PMID-sentid	Pub_year	Sent_text	comp_official_name	comp_offset	protein_name	organism	prot_offset
33915328-8	2021	A438079 promoted apoptosis via the Bcl-2/caspase9/caspase3 pathway and inhibited pyroptosis through the NLRP3/caspase1 pathway by inhibiting P2X7R in vitro and in vivo.	3-(5-(2,3-dichlorophenyl)-1H-tetrazol-1-yl)methylpyridine	0-7	caspase 1	Homo sapiens	110-118
6246161-3	1980	The percentage suppression of each given steroid was constant over the age groups from 6-9 years to P4-5 Tanner"s stage, while lower suppression was found in 17P, P and DHA in 2-5 year old girls and in 17P, DHA and E2 in adult women.	Steroids	41-48	caspase 1	Homo sapiens	100-104
33955754-0	2021	Cannabidiol Protects Human Skin Keratinocytes from Hydrogen-Peroxide-Induced Oxidative Stress via Modulation of the Caspase-1-IL-1beta Axis.	Cannabidiol	0-11	caspase 1	Homo sapiens	116-125
34000467-5	2021	Our results indicated that the activation of caspase-1 and the subsequent secretion of IL-1beta were significantly enhanced in infected macrophages under 1% oxygen, compared with those under a normal 20% oxygen concentration.	Oxygen	157-163	caspase 1	Homo sapiens	45-54
34000467-5	2021	Our results indicated that the activation of caspase-1 and the subsequent secretion of IL-1beta were significantly enhanced in infected macrophages under 1% oxygen, compared with those under a normal 20% oxygen concentration.	Oxygen	204-210	caspase 1	Homo sapiens	45-54
33955754-5	2021	CBD treatment down-regulated the mRNA expression levels of CASP1 and IL1B (by 32.9 and 51.0%, respectively) and reduced IL-1beta level (by 16.2%) in H2O2-stimulated HaCaT cells.	Cannabidiol	0-3	caspase 1	Homo sapiens	59-64
33955754-6	2021	Furthermore, CBD inhibited the activity of caspase-1 enzyme (by 15.7%) via direct binding to caspase-1 protein, which was supported by data from a biophysical binding assay (surface plasmon resonance) and a computational docking experiment.	Cannabidiol	13-16	caspase 1	Homo sapiens	43-52
33955754-6	2021	Furthermore, CBD inhibited the activity of caspase-1 enzyme (by 15.7%) via direct binding to caspase-1 protein, which was supported by data from a biophysical binding assay (surface plasmon resonance) and a computational docking experiment.	Cannabidiol	13-16	caspase 1	Homo sapiens	93-102
33955754-8	2021	The findings from the current study suggest that CBD exerts protective effects in human keratinocytes via the modulation of the caspase-1-IL-1beta axis, supporting its potential skin health applications.	Cannabidiol	49-52	caspase 1	Homo sapiens	128-137
33159713-12	2021	Western blot and immunofluorescence results confirmed that MEHP markedly augmented Caspase-1 expression in HEMECs.	mono-(2-ethylhexyl)phthalate	59-63	caspase 1	Homo sapiens	83-92
34011327-12	2021	SAL also attenuated LPS-induced activation of NLRP3 inflammasome, reduced the protein expression of NLRP3-related proteins, including ASC and caspase-1.	rhodioloside	0-3	caspase 1	Homo sapiens	142-151
34004605-8	2021	Bound caspases-4/5 oligomerize and trigger the assembly of the nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing-3 inflammasome followed by the activation of inflammatory caspase-1 resulting in subsequent release of interleukin-1beta.	Leucine	90-97	caspase 1	Homo sapiens	204-213
33982180-6	2021	Inhibition of caspase-1 by Belnacasan (VX-765) suppressed the transcription of IL-1beta, reduced cell lysis, and significantly promoted IBDV replication in DF-1 cells.	belnacasan	27-37	caspase 1	Homo sapiens	14-23
33982180-6	2021	Inhibition of caspase-1 by Belnacasan (VX-765) suppressed the transcription of IL-1beta, reduced cell lysis, and significantly promoted IBDV replication in DF-1 cells.	belnacasan	39-45	caspase 1	Homo sapiens	14-23
33454984-0	2021	Nitrosonisoldipine is a selective inhibitor of inflammatory caspases and protects against pyroptosis and related septic shock.	nitrosonisoldipine	0-18	caspase 1	Homo sapiens	60-68
33454984-5	2021	Using murine immortalized bone-marrow derived macrophage and human THP-1 cell line, we further discovered that NTS not only inhibits non-canonical pyroptosis mediated by caspase-11 or caspase-4, but also canonical pyroptosis mediated by caspase-1.	nts	111-114	caspase 1	Homo sapiens	170-179
33454984-6	2021	Mechanistically, NTS directly inhibits the enzyme activities of these inflammatory caspases, and these inhibitory effects persist despite extensive washout of the drug.	nts	17-20	caspase 1	Homo sapiens	83-91
33909257-5	2021	Bavachin boosts the secretion of IL-1beta and caspase-1 caused by ATP or nigericin but not those induced by poly(I:C), monosodium urate crystal, or intracellular lipopolysaccharide.	bavachin	0-8	caspase 1	Homo sapiens	46-55
33760137-3	2021	The present study identified tanshinone IIA as a potent drug that could suppress the proliferation of HK1 cells by enhancing pyroptosis via regulation of the miR-125b/foxp3/caspase-1 signaling pathway.	tanshinone	29-43	caspase 1	Homo sapiens	173-182
33760137-9	2021	In conclusion, the present study demonstrates that tanshinone IIA enhances pyroptosis and inhibits the proliferation of HK1 cells by modulating miR-125b/foxp3/caspase-1/GSDMD signaling.	tanshinone	51-65	caspase 1	Homo sapiens	159-168
33909257-5	2021	Bavachin boosts the secretion of IL-1beta and caspase-1 caused by ATP or nigericin but not those induced by poly(I:C), monosodium urate crystal, or intracellular lipopolysaccharide.	Adenosine Triphosphate	66-69	caspase 1	Homo sapiens	46-55
33909257-5	2021	Bavachin boosts the secretion of IL-1beta and caspase-1 caused by ATP or nigericin but not those induced by poly(I:C), monosodium urate crystal, or intracellular lipopolysaccharide.	Nigericin	73-82	caspase 1	Homo sapiens	46-55
33902703-11	2021	Furthermore, cleaved caspase-1 was induced in the cellular lysates of CIRP/MSU-treated neutrophils.	Uric Acid	75-78	caspase 1	Homo sapiens	21-30
33741688-3	2021	In this study, we show that extracellular heme engages the human inflammatory caspases, caspase-1, caspase-4, and caspase-5, resulting in the release of IL-1beta.	Heme	42-46	caspase 1	Homo sapiens	78-86
33848524-7	2021	RESULTS: Inflammasome activation and oxidative stress were elevated in CECs following exposure to TNF-alpha and IFN-gamma, which resulted in cell death by pyroptosis as determined by LDH release which was inhibited by the caspase-1 inhibitor Ac-YVAD-cmk.	ac-yvad	242-249	caspase 1	Homo sapiens	222-231
33741688-3	2021	In this study, we show that extracellular heme engages the human inflammatory caspases, caspase-1, caspase-4, and caspase-5, resulting in the release of IL-1beta.	Heme	42-46	caspase 1	Homo sapiens	88-97
33741688-5	2021	In human primary macrophages, heme activated caspase-1 in an inflammasome-dependent manner, but heme-induced activation of caspase-4 and caspase-5 was independent of canonical inflammasomes.	Heme	30-34	caspase 1	Homo sapiens	45-54
33835494-3	2021	Here we show that NLR family pyrin domain containing 3 (NLRP3) and caspase 1 (CASP1) are indirectly modulated by the intracellular Cl- concentration, showing maximal expression and activity at 75 mM Cl- , in the presence of the ionophores nigericin and tributyltin.	Nigericin	239-248	caspase 1	Homo sapiens	67-76
33835494-3	2021	Here we show that NLR family pyrin domain containing 3 (NLRP3) and caspase 1 (CASP1) are indirectly modulated by the intracellular Cl- concentration, showing maximal expression and activity at 75 mM Cl- , in the presence of the ionophores nigericin and tributyltin.	Nigericin	239-248	caspase 1	Homo sapiens	78-83
33835494-3	2021	Here we show that NLR family pyrin domain containing 3 (NLRP3) and caspase 1 (CASP1) are indirectly modulated by the intracellular Cl- concentration, showing maximal expression and activity at 75 mM Cl- , in the presence of the ionophores nigericin and tributyltin.	tributyltin	253-264	caspase 1	Homo sapiens	67-76
33835494-3	2021	Here we show that NLR family pyrin domain containing 3 (NLRP3) and caspase 1 (CASP1) are indirectly modulated by the intracellular Cl- concentration, showing maximal expression and activity at 75 mM Cl- , in the presence of the ionophores nigericin and tributyltin.	tributyltin	253-264	caspase 1	Homo sapiens	78-83
33835494-5	2021	The CASP1 inhibitor VX-765 and the NLRP3 inflammasome inhibitor MCC950 completely blocked the Cl- -stimulated IL-1beta mRNA expression and partially the IL-1beta secretion.	belnacasan	20-26	caspase 1	Homo sapiens	4-9
33118609-5	2021	The influence conferred by hyphae-treated HCECs or TSLP treatment was rescued by TSLP neutralizing antibody or VX-765 (caspase-1 inhibitor) treatment.	belnacasan	111-117	caspase 1	Homo sapiens	119-128
32779379-0	2021	Exposure to environmental black carbon exacerbates nasal epithelial inflammation via the reactive oxygen species (ROS)-nucleotide-binding, oligomerization domain-like receptor family, pyrin domain containing 3 (NLRP3)-caspase-1-interleukin 1beta (IL-1beta) pathway.	Carbon	32-38	caspase 1	Homo sapiens	218-227
33830232-4	2021	ACA inhibited Caspase-1 activation and IL-1beta production by NLRP3 agonists such as nigericin, monosodium urate (MSU) crystals, and ATP.	Acetates	0-3	caspase 1	Homo sapiens	14-23
33830232-4	2021	ACA inhibited Caspase-1 activation and IL-1beta production by NLRP3 agonists such as nigericin, monosodium urate (MSU) crystals, and ATP.	Nigericin	85-94	caspase 1	Homo sapiens	14-23
33830232-4	2021	ACA inhibited Caspase-1 activation and IL-1beta production by NLRP3 agonists such as nigericin, monosodium urate (MSU) crystals, and ATP.	Uric Acid	96-112	caspase 1	Homo sapiens	14-23
33830232-4	2021	ACA inhibited Caspase-1 activation and IL-1beta production by NLRP3 agonists such as nigericin, monosodium urate (MSU) crystals, and ATP.	Uric Acid	114-117	caspase 1	Homo sapiens	14-23
33830232-4	2021	ACA inhibited Caspase-1 activation and IL-1beta production by NLRP3 agonists such as nigericin, monosodium urate (MSU) crystals, and ATP.	Adenosine Triphosphate	133-136	caspase 1	Homo sapiens	14-23
33450497-5	2021	Further mechanistic studies revealed that the alleviation of pulmonary toxicity in 6"-DO-BLM Z by a slight change in the sugar moiety could attribute to the decrease of ROS production and thereby reduce the subsequent caspase-1 activity and resulting inflammatory response.	Sugars	121-126	caspase 1	Homo sapiens	218-227
