ammonium ferrous sulfate	11-14	caspase 8	Homo sapiens	96-101
12010809-1	2002	Caspase-8 (Fas-associating protein with death domain-like interleukin-1beta- converting enzyme [FLICE]/MACH/Mch5) belongs to a family of cysteine proteases presumed to be the apex of the apoptotic signaling pathways.	ammonium ferrous sulfate	11-14	caspase 8	Homo sapiens	108-112
12010809-8	2002	Moreover, Fas-mediated apoptosis was inhibited in caspase-8L-transfected Jurkat cells, which were associated with a reduction in the caspase-8 catalytic activity.	ammonium ferrous sulfate	10-13	caspase 8	Homo sapiens	50-57
12010809-8	2002	Moreover, Fas-mediated apoptosis was inhibited in caspase-8L-transfected Jurkat cells, which were associated with a reduction in the caspase-8 catalytic activity.	ammonium ferrous sulfate	10-13	caspase 8	Homo sapiens	50-59
12010809-9	2002	In vitro binding assays demonstrated that caspase-8L bound to FADD (Fas-associating protein with death domain) and caspase-8a and blocked the binding of caspase-8 to FADD.	ammonium ferrous sulfate	68-71	caspase 8	Homo sapiens	42-51
11992538-9	2002	Furthermore, Apo2L/TRAIL-induced apoptosis and its augmentation by chemotherapy was effectively inhibited by caspase-8 zIETD-fmk and caspase-3 zDEVD-fmk protease inhibitors and by the pan-caspase inhibitor zVAD-fmk.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	119-128	caspase 8	Homo sapiens	109-118
11984520-1	2002	BACKGROUND &amp; AIMS: Caspases are critical mediators of apoptosis and proliferation of peripheral blood T cells (PBT), but their role in lamina propria T cells (LPT), a cell population highly susceptible to apoptosis, has not been explored.	Adenosine Monophosphate	12-15	caspase 8	Homo sapiens	23-31
11987151-10	2002	As predicted, overexpression of FADD-DN prevented activation of caspase-8 and Bid cleavage and attenuated the release of cytochrome c and activation of caspases -2, -7, and -9.	fadd-dn	32-39	caspase 8	Homo sapiens	64-73
11880365-5	2002	CDDO in combination with TNF caused a dramatic increase in apoptosis in ML-1 leukemia cells that was associated with activation of caspase-8, cleavage of Bid, translocation of Bax, cytochrome c release, and caspase-3 activation.	2-cyano-3,12-dioxoolean-1,9-dien-28-oic acid	0-4	caspase 8	Homo sapiens	131-140
12432279-6	2002	Selenium upregulation of DR5 was coupled with caspase 8 activation and Bid cleavage thereby suggesting the existence of a potential cross-talk between the DR5 and the mitochondrial pathways.	Selenium	0-8	caspase 8	Homo sapiens	46-55
11984520-4	2002	RESULTS: In RA(+) and RO(+) PBT, activation leads to significant increase of caspase activity but not cell death, whereas in LPT a lower elevation of caspase activity was followed by a marked degree of apoptosis.	ro(+) pbt	22-31	caspase 8	Homo sapiens	77-84
12041673-0	2002	Sodium salicylate-triggered apoptosis in HL-60 cells depends on caspase-8 activation.	Sodium Salicylate	0-17	caspase 8	Homo sapiens	64-73
11956588-10	2002	DOX treatment significantly activated caspase-8, -6, and -3 in LNCaP cells.	Doxorubicin	0-3	caspase 8	Homo sapiens	38-59
12041673-2	2002	Apoptosis was identified and analyzed with the help of transmission electron microscopy, annexin V staining, and DNA gel electrophoresis, and the association of caspase-8 activation with apoptosis was determined with the specific protease inhibitor IETD-fmk.	isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	249-257	caspase 8	Homo sapiens	161-170
12041673-8	2002	The findings presented herein strongly suggest that Na-Sal can exert potent killing and proapoptotic activity against HL-60 cells, and this effect appears to depend on caspase-8 activation.	Sodium Salicylate	52-58	caspase 8	Homo sapiens	168-177
11937560-8	2002	Inhibitors of both caspase-8 and caspase-9 partially prevented the apoptotic effect of morphine on macrophages.	Morphine	87-95	caspase 8	Homo sapiens	19-28
11983548-0	2002	Endogenous endothelium-derived nitric oxide inhibits myocardial caspase activity: implications for treatment of end-stage heart failure.	Nitric Oxide	31-43	caspase 8	Homo sapiens	64-71
11948413-7	2002	Moreover, ectopic expression of IRF1 induced caspase-8 expression thereby sensitizing cells for TRAIL-, APO1- or doxorubicin-induced apoptosis.	Doxorubicin	113-124	caspase 8	Homo sapiens	45-54
12018840-5	2002	Cisplatin induced apoptosis with the cytochrome c release and caspase-3 activation in both wild-type and caspase-8-deficient JB-6 cells, while the Fas antibody induced these apoptotic events only in wild-type cells.	Cisplatin	0-9	caspase 8	Homo sapiens	105-114
12018840-10	2002	These data suggest that the cisplatin-induced apoptotic signal is initiated by the caspase-8-independent cytochrome c release, and the JNK activation protects cells from cisplatin-induced apoptosis via the metallothionein expression.	Cisplatin	28-37	caspase 8	Homo sapiens	83-92
12452010-3	2002	METHODS: The cytotoxic effect of TPT on K562 cells was determined using MTT assay; TPT-induced apoptosis in K562 cells was identified by morphological analysis and Annexin V FITC staining; correlation between TPT-mediated killing or apoptosis and caspase-8 activation was investigated using caspase-8 inhibitor IETD-fmk.	9 alpha,11 alpha,15 alpha-trihydroxy-16-phenoxy-17,18,19,20-tetranorprosta-4,5,13-trienoic acid	83-86	caspase 8	Homo sapiens	247-256
12452010-3	2002	METHODS: The cytotoxic effect of TPT on K562 cells was determined using MTT assay; TPT-induced apoptosis in K562 cells was identified by morphological analysis and Annexin V FITC staining; correlation between TPT-mediated killing or apoptosis and caspase-8 activation was investigated using caspase-8 inhibitor IETD-fmk.	9 alpha,11 alpha,15 alpha-trihydroxy-16-phenoxy-17,18,19,20-tetranorprosta-4,5,13-trienoic acid	83-86	caspase 8	Homo sapiens	291-300
12452010-3	2002	METHODS: The cytotoxic effect of TPT on K562 cells was determined using MTT assay; TPT-induced apoptosis in K562 cells was identified by morphological analysis and Annexin V FITC staining; correlation between TPT-mediated killing or apoptosis and caspase-8 activation was investigated using caspase-8 inhibitor IETD-fmk.	9 alpha,11 alpha,15 alpha-trihydroxy-16-phenoxy-17,18,19,20-tetranorprosta-4,5,13-trienoic acid	83-86	caspase 8	Homo sapiens	247-256
12452010-3	2002	METHODS: The cytotoxic effect of TPT on K562 cells was determined using MTT assay; TPT-induced apoptosis in K562 cells was identified by morphological analysis and Annexin V FITC staining; correlation between TPT-mediated killing or apoptosis and caspase-8 activation was investigated using caspase-8 inhibitor IETD-fmk.	9 alpha,11 alpha,15 alpha-trihydroxy-16-phenoxy-17,18,19,20-tetranorprosta-4,5,13-trienoic acid	83-86	caspase 8	Homo sapiens	291-300
12452010-7	2002	CONCLUSION: Topoisomerase I inhibitor TPT possess killing activity and was induce apoptosis to K562 cells, which could be dependent on activation of caspase-8.	9 alpha,11 alpha,15 alpha-trihydroxy-16-phenoxy-17,18,19,20-tetranorprosta-4,5,13-trienoic acid	38-41	caspase 8	Homo sapiens	149-158
11984078-11	2002	Isothiocyanates also induced apoptosis of pre-cancerous cells and tumor cells activated by caspase-8 and potentiated by JNK1.	Isothiocyanates	0-15	caspase 8	Homo sapiens	91-100
11935314-13	2002	Norcantharidin-treated cells showed the activation of caspase 8.	norcantharidin	0-14	caspase 8	Homo sapiens	54-63
11865194-7	2002	All the anti-Fas antibody-mediated signals for apoptosis induction in NOS4 cells were completely blocked by a caspase-8-specific inhibitor, Z-IETD-FMK.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	140-150	caspase 8	Homo sapiens	110-119
11894131-1	2002	Fas engagement rapidly induces formation of the death-inducing signaling complex (DISC) that consists of Fas, FADD and pro-caspase-8.	ammonium ferrous sulfate	0-3	caspase 8	Homo sapiens	123-132
11894131-6	2002	In addition, CH-11-induced activation of caspase-8-like protease in AIDS-KS cells was much less pronounced compared with that in Hut 78; however, a caspase-8 inhibitor, zIETD-fmk, completely blocked the apoptosis.	4-dimethylamino-3',4'-dimethoxychalcone	13-18	caspase 8	Homo sapiens	41-50
11894131-6	2002	In addition, CH-11-induced activation of caspase-8-like protease in AIDS-KS cells was much less pronounced compared with that in Hut 78; however, a caspase-8 inhibitor, zIETD-fmk, completely blocked the apoptosis.	4-dimethylamino-3',4'-dimethoxychalcone	13-18	caspase 8	Homo sapiens	148-157
11894131-6	2002	In addition, CH-11-induced activation of caspase-8-like protease in AIDS-KS cells was much less pronounced compared with that in Hut 78; however, a caspase-8 inhibitor, zIETD-fmk, completely blocked the apoptosis.	Potassium	73-75	caspase 8	Homo sapiens	41-50
11894131-6	2002	In addition, CH-11-induced activation of caspase-8-like protease in AIDS-KS cells was much less pronounced compared with that in Hut 78; however, a caspase-8 inhibitor, zIETD-fmk, completely blocked the apoptosis.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	169-178	caspase 8	Homo sapiens	41-50
11915023-6	2002	The potentiation of DCA- and CDCA-induced apoptosis by MEK1/2 inhibitors correlated with cleavage of procaspase 3, which was blocked by inhibitors of caspase 8 (ile-Glu-Thr-Asp-p-nitroanilide [IETD]) and caspase 3 (DEVD).	Deoxycholic Acid	20-23	caspase 8	Homo sapiens	150-159
11915023-6	2002	The potentiation of DCA- and CDCA-induced apoptosis by MEK1/2 inhibitors correlated with cleavage of procaspase 3, which was blocked by inhibitors of caspase 8 (ile-Glu-Thr-Asp-p-nitroanilide [IETD]) and caspase 3 (DEVD).	Chenodeoxycholic Acid	29-33	caspase 8	Homo sapiens	150-159
11915023-6	2002	The potentiation of DCA- and CDCA-induced apoptosis by MEK1/2 inhibitors correlated with cleavage of procaspase 3, which was blocked by inhibitors of caspase 8 (ile-Glu-Thr-Asp-p-nitroanilide [IETD]) and caspase 3 (DEVD).	Ile-Glu-Thr-Asp-p-nitroanilide	161-191	caspase 8	Homo sapiens	150-159
11915023-6	2002	The potentiation of DCA- and CDCA-induced apoptosis by MEK1/2 inhibitors correlated with cleavage of procaspase 3, which was blocked by inhibitors of caspase 8 (ile-Glu-Thr-Asp-p-nitroanilide [IETD]) and caspase 3 (DEVD).	IETD	193-197	caspase 8	Homo sapiens	150-159
11894131-6	2002	In addition, CH-11-induced activation of caspase-8-like protease in AIDS-KS cells was much less pronounced compared with that in Hut 78; however, a caspase-8 inhibitor, zIETD-fmk, completely blocked the apoptosis.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	169-178	caspase 8	Homo sapiens	148-157
11894131-12	2002	Altogether, the present data provide evidence that the Fas signal in AIDS-KS cells is preferentially transduced through the mitochondria-dependent pathway, which is initiated by caspase-8 activation.	ammonium ferrous sulfate	55-58	caspase 8	Homo sapiens	178-187
11918220-9	2002	Moreover, daidzein and estradiol promoted caspase-8 and caspase-3 cleavage and DNA fragmentation of monocytic bone marrow cells.	daidzein	10-18	caspase 8	Homo sapiens	42-51
11918220-9	2002	Moreover, daidzein and estradiol promoted caspase-8 and caspase-3 cleavage and DNA fragmentation of monocytic bone marrow cells.	Estradiol	23-32	caspase 8	Homo sapiens	42-51
11935314-14	2002	Both zVAD-FMK (a broad range caspase inhibitor) and IETD-FMK (a caspase-8 inhibitor) showed apparent inhibition of the apoptosis-inducing effect.	isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	52-60	caspase 8	Homo sapiens	64-73
11925595-0	2002	JTE-522-induced apoptosis in human gastric adenocarcinoma [correction of adenocarcinoma] cell line AGS cells by caspase activation accompanying cytochrome C release, membrane translocation of Bax and loss of mitochondrial membrane potential.	4-(4-cyclohexyl-2-methyloxazol-5-yl)-2-fluorobenzenesulfonamide	0-7	caspase 8	Homo sapiens	112-119
11948397-7	2002	Since Fas/CD95 and caspase-8 were only slightly activated we conclude GCV-induced apoptosis to occur in this cell system mainly by activating the mitochondrial damage pathway.	Ganciclovir	70-73	caspase 8	Homo sapiens	19-28
11751897-4	2002	We find that GluR1, but not GluR2 or GluR3, is a substrate for agonist (alpha-amino-3-hydroxy-5-methyl-isoxazole-4-propionic acid)-initiated rapid proteolytic cleavage at aspartic acid 865 through the activation of caspase 8-like activity that is independent of membrane fusion and is not coincident with apoptosis.	alpha-amino-3-hydroxy-5-methyl-isoxazole-4-propionic acid	72-129	caspase 8	Homo sapiens	215-224
11751897-5	2002	Dose-dependent nicotine preconditioning for 24 h antagonizes agonist-initiated caspase cleavage of GluR1 through a mechanism that is coincident with desensitization of both nAChRalpha4beta2 and nAChRalpha7 receptors and the delayed activation of a caspase 8-like activity.	Nicotine	15-23	caspase 8	Homo sapiens	248-257
11836578-3	2002	The participation of the Fas-mediated apoptotic pathway was suggested by the upregulation of the surface Fas molecule, the reduction of the apoptotic cell fraction after inhibition of caspase 8 which is a Fas-related initiator caspase, and the changes in Fas-related genes after irradiation.	ammonium ferrous sulfate	25-28	caspase 8	Homo sapiens	184-193
11790791-2	2002	The caspase-8 inhibitor benzyloxycarbonyl-Ile-Glu(OMe)-Thr-Asp(OMe)-CH(2)F (IETD) prevented the cleavage of Bid and the loss of viability.	benzyloxycarbonyl-ile-glu	24-49	caspase 8	Homo sapiens	4-13
11790791-2	2002	The caspase-8 inhibitor benzyloxycarbonyl-Ile-Glu(OMe)-Thr-Asp(OMe)-CH(2)F (IETD) prevented the cleavage of Bid and the loss of viability.	Threonine	55-58	caspase 8	Homo sapiens	4-13
11790791-2	2002	The caspase-8 inhibitor benzyloxycarbonyl-Ile-Glu(OMe)-Thr-Asp(OMe)-CH(2)F (IETD) prevented the cleavage of Bid and the loss of viability.	Aspartic Acid	59-62	caspase 8	Homo sapiens	4-13
11883953-3	2002	ML-1 cells incubated with either anisomycin or staurosporine exhibited Bax translocation, cytochrome c release, caspase 8 activation, and Bid cleavage; only the latter two events were caspase-dependent, confirming that they are consequences in this apoptotic pathway.	Anisomycin	33-43	caspase 8	Homo sapiens	112-121
11883953-3	2002	ML-1 cells incubated with either anisomycin or staurosporine exhibited Bax translocation, cytochrome c release, caspase 8 activation, and Bid cleavage; only the latter two events were caspase-dependent, confirming that they are consequences in this apoptotic pathway.	Staurosporine	47-60	caspase 8	Homo sapiens	112-121
11866444-2	2002	HLE cells underwent apoptosis at 2 microM ATO, which was executed by the activation of caspase-3 through the mitochondrial pathway mediated by caspase-8 activation and Bid truncation.	Arsenic Trioxide	42-45	caspase 8	Homo sapiens	143-152
11872042-9	2002	Of 1176 different human cDNA transcripts in cisplatin-treated TTSC-3, three genes (tumour necrosis factor receptor 1, caspase 8 and Apaf1), which are associated with apoptosis, were expressed markedly more than after saline injection.	Cisplatin	44-53	caspase 8	Homo sapiens	118-127
11872042-9	2002	Of 1176 different human cDNA transcripts in cisplatin-treated TTSC-3, three genes (tumour necrosis factor receptor 1, caspase 8 and Apaf1), which are associated with apoptosis, were expressed markedly more than after saline injection.	Sodium Chloride	217-223	caspase 8	Homo sapiens	118-127
11859411-9	2002	Investigation of the mechanism by which a combination of drugs plus CD95 ligation can increase cell death showed that caspase-8 was activated in cells exposed to a combination of cisplatin and anti-CD95, but not in cells exposed to either agent alone.	Cisplatin	179-188	caspase 8	Homo sapiens	118-127
12429924-4	2002	The pan- caspase inhibitor Boc-fmk and the caspase-8 inhibitor lETD-fmk opposed CGP74514A-induced caspase-9 activation and PARP degradation, but not cytochrome c or Smac/DIABLO release.	letd-fmk	63-71	caspase 8	Homo sapiens	43-52
12429924-4	2002	The pan- caspase inhibitor Boc-fmk and the caspase-8 inhibitor lETD-fmk opposed CGP74514A-induced caspase-9 activation and PARP degradation, but not cytochrome c or Smac/DIABLO release.	N(2)-(2-aminocyclohexyl)-N(6)-(3-chlorophenyl)-9-ethyl-9H-purine-2,6-diamine	80-89	caspase 8	Homo sapiens	43-52
11896617-7	2002	However, approximately 20% of the neuroblastoma cell lines with methylated CASP8 alleles are also highly resistant to staurosporine (STS)- and radiation-induced cell death, presumably because cytochrome c is not released from mitochondria.	Staurosporine	118-131	caspase 8	Homo sapiens	75-80
11896617-7	2002	However, approximately 20% of the neuroblastoma cell lines with methylated CASP8 alleles are also highly resistant to staurosporine (STS)- and radiation-induced cell death, presumably because cytochrome c is not released from mitochondria.	Staurosporine	133-136	caspase 8	Homo sapiens	75-80
12170777-8	2002	Inhibition of caspase function using a pan-caspase inhibitor ZVAD blocked the enhanced apoptotic response at 24 h. Selective inhibition of caspase 9 with LEHD or caspase 8 with IETD partially blunted the apoptotic response in MDA-MB-231, DU145 and A431 cells, whereas inhibition of both caspases reduced the response by &gt; 90%.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	61-65	caspase 8	Homo sapiens	14-21
12170777-8	2002	Inhibition of caspase function using a pan-caspase inhibitor ZVAD blocked the enhanced apoptotic response at 24 h. Selective inhibition of caspase 9 with LEHD or caspase 8 with IETD partially blunted the apoptotic response in MDA-MB-231, DU145 and A431 cells, whereas inhibition of both caspases reduced the response by &gt; 90%.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	61-65	caspase 8	Homo sapiens	43-50
12170777-8	2002	Inhibition of caspase function using a pan-caspase inhibitor ZVAD blocked the enhanced apoptotic response at 24 h. Selective inhibition of caspase 9 with LEHD or caspase 8 with IETD partially blunted the apoptotic response in MDA-MB-231, DU145 and A431 cells, whereas inhibition of both caspases reduced the response by &gt; 90%.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	61-65	caspase 8	Homo sapiens	162-171
12170777-8	2002	Inhibition of caspase function using a pan-caspase inhibitor ZVAD blocked the enhanced apoptotic response at 24 h. Selective inhibition of caspase 9 with LEHD or caspase 8 with IETD partially blunted the apoptotic response in MDA-MB-231, DU145 and A431 cells, whereas inhibition of both caspases reduced the response by &gt; 90%.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	61-65	caspase 8	Homo sapiens	287-295
11836578-3	2002	The participation of the Fas-mediated apoptotic pathway was suggested by the upregulation of the surface Fas molecule, the reduction of the apoptotic cell fraction after inhibition of caspase 8 which is a Fas-related initiator caspase, and the changes in Fas-related genes after irradiation.	ammonium ferrous sulfate	105-108	caspase 8	Homo sapiens	184-193
11836578-3	2002	The participation of the Fas-mediated apoptotic pathway was suggested by the upregulation of the surface Fas molecule, the reduction of the apoptotic cell fraction after inhibition of caspase 8 which is a Fas-related initiator caspase, and the changes in Fas-related genes after irradiation.	ammonium ferrous sulfate	105-108	caspase 8	Homo sapiens	184-193
12011585-8	2002	Nicotinamide not only maintains the mitochondrial membrane potential and the prevention of cytochrome c release, but also prevents the induction of caspase-8-, caspase-1- and caspase-3-like activities linked to the DNA repair enzyme poly(ADP-ribose) polymerase through mechanisms that are independent from the MAP kinase systems of p38 and JNK.	Niacinamide	0-12	caspase 8	Homo sapiens	148-157
11880503-2	2002	In pheochromocytoma cells, MMT exposure resulted in rapid increase in generation of reactive oxygen species (ROS) within 5--15 min, followed by release of mitochondrial cytochrome C into cytoplasm and subsequent activation of cysteine proteases, caspase-9 (twofold to threefold) and caspase-3 (15- to 25-fold), but not caspase-8, in a time- and dose-dependent manner.	2-methylcyclopentadienyl manganese tricarbonyl	27-30	caspase 8	Homo sapiens	319-328
11861801-4	2002	Pretreatment with a broad caspase inhibitor [benzyloxycarbonyl-Val-Ala-Asp-(Ome) fluoromethyl ketone] markedly decreased the incidence of apoptotic cells induced by FTY720, etoposide, and anti-Fas antibody, through the abrogation of cleavage of Bid, poly(ADP-ribose) polymerase, and caspases 3, 8, and 9.	benzyloxycarbonyl-val-ala-asp-(ome) fluoromethyl ketone	45-100	caspase 8	Homo sapiens	26-33
11861801-4	2002	Pretreatment with a broad caspase inhibitor [benzyloxycarbonyl-Val-Ala-Asp-(Ome) fluoromethyl ketone] markedly decreased the incidence of apoptotic cells induced by FTY720, etoposide, and anti-Fas antibody, through the abrogation of cleavage of Bid, poly(ADP-ribose) polymerase, and caspases 3, 8, and 9.	Etoposide	173-182	caspase 8	Homo sapiens	26-33
11734564-0	2002	Glutathione dependence of caspase-8 activation at the death-inducing signaling complex.	Glutathione	0-11	caspase 8	Homo sapiens	26-35
22692436-9	2002	Treatment with cytotoxic doses of tocotrienol resulted in a large increase in caspase-8 and caspase-3, but not caspase-9 activity.	Tocotrienols	34-45	caspase 8	Homo sapiens	78-87
22692436-10	2002	Combined treatment of tocotrienol with selective caspase-8 or caspase-3 inhibitors completely blocked tocotrieno-linduced apoptosis and activation of caspase-8 and caspase-3, respectively.	Tocotrienols	22-33	caspase 8	Homo sapiens	49-58
22692436-10	2002	Combined treatment of tocotrienol with selective caspase-8 or caspase-3 inhibitors completely blocked tocotrieno-linduced apoptosis and activation of caspase-8 and caspase-3, respectively.	Tocotrienols	22-33	caspase 8	Homo sapiens	150-159
22692436-10	2002	Combined treatment of tocotrienol with selective caspase-8 or caspase-3 inhibitors completely blocked tocotrieno-linduced apoptosis and activation of caspase-8 and caspase-3, respectively.	tocotrieno	22-32	caspase 8	Homo sapiens	49-58
22692436-10	2002	Combined treatment of tocotrienol with selective caspase-8 or caspase-3 inhibitors completely blocked tocotrieno-linduced apoptosis and activation of caspase-8 and caspase-3, respectively.	tocotrieno	22-32	caspase 8	Homo sapiens	150-159
22692436-11	2002	These findings demonstrate that tocotrienol-induced apoptosis in highly malignant mammary epithelial cells is mediated through caspase-8 activation, and may provide essential information necessary for understanding the potential health benefits of these compounds in preventing and/or reducing the risk of breast cancer in women.	Tocotrienols	32-43	caspase 8	Homo sapiens	127-136
11734564-2	2002	We investigated differential effects of glutathione depletion on CD95-triggered apoptosis in T and B cell lines as well as the glutathione dependence of caspase-8 activation.	Glutathione	127-138	caspase 8	Homo sapiens	153-162
11734564-9	2002	Our data indicate that the activation of caspase-8 at the DISC and hence CD95-mediated apoptosis induction shows a cell-specific requirement for intracellular glutathione.	Glutathione	159-170	caspase 8	Homo sapiens	41-50
11840266-5	2002	Activation of caspases was necessary for ajoene-induced apoptosis since the broad-range caspase inhibitor zVAD-fmk completely abrogated ajoene-mediated DNA fragmentation.	ajoene	41-47	caspase 8	Homo sapiens	14-22
11839682-1	2002	PURPOSE: Here we report on the role of mitochondria, death receptors (DRs), and caspases in exerting the cytotoxic effect of clinically relevant concentrations of paclitaxel in the non-small cell lung cancer cell line NCI-H460.	Paclitaxel	163-173	caspase 8	Homo sapiens	80-88
11779361-5	2002	Cycloheximide also inhibited the activation of caspases and AP-1, the expression of Fas, the formation of DISC and the release of cytochrome-C, but not the activation of SAPK/JNK in X-irradiated MOLT-4 cells.	Cycloheximide	0-13	caspase 8	Homo sapiens	47-55
11788820-6	2002	We propose that Htt polyglutamine expansion liberates Hip-1 so that it can form a caspase-8 recruitment complex with Hippi.	polyglutamine	20-33	caspase 8	Homo sapiens	82-91
11756235-0	2002	Curcumin (diferuloylmethane) induces apoptosis through activation of caspase-8, BID cleavage and cytochrome c release: its suppression by ectopic expression of Bcl-2 and Bcl-xl.	Curcumin	0-8	caspase 8	Homo sapiens	69-78
11756235-0	2002	Curcumin (diferuloylmethane) induces apoptosis through activation of caspase-8, BID cleavage and cytochrome c release: its suppression by ectopic expression of Bcl-2 and Bcl-xl.	Curcumin	10-27	caspase 8	Homo sapiens	69-78
11756235-6	2002	Curcumin activated caspase-8 and caspase-3 in HL-60 neo cells but not in Bcl-2 and Bcl-xl-transfected cells.	Curcumin	0-8	caspase 8	Homo sapiens	19-28
11756235-10	2002	Because DN-FLICE blocked curcumin-induced apoptosis, caspase-8 must play a critical role.	Curcumin	25-33	caspase 8	Homo sapiens	11-16
11756235-11	2002	Overall, our results indicate that curcumin induces apoptosis through mitochondrial pathway involving caspase-8, BID cleavage, cytochrome c release, and caspase-3 activation.	Curcumin	35-43	caspase 8	Homo sapiens	102-111
11782443-5	2002	Release of Smac/DIABLO from mitochondria through the TRAIL-caspase-8-tBid-Bax cascade is required to remove the inhibitory effect of XIAP and allow apoptosis to proceed.	tBID	69-73	caspase 8	Homo sapiens	59-68
11846806-7	2002	The DENSPM-induced cell death was dependent on the activation of the caspases as it was inhibited by the general caspase inhibitor Z-Val-Ala-Asp fluoromethyl ketone.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	131-164	caspase 8	Homo sapiens	69-77
11846806-7	2002	The DENSPM-induced cell death was dependent on the activation of the caspases as it was inhibited by the general caspase inhibitor Z-Val-Ala-Asp fluoromethyl ketone.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	131-164	caspase 8	Homo sapiens	69-76
11859461-5	2002	The cell death by DMHS was partially prevented by the caspase inhibitor, zVAD-fmk.	dmhs	18-22	caspase 8	Homo sapiens	54-61
11859461-5	2002	The cell death by DMHS was partially prevented by the caspase inhibitor, zVAD-fmk.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	73-81	caspase 8	Homo sapiens	54-61
11859461-6	2002	DMHS caused activation of caspases such as caspase-3, -8, and -9.	dmhs	0-4	caspase 8	Homo sapiens	26-34
12630765-9	2002	In addition, 15d-PGJ2 treatment induced apoptosis through activation of caspase-8, -9, and -3.	15-deoxy-delta(12,14)-prostaglandin J2	13-21	caspase 8	Homo sapiens	72-93
11840266-5	2002	Activation of caspases was necessary for ajoene-induced apoptosis since the broad-range caspase inhibitor zVAD-fmk completely abrogated ajoene-mediated DNA fragmentation.	ajoene	41-47	caspase 8	Homo sapiens	14-21
11840266-5	2002	Activation of caspases was necessary for ajoene-induced apoptosis since the broad-range caspase inhibitor zVAD-fmk completely abrogated ajoene-mediated DNA fragmentation.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	106-114	caspase 8	Homo sapiens	14-22
11840266-5	2002	Activation of caspases was necessary for ajoene-induced apoptosis since the broad-range caspase inhibitor zVAD-fmk completely abrogated ajoene-mediated DNA fragmentation.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	106-114	caspase 8	Homo sapiens	14-21
11840266-5	2002	Activation of caspases was necessary for ajoene-induced apoptosis since the broad-range caspase inhibitor zVAD-fmk completely abrogated ajoene-mediated DNA fragmentation.	ajoene	136-142	caspase 8	Homo sapiens	14-22
11840266-5	2002	Activation of caspases was necessary for ajoene-induced apoptosis since the broad-range caspase inhibitor zVAD-fmk completely abrogated ajoene-mediated DNA fragmentation.	ajoene	136-142	caspase 8	Homo sapiens	14-21
11840266-7	2002	Furthermore, ajoene induced the release of cytochrome c, which was not inhibited by zVAD-fmk indicating that cytochrome c release precedes caspase activation.	ajoene	13-19	caspase 8	Homo sapiens	139-146
11840266-9	2002	Overexpression of Bcl-x(L) clearly diminished ajoene-induced caspase activation as well as apoptosis.	ajoene	46-52	caspase 8	Homo sapiens	61-68
11840266-10	2002	These results indicate that apoptosis in leukemia cells triggered by ajoene is based on the activation of a mitochondria-dependent caspase cascade which includes also the activation of the initiator caspase-8.	ajoene	69-75	caspase 8	Homo sapiens	131-138
11840266-10	2002	These results indicate that apoptosis in leukemia cells triggered by ajoene is based on the activation of a mitochondria-dependent caspase cascade which includes also the activation of the initiator caspase-8.	ajoene	69-75	caspase 8	Homo sapiens	199-208
11795493-0	2001	Activation of caspase-8 in 3-deazaadenosine-induced apoptosis of U-937 cells occurs downstream of caspase-3 and caspase-9 without Fas receptor-ligand interaction.	3-deazaadenosine	27-43	caspase 8	Homo sapiens	14-23
12005112-0	2002	Acetaminophen induces a caspase-dependent and Bcl-XL sensitive apoptosis in human hepatoma cells and lymphocytes.	Acetaminophen	0-13	caspase 8	Homo sapiens	24-31
12005112-11	2002	These results demonstrate that acetaminophen induces caspases-dependent apoptosis with mitochondria as a primary target.	Acetaminophen	31-44	caspase 8	Homo sapiens	53-61
11795493-2	2001	In this study, we analyzed the activation pathway of the caspase cascade involved in the DZA-induced apoptosis using specific inhibitors of caspases.	3-deazaadenosine	89-92	caspase 8	Homo sapiens	57-64
11795493-8	2001	Taken together, these results suggest that in the DZA-induced apoptosis, caspase-8 may serve as an executioner caspase and be activated downstream of both caspase-3 and caspase-9, independently of Fas receptor-ligand interaction.	3-deazaadenosine	50-53	caspase 8	Homo sapiens	73-82
11795493-2	2001	In this study, we analyzed the activation pathway of the caspase cascade involved in the DZA-induced apoptosis using specific inhibitors of caspases.	3-deazaadenosine	89-92	caspase 8	Homo sapiens	140-148
11795493-8	2001	Taken together, these results suggest that in the DZA-induced apoptosis, caspase-8 may serve as an executioner caspase and be activated downstream of both caspase-3 and caspase-9, independently of Fas receptor-ligand interaction.	3-deazaadenosine	50-53	caspase 8	Homo sapiens	73-80
11795493-4	2001	zDEVD-Fmk, a specific inhibitor of caspase-3, and zLEHD-Fmk, a specific inhibitor of caspase-9, prevented the activation of caspase-8 but neither caspase-3 nor caspase-9, indicating that caspase-8 is downstream of both caspase-3 and caspase-9, which are activated by independent pathways.	benzoylcarbonyl-aspartyl-glutamyl-valyl-aspartyl-fluoromethyl ketone	0-9	caspase 8	Homo sapiens	124-133
11795493-4	2001	zDEVD-Fmk, a specific inhibitor of caspase-3, and zLEHD-Fmk, a specific inhibitor of caspase-9, prevented the activation of caspase-8 but neither caspase-3 nor caspase-9, indicating that caspase-8 is downstream of both caspase-3 and caspase-9, which are activated by independent pathways.	benzyloxycarbonyl-leucyl-glutamyl-histidyl-aspartic acid fluoromethyl ketone	50-59	caspase 8	Homo sapiens	124-133
11795493-5	2001	zVAD-Fmk, a universal inhibitor of caspases, kept the caspase-3 from being activated but not caspase-9.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	0-8	caspase 8	Homo sapiens	35-43
11716543-0	2001	Curcumin induces apoptosis in human melanoma cells through a Fas receptor/caspase-8 pathway independent of p53.	Curcumin	0-8	caspase 8	Homo sapiens	74-83
11735112-6	2001	Promyelocytic HL-60 cells mainly expressed caspase-8 mRNAs with the normal exon 8, but the splicing pattern was changed to the distant exon 8 splice site during DMSO-induced differentiation of HL-60 cells.	Dimethyl Sulfoxide	161-165	caspase 8	Homo sapiens	43-52
11716543-6	2001	Both a caspase-8 and broad-based caspase inhibitor, but not a caspase-9 specific inhibitor, suppressed curcumin-induced cell death.	Curcumin	103-111	caspase 8	Homo sapiens	7-16
11595831-4	2001	Pretreatment of T lymphocytes with caspase inhibitors Z-VAD.fmk or DEVD.fmk prevented DNA fragmentation in response to TPEN indicating that apoptosis triggered by zinc deficiency is entirely dependent on activation of caspase family members.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	54-63	caspase 8	Homo sapiens	35-42
11739185-5	2001	Fas signaling can be interrupted at 3 mains levels: Fas clustering, alteration of death-inducing-signaling-complex (DISC) formation, and effector caspase inhibition of downstream caspase-8.	ammonium ferrous sulfate	0-3	caspase 8	Homo sapiens	179-188
11739185-7	2001	However, pretreatment with chelerythrin, but not with calphostin C, resulted in the restoration of Fas-induced caspase-8 activation and cytotoxicity, suggesting that some atypical protein kinase C (PKC) isoforms contributed to the lack of DISC formation.	chelerythrin	27-39	caspase 8	Homo sapiens	111-120
11739185-7	2001	However, pretreatment with chelerythrin, but not with calphostin C, resulted in the restoration of Fas-induced caspase-8 activation and cytotoxicity, suggesting that some atypical protein kinase C (PKC) isoforms contributed to the lack of DISC formation.	ammonium ferrous sulfate	99-102	caspase 8	Homo sapiens	111-120
11739185-8	2001	Indeed, treatment with antisense oligonucleotides directed against PKC zeta and enforced expression of Par-4, a negative regulator of PKC zeta activity, restored Fas-induced caspase-8 activity and apoptosis.	Oligonucleotides	33-49	caspase 8	Homo sapiens	174-183
11595831-4	2001	Pretreatment of T lymphocytes with caspase inhibitors Z-VAD.fmk or DEVD.fmk prevented DNA fragmentation in response to TPEN indicating that apoptosis triggered by zinc deficiency is entirely dependent on activation of caspase family members.	devd.fmk	67-75	caspase 8	Homo sapiens	35-42
11595831-4	2001	Pretreatment of T lymphocytes with caspase inhibitors Z-VAD.fmk or DEVD.fmk prevented DNA fragmentation in response to TPEN indicating that apoptosis triggered by zinc deficiency is entirely dependent on activation of caspase family members.	devd.fmk	67-75	caspase 8	Homo sapiens	218-225
11595831-4	2001	Pretreatment of T lymphocytes with caspase inhibitors Z-VAD.fmk or DEVD.fmk prevented DNA fragmentation in response to TPEN indicating that apoptosis triggered by zinc deficiency is entirely dependent on activation of caspase family members.	N,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamine	119-123	caspase 8	Homo sapiens	35-42
11595831-4	2001	Pretreatment of T lymphocytes with caspase inhibitors Z-VAD.fmk or DEVD.fmk prevented DNA fragmentation in response to TPEN indicating that apoptosis triggered by zinc deficiency is entirely dependent on activation of caspase family members.	N,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamine	119-123	caspase 8	Homo sapiens	218-225
11732001-0	2001	Activation of caspase-8 during N-(4-hydroxyphenyl)retinamide-induced apoptosis in Fas-defective hepatoma cells.	Fenretinide	31-60	caspase 8	Homo sapiens	14-23
11800021-0	2001	Doxorubicin-induced apoptosis in caspase-8-deficient neuroblastoma cells is mediated through direct action on mitochondria.	Doxorubicin	0-11	caspase 8	Homo sapiens	33-42
11800021-2	2001	PURPOSE: The aim of this study was to determine whether doxorubicin could induce apoptosis in caspase-8-deficient neuroblastoma cells and to define its mechanism of action.	Doxorubicin	56-67	caspase 8	Homo sapiens	94-103
11800021-3	2001	METHODS: The caspase-8-deficient human neuroblastoma cell line, SKN-SH, was incubated with doxorubicin and the apoptotic response, as well as expression of apoptotic molecules in the p53/ Fas/caspase-8 pathway, were determined.	Doxorubicin	91-102	caspase 8	Homo sapiens	13-22
11800021-10	2001	Thus, mitochondria and downstream apoptotic signaling intermediates may be considered as key targets for doxorubicin-induced apoptosis in neuroblastoma tumors having deficiencies in the Fas/caspase-8 system.	Doxorubicin	105-116	caspase 8	Homo sapiens	190-199
11753570-7	2001	Our results indicate that the apoptosis induced by SVNI is mediated by activation of caspase-8, and that TNF-alpha plays an important role in the apoptotic response.	svni	51-55	caspase 8	Homo sapiens	85-94
11737081-11	2001	These agents also reduced the period of resistance to Fas-mediated apoptosis after T cell activation, possibly by reducing expression of c-FLIP, allowing early activation of caspase 8 in alloreactive T cells.	ammonium ferrous sulfate	54-57	caspase 8	Homo sapiens	174-183
11925935-5	2001	In the present study, we demonstrate that caspase-8 is cleaved in control transfectant KB cells early on during Fas-induced apoptosis.	ammonium ferrous sulfate	112-115	caspase 8	Homo sapiens	42-51
11581255-7	2001	Here we report that PKC alters Fas/CD95 signaling from the plasma membrane to the activation of caspases by exerting a profound action on survival/cell death decisions.	ammonium ferrous sulfate	31-34	caspase 8	Homo sapiens	96-104
11925935-7	2001	In contrast, Fas-induced caspase-8 cleavage is inhibited in KB/TP cells, which lead to inhibition of the downstream apoptotic cascade and inhibition of apoptosis.	ammonium ferrous sulfate	13-16	caspase 8	Homo sapiens	25-34
12160093-1	2001	Structure-based design of a combinatorial array was carried out in order to identify non-peptidic thiomethylketone inhibitors of caspases 3 and 8.	1,3-bis(sulfanyl)propan-2-one	98-114	caspase 8	Homo sapiens	129-137
11753607-0	2001	Sensitization to TRAIL-induced apoptosis and modulation of FLICE-inhibitory protein in B chronic lymphocytic leukemia by actinomycin D.	Dactinomycin	121-134	caspase 8	Homo sapiens	59-64
11698497-6	2001	We conclude that caspase-8 and caspase-3 activation, but not MPTP opening, mediate Fas-induced eosinophil apoptosis and are the main targets for the protective effect of IL-5 and IFN-gamma.	ammonium ferrous sulfate	83-86	caspase 8	Homo sapiens	17-26
11673515-1	2001	Previous studies of thymocyte apoptosis using a series of cell-permeable fluorogenic peptide substrates showed that Fas cross-linking triggered a caspase cascade in which cleavage of the IETDase (caspase 8-selective) substrate was the earliest caspase activity measured by flow cytometry.	ammonium ferrous sulfate	116-119	caspase 8	Homo sapiens	196-205
11703590-5	2001	RESULTS: The activation of initiator caspases-8, -9 and -2, and executioner caspase-3 began after eight hours of cisplatin treatment, thereafter markedly increased in a time (8 to 24 hours) and dose-dependent manner (0 to 200 micromol/L).	Cisplatin	113-122	caspase 8	Homo sapiens	37-58
11507096-5	2001	Apoptosis and mitochondrial cytochrome c release were inhibited by transfection with dominant negative FADD, CrmA transfection, or treatment with the selective caspase 8 inhibitor IETD-CHO.	IETD-CHO	180-188	caspase 8	Homo sapiens	160-169
11765224-0	2001	Expression of Fas-associated death domain-like interleukin-1beta-converting enzyme (FLICE) inhibitory protein (FLIP) in human articular chondrocytes: possible contribution to the resistance to Fas-mediated death of in vitro cultured human articular chondrocytes.	ammonium ferrous sulfate	14-17	caspase 8	Homo sapiens	84-89
11813492-5	2001	Caspase 8 activity (Flice) was detected in the heart muscle in congenital heart disease in a two-week old infant but also in ischaemia in a 58-year old woman with thrombosis of the coronary artery or in acute circulatory failure after an overdosage of pervitin in a 39-year-old drug addict.	Methamphetamine	252-260	caspase 8	Homo sapiens	0-9
11514566-3	2001	In this report, we demonstrate that indomethacin and sulindac sulfide induce apoptosis of human leukemic Jurkat cells by a mechanism that requires the Fas-associated Death Domain Protein-mediated activation of a caspase-8-dependent pathway.	Indomethacin	36-48	caspase 8	Homo sapiens	212-221
11588206-3	2001	17-beta-estradiol-treated neuronal extracts directly inhibit recombinant active caspase-6, caspase-3, caspase-7, and caspase-8 in vitro.	Estradiol	0-17	caspase 8	Homo sapiens	117-126
11514566-3	2001	In this report, we demonstrate that indomethacin and sulindac sulfide induce apoptosis of human leukemic Jurkat cells by a mechanism that requires the Fas-associated Death Domain Protein-mediated activation of a caspase-8-dependent pathway.	sulindac sulfide	53-69	caspase 8	Homo sapiens	212-221
11431480-7	2001	The results show that the activation of caspase-8, but not caspase-9, is necessary for Fas-induced apoptosis.	ammonium ferrous sulfate	87-90	caspase 8	Homo sapiens	40-49
11709711-0	2001	Protein kinase C inhibits singlet oxygen-induced apoptosis by decreasing caspase-8 activation.	Singlet Oxygen	26-40	caspase 8	Homo sapiens	73-82
11709711-2	2001	We have shown previously that caspase-8 and p38 mediate singlet oxygen-induced apoptosis in HL-60 cells.	Singlet Oxygen	56-70	caspase 8	Homo sapiens	30-39
11709711-3	2001	In this study, we investigated the influence of PKC on regulation of the caspase and p38 pathways initiated by singlet oxygen.	Singlet Oxygen	111-125	caspase 8	Homo sapiens	73-80
11709711-4	2001	Singlet oxygen induced Fas clustering and subsequent recruitment of FADD and caspase-8.	Singlet Oxygen	0-14	caspase 8	Homo sapiens	77-86
11709711-6	2001	Surprisingly, under the same conditions PKC activation was still able to prevent singlet oxygen-induced activation of caspase-8 and block its downstream signaling events including cleavage of Bid and caspase-3, decrease in mitochondrial transmembrane potential and release of cytochrome c from mitochondria.	Singlet Oxygen	81-95	caspase 8	Homo sapiens	118-127
11431480-0	2001	Differential involvement of initiator caspases in apoptotic volume decrease and potassium efflux during Fas- and UV-induced cell death.	Potassium	80-89	caspase 8	Homo sapiens	38-46
12067476-9	2001	We also showed that cell death triggered through Fas receptor was caspase dependent, hence it was blocked by a selective caspase-8 inhibitor (IETD-fmk).	isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	142-150	caspase 8	Homo sapiens	121-130
11585752-7	2001	The involvement of the TRAIL pathway was further confirmed by the activation of caspase-8 in Mifepristone-treated cells.	Mifepristone	93-105	caspase 8	Homo sapiens	80-89
11600533-0	2001	Cytochrome c release is upstream to activation of caspase-9, caspase-8, and caspase-3 in the enhanced apoptosis of anaplastic thyroid cancer cells induced by manumycin and paclitaxel.	manumycin	158-167	caspase 8	Homo sapiens	61-70
11600533-0	2001	Cytochrome c release is upstream to activation of caspase-9, caspase-8, and caspase-3 in the enhanced apoptosis of anaplastic thyroid cancer cells induced by manumycin and paclitaxel.	Paclitaxel	172-182	caspase 8	Homo sapiens	61-70
11600533-3	2001	In ARO and KAT-4 cells, manumycin- plus paclitaxel-induced DNA fragmentation was blocked by the inhibitors of caspase-9, caspase-8, and caspase-3.	manumycin	24-33	caspase 8	Homo sapiens	121-130
11709711-9	2001	These data indicate that PKC inhibits singlet oxygen-induced apoptosis by blocking activation of caspase-8.	Singlet Oxygen	38-52	caspase 8	Homo sapiens	97-106
11600533-3	2001	In ARO and KAT-4 cells, manumycin- plus paclitaxel-induced DNA fragmentation was blocked by the inhibitors of caspase-9, caspase-8, and caspase-3.	Paclitaxel	40-50	caspase 8	Homo sapiens	121-130
11600533-8	2001	We concluded that the cytochrome c release was upstream of the activation of caspase-9, caspase-8, and caspase-3 in the enhanced apoptosis of anaplastic thyroid cancer cells treated with manumycin plus paclitaxel, and that the interaction between manumycin and paclitaxel occurred at or upstream of cytochrome c in the apoptosis regulatory pathway in anaplastic thyroid cancer cells.	manumycin	187-196	caspase 8	Homo sapiens	88-97
11600533-8	2001	We concluded that the cytochrome c release was upstream of the activation of caspase-9, caspase-8, and caspase-3 in the enhanced apoptosis of anaplastic thyroid cancer cells treated with manumycin plus paclitaxel, and that the interaction between manumycin and paclitaxel occurred at or upstream of cytochrome c in the apoptosis regulatory pathway in anaplastic thyroid cancer cells.	Paclitaxel	202-212	caspase 8	Homo sapiens	88-97
11525634-4	2001	Altogether, our observations establish that caspase-8 is actively processed in both receptor-mediated and DDA-induced cell death.	dda	106-109	caspase 8	Homo sapiens	44-53
11746819-5	2001	Pretreatment of the cells with ZB4 (which disrupts the Fas response mechanism) also decreased the subsequent magnolol-induced caspase-8 activation and reduced the occurrence of apoptosis.	N-{(1S,2S)-2-[4-(2-methoxyphenyl)piperazin-1-yl]cyclohexyl}benzenesulfonamide	31-34	caspase 8	Homo sapiens	126-135
11746819-5	2001	Pretreatment of the cells with ZB4 (which disrupts the Fas response mechanism) also decreased the subsequent magnolol-induced caspase-8 activation and reduced the occurrence of apoptosis.	magnolol	109-117	caspase 8	Homo sapiens	126-135
11549272-2	2001	In the present study, by using the human leukemic U937 cell line, we demonstrate that the cytochrome c release is caspase-8-dependent and can be blocked by an inhibitor of caspase-8, Z-Ile-Glu (OMe)-Thr-Asp(OMe)-fluoromethyl ketone (Z-IETD.fmk), or a pan caspase inhibitor, benzyloxycarbonyl-Val-Ala-Asp-fluoromethyl ketone (Z-VAD.fmk).	z-ile-glu	183-192	caspase 8	Homo sapiens	114-123
11549272-2	2001	In the present study, by using the human leukemic U937 cell line, we demonstrate that the cytochrome c release is caspase-8-dependent and can be blocked by an inhibitor of caspase-8, Z-Ile-Glu (OMe)-Thr-Asp(OMe)-fluoromethyl ketone (Z-IETD.fmk), or a pan caspase inhibitor, benzyloxycarbonyl-Val-Ala-Asp-fluoromethyl ketone (Z-VAD.fmk).	Threonine	199-202	caspase 8	Homo sapiens	114-123
11549272-2	2001	In the present study, by using the human leukemic U937 cell line, we demonstrate that the cytochrome c release is caspase-8-dependent and can be blocked by an inhibitor of caspase-8, Z-Ile-Glu (OMe)-Thr-Asp(OMe)-fluoromethyl ketone (Z-IETD.fmk), or a pan caspase inhibitor, benzyloxycarbonyl-Val-Ala-Asp-fluoromethyl ketone (Z-VAD.fmk).	Threonine	199-202	caspase 8	Homo sapiens	172-181
11549272-2	2001	In the present study, by using the human leukemic U937 cell line, we demonstrate that the cytochrome c release is caspase-8-dependent and can be blocked by an inhibitor of caspase-8, Z-Ile-Glu (OMe)-Thr-Asp(OMe)-fluoromethyl ketone (Z-IETD.fmk), or a pan caspase inhibitor, benzyloxycarbonyl-Val-Ala-Asp-fluoromethyl ketone (Z-VAD.fmk).	asp(ome)-fluoromethyl ketone	203-231	caspase 8	Homo sapiens	114-123
11549272-2	2001	In the present study, by using the human leukemic U937 cell line, we demonstrate that the cytochrome c release is caspase-8-dependent and can be blocked by an inhibitor of caspase-8, Z-Ile-Glu (OMe)-Thr-Asp(OMe)-fluoromethyl ketone (Z-IETD.fmk), or a pan caspase inhibitor, benzyloxycarbonyl-Val-Ala-Asp-fluoromethyl ketone (Z-VAD.fmk).	asp(ome)-fluoromethyl ketone	203-231	caspase 8	Homo sapiens	172-181
11549272-2	2001	In the present study, by using the human leukemic U937 cell line, we demonstrate that the cytochrome c release is caspase-8-dependent and can be blocked by an inhibitor of caspase-8, Z-Ile-Glu (OMe)-Thr-Asp(OMe)-fluoromethyl ketone (Z-IETD.fmk), or a pan caspase inhibitor, benzyloxycarbonyl-Val-Ala-Asp-fluoromethyl ketone (Z-VAD.fmk).	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	233-243	caspase 8	Homo sapiens	114-123
11549272-2	2001	In the present study, by using the human leukemic U937 cell line, we demonstrate that the cytochrome c release is caspase-8-dependent and can be blocked by an inhibitor of caspase-8, Z-Ile-Glu (OMe)-Thr-Asp(OMe)-fluoromethyl ketone (Z-IETD.fmk), or a pan caspase inhibitor, benzyloxycarbonyl-Val-Ala-Asp-fluoromethyl ketone (Z-VAD.fmk).	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	233-243	caspase 8	Homo sapiens	172-181
11549272-2	2001	In the present study, by using the human leukemic U937 cell line, we demonstrate that the cytochrome c release is caspase-8-dependent and can be blocked by an inhibitor of caspase-8, Z-Ile-Glu (OMe)-Thr-Asp(OMe)-fluoromethyl ketone (Z-IETD.fmk), or a pan caspase inhibitor, benzyloxycarbonyl-Val-Ala-Asp-fluoromethyl ketone (Z-VAD.fmk).	Caspase Inhibitor VI	274-323	caspase 8	Homo sapiens	114-123
11549272-2	2001	In the present study, by using the human leukemic U937 cell line, we demonstrate that the cytochrome c release is caspase-8-dependent and can be blocked by an inhibitor of caspase-8, Z-Ile-Glu (OMe)-Thr-Asp(OMe)-fluoromethyl ketone (Z-IETD.fmk), or a pan caspase inhibitor, benzyloxycarbonyl-Val-Ala-Asp-fluoromethyl ketone (Z-VAD.fmk).	Caspase Inhibitor VI	274-323	caspase 8	Homo sapiens	172-181
11549272-2	2001	In the present study, by using the human leukemic U937 cell line, we demonstrate that the cytochrome c release is caspase-8-dependent and can be blocked by an inhibitor of caspase-8, Z-Ile-Glu (OMe)-Thr-Asp(OMe)-fluoromethyl ketone (Z-IETD.fmk), or a pan caspase inhibitor, benzyloxycarbonyl-Val-Ala-Asp-fluoromethyl ketone (Z-VAD.fmk).	z-vad	325-330	caspase 8	Homo sapiens	114-123
11549272-2	2001	In the present study, by using the human leukemic U937 cell line, we demonstrate that the cytochrome c release is caspase-8-dependent and can be blocked by an inhibitor of caspase-8, Z-Ile-Glu (OMe)-Thr-Asp(OMe)-fluoromethyl ketone (Z-IETD.fmk), or a pan caspase inhibitor, benzyloxycarbonyl-Val-Ala-Asp-fluoromethyl ketone (Z-VAD.fmk).	z-vad	325-330	caspase 8	Homo sapiens	172-181
11549272-2	2001	In the present study, by using the human leukemic U937 cell line, we demonstrate that the cytochrome c release is caspase-8-dependent and can be blocked by an inhibitor of caspase-8, Z-Ile-Glu (OMe)-Thr-Asp(OMe)-fluoromethyl ketone (Z-IETD.fmk), or a pan caspase inhibitor, benzyloxycarbonyl-Val-Ala-Asp-fluoromethyl ketone (Z-VAD.fmk).	FMK	240-243	caspase 8	Homo sapiens	114-123
11549272-2	2001	In the present study, by using the human leukemic U937 cell line, we demonstrate that the cytochrome c release is caspase-8-dependent and can be blocked by an inhibitor of caspase-8, Z-Ile-Glu (OMe)-Thr-Asp(OMe)-fluoromethyl ketone (Z-IETD.fmk), or a pan caspase inhibitor, benzyloxycarbonyl-Val-Ala-Asp-fluoromethyl ketone (Z-VAD.fmk).	FMK	240-243	caspase 8	Homo sapiens	172-181
11598198-9	2001	Indeed, TGFbeta-induced activation of p38 and two different inhibitors specific for this mitogen-activated protein kinase pathway (SB203580 and PD169316) prevented TGFbeta-mediated caspase-8 activation as well as the loss of mitochondrial membrane potential and apoptosis.	SB 203580	131-139	caspase 8	Homo sapiens	181-190
11598198-9	2001	Indeed, TGFbeta-induced activation of p38 and two different inhibitors specific for this mitogen-activated protein kinase pathway (SB203580 and PD169316) prevented TGFbeta-mediated caspase-8 activation as well as the loss of mitochondrial membrane potential and apoptosis.	2-(4-nitrophenyl)-4-(4-fluorophenyl)-5-(4-pyridinyl)-1H-imidazole	144-152	caspase 8	Homo sapiens	181-190
11559570-0	2001	Sulindac sulfide-induced apoptosis involves death receptor 5 and the caspase 8-dependent pathway in human colon and prostate cancer cells.	sulindac sulfide	0-16	caspase 8	Homo sapiens	69-78
11559570-5	2001	Sulindac sulfide up-regulated DR5 and activated the proximal caspase 8 in various different colon and prostate cancer cell lines.	sulindac sulfide	0-16	caspase 8	Homo sapiens	61-70
11559570-11	2001	Thus, our results demonstrate that sulindac sulfide also engages the membrane DR pathway involving DR5 and proximal caspase 8 to induce apoptosis.	sulindac sulfide	35-51	caspase 8	Homo sapiens	116-125
11461927-3	2001	In contrast, TRAIL-induced NF-kappaB activation occurred in HeLa cells only upon pretreatment with the caspase inhibitor, benzyloxycarbonyl-Val-Ala-Asp-(OMe) fluoromethyl ketone (z-VAD.fmk), indicating that this was due to a caspase-sensitive component of TRAIL-induced NF-kappaB activation.	benzyloxycarbonyl-val-ala-asp-(ome) fluoromethyl ketone	122-177	caspase 8	Homo sapiens	103-110
11461927-3	2001	In contrast, TRAIL-induced NF-kappaB activation occurred in HeLa cells only upon pretreatment with the caspase inhibitor, benzyloxycarbonyl-Val-Ala-Asp-(OMe) fluoromethyl ketone (z-VAD.fmk), indicating that this was due to a caspase-sensitive component of TRAIL-induced NF-kappaB activation.	benzyloxycarbonyl-val-ala-asp-(ome) fluoromethyl ketone	122-177	caspase 8	Homo sapiens	225-232
11461927-3	2001	In contrast, TRAIL-induced NF-kappaB activation occurred in HeLa cells only upon pretreatment with the caspase inhibitor, benzyloxycarbonyl-Val-Ala-Asp-(OMe) fluoromethyl ketone (z-VAD.fmk), indicating that this was due to a caspase-sensitive component of TRAIL-induced NF-kappaB activation.	z-vad	179-184	caspase 8	Homo sapiens	103-110
11461927-3	2001	In contrast, TRAIL-induced NF-kappaB activation occurred in HeLa cells only upon pretreatment with the caspase inhibitor, benzyloxycarbonyl-Val-Ala-Asp-(OMe) fluoromethyl ketone (z-VAD.fmk), indicating that this was due to a caspase-sensitive component of TRAIL-induced NF-kappaB activation.	FMK	185-188	caspase 8	Homo sapiens	103-110
11566177-6	2001	Ac-LEHD-CHO, a caspase-9 inhibitor or Ac-IETD-CHO, a caspase-8 inhibitor, inhibited cisplatin-induced caspase-3 activation and apoptosis similarly in both cell lines.	Ac-IETD-CHO	38-49	caspase 8	Homo sapiens	53-62
11566177-6	2001	Ac-LEHD-CHO, a caspase-9 inhibitor or Ac-IETD-CHO, a caspase-8 inhibitor, inhibited cisplatin-induced caspase-3 activation and apoptosis similarly in both cell lines.	Cisplatin	84-93	caspase 8	Homo sapiens	53-62
11566177-13	2001	These results indicate that apoptosis and caspases are less induced in cisplatin-selected HeLa cells.	Cisplatin	71-80	caspase 8	Homo sapiens	42-50
11525634-5	2001	However, while Fas-dependent apoptosis absolutely required caspase-8 activity, it is not necessary for completion of the apoptotic program induced by IR and MMC.	ammonium ferrous sulfate	15-18	caspase 8	Homo sapiens	59-68
11525634-6	2001	Experiments performed to understand the molecular pathway(s) of the caspase-8 activation after DDA demonstrated that for both IR and MMC, the Fas/Fas-L interaction is dispensable.	dda	95-98	caspase 8	Homo sapiens	68-77
11593392-5	2001	Treatment with the demethylation agent 5-Aza-2"-deoxycytidine (5-dAzaC) reversed hypermethylation of caspase-8 resulting in restoration of caspase-8 expression and recruitment and activation of caspase-8 at the CD95 DISC upon receptor cross-linking thereby sensitizing for death receptor-, and importantly, also for drug-induced apoptosis.	Decitabine	39-61	caspase 8	Homo sapiens	101-110
11593392-5	2001	Treatment with the demethylation agent 5-Aza-2"-deoxycytidine (5-dAzaC) reversed hypermethylation of caspase-8 resulting in restoration of caspase-8 expression and recruitment and activation of caspase-8 at the CD95 DISC upon receptor cross-linking thereby sensitizing for death receptor-, and importantly, also for drug-induced apoptosis.	Decitabine	39-61	caspase 8	Homo sapiens	139-148
11525634-7	2001	Data obtained from caspase inhibitors and from lymphoblasts carrying mutations in ATM and FANCC proteins, involved in DDA response, clearly showed that distinct mechanisms are responsible for caspase-8 activation by IR and MMC in B-lymphoblasts.	dda	118-121	caspase 8	Homo sapiens	192-201
11593392-5	2001	Treatment with the demethylation agent 5-Aza-2"-deoxycytidine (5-dAzaC) reversed hypermethylation of caspase-8 resulting in restoration of caspase-8 expression and recruitment and activation of caspase-8 at the CD95 DISC upon receptor cross-linking thereby sensitizing for death receptor-, and importantly, also for drug-induced apoptosis.	Decitabine	39-61	caspase 8	Homo sapiens	139-148
11525634-9	2001	Caspase-8 activation by MMC evokes the mitochondrial pathways involving FANCC but not ATM.	Mitomycin	24-27	caspase 8	Homo sapiens	0-9
11593392-5	2001	Treatment with the demethylation agent 5-Aza-2"-deoxycytidine (5-dAzaC) reversed hypermethylation of caspase-8 resulting in restoration of caspase-8 expression and recruitment and activation of caspase-8 at the CD95 DISC upon receptor cross-linking thereby sensitizing for death receptor-, and importantly, also for drug-induced apoptosis.	5-dazac	63-70	caspase 8	Homo sapiens	101-110
11593392-5	2001	Treatment with the demethylation agent 5-Aza-2"-deoxycytidine (5-dAzaC) reversed hypermethylation of caspase-8 resulting in restoration of caspase-8 expression and recruitment and activation of caspase-8 at the CD95 DISC upon receptor cross-linking thereby sensitizing for death receptor-, and importantly, also for drug-induced apoptosis.	5-dazac	63-70	caspase 8	Homo sapiens	139-148
11593392-5	2001	Treatment with the demethylation agent 5-Aza-2"-deoxycytidine (5-dAzaC) reversed hypermethylation of caspase-8 resulting in restoration of caspase-8 expression and recruitment and activation of caspase-8 at the CD95 DISC upon receptor cross-linking thereby sensitizing for death receptor-, and importantly, also for drug-induced apoptosis.	5-dazac	63-70	caspase 8	Homo sapiens	139-148
11593392-6	2001	Inhibition of caspase-8 activity also inhibited apoptosis sensitization by 5-dAzaC.	5-dazac	75-82	caspase 8	Homo sapiens	14-23
11553704-8	2001	In agreement with FAS-mediated cell killing, inhibition of caspase function with the use of dominant negative Fas-associated protein with death domain, a caspase 8 inhibitor (Ile-Glu-Thr-Asp-p-nitroanilide [IETD]) or dominant negative procaspase 8 blocked the potentiation of bile acid-induced apoptosis.	Threonine	183-186	caspase 8	Homo sapiens	154-163
11572758-0	2001	Geranylgeraniol, an intermediate product in mevalonate pathway, induces apoptotic cell death in human hepatoma cells: death receptor-independent activation of caspase-8 with down-regulation of Bcl-xL expression.	geranylgeraniol	0-15	caspase 8	Homo sapiens	159-168
11572758-4	2001	Activation of caspase-8 /-9 /-3 in HuH-7 cells was found after 8 h treatment with GGOH, at which time DNA fragmentation and loss of mitochondrial transmembrane potential (Deltaphim) occurred.	ggoh	82-86	caspase 8	Homo sapiens	14-27
11572758-8	2001	Activation of caspase-8 /-9 /-3, as well as Deltaphim, by GGOH treatment was suppressed by addition of UDCA.	ggoh	58-62	caspase 8	Homo sapiens	14-23
11604558-7	2001	Hence, this study provides support for caspase-8-mediated apoptosis in U-937 GTB when exposed to etoposide.	u-937 gtb	71-80	caspase 8	Homo sapiens	39-48
11604558-7	2001	Hence, this study provides support for caspase-8-mediated apoptosis in U-937 GTB when exposed to etoposide.	Etoposide	97-106	caspase 8	Homo sapiens	39-48
11553704-11	2001	Treatment of hepatocytes with DCA transiently increased expression of the caspase 8 inhibitor proteins c-FLIP-(S) and c-FLIP-(L) that were reduced by inhibition of MAPK or PI(3) kinase.	Deoxycholic Acid	30-33	caspase 8	Homo sapiens	74-83
11716366-6	2001	Paclitaxel induced apoptosis through activation of both caspase-8 and caspase-3.	Paclitaxel	0-10	caspase 8	Homo sapiens	56-65
11513883-3	2001	Using wild-type Jurkat T cells, we show that the proteasome inhibitors MG132 and lactacystin promote the cleavage of eIF4G, activate caspase-8 and caspase-3-like activities and decrease cell viability.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	71-76	caspase 8	Homo sapiens	133-142
11522296-7	2001	In addition, proteasome inhibitor-induced apoptosis was prevented by the addition of antagonistic anti-FasL antibody (4A5) or z-IETD.fmk, a potent inhibitor of caspase-8, indicating the involvement of the Fas receptor-ligand apoptotic signaling system in proteasome inhibitor-mediated apoptosis.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	126-136	caspase 8	Homo sapiens	160-169
11506817-7	2001	However, increasing the concentrations of these compounds such as BHA, the activities of cell death signaling molecules, caspases, were stimulated and resulted in apoptotic cell death.	bha	66-69	caspase 8	Homo sapiens	121-129
11402050-2	2001	Upon caspase cleavage at Asp-87, the 10- and 25-kDa cleavage products of P35 remain tightly associated with the inhibited caspase.	Aspartic Acid	25-28	caspase 8	Homo sapiens	5-12
11402050-2	2001	Upon caspase cleavage at Asp-87, the 10- and 25-kDa cleavage products of P35 remain tightly associated with the inhibited caspase.	Aspartic Acid	25-28	caspase 8	Homo sapiens	122-129
11513883-3	2001	Using wild-type Jurkat T cells, we show that the proteasome inhibitors MG132 and lactacystin promote the cleavage of eIF4G, activate caspase-8 and caspase-3-like activities and decrease cell viability.	lactacystin	81-92	caspase 8	Homo sapiens	133-142
11513883-4	2001	Furthermore, MG132 also promotes the cleavage of eIF4G and the activation of caspase-3-like activity in a caspase-8-deficient Jurkat cell line which is resistant to anti-Fas-mediated apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-18	caspase 8	Homo sapiens	106-115
11505393-6	2001	Thus, another objective of this study was to evaluate the relation between cell cycle arrest, ROS formation, and caspase activity levels after 2-Me treatment in gastric carcinoma cells.	2-Methoxyestradiol	143-147	caspase 8	Homo sapiens	113-120
11521188-9	2001	These data place potentiating effects of CHX (i) to the activation of caspase 8 at the receptor in LN-229 cells as well as (ii) to a down-stream target at least in LN-18 cells, but probably both cell lines, that may be identical with p21Waf/Cip1.	Cycloheximide	41-44	caspase 8	Homo sapiens	70-79
11478767-4	2001	The EGCG treatment of human monocytic leukemia U937 cells resulted in elevation of caspase 8 activity and fragmentation of caspase 8.	epigallocatechin gallate	4-8	caspase 8	Homo sapiens	83-92
11478767-4	2001	The EGCG treatment of human monocytic leukemia U937 cells resulted in elevation of caspase 8 activity and fragmentation of caspase 8.	epigallocatechin gallate	4-8	caspase 8	Homo sapiens	123-132
11478767-5	2001	The DNA ladder formation caused by the EGCG treatment was inhibited by the caspase 8 inhibitor.	epigallocatechin gallate	39-43	caspase 8	Homo sapiens	75-84
11505393-7	2001	METHODS: It was determined whether 2-Me directly induced apoptosis in two gastric carcinoma cell lines (SC-M1 and NUGC-3) through caspase-3 and caspase-8 activation and, eventually, induced DNA fragmentation.	2-Methoxyestradiol	35-39	caspase 8	Homo sapiens	144-153
11505393-10	2001	RESULTS: It was found that 2-Me treatment resulted in G(2)/M-cycle arrest, caspase-8 and caspase-3 activation, and DNA fragmentation.	2-Methoxyestradiol	27-31	caspase 8	Homo sapiens	75-84
11505393-15	2001	CONCLUSIONS: These results suggest that the 2-Me-induced apoptosis of gastric carcinoma cells by DNA fragmentation accompanied caspase activation.	2-Methoxyestradiol	44-48	caspase 8	Homo sapiens	127-134
11473025-5	2001	In vitro exposure of islets from nondiabetic organ donors to high glucose levels induced Fas expression, caspase-8 and -3 activation, and beta-cell apoptosis.	Glucose	66-73	caspase 8	Homo sapiens	105-121
11410864-2	2001	JNK activation was completely dependent on the activation of caspases in type I and type II cells, as revealed by the inhibitory effects of the caspase inhibitors zVAD-fmk or the cowpoxvirus-encoded CrmA protein.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	163-171	caspase 8	Homo sapiens	61-69
11466626-9	2001	A missense mutation was detected at codon 96, GCT (Alanine) to GTT (Valine), of the caspase 8 gene in one of the NB cell lines lacking caspase 8 expression.	Alanine	51-58	caspase 8	Homo sapiens	84-93
11466626-9	2001	A missense mutation was detected at codon 96, GCT (Alanine) to GTT (Valine), of the caspase 8 gene in one of the NB cell lines lacking caspase 8 expression.	Valine	68-74	caspase 8	Homo sapiens	84-93
11466626-9	2001	A missense mutation was detected at codon 96, GCT (Alanine) to GTT (Valine), of the caspase 8 gene in one of the NB cell lines lacking caspase 8 expression.	Valine	68-74	caspase 8	Homo sapiens	135-144
11410864-2	2001	JNK activation was completely dependent on the activation of caspases in type I and type II cells, as revealed by the inhibitory effects of the caspase inhibitors zVAD-fmk or the cowpoxvirus-encoded CrmA protein.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	163-171	caspase 8	Homo sapiens	61-68
11437602-4	2001	Amino-terminal sequence analysis of the caspase 3 polypeptides proved that caspase 8 had specifically cleaved the Asp(175)-Ser(176) bond to yield the expected p18 and p12 subunits, with partial cleavage at the Asp(28)-Ser(29) bond to release the prosegment.	Aspartic Acid	114-117	caspase 8	Homo sapiens	75-84
11427719-2	2001	vICA inhibits Fas-mediated apoptosis by binding to the pro-domain of caspase-8 and preventing its activation.	vica	0-4	caspase 8	Homo sapiens	69-78
11427719-2	2001	vICA inhibits Fas-mediated apoptosis by binding to the pro-domain of caspase-8 and preventing its activation.	ammonium ferrous sulfate	14-17	caspase 8	Homo sapiens	69-78
11465715-11	2001	Furthermore, apoptosis induced by CD95 stimulation and proteasome inhibitors was blocked by the caspase 8-specific inhibitor Ac-IETD-CHO.	Ac-IETD-CHO	125-136	caspase 8	Homo sapiens	96-105
11469678-10	2001	RESULTS: Caspase-8 activity increased significantly threefold (P &lt; 0.005) after 12 h incubation of HepG2 cells with 1 mM ethanol whereas no change was observed in control cells.	Ethanol	124-131	caspase 8	Homo sapiens	9-18
11469678-11	2001	Incubation with caspase-8 inhibitor completely prevented apoptosis induced by ethanol (P &lt; 0.001).	Ethanol	78-85	caspase 8	Homo sapiens	16-25
11469678-15	2001	CONCLUSIONS: These findings show that apoptosis induced by low concentrations of ethanol in human HepG2 cells is associated with Fas-receptor activation and subsequent caspase-8 activation.	Ethanol	81-88	caspase 8	Homo sapiens	168-177