33450497-5	2021	Further mechanistic studies revealed that the alleviation of pulmonary toxicity in 6"-DO-BLM Z by a slight change in the sugar moiety could attribute to the decrease of ROS production and thereby reduce the subsequent caspase-1 activity and resulting inflammatory response.	ros	169-172	caspase 1	Homo sapiens	218-227
32779379-0	2021	Exposure to environmental black carbon exacerbates nasal epithelial inflammation via the reactive oxygen species (ROS)-nucleotide-binding, oligomerization domain-like receptor family, pyrin domain containing 3 (NLRP3)-caspase-1-interleukin 1beta (IL-1beta) pathway.	Reactive Oxygen Species	89-112	caspase 1	Homo sapiens	218-227
32779379-0	2021	Exposure to environmental black carbon exacerbates nasal epithelial inflammation via the reactive oxygen species (ROS)-nucleotide-binding, oligomerization domain-like receptor family, pyrin domain containing 3 (NLRP3)-caspase-1-interleukin 1beta (IL-1beta) pathway.	Reactive Oxygen Species	114-117	caspase 1	Homo sapiens	218-227
33731932-1	2021	Nucleotide-binding domain and leucine-rich repeat pyrin-domain containing protein 1 (NLRP1) is an inflammasome sensor that mediates the activation of caspase-1 to induce cytokine maturation and pyroptosis1-4.	Leucine	30-37	caspase 1	Homo sapiens	150-159
32779379-9	2021	NLRP3 and Caspase-1 inhibitors (MCC950 and YVAD) significantly inhibited IL-1beta expression and NLRP3 activation, but not NLRP3 expression following exposure to BC +- pollen.	YVAD	43-47	caspase 1	Homo sapiens	10-19
32779379-10	2021	CONCLUSION: These findings suggest that exposure to BC and pollen can exaggerate oxidative stress and significantly increase the expression of IL-1beta in hNECs, and that this may involve a pathway integrating ROS-NLRP3-Caspase-1-IL-1beta signaling.	Reactive Oxygen Species	210-213	caspase 1	Homo sapiens	220-229
33043385-0	2021	Cardamonin inhibits cell proliferation by caspase-mediated cleavage of Raptor.	cardamonin	0-10	caspase 1	Homo sapiens	42-49
33043385-2	2021	We investigated the mechanism that cardamonin decreases Raptor expression through caspase-mediated protein degradation.	cardamonin	35-45	caspase 1	Homo sapiens	82-89
33043385-4	2021	We analyzed the gene expression of caspases based on TCGA and GTEx gene expression data in serous cystadenocarcinoma and normal tissues, monitored caspase activity by caspase colorimetric assay kit, detected expression of mTORC1-associated proteins and apoptosis-associated proteins by western blotting, and finally detected cell viability by methyl thiazolyl tetrazolium (MTT) assay.	monooxyethylene trimethylolpropane tristearate	373-376	caspase 1	Homo sapiens	35-42
33741902-0	2021	N6-methyladenosine modification of circCUX1 confers radioresistance of hypopharyngeal squamous cell carcinoma through caspase1 pathway.	N-methyladenosine	0-18	caspase 1	Homo sapiens	118-126
33043385-6	2021	Raptor was cleaved when caspases were activated by cisplatin and caspase-6/caspase-8 was activated by cardamonin in SKOV3 cells.	Cisplatin	51-60	caspase 1	Homo sapiens	24-32
33677475-6	2021	In addition, the volume-sensitive chloride current of OA chondrocytes decreased significantly with the increase of the expression levels of inflammation-related proteins caspase-1, caspase-3, and NLRP3.	Chlorides	34-42	caspase 1	Homo sapiens	170-179
33043385-3	2021	SKOV3 cells and HeLa cells were pretreated with caspase inhibitor z-VAD-fmk for 30 min and then exposed to different doses of cardamonin and cisplatin, respectively.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	66-75	caspase 1	Homo sapiens	48-55
33043385-4	2021	We analyzed the gene expression of caspases based on TCGA and GTEx gene expression data in serous cystadenocarcinoma and normal tissues, monitored caspase activity by caspase colorimetric assay kit, detected expression of mTORC1-associated proteins and apoptosis-associated proteins by western blotting, and finally detected cell viability by methyl thiazolyl tetrazolium (MTT) assay.	methyl thiazolyl tetrazolium	343-371	caspase 1	Homo sapiens	35-43
33043385-4	2021	We analyzed the gene expression of caspases based on TCGA and GTEx gene expression data in serous cystadenocarcinoma and normal tissues, monitored caspase activity by caspase colorimetric assay kit, detected expression of mTORC1-associated proteins and apoptosis-associated proteins by western blotting, and finally detected cell viability by methyl thiazolyl tetrazolium (MTT) assay.	methyl thiazolyl tetrazolium	343-371	caspase 1	Homo sapiens	35-42
33043385-4	2021	We analyzed the gene expression of caspases based on TCGA and GTEx gene expression data in serous cystadenocarcinoma and normal tissues, monitored caspase activity by caspase colorimetric assay kit, detected expression of mTORC1-associated proteins and apoptosis-associated proteins by western blotting, and finally detected cell viability by methyl thiazolyl tetrazolium (MTT) assay.	monooxyethylene trimethylolpropane tristearate	373-376	caspase 1	Homo sapiens	35-43
33738798-1	2021	The nucleotide-binding domain leucine-rich repeat (LRR)-containing protein family pyrin domain (PYD)-containing protein 1 (NLRP1) forms an inflammasome complex with apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC) and caspase-1.	Leucine	30-37	caspase 1	Homo sapiens	255-264
33720048-6	2021	Mechanistically, caspase-1 activation closely correlated with the inflammatory marker expression and was shown to occur through NLRP3 inflammasome activation driven by virus-dependent and/or -independent ROS production, while caspase-3 activation in CD4+ T cells was more closely related to T cell activation status.	ros	204-207	caspase 1	Homo sapiens	17-26
33724611-9	2021	Subsequently, we found that TRIM24 negatively regulated NLRP3/Caspase-1/IL-1beta-mediated pyroptosis and cell migration of hESC, and CY-09, the specific inhibitor of NLRP3, could reverse the promoted pyroptosis and cell migration induced by siTRIM24.	sitrim24	241-249	caspase 1	Homo sapiens	62-71
33691097-5	2021	Mechanistically, itaconate accumulation upon prolonged inflammatory stimulation prevents full caspase-1 activation and processing of gasdermin D, which we demonstrate to be post-translationally modified by endogenous itaconate.	itaconic acid	17-26	caspase 1	Homo sapiens	94-103
33683342-6	2021	Unexpectedly, the CD66b+CD16dim granulocytes had decreased nigericin-triggered caspase-1 activation potential associated with an increased percentage of NLRP3 inflammasome impaired immature neutrophils and a loss of eosinophils in the blood.	Nigericin	59-68	caspase 1	Homo sapiens	79-88
33683342-7	2021	In patients who recovered from COVID-19, nigericin-triggered caspase-1 activation potential in CD66b+CD16dim cells was restored and the proportion of immature neutrophils was similar to control.	Nigericin	41-50	caspase 1	Homo sapiens	61-70
33650689-6	2021	Human oral keratinocyte (HOK) was stimulated with normal and high glucose, and pre-treated with Z-YVAD-FMK (Caspase-1 inhibitor) prior to evaluating cellular senescence, SASP secretion, and inflammasome activation.	benzyloxycarbonyltyrosyl-valyl-alanyl-aspartic acid fluoromethyl ketone	96-106	caspase 1	Homo sapiens	108-117
33747105-13	2021	It was found that GLGZG could inhibit OGD/R-induced cell apoptosis, increase neuronal cell viability, decrease the production of IL-18 and IL-1beta, and downregulate the expression levels of pyroptosis markers (NLRP3, ASC, and caspase-1).	glgzg	18-23	caspase 1	Homo sapiens	227-236
33747919-4	2021	Recent studies have shown a potential role of EMP1, CASP1, and NLRP3 genes in prednisolone response.	Prednisolone	78-90	caspase 1	Homo sapiens	52-57
33663554-5	2021	ROS scavenger N-acetyl-L-cysteine (NAC) and caspase-1 inhibitor VX-765 were used to intervene in PM2.5-induced damages.	belnacasan	64-70	caspase 1	Homo sapiens	44-53
33650689-9	2021	In vitro, high glucose-induced the inflammaging in HOK, and blocking inflammasome activation through inhibiting Caspase-1 and glucose-induced inflammaging.	Glucose	15-22	caspase 1	Homo sapiens	112-121
33605079-11	2021	Furthermore, LPZ deteriorated cisplatin-induced inflammation, as revealed by the increased mRNA expression of pro-inflammatory factors including, NLRP3, IL-1beta, TNF-alpha and caspase 1, as well as neutrophil infiltration.	Lansoprazole	13-16	caspase 1	Homo sapiens	177-186
33187650-8	2021	DBDPE not only induced cytotoxicity and reactive oxygen species (ROS) generation in HAECs but also caused HAECs pyroptosis, which was evidenced by the elevated expression of Nod-like receptor protein -3 (NLRP3), ASC, and caspase-1 in DBDPE-treated group.	decabromodiphenyl ethane	0-5	caspase 1	Homo sapiens	221-230
33433347-5	2021	Simultaneously, Mo or/and Cd upregulated ASC, NLRP3, NEK7, Caspase-1, GSDMA, GSDME, IL-18 and IL-1beta mRNA levels and Caspase-1 p20, NLRP3, ASC, GSDMD protein levels, increased the percentage of pyroptotic cells, LDH, NO, IL-18 and IL-1beta releases as well as relative conductivity.	Cadmium	26-28	caspase 1	Homo sapiens	59-68
33433347-5	2021	Simultaneously, Mo or/and Cd upregulated ASC, NLRP3, NEK7, Caspase-1, GSDMA, GSDME, IL-18 and IL-1beta mRNA levels and Caspase-1 p20, NLRP3, ASC, GSDMD protein levels, increased the percentage of pyroptotic cells, LDH, NO, IL-18 and IL-1beta releases as well as relative conductivity.	Cadmium	26-28	caspase 1	Homo sapiens	119-128
32896537-8	2021	This was in contrast to the methotrexate-treated patients who exhibited persistent, increased caspase-1 reactivity.	Methotrexate	28-40	caspase 1	Homo sapiens	94-103
33422385-11	2021	Caspase1 correlated positively with Isoleucine, GABA, Carnitine, and PC34:2.	Isoleucine	36-46	caspase 1	Homo sapiens	0-8
33422385-11	2021	Caspase1 correlated positively with Isoleucine, GABA, Carnitine, and PC34:2.	gamma-Aminobutyric Acid	48-52	caspase 1	Homo sapiens	0-8
33422385-11	2021	Caspase1 correlated positively with Isoleucine, GABA, Carnitine, and PC34:2.	Carnitine	54-63	caspase 1	Homo sapiens	0-8
33389490-4	2021	NLRP3 (NOD-, LRR-, and pyrin domain-containing 3) senses the stimuli signal of excessive uric acid and then it recruits apoptosis-related specular protein (ASC) as well as aspartic acid-specific cysteine protease (caspase)-1 precursor to form NLRP3 inflammasome.	Uric Acid	89-98	caspase 1	Homo sapiens	195-224