11437602-4	2001	Amino-terminal sequence analysis of the caspase 3 polypeptides proved that caspase 8 had specifically cleaved the Asp(175)-Ser(176) bond to yield the expected p18 and p12 subunits, with partial cleavage at the Asp(28)-Ser(29) bond to release the prosegment.	Serine	218-221	caspase 8	Homo sapiens	75-84
11439090-2	2001	In the highly sensitive Jurkat cell line, early caspase-8 activation, observed from 2 h after treatment, was chronologically associated with an acute depletion of glutathione and the cleavage of caspase-3 and poly-ADP ribosyl polymerase (PARP), followed by a progressive fall in the mitochondrial transmembrane potential (Delta(psi)m), between 4 and 48 h after treatment.	Glutathione	163-174	caspase 8	Homo sapiens	48-57
11331281-7	2001	A mutant TR, lacking the active site cysteines, inhibits the cell death induced by caspase 8.	Cysteine	37-46	caspase 8	Homo sapiens	83-92
11445067-0	2001	Caspases are reversibly inactivated by hydrogen peroxide.	Hydrogen Peroxide	39-56	caspase 8	Homo sapiens	0-8
11445067-2	2001	We found that H2O2 inhibited the activity of recombinant caspase-3 and caspase-8, half-inhibition occurring at about 17 microM H2O2.	Hydrogen Peroxide	14-18	caspase 8	Homo sapiens	71-80
11445067-2	2001	We found that H2O2 inhibited the activity of recombinant caspase-3 and caspase-8, half-inhibition occurring at about 17 microM H2O2.	Hydrogen Peroxide	127-131	caspase 8	Homo sapiens	71-80
11445067-4	2001	100-200 microM H2O2 added to macrophages after induction of caspase activation by nitric oxide or serum withdrawal substantially inhibited caspase activity.	Hydrogen Peroxide	15-19	caspase 8	Homo sapiens	60-67
11445067-4	2001	100-200 microM H2O2 added to macrophages after induction of caspase activation by nitric oxide or serum withdrawal substantially inhibited caspase activity.	Hydrogen Peroxide	15-19	caspase 8	Homo sapiens	139-146
11445067-4	2001	100-200 microM H2O2 added to macrophages after induction of caspase activation by nitric oxide or serum withdrawal substantially inhibited caspase activity.	Nitric Oxide	82-94	caspase 8	Homo sapiens	60-67
11445067-4	2001	100-200 microM H2O2 added to macrophages after induction of caspase activation by nitric oxide or serum withdrawal substantially inhibited caspase activity.	Nitric Oxide	82-94	caspase 8	Homo sapiens	139-146
11445067-6	2001	The data suggest that the activity of caspases in cells can be directly but reversibly inhibited by H2O2.	Hydrogen Peroxide	100-104	caspase 8	Homo sapiens	38-46
11410792-2	2001	We have previously reported that the activation of caspase-3 and caspase-8 plays a crucial role in paclitaxel-induced apoptosis.	Paclitaxel	99-109	caspase 8	Homo sapiens	65-74
11437602-6	2001	This mutant procaspase 3, which we call m-pro3, serves as a useful reagent with which to test the efficacy of caspase 8 inhibitors in blocking processing of the natural polypeptide substrate of this enzyme and may be valuable as a source of "proenzyme" for crystallographic analysis.	m-pro3	40-46	caspase 8	Homo sapiens	110-119
11437602-4	2001	Amino-terminal sequence analysis of the caspase 3 polypeptides proved that caspase 8 had specifically cleaved the Asp(175)-Ser(176) bond to yield the expected p18 and p12 subunits, with partial cleavage at the Asp(28)-Ser(29) bond to release the prosegment.	Serine	123-126	caspase 8	Homo sapiens	75-84
11437602-4	2001	Amino-terminal sequence analysis of the caspase 3 polypeptides proved that caspase 8 had specifically cleaved the Asp(175)-Ser(176) bond to yield the expected p18 and p12 subunits, with partial cleavage at the Asp(28)-Ser(29) bond to release the prosegment.	Aspartic Acid	210-213	caspase 8	Homo sapiens	75-84
11439335-8	2001	A Fas-antagonistic mAb (ZB-4) inhibited the Fas-agonistic mAb CH-11-induced caspase-8 activation and apoptosis in Jurkat T-leukemic cells (used as positive control), but had no effect on mAb 225-induced activation of caspase-8 and apoptosis in DiFi cells.	ammonium ferrous sulfate	2-5	caspase 8	Homo sapiens	76-85
11439335-2	2001	In the current study, we found that pretreatment of DiFi cells with the caspase-8-specific inhibitor z-IETD-fmk but not pretreatment with the caspase-9-specific inhibitor z-LEHD-fmk inhibited mAb 225-induced apoptosis, indicating that caspase-8 plays an essential role in initiating mAb 225-induced apoptosis.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	101-111	caspase 8	Homo sapiens	72-81
11439165-9	2001	When studying the activity of some of these isoforms, including FLIPR, they all efficiently inhibited Fas-mediated apoptosis in A20 B lymphoma cells by impeding caspase-8, -3 and -7 activity as well as poly(ADP-ribose) polymerase (PARP) cleavage.	ammonium ferrous sulfate	102-105	caspase 8	Homo sapiens	161-181
11439335-8	2001	A Fas-antagonistic mAb (ZB-4) inhibited the Fas-agonistic mAb CH-11-induced caspase-8 activation and apoptosis in Jurkat T-leukemic cells (used as positive control), but had no effect on mAb 225-induced activation of caspase-8 and apoptosis in DiFi cells.	ammonium ferrous sulfate	2-5	caspase 8	Homo sapiens	217-226
11439335-2	2001	In the current study, we found that pretreatment of DiFi cells with the caspase-8-specific inhibitor z-IETD-fmk but not pretreatment with the caspase-9-specific inhibitor z-LEHD-fmk inhibited mAb 225-induced apoptosis, indicating that caspase-8 plays an essential role in initiating mAb 225-induced apoptosis.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	101-111	caspase 8	Homo sapiens	235-244
11439335-8	2001	A Fas-antagonistic mAb (ZB-4) inhibited the Fas-agonistic mAb CH-11-induced caspase-8 activation and apoptosis in Jurkat T-leukemic cells (used as positive control), but had no effect on mAb 225-induced activation of caspase-8 and apoptosis in DiFi cells.	ZB-4	24-28	caspase 8	Homo sapiens	76-85
11439335-8	2001	A Fas-antagonistic mAb (ZB-4) inhibited the Fas-agonistic mAb CH-11-induced caspase-8 activation and apoptosis in Jurkat T-leukemic cells (used as positive control), but had no effect on mAb 225-induced activation of caspase-8 and apoptosis in DiFi cells.	ZB-4	24-28	caspase 8	Homo sapiens	217-226
11439335-8	2001	A Fas-antagonistic mAb (ZB-4) inhibited the Fas-agonistic mAb CH-11-induced caspase-8 activation and apoptosis in Jurkat T-leukemic cells (used as positive control), but had no effect on mAb 225-induced activation of caspase-8 and apoptosis in DiFi cells.	ammonium ferrous sulfate	44-47	caspase 8	Homo sapiens	76-85
11439335-8	2001	A Fas-antagonistic mAb (ZB-4) inhibited the Fas-agonistic mAb CH-11-induced caspase-8 activation and apoptosis in Jurkat T-leukemic cells (used as positive control), but had no effect on mAb 225-induced activation of caspase-8 and apoptosis in DiFi cells.	ammonium ferrous sulfate	44-47	caspase 8	Homo sapiens	217-226
11439335-8	2001	A Fas-antagonistic mAb (ZB-4) inhibited the Fas-agonistic mAb CH-11-induced caspase-8 activation and apoptosis in Jurkat T-leukemic cells (used as positive control), but had no effect on mAb 225-induced activation of caspase-8 and apoptosis in DiFi cells.	4-dimethylamino-3',4'-dimethoxychalcone	62-67	caspase 8	Homo sapiens	76-85
11439335-8	2001	A Fas-antagonistic mAb (ZB-4) inhibited the Fas-agonistic mAb CH-11-induced caspase-8 activation and apoptosis in Jurkat T-leukemic cells (used as positive control), but had no effect on mAb 225-induced activation of caspase-8 and apoptosis in DiFi cells.	4-dimethylamino-3',4'-dimethoxychalcone	62-67	caspase 8	Homo sapiens	217-226
11406564-7	2001	In vitro down-regulation of bcl-2 with antisense oligonucleotides allowed the release of cytochrome c from mitochondria and the activation of caspases 8 and 3 upon Fas activation as well as sensitized neuroblastoma cells to Fas-mediated apoptosis.	Oligonucleotides	49-65	caspase 8	Homo sapiens	142-158
11406564-7	2001	In vitro down-regulation of bcl-2 with antisense oligonucleotides allowed the release of cytochrome c from mitochondria and the activation of caspases 8 and 3 upon Fas activation as well as sensitized neuroblastoma cells to Fas-mediated apoptosis.	ammonium ferrous sulfate	164-167	caspase 8	Homo sapiens	142-158
11406564-10	2001	These data indicate that Fas-mediated apoptosis in neuroblastoma cells is mitochondria-dependent and inhibited both at the mitochondrial level and at the level of caspase 8 activation.	ammonium ferrous sulfate	25-28	caspase 8	Homo sapiens	163-172
11399061-7	2001	The fact that spermine inhibited caspase activation only in the thymocytes implies that spermine inhibited dexamethasone-induced apoptosis upstream of caspase-9 activation.	Spermine	14-22	caspase 8	Homo sapiens	33-40
11399061-7	2001	The fact that spermine inhibited caspase activation only in the thymocytes implies that spermine inhibited dexamethasone-induced apoptosis upstream of caspase-9 activation.	Spermine	88-96	caspase 8	Homo sapiens	33-40
11399061-7	2001	The fact that spermine inhibited caspase activation only in the thymocytes implies that spermine inhibited dexamethasone-induced apoptosis upstream of caspase-9 activation.	Dexamethasone	107-120	caspase 8	Homo sapiens	33-40
11355877-6	2001	However, 100 microM Z-VAD.fmk, a pan caspase inhibitor, completely blocked TRAIL-initiated mitochondrial alterations and cleavages of caspases and Bid.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	20-29	caspase 8	Homo sapiens	37-44
11352849-7	2001	Incubation with the caspase 8 inhibitor IETD ameliorated the albumin-induced apoptosis.	IETD	40-44	caspase 8	Homo sapiens	20-29
11599886-0	2001	Fas-independent apoptosis induced by UVC in p53-mutated human epithelial tumor A431 cells through activation of caspase-8 and JNK/SAPK.	ammonium ferrous sulfate	0-3	caspase 8	Homo sapiens	112-121
11599886-12	2001	An inhibitor of caspase-8, Ac-IETD-CHO, partially inhibited UVC-induced apoptosis.	Ac-IETD-CHO	27-38	caspase 8	Homo sapiens	16-25
11350795-3	2001	TNF-alpha also triggered endothelial cell apoptosis beginning at 4 h, which was attenuated by the caspase inhibitor Z-Val-Ala-Asp-fluoromethylketone.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	116-148	caspase 8	Homo sapiens	98-105
11355877-6	2001	However, 100 microM Z-VAD.fmk, a pan caspase inhibitor, completely blocked TRAIL-initiated mitochondrial alterations and cleavages of caspases and Bid.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	20-29	caspase 8	Homo sapiens	134-142
11274139-6	2001	In S-100 cytosolic extracts treated with cytochrome c/dATP or caspase-8, alphaB-crystallin inhibits the autoproteolytic maturation of the p24 partially processed caspase-3 intermediate.	alphab-crystallin	73-90	caspase 8	Homo sapiens	62-71
11375056-8	2001	In these subjects the Fas-related caspase 8 (FLICE) was significantly increased in cells treated with the recombinant Fas.	ammonium ferrous sulfate	22-25	caspase 8	Homo sapiens	45-50
11278665-7	2001	However, when the cells were sensitized with cycloheximide, which is sufficient to sensitize the cells also to apoptosis by TNF-R1 stimulation, we noticed that adenovirus-mediated expression of constitutively active MKK1 could rescue the cells from apoptosis induced by the respective receptors by preventing caspase-8 activation.	Cycloheximide	45-58	caspase 8	Homo sapiens	309-318
11375056-8	2001	In these subjects the Fas-related caspase 8 (FLICE) was significantly increased in cells treated with the recombinant Fas.	ammonium ferrous sulfate	118-121	caspase 8	Homo sapiens	45-50
11497260-0	2001	Irofulven (6-hydroxymethylacylfulvene, MGI 114) induces caspase 8 and 9-mediated apoptosis in human pancreatic adenocarcinoma cells.	irofulven	0-9	caspase 8	Homo sapiens	56-65
11497260-0	2001	Irofulven (6-hydroxymethylacylfulvene, MGI 114) induces caspase 8 and 9-mediated apoptosis in human pancreatic adenocarcinoma cells.	irofulven	11-37	caspase 8	Homo sapiens	56-65
11497260-0	2001	Irofulven (6-hydroxymethylacylfulvene, MGI 114) induces caspase 8 and 9-mediated apoptosis in human pancreatic adenocarcinoma cells.	irofulven	39-46	caspase 8	Homo sapiens	56-65
11277999-0	2001	Hypericin photo-induced apoptosis involves the tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and activation of caspase-8.	hypericin	0-9	caspase 8	Homo sapiens	129-138
11376876-12	2001	In HL-60 cells, upstream caspase 8 is processed in response to didox, whereas caspases 8 and 9 are processed upon amidox treatment.	3,4-dihydroxybenzohydroxamic acid	63-68	caspase 8	Homo sapiens	25-34
11376876-12	2001	In HL-60 cells, upstream caspase 8 is processed in response to didox, whereas caspases 8 and 9 are processed upon amidox treatment.	Amidox	114-120	caspase 8	Homo sapiens	78-94
11381362-7	2001	Apoptosis induction in HT29 cells was concomitant with processing of caspases 3, 7, 8, and 9 and was inhibited by the caspase inhibitor ZVAD.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	136-140	caspase 8	Homo sapiens	69-77
11381362-7	2001	Apoptosis induction in HT29 cells was concomitant with processing of caspases 3, 7, 8, and 9 and was inhibited by the caspase inhibitor ZVAD.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	136-140	caspase 8	Homo sapiens	69-76
11306692-3	2001	Overexpression of the caspase-8 inhibitor CrmA blocked CDDO-induced cytochrome c release and apoptosis.	crma	42-46	caspase 8	Homo sapiens	22-31
11306692-3	2001	Overexpression of the caspase-8 inhibitor CrmA blocked CDDO-induced cytochrome c release and apoptosis.	2-cyano-3,12-dioxoolean-1,9-dien-28-oic acid	55-59	caspase 8	Homo sapiens	22-31
11306692-5	2001	In concert with these findings, we demonstrate that CDDO: 1) activates caspase-8 and thereby caspase-3 by a cytochrome c-independent mechanism and 2) induces cytochrome c release by caspase-8-dependent cleavage of Bid.	2-cyano-3,12-dioxoolean-1,9-dien-28-oic acid	52-56	caspase 8	Homo sapiens	71-80
11306692-5	2001	In concert with these findings, we demonstrate that CDDO: 1) activates caspase-8 and thereby caspase-3 by a cytochrome c-independent mechanism and 2) induces cytochrome c release by caspase-8-dependent cleavage of Bid.	2-cyano-3,12-dioxoolean-1,9-dien-28-oic acid	52-56	caspase 8	Homo sapiens	182-191
11306692-7	2001	These findings demonstrate that CDDO induces both osteoblastic differentiation and apoptosis by caspase-8-dependent mechanisms.	2-cyano-3,12-dioxoolean-1,9-dien-28-oic acid	32-36	caspase 8	Homo sapiens	96-105
11877079-0	2001	[Indomethacin induces apoptosis of K562 cells through activation of caspases and elevation of intracellular free calcium].	Indomethacin	1-13	caspase 8	Homo sapiens	68-76
11264006-8	2001	The expression of Fas-associated death domain-like interleukin 1-converting enzyme-inhibitory protein (FLIP), which acts as an inhibitor of an initiator caspase (caspase-8), was down-regulated by 5-FU treatment in cl-1 cells.	Fluorouracil	196-200	caspase 8	Homo sapiens	162-171
11295044-0	2001	Apoptotic activity of novel bile acid derivatives in human leukemic T cells through the activation of caspases.	Bile Acids and Salts	28-37	caspase 8	Homo sapiens	102-110
11306692-0	2001	The novel triterpenoid CDDO induces apoptosis and differentiation of human osteosarcoma cells by a caspase-8 dependent mechanism.	triterpenoid TP-222	10-22	caspase 8	Homo sapiens	99-108
11306692-0	2001	The novel triterpenoid CDDO induces apoptosis and differentiation of human osteosarcoma cells by a caspase-8 dependent mechanism.	2-cyano-3,12-dioxoolean-1,9-dien-28-oic acid	23-27	caspase 8	Homo sapiens	99-108
11281652-8	2001	Moreover, Bax translocation, cytochrome c release, and caspase 9 activation were blocked by the broad-spectrum caspase inhibitor, Z-VAD-fmk and the caspase 8-preferential inhibitor, Ac-IETD-CHO, suggesting that the mitochondria might participate in apoptosis by amplifying the upstream death signals.	Ac-IETD-CHO	182-193	caspase 8	Homo sapiens	148-157
11306488-0	2001	Caspases as key executors of methyl selenium-induced apoptosis (anoikis) of DU-145 prostate cancer cells.	dimethylselenide	29-44	caspase 8	Homo sapiens	0-8
11306488-3	2001	To explore the role of caspases in cancer cell apoptosis induced by selenium, we examined the involvement of these molecules in the death of the DU-145 human prostate carcinoma cells induced by methylseleninic acid (MSeA), a novel penultimate precursor of the putative critical anticancer metabolite CH3SeH.	Selenium	68-76	caspase 8	Homo sapiens	23-31
11306488-11	2001	Taken together, the data support a methyl selenium-specific induction of DU-145 cell apoptosis that involves cell detachment as a prerequisite (anoikis) and is executed principally through caspase-8 activation and its cross-talk with multiple caspases.	dimethylselenide	35-50	caspase 8	Homo sapiens	189-198
11306488-11	2001	Taken together, the data support a methyl selenium-specific induction of DU-145 cell apoptosis that involves cell detachment as a prerequisite (anoikis) and is executed principally through caspase-8 activation and its cross-talk with multiple caspases.	dimethylselenide	35-50	caspase 8	Homo sapiens	243-251
11550089-0	2001	Extended polyglutamine selectively interacts with caspase-8 and -10 in nuclear aggregates.	polyglutamine	9-22	caspase 8	Homo sapiens	50-67
11550089-3	2001	We and others previously demonstrated that caspase-8 was activated by proteolysis in association with the expression of extended polyglutamine.	polyglutamine	129-142	caspase 8	Homo sapiens	43-52
11550089-6	2001	Caspase-8 and -10 were recruited into nuclear aggregates of extended polyglutamine, where at least a fraction of these caspases was converted to the activated forms.	polyglutamine	69-82	caspase 8	Homo sapiens	0-17
11550089-7	2001	Caspase-8 and -10 were co-immunoprecipitated with polyglutamine only when the polyglutamine was pathologically extended, whereas caspase-2, -3, -6, -7 and -9 were not co-immunoprecipitated with polyglutamine regardless of its size.	polyglutamine	50-63	caspase 8	Homo sapiens	0-17
11550089-7	2001	Caspase-8 and -10 were co-immunoprecipitated with polyglutamine only when the polyglutamine was pathologically extended, whereas caspase-2, -3, -6, -7 and -9 were not co-immunoprecipitated with polyglutamine regardless of its size.	polyglutamine	78-91	caspase 8	Homo sapiens	0-17
11550089-7	2001	Caspase-8 and -10 were co-immunoprecipitated with polyglutamine only when the polyglutamine was pathologically extended, whereas caspase-2, -3, -6, -7 and -9 were not co-immunoprecipitated with polyglutamine regardless of its size.	polyglutamine	78-91	caspase 8	Homo sapiens	0-17
11550089-8	2001	A dominant-negative form of caspase-8 with a mutation at the catalytic cysteine residue inhibited polyglutamine-mediated nuclear apoptotic phenotype.	Cysteine	71-79	caspase 8	Homo sapiens	28-37
11550089-8	2001	A dominant-negative form of caspase-8 with a mutation at the catalytic cysteine residue inhibited polyglutamine-mediated nuclear apoptotic phenotype.	polyglutamine	98-111	caspase 8	Homo sapiens	28-37
11259623-9	2001	beta-Lapachone promotes the expression of cyclin-dependent kinase (cdk) inhibitors (p21(WAF1) and p27(Kip1)), induces bak expression, and subsequently stimulates the activation of caspase-7 but not of caspase-3 or caspase-8 during the apoptosis of HPC cells.	beta-lapachone	0-14	caspase 8	Homo sapiens	214-223
11277999-4	2001	Both photoactivated HYP and PXL similarly increased the activity of caspase-8 and caspase-3, and drug-induced apoptosis of Jurkat cells was completely blocked by inhibitors of caspase-8 (Z-IETD-FMK) and caspase-3 (Z-DEVD-FMK).	benzoylcarbonyl-aspartyl-glutamyl-valyl-aspartyl-fluoromethyl ketone	214-224	caspase 8	Homo sapiens	176-185
11102441-6	2001	Pro-caspase-8 and cytochrome c were released from isolated mitochondria that were treated with an inhibitor of the ADP/ATP carrier atractyloside, which opens the mitochondria permeability transition pore.	Adenosine Diphosphate	115-118	caspase 8	Homo sapiens	4-13
11222383-1	2001	The activation of caspase-8, a crucial upstream mediator of death receptor signaling, was investigated in epirubicin- and Taxol-induced apoptosis of B-lymphoma cells.	Epirubicin	106-116	caspase 8	Homo sapiens	18-27
11102441-6	2001	Pro-caspase-8 and cytochrome c were released from isolated mitochondria that were treated with an inhibitor of the ADP/ATP carrier atractyloside, which opens the mitochondria permeability transition pore.	Adenosine Triphosphate	119-122	caspase 8	Homo sapiens	4-13
11102441-6	2001	Pro-caspase-8 and cytochrome c were released from isolated mitochondria that were treated with an inhibitor of the ADP/ATP carrier atractyloside, which opens the mitochondria permeability transition pore.	Atractyloside	131-144	caspase 8	Homo sapiens	4-13
11102441-12	2001	These results suggest that pro-caspase-8 is predominantly localized in mitochondria and is released upon apoptotic stimulation through a CsA-sensitive mechanism.	Cyclosporine	137-140	caspase 8	Homo sapiens	31-40
11106658-6	2001	Dominant negative-FADD and caspase-8 inhibitor benzyloxycarbonyl-Ile-Glu-Thr-Asp effectively inhibited MKK7-induced cell death, supporting a major involvement of FADD cascade.	Threonine	73-76	caspase 8	Homo sapiens	27-36
11238127-10	2001	These results suggest that the long isoform of caspase-2 plays a role in the Fas-mediated pathway to cell death by contributing to caspase-8 activation at the DISC level.	ammonium ferrous sulfate	77-80	caspase 8	Homo sapiens	131-140
11275978-4	2001	Our data indicated that the resistance of 2 selected Fas-transfected clones to CD95-mediated lysis correlated with down-regulation of caspase-8 or its lack of cleavage and subsequent activation.	ammonium ferrous sulfate	53-56	caspase 8	Homo sapiens	134-143
11396178-6	2001	Curcumin also stimulated the activity of caspase-8, which initiates Fas signalling pathway of apoptosis.	Curcumin	0-8	caspase 8	Homo sapiens	41-50
11222383-1	2001	The activation of caspase-8, a crucial upstream mediator of death receptor signaling, was investigated in epirubicin- and Taxol-induced apoptosis of B-lymphoma cells.	Paclitaxel	122-127	caspase 8	Homo sapiens	18-27
11222383-3	2001	Indeed, active caspase-8 was readily detected after treatment of mature and immature B-lymphoid cells with epirubicin or Taxol.	Epirubicin	107-117	caspase 8	Homo sapiens	15-24
11222383-3	2001	Indeed, active caspase-8 was readily detected after treatment of mature and immature B-lymphoid cells with epirubicin or Taxol.	Paclitaxel	121-126	caspase 8	Homo sapiens	15-24
11222383-7	2001	This assumption was confirmed in 2 experimental systems-zDEVD-fmk, a cell-permeable inhibitor of caspase-3-like activity, blocked drug-induced caspase-8 cleavage, and depletion of caspase-3 from cell extracts impaired caspase-8 cleavage after in vitro activation with dATP and cytochrome c.	benzoylcarbonyl-aspartyl-glutamyl-valyl-aspartyl-fluoromethyl ketone	56-65	caspase 8	Homo sapiens	143-152
11222383-7	2001	This assumption was confirmed in 2 experimental systems-zDEVD-fmk, a cell-permeable inhibitor of caspase-3-like activity, blocked drug-induced caspase-8 cleavage, and depletion of caspase-3 from cell extracts impaired caspase-8 cleavage after in vitro activation with dATP and cytochrome c.	benzoylcarbonyl-aspartyl-glutamyl-valyl-aspartyl-fluoromethyl ketone	56-65	caspase 8	Homo sapiens	218-227
11223917-0	2001	Low concentrations of 1-methyl-4-phenylpyridinium ion induce caspase-mediated apoptosis in human SH-SY5Y neuroblastoma cells.	1-Methyl-4-phenylpyridinium	22-49	caspase 8	Homo sapiens	61-68
11241739-7	2001	Although we could induce caspase 8 in HFA with the inflammatory cytokines IFNgamma and TNFalpha, HFA remained resistant to Fas-mediated injury.	hfa	38-41	caspase 8	Homo sapiens	25-34
11241739-10	2001	Our findings indicate that caspase 8 and its regulators play a central role in determining the response to Fas ligation of HFA and support a role for Fas signaling in the developing central nervous system other than related to cytotoxicity.	hfa	123-126	caspase 8	Homo sapiens	27-36
11238216-0	2001	Butyric acid-induced T-cell apoptosis is mediated by caspase-8 and -9 activation in a Fas-independent manner.	Butyric Acid	0-12	caspase 8	Homo sapiens	53-69
11238216-0	2001	Butyric acid-induced T-cell apoptosis is mediated by caspase-8 and -9 activation in a Fas-independent manner.	ammonium ferrous sulfate	86-89	caspase 8	Homo sapiens	53-69
11238216-8	2001	Time-dependent activation of caspase-8 and -9 was recognized in butyric acid- as well as Fas-mediated apoptosis.	Butyric Acid	64-76	caspase 8	Homo sapiens	29-45
11238216-8	2001	Time-dependent activation of caspase-8 and -9 was recognized in butyric acid- as well as Fas-mediated apoptosis.	ammonium ferrous sulfate	89-92	caspase 8	Homo sapiens	29-45
11238216-9	2001	IETD-CHO and LEHD-CHO, specific inhibitors of caspase-8 and -9, respectively, completely blocked Fas-mediated apoptosis and partially prevented butyric acid-induced apoptosis.	ammonium ferrous sulfate	97-100	caspase 8	Homo sapiens	46-62
11238216-9	2001	IETD-CHO and LEHD-CHO, specific inhibitors of caspase-8 and -9, respectively, completely blocked Fas-mediated apoptosis and partially prevented butyric acid-induced apoptosis.	Butyric Acid	144-156	caspase 8	Homo sapiens	46-62
11238216-10	2001	These results suggest that the Fas-FasL interaction is not involved in butyric acid-induced apoptosis and that caspase-8 and -9-dependent apoptosis plays an important role in butyric acid-induced apoptosis, as well as Fas-induced apoptosis.	Butyric Acid	175-187	caspase 8	Homo sapiens	111-127
11313826-4	2001	Ectopic expression of the preferential caspase 8 inhibitor, crm-A, inhibits Ad-CD95L-induced cell death but has no effect on TK/GCV cytotoxicity.	crm-a	60-65	caspase 8	Homo sapiens	39-48
11223917-5	2001	The MPP(+)-induced apoptosis was completely prevented by the broad caspase inhibitor zVAD.fmk but not by the caspase-8 inhibitor IETD.fmk.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	85-89	caspase 8	Homo sapiens	67-74
11223917-5	2001	The MPP(+)-induced apoptosis was completely prevented by the broad caspase inhibitor zVAD.fmk but not by the caspase-8 inhibitor IETD.fmk.	FMK	90-93	caspase 8	Homo sapiens	67-74
11223917-10	2001	We conclude that MPP(+) can induce caspase-mediated apoptosis, which is prevented by caspase inhibition, at concentrations lower than those needed to trigger mitochondrial dysfunction and closer to those found in the brains of MPTP-treated animals.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	227-231	caspase 8	Homo sapiens	35-42
11223917-10	2001	We conclude that MPP(+) can induce caspase-mediated apoptosis, which is prevented by caspase inhibition, at concentrations lower than those needed to trigger mitochondrial dysfunction and closer to those found in the brains of MPTP-treated animals.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	227-231	caspase 8	Homo sapiens	85-92
11163331-13	2001	The recent demonstration of a critical role for activation of caspase-8 in phenethyl isothiocyanate-induced apoptosis suggests that this thiocarbamoylation directly or indirectly leads to functional activation of a cell death receptor/adaptor protein complex.	phenethyl isothiocyanate	75-99	caspase 8	Homo sapiens	62-71
11178964-2	2001	Caspases, the major effectors of apoptosis, are cysteine proteases that cleave crucial substrate proteins exclusively after aspartate residues.	Aspartic Acid	124-133	caspase 8	Homo sapiens	0-8
11063743-4	2001	The Fas pathway was blocked at the level of caspase-8, whereas the intrinsic pathway was blocked at the mitochondria.	ammonium ferrous sulfate	4-7	caspase 8	Homo sapiens	44-53
11221844-6	2001	Z-IETD-fmk, a caspase-8 inhibitor, completely blocked caspase-8 activation and resulted in inhibition of caspase-3 (a caspase-3-like protease) activation and apoptotic cell death.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	0-10	caspase 8	Homo sapiens	14-23
11221844-6	2001	Z-IETD-fmk, a caspase-8 inhibitor, completely blocked caspase-8 activation and resulted in inhibition of caspase-3 (a caspase-3-like protease) activation and apoptotic cell death.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	0-10	caspase 8	Homo sapiens	54-63
11221844-8	2001	Caspase-8-deficient Jurkat cells were resistant to both TRAIL and Fas-induced apoptosis, whereas wild-type Jurkat cells were susceptible to both TRAIL- and Fas-induced apoptosis.	ammonium ferrous sulfate	66-69	caspase 8	Homo sapiens	0-9
11221844-8	2001	Caspase-8-deficient Jurkat cells were resistant to both TRAIL and Fas-induced apoptosis, whereas wild-type Jurkat cells were susceptible to both TRAIL- and Fas-induced apoptosis.	ammonium ferrous sulfate	156-159	caspase 8	Homo sapiens	0-9
11234897-9	2001	The combination of actinomycin D and TRAIL induced an almost complete lysis of Aspc1 cells, whereas actinomycin D alone had no effect on cell survival but inhibited the expression of the Flice inhibitory protein, which is assumed to play a role in the apoptotic pathway of TRAIL.	Dactinomycin	19-32	caspase 8	Homo sapiens	187-192
11234897-9	2001	The combination of actinomycin D and TRAIL induced an almost complete lysis of Aspc1 cells, whereas actinomycin D alone had no effect on cell survival but inhibited the expression of the Flice inhibitory protein, which is assumed to play a role in the apoptotic pathway of TRAIL.	Dactinomycin	100-113	caspase 8	Homo sapiens	187-192
11145719-10	2001	Costimulation with the GC receptor antagonist mifepristone diminished monocyte apoptosis as well as CD95/CD95L expression and subsequent caspase-8 and caspase-3 activation.	Mifepristone	46-58	caspase 8	Homo sapiens	137-146
11222103-6	2001	To explore this possibility, we analyzed whether the poxvirus caspase-8 inhibitor, CrmA, was able to inhibit IFN or PKR/dsRNA-mediated apoptosis.	crma	83-87	caspase 8	Homo sapiens	62-71
11245427-8	2001	Treatment with 5-aza-2"-deoxycytidine restored mRNA and protein expression of caspase-8 and TRAIL sensitivity of resistant cell lines, suggesting that gene methylation is involved in caspase inactivation.	Decitabine	15-37	caspase 8	Homo sapiens	78-87
11157988-5	2001	Matrix attachment modulates Fas-mediated apoptosis at two different levels: by regulating the expression level of Fas, and by regulating the expression level of c-Flip, an endogenous antagonist of caspase-8.	ammonium ferrous sulfate	28-31	caspase 8	Homo sapiens	197-206
11042212-0	2001	Regulation of apoptosis by phosphatidylinositol 4,5-bisphosphate inhibition of caspases, and caspase inactivation of phosphatidylinositol phosphate 5-kinases.	Phosphatidylinositol 4,5-Diphosphate	27-64	caspase 8	Homo sapiens	79-87
11042212-2	2001	We now report that another phosphoinositide, phosphatidylinositol 4,5-bisphosphate (PIP2) is a direct inhibitor of initiator caspases 8 and 9, and their common effector caspase 3.	Phosphatidylinositols	27-43	caspase 8	Homo sapiens	125-141
11042212-2	2001	We now report that another phosphoinositide, phosphatidylinositol 4,5-bisphosphate (PIP2) is a direct inhibitor of initiator caspases 8 and 9, and their common effector caspase 3.	Phosphatidylinositol 4,5-Diphosphate	45-82	caspase 8	Homo sapiens	125-141
11042212-2	2001	We now report that another phosphoinositide, phosphatidylinositol 4,5-bisphosphate (PIP2) is a direct inhibitor of initiator caspases 8 and 9, and their common effector caspase 3.	Phosphatidylinositol 4,5-Diphosphate	84-88	caspase 8	Homo sapiens	125-141
11042212-13	2001	This novel feedforward amplification mechanism for maintaining the balance between life and death of a cell works through phosphoinositide regulation of caspases and caspase regulation of phosphoinositide synthesis.	Phosphatidylinositols	122-138	caspase 8	Homo sapiens	153-161
11042212-13	2001	This novel feedforward amplification mechanism for maintaining the balance between life and death of a cell works through phosphoinositide regulation of caspases and caspase regulation of phosphoinositide synthesis.	Phosphatidylinositols	188-204	caspase 8	Homo sapiens	153-161
11145719-11	2001	In contrast, the caspase inhibitor N:-acetyl-Asp-Glu-Val-Asp-aldehyde suppressed caspase-3 activation and apoptosis, but did not down-regulate caspase-8 activation and expression of CD95 and CD95L.	n:-acetyl-asp-glu-val-asp-aldehyde	35-69	caspase 8	Homo sapiens	17-24
11459518-0	2001	Pathological apoptosis by xanthurenic acid, a tryptophan metabolite: activation of cell caspases but not cytoskeleton breakdown.	xanthurenic acid	26-42	caspase 8	Homo sapiens	88-96
11212279-4	2001	Cotreatment with the caspase-8 inhibitor z-IETD-fmk or DR4:Fc significantly inhibited Apo-2L/TRAIL-induced apoptosis.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	41-51	caspase 8	Homo sapiens	21-30
11146107-0	2000	Staurosporine- and H-7-induced cell death in SH-SY5Y neuroblastoma cells is associated with caspase-2 and caspase-3 activation, but not with activation of the FAS/FAS-L-caspase-8 signaling pathway.	1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine	19-22	caspase 8	Homo sapiens	169-178