33389490-4	2021	NLRP3 (NOD-, LRR-, and pyrin domain-containing 3) senses the stimuli signal of excessive uric acid and then it recruits apoptosis-related specular protein (ASC) as well as aspartic acid-specific cysteine protease (caspase)-1 precursor to form NLRP3 inflammasome.	Aspartic Acid	172-185	caspase 1	Homo sapiens	195-224
33626512-4	2021	Treating bone marrow-derived macrophages (BMDMs) with nicotine in vitro led to enhanced lipid phagocytosis, chemotaxis, and increased production of reactive oxygen species (ROS), which activated TXNIP/NLRP3 inflammasome signaling and promoted pyroptosis, as evidenced by caspase-1 cleavage and increased production of IL-1beta, IL-18, and gasdermin D.	Nicotine	54-62	caspase 1	Homo sapiens	271-280
33383234-0	2021	Reduced intracellular antioxidant capacity in platelets contributes to primary immune thrombocytopenia via ROS-NLRP3-caspase-1 pathway.	ros	107-110	caspase 1	Homo sapiens	117-126
33383234-11	2021	Pretreating ITP platelets with NLRP3 inhibitor MCC950 or caspase-1 inhibitor Z-YVAD-FMK significantly reduced the proportion of pyroptotic cells in H2O2-treated ITP platelets and suppressed IL-1beta secretion in supernatants.	benzyloxycarbonyltyrosyl-valyl-alanyl-aspartic acid fluoromethyl ketone	77-87	caspase 1	Homo sapiens	57-66
33383234-11	2021	Pretreating ITP platelets with NLRP3 inhibitor MCC950 or caspase-1 inhibitor Z-YVAD-FMK significantly reduced the proportion of pyroptotic cells in H2O2-treated ITP platelets and suppressed IL-1beta secretion in supernatants.	Hydrogen Peroxide	148-152	caspase 1	Homo sapiens	57-66
33279259-8	2021	RESULTS: Significantly raised levels of caspase-1, BNIP3, and NADPH oxidase mRNA expression were identified in cardiac chambers from BDD hearts compared to DCD hearts, and these differences were exaggerated in older donors.	7,7'-dimethoxy-(4,4'-bi-1,3-benzodioxole)-5,5'-dicarboxylic acid dimethyl ester	133-136	caspase 1	Homo sapiens	40-49
33626512-4	2021	Treating bone marrow-derived macrophages (BMDMs) with nicotine in vitro led to enhanced lipid phagocytosis, chemotaxis, and increased production of reactive oxygen species (ROS), which activated TXNIP/NLRP3 inflammasome signaling and promoted pyroptosis, as evidenced by caspase-1 cleavage and increased production of IL-1beta, IL-18, and gasdermin D.	Reactive Oxygen Species	173-176	caspase 1	Homo sapiens	271-280
33559194-6	2021	METHODS: Recently, work has published demonstrating that Normal Human Epidermal Keratinocytes (NHEKs) can be activated by UVB and ATP to express active Caspase-1 via NLRP inflammasome-mediated pathways.	Adenosine Triphosphate	130-133	caspase 1	Homo sapiens	152-161
33385416-12	2021	CONCLUSIONS: /interpretation: Taken together, our study showed that miR-21-3p aggravates STZ-induced diabetic cardiac fibrosis through the caspase1 pathways by suppressing AR expression.	Streptozocin	89-92	caspase 1	Homo sapiens	139-147
33559194-7	2021	There was a strong interest to see if, highly purified Cannabidiol Isolate (>99% purity) might function to control release of active Caspase-1 by testing of NHEKs using the previously described models.	Cannabidiol	55-66	caspase 1	Homo sapiens	133-142
33546151-7	2021	We report novel functions for AgNPs-affected autophagy, represented by the control of the release of IL-1beta, caspase-1, adaptor protein apoptosis-associated speck-like protein containing a CARD (ASC), and NLRP3 in BMDMs following treatment with LPS+ATP.	Adenosine Triphosphate	251-254	caspase 1	Homo sapiens	111-195
33559194-11	2021	CONCLUSIONS: Data presented suggests that if Cannabidiol functions as an anti-inflammatory, it does so through pathways not associated with either the NLRP inflammasome-mediated expression of Caspase-1 or through the more commonly known expression of interleukin or prostaglandin inflammatory pathways.	Cannabidiol	45-56	caspase 1	Homo sapiens	192-201
33430331-7	2021	Caspase-1 activity was measured with a fluorescent labeled inhibitor of caspase-1 (FLICA; FAM-YVAD-FMK) and detected microscopically.	fam-yvad-fmk	90-102	caspase 1	Homo sapiens	0-9
32396707-0	2021	Resibufogenin Suppresses Growth and Metastasis through Inducing Caspase-1-Dependent Pyroptosis via ROS-Mediated NF-kappaB Suppression in Non-Small Cell Lung Cancer.	bufogenin	0-13	caspase 1	Homo sapiens	64-73
32396707-12	2021	Further study demonstrated that RB induced pyroptosis in a caspase-1-dependent manner, as evidenced by the finding that VX765 effectively reversed the effects of RB on A549 and H520 cells.	bufogenin	32-34	caspase 1	Homo sapiens	59-68
32396707-13	2021	We also found that RB could trigger caspase-1-dependent pyroptosis through ROS-mediated NF-kappaB suppression.	Reactive Oxygen Species	75-78	caspase 1	Homo sapiens	36-45
32966618-10	2021	The miR-223 inhibitor further promoted ATP plus LPS-induced NLRP3/CASP1 inflammasome pathway activation compared to the ATP plus LPS-induced group (p<0.05).	Adenosine Triphosphate	39-42	caspase 1	Homo sapiens	66-71
33469482-7	2021	Quercetin inhibited angiogenesis of HRMECs as well as the expressions of NLRP3, ASC, Caspase-1, IL-1beta, IL-18, LC3, Beclin-1, and autophagy of HRMECs under a HG condition.	Quercetin	0-9	caspase 1	Homo sapiens	85-94
33157513-0	2021	Inhibition of ROS/NLRP3/Caspase-1 mediated pyroptosis alleviates excess molybdenum-induced apoptosis in duck renal tubular epithelial cells.	Molybdenum	72-82	caspase 1	Homo sapiens	24-33
32966618-11	2021	In contrast, the miR-223 mimic significantly inhibited the NLRP3/CASP1 inflammasome pathway activation induced by ATP plus LPS compared to the ATP plus LPS-induced group (p<0.05).	Adenosine Triphosphate	114-117	caspase 1	Homo sapiens	65-70
33470533-9	2021	In the Langendorff model, PD98059 inhibited ERK1/2 and up-regulated the expression of NOX4, NLRP3, caspase-1 and IL-1beta, which exacerbated oxidative stress and inflammation.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	26-33	caspase 1	Homo sapiens	99-108
33430857-13	2021	miR-107 overexpression down-regulated the expression of caspase-1, c-caspase-1, GSDMD-N, and TLR4 in chondrocytes induced by LPS and ATP.	Adenosine Triphosphate	133-136	caspase 1	Homo sapiens	56-65
33325949-0	2021	Taxifolin ameliorate high-fat-diet feeding plus acute ethanol binge-induced steatohepatitis through inhibiting inflammatory caspase-1-dependent pyroptosis.	taxifolin	0-9	caspase 1	Homo sapiens	124-133
33325949-6	2021	In addition, TAX inhibited the expression of P2X7R, IL-1beta, and caspase-1.	taxifolin	13-16	caspase 1	Homo sapiens	66-75
33325949-7	2021	Moreover, TAX reduced the expression of caspase-1 activation; thereby inhibiting the recruitment of macrophages and neutrophils.	taxifolin	10-13	caspase 1	Homo sapiens	40-49
33065089-10	2021	MIAT antagonized the effect of miR-342-3p on the depression of its target CASP1 and promoted AGE-BSA-induced pericyte pyroptosis.	mir-342-3p	31-41	caspase 1	Homo sapiens	74-79
33325949-8	2021	TAX also improved the inflammatory response caused by caspase-1 activation in steatotic hepatocytes.	taxifolin	0-3	caspase 1	Homo sapiens	54-63
33325949-9	2021	TAX exhibited an inhibitory effect on lipid accumulation and caspase-1-related pyroptosis.	taxifolin	0-3	caspase 1	Homo sapiens	61-70
33325949-10	2021	Collectively, TAX has therapeutic potential as an intervention of steatohepatitis induced by alcohol combined with HFD and for preventing non-alcoholic fatty liver degeneration targeting caspase-1-dependent pyroptosis.	taxifolin	14-17	caspase 1	Homo sapiens	187-196
33160017-0	2021	The SGLT2 inhibitor Empagliflozin attenuates interleukin-17A-induced human aortic smooth muscle cell proliferation and migration by targeting TRAF3IP2/ROS/NLRP3/Caspase-1-dependent IL-1beta and IL-18 secretion.	empagliflozin	20-33	caspase 1	Homo sapiens	161-170
33160017-6	2021	Importantly, SMC express SGLT2, and pre-treatment with EMPA attenuated IL-17A/TRAF3IP2-dependent oxidative stress, NLRP3 expression, caspase-1 activation, IL-1beta and IL-18 secretion, and SMC proliferation and migration.	empagliflozin	55-59	caspase 1	Homo sapiens	133-142
33402173-15	2021	Moreover, isoliquiritin protected primary microglia against LPS and adenosine triphosphate (ATP) elicited NLRP3 inflammasome activation in vitro, evidenced by declined protein levels of p-NF-kappaB, NLRP3; cleaved Caspase-1, IL-1beta, and GSDMD-N; upregulated miRNA-27a mRNA expression; and decreased the mRNA and protein levels of SYK.	neoisoliquiritin	10-23	caspase 1	Homo sapiens	214-223
33402173-15	2021	Moreover, isoliquiritin protected primary microglia against LPS and adenosine triphosphate (ATP) elicited NLRP3 inflammasome activation in vitro, evidenced by declined protein levels of p-NF-kappaB, NLRP3; cleaved Caspase-1, IL-1beta, and GSDMD-N; upregulated miRNA-27a mRNA expression; and decreased the mRNA and protein levels of SYK.	Adenosine Triphosphate	92-95	caspase 1	Homo sapiens	214-223
33470344-7	2021	Moreover, high glucose upregulated the protein expression of interleukin-1beta, ionized calcium-binding adapter molecule-1, NOD-like receptor family pyrin domain containing 3, cleaved caspase-1, and cleaved gasdermin D.	Glucose	15-22	caspase 1	Homo sapiens	184-193
33049092-4	2021	METHODS: Human THP-1 cells or primary human monocytes were differentiated, treated with APC or PAR-derived peptides, and then stimulated with LPS and ATP to induce caspase-1 activity, a product of inflammasome activation.	Adenosine Triphosphate	150-153	caspase 1	Homo sapiens	164-173
33189612-4	2021	This study found that lipopolysaccharide + ATP upregulated Meg3, promoted microglia activation, Nlrp3/caspase1 activation and inflammation, and markedly reduced miR-7a-5p.	Adenosine Triphosphate	43-46	caspase 1	Homo sapiens	102-110
33199234-0	2021	Suppressing ROS generation by apocynin inhibited cyclic stretch-induced inflammatory reaction in HPDLCs via a caspase-1 dependent pathway.	Reactive Oxygen Species	12-15	caspase 1	Homo sapiens	110-119
33199234-0	2021	Suppressing ROS generation by apocynin inhibited cyclic stretch-induced inflammatory reaction in HPDLCs via a caspase-1 dependent pathway.	acetovanillone	30-38	caspase 1	Homo sapiens	110-119
33199234-6	2021	The cyclic stretch also induced the expression of caspase-1 and NLRP3 inflammasome, which could also be inhibited by apocynin.	acetovanillone	117-125	caspase 1	Homo sapiens	50-59
33199234-8	2021	Collectively, it is the first time that increased intracellular ROS was proved to play as an intermediate signal in the cyclic stretch-induced inflammatory reaction in HPDLCs, via a caspase-1-dependent pathway.	Reactive Oxygen Species	64-67	caspase 1	Homo sapiens	182-191
34033101-6	2021	These include cleavage of GSDM D and E, activation and release of IL-1beta and IL-18, and activation of cysteinyl aspartate specific proteinase (caspase-1, -3, -4, -5, and -11).	lysyl-cysteinyl-cysteinyl-arginyl-cysteinyl-lysine	104-113	caspase 1	Homo sapiens	145-175
34033101-6	2021	These include cleavage of GSDM D and E, activation and release of IL-1beta and IL-18, and activation of cysteinyl aspartate specific proteinase (caspase-1, -3, -4, -5, and -11).	Aspartic Acid	114-123	caspase 1	Homo sapiens	145-175
33379407-7	2020	RSV down-regulated nuclear factor-kappaB activation, IkappaBalpha phosphorylation as well as activation of receptor-interacting protein2 and caspase-1 in HMC-1 cells.	Resveratrol	0-3	caspase 1	Homo sapiens	141-150
33500734-7	2021	Results: Exposure to the PPARgamma agonist, rosiglitazone, during the second signal of NLRP3 inflammasome activation attenuated caspase-1 and IL-1beta maturation.	Rosiglitazone	44-57	caspase 1	Homo sapiens	128-137
33396676-6	2020	However, NLRP3 and cleaved caspase-1 complex formation increased with hyperglycemia and cytokine challenge but was inhibited by tonabersat treatment.	tonabersat	128-138	caspase 1	Homo sapiens	27-36
33456483-6	2020	To determine how aldosterone (Aldo) activated the mineralocorticoid receptor (MR) and then induced mesangial cell pyroptosis with NLRP3-caspase-1-IL-1beta pathway, human mesangial cells (HMCs) were treated with HJHR and eplerenone, which were examined to detect the expression of NLRP3 inflammasome-associated proteins following treatment with Aldo.	Aldosterone	30-34	caspase 1	Homo sapiens	136-145
32621119-6	2020	MLKL-induced caspase-1 activation and IL-1beta maturation were abolished by NLR family, pyrin domain-containing 3 (NLRP3) specific inhibitor MCC950, or extracellular high potassium concentration.	Potassium	171-180	caspase 1	Homo sapiens	13-22
33332241-6	2021	In this study, melatonin attenuated the expression of pyroptosis-related genes, including NLRP3, caspase-1 and IL-1beta, in human umbilical vein endothelial cells treated with oxidised low-density lipoprotein.	Melatonin	15-24	caspase 1	Homo sapiens	97-106
33318544-7	2020	Furthermore, inhibition of caspase-1 and NLRP3 activation increased neutrophil ROS-production, phagocytosis and the ability of neutrophils to suppress UPEC growth.	ros	79-82	caspase 1	Homo sapiens	27-36
32098511-8	2020	Doxofylline inhibits LPS-induced NLRP3-TXNIP inflammasome activation as revealed by its inhibitive effect on NLRP3, caspase 1 (P10 unit), and TXNIP induction as well as weakened induction of IL-1beta and IL-18.	doxofylline	0-11	caspase 1	Homo sapiens	116-125
33208362-5	2020	We further demonstrate that GSDMD inactivation by apoptotic caspases at aspartate 88 (D88) suppresses TNF-induced lethality but promotes anti-Yersinia defense.	Aspartic Acid	72-81	caspase 1	Homo sapiens	60-68
33145937-8	2020	Moreover, miR-223-3p showed a notable inhibitory effect on recombinant Tp17 (rTP17)-induced caspase-1 activation, resulting in decrease in IL-1beta production and pyroptosis, which was accompanied by the release of lactate dehydrogenase (LDH) in HUVECs.	mir-223-3p	10-20	caspase 1	Homo sapiens	92-101
33208362-5	2020	We further demonstrate that GSDMD inactivation by apoptotic caspases at aspartate 88 (D88) suppresses TNF-induced lethality but promotes anti-Yersinia defense.	NLVSGLIEARKYLEQLHRKLKNRKV	86-89	caspase 1	Homo sapiens	60-68
33168816-1	2020	Accumulating data indicate caspase-1 (CASP1), one of the inflammatory caspases, promotes hepatocellular carcinoma (HCC) progression in tumor proliferation, invasion, EMT phenotype and sorafenib resistance.	Sorafenib	184-193	caspase 1	Homo sapiens	27-36
33196459-7	2020	In retinoic acid-differentiated ATXN3/Q75-GFP SH-SY5Y cells inflamed with IFN-gamma-primed HMC3 conditioned medium, treatment with the tested compounds mitigated the increased caspase 1 activity and lactate dehydrogenase release, reduced polyQ aggregation and ROS and/or promoted neurite outgrowth.	Tretinoin	3-16	caspase 1	Homo sapiens	176-185
33168816-1	2020	Accumulating data indicate caspase-1 (CASP1), one of the inflammatory caspases, promotes hepatocellular carcinoma (HCC) progression in tumor proliferation, invasion, EMT phenotype and sorafenib resistance.	Sorafenib	184-193	caspase 1	Homo sapiens	38-43
33168816-1	2020	Accumulating data indicate caspase-1 (CASP1), one of the inflammatory caspases, promotes hepatocellular carcinoma (HCC) progression in tumor proliferation, invasion, EMT phenotype and sorafenib resistance.	Sorafenib	184-193	caspase 1	Homo sapiens	70-78
33152658-7	2020	HBC treatment with both LPS and ATP induced caspase-1 activation, gasdermin D (GSDMD) cleavage, which mediates pyroptosis, and IL-1beta processing.	Adenosine Triphosphate	32-35	caspase 1	Homo sapiens	44-53
32506648-15	2020	In conclusion, Arha inhibited UA transport as well as preventing inflammation and pyroptosis via activating PPARgamma thereby blocking caspase-1 activation of HUA in vitro.	arhalofenate	15-19	caspase 1	Homo sapiens	135-144
32769069-6	2020	EGCG prevented caspase-1 activity and decreased transcriptional activity of nuclear factor (NF)-kappaB by suppressing inhibitory protein kappaBalpha phosphorylation in RANKL-stimulated HMC-1 cells.	epigallocatechin gallate	0-4	caspase 1	Homo sapiens	15-24
32769069-9	2020	Overall, these results suggest that EGCG acts as a natural agent for preventing and treating RANKL-mediated inflammatory diseases by targeting PI3 Kinase, MAP Kinase, caspase-1, and NF-kappaB signaling cascade in mast cells.	epigallocatechin gallate	36-40	caspase 1	Homo sapiens	167-176
33050989-2	2020	We had previously reported that TG-induced macrophage death is triggered by caspase-1 and -2, therefore we investigated the mechanism underlying this phenomenon.	Triglycerides	32-34	caspase 1	Homo sapiens	76-92
33050989-3	2020	We found that potassium efflux is increased in TG-treated THP-1 macrophages and that the inhibition of potassium efflux blocks TG-induced cell death as well as caspase-1 and -2 activation.	Potassium	14-23	caspase 1	Homo sapiens	160-176
33050989-3	2020	We found that potassium efflux is increased in TG-treated THP-1 macrophages and that the inhibition of potassium efflux blocks TG-induced cell death as well as caspase-1 and -2 activation.	Triglycerides	47-49	caspase 1	Homo sapiens	160-176
33050989-3	2020	We found that potassium efflux is increased in TG-treated THP-1 macrophages and that the inhibition of potassium efflux blocks TG-induced cell death as well as caspase-1 and -2 activation.	Potassium	103-112	caspase 1	Homo sapiens	160-176
33050989-4	2020	Furthermore, reducing ATP concentration (known to induce potassium efflux), restored cell viability and caspase-1 and -2 activity.	Adenosine Triphosphate	22-25	caspase 1	Homo sapiens	104-120
33050989-4	2020	Furthermore, reducing ATP concentration (known to induce potassium efflux), restored cell viability and caspase-1 and -2 activity.	Potassium	57-66	caspase 1	Homo sapiens	104-120
33050989-6	2020	Inhibition of pannexin-1 activity using its inhibitor, probenecid, recovered cell viability and blocked the activation of caspase-1 and -2 in TG-treated macrophages.	Probenecid	55-65	caspase 1	Homo sapiens	122-138
33050989-6	2020	Inhibition of pannexin-1 activity using its inhibitor, probenecid, recovered cell viability and blocked the activation of caspase-1 and -2 in TG-treated macrophages.	Triglycerides	142-144	caspase 1	Homo sapiens	122-138
32506648-0	2020	The mechanism of Arhalofenate in alleviating hyperuricemia-Activating PPARgamma thereby reducing caspase-1 activity.	arhalofenate	17-29	caspase 1	Homo sapiens	97-106
32506648-14	2020	Besides, the co-treatment of Mifobate blunted the effects of Arha on cell viability and expression of GSDMD, TLR4, and caspase-1.	mifobate	29-37	caspase 1	Homo sapiens	119-128
32506648-14	2020	Besides, the co-treatment of Mifobate blunted the effects of Arha on cell viability and expression of GSDMD, TLR4, and caspase-1.	arhalofenate	61-65	caspase 1	Homo sapiens	119-128
33117829-0	2020	Ethyl Pyruvate Reduces Systemic Leukocyte Activation via Caspase-1 and NF-kappaB After Blunt Chest Trauma and Haemorrhagic Shock.	ethyl pyruvate	0-14	caspase 1	Homo sapiens	57-66
32497199-5	2020	Consistently, other HSP90 inhibitors, including Radicicol, 17-DMAG and 17-AAG, all ameliorated pyroptosis in THP-1 cells by suppressing the inflammasome/Caspase-1/GSDMD signal pathway in pyroptosis.	monorden	48-57	caspase 1	Homo sapiens	153-162
32497199-5	2020	Consistently, other HSP90 inhibitors, including Radicicol, 17-DMAG and 17-AAG, all ameliorated pyroptosis in THP-1 cells by suppressing the inflammasome/Caspase-1/GSDMD signal pathway in pyroptosis.	17-(dimethylaminoethylamino)-17-demethoxygeldanamycin	59-66	caspase 1	Homo sapiens	153-162
32497199-5	2020	Consistently, other HSP90 inhibitors, including Radicicol, 17-DMAG and 17-AAG, all ameliorated pyroptosis in THP-1 cells by suppressing the inflammasome/Caspase-1/GSDMD signal pathway in pyroptosis.	tanespimycin	71-77	caspase 1	Homo sapiens	153-162
33497945-0	2020	Inhibition of ROS/NLRP3/Caspase-1 mediated pyroptosis attenuates cadmium-induced apoptosis in duck renal tubular epithelial cells.	Cadmium	65-72	caspase 1	Homo sapiens	24-33
33497945-4	2020	Simultaneously, Cd also markedly upregulated NLRP3, Caspase-1, ASC, NEK7, IL-1beta and IL-18 mRNA levels and NLRP3, Caspase-1 p20, GSDMD and ASC protein levels.	Cadmium	16-18	caspase 1	Homo sapiens	52-61
33497945-4	2020	Simultaneously, Cd also markedly upregulated NLRP3, Caspase-1, ASC, NEK7, IL-1beta and IL-18 mRNA levels and NLRP3, Caspase-1 p20, GSDMD and ASC protein levels.	Cadmium	16-18	caspase 1	Homo sapiens	116-125
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 1	Homo sapiens	21-30
33066043-8	2020	Cells treated with D089 in addition to either a caspase 1 inhibitor or siRNA-caspase 1 showed increased IC50 values, indicating a contribution of cleaved caspase 1 to cell death.	d089	19-23	caspase 1	Homo sapiens	48-57
33066043-8	2020	Cells treated with D089 in addition to either a caspase 1 inhibitor or siRNA-caspase 1 showed increased IC50 values, indicating a contribution of cleaved caspase 1 to cell death.	d089	19-23	caspase 1	Homo sapiens	77-86