11180403-4	2001	In addition, the inhibition assay revealed that caspase-8 is located upstream of both caspase-3 and -7, suggesting that Stx1-mediated apoptosis utilizes a similar caspase cascade to that involved in Fas-mediated apoptosis.	ammonium ferrous sulfate	199-202	caspase 8	Homo sapiens	48-57
11180403-4	2001	In addition, the inhibition assay revealed that caspase-8 is located upstream of both caspase-3 and -7, suggesting that Stx1-mediated apoptosis utilizes a similar caspase cascade to that involved in Fas-mediated apoptosis.	ammonium ferrous sulfate	199-202	caspase 8	Homo sapiens	48-55
11134292-7	2001	Furthermore, E4orf4 induces accumulation of reactive oxygen species (ROS) in a caspase-8- and FADD/MORT1-dependent manner, and inhibition of ROS generation by 4,5-dihydroxy-1, 3-benzene-disulfonic acid (Tiron) inhibits E4orf4-induced apoptosis.	e4orf4	13-19	caspase 8	Homo sapiens	79-88
11134292-7	2001	Furthermore, E4orf4 induces accumulation of reactive oxygen species (ROS) in a caspase-8- and FADD/MORT1-dependent manner, and inhibition of ROS generation by 4,5-dihydroxy-1, 3-benzene-disulfonic acid (Tiron) inhibits E4orf4-induced apoptosis.	Reactive Oxygen Species	44-67	caspase 8	Homo sapiens	79-88
11134292-7	2001	Furthermore, E4orf4 induces accumulation of reactive oxygen species (ROS) in a caspase-8- and FADD/MORT1-dependent manner, and inhibition of ROS generation by 4,5-dihydroxy-1, 3-benzene-disulfonic acid (Tiron) inhibits E4orf4-induced apoptosis.	Reactive Oxygen Species	69-72	caspase 8	Homo sapiens	79-88
11146107-3	2000	The process is inhibited with DEVD-fmk, a potent caspase-3 (and caspase-8) inhibitor, thus indicating that staurosporine- and H-7-induced cell death in SH-SY5Y is mediated by caspase activation.	1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine	126-129	caspase 8	Homo sapiens	64-73
11146107-3	2000	The process is inhibited with DEVD-fmk, a potent caspase-3 (and caspase-8) inhibitor, thus indicating that staurosporine- and H-7-induced cell death in SH-SY5Y is mediated by caspase activation.	devd-fmk	30-38	caspase 8	Homo sapiens	64-73
11146107-3	2000	The process is inhibited with DEVD-fmk, a potent caspase-3 (and caspase-8) inhibitor, thus indicating that staurosporine- and H-7-induced cell death in SH-SY5Y is mediated by caspase activation.	Staurosporine	107-120	caspase 8	Homo sapiens	64-73
11156422-3	2000	Using the NSCLC cell line NCI-H460 (H460), here, we studied the effect of stable expression of various caspase inhibitors on apoptosis induced by the anticancer drugs cisplatin, topotecan, and gemcitabine.	Cisplatin	167-176	caspase 8	Homo sapiens	103-110
10970901-5	2000	Caspase inhibitors suppressed the DNA fragmentation in the order of Z-VAD-FMK &gt; caspase-8 inhibitor &gt; caspase-3 inhibitor.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	68-77	caspase 8	Homo sapiens	83-92
11110692-7	2000	Treatment of FA cells with the fluoromethyl ketone tetrapeptide caspase 8 inhibitor (ac-IETD-FMK) did suppress caspase 3 activation.	1,3-Difluoroacetone	31-50	caspase 8	Homo sapiens	64-73
11110692-7	2000	Treatment of FA cells with the fluoromethyl ketone tetrapeptide caspase 8 inhibitor (ac-IETD-FMK) did suppress caspase 3 activation.	Ac-IETD-fmk	85-96	caspase 8	Homo sapiens	64-73
11110692-9	2000	Therefore fas-induced apoptosis in Fanconi anemia cells of the C type involves the activation of caspase 8, which controls activation of caspase 3 family members and one direct or indirect function of the FANCC protein is to suppress apoptotic responses to IFN-gamma upstream of caspase 3 activation.	ammonium ferrous sulfate	10-13	caspase 8	Homo sapiens	97-106
11112424-6	2000	The activation of these caspases was potentiated by the PKC inhibitor bisindolylmaleimide (BIM) which downregulates PKC eta and sensitizes cells to TNF.	bisindolylmaleimide	70-89	caspase 8	Homo sapiens	24-32
11112424-6	2000	The activation of these caspases was potentiated by the PKC inhibitor bisindolylmaleimide (BIM) which downregulates PKC eta and sensitizes cells to TNF.	bisindolylmaleimide	91-94	caspase 8	Homo sapiens	24-32
11187905-6	2000	However, activation of both caspase-8 and caspase-3 was achieved in BR97 cells treated with staurosporine.	Staurosporine	92-105	caspase 8	Homo sapiens	28-37
11077052-8	2000	DEVD-FMK, a caspase-3 inhibitor, and VEID-FMK, a caspase-6 inhibitor, partially inhibited 3-BAABE-induced apoptosis, whereas exposure to IETD-FMK, a caspase-8 inhibitor, had no effect.	isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	137-145	caspase 8	Homo sapiens	149-158
11121139-11	2000	Silicon phthalocyanine 4 photodynamic therapy also caused a significant activation of FLICE, as evident from the appearance of cleaved products of pro-caspase 8.	silicon phthalocyanine	0-24	caspase 8	Homo sapiens	86-91
11077039-0	2000	Caspase-8 activation independent of CD95/CD95-L interaction during paclitaxel-induced apoptosis in human colon cancer cells (HT29-D4).	Paclitaxel	67-77	caspase 8	Homo sapiens	0-9
11077039-4	2000	By using both enzymatic assay and immunoblot detection of cleaved fragments, we showed that caspase-8, a central component of the CD95-induced apoptotic pathway, was significantly activated during paclitaxel exposure, contemporary to apoptosis occurrence.	Paclitaxel	197-207	caspase 8	Homo sapiens	92-101
11121139-11	2000	Silicon phthalocyanine 4 photodynamic therapy also caused a significant activation of FLICE, as evident from the appearance of cleaved products of pro-caspase 8.	silicon phthalocyanine	0-24	caspase 8	Homo sapiens	151-160
11187905-7	2000	Furthermore, protein synthesis inhibition by cycloheximide restored sensitivity to CD95-mediated apoptosis and allowed activation of both caspase-8 and caspase-3 in BR97 cells.	Cycloheximide	45-58	caspase 8	Homo sapiens	138-147
11107127-8	2000	CONCLUSIONS: Treatment with 5-aza-2"-deoxycytidine restored mRNA expression of caspase-8 and -10 and TRAIL sensitivity of resistant cell lines, suggesting that gene methylation is involved in caspase inactivation.	Decitabine	28-50	caspase 8	Homo sapiens	79-96
11067917-7	2000	The pan caspase inhibitor z-Val-Ala-Asp-fluoromethylketone (zVAD-fmk) and the inhibitor of caspase-8 (z-Ile-Glu-Thr-Asp-fluoromethylketone; zIETD-fmk) blocked changes in MMP and apoptosis, suggesting that the changes in MMP were dependent on activation of caspase-8.	benzyloxycarbonyl-Ile-Glu-Thr-Asp-fluoromethyl ketone	102-138	caspase 8	Homo sapiens	91-100
11099414-2	2000	The pro-apoptotic protein BID underwent posttranslational (rather than classic cotranslational) N-myristoylation when cleavage by caspase 8 caused exposure of a glycine residue.	Glycine	161-168	caspase 8	Homo sapiens	130-139
11070498-0	2000	Caspases that are activated during generation of nuclear polyglutamine aggregates are necessary for DNA fragmentation but not sufficient for cell death.	polyglutamine	57-70	caspase 8	Homo sapiens	0-8
11073986-7	2000	Addition of a general caspase inhibitor, z-VAD.	z-vad	41-46	caspase 8	Homo sapiens	22-29
11101870-0	2000	Fas triggers an alternative, caspase-8-independent cell death pathway using the kinase RIP as effector molecule.	ammonium ferrous sulfate	0-3	caspase 8	Homo sapiens	29-38
11067917-7	2000	The pan caspase inhibitor z-Val-Ala-Asp-fluoromethylketone (zVAD-fmk) and the inhibitor of caspase-8 (z-Ile-Glu-Thr-Asp-fluoromethylketone; zIETD-fmk) blocked changes in MMP and apoptosis, suggesting that the changes in MMP were dependent on activation of caspase-8.	benzyloxycarbonyl-Ile-Glu-Thr-Asp-fluoromethyl ketone	102-138	caspase 8	Homo sapiens	256-265
11070498-2	2000	Although it has been shown recently that caspase-8 coaggregates with polyQ and is activated during polyQ-mediated cell death, little is known of the location and timing of caspase-8 activation by nuclear polyQ aggregates.	polyglutamine	99-104	caspase 8	Homo sapiens	41-50
11070498-2	2000	Although it has been shown recently that caspase-8 coaggregates with polyQ and is activated during polyQ-mediated cell death, little is known of the location and timing of caspase-8 activation by nuclear polyQ aggregates.	polyglutamine	99-104	caspase 8	Homo sapiens	41-50
11103780-5	2000	Both HCT116 and SW480 cells were protected from TRAIL by the caspase 8 inhibitor Z-IETD-FMK, dominant-negative FADD and cellular FLIP-s and interestingly both cell lines displayed caspase 9 cleavage to a similar extent after TRAIL exposure.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	81-91	caspase 8	Homo sapiens	61-70
11070498-7	2000	Furthermore, we showed that the caspase inhibitor z-VAD-fmk inhibited DNA fragmentation, but only partially inhibited the appearance of apoptotic morphology.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	50-59	caspase 8	Homo sapiens	32-39
11070498-8	2000	Thus, caspase activation, including caspase-8 and -3, is necessary for polyQ-mediated DNA fragmentation but not sufficient for polyQ-mediated cell death in P19 EC cells.	polyglutamine	71-76	caspase 8	Homo sapiens	6-13
11070498-8	2000	Thus, caspase activation, including caspase-8 and -3, is necessary for polyQ-mediated DNA fragmentation but not sufficient for polyQ-mediated cell death in P19 EC cells.	polyglutamine	71-76	caspase 8	Homo sapiens	36-52
10896673-5	2000	Our results suggest that flavopiridol can induce apoptosis through different pathways of caspase activation with caspase 8 playing a pivotal role.	alvocidib	25-37	caspase 8	Homo sapiens	89-96
11044257-5	2000	Using various tetrapeptide inhibitors for caspase and its associated factor, we additionally demonstrated that inhibitors for caspase 3 (Ac-DEVD-CHO) and caspase 8/granzyme B (Ac-IETD-CHO) suppressed CTL-induced cell death, but an inhibitor for Fas-activated serine proteinase, which acts for the caspase 3 activator, did not, suggesting that CTL-induced cell death was initiated by the Perforin/Granzyme B system, rather than the Fas ligand/Fas system.	Ac-IETD-CHO	176-187	caspase 8	Homo sapiens	154-163
11032723-4	2000	Acetyl-IETD-fluoromethylketone, a caspase-8 inhibitor, potently suppressed TRAIL-induced cell death compared to acetyl-DEVD-fluoromethylketone and acetyl-LEHD-fluoromethylketone, inhibitors of caspase-3 and caspase-9, respectively.	acetyl-ietd-fluoromethylketone	0-30	caspase 8	Homo sapiens	34-43
10896673-5	2000	Our results suggest that flavopiridol can induce apoptosis through different pathways of caspase activation with caspase 8 playing a pivotal role.	alvocidib	25-37	caspase 8	Homo sapiens	113-122
10913120-6	2000	Death induced in the presence of Z-VAD-fmk was associated with a partial inhibition of caspase-8, whereas no effects on cytochrome c release, DEVDase activity, and intranucleosomal DNA cleavage were observed.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	33-42	caspase 8	Homo sapiens	87-96
10930419-7	2000	The results also demonstrate that ara-C induces cleavage of procaspase-3 by a caspase-8-dependent mechanism and that XIAP inhibits caspase-3 activity.	Cytarabine	34-39	caspase 8	Homo sapiens	78-87
11010806-6	2000	Fas-mediated apoptosis of senescent fibroblasts was evidenced by chromosome condensation and by activation of caspase-8 and -3, proteases crucial for the execution of the Fas apoptosis pathway.	ammonium ferrous sulfate	0-3	caspase 8	Homo sapiens	110-126
10913120-7	2000	Thus, Z-VAD-fmk is likely weakening the death-inducing signaling complex-mediated activation of caspase-8 and diverting cells to a Type II pathway.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	6-15	caspase 8	Homo sapiens	96-105
11012613-0	2000	Role of caspases in dexamethasone-induced apoptosis and activation of c-Jun NH2-terminal kinase and p38 mitogen-activated protein kinase in human eosinophils.	Dexamethasone	20-33	caspase 8	Homo sapiens	8-16
10960761-2	2000	Caspase-8 and caspase-3 were activated in MMC-treated cells whereas caspase-1 was not activated, and cytochrome c was released from mitochondrial membrane to cytosol suggesting that caspase-9 was activated during the MMC-induced apoptotic process.	Mitomycin	42-45	caspase 8	Homo sapiens	0-9
10960761-5	2000	Activation of caspase-8 in response to Fas triggering by recruitment of caspase-8 to the Fas has also been found, however, MMC did not induce FasL and Fas expression, as evidenced by reverse transcriptase-polymerase chain reaction and Western blotting.	ammonium ferrous sulfate	39-42	caspase 8	Homo sapiens	14-23
10960761-5	2000	Activation of caspase-8 in response to Fas triggering by recruitment of caspase-8 to the Fas has also been found, however, MMC did not induce FasL and Fas expression, as evidenced by reverse transcriptase-polymerase chain reaction and Western blotting.	ammonium ferrous sulfate	39-42	caspase 8	Homo sapiens	72-81
10960761-5	2000	Activation of caspase-8 in response to Fas triggering by recruitment of caspase-8 to the Fas has also been found, however, MMC did not induce FasL and Fas expression, as evidenced by reverse transcriptase-polymerase chain reaction and Western blotting.	Mitomycin	123-126	caspase 8	Homo sapiens	14-23
10960761-6	2000	Taken together, these findings indicate that MMC-induced apoptosis in SNU-16 cells was mediated by caspase-8, caspase-9, and caspase-3 activation independently of FasL/Fas interactions.	Mitomycin	45-48	caspase 8	Homo sapiens	99-108
11279540-7	2000	In addition, expression of Toso, a cell surface apoptosis regulator, seemed to block activation of caspase-8 by TRAIL via enhanced expression of FLIPL in granulocytic differentiated cells.	toso	27-31	caspase 8	Homo sapiens	99-108
11032765-10	2000	In addition, pretreatment with the caspase-3 inhibitor Ac-DEVD-CHO and the caspase-8 inhibitor Ac-IETD-CHO (25 microM, 8 h) significantly decreased caspase-3 activation following exposure to 1 mM PSP and parathion (p &lt; 0.05).	Ac-IETD-CHO	95-106	caspase 8	Homo sapiens	75-84
11032765-10	2000	In addition, pretreatment with the caspase-3 inhibitor Ac-DEVD-CHO and the caspase-8 inhibitor Ac-IETD-CHO (25 microM, 8 h) significantly decreased caspase-3 activation following exposure to 1 mM PSP and parathion (p &lt; 0.05).	Parathion	204-213	caspase 8	Homo sapiens	75-84
11012613-10	2000	We therefore conclude that dexamethasone-induced apoptosis and activation of JNK and p38 MAPK activity in eosinophils are regulated by caspases but not through the common apoptosis-related caspase-3, -8 as in other cell types.	Dexamethasone	27-40	caspase 8	Homo sapiens	189-202
10958671-3	2000	To examine the consequences of maintaining the structural integrity of BAP31 during apoptosis, the caspase recognition aspartate residues were mutated to alanine residues, and Fas-mediated activation of caspase 8 and cell death were examined in human KB epithelial cells stably expressing the caspase-resistant mutant crBAP31.	ammonium ferrous sulfate	176-179	caspase 8	Homo sapiens	203-212
11004695-1	2000	Lymphoma cells often display in vitro resistance to FAS-induced apoptosis, in which caspases act as crucial cell death effectors.	ammonium ferrous sulfate	52-55	caspase 8	Homo sapiens	84-92
11004695-3	2000	To investigate the mechanism of FAS resistance, the expression of caspase-8 was analysed by immunohistochemistry, together with that of the substrates caspase-3 and ICAD, in 52 representative samples from non Hodgkin"s lymphoma (NHL), 12 from Hodgkin"s disease (HD), and eight benign lymphoid tissues.	ammonium ferrous sulfate	32-35	caspase 8	Homo sapiens	66-75
11030149-7	2000	Treatment with the methyltransferase inhibitor 5-aza-2"-deoxycytidine restored mRNA expression of caspase-8 and TRAIL-sensitivity in formerly TRAIL-resistant PNET cells, suggesting that gene methylation inhibits caspase-8 transcription in these cells.	Decitabine	47-69	caspase 8	Homo sapiens	98-107
11030149-7	2000	Treatment with the methyltransferase inhibitor 5-aza-2"-deoxycytidine restored mRNA expression of caspase-8 and TRAIL-sensitivity in formerly TRAIL-resistant PNET cells, suggesting that gene methylation inhibits caspase-8 transcription in these cells.	Decitabine	47-69	caspase 8	Homo sapiens	212-221
10964557-0	2000	Caspase-8 specificity probed at subsite S(4): crystal structure of the caspase-8-Z-DEVD-cho complex.	8-z-devd-cho	79-91	caspase 8	Homo sapiens	0-9
10964557-1	2000	Caspase-8 is an initiator enzyme in the Fas-mediated pathway of which the downstream executioner caspase-3 is a physiological target.	ammonium ferrous sulfate	40-43	caspase 8	Homo sapiens	0-9
10964557-2	2000	Caspases are cysteine proteases that are specific for substrates with an aspartic acid residue at the P(1) position and have an optimal recognition motif that incorporates four amino acid residues N-terminal to the cleavage site.	Aspartic Acid	73-86	caspase 8	Homo sapiens	0-8
10964557-4	2000	We report the X-ray crystallographic structure of caspase-8 in complex with benzyloxycarbonyl-Asp-Glu-Val-Asp-aldehyde (Z-DEVD), a specific group II caspase inhibitor.	SCHEMBL6657994	76-118	caspase 8	Homo sapiens	50-59
10964557-4	2000	We report the X-ray crystallographic structure of caspase-8 in complex with benzyloxycarbonyl-Asp-Glu-Val-Asp-aldehyde (Z-DEVD), a specific group II caspase inhibitor.	z-devd	120-126	caspase 8	Homo sapiens	50-59
10964557-6	2000	Kinetic data reveal that Z-DEVD (K(i) 2 nM) is an almost equally potent inhibitor of caspase-8 as the specific group III inhibitor Boc-IETD-aldehyde (K(i) 1 nM).	z-devd	25-31	caspase 8	Homo sapiens	85-94
10964557-7	2000	In view of this finding, the original classification of caspases into three specificity groups needs to be modified, at least for caspase-8, which tolerates small hydrophobic residues as well as the acidic residue Asp in subsite S(4).	Aspartic Acid	214-217	caspase 8	Homo sapiens	56-64
10964557-7	2000	In view of this finding, the original classification of caspases into three specificity groups needs to be modified, at least for caspase-8, which tolerates small hydrophobic residues as well as the acidic residue Asp in subsite S(4).	Aspartic Acid	214-217	caspase 8	Homo sapiens	130-139
11042678-4	2000	Furthermore, a caspase-8-negative, Fas-resistant Jurkat cell line was sensitive to resveratrol-induced apoptosis which could be strongly inhibited in the Jurkat as well as in the CEM cell line by z-VAD-fmk and z-IETD-fmk.	ammonium ferrous sulfate	35-38	caspase 8	Homo sapiens	15-24
11042678-4	2000	Furthermore, a caspase-8-negative, Fas-resistant Jurkat cell line was sensitive to resveratrol-induced apoptosis which could be strongly inhibited in the Jurkat as well as in the CEM cell line by z-VAD-fmk and z-IETD-fmk.	Resveratrol	83-94	caspase 8	Homo sapiens	15-24
11042678-4	2000	Furthermore, a caspase-8-negative, Fas-resistant Jurkat cell line was sensitive to resveratrol-induced apoptosis which could be strongly inhibited in the Jurkat as well as in the CEM cell line by z-VAD-fmk and z-IETD-fmk.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	196-205	caspase 8	Homo sapiens	15-24
11042678-4	2000	Furthermore, a caspase-8-negative, Fas-resistant Jurkat cell line was sensitive to resveratrol-induced apoptosis which could be strongly inhibited in the Jurkat as well as in the CEM cell line by z-VAD-fmk and z-IETD-fmk.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	210-220	caspase 8	Homo sapiens	15-24
11034327-6	2000	Therefore, aspirin-induced apoptosis involves caspase activation through cytochrome c release.	Aspirin	11-18	caspase 8	Homo sapiens	46-53
11210827-6	2000	A broad-spectrum caspase inhibitor, z-VAD-fmk, completely prevented all apoptotic changes, except for the depletion of delta psi m. Both Ac-DEVD-CHO and Ac-IETD-CHO, inhibitors of caspase -3 and -8, respectively, effectively inhibited typical chromatin condensation to almost the same extent.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	36-45	caspase 8	Homo sapiens	17-24
11210827-6	2000	A broad-spectrum caspase inhibitor, z-VAD-fmk, completely prevented all apoptotic changes, except for the depletion of delta psi m. Both Ac-DEVD-CHO and Ac-IETD-CHO, inhibitors of caspase -3 and -8, respectively, effectively inhibited typical chromatin condensation to almost the same extent.	acetyl-aspartyl-glutamyl-valyl-aspartal	137-148	caspase 8	Homo sapiens	17-24
11210827-6	2000	A broad-spectrum caspase inhibitor, z-VAD-fmk, completely prevented all apoptotic changes, except for the depletion of delta psi m. Both Ac-DEVD-CHO and Ac-IETD-CHO, inhibitors of caspase -3 and -8, respectively, effectively inhibited typical chromatin condensation to almost the same extent.	Ac-IETD-CHO	153-164	caspase 8	Homo sapiens	17-24
11021749-0	2000	Involvement of CD95-independent caspase 8 activation in arsenic trioxide-induced apoptosis.	Arsenic Trioxide	56-72	caspase 8	Homo sapiens	32-41
11021749-7	2000	Caspase 8 and Bid were also activated by As2O3 in NB4 but not in NB4/As.	Arsenic Trioxide	41-46	caspase 8	Homo sapiens	0-9
11021749-14	2000	These findings suggest that the As2O3 treatment activates caspase 8 in a CD95-independent but GSH concentration-dependent manner.	Arsenic Trioxide	32-37	caspase 8	Homo sapiens	58-67
11021749-14	2000	These findings suggest that the As2O3 treatment activates caspase 8 in a CD95-independent but GSH concentration-dependent manner.	Glutathione	94-97	caspase 8	Homo sapiens	58-67
10964568-8	2000	The properties of the FADD-DD structure are discussed with respect to previously reported mutagenesis data and emerging models for FasL-induced FADD recruitment to Fas and caspase-8 activation.	ammonium ferrous sulfate	131-134	caspase 8	Homo sapiens	172-181
11062731-8	2000	These findings suggested that 5-FU induced apoptosis was mediated by the activation of a caspase cascade involving caspase 1, 3 and 8.	Fluorouracil	30-34	caspase 8	Homo sapiens	115-133
10871865-6	2000	The first pathway is utilized by lymphoid cells stimulated through Fas, is abrogated in a caspase-8-deficient T-cell line, and is blocked by the caspase inhibitors Z-VAD-fmk and Boc-D-fmk.	ammonium ferrous sulfate	67-70	caspase 8	Homo sapiens	90-99
10849426-4	2000	We found that benzyloxycarbonyl-Val-Ala-Asp-fluoromethyl ketone (zVAD-fmk), a broad-spectrum caspase inhibitor, mostly inhibited ASK1-induced cell death, suggesting that caspases are required for ASK1-induced apoptosis.	Caspase Inhibitor VI	14-63	caspase 8	Homo sapiens	170-178
10849426-4	2000	We found that benzyloxycarbonyl-Val-Ala-Asp-fluoromethyl ketone (zVAD-fmk), a broad-spectrum caspase inhibitor, mostly inhibited ASK1-induced cell death, suggesting that caspases are required for ASK1-induced apoptosis.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	65-73	caspase 8	Homo sapiens	170-178
10962570-5	2000	Although the caspase 8 specific inhibitor z-IETD.fmk did not affect translocation of BAX to the mitochondrial membrane and cytochrome C release it almost completely blocked cleavage of the prototype caspase substrate PARP and DNA fragmentation while enforcing mitochondrial depolarization and production of reactive oxygene species (ROS).	z-ietd	42-48	caspase 8	Homo sapiens	13-22
10962570-5	2000	Although the caspase 8 specific inhibitor z-IETD.fmk did not affect translocation of BAX to the mitochondrial membrane and cytochrome C release it almost completely blocked cleavage of the prototype caspase substrate PARP and DNA fragmentation while enforcing mitochondrial depolarization and production of reactive oxygene species (ROS).	z-ietd	42-48	caspase 8	Homo sapiens	13-20
10962570-5	2000	Although the caspase 8 specific inhibitor z-IETD.fmk did not affect translocation of BAX to the mitochondrial membrane and cytochrome C release it almost completely blocked cleavage of the prototype caspase substrate PARP and DNA fragmentation while enforcing mitochondrial depolarization and production of reactive oxygene species (ROS).	FMK	49-52	caspase 8	Homo sapiens	13-22
10962570-5	2000	Although the caspase 8 specific inhibitor z-IETD.fmk did not affect translocation of BAX to the mitochondrial membrane and cytochrome C release it almost completely blocked cleavage of the prototype caspase substrate PARP and DNA fragmentation while enforcing mitochondrial depolarization and production of reactive oxygene species (ROS).	FMK	49-52	caspase 8	Homo sapiens	13-20
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	caspase 8	Homo sapiens	63-72
10891390-5	2000	In addition, the expression of TRAF-2 and cIAP-1, which are transcriptionally regulated by NF-kappaB and function as anti-apoptotic molecules through the interruption of caspase pathway, was also inhibited by 5-FU.	Fluorouracil	209-213	caspase 8	Homo sapiens	170-177
10891390-6	2000	Finally, the activity of caspase-8 and caspase-3 showed a significant increase in response to 5-FU.	Fluorouracil	94-98	caspase 8	Homo sapiens	25-34
10915556-5	2000	Moreover, despite the specific caspase-8 inhibitor z-IETD-fmk substantially protecting transformed CL-01 B cells from CD95L fp-mediated apoptosis and permitting their ongoing proliferation, caspase-8 inhibition had no protective effects on CD95L fp-mediated inhibition of constitutive IgM production by CL-01 B cells.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	51-61	caspase 8	Homo sapiens	31-40
10837470-6	2000	In contrast, blockade of caspase-8 with Ile-Glu-Thr-Asp-fluoromethyl ketone is sufficient to prevent formation of DNA fragments and to inhibit all the above signaling events, with exception of p38 phosphorylation, in both singlet oxygen- and H(2)O(2)-treated cells.	Isoleucine	40-43	caspase 8	Homo sapiens	25-34
10837470-6	2000	In contrast, blockade of caspase-8 with Ile-Glu-Thr-Asp-fluoromethyl ketone is sufficient to prevent formation of DNA fragments and to inhibit all the above signaling events, with exception of p38 phosphorylation, in both singlet oxygen- and H(2)O(2)-treated cells.	Glutamic Acid	44-47	caspase 8	Homo sapiens	25-34
10837470-6	2000	In contrast, blockade of caspase-8 with Ile-Glu-Thr-Asp-fluoromethyl ketone is sufficient to prevent formation of DNA fragments and to inhibit all the above signaling events, with exception of p38 phosphorylation, in both singlet oxygen- and H(2)O(2)-treated cells.	Threonine	48-51	caspase 8	Homo sapiens	25-34
10837470-6	2000	In contrast, blockade of caspase-8 with Ile-Glu-Thr-Asp-fluoromethyl ketone is sufficient to prevent formation of DNA fragments and to inhibit all the above signaling events, with exception of p38 phosphorylation, in both singlet oxygen- and H(2)O(2)-treated cells.	asp-fluoromethyl ketone	52-75	caspase 8	Homo sapiens	25-34
10837470-6	2000	In contrast, blockade of caspase-8 with Ile-Glu-Thr-Asp-fluoromethyl ketone is sufficient to prevent formation of DNA fragments and to inhibit all the above signaling events, with exception of p38 phosphorylation, in both singlet oxygen- and H(2)O(2)-treated cells.	Singlet Oxygen	222-236	caspase 8	Homo sapiens	25-34
10837470-6	2000	In contrast, blockade of caspase-8 with Ile-Glu-Thr-Asp-fluoromethyl ketone is sufficient to prevent formation of DNA fragments and to inhibit all the above signaling events, with exception of p38 phosphorylation, in both singlet oxygen- and H(2)O(2)-treated cells.	Hydrogen Peroxide	242-250	caspase 8	Homo sapiens	25-34
10837470-7	2000	These data suggest that caspase-3 activation is regulated through redundant signaling pathways that involve p38 and caspase-8 acting upstream of Bid during singlet oxygen-induced apoptosis, whereas the activation of caspase-3 by H(2)O(2) is only governed by a caspase-8-mediated apoptotic pathway.	Singlet Oxygen	156-170	caspase 8	Homo sapiens	116-125
10837470-7	2000	These data suggest that caspase-3 activation is regulated through redundant signaling pathways that involve p38 and caspase-8 acting upstream of Bid during singlet oxygen-induced apoptosis, whereas the activation of caspase-3 by H(2)O(2) is only governed by a caspase-8-mediated apoptotic pathway.	Singlet Oxygen	156-170	caspase 8	Homo sapiens	260-269
10913000-6	2000	Moreover, we demonstrate that peroxynitrite treatment stimulated activation of caspases 8 and 9, two initial caspases in the apoptotic signaling pathway, and preincubation of cells with their inhibitor, IETD-FMK, inhibited activation of caspase 3-like proteases and caspase 2 at the concentration that prevents the apoptosis.	Peroxynitrous Acid	30-43	caspase 8	Homo sapiens	79-95
10913000-6	2000	Moreover, we demonstrate that peroxynitrite treatment stimulated activation of caspases 8 and 9, two initial caspases in the apoptotic signaling pathway, and preincubation of cells with their inhibitor, IETD-FMK, inhibited activation of caspase 3-like proteases and caspase 2 at the concentration that prevents the apoptosis.	isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	203-211	caspase 8	Homo sapiens	79-95
10913000-7	2000	These observations, together, suggest that caspase 8 and/or caspase 9 mediates activation of caspase 3-like proteases and caspase 2 during the apoptosis induced by peroxynitrite in HL-60 cells.	Peroxynitrous Acid	164-177	caspase 8	Homo sapiens	43-52
10891503-5	2000	Plectin was quantitatively cleaved by caspase 8 at Asp 2395 in the center of the molecule in all cells tested.	Aspartic Acid	51-54	caspase 8	Homo sapiens	38-47
10922462-0	2000	Regulation of the activity of caspases by L-carnitine and palmitoylcarnitine.	Carnitine	42-53	caspase 8	Homo sapiens	30-38
10922462-0	2000	Regulation of the activity of caspases by L-carnitine and palmitoylcarnitine.	Palmitoylcarnitine	58-76	caspase 8	Homo sapiens	30-38
10922462-5	2000	In addition, 5 mM carnitine potently inhibited the activity of recombinant caspases 3, 7 and 8, whereas its long-chain fatty acid derivative palmitoylcarnitine stimulated the activity of all the caspases.	Carnitine	18-27	caspase 8	Homo sapiens	75-83
10825467-7	2000	Activities of caspase-3 and caspase-8 were increased during isothiocyanate-induced apoptosis, but caspase-1 activity was not.	isothiocyanic acid	60-74	caspase 8	Homo sapiens	28-37
10825467-8	2000	The general caspase inhibitor N-benzyloxycarbonyl-Val-Ala-Asp(OMe)-fluoromethylketone and the specific caspase-8 inhibitor N-benzyloxycarbonyl-Ile-Glu(OMe)-Thr-Asp(OMe)-fluoromethylketone inhibited apoptosis, but specific caspase-1 and caspase-3 inhibitors did not.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	123-187	caspase 8	Homo sapiens	103-112
10825467-10	2000	This suggests that caspase-8 has a critical role, and caspase-3 a supporting role, in isothiocyanate-induced apoptosis in which p53 is not an obligatory participant.	isothiocyanic acid	86-100	caspase 8	Homo sapiens	19-28
10919654-5	2000	Oleandrin also promoted caspase activation, detected by cleavage poly(ADP-ribose) polymerase and hydrolysis of a peptide substrate (DEVD-pNA).	oleandrin	0-9	caspase 8	Homo sapiens	24-31
10919654-5	2000	Oleandrin also promoted caspase activation, detected by cleavage poly(ADP-ribose) polymerase and hydrolysis of a peptide substrate (DEVD-pNA).	aspartyl-glutamyl-valyl-aspartyl-p-nitroanilide	132-140	caspase 8	Homo sapiens	24-31
10871865-6	2000	The first pathway is utilized by lymphoid cells stimulated through Fas, is abrogated in a caspase-8-deficient T-cell line, and is blocked by the caspase inhibitors Z-VAD-fmk and Boc-D-fmk.	ammonium ferrous sulfate	67-70	caspase 8	Homo sapiens	90-97
10871865-6	2000	The first pathway is utilized by lymphoid cells stimulated through Fas, is abrogated in a caspase-8-deficient T-cell line, and is blocked by the caspase inhibitors Z-VAD-fmk and Boc-D-fmk.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	164-173	caspase 8	Homo sapiens	90-99
10871865-6	2000	The first pathway is utilized by lymphoid cells stimulated through Fas, is abrogated in a caspase-8-deficient T-cell line, and is blocked by the caspase inhibitors Z-VAD-fmk and Boc-D-fmk.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	164-173	caspase 8	Homo sapiens	90-97
10871865-6	2000	The first pathway is utilized by lymphoid cells stimulated through Fas, is abrogated in a caspase-8-deficient T-cell line, and is blocked by the caspase inhibitors Z-VAD-fmk and Boc-D-fmk.	Boc-D-FMK	178-187	caspase 8	Homo sapiens	90-99
10871865-6	2000	The first pathway is utilized by lymphoid cells stimulated through Fas, is abrogated in a caspase-8-deficient T-cell line, and is blocked by the caspase inhibitors Z-VAD-fmk and Boc-D-fmk.	Boc-D-FMK	178-187	caspase 8	Homo sapiens	90-97
10747891-1	2000	Exposure to anti-Fas antibody in Jurkat cells (type II cells), which are characterized by a weak caspase-8 activation at the death-inducing signaling complex (DISC), induced a biphasic increase in ceramide levels.	Ceramides	197-205	caspase 8	Homo sapiens	97-106
10972087-10	2000	By exploring the Fas pathway in Jurkat cells, we found that both apoptosis inducers acted through Fas, since Fas-L, as well as CPP32 and FLICE were activated.	ammonium ferrous sulfate	17-20	caspase 8	Homo sapiens	137-142
10747891-4	2000	Exogenous sphingosine, as well as cell-permeable C(2)-ceramide, induced cytochrome c release from mitochondria in a caspase-independent fashion leading to activation of caspase-9 and executioner caspases and, surprisingly, activation of the initiator caspase-8 and processing of its substrate Bid.	Sphingosine	10-21	caspase 8	Homo sapiens	251-260