33066043-8	2020	Cells treated with D089 in addition to either a caspase 1 inhibitor or siRNA-caspase 1 showed increased IC50 values, indicating a contribution of cleaved caspase 1 to cell death.	d089	19-23	caspase 1	Homo sapiens	77-86
32970791-2	2020	We show that increases in exosome secretion induced by either viral infection or LPS/ATP exposure result from inflammasome activation and subsequent caspase-1-dependent cleavage of the trafficking adaptor protein RILP.	Adenosine Triphosphate	85-88	caspase 1	Homo sapiens	149-158
33497945-7	2020	Taken together, Cd exposure induces duck renal tubular epithelial cell pyroptosis through ROS/NLRP3/Caspase-1 signaling pathway, and inhibiting Caspase-1 dependent pyroptosis attenuates Cd-induced apoptosis.	Cadmium	16-18	caspase 1	Homo sapiens	100-109
33497945-7	2020	Taken together, Cd exposure induces duck renal tubular epithelial cell pyroptosis through ROS/NLRP3/Caspase-1 signaling pathway, and inhibiting Caspase-1 dependent pyroptosis attenuates Cd-induced apoptosis.	Cadmium	16-18	caspase 1	Homo sapiens	144-153
33497945-7	2020	Taken together, Cd exposure induces duck renal tubular epithelial cell pyroptosis through ROS/NLRP3/Caspase-1 signaling pathway, and inhibiting Caspase-1 dependent pyroptosis attenuates Cd-induced apoptosis.	Cadmium	186-188	caspase 1	Homo sapiens	144-153
32941596-3	2020	Nucleotide-binding and leucine-rich repeat-containing receptors (NLRs) encompass a large number of innate immune sensors and receptors, which mediate the activation of Caspase-1 and the subsequent release of mature interleukin-1beta and interleukin-18.	Leucine	23-30	caspase 1	Homo sapiens	168-177
32659366-14	2020	SIGNIFICANCE: FL118 restrains the growth and metastasis of colorectal cancer by inducing NLRP3-ASC-Caspase-1 mediated pyroptosis, which provides important evidence in the study on the role of pyroptosis and different tumors.	7-ethyl-7-hydroxy-10H-1,3-Dioxolo(4,5-g)pyrano(3',4':6,7)indolizino(1,2-b)quinoline-8,11(7H,12H)-dione	14-19	caspase 1	Homo sapiens	99-108
31993881-0	2020	The role of Caspase-1/GSDMD-mediated pyroptosis in Taxol-induced cell death and a Taxol-resistant phenotype in nasopharyngeal carcinoma regulated by autophagy.	Paclitaxel	51-56	caspase 1	Homo sapiens	12-21
31993881-5	2020	In this study, we observed that Taxol treatment caused pyroptotic cell death, along with activation of Caspase-1 and maturation of IL-1beta, as well as cleavage of GSDMD, which is the canonical pyroptosis executor.	Paclitaxel	32-37	caspase 1	Homo sapiens	103-112
31993881-6	2020	Furthermore, Taxol-induced pyroptotic cell death could be suppressed by Caspase-1 inhibitor (Z-YVAD-FMK) and GSDMD knockout.	Paclitaxel	13-18	caspase 1	Homo sapiens	72-81
31993881-6	2020	Furthermore, Taxol-induced pyroptotic cell death could be suppressed by Caspase-1 inhibitor (Z-YVAD-FMK) and GSDMD knockout.	tyrosyl-valyl-alanyl-aspartic acid fluoromethyl ketone	93-103	caspase 1	Homo sapiens	72-81
31993881-7	2020	Moreover, NPC parental cells demonstrated higher levels of pyroptosis than Taxol-resistant cells, and pyroptosis mediated by Caspase-1/GSDMD suppression induced by a Caspase-1 inhibitor and GSDMD knockout could induce a Taxol-resistant phenotype in vitro and in vivo.	Paclitaxel	75-80	caspase 1	Homo sapiens	125-134
31993881-7	2020	Moreover, NPC parental cells demonstrated higher levels of pyroptosis than Taxol-resistant cells, and pyroptosis mediated by Caspase-1/GSDMD suppression induced by a Caspase-1 inhibitor and GSDMD knockout could induce a Taxol-resistant phenotype in vitro and in vivo.	Paclitaxel	220-225	caspase 1	Homo sapiens	125-134
31993881-8	2020	By transfecting an siRNA targeting Beclin-1 into NPC Taxol-resistant cells, we discovered that autophagy could negatively regulate pyroptosis by inhibiting Caspase-1/GSDMD activation.	Paclitaxel	53-58	caspase 1	Homo sapiens	156-165
31993881-9	2020	Taken together, our results indicated that Caspase-1/GSDMD mediated Taxol-induced pyroptosis and a Taxol-resistant phenotype in NPC cell lines, which may be regulated by autophagy.	Paclitaxel	68-73	caspase 1	Homo sapiens	43-52
31993881-9	2020	Taken together, our results indicated that Caspase-1/GSDMD mediated Taxol-induced pyroptosis and a Taxol-resistant phenotype in NPC cell lines, which may be regulated by autophagy.	Paclitaxel	99-104	caspase 1	Homo sapiens	43-52
32794617-4	2020	Uric acid sodium salt induces caspase-1 activation, cell death, and the expression of proinflammatory cytokines, including IL-1alpha, IL-6, and IL-8, in the human keratinocyte HOK-16B cell line.	Uric acid sodium salt	0-21	caspase 1	Homo sapiens	30-39
32651843-7	2020	Thirdly, further evaluation of the major components of the NLRP3 inflammasome revealed that PNX-20 inhibited LPS-mediated upregulation of NLRP3, ASC, and cleaved caspase-1 (P10).	pnx-20	92-98	caspase 1	Homo sapiens	162-171
33134423-3	2020	Six months of elvitegravir/cobicistat/emtricitabine/tenofovir disoproxil fumarate significantly decreased caspase-1 levels in association with CD4+/CD8+ ratio recovery.	Elvitegravir, Cobicistat, Emtricitabine, Tenofovir Disoproxil Fumarate Drug Combination	14-81	caspase 1	Homo sapiens	106-115
32711374-8	2020	Moreover, the levels of pro-cytokines were positively correlated with caspase-1 and serum cotinine, corroborating the secretion of cytokines in a caspase-1-dependent manner.	Cotinine	90-98	caspase 1	Homo sapiens	146-155
32945495-9	2020	Furthermore, NAC reduced the expression of ASC, NLRP3, caspase-1 and TXNIP, but enhanced that of TRX.	Acetylcysteine	13-16	caspase 1	Homo sapiens	55-64
32390268-10	2020	However, PRBC-SN alone increased caspase-1 production.	prbc-sn	9-16	caspase 1	Homo sapiens	33-42
32390268-12	2020	PRBC-SN augmented LPS-driven IL-1beta and caspase-1 production.	prbc-sn	0-7	caspase 1	Homo sapiens	42-51
32983576-7	2020	Bafilomycin-A1 treatment significantly increased caspase-1 and Pro-IL-1beta expression in normal and MCD keratocytes.	bafilomycin	0-11	caspase 1	Homo sapiens	49-58
32983576-8	2020	Nod-like receptors pyrins-3 (NLRP3), caspase-1, Pro-IL-1beta, and IL-1beta levels were pronouncedly elevated in cells exposed to H2O2.	Hydrogen Peroxide	129-133	caspase 1	Homo sapiens	37-46
32907600-6	2020	Caspase-1 pathway was studied by measurements of its activation state and its role in PBMCs adhesion, transmigration, and BBB permeability were investigated using the specific caspase-1 inhibitor, VX-765.	belnacasan	197-203	caspase 1	Homo sapiens	0-9
32917871-7	2020	These results suggest that Caspase-1-mediated inflammation occurs early in the disease and raise hope that VX-765, a previously Food and Drug Administration-approved drug for human CNS clinical trials, may be a useful drug to prevent the onset of cognitive deficits and brain inflammation in AD.	belnacasan	107-113	caspase 1	Homo sapiens	27-36
33005686-8	2020	Finally, Caspase1 gene was significantly upmodulated in response to HAnano  and it suggests an involvement of the inflammasome complex.	hanano	68-74	caspase 1	Homo sapiens	9-17
32804985-0	2020	Lactic acid bacterium, Lactobacillus paracasei KW3110, suppresses inflammatory stress-induced caspase-1 activation by promoting interleukin-10 production in mouse and human immune cells.	Lactic Acid	0-11	caspase 1	Homo sapiens	94-103
32750036-8	2020	Targeting aberrant glucose metabolism with shikonin, a pyruvate kinase M2 inhibitor, dampened NLRP3-mediated inflammation (caspase-1 (p<0.05), IL1beta (p<0.01)) and improved healing in vivo.	shikonin	43-51	caspase 1	Homo sapiens	123-132
32507974-7	2020	RESULTS: LPS-induced inflammation in the presence of ATP activates NLRP3 that subsequently increases pancreatic cancer cell proliferation by increasing caspase-1 activity leading to overall production of IL-1beta.	Adenosine Triphosphate	53-56	caspase 1	Homo sapiens	152-161
32716363-4	2020	We found that NLRP3 inflammasome-mediated caspase-1 activation and subsequent IL-1beta production were reduced in beta-glucan-reprogrammed macrophages.	beta-Glucans	114-125	caspase 1	Homo sapiens	42-51
32716585-5	2020	miR-375-3p blocks the Wnt/beta-catenin pathway and downstream molecules Cyclin D1 and c-Myc by inhibiting the expression of FZD8 directly, it could increase caspase 1 and caspase 3 expression and promote T24 cell apoptosis as well.	mir-375-3p	0-10	caspase 1	Homo sapiens	157-166
32716363-6	2020	Importantly, beta-glucan-induced memory in macrophages resulted in a remarkable attenuation of IL-1beta secretion and caspase-1 activation in patients with an NLRP3-associated autoinflammatory disease, cryopyrin-associated periodic syndromes (CAPS).	beta-Glucans	13-24	caspase 1	Homo sapiens	118-127
32035094-7	2020	Treatment with ATP caused the activation of caspase-1 as well as the production of active forms of IL-1beta and IL-18 via P2X7 receptor (P2X7R) in keratinocytes and melanocytes.	Adenosine Triphosphate	15-18	caspase 1	Homo sapiens	44-53
32929357-10	2020	Cholesterol stimulated the protein expression of NLRP3 inflammasome components ASC, caspase-1 and IL-1beta, and decreased AQP2 protein abundance in vitro, which was markedly prevented by statins, likely through the enhancement of ASC speck degradation via autophagy.	Cholesterol	0-11	caspase 1	Homo sapiens	84-93
32804985-0	2020	Lactic acid bacterium, Lactobacillus paracasei KW3110, suppresses inflammatory stress-induced caspase-1 activation by promoting interleukin-10 production in mouse and human immune cells.	kw3110	47-53	caspase 1	Homo sapiens	94-103
32804985-9	2020	Our findings reveal a novel anti-inflammatory mechanism of LAB and the effect of KW3110 on caspase-1 activation is expected to contribute to constructing future preventive strategies for inflammation-related disorders using food ingredients.	kw3110	81-87	caspase 1	Homo sapiens	91-100
32787872-13	2020	Ethanol-induced JNK1 phosphorylation activated the NLRP3 inflammasome that induced caspase-1 dependent mitophagy inhibition, thereby exacerbating ROS accumulation and causing cell death.	Ethanol	0-7	caspase 1	Homo sapiens	83-92
32855770-9	2020	In addition, pretreatment with BB extracts was able to prevent ozone-induced ROS production and inflammasome activation measured as NRLP1-ASC scaffold formation and also prevent the transcripts of key inflammasome players such as CASP1 and IL-18, suggesting that this approach as a possible new technology to prevent cutaneous pollution damage.	Ozone	63-68	caspase 1	Homo sapiens	230-235
32787872-14	2020	Suppressing caspase-1 induced mitophagy and reversed the ethanol-induced apoptosis in neuronal cells.	Ethanol	57-64	caspase 1	Homo sapiens	12-21
32554464-10	2020	We propose that P1"-P4"-based inhibitors could be exploited to specifically target inflammatory caspases.	p1"-p4"	16-23	caspase 1	Homo sapiens	96-104
32239395-12	2020	Nicardipine also mitigated caspase-1 activation, inhibited ASC oligomerization, and reduced NLRP3 expression.	Nicardipine	0-11	caspase 1	Homo sapiens	27-36
32832566-4	2020	NLRP11 was significantly upregulated after induction with adenosine at both the mRNA and protein levels, which led to the interaction of endogenous NLRP11 with the ASC adaptor protein; however, this interaction did not result in the activation of the caspase-1 enzyme.	Adenosine	58-67	caspase 1	Homo sapiens	251-260
32968631-14	2020	Cur attenuated DOX-induced cardiomyocyte pyroptosis as evidenced by NLR family pyrin domain containing 3 (NLRP3), Caspase-1, and interleukin-18 levels.	Doxorubicin	15-18	caspase 1	Homo sapiens	114-123
32764386-7	2020	Negatively charged sulfonate-functionalized polystyrene nanoparticles demonstrated a size-related trend for the inhibition of caspase-1, which was not observed for amine-functionalized polystyrene of similar sizes.	Alkanesulfonates	19-28	caspase 1	Homo sapiens	126-135
32764386-7	2020	Negatively charged sulfonate-functionalized polystyrene nanoparticles demonstrated a size-related trend for the inhibition of caspase-1, which was not observed for amine-functionalized polystyrene of similar sizes.	Polystyrenes	44-55	caspase 1	Homo sapiens	126-135
32764386-7	2020	Negatively charged sulfonate-functionalized polystyrene nanoparticles demonstrated a size-related trend for the inhibition of caspase-1, which was not observed for amine-functionalized polystyrene of similar sizes.	Amines	164-169	caspase 1	Homo sapiens	126-135
32764386-7	2020	Negatively charged sulfonate-functionalized polystyrene nanoparticles demonstrated a size-related trend for the inhibition of caspase-1, which was not observed for amine-functionalized polystyrene of similar sizes.	Polystyrenes	185-196	caspase 1	Homo sapiens	126-135
32335355-8	2020	We found decreased IL-1beta secretion 2154 pg/ml to 854 pg/ml IL-1beta secretion using Y-VAD and we observed decrease from 2154 pg/ml to 22.33 pg/ml with Z-VAD, and this inhibition was followed by diminished viral replication from 2.25 x 107 to 2.1 x 105 CCID50, which suggests that caspase 1-dependent secretion of the IL-1beta active molecule is important for viral replication.	z-vad	154-159	caspase 1	Homo sapiens	283-292
32124392-14	2020	CONCLUSION: Our finding confirmed that ChIV provides a neuroprotective effect against sevoflurane-induced neuroinflammation and cognitive impairment by blocking the NLRP3/caspase-1 pathway, which may be an effective strategy for the clinical treatment of elderly patients with POCD induced by anesthesia.	Sevoflurane	86-97	caspase 1	Homo sapiens	171-180
32698510-12	2020	Ruxolitinib reverted IFN-gamma-induced expression of caspase-1, IL-1beta, IL-15, and IL-18, and stimulated several growth factors, such as FGF7.	ruxolitinib	0-11	caspase 1	Homo sapiens	53-62
32584575-7	2020	Analysis of IL-1beta and caspase-1 expression revealed that the new diterpenoids 15 and 18 are selective inhibitors of the NLRP3 inflammasome, reinforcing the previously demonstrated anti-inflammatory properties of hispanolone derivatives.	Diterpenes	68-80	caspase 1	Homo sapiens	25-34
32808940-4	2020	Studies show that colchicine, among other actions, inhibits the assembly of NLRP3 complex that is responsible for generating the active form of Caspase-1 that will convert Pro-IL-1beta and Pro-IL-18 into their active forms.	Colchicine	18-28	caspase 1	Homo sapiens	144-153
32202959-7	2020	Stimulation of THP-1 macrophage-like cells with every periodontopathic bacteria induced IL-1beta secretion without cell death, which was suppressed by the NLRP3 inhibitor, MCC950, and caspase-1 inhibitor, z-YVAD-FMK.	benzyloxycarbonyltyrosyl-valyl-alanyl-aspartic acid fluoromethyl ketone	205-215	caspase 1	Homo sapiens	184-193
32315958-8	2020	RESULTS: Following butyrate supplementation, the relative expression levels of TLR2/4, NF-kappaB1, Caspase-1, NLRP3, IL-1beta & IL-18 were significantly downregulated (p < 0.05).	Butyrates	19-27	caspase 1	Homo sapiens	99-108
32640751-9	2020	In immune cells and AML (acute myeloid leukemia) cells, the anti-cancer drug talabostat induces CARD8 activation and causes caspase-1-dependent pyroptosis.	talabostat	77-87	caspase 1	Homo sapiens	124-133
32321163-5	2020	These investigations revealed rapid caspase-1 activation and mature IL-1beta secretion in the skin and draining lymph nodes (dLNs) after 1.5 and 3% triclosan exposure.	Triclosan	148-157	caspase 1	Homo sapiens	36-45
32616234-6	2020	After 7-D ammonia exposure, the proportion of the phylum Proteobacteria and the genus Escherichia/Shigella in lung tissue was significantly increased, the expression levels of NLRP3 and caspase-1 mRNA were significantly increased, and the content of IL-1beta in lung tissue and serum was higher than that in the control group.	Ammonia	10-17	caspase 1	Homo sapiens	186-195
32054994-12	2020	Enhanced expression of TNF and the activation of NLRP3 and CASP1 followed by the increased generation of IL-1beta and nuclear translocation of the NF-kappabeta transcription factor occurred in response to hemoglobin-derived peptides, and ferryl hemoglobin in endothelium was upregulated in both pathologies.	ferryl iron	238-244	caspase 1	Homo sapiens	59-64
32103153-5	2020	Consistent with this finding, we showed that TSLP reduces caspase-1 and caspase-3 activity levels in primary human bronchial epithelial cells treated with bleomycin via Bcl-xL up-regulation.	Bleomycin	155-164	caspase 1	Homo sapiens	58-67
32022249-11	2020	The expression of P2X7R, caspase-1 and NF-kappaB, the release of IL-1beta, calcium influx and PI uptake were reduced by 2354glu in macrophages stimulated with LPS/ATP.	seclazone	120-127	caspase 1	Homo sapiens	25-34
32577124-0	2020	RalB degradation by dihydroartemisinin induces autophagy and IFI16/caspase-1 inflammasome depression in the human laryngeal squamous cell carcinoma.	artenimol	20-38	caspase 1	Homo sapiens	67-76
32577124-15	2020	Furthermore, DHA promotes autophagy, which suppresses the activation of IFI16/caspase-1 inflammasome and IL-1beta production.	artenimol	13-16	caspase 1	Homo sapiens	78-87
32577124-16	2020	Conclusions: Therefore, our findings demonstrate that DHA may act as a RalB inhibitor to regulate the crosstalk between autophagy and IFI16/caspase-1 inflammasome, which inhibits IL-1beta production in tumor microenvironment.	artenimol	54-57	caspase 1	Homo sapiens	140-149
32676145-0	2020	3-Difluoroalkyl Quaternary Oxindoles Inhibit Macrophage Pyroptosis by Blocking Inflammasome Recruitment of Caspase-1.	3-difluoroalkyl quaternary oxindoles	0-36	caspase 1	Homo sapiens	107-116
32676145-4	2020	In current study, we identify 3-difluoroalkyl quaternary oxindoles as chemical inhibitors of caspase-1, the pyroptosis driving caspase.	3-difluoroalkyl quaternary oxindoles	30-66	caspase 1	Homo sapiens	93-102
32676145-4	2020	In current study, we identify 3-difluoroalkyl quaternary oxindoles as chemical inhibitors of caspase-1, the pyroptosis driving caspase.	3-difluoroalkyl quaternary oxindoles	30-66	caspase 1	Homo sapiens	93-100
32392065-0	2020	Effects of Inorganic Ions on Ice Nucleation by the Al-Surface of Kaolinite Immersed in Water.	Aluminum	51-53	caspase 1	Homo sapiens	29-32
32392065-0	2020	Effects of Inorganic Ions on Ice Nucleation by the Al-Surface of Kaolinite Immersed in Water.	Kaolin	65-74	caspase 1	Homo sapiens	29-32
32392065-0	2020	Effects of Inorganic Ions on Ice Nucleation by the Al-Surface of Kaolinite Immersed in Water.	Water	87-92	caspase 1	Homo sapiens	29-32
32392065-1	2020	Molecular dynamics simulations are employed to investigate the influence of inorganic salts on ice nucleation by the Al-surface of kaolinite, terminated with hydroxyl groups.	inorganic salts	76-91	caspase 1	Homo sapiens	95-98
32392065-1	2020	Molecular dynamics simulations are employed to investigate the influence of inorganic salts on ice nucleation by the Al-surface of kaolinite, terminated with hydroxyl groups.	Aluminum	117-119	caspase 1	Homo sapiens	95-98
32392065-1	2020	Molecular dynamics simulations are employed to investigate the influence of inorganic salts on ice nucleation by the Al-surface of kaolinite, terminated with hydroxyl groups.	Kaolin	131-140	caspase 1	Homo sapiens	95-98
32392065-6	2020	At a supercooling of 26 K (taking account of freezing point depression), 1 M salt solutions slowed ice nucleation by a factor of 2-3 compared with pure water, and significantly reduced the rate of ice growth after nucleation.	Salts	77-81	caspase 1	Homo sapiens	99-102
32392065-6	2020	At a supercooling of 26 K (taking account of freezing point depression), 1 M salt solutions slowed ice nucleation by a factor of 2-3 compared with pure water, and significantly reduced the rate of ice growth after nucleation.	Salts	77-81	caspase 1	Homo sapiens	197-200
32392065-7	2020	All salt solutions had similar influences on ice nucleation, and no specific ion effects were identified.	Salts	4-8	caspase 1	Homo sapiens	45-48
32392065-8	2020	Ice nucleation simulations for 1 M NaI(Cl), KI(Cl), and LiI solutions were performed for a range temperatures.	nai	35-38	caspase 1	Homo sapiens	0-3
32392065-8	2020	Ice nucleation simulations for 1 M NaI(Cl), KI(Cl), and LiI solutions were performed for a range temperatures.	KS I	44-46	caspase 1	Homo sapiens	0-3
32392065-8	2020	Ice nucleation simulations for 1 M NaI(Cl), KI(Cl), and LiI solutions were performed for a range temperatures.	lii	56-59	caspase 1	Homo sapiens	0-3
32392065-9	2020	In all cases, the supercooling required for ice nucleation was larger by 1 - 6 K, after accounting for freezing point depression, than that required for pure water.	Water	158-163	caspase 1	Homo sapiens	44-47
32392065-10	2020	For 1 M LiI solution an earlier laboratory study using kaolin as ice nucleating particles (INP) reported that the supercooling required for ice nucleation was 11 K smaller than that required for pure water.	Kaolin	55-61	caspase 1	Homo sapiens	65-68