10799503-0	2000	The prodomain of caspase-1 enhances Fas-mediated apoptosis through facilitation of caspase-8 activation.	ammonium ferrous sulfate	36-39	caspase 8	Homo sapiens	83-92
10811898-9	2000	Because BA prevented NMDA-induced caspase-3 activation and apoptosis, the presence of Cyt c in the neuronal cytoplasm is not sufficient for the induction of caspase activity or apoptosis.	N-Methylaspartate	21-25	caspase 8	Homo sapiens	34-41
10811898-11	2000	Additionally, staurosporine-induced, but not NMDA-induced, apoptosis was associated with activation of caspase-8.	Staurosporine	14-27	caspase 8	Homo sapiens	103-112
10779637-0	2000	Morphological change, loss of deltapsi(m) and activation of caspases upon apoptosis of colorectal adenocarcinoma induced by 5-FU.	Fluorouracil	124-128	caspase 8	Homo sapiens	60-68
10799503-5	2000	This enhancement of Fas-mediated apoptosis was abolished by inhibitors of caspase-8 (Ile-Glu-Thr-Asp-fluoromethyl ketone) and caspase-3 (Asp-Glu-Val-Asp-aldehyde) but was only slightly diminished by an inhibitor of caspase-1 (acetyl-Tyr-Val-Ala-Asp-chloromethyl ketone).	ammonium ferrous sulfate	20-23	caspase 8	Homo sapiens	74-83
10799503-5	2000	This enhancement of Fas-mediated apoptosis was abolished by inhibitors of caspase-8 (Ile-Glu-Thr-Asp-fluoromethyl ketone) and caspase-3 (Asp-Glu-Val-Asp-aldehyde) but was only slightly diminished by an inhibitor of caspase-1 (acetyl-Tyr-Val-Ala-Asp-chloromethyl ketone).	isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	85-120	caspase 8	Homo sapiens	74-83
10799503-5	2000	This enhancement of Fas-mediated apoptosis was abolished by inhibitors of caspase-8 (Ile-Glu-Thr-Asp-fluoromethyl ketone) and caspase-3 (Asp-Glu-Val-Asp-aldehyde) but was only slightly diminished by an inhibitor of caspase-1 (acetyl-Tyr-Val-Ala-Asp-chloromethyl ketone).	N-acetyl-tyrosyl-valyl-alanyl-aspartyl chloromethyl ketone	226-268	caspase 8	Homo sapiens	74-83
10822379-4	2000	After triggering massive ER dilation due to an inhibition of secretion, the drug brefeldin A (BFA) induces the release of cytochrome c from mitochondria in a caspase-8- and Bid-independent manner.	Brefeldin A	81-92	caspase 8	Homo sapiens	158-167
10822379-4	2000	After triggering massive ER dilation due to an inhibition of secretion, the drug brefeldin A (BFA) induces the release of cytochrome c from mitochondria in a caspase-8- and Bid-independent manner.	Brefeldin A	94-97	caspase 8	Homo sapiens	158-167
10792026-6	2000	In combination with TNF-alpha, however, ceramide potentiated, whereas NO inhibited, TNF-alpha-induced TRADD recruitment and caspase 8 activity.	Ceramides	40-48	caspase 8	Homo sapiens	124-133
10733510-0	2000	HMBA induces activation of a caspase-independent cell death pathway to overcome P-glycoprotein-mediated multidrug resistance.	hexamethylene bisacetamide	0-4	caspase 8	Homo sapiens	29-36
10845427-0	2000	The novel triterpenoid 2-cyano-3,12-dioxoolean-1,9-dien-28-oic acid induces apoptosis of human myeloid leukemia cells by a caspase-8-dependent mechanism.	triterpenoid TP-222	10-22	caspase 8	Homo sapiens	123-132
10845427-0	2000	The novel triterpenoid 2-cyano-3,12-dioxoolean-1,9-dien-28-oic acid induces apoptosis of human myeloid leukemia cells by a caspase-8-dependent mechanism.	2-cyano-3,12-dioxoolean-1,9-dien-28-oic acid	23-67	caspase 8	Homo sapiens	123-132
10845427-6	2000	In concert with these findings, we demonstrate that CDDO, but not ara-C, activates caspase-8 and thereby caspase-3 by a cytochrome c-independent mechanism.	2-cyano-3,12-dioxoolean-1,9-dien-28-oic acid	52-56	caspase 8	Homo sapiens	83-92
10845427-7	2000	The results also show that CDDO-induced cytochrome c release is mediated by caspase-8-dependent cleavage of Bid.	2-cyano-3,12-dioxoolean-1,9-dien-28-oic acid	27-31	caspase 8	Homo sapiens	76-85
10887967-7	2000	In caspase-3-expressing breast cancer cells, cytochrome c-induced processing of nuclear procaspase-9 is blocked by the caspase inhibitors z-VAD and DEVD but not by YVAD.	z-vad	138-143	caspase 8	Homo sapiens	3-10
10887967-7	2000	In caspase-3-expressing breast cancer cells, cytochrome c-induced processing of nuclear procaspase-9 is blocked by the caspase inhibitors z-VAD and DEVD but not by YVAD.	DEVD	148-152	caspase 8	Homo sapiens	3-10
10802708-5	2000	Caspase 8-null neuroblastoma cells were resistant to death receptor- and doxorubicin-mediated apoptosis, deficits that were corrected by programmed expression of the enzyme.	Doxorubicin	73-84	caspase 8	Homo sapiens	0-9
10852976-6	2000	Interestingly, Fas ligation activated caspase-8 and caspase-3 with the cleavage of poly(ADP-ribose) polymerase (PARP), corresponding to apoptosis of RA synoviocytes.	ammonium ferrous sulfate	15-18	caspase 8	Homo sapiens	38-47
10852976-7	2000	Furthermore, specific inhibitors for caspase-3 and caspase-8 but not caspase-1 suppressed Fas-induced apoptosis of RA synoviocytes in a dose- and time-dependent manner.	ammonium ferrous sulfate	90-93	caspase 8	Homo sapiens	51-60
10852976-10	2000	CONCLUSION: Our findings suggest that Fas-mediated apoptosis in synoviocytes may be regulated at the level of recruitment of FADD to the DISC, subsequently leading to the activation of the FADD/caspase-8/caspase-3 signalling pathway.	ammonium ferrous sulfate	38-41	caspase 8	Homo sapiens	194-203
10744730-8	2000	In addition Mad1 interfered with Fas-, TRAIL-, and UV-induced apoptosis, which coincided with a reduced activation of caspase-8 during Fas-mediated apoptosis in response to Mad1 expression.	ammonium ferrous sulfate	33-36	caspase 8	Homo sapiens	118-127
10822385-5	2000	Hyperthermia does not overcome resistance to apoptosis conferred by the viral caspase inhibitor, crm-A, indicating the absolute requirement for the activation of crm-A-sensitive caspases, probably caspase 8, for apoptosis.	crm-a	162-167	caspase 8	Homo sapiens	197-206
10830721-7	2000	In U251 and U-373 MG glioma cells, adenovirus-mediated transduction of the Bax gene combined with caspase-8 gene induced enhanced apoptosis and cell death as determined by morphological analysis and assay for dead cells, hypodiploid cells, and DNA fragmentation (terminal deoxynucleotidyltransferase-mediated deoxyuridine triphosphate nick end labeling method).	deoxyuridine triphosphate	309-334	caspase 8	Homo sapiens	98-107
10863977-0	2000	Lactacystin activates FLICE (caspase 8) protease and induces apoptosis in Fas-resistant adult T-cell leukemia cell lines.	lactacystin	0-11	caspase 8	Homo sapiens	22-27
10863977-0	2000	Lactacystin activates FLICE (caspase 8) protease and induces apoptosis in Fas-resistant adult T-cell leukemia cell lines.	lactacystin	0-11	caspase 8	Homo sapiens	29-38
10863977-5	2000	Moreover, LC induced the activation of caspase 8 (FLICE) protease, which is the initiator of the Fas-mediated apoptotic cascade.	ammonium ferrous sulfate	97-100	caspase 8	Homo sapiens	39-48
10863977-5	2000	Moreover, LC induced the activation of caspase 8 (FLICE) protease, which is the initiator of the Fas-mediated apoptotic cascade.	ammonium ferrous sulfate	97-100	caspase 8	Homo sapiens	50-55
10793331-7	2000	The pretreatment of cells with pan-caspase inhibitor Z-VAD-fmk markedly prevented CBDCA-mediated cytotoxicity/apoptosis and the modulation of Bcl-2 family proteins (generation of p18 Bax-alpha and p16 Bcl-x(L) ) with only slight prevention of decline of Deltapsi(m).	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	53-62	caspase 8	Homo sapiens	35-42
10793331-7	2000	The pretreatment of cells with pan-caspase inhibitor Z-VAD-fmk markedly prevented CBDCA-mediated cytotoxicity/apoptosis and the modulation of Bcl-2 family proteins (generation of p18 Bax-alpha and p16 Bcl-x(L) ) with only slight prevention of decline of Deltapsi(m).	Carboplatin	82-87	caspase 8	Homo sapiens	35-42
10793331-8	2000	Taken together, these results may suggest that activation of several caspases, including caspase-3 and -8, plays some role in CBDCA-mediated apoptosis, probably through the modification of Bcl-2 family proteins, Bax-alpha and Bcl-x(L).	Carboplatin	126-131	caspase 8	Homo sapiens	69-77
10753878-5	2000	NF-kappaB activation by FADD and Casper is inhibited by the caspase-specific inhibitors crmA and BD-fmk, suggesting that FADD- and Casper-induced NF-kappaB activation is mediated by caspase-8.	crma	88-92	caspase 8	Homo sapiens	182-191
10753878-5	2000	NF-kappaB activation by FADD and Casper is inhibited by the caspase-specific inhibitors crmA and BD-fmk, suggesting that FADD- and Casper-induced NF-kappaB activation is mediated by caspase-8.	bd-fmk	97-103	caspase 8	Homo sapiens	182-191
10753878-8	2000	A mutant of Casper and the caspase-specific inhibitors crmA and BD-fmk partially inhibit TNF-R1-, TRADD, and TNF-induced NF-kappaB activation, suggesting that FADD, Casper, and caspase-8 function downstream of TRADD and contribute to TNF-R1-induced NF-kappaB activation.	bd-fmk	64-70	caspase 8	Homo sapiens	177-186
10733510-2	2000	As well as effluxing xenotoxins, functional P-gp can confer resistance to caspase-dependent apoptosis induced by a range of different stimuli, including Fas ligand, tumor necrosis factor, UV irradiation, and serum starvation.	xenotoxins	21-31	caspase 8	Homo sapiens	74-81
10792503-4	2000	PMA stimulation also increased the expression of both pro-caspase-8 and pro-caspase-3 in U937, but not apoptosis or intracellular caspase-3 activity.	Tetradecanoylphorbol Acetate	0-3	caspase 8	Homo sapiens	58-67
10792503-5	2000	PMA also increased the expression of X-chromosome-linked inhibitor of apoptosis protein (XIAP) in U937, suggesting an inhibitory action for XIAP on the caspase cascade in PMA-stimulated U937.	Tetradecanoylphorbol Acetate	0-3	caspase 8	Homo sapiens	152-159
10792503-7	2000	When a potent NF-kappaB inhibitor, pyrrolidine dithiocarbamate (PDTC), was added to U937 cell culture in the presence of PMA, apoptosis was triggered by activation of caspase-3, which was induced by caspase-8 activation.	pyrrolidine dithiocarbamic acid	35-62	caspase 8	Homo sapiens	199-208
10792503-7	2000	When a potent NF-kappaB inhibitor, pyrrolidine dithiocarbamate (PDTC), was added to U937 cell culture in the presence of PMA, apoptosis was triggered by activation of caspase-3, which was induced by caspase-8 activation.	pyrrolidine dithiocarbamic acid	64-68	caspase 8	Homo sapiens	199-208
10792503-7	2000	When a potent NF-kappaB inhibitor, pyrrolidine dithiocarbamate (PDTC), was added to U937 cell culture in the presence of PMA, apoptosis was triggered by activation of caspase-3, which was induced by caspase-8 activation.	Tetradecanoylphorbol Acetate	121-124	caspase 8	Homo sapiens	199-208
10792503-9	2000	The inhibitors of caspase-8 and caspase-3 mostly inhibited apoptosis of U937 treated with PMA in the presence of PDTC.	Tetradecanoylphorbol Acetate	90-93	caspase 8	Homo sapiens	18-27
10745077-8	2000	Based on the X-ray structural analysis of caspase-8, a main chain carbonyl oxygen appears to be involved in a catalytic triad with the active site Cys and His residues.	Histidine	155-158	caspase 8	Homo sapiens	42-51
10733893-9	2000	SDS-PAGE, protein sequencing, and mass spectrometric analysis of these extracts showed complete conversion of the 33-kDa procaspase 8 to the 19- and 11-kDa subunits of activated caspase 8.	Sodium Dodecyl Sulfate	0-3	caspase 8	Homo sapiens	124-133
10673748-3	2000	These apoptotic phenomena induced by 2CdA were inhibited by cycloheximide (CHX; a protein synthesis inhibitor), deoxycytidine (dC; a substrate of deoxycytidine kinase), acetyl Ile-Glu-Thr-Asp aldehyde (Ac-IETD-CHO; a caspase-8 inhibitor) and acetyl Asp-Glu-Val-Asp aldehyde (Ac-DEVD-CHO; a caspase-3 inhibitor).	Cladribine	37-41	caspase 8	Homo sapiens	217-226
10734062-7	2000	(iii) Decrease in pH(i) is necessary to induce reduction in mitochondrial membrane potential, cyt c release and caspase-9 activation and (iv) depletion of ATP ablates SST-induced cyt c release and caspase-9 activation, but not its ability to induce effector caspases and apoptosis.	Adenosine Triphosphate	155-158	caspase 8	Homo sapiens	258-266
10734071-0	2000	Caspase-8 activation and bid cleavage contribute to MCF7 cellular execution in a caspase-3-dependent manner during staurosporine-mediated apoptosis.	Staurosporine	115-128	caspase 8	Homo sapiens	0-9
10749135-6	2000	This conclusion is supported by the observation that in HL-60/Apaf-1 cells, ectopic expression of dominant negative caspase-9, its inhibitory short isoform caspase-9b, or XIAP or treatment with the caspase inhibitor zVAD (50 microM) inhibited Apaf-1-induced caspase-8 and Bid cleavage, mitochondrial deltapsim, release of cyt c, and apoptosis.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	216-220	caspase 8	Homo sapiens	116-123
10749135-7	2000	In contrast, a transient transfection of dominant negative caspase-8 or CrmA or exposure to caspase-8 inhibitor zIETD-fmk inhibited the processing of procaspase-8 and Bid but did not inhibit the cytosolic accumulation of cyt c in either the untreated HL-60/Apaf-1 cells or the etoposide-treated HL-60/Apaf-1 and HL-60/neo cells.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	112-121	caspase 8	Homo sapiens	92-101
10749135-7	2000	In contrast, a transient transfection of dominant negative caspase-8 or CrmA or exposure to caspase-8 inhibitor zIETD-fmk inhibited the processing of procaspase-8 and Bid but did not inhibit the cytosolic accumulation of cyt c in either the untreated HL-60/Apaf-1 cells or the etoposide-treated HL-60/Apaf-1 and HL-60/neo cells.	Etoposide	277-286	caspase 8	Homo sapiens	59-68
10749135-7	2000	In contrast, a transient transfection of dominant negative caspase-8 or CrmA or exposure to caspase-8 inhibitor zIETD-fmk inhibited the processing of procaspase-8 and Bid but did not inhibit the cytosolic accumulation of cyt c in either the untreated HL-60/Apaf-1 cells or the etoposide-treated HL-60/Apaf-1 and HL-60/neo cells.	Etoposide	277-286	caspase 8	Homo sapiens	92-101
10721769-3	2000	In addition to the involvement of caspase 3 in arsenic trioxide-induced apoptosis of NB4 cells, the activation of caspase 8 was also shown to be involved by Western blot analysis or by apoptosis inhibition assay using caspase 8 inhibitor Ac-IETD-CHO.	Ac-IETD-CHO	238-249	caspase 8	Homo sapiens	114-123
10690508-11	2000	In TRAIL-sensitive cells, caspases 8, 9, and 3 were activated after TRAIL treatment, but in TRAIL-resistant cells, they were activated only by the combination of TRAIL and doxorubicin.	Doxorubicin	172-183	caspase 8	Homo sapiens	26-46
10690508-12	2000	Our results suggest: (a) evaluation of tumor DR4 and FLIP expression and host DR4 codon 441 status could be potentially useful predictors of TRAIL sensitivity, and (b) doxorubicin, in combination with TRAIL, may effectively promote caspase activation in TRAIL-resistant tumors.	Doxorubicin	168-179	caspase 8	Homo sapiens	232-239
10745077-8	2000	Based on the X-ray structural analysis of caspase-8, a main chain carbonyl oxygen appears to be involved in a catalytic triad with the active site Cys and His residues.	Oxygen	75-81	caspase 8	Homo sapiens	42-51
10745077-8	2000	Based on the X-ray structural analysis of caspase-8, a main chain carbonyl oxygen appears to be involved in a catalytic triad with the active site Cys and His residues.	Cysteine	147-150	caspase 8	Homo sapiens	42-51
10722705-7	2000	Limited pro-caspase 8 overexpression also increased ceramide levels 2.7 +/- 0.2-fold, yet failed, without CHX, to initiate apoptosis.	Ceramides	52-60	caspase 8	Homo sapiens	12-21
10722705-8	2000	Expression of membrane-targeted oligomerized CD-8 caspase 8 induced apoptosis without CHX, yet elevated ceramide only to a level equivalent to limited pro-caspase 8 transfection.	Ceramides	104-112	caspase 8	Homo sapiens	50-59
10706869-5	2000	Overexpression of CrmA, an inhibitor of caspase-1 and caspase-8, partially inhibited tumor-induced T-cell death.	crma	18-22	caspase 8	Homo sapiens	54-63
10652256-7	2000	The HNE-mediated activation of caspases, cleavage of PARP and DNA fragmentation were blocked by antioxidants cysteine, N-acety-L-cysteine and dithiothreitol, but not by two other HNE-reactive amino acids lysine and histidine, or by cystine, the oxidized form of cysteine.	4-hydroxy-2-nonenal	4-7	caspase 8	Homo sapiens	31-39
10652256-7	2000	The HNE-mediated activation of caspases, cleavage of PARP and DNA fragmentation were blocked by antioxidants cysteine, N-acety-L-cysteine and dithiothreitol, but not by two other HNE-reactive amino acids lysine and histidine, or by cystine, the oxidized form of cysteine.	Cysteine	109-117	caspase 8	Homo sapiens	31-39
10652256-7	2000	The HNE-mediated activation of caspases, cleavage of PARP and DNA fragmentation were blocked by antioxidants cysteine, N-acety-L-cysteine and dithiothreitol, but not by two other HNE-reactive amino acids lysine and histidine, or by cystine, the oxidized form of cysteine.	Acetylcysteine	119-137	caspase 8	Homo sapiens	31-39
10652256-7	2000	The HNE-mediated activation of caspases, cleavage of PARP and DNA fragmentation were blocked by antioxidants cysteine, N-acety-L-cysteine and dithiothreitol, but not by two other HNE-reactive amino acids lysine and histidine, or by cystine, the oxidized form of cysteine.	Dithiothreitol	142-156	caspase 8	Homo sapiens	31-39
10652256-7	2000	The HNE-mediated activation of caspases, cleavage of PARP and DNA fragmentation were blocked by antioxidants cysteine, N-acety-L-cysteine and dithiothreitol, but not by two other HNE-reactive amino acids lysine and histidine, or by cystine, the oxidized form of cysteine.	Lysine	204-210	caspase 8	Homo sapiens	31-39
10652256-7	2000	The HNE-mediated activation of caspases, cleavage of PARP and DNA fragmentation were blocked by antioxidants cysteine, N-acety-L-cysteine and dithiothreitol, but not by two other HNE-reactive amino acids lysine and histidine, or by cystine, the oxidized form of cysteine.	Histidine	215-224	caspase 8	Homo sapiens	31-39
10652256-7	2000	The HNE-mediated activation of caspases, cleavage of PARP and DNA fragmentation were blocked by antioxidants cysteine, N-acety-L-cysteine and dithiothreitol, but not by two other HNE-reactive amino acids lysine and histidine, or by cystine, the oxidized form of cysteine.	Cystine	232-239	caspase 8	Homo sapiens	31-39
10652256-7	2000	The HNE-mediated activation of caspases, cleavage of PARP and DNA fragmentation were blocked by antioxidants cysteine, N-acety-L-cysteine and dithiothreitol, but not by two other HNE-reactive amino acids lysine and histidine, or by cystine, the oxidized form of cysteine.	Cysteine	129-137	caspase 8	Homo sapiens	31-39
10673748-6	2000	Increases in the activities of caspases-8 and -3 were observed after 2CdA treatment.	Cladribine	69-73	caspase 8	Homo sapiens	31-48
10673748-8	2000	These results indicated that 2CdA-induced apoptosis was triggered by phosphorylation of 2CdA followed by the protein synthesis-dependent expression of Fas and Fas-L and activation of caspases-8 and -3.	Cladribine	29-33	caspase 8	Homo sapiens	183-200
10663637-0	2000	Cisplatin (CDDP) specifically induces apoptosis via sequential activation of caspase-8, -3 and -6 in osteosarcoma.	Cisplatin	0-9	caspase 8	Homo sapiens	77-97
10663637-0	2000	Cisplatin (CDDP) specifically induces apoptosis via sequential activation of caspase-8, -3 and -6 in osteosarcoma.	Cisplatin	11-15	caspase 8	Homo sapiens	77-97
10663637-20	2000	It also demonstrates that caspase-8 is a key molecule in the earliest stage of the signaling pathway of CDDP-induced apoptosis of HOS cells, and caspase-3 works downstream of caspase-8.	Cisplatin	104-108	caspase 8	Homo sapiens	26-35
10663637-20	2000	It also demonstrates that caspase-8 is a key molecule in the earliest stage of the signaling pathway of CDDP-induced apoptosis of HOS cells, and caspase-3 works downstream of caspase-8.	Cisplatin	104-108	caspase 8	Homo sapiens	175-184
10534343-7	1999	Addition of an inhibitor of caspase-8 or caspase-3 (IETD-FMK or DEVD-CHO) markedly inhibited TGF-beta1-induced apoptosis of HuH-7 cells.	isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	52-60	caspase 8	Homo sapiens	28-37
10587358-3	1999	FLICE (Fas-associated death domain-like interleukin 1beta-converting enzyme)-inhibitory protein (Flip), a naturally occurring caspase-inhibitory protein that lacks the critical cysteine domain necessary for catalytic activity, is a negative regulator of Fas-induced apoptosis.	Cysteine	177-185	caspase 8	Homo sapiens	0-5
10568827-0	1999	Apoptosis of colorectal adenocarcinoma induced by 5-FU and/or IFN-gamma through caspase 3 and caspase 8.	Fluorouracil	50-54	caspase 8	Homo sapiens	94-103
10568827-2	1999	We examined the role of caspases on the apoptosis induction of 5-FU and IFN-gamma using a colorectal adenocarcinoma cell line.	Fluorouracil	63-67	caspase 8	Homo sapiens	24-32
10568827-3	1999	The activities of caspase 3 and caspase 8 increased when apoptosis was induced by 5-FU and/or IFN-gamma.	Fluorouracil	82-86	caspase 8	Homo sapiens	32-41
10568827-6	1999	Thus, caspase 3 and caspase 8 play crucial roles in apoptosis induced by 5-FU and/or IFN-gamma, regardless of the Fas-Fas ligand system.	Fluorouracil	73-77	caspase 8	Homo sapiens	20-29
10548502-3	1999	SDS-PAGE and Western blot analysis showed that cleavage of Bid was induced by a 1-h incubation of BJAB cells with TRAIL and was blocked by a caspase-8 inhibitor.	Sodium Dodecyl Sulfate	0-3	caspase 8	Homo sapiens	141-150
10579724-3	1999	In the absence of trophic factors, many motoneurons die in culture within 2 d. Most (75%) of these were saved by Fas-Fc receptor body, which blocks interactions between Fas and FasL, or by the caspase-8 inhibitor tetrapeptide IETD.	IETD	226-230	caspase 8	Homo sapiens	193-202
10534343-7	1999	Addition of an inhibitor of caspase-8 or caspase-3 (IETD-FMK or DEVD-CHO) markedly inhibited TGF-beta1-induced apoptosis of HuH-7 cells.	aspartyl-glutamyl-valyl-aspartal	64-72	caspase 8	Homo sapiens	28-37
10527810-3	1999	We demonstrate that the selective caspase-8 inhibitor IETD-fmk blocks neuronal death induced by beta-amyloid.	isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	54-62	caspase 8	Homo sapiens	34-43
10535957-3	1999	vMIA, a product of the viral UL37 gene, inhibits Fas-mediated apoptosis at a point downstream of caspase-8 activation and Bid cleavage but upstream of cytochrome c release, while residing in mitochondria and associating with adenine nucleotide translocator.	ammonium ferrous sulfate	49-52	caspase 8	Homo sapiens	97-106
10509663-9	1999	Furthermore, the authors observed that treatment of retinal cells with inhibitors of caspases, including B-D-FMK and Z-IETD-FMK, blocked the apoptotic cell death induced by different stimuli.	b-d-fmk	105-112	caspase 8	Homo sapiens	85-93
10509663-9	1999	Furthermore, the authors observed that treatment of retinal cells with inhibitors of caspases, including B-D-FMK and Z-IETD-FMK, blocked the apoptotic cell death induced by different stimuli.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	117-127	caspase 8	Homo sapiens	85-93
10477698-8	1999	Our results imply that the relative levels of caspase-8 and FLIP(L) are an important determinant of susceptibility to Fas-mediated apoptosis.	ammonium ferrous sulfate	118-121	caspase 8	Homo sapiens	46-55
10508784-1	1999	BACKGROUND: In the initial stages of Fas-mediated apoptosis the cysteine protease caspase-8 is recruited to the cell receptor as a zymogen (procaspase-8) and is incorporated into the death-signalling complex.	ammonium ferrous sulfate	37-40	caspase 8	Homo sapiens	82-91
10508784-4	1999	RESULTS: We report here the crystal structure of a complex of the activated human caspase-8 (proteolytic domain) with the irreversible peptidic inhibitor Z-Glu-Val-Asp-dichloromethylketone at 2.8 A resolution.	z-glu-val-asp-dichloromethylketone	154-188	caspase 8	Homo sapiens	82-91
10508785-3	1999	Caspase-8 is designated as an initiator caspase and is believed to sit at the apex of the Fas- or TNF-mediated apoptotic cascade.	ammonium ferrous sulfate	90-93	caspase 8	Homo sapiens	0-9
10508785-5	1999	RESULTS: The structure of recombinant human caspase-8, covalently modified with the inhibitor acetyl-Ile-Glu-Thr-Asp-aldehyde, has been determined by X-ray crystallography to 1.2 A resolution.	acetyl-ile-glu	94-108	caspase 8	Homo sapiens	44-53
10508785-5	1999	RESULTS: The structure of recombinant human caspase-8, covalently modified with the inhibitor acetyl-Ile-Glu-Thr-Asp-aldehyde, has been determined by X-ray crystallography to 1.2 A resolution.	Threonine	109-112	caspase 8	Homo sapiens	44-53
10508785-5	1999	RESULTS: The structure of recombinant human caspase-8, covalently modified with the inhibitor acetyl-Ile-Glu-Thr-Asp-aldehyde, has been determined by X-ray crystallography to 1.2 A resolution.	asp-aldehyde	113-125	caspase 8	Homo sapiens	44-53
10508785-9	1999	CONCLUSIONS: The catalytic triad in caspase-8 comprises Cys360, His317 and the backbone carbonyl oxygen atom of Arg258, which points towards the Nepsilon atom of His317.	Oxygen	97-103	caspase 8	Homo sapiens	36-45
10438583-6	1999	These results suggest that Bcl-2 blocked Fas-mediated cell death by acting downstream of caspase-8, which is in contrast to staurosporine-induced apoptosis where Bcl-2 is acting upstream of caspase-8.	Staurosporine	124-137	caspase 8	Homo sapiens	190-199
10480431-6	1999	Coculture with increasing amounts of DC prevented CD95/Fas-triggered apoptosis in a dose-dependent fashion by inhibiting activation of caspase 8 and caspase 3.	ammonium ferrous sulfate	55-58	caspase 8	Homo sapiens	135-144
10447681-4	1999	Inhibition of tyrosine phosphatases delayed the cleavage and activation of caspase-8 and caspase-3 and antagonized the tyrosine dephosphorylation of the CD95 receptor-associated phosphoproteins p61 and p89/92.	Tyrosine	14-22	caspase 8	Homo sapiens	75-84
10444259-2	1999	In this study, we have examined the role of downstream mediators, including caspases, in Fas-mediated apoptosis in lymphocytes from ageing humans.	ammonium ferrous sulfate	89-92	caspase 8	Homo sapiens	76-84
10216102-7	1999	A potent activation of caspase-8 was also induced by cycloheximide, indicating that it was independent of protein synthesis.	Cycloheximide	53-66	caspase 8	Homo sapiens	23-32
10419518-7	1999	Furthermore, maintaining a normal intracellular potassium concentration represses the cell death process by inhibiting the activity of apoptotic nucleases and suppressing the activation of effector caspases (Hughes, F. M., Jr., Bortner, C. D. Purdy, G. D., and Cidlowski, J.	Potassium	48-57	caspase 8	Homo sapiens	198-206
10419518-17	1999	Treatment of Jurkat cells with various apoptotic agents in the presence of either the caspase-3 inhibitor DEVD, or the caspase-8 inhibitor IETD also blocked DNA degradation, but failed to prevent other characteristics of apoptosis.	IETD	139-143	caspase 8	Homo sapiens	119-128
10469173-6	1999	The IDVD/V site can be cleaved by caspase-8 in vitro, and its cleavage is less sensitive to DEVD-CHO and Bcl-2 over-expression than that of the DSVD/F site in Jurkat cells.	aspartyl-glutamyl-valyl-aspartal	92-100	caspase 8	Homo sapiens	34-43
10527889-0	1999	A crucial role of caspase 3 and caspase 8 in paclitaxel-induced apoptosis.	Paclitaxel	45-55	caspase 8	Homo sapiens	32-41
10527889-6	1999	The cleavage of caspase 3, caspase 8, and DFF45/ICAD was also observed in paclitaxel-induced apoptosis, and the inhibitor of caspase 3 and caspase 8 inhibited both antitumor effects and apoptosis induced by paclitaxel.	Paclitaxel	74-84	caspase 8	Homo sapiens	27-36
10527889-6	1999	The cleavage of caspase 3, caspase 8, and DFF45/ICAD was also observed in paclitaxel-induced apoptosis, and the inhibitor of caspase 3 and caspase 8 inhibited both antitumor effects and apoptosis induced by paclitaxel.	Paclitaxel	74-84	caspase 8	Homo sapiens	139-148
10527889-6	1999	The cleavage of caspase 3, caspase 8, and DFF45/ICAD was also observed in paclitaxel-induced apoptosis, and the inhibitor of caspase 3 and caspase 8 inhibited both antitumor effects and apoptosis induced by paclitaxel.	Paclitaxel	207-217	caspase 8	Homo sapiens	139-148
10361106-0	1999	Purified photoproducts of merocyanine 540 trigger cytochrome C release and caspase 8-dependent apoptosis in human leukemia and melanoma cells.	merocyanine	26-37	caspase 8	Homo sapiens	75-84
10361106-2	1999	We have shown that photoactivated merocyanine 540 (pMC540) triggers caspase-mediated apoptosis in HL60 leukemia and M14 melanoma cells.	merocyanine	34-45	caspase 8	Homo sapiens	68-75
10358093-6	1999	Affinity labeling with biotin-VAD-fmk of all active caspase species in TNFalpha-mediated apoptosis identified four newly labeled spots (activated caspases) present exclusively in TNFalpha/ActD-treated cells.	Biotin-VAD-FMK	23-37	caspase 8	Homo sapiens	146-154
10358093-7	1999	Both NO and the caspase inhibitor, Ac-DEVD-CHO, prevented the appearance of the four newly labeled spots or active caspases.	acetyl-aspartyl-glutamyl-valyl-aspartal	35-46	caspase 8	Homo sapiens	115-123
10399962-11	1999	Inhibition of caspase cleavage by the broad-range caspase inhibitor zVAD.fmk strongly reduced Bet-A-induced apoptosis, indicating that apoptosis was mediated by activation of caspases.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	68-72	caspase 8	Homo sapiens	14-21
10399962-11	1999	Inhibition of caspase cleavage by the broad-range caspase inhibitor zVAD.fmk strongly reduced Bet-A-induced apoptosis, indicating that apoptosis was mediated by activation of caspases.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	68-72	caspase 8	Homo sapiens	50-57
10399962-11	1999	Inhibition of caspase cleavage by the broad-range caspase inhibitor zVAD.fmk strongly reduced Bet-A-induced apoptosis, indicating that apoptosis was mediated by activation of caspases.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	68-72	caspase 8	Homo sapiens	175-183
10399962-11	1999	Inhibition of caspase cleavage by the broad-range caspase inhibitor zVAD.fmk strongly reduced Bet-A-induced apoptosis, indicating that apoptosis was mediated by activation of caspases.	FMK	73-76	caspase 8	Homo sapiens	14-21
10399962-11	1999	Inhibition of caspase cleavage by the broad-range caspase inhibitor zVAD.fmk strongly reduced Bet-A-induced apoptosis, indicating that apoptosis was mediated by activation of caspases.	FMK	73-76	caspase 8	Homo sapiens	50-57
10399962-11	1999	Inhibition of caspase cleavage by the broad-range caspase inhibitor zVAD.fmk strongly reduced Bet-A-induced apoptosis, indicating that apoptosis was mediated by activation of caspases.	FMK	73-76	caspase 8	Homo sapiens	175-183
10411938-0	1999	Herpes simplex virus thymidine kinase/ganciclovir-induced apoptosis involves ligand-independent death receptor aggregation and activation of caspases.	Ganciclovir	38-49	caspase 8	Homo sapiens	141-149
10411938-3	1999	TK/GCV-induced apoptosis involves CD95-L-independent CD95 aggregation leading to the formation of a Fas-associated death domain protein (FADD) and caspase-8-containing, death-inducing signaling complex.	Ganciclovir	3-6	caspase 8	Homo sapiens	147-156
10388534-0	1999	Caspase-8 mediates caspase-3 activation and cytochrome c release during singlet oxygen-induced apoptosis of HL-60 cells.	Singlet Oxygen	72-86	caspase 8	Homo sapiens	0-9
10388534-5	1999	Further studies showed that singlet oxygen induced an increase in caspase-8 activity and a reduction in mitochondrial cytochrome c.	Singlet Oxygen	28-42	caspase 8	Homo sapiens	66-75
10388534-7	1999	In addition, blockade of caspase-8 by Z-IETD-FMK inhibited cleavage of pro-caspase-3 and prevented loss of mitochondrial cytochrome c.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	38-48	caspase 8	Homo sapiens	25-34
10388534-8	1999	These results suggest that caspase-8 mediates caspase-3 activation and cytochrome c release during singlet oxygen-induced apoptosis in HL-60 cells.	Singlet Oxygen	99-113	caspase 8	Homo sapiens	27-36
10527889-7	1999	These results suggest that activation of caspase 3 and caspase 8 plays a crucial role in paclitaxel-induced apoptosis under any concentrations of paclitaxel.	Paclitaxel	89-99	caspase 8	Homo sapiens	55-64
10527889-7	1999	These results suggest that activation of caspase 3 and caspase 8 plays a crucial role in paclitaxel-induced apoptosis under any concentrations of paclitaxel.	Paclitaxel	146-156	caspase 8	Homo sapiens	55-64
10403377-7	1999	The mitochondrial stabilising agent bongkrekic acid also inhibited caspase activation and apoptosis.	Bongkrekic Acid	36-51	caspase 8	Homo sapiens	67-74
10358093-6	1999	Affinity labeling with biotin-VAD-fmk of all active caspase species in TNFalpha-mediated apoptosis identified four newly labeled spots (activated caspases) present exclusively in TNFalpha/ActD-treated cells.	Biotin-VAD-FMK	23-37	caspase 8	Homo sapiens	52-59
10318846-0	1999	Common regulation of apoptosis signaling induced by CD95 and the DNA-damaging stimuli etoposide and gamma-radiation downstream from caspase-8 activation.	Etoposide	86-95	caspase 8	Homo sapiens	132-141
10216102-3	1999	Because apoptosis induced by anticancer drugs has been proposed to involve CD95/CD95 ligand interaction, we investigated the mechanism of caspase activation by daunorubicin, doxorubicin, etoposide, and mitomycin C.	Daunorubicin	160-172	caspase 8	Homo sapiens	138-145
10216102-3	1999	Because apoptosis induced by anticancer drugs has been proposed to involve CD95/CD95 ligand interaction, we investigated the mechanism of caspase activation by daunorubicin, doxorubicin, etoposide, and mitomycin C.	Doxorubicin	174-185	caspase 8	Homo sapiens	138-145
10216102-3	1999	Because apoptosis induced by anticancer drugs has been proposed to involve CD95/CD95 ligand interaction, we investigated the mechanism of caspase activation by daunorubicin, doxorubicin, etoposide, and mitomycin C.	Etoposide	187-196	caspase 8	Homo sapiens	138-145
10216102-3	1999	Because apoptosis induced by anticancer drugs has been proposed to involve CD95/CD95 ligand interaction, we investigated the mechanism of caspase activation by daunorubicin, doxorubicin, etoposide, and mitomycin C.	Mitomycin	202-213	caspase 8	Homo sapiens	138-145
10216102-6	1999	The broad caspase inhibitor benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone prevented apoptosis and caspase-8 activation in response to CD95 and drug treatment, whereas a neutralizing CD95 decoy as well as a dominant-negative FADD construct selectively abrogated CD95, but not drug-induced effects.	Caspase Inhibitor VI	28-76	caspase 8	Homo sapiens	10-17
10216102-6	1999	The broad caspase inhibitor benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone prevented apoptosis and caspase-8 activation in response to CD95 and drug treatment, whereas a neutralizing CD95 decoy as well as a dominant-negative FADD construct selectively abrogated CD95, but not drug-induced effects.	Caspase Inhibitor VI	28-76	caspase 8	Homo sapiens	101-110
10328578-3	1999	We have recently found that Fas-mediated apoptosis of RA synoviocytes is associated with activation of two signaling pathways, the c-Jun amino-terminal kinase (JNK)/activator protein-1 (AP-1) pathway, and the FADD (Fas-associated death domain protein)/Caspase-8/Caspase-3/PARP (poly(ADP-ribose)polymerase) pathway.	ammonium ferrous sulfate	28-31	caspase 8	Homo sapiens	252-261
10228045-6	1999	Apo-2L induced apoptosis in &gt;80% of AIDS-KS cells pretreated with Act D. The caspase inhibitors, zIETD-fmk and zDEVD-fmk, inhibited apoptosis in AIDS-KS by sApo-2L, suggesting that caspase 3-like and caspase 8 or 10 activities are essential for Apo-2L-mediated apoptosis.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	100-109	caspase 8	Homo sapiens	80-87
10228045-6	1999	Apo-2L induced apoptosis in &gt;80% of AIDS-KS cells pretreated with Act D. The caspase inhibitors, zIETD-fmk and zDEVD-fmk, inhibited apoptosis in AIDS-KS by sApo-2L, suggesting that caspase 3-like and caspase 8 or 10 activities are essential for Apo-2L-mediated apoptosis.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	100-109	caspase 8	Homo sapiens	184-212
10228045-6	1999	Apo-2L induced apoptosis in &gt;80% of AIDS-KS cells pretreated with Act D. The caspase inhibitors, zIETD-fmk and zDEVD-fmk, inhibited apoptosis in AIDS-KS by sApo-2L, suggesting that caspase 3-like and caspase 8 or 10 activities are essential for Apo-2L-mediated apoptosis.	sapo-2l	159-166	caspase 8	Homo sapiens	80-87
10228045-6	1999	Apo-2L induced apoptosis in &gt;80% of AIDS-KS cells pretreated with Act D. The caspase inhibitors, zIETD-fmk and zDEVD-fmk, inhibited apoptosis in AIDS-KS by sApo-2L, suggesting that caspase 3-like and caspase 8 or 10 activities are essential for Apo-2L-mediated apoptosis.	benzoylcarbonyl-aspartyl-glutamyl-valyl-aspartyl-fluoromethyl ketone	114-123	caspase 8	Homo sapiens	80-87
10194469-2	1999	The Cer response to all three stimuli was mapped in between caspases sensitive to benzoyloxycarbonyl-VAD-fluoromethylketone (zVAD-fmk) and acetyl-DEVD-aldehyde (DEVD-CHO).	benzoyloxycarbonyl-vad-fluoromethylketone	82-123	caspase 8	Homo sapiens	60-68
10355595-8	1999	These results indicate that the elevation of levels of endogenous intracellular cyclic AMP and subsequent activation of protein kinase A play a crucial role in the prevention of apoptosis triggered by TNF-alpha/cycloheximide in human neutrophils, and that the possible target of cyclic AMP is a product in the metabolic pathway between caspase-8 and caspase-3.	Cyclic AMP	80-90	caspase 8	Homo sapiens	336-345
10207055-11	1999	Furthermore, an increase of rhodamine-123 uptake into intact cells, which has been explained by mitochondrial swelling, occurred considerably later than the caspase activation and was blocked by Z-VAD-fmk.	Rhodamine 123	28-41	caspase 8	Homo sapiens	157-164
10207055-11	1999	Furthermore, an increase of rhodamine-123 uptake into intact cells, which has been explained by mitochondrial swelling, occurred considerably later than the caspase activation and was blocked by Z-VAD-fmk.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	195-204	caspase 8	Homo sapiens	157-164
10208851-0	1999	Expression of extended polyglutamine sequentially activates initiator and effector caspases.	polyglutamine	23-36	caspase 8	Homo sapiens	83-91
10208851-7	1999	This is the first direct evidence that the expression of extended polyQ activates caspases and together with the previous findings that some of the products of genes responsible for CAG repeat diseases are substrates of caspase-3 indicates an important role of caspases in the pathogenesis of these diseases.	polyglutamine	66-71	caspase 8	Homo sapiens	82-90
10208851-7	1999	This is the first direct evidence that the expression of extended polyQ activates caspases and together with the previous findings that some of the products of genes responsible for CAG repeat diseases are substrates of caspase-3 indicates an important role of caspases in the pathogenesis of these diseases.	polyglutamine	66-71	caspase 8	Homo sapiens	261-269
10194469-2	1999	The Cer response to all three stimuli was mapped in between caspases sensitive to benzoyloxycarbonyl-VAD-fluoromethylketone (zVAD-fmk) and acetyl-DEVD-aldehyde (DEVD-CHO).	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	125-133	caspase 8	Homo sapiens	60-68
10194469-6	1999	These results indicate that the caspases required for the Cer response to etoposide and IR reside at or downstream from the mitochondria.	Etoposide	74-83	caspase 8	Homo sapiens	32-40
10201902-7	1999	Furthermore, we have observed that TCR-mediated neosynthesis of FLICE-like inhibitory protein mRNA is suppressed either by protein tyrosine kinase inhibitors or cyclosporin A.	Cyclosporine	161-174	caspase 8	Homo sapiens	64-69
10066378-4	1999	We demonstrate that cytochrome c is released from mitochondria of Jurkat cells in response to both staurosporine and an agonistic anti-Fas antibody and that only the latter is inhibited by the caspase inhibitor z-VAD-FMK.	Staurosporine	99-112	caspase 8	Homo sapiens	193-200
10066378-4	1999	We demonstrate that cytochrome c is released from mitochondria of Jurkat cells in response to both staurosporine and an agonistic anti-Fas antibody and that only the latter is inhibited by the caspase inhibitor z-VAD-FMK.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	211-220	caspase 8	Homo sapiens	193-200
10066378-5	1999	This suggests that an upstream caspase such as caspase-8 is required for the Fas-mediated release of mitochondrial cytochrome c.	ammonium ferrous sulfate	77-80	caspase 8	Homo sapiens	31-38
10066378-5	1999	This suggests that an upstream caspase such as caspase-8 is required for the Fas-mediated release of mitochondrial cytochrome c.	ammonium ferrous sulfate	77-80	caspase 8	Homo sapiens	47-56
10088775-10	1999	A gradual up-regulation of caspase 8 and caspase 3, which played a role in the caspase cascade for Fas-mediated apoptosis, was observed in TNFalpha-treated cultured OA synoviocytes.	ammonium ferrous sulfate	99-102	caspase 8	Homo sapiens	27-36
10088775-12	1999	More importantly, Z-IETD-FMK, a caspase 8 inhibitor, and Ac-DEVD-CHO, a caspase 3 inhibitor, almost completely inhibited Fas-mediated apoptosis of TNFalpha-treated cultured OA synoviocytes, whereas Ac-YVAD-CHO, a caspase 1 inhibitor, did not.	ammonium ferrous sulfate	121-124	caspase 8	Homo sapiens	32-41
10050884-5	1999	Apoptosis depended on mitochondrial permeability transition and activation of caspases, since the mitochondrion-specific inhibitor bongkrekic acid and the caspase inhibitor zVAD-fmk almost completely abrogated apoptosis.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	173-181	caspase 8	Homo sapiens	78-86
9971775-7	1999	In addition, we show that HIV-1Deltaenv infection and Tat expression increased the sensitivity of cells to Fas-mediated apoptosis, an apoptotic pathway that signals via casp-8.	ammonium ferrous sulfate	107-110	caspase 8	Homo sapiens	169-175
9988752-6	1999	However, Z-VAD.FMK inhibits chemical-induced apoptosis at a stage after commitment to cell death by inhibiting the initiator caspase-9 and the resultant postmitochondrial activation of effector caspases.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	9-18	caspase 8	Homo sapiens	194-202
10050884-5	1999	Apoptosis depended on mitochondrial permeability transition and activation of caspases, since the mitochondrion-specific inhibitor bongkrekic acid and the caspase inhibitor zVAD-fmk almost completely abrogated apoptosis.	Bongkrekic Acid	131-146	caspase 8	Homo sapiens	78-86
10050884-5	1999	Apoptosis depended on mitochondrial permeability transition and activation of caspases, since the mitochondrion-specific inhibitor bongkrekic acid and the caspase inhibitor zVAD-fmk almost completely abrogated apoptosis.	Bongkrekic Acid	131-146	caspase 8	Homo sapiens	78-85
10197541-0	1999	Caspase-8 is required for cell death induced by expanded polyglutamine repeats.	polyglutamine	57-70	caspase 8	Homo sapiens	0-9
10197541-3	1999	Inhibition of caspase-8 blocked polyglutamine-induced cell death.	polyglutamine	32-45	caspase 8	Homo sapiens	14-23
10050884-5	1999	Apoptosis depended on mitochondrial permeability transition and activation of caspases, since the mitochondrion-specific inhibitor bongkrekic acid and the caspase inhibitor zVAD-fmk almost completely abrogated apoptosis.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	173-181	caspase 8	Homo sapiens	78-85
9880544-5	1999	BTK associates with Fas via its kinase and PH domains and prevents the FAS-FADD interaction, which is essential for the recruitment and activation of FLICE by Fas during the apoptotic signal.	ammonium ferrous sulfate	20-23	caspase 8	Homo sapiens	150-155
9973490-9	1999	In addition, there was an early and increased activation of caspases (caspase-8 and caspase-3) involved in TNFR/TNF signaling pathway, as evident by early cleavage of caspase-8, poly(ADP-ribose) polymerase (PARP), and caspase-3 substrate DEVD-p-nitroamilide NA.	devd-p-nitroamilide	238-257	caspase 8	Homo sapiens	60-68
9973490-9	1999	In addition, there was an early and increased activation of caspases (caspase-8 and caspase-3) involved in TNFR/TNF signaling pathway, as evident by early cleavage of caspase-8, poly(ADP-ribose) polymerase (PARP), and caspase-3 substrate DEVD-p-nitroamilide NA.	devd-p-nitroamilide	238-257	caspase 8	Homo sapiens	70-79
9973403-7	1999	Overexpression of TAL accelerated Fas-induced mitochondrial ROI production, Deltapsim elevation, activation of caspase-8 and caspase-3, proteolysis of poly(A)DP-ribose polymerase, and PS externalization.	ammonium ferrous sulfate	34-37	caspase 8	Homo sapiens	111-120
9891071-4	1999	The addition of purified caspase 3, caspase 7, or caspase 8 to the cytosolic extract from Bcl-2:HL-60 cells, however, restored Cif activity, demonstrating that the inhibition of Cif by Bcl-2 overexpression could be overcome by activated caspases.	cif	127-130	caspase 8	Homo sapiens	50-59
9891071-4	1999	The addition of purified caspase 3, caspase 7, or caspase 8 to the cytosolic extract from Bcl-2:HL-60 cells, however, restored Cif activity, demonstrating that the inhibition of Cif by Bcl-2 overexpression could be overcome by activated caspases.	cif	178-181	caspase 8	Homo sapiens	50-59
9891071-5	1999	Moreover, the addition of purified caspases to cytosolic extracts prepared from parental HL-60 cells was also sufficient to cause Cif activation, suggesting that caspases might be required for Cif activation.	cif	130-133	caspase 8	Homo sapiens	35-43
9891071-5	1999	Moreover, the addition of purified caspases to cytosolic extracts prepared from parental HL-60 cells was also sufficient to cause Cif activation, suggesting that caspases might be required for Cif activation.	cif	130-133	caspase 8	Homo sapiens	162-170
9891071-6	1999	Consistent with these observations, Fas-induced apoptosis in Jurkat cells resulted in caspase 8 activation and subsequently in activation of Cif.	ammonium ferrous sulfate	36-39	caspase 8	Homo sapiens	86-95
9891071-8	1999	Taken together, these results indicate that Cif is identical to Bid and that it can be inhibited by Bcl-2 and activated by caspases.	cif	44-47	caspase 8	Homo sapiens	123-131
9880544-5	1999	BTK associates with Fas via its kinase and PH domains and prevents the FAS-FADD interaction, which is essential for the recruitment and activation of FLICE by Fas during the apoptotic signal.	ammonium ferrous sulfate	159-162	caspase 8	Homo sapiens	150-155
10022243-1	1998	Apoptosis, induced in human monocytic THP.1 cells by etoposide and N-tosyl-L-phenylalanyl chloromethyl ketone, was accompanied by the processing/activation of caspases, externalisation of phosphatidylserine (PS) and reduction in mitochondrial membrane potential (delta psi(m)).	Etoposide	53-62	caspase 8	Homo sapiens	159-167
9847376-3	1999	Incubation of infected cells with the peptide inhibitor z-VAD-fmk abrogated SV-induced apoptosis, indicating that proteases of the caspase family were involved.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	56-65	caspase 8	Homo sapiens	131-138
10022243-1	1998	Apoptosis, induced in human monocytic THP.1 cells by etoposide and N-tosyl-L-phenylalanyl chloromethyl ketone, was accompanied by the processing/activation of caspases, externalisation of phosphatidylserine (PS) and reduction in mitochondrial membrane potential (delta psi(m)).	Tosylphenylalanyl Chloromethyl Ketone	67-109	caspase 8	Homo sapiens	159-167
10022243-3	1998	The caspase inhibitor, benzyloxycarbonyl-Val-Ala-Asp (OMe) fluoromethyl ketone (Z-VAD.fmk) blocked the activation of caspases, PS exposure and the reduction in delta psi(m) as well as the morphological changes associated with apoptosis but it did not inhibit the release of mitochondrial cytochrome c.	benzyloxycarbonyl-val-ala-asp (ome) fluoromethyl ketone	23-78	caspase 8	Homo sapiens	4-11
10022243-3	1998	The caspase inhibitor, benzyloxycarbonyl-Val-Ala-Asp (OMe) fluoromethyl ketone (Z-VAD.fmk) blocked the activation of caspases, PS exposure and the reduction in delta psi(m) as well as the morphological changes associated with apoptosis but it did not inhibit the release of mitochondrial cytochrome c.	benzyloxycarbonyl-val-ala-asp (ome) fluoromethyl ketone	23-78	caspase 8	Homo sapiens	117-125
9852046-3	1998	In isolated mitochondria, BetA directly induces loss of transmembrane potential independent of a benzyloxycarbonyl-Val-Ala-Asp-fluoromethyl ketone-inhibitable caspase.	val-ala-asp-fluoromethyl ketone	115-146	caspase 8	Homo sapiens	159-166
10022243-3	1998	The caspase inhibitor, benzyloxycarbonyl-Val-Ala-Asp (OMe) fluoromethyl ketone (Z-VAD.fmk) blocked the activation of caspases, PS exposure and the reduction in delta psi(m) as well as the morphological changes associated with apoptosis but it did not inhibit the release of mitochondrial cytochrome c.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	80-89	caspase 8	Homo sapiens	4-11
10022243-3	1998	The caspase inhibitor, benzyloxycarbonyl-Val-Ala-Asp (OMe) fluoromethyl ketone (Z-VAD.fmk) blocked the activation of caspases, PS exposure and the reduction in delta psi(m) as well as the morphological changes associated with apoptosis but it did not inhibit the release of mitochondrial cytochrome c.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	80-89	caspase 8	Homo sapiens	117-125
9837855-5	1998	In addition, cell treatment with GSH impaired cytochrome c release into the cytosol and degradation of caspase-8 occurring during cell death.	Glutathione	33-36	caspase 8	Homo sapiens	103-112
9865748-0	1998	Fas-mediated apoptosis in human prostatic carcinoma cell lines occurs via activation of caspase-8 and caspase-7.	ammonium ferrous sulfate	0-3	caspase 8	Homo sapiens	88-97
9865748-6	1998	In experiments with caspase inhibitors we show that Fas-mediated apoptosis in PC3 is mainly executed by the caspase-3 subfamily, but another member(s) of the caspase family may be involved in Fas-mediated apoptosis in ALVA31, DU145, and JCA1.	ammonium ferrous sulfate	52-55	caspase 8	Homo sapiens	20-27
9865748-6	1998	In experiments with caspase inhibitors we show that Fas-mediated apoptosis in PC3 is mainly executed by the caspase-3 subfamily, but another member(s) of the caspase family may be involved in Fas-mediated apoptosis in ALVA31, DU145, and JCA1.	ammonium ferrous sulfate	52-55	caspase 8	Homo sapiens	108-115
9865748-6	1998	In experiments with caspase inhibitors we show that Fas-mediated apoptosis in PC3 is mainly executed by the caspase-3 subfamily, but another member(s) of the caspase family may be involved in Fas-mediated apoptosis in ALVA31, DU145, and JCA1.	ammonium ferrous sulfate	192-195	caspase 8	Homo sapiens	20-27
9865748-8	1998	The activated form of caspase-8 was detected in DU145 only after 4 h of simultaneous treatment with CHX and anti-Fas mAb, whereas in PC3 caspase-8 was found to be activated after 1 h of Fas-ligation.	ammonium ferrous sulfate	113-116	caspase 8	Homo sapiens	22-31
9829999-8	1998	The cowpox serpin CrmA is a potent (Ki &lt; 20 nM) and selective inhibitor of Group I caspases (caspase-1, -4, and -5) and most Group III caspases (caspase-8, -9, and -10), suggesting that this virus facilitates infection through inhibition of both apoptosis and the host inflammatory response.	crma	18-22	caspase 8	Homo sapiens	148-170
9830064-6	1998	In these cells, TRAIL-induced cell death and activation of the apoptosis executioner caspase-8 (FLICE/MACH) and caspase-3 (YAMA, CPP-32, Apopain), that belong to caspase subfamily of cysteine proteases, were abrogated, whereas JNK activation remained unaffected and was still sensitive toward z-VAD-fmk.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	293-302	caspase 8	Homo sapiens	85-94
9830064-6	1998	In these cells, TRAIL-induced cell death and activation of the apoptosis executioner caspase-8 (FLICE/MACH) and caspase-3 (YAMA, CPP-32, Apopain), that belong to caspase subfamily of cysteine proteases, were abrogated, whereas JNK activation remained unaffected and was still sensitive toward z-VAD-fmk.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	293-302	caspase 8	Homo sapiens	85-92
9804161-10	1998	The caspase-3 inhibitor DEVD-fmk blocked caspase-8 and Bap31 cleavage suggesting that caspase-8 and Bap31 processing occur downstream of caspase-3 activation in PDT-induced apoptosis.	devd-fmk	24-32	caspase 8	Homo sapiens	41-50
9840917-3	1998	In this report, we show that Fas activation induced the processing of caspase 8 in Jurkat cells with a time frame similar to the activation of caspase 3 and the proteolysis of nuclear proteins.	ammonium ferrous sulfate	29-32	caspase 8	Homo sapiens	70-79
9840917-6	1998	Furthermore, although caspase 8 was recruited to Fas upon Fas activation in the parental Jurkat cells, the recruitment of caspase 8 to Fas was inhibited in the transformants overexpressing Bcl-2.	ammonium ferrous sulfate	49-52	caspase 8	Homo sapiens	22-31
9840917-6	1998	Furthermore, although caspase 8 was recruited to Fas upon Fas activation in the parental Jurkat cells, the recruitment of caspase 8 to Fas was inhibited in the transformants overexpressing Bcl-2.	ammonium ferrous sulfate	58-61	caspase 8	Homo sapiens	22-31
9840917-6	1998	Furthermore, although caspase 8 was recruited to Fas upon Fas activation in the parental Jurkat cells, the recruitment of caspase 8 to Fas was inhibited in the transformants overexpressing Bcl-2.	ammonium ferrous sulfate	58-61	caspase 8	Homo sapiens	22-31
9840917-7	1998	These results suggest that Bcl-2 inhibits Fas-induced apoptosis by preventing the formation of the death-inducing signaling complex that is composed of Fas, FADD/MORT1, and caspase 8.	ammonium ferrous sulfate	42-45	caspase 8	Homo sapiens	173-182
9804161-10	1998	The caspase-3 inhibitor DEVD-fmk blocked caspase-8 and Bap31 cleavage suggesting that caspase-8 and Bap31 processing occur downstream of caspase-3 activation in PDT-induced apoptosis.	devd-fmk	24-32	caspase 8	Homo sapiens	86-95
10203687-5	1998	Apoptosis depended on activation of caspases (interleukin 1beta-converting enzyme/Ced-3 like proteases) as it was almost completely abrograted by the broad range caspase inhibitor benzyloxycarbonyl-Val-Ala-Asp-fluoromethyl ketone.	Caspase Inhibitor VI	180-229	caspase 8	Homo sapiens	36-44
9766678-4	1998	After Doxo treatment, enhanced CD95/CD95-L expression and caspase-8 activation were not blocked by Bcl-2 or Bcl-X(L) and were found in cells with a mitochondrial transmembrane potential (delta psi(m)) that was still normal (delta psi(m)high cells).	Doxorubicin	6-10	caspase 8	Homo sapiens	58-67
9766678-6	1998	Mitochondria from cells treated with either Doxo or Bet A induced cleavage of both caspase-8 and caspase-3 in cytosolic extracts.	Doxorubicin	44-48	caspase 8	Homo sapiens	83-92
9766678-6	1998	Mitochondria from cells treated with either Doxo or Bet A induced cleavage of both caspase-8 and caspase-3 in cytosolic extracts.	betulinic acid	52-57	caspase 8	Homo sapiens	83-92
10203695-3	1998	Here, we report that caspase 8 and 3 activation, poly(ADP-ribose)polymerase cleavage and apoptosis are inhibited by the lipoxygenase inhibitor, nordihydroguaretic acid (NDGA), or ectopic expression of crm-A or bcl-2.	Masoprocol	144-167	caspase 8	Homo sapiens	21-30
9694885-10	1998	Our results demonstrate that whereas Fas-mediated activation of caspase 3 requires an upstream caspase activity that is zVAD-fmk-sensitive, the initial cleavage of caspase 3 during granule-mediated cell death is insensitive to zVAD-fmk, suggesting that caspase 3 is cleaved directly by granzyme B in vivo.	ammonium ferrous sulfate	37-40	caspase 8	Homo sapiens	64-71
10203695-3	1998	Here, we report that caspase 8 and 3 activation, poly(ADP-ribose)polymerase cleavage and apoptosis are inhibited by the lipoxygenase inhibitor, nordihydroguaretic acid (NDGA), or ectopic expression of crm-A or bcl-2.	Masoprocol	169-173	caspase 8	Homo sapiens	21-30
9730899-0	1998	Differential regulation and ATP requirement for caspase-8 and caspase-3 activation during CD95- and anticancer drug-induced apoptosis.	Adenosine Triphosphate	28-31	caspase 8	Homo sapiens	48-57
9730899-7	1998	Prevention of ATP production completely inhibited caspase activation and apoptosis in response to chemotherapeutic drugs and staurosporine.	Adenosine Triphosphate	14-17	caspase 8	Homo sapiens	50-57
9730899-7	1998	Prevention of ATP production completely inhibited caspase activation and apoptosis in response to chemotherapeutic drugs and staurosporine.	Staurosporine	125-138	caspase 8	Homo sapiens	50-57
9730899-8	1998	Interestingly, caspase-8, whose function appeared to be restricted to death receptors, was also activated by these drugs under normal conditions, but not after ATP depletion.	Adenosine Triphosphate	160-163	caspase 8	Homo sapiens	15-24
9727492-3	1998	tBID induces first the clustering of mitochondria around the nuclei and release of cytochrome c independent of caspase activity, and then the loss of mitochondrial membrane potential, cell shrinkage, and nuclear condensation in a caspase-dependent fashion.	tBID	0-4	caspase 8	Homo sapiens	111-118
9727492-3	1998	tBID induces first the clustering of mitochondria around the nuclei and release of cytochrome c independent of caspase activity, and then the loss of mitochondrial membrane potential, cell shrinkage, and nuclear condensation in a caspase-dependent fashion.	tBID	0-4	caspase 8	Homo sapiens	230-237
9740801-0	1998	Essential requirement for caspase-8/FLICE in the initiation of the Fas-induced apoptotic cascade.	ammonium ferrous sulfate	67-70	caspase 8	Homo sapiens	26-35
9740801-0	1998	Essential requirement for caspase-8/FLICE in the initiation of the Fas-induced apoptotic cascade.	ammonium ferrous sulfate	67-70	caspase 8	Homo sapiens	36-41
9740801-5	1998	RESULTS: In a genetic screen for essential components of the Fas-mediated apoptotic cascade, we isolated a Jurkat T lymphocyte cell line deficient in caspase-8 that was completely resistant to Fas-induced apoptosis.	ammonium ferrous sulfate	61-64	caspase 8	Homo sapiens	150-159
9740801-5	1998	RESULTS: In a genetic screen for essential components of the Fas-mediated apoptotic cascade, we isolated a Jurkat T lymphocyte cell line deficient in caspase-8 that was completely resistant to Fas-induced apoptosis.	ammonium ferrous sulfate	193-196	caspase 8	Homo sapiens	150-159
9740801-7	1998	Fas activation of multiple caspases and of the stress kinase p38 and c-Jun NH2-terminal kinase (JNK) was completely blocked in the caspase-8-deficient cell line.	ammonium ferrous sulfate	0-3	caspase 8	Homo sapiens	27-35
9740801-7	1998	Fas activation of multiple caspases and of the stress kinase p38 and c-Jun NH2-terminal kinase (JNK) was completely blocked in the caspase-8-deficient cell line.	ammonium ferrous sulfate	0-3	caspase 8	Homo sapiens	131-140
9740801-9	1998	CONCLUSIONS: This study provides the first genetic evidence that caspase-8 occupies an essential and apical position in the Fas signaling pathway and suggests that caspase-8 may participate broadly in multiple apoptotic pathways.	ammonium ferrous sulfate	124-127	caspase 8	Homo sapiens	65-74
9740801-9	1998	CONCLUSIONS: This study provides the first genetic evidence that caspase-8 occupies an essential and apical position in the Fas signaling pathway and suggests that caspase-8 may participate broadly in multiple apoptotic pathways.	ammonium ferrous sulfate	124-127	caspase 8	Homo sapiens	164-173
9694885-3	1998	Both pathways involve the activation of a family of cysteine proteinases, the caspases, that cleave substrates at aspartic acid and are themselves activated by cleavage at internal aspartate residues.	Aspartic Acid	114-127	caspase 8	Homo sapiens	78-86
9694885-3	1998	Both pathways involve the activation of a family of cysteine proteinases, the caspases, that cleave substrates at aspartic acid and are themselves activated by cleavage at internal aspartate residues.	Aspartic Acid	181-190	caspase 8	Homo sapiens	78-86
9606216-0	1998	E1B 19K inhibits Fas-mediated apoptosis through FADD-dependent sequestration of FLICE.	ammonium ferrous sulfate	17-20	caspase 8	Homo sapiens	80-85
9606216-8	1998	Thus, E1B 19K may inhibit Fas-mediated cell death downstream of FADD recruitment of FLICE but upstream of FLICE activation by disrupting FADD oligomerization and sequestering an essential component of the DISC.	ammonium ferrous sulfate	26-29	caspase 8	Homo sapiens	84-89
9633517-6	1998	Initial studies on proteases activation tend to exclude a direct role of ICE and CPP32 in the induction of apoptosis in these cells and show a paclitaxel-dependent increase in FLICE levels, whose biological relevance is however at present not defined.	Paclitaxel	143-153	caspase 8	Homo sapiens	176-181
9426218-6	1997	Moreover, the subsite contacts between caspase-8 and the covalently linked inhibitor, Ac-DEVD-aldehyde, are only slightly different from those seen in the caspase-3 enzyme/inhibitor complex.	ac-devd-aldehyde	86-102	caspase 8	Homo sapiens	39-48
9654089-2	1998	In apoptosis triggered by Fas, a subset of cysteine proteases designated caspases is activated, playing a central role as effector molecules.	ammonium ferrous sulfate	26-29	caspase 8	Homo sapiens	73-81
9654089-3	1998	Among these caspases, human caspase-8 (FLICE/MACH/Mch5) has been isolated and shown to be indispensable for Fas-mediated apoptotic signaling.	ammonium ferrous sulfate	108-111	caspase 8	Homo sapiens	12-20
9654089-3	1998	Among these caspases, human caspase-8 (FLICE/MACH/Mch5) has been isolated and shown to be indispensable for Fas-mediated apoptotic signaling.	ammonium ferrous sulfate	108-111	caspase 8	Homo sapiens	28-37
9654089-3	1998	Among these caspases, human caspase-8 (FLICE/MACH/Mch5) has been isolated and shown to be indispensable for Fas-mediated apoptotic signaling.	ammonium ferrous sulfate	108-111	caspase 8	Homo sapiens	39-44
9654089-3	1998	Among these caspases, human caspase-8 (FLICE/MACH/Mch5) has been isolated and shown to be indispensable for Fas-mediated apoptotic signaling.	ammonium ferrous sulfate	108-111	caspase 8	Homo sapiens	50-54
9541007-8	1998	Z-IETD-FMK, which inhibits caspase 8/FLICE also inhibited Sph/DMS induced apoptosis with no inhibition of apoptosis induced by either ceramide.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	0-10	caspase 8	Homo sapiens	27-36
9541007-8	1998	Z-IETD-FMK, which inhibits caspase 8/FLICE also inhibited Sph/DMS induced apoptosis with no inhibition of apoptosis induced by either ceramide.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	0-10	caspase 8	Homo sapiens	37-42
9541007-8	1998	Z-IETD-FMK, which inhibits caspase 8/FLICE also inhibited Sph/DMS induced apoptosis with no inhibition of apoptosis induced by either ceramide.	Sphingosine	58-61	caspase 8	Homo sapiens	27-36
9541007-8	1998	Z-IETD-FMK, which inhibits caspase 8/FLICE also inhibited Sph/DMS induced apoptosis with no inhibition of apoptosis induced by either ceramide.	Sphingosine	58-61	caspase 8	Homo sapiens	37-42
9541007-8	1998	Z-IETD-FMK, which inhibits caspase 8/FLICE also inhibited Sph/DMS induced apoptosis with no inhibition of apoptosis induced by either ceramide.	dms	62-65	caspase 8	Homo sapiens	27-36
9541007-8	1998	Z-IETD-FMK, which inhibits caspase 8/FLICE also inhibited Sph/DMS induced apoptosis with no inhibition of apoptosis induced by either ceramide.	dms	62-65	caspase 8	Homo sapiens	37-42
9541007-9	1998	Together, these data indicate that Sph/DMS act independently from ceramide in the apoptosis pathway and further suggest that Sph/DMS act earlier in the pathway than ceramide and are involved upstream of even the early proteases, whereas the point of action for ceramide is downstream of the early proteases but upstream from the late caspases.	Ceramides	165-173	caspase 8	Homo sapiens	334-342
9541007-9	1998	Together, these data indicate that Sph/DMS act independently from ceramide in the apoptosis pathway and further suggest that Sph/DMS act earlier in the pathway than ceramide and are involved upstream of even the early proteases, whereas the point of action for ceramide is downstream of the early proteases but upstream from the late caspases.	Ceramides	165-173	caspase 8	Homo sapiens	334-342
9446604-1	1998	The assembly of the CD-95 (Fas/Apo-1) receptor death-inducing signaling complex occurs in a hierarchical manner; the death domain of CD-95 binds to the corresponding domain in the adapter molecule Fas-associated death domain (FADD) Mort-1, which in turn recruits the zymogen form of the death protease caspase-8 (FLICE/Mach-1) by a homophilic interaction involving the death effector domains.	ammonium ferrous sulfate	27-30	caspase 8	Homo sapiens	302-311
9446604-1	1998	The assembly of the CD-95 (Fas/Apo-1) receptor death-inducing signaling complex occurs in a hierarchical manner; the death domain of CD-95 binds to the corresponding domain in the adapter molecule Fas-associated death domain (FADD) Mort-1, which in turn recruits the zymogen form of the death protease caspase-8 (FLICE/Mach-1) by a homophilic interaction involving the death effector domains.	ammonium ferrous sulfate	27-30	caspase 8	Homo sapiens	313-318
9446604-7	1998	Cells transfected with Fpk3FLICE underwent apoptosis after exposure to FK1012H2; (ii) the creation of a nonprocessable zymogen form of FLICE that retained low but detectable protease activity.	FK 1012	71-79	caspase 8	Homo sapiens	27-32
14646514-0	1998	The anti-cancer drug etoposide can induce caspase-8 processing and apoptosis in the absence of CD95 receptor-ligand interaction.	Etoposide	21-30	caspase 8	Homo sapiens	42-51
14646514-2	1998	We find that, in Jurkat T cells, the DNA damaging anti-cancer drug etoposide induces apoptosis and, surprisingly, processing of caspase-8.	Etoposide	67-76	caspase 8	Homo sapiens	128-137
14646514-6	1998	Apparently, in Jurkat cells, etoposide can induce caspase-8 processing and apoptosis in a CD95-independent fashion.	Etoposide	29-38	caspase 8	Homo sapiens	50-59
9743944-4	1998	Drug-induced apoptosis critically depends on activation of caspases since apoptosis is almost completely abrogated by the caspase inhibitor zVAD-fmk.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	140-148	caspase 8	Homo sapiens	59-67