32392065-10	2020	For 1 M LiI solution an earlier laboratory study using kaolin as ice nucleating particles (INP) reported that the supercooling required for ice nucleation was 11 K smaller than that required for pure water.	Kaolin	55-61	caspase 1	Homo sapiens	140-143
32392065-10	2020	For 1 M LiI solution an earlier laboratory study using kaolin as ice nucleating particles (INP) reported that the supercooling required for ice nucleation was 11 K smaller than that required for pure water.	Water	200-205	caspase 1	Homo sapiens	140-143
32392065-13	2020	In our experiments ice nucleation in the LiI solution required the same supercooling as pure water, which is more consistent with our simulations.	Water	93-98	caspase 1	Homo sapiens	19-22
32321279-8	2020	Transfection of miR-887-3p into HPMECs altered gene expression, including the upregulation of several genes previously associated with ARDS (e.g., CXCL10, CCL5, CX3CL1, VCAM1, CASP1, IL1B, IFNB, and TLR2), and activation of cellular pathways relevant to the response to infection.	mir-887-3p	16-26	caspase 1	Homo sapiens	176-181
32129540-8	2020	Reactive oxygen species were generated in response to the hypoxia-mediated activation of caspase-1.	Oxygen	9-15	caspase 1	Homo sapiens	89-98
32629886-5	2020	Interestingly, NaHS also stimulated the caspase-1 inflammasome pathway, leading to increased secretion of the pro-inflammatory molecule interleukin-18 (IL-18).	sodium bisulfide	15-19	caspase 1	Homo sapiens	40-49
32371889-1	2020	Gasdermin-D (GSDMD) in inflammasome-activated macrophages is cleaved by caspase-1 to generate N-GSDMD fragments.	n-gsdmd	94-101	caspase 1	Homo sapiens	72-81
31778733-9	2020	Results clearly showed that O3 exposure increased both transcript and protein levels of the main inflammasome complex, such as ASC and caspase-1.	Superoxides	28-30	caspase 1	Homo sapiens	135-144
32361594-0	2020	GSDME-Dependent Incomplete Pyroptosis Permits Selective IL-1alpha Release under Caspase-1 Inhibition.	gsdme	0-5	caspase 1	Homo sapiens	80-89
32423023-1	2020	The NLRP3 (nucleotide-binding domain, leucine-rich-repeat-containing family, pyrin domain-containing 3) inflammasome senses pathogen-associated molecular patterns (PAMPs) and danger-associated molecular patterns (DAMPs), and activates caspase-1, which provokes release of proinflammatory cytokines such as interleukin-1beta (IL-1beta) and IL-18 as well as pyroptosis to engage in innate immune defense.	Leucine	38-45	caspase 1	Homo sapiens	235-244
32376492-7	2021	Aspirin or non-steroidal anti-inflammatory drugs (NSAIDs) remain the mainstay of therapy in RP, whereas colchicine is recommended on top of standard anti-inflammatory therapy, due to its role in inhibiting the IL-1 converting enzyme (caspase 1) within the inflammasome as well as the release of additional pro-inflammatory mediators and reactive oxygen species.	Colchicine	104-114	caspase 1	Homo sapiens	234-243
32397236-6	2020	Moreover, TNF-alpha or ATP increased protein levels of NLRC4, ASC, and caspase-1 in a P2Y2R-dependent manner in MDA-MB-231 and RT-R-MDA-MB-231 cells.	Adenosine Triphosphate	23-26	caspase 1	Homo sapiens	71-80
32397236-7	2020	In addition, P2Y2R activation by ATP induced the secretion of IL-1beta and VEGF-A, as well as invasion, in MDA-MB-231 and RT-R-MDA-MB-231 cells, which was inhibited by NLRC4, ASC, and caspase-1 small interfering RNA (siRNA).	Adenosine Triphosphate	33-36	caspase 1	Homo sapiens	184-193
32397236-8	2020	Taken together, this report suggests that P2Y2R activation by ATP induces tumor invasion and angiogenesis through inflammasome activation, specifically by regulating the inflammasome components NLRC4, ASC, and caspase-1.	Adenosine Triphosphate	62-65	caspase 1	Homo sapiens	210-219
32367435-8	2020	Treatment of human cardiomyocytes with GC7, an inhibitor of DHS, catalyzing the first step in hypusine biosynthesis led to a decrease in proinflammatory and proapoptotic myocardial caspase-1 activity in comparison to untreated cardiomyocytes.	hypusine	94-102	caspase 1	Homo sapiens	181-190
32014690-6	2020	Here we found that TDI induced pyroptosis in 16HBE cells, as evidenced by enhanced expressions of caspase-1 and elevated levels of LDH, IL-1beta and HMGB1.	Toluene 2,4-Diisocyanate	19-22	caspase 1	Homo sapiens	98-107
32018221-3	2020	Notably, we found that high-glucose (50 mM) increased the expression levels of Caspase-1, Gasdermin D, NLRP3, IL-1beta and IL-18 in ARPE-19 cells, which indicated that high-glucose triggered pyroptotic cell death.	Glucose	28-35	caspase 1	Homo sapiens	79-88
32018221-3	2020	Notably, we found that high-glucose (50 mM) increased the expression levels of Caspase-1, Gasdermin D, NLRP3, IL-1beta and IL-18 in ARPE-19 cells, which indicated that high-glucose triggered pyroptotic cell death.	Glucose	173-180	caspase 1	Homo sapiens	79-88
32317086-7	2020	Tamoxifen induced reactive oxygen species (ROS)-mediated autophagic cell death and caspase-1-mediated pyroptosis in RPE cells.	Tamoxifen	0-9	caspase 1	Homo sapiens	83-92
32319486-5	2020	Furthermore, Cr(vi) could induce the activation of the nuclear factor kappa B (NF-kappaB) signaling pathway, the accumulation of p65 in the nucleus, and the increase in the phosphorylation of IkappaB and the expression of cleaved caspase-1 and IL-1beta in THP-1 cells.	chromium hexavalent ion	13-19	caspase 1	Homo sapiens	230-239
32032660-2	2020	The death of A549 cells induced by A + N morphologically resembles inflammation-inducing pyroptosis - cell destruction triggered by activated caspase-1.	Nitrogen	39-40	caspase 1	Homo sapiens	142-151
32032660-3	2020	The treatment with A + N (or camptothecin) strongly upregulated caspase-1 and its two activators: IFI16 and NLRP1, however, caspase-1 activation was not detected.	Nitrogen	23-24	caspase 1	Homo sapiens	64-73
32032660-3	2020	The treatment with A + N (or camptothecin) strongly upregulated caspase-1 and its two activators: IFI16 and NLRP1, however, caspase-1 activation was not detected.	Nitrogen	23-24	caspase 1	Homo sapiens	124-133
32032660-3	2020	The treatment with A + N (or camptothecin) strongly upregulated caspase-1 and its two activators: IFI16 and NLRP1, however, caspase-1 activation was not detected.	Camptothecin	29-41	caspase 1	Homo sapiens	64-73
32094205-6	2020	This priming allowed for effective induction of caspase-1-dependent cell death upon treatment with muramyl tripeptide phosphatidylethanolamine (MTP-PE), a synthetic ligand for NOD2.	mifamurtide	99-142	caspase 1	Homo sapiens	48-57
32366053-0	2020	Short Exposure to Ethanol Diminishes Caspase-1 and ASC Activation in Human HepG2 Cells In Vitro.	Ethanol	18-25	caspase 1	Homo sapiens	37-46
32366053-8	2020	The co-stimulation with LPS and ATP induced a significant ASC speck formation, caspase-1 activation, cell death and ROS generation.	Adenosine Triphosphate	32-35	caspase 1	Homo sapiens	79-88
32252692-11	2020	The levels of inflammation related proteins NLRP3, ASC, caspase1, IL-1beta and IL-18 was also inhibited after the treatment of ripasudil.	K-115	127-136	caspase 1	Homo sapiens	56-64
32252692-13	2020	CONCLUSION: Ripasudil relieved the inflammatory injury of RPE cells by upregulating miR-136-5p, therefore inhibiting the expression of ROCK1, ROCK2, NLRP3, ASC, caspase1, IL-1beta and IL-18.	K-115	12-21	caspase 1	Homo sapiens	161-169
32076940-8	2020	Furthermore, SAL also decreased the activation of caspase-1 and inhibited the release of IL-1beta induced by lipopolysaccharide (LPS) and adenosine triphosphate (ATP) in human umbilical vein endothelial cell (HUVECs).	rhodioloside	13-16	caspase 1	Homo sapiens	50-59
32330868-11	2020	Importantly, Metformin reduced pyroptosis-related proteins, including NLRP3, cleaved caspase-1, and the N-terminus of GSDMD.	Metformin	13-22	caspase 1	Homo sapiens	85-94
32366053-9	2020	The inhibition of the ATP-dependent purinoreceptor P2X7 decreased the caspase-1 activation, whereas sodium orthovanadate significantly induced caspase-1.	Adenosine Triphosphate	22-25	caspase 1	Homo sapiens	70-79
32366053-9	2020	The inhibition of the ATP-dependent purinoreceptor P2X7 decreased the caspase-1 activation, whereas sodium orthovanadate significantly induced caspase-1.	Sodium orthovanadate	100-120	caspase 1	Homo sapiens	143-152
32366053-10	2020	Additional treatment with EtOH reversed the LPS and ATP-induced caspase-1 activation, ASC speck formation and ROS production.	Ethanol	26-30	caspase 1	Homo sapiens	64-73
32366053-10	2020	Additional treatment with EtOH reversed the LPS and ATP-induced caspase-1 activation, ASC speck formation and ROS production.	Adenosine Triphosphate	52-55	caspase 1	Homo sapiens	64-73
32366053-11	2020	The ASC speck formation and caspase-1 induction require a two-step signaling with LPS and ATP in HepG2 cells.	Adenosine Triphosphate	90-93	caspase 1	Homo sapiens	28-37
32420343-6	2020	Our data showed that high glucose induced NLRP3-caspase-1-GSDMD activation and pore formation in a dose- and time-dependent manner (p < 0.05) and resulted in the inflammatory cytokines IL-1beta and IL-18 and lactate dehydrogenase (LDH) release from HRPs (p < 0.05), which are all signs of HRP pyroptosis.	Glucose	26-33	caspase 1	Homo sapiens	48-57
32420343-9	2020	Taken together, our results firstly revealed that high glucose induced the loss of retinal pericytes partly via NLRP3-caspase-1-GSDMD-mediated pyroptosis.	Glucose	55-62	caspase 1	Homo sapiens	118-127
32271889-11	2020	Both caspase-1 activity and release of IL-1beta were reduced by cis-UCA.	cis-Urocanic acid	64-71	caspase 1	Homo sapiens	5-14
32271889-12	2020	Additionally, UV-B stimulated the caspase-1-independent production of IL-18, an effect also reduced by cis-UCA.	cis-Urocanic acid	103-110	caspase 1	Homo sapiens	34-43
31917290-9	2020	In addition, DEX suppressed the expression of taurine, TXNIP, NLRP3, ASC and cleaved caspase-1 and activated the expression of p-AMPK and p-GSK3beta.	Dexmedetomidine	13-16	caspase 1	Homo sapiens	85-94
32041439-6	2020	Binding mode of sulforaphane within caspase-1 was determined by molecular docking simulation.	sulforaphane	16-28	caspase 1	Homo sapiens	36-45
32041439-9	2020	In the molecular docking simulation and in vitro caspase-1 assays, sulforaphane regulated caspase-1 activity by docking with the identical binding site of caspase-1.	sulforaphane	67-79	caspase 1	Homo sapiens	49-58