9743944-4	1998	Drug-induced apoptosis critically depends on activation of caspases since apoptosis is almost completely abrogated by the caspase inhibitor zVAD-fmk.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	140-148	caspase 8	Homo sapiens	59-66
9586636-5	1998	We mapped the effect of Toso to inhibition of caspase-8 processing, the most upstream caspase activity in Fas-mediated signaling, potentially through activation of cFLIP.	toso	24-28	caspase 8	Homo sapiens	46-55
9586636-5	1998	We mapped the effect of Toso to inhibition of caspase-8 processing, the most upstream caspase activity in Fas-mediated signaling, potentially through activation of cFLIP.	toso	24-28	caspase 8	Homo sapiens	46-53
9190889-0	1997	Affinity labeling displays the stepwise activation of ICE-related proteases by Fas, staurosporine, and CrmA-sensitive caspase-8.	crma	103-107	caspase 8	Homo sapiens	118-127
9354463-3	1997	BA-induced apoptosis was independent of CD95-ligand/receptor interaction and accumulation of wild-type p53 protein, but it critically depended on activation of caspases (interleukin 1beta-converting enzyme/Ced-3-like proteases).	betulinic acid	0-2	caspase 8	Homo sapiens	160-168
9354463-5	1997	The broad-spectrum peptide inhibitor benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone, which blocked cleavage of FLICE and PARP, also completely abrogated BA-triggered apoptosis.	Caspase Inhibitor VI	37-85	caspase 8	Homo sapiens	113-118
9354463-5	1997	The broad-spectrum peptide inhibitor benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone, which blocked cleavage of FLICE and PARP, also completely abrogated BA-triggered apoptosis.	betulinic acid	155-157	caspase 8	Homo sapiens	113-118
9354463-6	1997	Cleavage of caspases was preceded by disturbance of mitochondrial membrane potential and by generation of reactive oxygen species.	Reactive Oxygen Species	106-129	caspase 8	Homo sapiens	12-20
9354463-8	1997	This suggested that mitochondrial alterations were involved in BA-induced activation of caspases.	betulinic acid	63-65	caspase 8	Homo sapiens	88-96
9354463-0	1997	Betulinic acid triggers CD95 (APO-1/Fas)- and p53-independent apoptosis via activation of caspases in neuroectodermal tumors.	betulinic acid	0-14	caspase 8	Homo sapiens	90-98
9190889-3	1997	YV(bio)KD-aomk identified six distinct polypeptides corresponding to active caspases in Fas-stimulated Jurkat T cells.	ammonium ferrous sulfate	88-91	caspase 8	Homo sapiens	76-84
9190889-9	1997	Overall, these findings provide evidence that caspase-8, a CrmA-sensitive protease, is responsible for initiating the stepwise activation of multiple caspases in Fas-stimulated cells.	ammonium ferrous sulfate	162-165	caspase 8	Homo sapiens	46-55
9190889-9	1997	Overall, these findings provide evidence that caspase-8, a CrmA-sensitive protease, is responsible for initiating the stepwise activation of multiple caspases in Fas-stimulated cells.	ammonium ferrous sulfate	162-165	caspase 8	Homo sapiens	150-158
8681377-3	1996	FLICE binds to the death effector domain of FADD and upon overexpression induces apoptosis that is blocked by the ICE family inhibitors, CrmA and z-VAD-fmk.	crma	137-141	caspase 8	Homo sapiens	0-5
9184224-10	1997	Activation of FLICE is blocked by the peptide inhibitors zVAD-fmk, zDEVD-fmk and zIETD-fmk, but not by crmA or Ac-YVAD-CHO.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	57-65	caspase 8	Homo sapiens	14-19
9184224-10	1997	Activation of FLICE is blocked by the peptide inhibitors zVAD-fmk, zDEVD-fmk and zIETD-fmk, but not by crmA or Ac-YVAD-CHO.	benzoylcarbonyl-aspartyl-glutamyl-valyl-aspartyl-fluoromethyl ketone	67-76	caspase 8	Homo sapiens	14-19
9184224-10	1997	Activation of FLICE is blocked by the peptide inhibitors zVAD-fmk, zDEVD-fmk and zIETD-fmk, but not by crmA or Ac-YVAD-CHO.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	81-90	caspase 8	Homo sapiens	14-19
8681377-3	1996	FLICE binds to the death effector domain of FADD and upon overexpression induces apoptosis that is blocked by the ICE family inhibitors, CrmA and z-VAD-fmk.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	146-155	caspase 8	Homo sapiens	0-5
33812418-19	2021	The inhibitory effect of YX-18 on the proliferation of Burkitt lymphoma cells may be related with the effect of Caspase apoptosis pathway, the proliferation and apoptosis-related molecules, such as C-MYC and Ki-67, and also to the inhibition of NF-kappaB pathway.	yx-18	25-30	caspase 8	Homo sapiens	112-119
33921647-7	2021	The specific inhibitors of p-JNK1/2 also reduced platyphyllenone-induced cleavage of PARP, caspase-3, and caspase -8, LC3-II and p62 protein expression.	PLATYPHYLLENONE	49-64	caspase 8	Homo sapiens	106-116
33801204-9	2021	Activation of these caspases were also confirmed by western blotting in which significant levels of cleaved forms of caspase 3, caspase 8, and PARP were detected in HOEA-treated U937 cells.	hoea	165-169	caspase 8	Homo sapiens	128-137
33800294-0	2021	Polymorphisms in the Gene Encoding Caspase 8 May Predict the Response to First-Line Platinum-Based Chemotherapy in Locally Advanced or Advanced Non-Small-Cell Lung Cancer.	Platinum	84-92	caspase 8	Homo sapiens	35-44
33763175-6	2021	According to the results of the apoptosis assay, a farrerol pretreatment decreased the protein expression of the Bax/Bcl-2, cleaved caspase-3, PARP, caspase-8, and caspase-9 proteins.	farrerol	51-59	caspase 8	Homo sapiens	149-158
33770100-3	2021	Here we show that TRAIL and the Smac mimetic LCL161 induce non-canonical NF-kappaB and IFN signaling in ER-positive MCF-7 cells and in CAMA-1 breast cancer cells when apoptosis is blocked by caspase inhibition.	LCL161	45-51	caspase 8	Homo sapiens	191-198
33804714-3	2021	Accordingly, the transcript levels of BAX, CASPASE-8, and CASPASE-3 in the cells treated with AI-EtE at IC50 dose were 1.55-, 1.62-, and 2.45-fold higher than those in the control cells, respectively.	ai-ete	94-100	caspase 8	Homo sapiens	43-52
33806566-0	2021	Betulinic Acid Restricts Human Bladder Cancer Cell Proliferation In Vitro by Inducing Caspase-Dependent Cell Death and Cell Cycle Arrest, and Decreasing Metastatic Potential.	betulinic acid	0-14	caspase 8	Homo sapiens	86-93
33806566-8	2021	However, pre-treatment of pan-caspase inhibitor markedly suppressed BA-induced apoptosis.	betulinic acid	68-70	caspase 8	Homo sapiens	30-37
33806566-12	2021	Furthermore, BA-induced apoptosis is regulated by caspase-dependent and ROS-independent pathways, and these results provide the underlying anti-proliferative molecular mechanism of BA in human bladder cancer cells.	betulinic acid	13-15	caspase 8	Homo sapiens	50-57
33817182-5	2019	Accordingly, upon ANDR treatment, the expression of caspase-8 was increased, whereas no significant induction of caspase-1 expression was observed.	andrographolide	18-22	caspase 8	Homo sapiens	52-61
33000266-12	2020	Additionally, the mRNA and protein levels of apoptosis-associated proteins (Fas, FADD, caspase-8 and caspase-3) and E-cadherin in HCT-116 cells were upregulated following treatment with curcumin in a dose-dependent manner.	Curcumin	186-194	caspase 8	Homo sapiens	87-96
22951985-7	2012	Exposure to BP did not increase expression of CD95, but led to augmented activation of caspase-8.	Benzo(a)pyrene	12-14	caspase 8	Homo sapiens	87-96
21380726-4	2011	Trichostatin A induced nuclear damage, decrease in Bid and Bcl-2 protein levels, increase in Bax levels, cytochrome c release, activation of caspases (8, 9, and 3) and increase in tumor suppressor p53 levels.	trichostatin A	0-14	caspase 8	Homo sapiens	141-149
23737847-0	2013	Inclusion Complex of Zerumbone with Hydroxypropyl- beta -Cyclodextrin Induces Apoptosis in Liver Hepatocellular HepG2 Cells via Caspase 8/BID Cleavage Switch and Modulating Bcl2/Bax Ratio.	zerumbone	21-30	caspase 8	Homo sapiens	128-137
23737847-0	2013	Inclusion Complex of Zerumbone with Hydroxypropyl- beta -Cyclodextrin Induces Apoptosis in Liver Hepatocellular HepG2 Cells via Caspase 8/BID Cleavage Switch and Modulating Bcl2/Bax Ratio.	2-Hydroxypropyl-beta-cyclodextrin	36-69	caspase 8	Homo sapiens	128-137
21380726-7	2011	Akt inhibitor may potentiate the apoptotic effect of trichostatin A on ovarian carcinoma cell lines by increasing the activation of the caspase-8-dependent pathway and the mitochondria-mediated cell death pathway, leading to caspase activation.	trichostatin A	53-67	caspase 8	Homo sapiens	136-145
34876259-0	2022	Corrigendum to "Dihydroartemisinin mediating PKM2-caspase-8/3-GSDME axis for pyroptosis in esophageal squamous cell carcinoma" (Chem.	artenimol	16-34	caspase 8	Homo sapiens	50-61
16287099-10	2006	MG132 plus rhTRAIL enhanced caspase 8 and caspase 3 activation and concomitant cleavage of X-linked inhibitor of apoptosis (XIAP), particularly in HeLa.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	caspase 8	Homo sapiens	28-37
34906906-7	2022	The stimulation of TLR3 or TLR9 and TAL treatment caused significantly more apoptosis in TNBC cells through the over-expression of caspase-3 and caspase-8.	talazoparib	36-39	caspase 8	Homo sapiens	145-154
34861471-4	2022	Arsenite exposure resulted in dose-dependent growth inhibition, which was associated with apoptosis, as demonstrated by depolarized mitochondrial membrane potential and cleavage of caspase-8, caspase-3, PARP-1, and Bax.	arsenite	0-8	caspase 8	Homo sapiens	181-190
34609723-7	2022	RESULTS: ATG5, BCL2L1, CASP3, CASP8, GAPDH were identified as key ARGs in our research.	args	66-70	caspase 8	Homo sapiens	30-35
34906906-4	2022	TAL alone and the combination of TAL with Poly I:C or CpG-ODN induced cell death were analyzed by water-soluble tetrazolium salt 1 (WST-1), Annexin V analysis, acridine orange staining and mRNA levels of caspase-3 and caspase-8 in HCC1937 and HCC1937-R (TAL resistant) TNBC cells.	talazoparib	33-36	caspase 8	Homo sapiens	218-227
34906906-4	2022	TAL alone and the combination of TAL with Poly I:C or CpG-ODN induced cell death were analyzed by water-soluble tetrazolium salt 1 (WST-1), Annexin V analysis, acridine orange staining and mRNA levels of caspase-3 and caspase-8 in HCC1937 and HCC1937-R (TAL resistant) TNBC cells.	Poly I	42-48	caspase 8	Homo sapiens	218-227
34588172-5	2021	Either inhibition or genetic depletion of CASP-8 decreased the CRBN cleavage upon Btz treatment, which could potentiate the anti-myeloma activity of IMiD lenalidomide (Len).	Bortezomib	82-85	caspase 8	Homo sapiens	42-48
34959709-10	2021	Thus, co-treatment with MLPE and PFT-alpha significantly increased caspase-3, caspase-8, and cytochrome c release, indicating that p53 deficiency caused the apoptosis.	pifithrin	33-42	caspase 8	Homo sapiens	78-87
34599991-5	2021	Moreover, the structures formed in the presence of SA recovered the viability of neuron-like cells (SH-SY5Y) through regulation of endoplasmic reticulum stress signaling pathway by downregulation of ATF-6, caspase-8 and caspase-3 mRNA.	syringic acid	51-53	caspase 8	Homo sapiens	206-215
34878630-7	2022	Transient or permanent MEN1 inactivation caused a decrease of caspase 8 activity in BON1, HPSC2.2 cells and MEN1-/- MEFs treated with staurosporine.	Staurosporine	134-147	caspase 8	Homo sapiens	62-71
34938196-9	2021	The expressions of Bax, Bcl-2, caspase-9, caspase-8, and cleaved caspase-3 proteins were evaluated to investigate the apoptotic mechanism of BBTPP-SDT.	bbtpp	141-146	caspase 8	Homo sapiens	42-51
34655567-0	2021	Dihydroartemisinin mediating PKM2-caspase-8/3-GSDME axis for pyroptosis in esophageal squamous cell carcinoma.	artenimol	0-18	caspase 8	Homo sapiens	34-45
34655567-4	2021	After applying DHA treatment to ESCC, we found that some dying cells exhibited the characteristic morphology of pyroptosis, such as blowing large bubbles from the cell membrane, accompanied by downregulation of pyruvate kinase isoform M2 (PKM2), activation of caspase-8/3, and production of GSDME-NT.	artenimol	15-18	caspase 8	Homo sapiens	260-271
34655567-6	2021	Both knockdown of GSDME and application of caspase-8/3 specific inhibitors (z-ITED-FMK/Ac-DEVD-CHO) significantly inhibited DHA-induced pyroptosis.	z-ited-fmk	76-86	caspase 8	Homo sapiens	43-54
34655567-6	2021	Both knockdown of GSDME and application of caspase-8/3 specific inhibitors (z-ITED-FMK/Ac-DEVD-CHO) significantly inhibited DHA-induced pyroptosis.	artenimol	124-127	caspase 8	Homo sapiens	43-54
34655567-10	2021	Therefore, the results suggest that DHA can induce pyroptosis of ESCC cells via the PKM2-caspase-8/3-GSDME pathway.	artenimol	36-39	caspase 8	Homo sapiens	89-100
34755444-7	2021	Both flavonoids induced apoptosis, accompanied by activation of caspase-3, caspase-7, caspase-8 and caspase-9.	Flavonoids	5-15	caspase 8	Homo sapiens	86-95
34588172-0	2021	Caspase-8 regulates the anti-myeloma activity of bortezomib and lenalidomide.	Bortezomib	49-59	caspase 8	Homo sapiens	0-9
34588172-0	2021	Caspase-8 regulates the anti-myeloma activity of bortezomib and lenalidomide.	Lenalidomide	64-76	caspase 8	Homo sapiens	0-9
34588172-5	2021	Either inhibition or genetic depletion of CASP-8 decreased the CRBN cleavage upon Btz treatment, which could potentiate the anti-myeloma activity of IMiD lenalidomide (Len).	Lenalidomide	168-171	caspase 8	Homo sapiens	42-48
34588172-6	2021	This work suggests that administration of CASP-8 inhibitors might enhance the overall effectiveness of Btz/Len-based therapeutic treatment for myeloma patients.	Bortezomib	103-106	caspase 8	Homo sapiens	42-48
34588172-6	2021	This work suggests that administration of CASP-8 inhibitors might enhance the overall effectiveness of Btz/Len-based therapeutic treatment for myeloma patients.	Lenalidomide	107-110	caspase 8	Homo sapiens	42-48
34588172-7	2021	Significance Statement Caspase-8 activation upon bortezomib treatment results in the cleavage of cereblon, a substrate receptor of the cullin 4-RING E3 ligase, which is responsible for the degradation of two transcription factors IKZF1 and IKZF3 in the presence of immunomodulatory drugs including lenalidomide.	Bortezomib	49-59	caspase 8	Homo sapiens	23-32
34588172-7	2021	Significance Statement Caspase-8 activation upon bortezomib treatment results in the cleavage of cereblon, a substrate receptor of the cullin 4-RING E3 ligase, which is responsible for the degradation of two transcription factors IKZF1 and IKZF3 in the presence of immunomodulatory drugs including lenalidomide.	Lenalidomide	298-310	caspase 8	Homo sapiens	23-32
34588172-8	2021	The administration of caspase-8 inhibitor may enhance the anti-myeloma activity of the combination therapy with bortezomib and lenalidomide to multiple myeloma.	Bortezomib	112-122	caspase 8	Homo sapiens	22-31
34588172-8	2021	The administration of caspase-8 inhibitor may enhance the anti-myeloma activity of the combination therapy with bortezomib and lenalidomide to multiple myeloma.	Lenalidomide	127-139	caspase 8	Homo sapiens	22-31
34256094-5	2021	Mechanistically, PDT may inhibit pyruvate kinase M2 (PKM2) and consequently, activate caspase-8 and caspase-3, which ultimately releases N-GSDME and triggers pyroptosis in ESCC.	n-gsdme	137-144	caspase 8	Homo sapiens	86-95
34941677-7	2021	As uremic toxins are drivers of inflammation and regulated cell death, we applied a monocyte- and macrophage-like THP-1 model system to demonstrate that the protein-bound uremic toxin indoxyl sulfate (IS) is an inducer of pyroptotic cell death, particularly engaging caspase-4/caspase-5 and to a lesser extent caspase-8 and caspase-1.	Indican	184-199	caspase 8	Homo sapiens	310-319
34839142-7	2021	While ONOO- increase is downstream of caspase-8 activation, it is involved in the upregulation of TMTC2, gene knockdown of which abrogated TRAIL-induced apoptotic execution.	onoo	6-10	caspase 8	Homo sapiens	38-47
34620029-5	2021	In the present paper, we reported the ultrastructural changes in GCTB cells exposed to quercetin and also determined the expression of RIP1K, Caspase 3 and Caspase 8 on the exposed cells.	Quercetin	87-96	caspase 8	Homo sapiens	156-165
34806141-0	2022	Curcumin induces apoptosis through caspase dependent pathway in human colon carcinoma cells.	Curcumin	0-8	caspase 8	Homo sapiens	35-42
34798907-8	2021	RESULTS: Pb was associated with decreased methylation of cg20608990 (CASP8) (FDR = 0.04), and Mn was associated with increased methylation of cg02042823 (A2BP1) in cord blood (FDR = 9.73 x 10-6).	Lead	9-11	caspase 8	Homo sapiens	69-74
34798907-8	2021	RESULTS: Pb was associated with decreased methylation of cg20608990 (CASP8) (FDR = 0.04), and Mn was associated with increased methylation of cg02042823 (A2BP1) in cord blood (FDR = 9.73 x 10-6).	cg20608990	57-67	caspase 8	Homo sapiens	69-74
34425189-4	2021	Further, a series of experiments were performed to measure the markers of intrinsic (Bax, cytochrome c and caspase-9), extrinsic (TNFR, FADR and caspase-8) and endoplasmic reticulum (ER) stress (protein ubiquitylation, calcium flux, Bip-2, CHOP and caspase-12) pathways in DSePA treated cells.	3,3'-diselenodipropionic acid	273-278	caspase 8	Homo sapiens	145-154
34486189-6	2021	Harpagoside prevented Ang II-induced apoptosis via keeping Bax/Bcl-2 balance, decreasing cytochrome c release, and inactivation of caspase-8, caspase-9, and caspase-3 (the mitochondria-dependent and death receptor-mediated apoptosis pathways).	harpagoside	0-11	caspase 8	Homo sapiens	131-140
34769290-10	2021	FLLL32 activates proteins such as caspase-8, caspase-9, caspase-3, PARP, and mitogen-activated protein kinases (MAPKs) in apoptosis-related molecular mechanisms.	FLLL 32	0-6	caspase 8	Homo sapiens	34-43
34337761-7	2021	Docking studies revealed the high binding affinity of Nuatigenin at significant sites with apoptotic proteins Bcl-2, Bax, caspase-3, caspase-8, p53 and apoptosis inducing factor along with cell surface receptors estrogen receptor, projesterone receptor, epidermal growth factor receptor, and human epidermal growth factor receptor-2.	nuatigenin	54-64	caspase 8	Homo sapiens	133-142
34490473-10	2021	In addition, naringenin notably inhibited the proliferation of RCC cells by decreasing Ki67 expression, blocked cell cycle progression in the G2 phase by regulating expression of cell cycle proteins, and increased apoptosis by upregulating caspase-8 expression, downregulating Bcl-2 expression and altering the cellular morphology.	naringenin	13-23	caspase 8	Homo sapiens	240-249
34681898-6	2021	Ardisianone also induced downstream signaling by activating caspase-8 and -3 and degradation in Bid, a caspase-8 substrate.	Ardisianone	0-11	caspase 8	Homo sapiens	60-76
34677776-11	2022	Moreover, SI-WmiRs inhibited pro-apoptotic BAX, Caspase 3 and Caspase 8 gene expression and protein levels to prevent apoptosis of UV-stressed HaCaT cells.	Silicon	10-12	caspase 8	Homo sapiens	62-71
34681913-9	2021	Quercetin also significantly enhanced vorinostat-induced apoptosis, caspase-3, caspase-8, and caspase-9 activity, and the loss of mitochondrial membrane potential.	Quercetin	0-9	caspase 8	Homo sapiens	79-88
34681898-6	2021	Ardisianone also induced downstream signaling by activating caspase-8 and -3 and degradation in Bid, a caspase-8 substrate.	Ardisianone	0-11	caspase 8	Homo sapiens	103-112
34660779-4	2021	Treatment with PAC and ATRA induced cell cycle arrest at the G2/M phase and apoptosis by upregulating p53 and caspase-8 expression and increased the intracellular calcium (Ca2+) level possibly by enhancing Ca2+ uptake via plasma membrane channels.	Paclitaxel	15-18	caspase 8	Homo sapiens	110-119
34660779-4	2021	Treatment with PAC and ATRA induced cell cycle arrest at the G2/M phase and apoptosis by upregulating p53 and caspase-8 expression and increased the intracellular calcium (Ca2+) level possibly by enhancing Ca2+ uptake via plasma membrane channels.	Tretinoin	23-27	caspase 8	Homo sapiens	110-119
34165247-8	2021	Proteins involved in the extrinsic and intrinsic pathways of apoptosis, such as death receptor, caspase-3, caspase-8, caspase-9, and Bcl-2 family proteins (Bax, t-Bid, Bcl-2, and Bcl-xL), were downregulated and upregulated after treatment with luteolin-7-O-glucoside, respectively.	luteolin-7-O-glucoside	244-266	caspase 8	Homo sapiens	107-116
34523215-6	2021	In-vitro investigations revealed that CoCl2 -induced hypoxia triggered activation of caspases, resulting in apoptosis dysfunction in cementoblasts.	cobaltous chloride	38-43	caspase 8	Homo sapiens	85-93
34302634-6	2021	Western blotting, reverse transcription polymerase chain reaction, and protein stability analyses were performed to analyze the effect of lactucin on the expression of apoptosis-related proteins such as B-cell lymphoma 2 (BCL-2) and CFLAR (CASP8 and FADD like apoptosis regulator) long isoform (CFLARL) in Caki-1 human renal cancer cells.	lactucin	138-146	caspase 8	Homo sapiens	240-245
34302634-8	2021	RESULTS: Lactucin treatment induced apoptosis in Caki-1 cells in a dose-dependent manner via activation of the caspase pathway.	lactucin	9-17	caspase 8	Homo sapiens	111-118
34302634-12	2021	CONCLUSIONS: Our study is the first to demonstrate that lactucin-induced apoptosis is mediated by ROS production, which in turn activates the caspase-dependent apoptotic pathway by inhibiting BCL-2 and CFLARL expression in Caki-1 cells.	lactucin	56-64	caspase 8	Homo sapiens	142-149
34302634-12	2021	CONCLUSIONS: Our study is the first to demonstrate that lactucin-induced apoptosis is mediated by ROS production, which in turn activates the caspase-dependent apoptotic pathway by inhibiting BCL-2 and CFLARL expression in Caki-1 cells.	Reactive Oxygen Species	98-101	caspase 8	Homo sapiens	142-149
34314869-4	2021	We examine two important aspects required for clinical application of the biomaterials, if SHH PA suppresses intrinsic (caspase 9) and extrinsic (caspase 8) apoptotic mechanisms, and if suppressing one apoptotic mechanism forces apoptosis to occur via a different mechanism.	Protactinium	95-97	caspase 8	Homo sapiens	146-155
34234270-0	2021	Resveratrol promotes skin wound healing by regulating the miR-212/CASP8 axis.	Resveratrol	0-11	caspase 8	Homo sapiens	66-71
34457060-10	2021	In addition, caspase-8 and -9 inhibitors, respectively, significantly decreased paclitaxel-induced apoptosis.	Paclitaxel	80-90	caspase 8	Homo sapiens	13-29
34482382-0	2021	Non-apoptotic function of caspase-8 confers prostate cancer enzalutamide resistance via NF-kappaB activation.	enzalutamide	60-72	caspase 8	Homo sapiens	26-35
34466155-7	2021	The protein expression levels of cellular FLICE (FADD-like IL-1beta-converting enzyme)-inhibitory protein (c-FLIP)(L) and Bcl-2, which were determined by western blotting, decreased after pioglitazone treatment in Caki cells.	Pioglitazone	188-200	caspase 8	Homo sapiens	42-47
34466155-8	2021	Flow cytometry and western blot analyses demonstrated that pioglitazone-mediated apoptosis was blocked following pretreatment with the pan-caspase inhibitor, z-VAD-fmk, indicating that pioglitazone-induced apoptosis was mediated via a caspase-dependent signaling pathway.	Pioglitazone	59-71	caspase 8	Homo sapiens	139-146
34466155-8	2021	Flow cytometry and western blot analyses demonstrated that pioglitazone-mediated apoptosis was blocked following pretreatment with the pan-caspase inhibitor, z-VAD-fmk, indicating that pioglitazone-induced apoptosis was mediated via a caspase-dependent signaling pathway.	Pioglitazone	59-71	caspase 8	Homo sapiens	235-242
34466155-8	2021	Flow cytometry and western blot analyses demonstrated that pioglitazone-mediated apoptosis was blocked following pretreatment with the pan-caspase inhibitor, z-VAD-fmk, indicating that pioglitazone-induced apoptosis was mediated via a caspase-dependent signaling pathway.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	158-167	caspase 8	Homo sapiens	139-146
34466155-8	2021	Flow cytometry and western blot analyses demonstrated that pioglitazone-mediated apoptosis was blocked following pretreatment with the pan-caspase inhibitor, z-VAD-fmk, indicating that pioglitazone-induced apoptosis was mediated via a caspase-dependent signaling pathway.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	158-167	caspase 8	Homo sapiens	235-242
34466155-8	2021	Flow cytometry and western blot analyses demonstrated that pioglitazone-mediated apoptosis was blocked following pretreatment with the pan-caspase inhibitor, z-VAD-fmk, indicating that pioglitazone-induced apoptosis was mediated via a caspase-dependent signaling pathway.	Pioglitazone	185-197	caspase 8	Homo sapiens	139-146
34466155-8	2021	Flow cytometry and western blot analyses demonstrated that pioglitazone-mediated apoptosis was blocked following pretreatment with the pan-caspase inhibitor, z-VAD-fmk, indicating that pioglitazone-induced apoptosis was mediated via a caspase-dependent signaling pathway.	Pioglitazone	185-197	caspase 8	Homo sapiens	235-242
34466155-11	2021	In conclusion, these findings indicated that pioglitazone-induced apoptosis is regulated through caspase-mediated degradation of FLIP(L) and reduction of Bcl-2 protein stability, suggesting that pioglitazone is a feasible apoptotic agent that could be used in the treatment of human RC.	Pioglitazone	45-57	caspase 8	Homo sapiens	97-104
34466155-11	2021	In conclusion, these findings indicated that pioglitazone-induced apoptosis is regulated through caspase-mediated degradation of FLIP(L) and reduction of Bcl-2 protein stability, suggesting that pioglitazone is a feasible apoptotic agent that could be used in the treatment of human RC.	Pioglitazone	195-207	caspase 8	Homo sapiens	97-104
34310992-3	2021	FADD depletion inhibited SEM-LA-elicited caspase-8 activation, t-Bid production, and cell death, indicating that SEM-LA activated death receptor-mediated apoptosis in U937 cells.	sem-la	25-31	caspase 8	Homo sapiens	41-50
34503423-7	2022	NU 9056 also induced apoptosis by upregulating DR4, DR5, and caspase 8 expressions.	1,2-bis(isothiazol-5-yl)disulfane	0-7	caspase 8	Homo sapiens	61-70
34482382-7	2021	Collectively, our work demonstrates that enzalutamide-resistance is mediated by caspase-8 upregulation and the consequent increase in NF-kappaB/IL-8 mediated survival signaling, highlighting caspase-8 and NF-kappaB as potential therapeutic targets to overcome enzalutamide-resistance in CRPC.	enzalutamide	41-53	caspase 8	Homo sapiens	191-200
34543231-5	2021	METHODS: HCT116 cells were treated with TS essential oil alone or with TRAIL, and then its anticancer effect was determined by using MTT assay, live dead assay, caspase activation and PARP cleavage.	ts essential oil	40-56	caspase 8	Homo sapiens	161-168
34576119-5	2021	While CBD alone did not have any major effects on keratinocytes, the UVB treatment activated the extrinsic apoptotic pathway, with enhanced caspase 8 expression in both healthy and psoriatic keratinocytes.	Cannabidiol	6-9	caspase 8	Homo sapiens	140-149
34576119-8	2021	Application of CBD partially attenuated these effects of UVB irradiation both in healthy and psoriatic keratinocytes, reducing the levels of 15-d-PGJ2, p-p38 and caspase 8 while increasing Bcl2 expression.	Cannabidiol	15-18	caspase 8	Homo sapiens	162-171
34482382-3	2021	By analyzing transcriptome of enzalutamide-resistant prostate cancer cells, we found that resistance was conferred by a mild caspase-8 upregulation that in turn led to NF-kappaB activation and the subsequent upregulation of the downstream IL-8.	enzalutamide	30-42	caspase 8	Homo sapiens	125-134
34482382-4	2021	Mechanistically, we found that the pro-survival and enzalutamide-resistance-promoting features of caspase-8 were independent of its proteolytic activity, using a catalytically-inactive caspase-8 mutant.	enzalutamide	52-64	caspase 8	Homo sapiens	98-107
34482382-7	2021	Collectively, our work demonstrates that enzalutamide-resistance is mediated by caspase-8 upregulation and the consequent increase in NF-kappaB/IL-8 mediated survival signaling, highlighting caspase-8 and NF-kappaB as potential therapeutic targets to overcome enzalutamide-resistance in CRPC.	enzalutamide	41-53	caspase 8	Homo sapiens	80-89
34217978-4	2021	The mechanism of cytotoxicity of Sonapatha was determined at the molecular level by estimation of caspase 8 and 3 activities and Western blot analysis of NF-kappaB, COX-2, Nrf2, and RASSF7 which are overexpressed in neoplastic cells.	sonapatha	33-42	caspase 8	Homo sapiens	98-113
34217978-6	2021	Ethanol extract of Sonapatha (0, 20, 40, and 80 mug/mL) reduced clonogenicity, increased DNA fragmentation, apoptotic and necrotic indices, lactate dehydrogenase release, caspase 8 and 3 activities and inhibited the overexpression of NF-kappaB, COX-2, Nrf2, and RASSF7 in HeLa cells concentration-dependently.	Ethanol	0-7	caspase 8	Homo sapiens	171-186
34217978-6	2021	Ethanol extract of Sonapatha (0, 20, 40, and 80 mug/mL) reduced clonogenicity, increased DNA fragmentation, apoptotic and necrotic indices, lactate dehydrogenase release, caspase 8 and 3 activities and inhibited the overexpression of NF-kappaB, COX-2, Nrf2, and RASSF7 in HeLa cells concentration-dependently.	sonapatha	19-28	caspase 8	Homo sapiens	171-186
34479917-7	2021	Furthermore, paclitaxel induced ROS-mediated DNA damage that triggered the activation of the extrinsic pathway of apoptosis via the up-regulation of death receptor (DR5) and caspase-8 activation.	Paclitaxel	13-23	caspase 8	Homo sapiens	174-183
34479917-7	2021	Furthermore, paclitaxel induced ROS-mediated DNA damage that triggered the activation of the extrinsic pathway of apoptosis via the up-regulation of death receptor (DR5) and caspase-8 activation.	Reactive Oxygen Species	32-35	caspase 8	Homo sapiens	174-183
34602453-6	2021	The cytotoxic effects of leonurine on HL-60 and U-937 cells were associated with an increased ratio of Bax/Bcl-2, activation of caspase-3, caspase-8 and caspase-9, and increased expression of cytochrome c in the cytoplasm.	leonurine	25-34	caspase 8	Homo sapiens	139-148
34658346-3	2021	MTT assay was used to assess the proliferation of BON-ELF4 cells and BON-Vector cells, and the cell apoptosis induced by treatment with epirubicin (0.1 mumol/L for 24 h) was analyzed by detecting the expressions of cleaved caspase-8, caspase-9, and PARP using Western blotting.	Epirubicin	136-146	caspase 8	Homo sapiens	223-232
34466099-6	2021	Combination rHuEPO and tamoxifen produced much lesser effect on the caspase-8 activity.	Tamoxifen	23-32	caspase 8	Homo sapiens	68-77
34466099-13	2021	The rHuEPO-tamoxifen treatment enhanced the caspase-independent apoptotic effects of tamoxifen on the spheroid MCF-7 cells.	Tamoxifen	11-20	caspase 8	Homo sapiens	44-51
34466099-13	2021	The rHuEPO-tamoxifen treatment enhanced the caspase-independent apoptotic effects of tamoxifen on the spheroid MCF-7 cells.	Tamoxifen	85-94	caspase 8	Homo sapiens	44-51
34502426-8	2021	The effect of resveratrol and IR enhanced the expression of apoptotic genes, such as Bax, p53, and caspase 8, leading to apoptosis.	Resveratrol	14-25	caspase 8	Homo sapiens	99-108
34363313-4	2021	We show that diverse stress stimuli, including etoposide, brefeldin A and paclitaxel, as well as heat stress and gamma-irradiation, caused formation of a complex containing ATG5-ATG12, FADD and caspase-8 leading to activation of downstream caspases in caspase-9-deficient cells.	Etoposide	47-56	caspase 8	Homo sapiens	194-203
34363313-4	2021	We show that diverse stress stimuli, including etoposide, brefeldin A and paclitaxel, as well as heat stress and gamma-irradiation, caused formation of a complex containing ATG5-ATG12, FADD and caspase-8 leading to activation of downstream caspases in caspase-9-deficient cells.	Etoposide	47-56	caspase 8	Homo sapiens	240-248
34363313-4	2021	We show that diverse stress stimuli, including etoposide, brefeldin A and paclitaxel, as well as heat stress and gamma-irradiation, caused formation of a complex containing ATG5-ATG12, FADD and caspase-8 leading to activation of downstream caspases in caspase-9-deficient cells.	Brefeldin A	58-69	caspase 8	Homo sapiens	194-203
34363313-4	2021	We show that diverse stress stimuli, including etoposide, brefeldin A and paclitaxel, as well as heat stress and gamma-irradiation, caused formation of a complex containing ATG5-ATG12, FADD and caspase-8 leading to activation of downstream caspases in caspase-9-deficient cells.	Brefeldin A	58-69	caspase 8	Homo sapiens	240-248
34363313-4	2021	We show that diverse stress stimuli, including etoposide, brefeldin A and paclitaxel, as well as heat stress and gamma-irradiation, caused formation of a complex containing ATG5-ATG12, FADD and caspase-8 leading to activation of downstream caspases in caspase-9-deficient cells.	Paclitaxel	74-84	caspase 8	Homo sapiens	194-203
34363313-4	2021	We show that diverse stress stimuli, including etoposide, brefeldin A and paclitaxel, as well as heat stress and gamma-irradiation, caused formation of a complex containing ATG5-ATG12, FADD and caspase-8 leading to activation of downstream caspases in caspase-9-deficient cells.	Paclitaxel	74-84	caspase 8	Homo sapiens	240-248
34363313-4	2021	We show that diverse stress stimuli, including etoposide, brefeldin A and paclitaxel, as well as heat stress and gamma-irradiation, caused formation of a complex containing ATG5-ATG12, FADD and caspase-8 leading to activation of downstream caspases in caspase-9-deficient cells.	fadd	185-189	caspase 8	Homo sapiens	240-248
34389694-5	2021	In cells co-cultured with TNFalpha to mimic an inflammatory tumor microenvironment, tolinapant induced caspase-8-dependent apoptosis in colorectal cancer cell line models; however, the extent of apoptosis was limited because of inhibition by the caspase-8 paralogs FLIP and, unexpectedly, caspase-10.	U 17660	84-94	caspase 8	Homo sapiens	103-112
34389694-8	2021	Further analyses revealed that caspase-8 knockout RIPK3-positive colorectal cancer models were sensitive to tolinapant-induced necroptosis, an effect that could be exploited in caspase-8-proficient models using the clinically relevant caspase inhibitor emricasan.	U 17660	108-118	caspase 8	Homo sapiens	31-40
34389694-8	2021	Further analyses revealed that caspase-8 knockout RIPK3-positive colorectal cancer models were sensitive to tolinapant-induced necroptosis, an effect that could be exploited in caspase-8-proficient models using the clinically relevant caspase inhibitor emricasan.	3-(2-(2-tert-butylphenylaminooxalyl)aminopropionylamino)-4-oxo-5-(2,3,5,6-tetrafluorophenoxy)pentanoic acid	253-262	caspase 8	Homo sapiens	31-40
34389694-8	2021	Further analyses revealed that caspase-8 knockout RIPK3-positive colorectal cancer models were sensitive to tolinapant-induced necroptosis, an effect that could be exploited in caspase-8-proficient models using the clinically relevant caspase inhibitor emricasan.	3-(2-(2-tert-butylphenylaminooxalyl)aminopropionylamino)-4-oxo-5-(2,3,5,6-tetrafluorophenoxy)pentanoic acid	253-262	caspase 8	Homo sapiens	177-186
34389694-8	2021	Further analyses revealed that caspase-8 knockout RIPK3-positive colorectal cancer models were sensitive to tolinapant-induced necroptosis, an effect that could be exploited in caspase-8-proficient models using the clinically relevant caspase inhibitor emricasan.	3-(2-(2-tert-butylphenylaminooxalyl)aminopropionylamino)-4-oxo-5-(2,3,5,6-tetrafluorophenoxy)pentanoic acid	253-262	caspase 8	Homo sapiens	235-242
34466064-7	2021	The Tilianin-triggered apoptosis in PA-1 cells was correlated with elevated generation of ROS, loss of mitochondrial membrane potential, alterations in pro-apoptotic (upregulated mRNA expression of Bax) and anti-apoptotic (downregulated mRNA expression of Bcl2) factors and activation of caspase-8, -9 and -3.	tilianin	4-12	caspase 8	Homo sapiens	288-308
34549714-1	2021	OBJECTIVE: To investigate the effect of DR5-mediated docetaxel-targeted lipid microbubbles (MBs) combined with ultrasound-targeted microbubble destruction on apoptosis and expressions of Bcl-2, nuclear factor-kappaB(NF-kappaB), caspase-8, and DR5 in human HepG2 cells.	Docetaxel	53-62	caspase 8	Homo sapiens	228-237
34384107-10	2021	Importantly, co-treatment of AMH plus leptin upregulates the expression of pro-apoptotic proteins, such as Bax, caspase-3, and caspase-8 after incubating with a high level of glucose.	Glucose	175-182	caspase 8	Homo sapiens	127-136
34492839-7	2021	Additionally, CuSO4 induced apoptosis which was featured by MMP depolarization and up-regulated levels of cleaved-caspase-3, cleaved-caspase-8, cleaved-caspase-9, caspase-12, cleaved-PARP and Bax, whereas down-regulated Bcl-2 expression.	Copper Sulfate	14-19	caspase 8	Homo sapiens	133-142
34388026-3	2021	This study investigated whether lentivirus-mediated Gag-CASP8 can effectively deliver activated CASP8 into primary human breast cancer cells overexpressing HER-2 to induce apoptosis and explore the underlying mechanism.	Glycosaminoglycans	52-55	caspase 8	Homo sapiens	56-61
34388026-3	2021	This study investigated whether lentivirus-mediated Gag-CASP8 can effectively deliver activated CASP8 into primary human breast cancer cells overexpressing HER-2 to induce apoptosis and explore the underlying mechanism.	Glycosaminoglycans	52-55	caspase 8	Homo sapiens	96-101
34388026-4	2021	Materials and Methods: HER-2-overexpressing primary human breast cancer cells were infected with lentivirus-like particles carrying Gag-CASP8.	Glycosaminoglycans	132-135	caspase 8	Homo sapiens	136-141
34388026-5	2021	Results: After a 48-h infection of primary human breast cancer cells with HER-2 by lentivirus-mediated Gag-CASP8, significant differences were observed in the survival rate, migration ability, S-phase number of cells, apoptosis rate, and intracellular activated CASP8 and caspase-3 levels in tumor cells compared with those in the control group (p < 0.05).	Glycosaminoglycans	103-106	caspase 8	Homo sapiens	107-112
34388026-5	2021	Results: After a 48-h infection of primary human breast cancer cells with HER-2 by lentivirus-mediated Gag-CASP8, significant differences were observed in the survival rate, migration ability, S-phase number of cells, apoptosis rate, and intracellular activated CASP8 and caspase-3 levels in tumor cells compared with those in the control group (p < 0.05).	Glycosaminoglycans	103-106	caspase 8	Homo sapiens	262-267
34388026-6	2021	Conclusions: Lentivirus-mediated Gag-CASP8 can deliver activated CASP8 into HER-2-overexpressing primary human breast cancer cells and induce apoptosis by activating caspase-3, a downstream apoptotic executive molecule.	Glycosaminoglycans	33-36	caspase 8	Homo sapiens	37-42
34388026-6	2021	Conclusions: Lentivirus-mediated Gag-CASP8 can deliver activated CASP8 into HER-2-overexpressing primary human breast cancer cells and induce apoptosis by activating caspase-3, a downstream apoptotic executive molecule.	Glycosaminoglycans	33-36	caspase 8	Homo sapiens	65-70
34388026-7	2021	By blocking the S-phase to inhibit cell proliferation and migration, lentivirus-mediated Gag-CASP8 provides a reference for tumor gene therapy.	Glycosaminoglycans	89-92	caspase 8	Homo sapiens	93-98
34381064-7	2021	RT-qPCR for apoptotic genes (BCL2, CASP3 and CASP8) and necrosis genes (MLKL, RIPK1 and RIPK3) did not show significant differences between control and treated cells of both types, with the exception of eugenol-treated HeLa cells in which expression of BCL2, MLKL and RIPK1 was significantly higher than controls.	Eugenol	203-210	caspase 8	Homo sapiens	45-50
34362880-5	2021	To investigate their functional properties and phenotypic effects, 18 HNSCC-associated caspase-8 mutants were expressed in doxycycline-inducible fashion in cell line models wherein the endogenous wild-type caspase-8 was deleted.	Doxycycline	123-134	caspase 8	Homo sapiens	87-96
34362880-9	2021	Doxycycline-induced expression of wild-type caspase-8 or a representative mutant led to an increased percentage of T and NKT cells in syngeneic HNSCC xenograft tumors.	Doxycycline	0-11	caspase 8	Homo sapiens	44-53
34401358-7	2021	Furthermore, the participation of caspase-8 in the possible mechanism of action of isoeleutherin, eleutherin, and eleutherol was also investigated through a docking study.	isoeleutherin	83-96	caspase 8	Homo sapiens	34-43
34126378-9	2021	Moreover, AEA induced an increase in caspase -3/-7 activities in both cell models, but in hGCs there was also an increase in caspase 8 activity.	aea	10-13	caspase 8	Homo sapiens	125-134
34401358-7	2021	Furthermore, the participation of caspase-8 in the possible mechanism of action of isoeleutherin, eleutherin, and eleutherol was also investigated through a docking study.	eleutherin	98-108	caspase 8	Homo sapiens	34-43
34401358-7	2021	Furthermore, the participation of caspase-8 in the possible mechanism of action of isoeleutherin, eleutherin, and eleutherol was also investigated through a docking study.	eleutherol	114-124	caspase 8	Homo sapiens	34-43
34401358-12	2021	Despite the results of cytotoxicity, in vitro studies demonstrated that the use of EEEp appears to be safe and cell death may involve its binding to caspase-8.	eeep	83-87	caspase 8	Homo sapiens	149-158
34330116-0	2021	Activating Caspase-8/Bid/ROS Signaling to Promote Apoptosis of Breast Cancer Cells by Folate-modified Albumin Baicalin-loaded Nanoparticles.	Folic Acid	86-92	caspase 8	Homo sapiens	11-20
34367939-3	2021	Initially, caspase-8 phosphorylated at tyrosine 380 by c-Src predominantly enhancing c-Src activation to facilitate metastasis through attaining epithelial-mesenchymal transition (EMT) phenotype in lung adenocarcinoma.	Tyrosine	39-47	caspase 8	Homo sapiens	11-20
34330116-14	2021	The mechanism of FA-BSANPs/BA promoting apoptosis of breast cancer may be due to its action on the caspase-8/Bid/ROS pathway.	baicalin	27-29	caspase 8	Homo sapiens	99-108
34330116-14	2021	The mechanism of FA-BSANPs/BA promoting apoptosis of breast cancer may be due to its action on the caspase-8/Bid/ROS pathway.	ros	113-116	caspase 8	Homo sapiens	99-108
34367939-4	2021	Mechanistically, the linkage of c-Src SH2 domain with phosphotyrosine 380 of caspase-8 and SH3 domain with "PDEP" motif of caspase-8 overactivates c-Src as compared with other c-Src-partner proteins.	Phosphotyrosine	54-69	caspase 8	Homo sapiens	77-86
34080659-9	2021	TRAIL in combination with amitriptyline or CQ significantly increased the expression of apoptosis-indicator proteins cleaved caspase-8 and caspase-3.	Amitriptyline	26-39	caspase 8	Homo sapiens	125-134
34299199-6	2021	The results showed that ruthenium compounds break partially or completely the cisplatin resistance by activating the caspase 8-dependent apoptosis pathway and loss of mitochondrial membrane potential.	Ruthenium Compounds	24-43	caspase 8	Homo sapiens	117-126
34299199-6	2021	The results showed that ruthenium compounds break partially or completely the cisplatin resistance by activating the caspase 8-dependent apoptosis pathway and loss of mitochondrial membrane potential.	Cisplatin	78-87	caspase 8	Homo sapiens	117-126
34182480-0	2021	Tetrandrine Enhances H2O2-Induced Apoptotic Cell Death Through Caspase-dependent Pathway in Human Keratinocytes.	tetrandrine	0-11	caspase 8	Homo sapiens	63-70
34080659-9	2021	TRAIL in combination with amitriptyline or CQ significantly increased the expression of apoptosis-indicator proteins cleaved caspase-8 and caspase-3.	Chloroquine	43-45	caspase 8	Homo sapiens	125-134
34209868-9	2021	The apoptosis-inducing activity of pancracine in MOLT-4 cells was evidenced by the significantly higher activity of caspases.	pancracine	35-45	caspase 8	Homo sapiens	116-124
34234678-11	2021	The combination treatment with CM and ponesimod reduced the expression of caspase-3, caspase-8, Bax, and Annexin V proteins and increased the relative BCL-2/Bax ratio, indicating inhibition of apoptosis as a possible mechanism of action.	ponesimod	38-47	caspase 8	Homo sapiens	85-94
34161670-7	2022	Moreover, PB induced G0/G1 cycle arrest and caspase-dependent apoptosis of HGC-27 cells.	physalin B	10-12	caspase 8	Homo sapiens	44-51
34161670-8	2022	Cleaved caspases 8, 3, and 7, poly(ADP)-ribose polymerase (PARP), and the cyclin-dependent kinase (CDK) inhibitor p-Chk2 was induced by PB in HGC-27 cells, while the cell cycle-related proteins cyclin D1, cyclin D3, CDK4, CDK6, cyclin E, and phosphorylated retinoblastoma tumor suppressor protein (p-Rb) were downregulated in a dose-dependent manner.	physalin B	136-138	caspase 8	Homo sapiens	8-28
34161670-9	2022	CONCLUSIONS: PB inhibits proliferation via cyclin-dependent kinase and induces caspase-dependent apoptosis in HGC-27 cells, suggesting that PB might be a novel and effective agent for undifferentiated GC therapy.	physalin B	13-15	caspase 8	Homo sapiens	79-86
34161670-9	2022	CONCLUSIONS: PB inhibits proliferation via cyclin-dependent kinase and induces caspase-dependent apoptosis in HGC-27 cells, suggesting that PB might be a novel and effective agent for undifferentiated GC therapy.	physalin B	140-142	caspase 8	Homo sapiens	79-86
34181325-10	2021	By the supplementation of CGM showed an increase in Bax and cleaved caspase-8 protein in HeLa cells after 48 h exposure.	cgm	26-29	caspase 8	Homo sapiens	68-77
34083287-10	2021	Furthermore, the expression of extrinsic pathway proteins, e.g. Fas/FasL, DR4/TRAIL, and Fas-associated protein with death domain, was increased by pemetrexed, which then activated caspase-8, caspase-9, and caspase-3 and induced poly (ADP-ribose) polymerase proteolysis.	Pemetrexed	148-158	caspase 8	Homo sapiens	181-190
34088893-7	2021	We investigated the in vitro effect of Smac-mimetic added to carboplatin and paclitaxel treatment of ovarian cancer cells expressing wild type and low Caspase 8 levels, which resulted in a 2-4-fold enhancement of cell death.	Paclitaxel	77-87	caspase 8	Homo sapiens	151-160
34071530-4	2021	Furthermore, both catechin nanoemulsions and extracts could raise caspase-8, caspase-9 and caspase-3 activities for DU-145 cell apoptosis, arresting the cell cycle at S and G2/M phases.	Catechin	18-26	caspase 8	Homo sapiens	66-75
34070401-8	2021	Treatment with PtMet2-PAMAM substantially increased apoptosis in a dose-dependent manner via caspase-9 (intrinsic pathway) and caspase-8 (extrinsic pathway) activation along with pro-apoptotic protein expression modulation.	ptmet2-pamam	15-27	caspase 8	Homo sapiens	127-136
34114395-0	2021	Celastrol induces caspase-dependent apoptosis of hepatocellular carcinoma cells by suppression of mammalian target of rapamycin.	celastrol	0-9	caspase 8	Homo sapiens	18-25
34114395-8	2021	Western blot assays indicated that celastrol up-regulated cleaved-caspase-3, cleaved-caspase-8, cleaved-caspase-9, and cleaved-PARP by inhibiting the phosphorylation of mTOR in HepG2 cells.	celastrol	35-44	caspase 8	Homo sapiens	85-94
34073459-0	2021	Pt(II)-Thiocarbohydrazone Complex as Cytotoxic Agent and Apoptosis Inducer in Caov-3 and HT-29 Cells through the P53 and Caspase-8 Pathways.	pt(ii)-thiocarbohydrazone	0-25	caspase 8	Homo sapiens	121-130
34073459-4	2021	Results demonstrated that the cytotoxic effect of the Pt(II)-thiocarbohydrazone complexes against Caov-3 and HT-29 cells was highly significant, and this effect triggered the activation of the p53 and caspase-8 pathways.	pt(ii)	54-60	caspase 8	Homo sapiens	201-210
34073459-4	2021	Results demonstrated that the cytotoxic effect of the Pt(II)-thiocarbohydrazone complexes against Caov-3 and HT-29 cells was highly significant, and this effect triggered the activation of the p53 and caspase-8 pathways.	thiocarbohydrazone	61-79	caspase 8	Homo sapiens	201-210
34114395-10	2021	Celastrol also induced caspase-dependent apoptosis (up-regulation of cleaved-caspase- 3, -8, -9, and cleaved-PARP) and inhibited the activation of mTOR in vivo.	celastrol	0-9	caspase 8	Homo sapiens	23-30
34066632-7	2021	Apoptosis triggered either by hyperthermia or hyperthermia/ethanol was almost completely abolished by a caspase-8 specific inhibitor, indicating that this caspase plays a main role in both conditions.	Ethanol	59-66	caspase 8	Homo sapiens	104-113
34114395-11	2021	CONCLUSION: Celastrol induces caspase-dependent apoptosis in HCC cells by inhibiting the activation of mTOR.	celastrol	12-21	caspase 8	Homo sapiens	30-37
34073773-5	2021	In addition to the effector caspase 3 and poly adenosine diphosphate-ribose polymerase, GO-Y078 significantly activated both initiators of extrinsic caspase 8 and intrinsic caspase 9, whereas cellular inhibitors of apoptosis 1 (cIAP-1) and X-chromosome-linked IAP (XIAP) in U2OS and 143B cells were significantly repressed.	GO-Y078	88-95	caspase 8	Homo sapiens	149-158
34073773-7	2021	Using inhibitors of JNK (JNK-in-8) and p38 (SB203580), GO-Y078"s increases in cleaved caspases 8, 9, and 3 could be expectedly suppressed, but they could not be affected by co-treatment with the ERK inhibitor (U0126).	SB 203580	44-52	caspase 8	Homo sapiens	86-106
34073773-7	2021	Using inhibitors of JNK (JNK-in-8) and p38 (SB203580), GO-Y078"s increases in cleaved caspases 8, 9, and 3 could be expectedly suppressed, but they could not be affected by co-treatment with the ERK inhibitor (U0126).	GO-Y078	55-62	caspase 8	Homo sapiens	86-106
34073773-7	2021	Using inhibitors of JNK (JNK-in-8) and p38 (SB203580), GO-Y078"s increases in cleaved caspases 8, 9, and 3 could be expectedly suppressed, but they could not be affected by co-treatment with the ERK inhibitor (U0126).	U 0126	210-215	caspase 8	Homo sapiens	86-106
35247515-8	2022	Together, the results herein reveal DDAs as the first small molecule, active site inhibitors of AGR2 and ERp44, and demonstrate roles for AGR2 and ERp44 in regulating the activity, stability, and localization of DR4 and DR5, and activation of Caspase 8.	ddas	36-40	caspase 8	Homo sapiens	243-252
34086162-0	2021	Dichloromethane fraction of Moringa oleifera leaf methanolic extract selectively inhibits breast cancer cells (MCF7) by induction of apoptosis via upregulation of Bax, p53 and caspase 8 expressions.	Methylene Chloride	0-15	caspase 8	Homo sapiens	176-185
34393434-11	2021	In the Molt-4 cells, D-carvone induced the apoptosis in a time and dose dependent manner by the activation of caspases-8, -9 and -3.	d-Carvone	21-30	caspase 8	Homo sapiens	110-131
34273265-7	2021	Platycodin D also increased caspase-9, caspase-8, caspase-3, and p53 expression and decreased Bcl-2 expression in tumour tissues.	platycodin D	0-12	caspase 8	Homo sapiens	39-48
35430982-6	2022	Caracasine increased CD95 expression (p<0.01 in Jurkat and p<0.05 in HL60) and caspase-8 activation (p <0.001 in Jurkat and p<0.05 in HL60).	caracasine	0-10	caspase 8	Homo sapiens	79-88
35601667-6	2022	VC inhibited neomycin-induced apoptosis, ameliorated neomycin reduced antiapoptotic Bcl-2 expression, and suppressed neomycin increased expression of proapoptotic Bax, caspase-3 cleavage and caspase-8.	Ascorbic Acid	0-2	caspase 8	Homo sapiens	191-200
35601667-6	2022	VC inhibited neomycin-induced apoptosis, ameliorated neomycin reduced antiapoptotic Bcl-2 expression, and suppressed neomycin increased expression of proapoptotic Bax, caspase-3 cleavage and caspase-8.	Neomycin	117-125	caspase 8	Homo sapiens	191-200
35478473-5	2022	In MCF-7 cells, atractylodin administration decreased Bcl-2 expression while activating the expression of p53, Bax, cleaved caspase-3, caspase-8, and caspase-9 apoptotic members.	atractylodin	16-28	caspase 8	Homo sapiens	135-144
35522455-4	2022	A specific inhibitor of caspase-8 (Z-IETD-FMK) was also used to verify the possible mechanisms.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	35-45	caspase 8	Homo sapiens	24-33
35505281-9	2022	Furthermore, as shown by our experimental findings, Risperidone treatment inhibited the differentiation and autophagy, and promoted the apoptosis of osteoblasts, as evidenced by elevated levels of OPG, p62, cleaved PARP1, cleaved caspase-3, cleaved caspase-8, and cleaved caspase-9, and reduced levels of LC3 II/I, Beclin1, collagen I, and RANKL.	Risperidone	52-63	caspase 8	Homo sapiens	249-258
35393392-7	2022	Co-treatment with specific necroptosis inhibitor necrostatin-1 (Nec-1) or Necrosulfonamide (NSA) prevented cell death caused by iPA treatment while the general caspase inhibitor Z-VAD-fluoromethylketone (z-VAD-fmk) did not elicit any effect, suggesting that this molecule induces caspase-independent necroptosis.	necrostatin-1	49-62	caspase 8	Homo sapiens	280-287
35431006-5	2022	In addition, HN5 cells were also treated with curcumin to evaluate its effect on the caspase-8, -9, Bcl-2, Bax, and Stat3 genes expression.	Curcumin	46-54	caspase 8	Homo sapiens	85-98
35393392-7	2022	Co-treatment with specific necroptosis inhibitor necrostatin-1 (Nec-1) or Necrosulfonamide (NSA) prevented cell death caused by iPA treatment while the general caspase inhibitor Z-VAD-fluoromethylketone (z-VAD-fmk) did not elicit any effect, suggesting that this molecule induces caspase-independent necroptosis.	N-(4-(N-(3-methoxypyrazin-2-yl)sulfamoyl)phenyl)-3-(5-nitrothiophene-2-yl)acrylamide	74-90	caspase 8	Homo sapiens	280-287
35393392-7	2022	Co-treatment with specific necroptosis inhibitor necrostatin-1 (Nec-1) or Necrosulfonamide (NSA) prevented cell death caused by iPA treatment while the general caspase inhibitor Z-VAD-fluoromethylketone (z-VAD-fmk) did not elicit any effect, suggesting that this molecule induces caspase-independent necroptosis.	ipa	128-131	caspase 8	Homo sapiens	280-287
35393392-7	2022	Co-treatment with specific necroptosis inhibitor necrostatin-1 (Nec-1) or Necrosulfonamide (NSA) prevented cell death caused by iPA treatment while the general caspase inhibitor Z-VAD-fluoromethylketone (z-VAD-fmk) did not elicit any effect, suggesting that this molecule induces caspase-independent necroptosis.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	178-202	caspase 8	Homo sapiens	160-167
35393392-7	2022	Co-treatment with specific necroptosis inhibitor necrostatin-1 (Nec-1) or Necrosulfonamide (NSA) prevented cell death caused by iPA treatment while the general caspase inhibitor Z-VAD-fluoromethylketone (z-VAD-fmk) did not elicit any effect, suggesting that this molecule induces caspase-independent necroptosis.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	178-202	caspase 8	Homo sapiens	280-287
35393392-7	2022	Co-treatment with specific necroptosis inhibitor necrostatin-1 (Nec-1) or Necrosulfonamide (NSA) prevented cell death caused by iPA treatment while the general caspase inhibitor Z-VAD-fluoromethylketone (z-VAD-fmk) did not elicit any effect, suggesting that this molecule induces caspase-independent necroptosis.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	204-213	caspase 8	Homo sapiens	160-167
35379808-4	2022	For Rnf31 we demonstrate that it protects tumor cells from TNF-mediated caspase 8 cleavage and subsequent apoptosis induction, a mechanism that is conserved in human PDA organoids.	pda organoids	166-179	caspase 8	Homo sapiens	72-81
35442463-17	2022	CONCLUSIONS: (1) Icariin, quercetin and luteolin may act on target proteins, including IL-6, ESR1, EGFR, MAPK8, VEGFA and CASP8, to participate in the regulation of the human cytomegalovirus infection pathway, the PI3K-Akt signaling pathway, the TNF signaling pathway and other signaling pathways in order to effectively treat CAD.	icariin	17-24	caspase 8	Homo sapiens	122-127
35086954-5	2022	High throughput drug-screening failed to identify genomic alterations associated with response to MEDI3039; however, transcriptomics anaysis revealed striking association between MEDI3039 sensitivity and expression of core components of the extrinsic apoptotic pathway, most notably its main apoptotic effector caspase-8 in solid tumor cell lines.	medi3039	179-187	caspase 8	Homo sapiens	311-320
35442463-17	2022	CONCLUSIONS: (1) Icariin, quercetin and luteolin may act on target proteins, including IL-6, ESR1, EGFR, MAPK8, VEGFA and CASP8, to participate in the regulation of the human cytomegalovirus infection pathway, the PI3K-Akt signaling pathway, the TNF signaling pathway and other signaling pathways in order to effectively treat CAD.	Quercetin	26-35	caspase 8	Homo sapiens	122-127
35442463-17	2022	CONCLUSIONS: (1) Icariin, quercetin and luteolin may act on target proteins, including IL-6, ESR1, EGFR, MAPK8, VEGFA and CASP8, to participate in the regulation of the human cytomegalovirus infection pathway, the PI3K-Akt signaling pathway, the TNF signaling pathway and other signaling pathways in order to effectively treat CAD.	Luteolin	40-48	caspase 8	Homo sapiens	122-127
35092733-0	2022	Role of caspase-8 and/or -9 as biomarkers that can distinguish the potential to cause toxic- and immune related-adverse event, for the progress of acetaminophen-induced liver injury.	Acetaminophen	147-160	caspase 8	Homo sapiens	8-17
35086954-6	2022	Further analyses of colorectal cell-lines and patient-derived xenografts, identified caspase-8 expression ratio to its endogenous regulator FLIP(L) as predictive of sensitivity to MEDI3039 in several major solid tumor types and a further subset indicated by caspase-8:MCL-1 ratio.	medi3039	180-188	caspase 8	Homo sapiens	85-94
35086954-6	2022	Further analyses of colorectal cell-lines and patient-derived xenografts, identified caspase-8 expression ratio to its endogenous regulator FLIP(L) as predictive of sensitivity to MEDI3039 in several major solid tumor types and a further subset indicated by caspase-8:MCL-1 ratio.	medi3039	180-188	caspase 8	Homo sapiens	258-267
35321428-0	2022	Caspase-8: Friend or Foe in Bortezomib/Lenalidomide-Based Therapy for Myeloma.	Bortezomib	28-38	caspase 8	Homo sapiens	0-9
35151092-5	2022	Importantly, the combination of poly(I:C) with proteasome inhibitors enhanced caspase-8 and caspase-9 activation, and synergistically induced cervical cancer cell apoptosis.	Poly I-C	32-41	caspase 8	Homo sapiens	78-87
35321428-3	2022	Bortezomib and lenalidomide activate caspase-8 and promote the apoptosis of myeloma cells.	Bortezomib	0-10	caspase 8	Homo sapiens	37-46
35455398-7	2022	The analysis of upstream signaling pathways revealed that dehydrocrenatidine induced caspase-mediated apoptosis by suppressing the phosphorylation of JNK1/2.	dehydrocrenatidine	58-76	caspase 8	Homo sapiens	85-92
35195559-8	2022	Furthermore, an ARG signature was established based on overall survival-related ARGs (CASP4, BAK1, PIK3R4, CASP8, BIRC5, RPTOR, and CAPN1) using least absolute shrinkage and selection operator (LASSO) regression.	Arginine	16-19	caspase 8	Homo sapiens	107-112
35321428-3	2022	Bortezomib and lenalidomide activate caspase-8 and promote the apoptosis of myeloma cells.	Lenalidomide	15-27	caspase 8	Homo sapiens	37-46
35321428-4	2022	However, caspase-8 inhibition potentiated the antiproliferative effect of lenalidomide and bortezomib in myeloma cells, suggesting that caspase-8 could regulate proliferation and apoptosis in the opposite pathway.	Lenalidomide	74-86	caspase 8	Homo sapiens	136-145
35321428-4	2022	However, caspase-8 inhibition potentiated the antiproliferative effect of lenalidomide and bortezomib in myeloma cells, suggesting that caspase-8 could regulate proliferation and apoptosis in the opposite pathway.	Bortezomib	91-101	caspase 8	Homo sapiens	136-145
35321428-5	2022	In this mini-review, I summarized recent advances in determining the molecular mechanisms of caspase-8 in bortezomib-lenalidomide-based therapy for myeloma and explored the possible functions of caspase-8 in the proliferation and apoptosis of myeloma cells.	Bortezomib	106-116	caspase 8	Homo sapiens	93-102
35402180-7	2022	Furthermore, the expression of caspase 8 and caspase 3 was positively correlated with the concentration of ligustrazine, and there was significant difference compared with the control group.	tetramethylpyrazine	107-119	caspase 8	Homo sapiens	31-40
35296559-8	2022	Additionally, loss of CFLAR (Caspase-8 and FADD Like Apoptosis Regulator), BCL2L1, and BID (BH3 Interacting Domain Death Agonist) induced profound changes in sensitivity to TCEs, indicating that key regulators of apoptosis, which are frequently altered in cancer, impact tumor responsiveness to BiTE therapy.	tces	173-177	caspase 8	Homo sapiens	29-38
35074343-5	2022	Compared with the negative control, the Y79 cells treated with PNS had significantly increased (P < 0.05) mRNA and protein expression of Bax, caspase-3, caspase-8, and caspase-9 and elevated levels of cleaved caspase-3, cleaved caspase-8, and cleaved caspase-9 proteins (P < 0.05).	4'-phosphopantetheine	63-66	caspase 8	Homo sapiens	153-162
35074343-5	2022	Compared with the negative control, the Y79 cells treated with PNS had significantly increased (P < 0.05) mRNA and protein expression of Bax, caspase-3, caspase-8, and caspase-9 and elevated levels of cleaved caspase-3, cleaved caspase-8, and cleaved caspase-9 proteins (P < 0.05).	4'-phosphopantetheine	63-66	caspase 8	Homo sapiens	228-237
35601780-6	2022	M. congesta essentials oil has the highest cytotoxic effect on gastric cancer (HGC-27) cells, decreases MMP2 and MMP9 expressions, and induces apoptosis with increasing the expression of caspase 3 and caspase 8 genes.	congesta essentials oil	3-26	caspase 8	Homo sapiens	201-210
35335908-8	2022	ASA significantly decreased the expression levels of miRNA155, NLRP3, and IL1B, and produced a significant decrease in caspase-8 immunoreaction in the neurons and glial cells of the frontal cortex with a reduction in the process of neuroinflammation and neuronal damage.	Aspirin	0-3	caspase 8	Homo sapiens	119-128
35215023-8	2022	Surprisingly, Cur@affi-F/GQs significantly enhance the expression and activity of apoptosis-associated proteins in Bcl-2/Bax-caspase 8, 9-caspase 3 apoptotic pathway, which is the main factor in the death of tumor cells induced by FUdR.	Floxuridine	231-235	caspase 8	Homo sapiens	125-134
35200638-7	2022	This effect was reversed by caspase inhibitors, suggesting caspase-mediated apoptosis in the (-)-agelasidine A-treated Hep3B cells.	agelasidine A	93-110	caspase 8	Homo sapiens	59-66
35203294-8	2022	Specifically, the intrinsic and extrinsic apoptotic caspase 9 and caspase 8 were overexpressed in OVCA cells following CPC treatment.	cryptocaryone	119-122	caspase 8	Homo sapiens	66-75
35070983-14	2021	Furthermore, quercetin combined with cisplatin downregulated the expression of EGFR, MYC, CCND1, and ERBB2 proteins and upregulated CASP8 expression in HeLa and SiHa cells.	Quercetin	13-22	caspase 8	Homo sapiens	132-137
34994335-10	2022	These compounds combined with cisplatin caused upregulation in the pro-apoptotic Bax, Bid, caspase-3, caspase-8, caspase-9, Fas, and p53 gene expressions while downregulating anti-apoptotic DFFA, NFkB1, and Bcl2 gene expressions.	Cisplatin	30-39	caspase 8	Homo sapiens	102-111
35070983-14	2021	Furthermore, quercetin combined with cisplatin downregulated the expression of EGFR, MYC, CCND1, and ERBB2 proteins and upregulated CASP8 expression in HeLa and SiHa cells.	Cisplatin	37-46	caspase 8	Homo sapiens	132-137
34908079-1	2022	In this study we self-assembled the four-armed porphyrin hetero dimer capsule Cap4, stabilized through amidinium-carboxylate salt bridges, in CH2Cl2 and CHCl3.	Porphyrins	47-56	caspase 8	Homo sapiens	78-82
34908079-1	2022	In this study we self-assembled the four-armed porphyrin hetero dimer capsule Cap4, stabilized through amidinium-carboxylate salt bridges, in CH2Cl2 and CHCl3.	amidinium	103-112	caspase 8	Homo sapiens	78-82
34908079-1	2022	In this study we self-assembled the four-armed porphyrin hetero dimer capsule Cap4, stabilized through amidinium-carboxylate salt bridges, in CH2Cl2 and CHCl3.	carboxylate	113-124	caspase 8	Homo sapiens	78-82
34908079-1	2022	In this study we self-assembled the four-armed porphyrin hetero dimer capsule Cap4, stabilized through amidinium-carboxylate salt bridges, in CH2Cl2 and CHCl3.	Salts	125-129	caspase 8	Homo sapiens	78-82
34908079-1	2022	In this study we self-assembled the four-armed porphyrin hetero dimer capsule Cap4, stabilized through amidinium-carboxylate salt bridges, in CH2Cl2 and CHCl3.	Methylene Chloride	142-148	caspase 8	Homo sapiens	78-82
34908079-1	2022	In this study we self-assembled the four-armed porphyrin hetero dimer capsule Cap4, stabilized through amidinium-carboxylate salt bridges, in CH2Cl2 and CHCl3.	Chloroform	153-158	caspase 8	Homo sapiens	78-82
34908079-3	2022	The number of arms strongly influenced their recognition behaviour; guests possessing small aromatic faces (e.g., 1,3,5-trinitrobenzene) preferred residing in the cavity of the two-armed capsule Cap2, rather than in Cap4, both thermodynamically and kinetically; in contrast, large aromatic guests (e.g., 9,10-dibromoanthracene) were encapsulated predominantly by Cap4 because of favourable entropic effects.	sym-trinitrobenzene	114-135	caspase 8	Homo sapiens	216-220
34908079-3	2022	The number of arms strongly influenced their recognition behaviour; guests possessing small aromatic faces (e.g., 1,3,5-trinitrobenzene) preferred residing in the cavity of the two-armed capsule Cap2, rather than in Cap4, both thermodynamically and kinetically; in contrast, large aromatic guests (e.g., 9,10-dibromoanthracene) were encapsulated predominantly by Cap4 because of favourable entropic effects.	sym-trinitrobenzene	114-135	caspase 8	Homo sapiens	363-367
34908079-3	2022	The number of arms strongly influenced their recognition behaviour; guests possessing small aromatic faces (e.g., 1,3,5-trinitrobenzene) preferred residing in the cavity of the two-armed capsule Cap2, rather than in Cap4, both thermodynamically and kinetically; in contrast, large aromatic guests (e.g., 9,10-dibromoanthracene) were encapsulated predominantly by Cap4 because of favourable entropic effects.	9,10-Dibromoanthracene	304-326	caspase 8	Homo sapiens	363-367
34908079-4	2022	The number of arms enabled self-sorting behaviour of the dimer formation; complexation studies using an equimolar mixture of the four porphyrin constituents of the two capsules revealed the quantitative formation of the corresponding dimers Cap2 and Cap4.	Porphyrins	134-143	caspase 8	Homo sapiens	250-254