32041439-9	2020	In the molecular docking simulation and in vitro caspase-1 assays, sulforaphane regulated caspase-1 activity by docking with the identical binding site of caspase-1.	sulforaphane	67-79	caspase 1	Homo sapiens	90-99
32041439-9	2020	In the molecular docking simulation and in vitro caspase-1 assays, sulforaphane regulated caspase-1 activity by docking with the identical binding site of caspase-1.	sulforaphane	67-79	caspase 1	Homo sapiens	90-99
32041439-12	2020	Furthermore, phosphorylation of mitogen-activated protein kinases (MAPK) was down-regulated by treatment with sulforaphane or WE.Conclusion: Our findings suggest that sulforaphane and WE have anti-allergic inflammatory effects by intercepting caspase-1/NF-kappaB/MAPKs signaling pathways.	sulforaphane	110-122	caspase 1	Homo sapiens	243-252
32041439-12	2020	Furthermore, phosphorylation of mitogen-activated protein kinases (MAPK) was down-regulated by treatment with sulforaphane or WE.Conclusion: Our findings suggest that sulforaphane and WE have anti-allergic inflammatory effects by intercepting caspase-1/NF-kappaB/MAPKs signaling pathways.	sulforaphane	167-179	caspase 1	Homo sapiens	243-252
32094205-6	2020	This priming allowed for effective induction of caspase-1-dependent cell death upon treatment with muramyl tripeptide phosphatidylethanolamine (MTP-PE), a synthetic ligand for NOD2.	mifamurtide	144-150	caspase 1	Homo sapiens	48-57
32296327-4	2020	Results: TBA inhibited 6-OHDA-induced NLRP3 activation, as demonstrated by decreased expressions of NLRP3 and matured caspase-1 and IL-1beta, and also alleviated glial proliferation and dopaminergic neuronal degeneration.	tubastatin A	9-12	caspase 1	Homo sapiens	118-127
32296327-4	2020	Results: TBA inhibited 6-OHDA-induced NLRP3 activation, as demonstrated by decreased expressions of NLRP3 and matured caspase-1 and IL-1beta, and also alleviated glial proliferation and dopaminergic neuronal degeneration.	Oxidopamine	23-29	caspase 1	Homo sapiens	118-127
32118580-7	2020	In (LPS/ATP-stimulated) PBMCs, IL-18/TNF/caspase-1 were all significantly decreased and IL-10 was increased with both combinations.	Adenosine Triphosphate	8-11	caspase 1	Homo sapiens	41-50
32222695-11	2020	In vitro experiments indicated that DOP increased the LO2 cell viability; prevented LDH release prominently; reduced the secretion of IL-1beta, IL-6, and TNF-alpha; and reversed the expression of IL-1beta, IL-6, TNF-alpha, caspase 1, NLRP3, p-NF-kappaB, and TLR4.	Diethylhexyl Phthalate	36-39	caspase 1	Homo sapiens	223-232
32194991-8	2020	Furthermore, inhibitors of AMPK and SIRT1 abrogated the downregulation of caspase-1 induced by metformin treatment, indicating that AMPK and SIRT1 are essential for the inhibitory effect on NLRP3 inflammasome in NHEKs.	Metformin	95-104	caspase 1	Homo sapiens	74-83
32057231-3	2020	The ultrasmall-size (<10 nm) Au nanoparticles preferentially activate the NLRP3 inflammasome for Caspase-1 maturation and interleukin-1beta production, while the larger-size Au nanoparticles (>10 nm) trigger the NF-kappaB signaling pathway.	Gold	29-31	caspase 1	Homo sapiens	97-106
32209983-7	2020	LPS-stimulated caspase-1 activation increased following glucose ingestion (main effect of time; p = 0.032), with no differences between conditions.	Glucose	56-63	caspase 1	Homo sapiens	15-24
32209983-10	2020	In individuals with obesity, an excursion into hyperglycemia following ingestion of a glucose load augments LPS-induced activation of caspase-1 in monocytes with no apparent impact of raising circulating beta-OHB concentration via ingestion of exogenous ketones.	Glucose	86-93	caspase 1	Homo sapiens	134-143
32130533-0	2020	Exploring the ring potential of 2,4-diaminopyrimidine derivatives towards the identification of novel caspase-1 inhibitors in Alzheimer"s disease therapy.	2,4-diaminopyrimidine	32-53	caspase 1	Homo sapiens	102-111
32130533-2	2020	A recent report highlighted 2,4-diaminopyrimidine ring as an essential fragment in the inhibition of human caspase-1.	2,4-diaminopyrimidine	28-49	caspase 1	Homo sapiens	107-116
32130533-4	2020	The purpose of this study is therefore in twofold: (1) to understand the enzyme binding mechanism of the 2,4-diaminopyrimidine ring and (2) to search for more potent caspase-1 inhibitors that contain the ring, using integrative per-residue energy decomposition (PRED) pharmacophore modeling.	2,4-diaminopyrimidine	105-126	caspase 1	Homo sapiens	166-175
32130533-5	2020	Ligand interaction profile of a reference compound revealed a peculiar hydrogen formation of the amino group of 2,4-diaminopyrimidine with active site residue Arg341, possibly forming the bases for its inhibitory prowess against caspase-1.	Hydrogen	71-79	caspase 1	Homo sapiens	229-238
32130533-5	2020	Ligand interaction profile of a reference compound revealed a peculiar hydrogen formation of the amino group of 2,4-diaminopyrimidine with active site residue Arg341, possibly forming the bases for its inhibitory prowess against caspase-1.	2,4-diaminopyrimidine	112-133	caspase 1	Homo sapiens	229-238
32130533-6	2020	A generated pharmacophore model for structure-based virtual screening identified compounds, ZINC724667, ZINC09908119, and ZINC09933770, as potential caspase-1 inhibitors that possessed desirable pharmacokinetic and physiochemical properties.	CHEMBL4126243	92-102	caspase 1	Homo sapiens	149-158
32130533-6	2020	A generated pharmacophore model for structure-based virtual screening identified compounds, ZINC724667, ZINC09908119, and ZINC09933770, as potential caspase-1 inhibitors that possessed desirable pharmacokinetic and physiochemical properties.	zinc09908119	104-116	caspase 1	Homo sapiens	149-158
32130533-6	2020	A generated pharmacophore model for structure-based virtual screening identified compounds, ZINC724667, ZINC09908119, and ZINC09933770, as potential caspase-1 inhibitors that possessed desirable pharmacokinetic and physiochemical properties.	zinc09933770	122-134	caspase 1	Homo sapiens	149-158
31506572-0	2020	Isosibiricin inhibits microglial activation by targeting the dopamine D1/D2 receptor-dependent NLRP3/caspase-1 inflammasome pathway.	Isosibiricin	0-12	caspase 1	Homo sapiens	101-110
31951974-8	2020	These findings indicate that PKR/JNK/NF-kappaB signal is essential for casticin-induced caspase-1 inflammasome formation and inflammatory cytokines release in 5-8F cell.	casticin	71-79	caspase 1	Homo sapiens	88-97
31927504-0	2020	Uric acid increases IL-1beta secretion and Caspase-1 activation in PBMCs of Behcet"s disease patients: The in vitro immunomodulatory effect of xanthine oxidase inhibitor Allopurinol.	Uric Acid	0-9	caspase 1	Homo sapiens	43-52
31927504-9	2020	Additionally, while UA has markedly increased NO, IL-1beta, and Caspase-1 activity levels in PBMCs of BD patients, Allopurinol has exerted an immunomodulatory effect resulting in reduced NO, IL-1beta and Caspase-1 levels in PBMCs of BD patients particularly during the active stages.	Uric Acid	20-22	caspase 1	Homo sapiens	64-73
32103904-12	2020	Moreover, HG treatment increased the protein levels of pro-inflammatory cytokines, caspase-1 and phosphorylated JNK, which was significantly attenuated by H2S or Y-P 740.	Hydrogen Sulfide	155-158	caspase 1	Homo sapiens	83-115
31734269-3	2020	THP-1 macrophages exposed to Cinacalcet (CaSR activator, 2 muM, 4 h) showed elevated proinflammatory marker and NLRP3 inflammasome mRNA, pro-IL-1beta protein and caspase-1 activity, whereas preincubation with CaSR negative modulators prevented these effects.	cina	29-39	caspase 1	Homo sapiens	162-171
32104285-12	2020	Under LPS treatment, the NF-kappaB pathway inhibitor BAY11-7082 further enhanced the inhibitory effects of rapamycin, but inhibited the promoting effects of 3-MA on the protein expression levels of IL-1beta and caspase-1.	3-(4-methylphenylsulfonyl)-2-propenenitrile	53-63	caspase 1	Homo sapiens	211-220
32104285-12	2020	Under LPS treatment, the NF-kappaB pathway inhibitor BAY11-7082 further enhanced the inhibitory effects of rapamycin, but inhibited the promoting effects of 3-MA on the protein expression levels of IL-1beta and caspase-1.	3-methyladenine	157-161	caspase 1	Homo sapiens	211-220
31780258-8	2020	Furthermore, caspase-1 inhibitor was co-administered with high glucose in ME3T3-E1 cells, which shows that caspase-1 inhibitor could repress effect of high glucose on the proliferation and differentiation of osteoblast.	Glucose	63-70	caspase 1	Homo sapiens	13-22
31780258-8	2020	Furthermore, caspase-1 inhibitor was co-administered with high glucose in ME3T3-E1 cells, which shows that caspase-1 inhibitor could repress effect of high glucose on the proliferation and differentiation of osteoblast.	Glucose	63-70	caspase 1	Homo sapiens	107-116
31780258-8	2020	Furthermore, caspase-1 inhibitor was co-administered with high glucose in ME3T3-E1 cells, which shows that caspase-1 inhibitor could repress effect of high glucose on the proliferation and differentiation of osteoblast.	Glucose	156-163	caspase 1	Homo sapiens	13-22
31780258-8	2020	Furthermore, caspase-1 inhibitor was co-administered with high glucose in ME3T3-E1 cells, which shows that caspase-1 inhibitor could repress effect of high glucose on the proliferation and differentiation of osteoblast.	Glucose	156-163	caspase 1	Homo sapiens	107-116
31935365-7	2020	While LPS increased inflammasome assembling and caspase-1 activation, AC treatment inhibited caspase-1 activation in D-HAEC (P &lt;= 0.05).	Anthocyanins	70-72	caspase 1	Homo sapiens	93-102
32010254-9	2020	The expression levels of NLRP3, caspase-1 and IL-1beta were inhibited after the addition of autophagy inhibitor 3-MA.	3-methyladenine	112-116	caspase 1	Homo sapiens	32-41
31549730-11	2020	In addition, ADP altered mitochondrial membrane potential in combination with ATP and increased the number of caspase-1 positive cells through the P2Y12 receptor.	Adenosine Diphosphate	13-16	caspase 1	Homo sapiens	110-119
31646445-3	2020	Accumulating investigations imply that chloride efflux-dependent ASC speck oligomerization and potassium efflux-dependent activation of caspase-1 are the two relatively independent, but indispensable events for NLRP3 inflammasome activation.	Chlorides	39-47	caspase 1	Homo sapiens	136-145
31646445-3	2020	Accumulating investigations imply that chloride efflux-dependent ASC speck oligomerization and potassium efflux-dependent activation of caspase-1 are the two relatively independent, but indispensable events for NLRP3 inflammasome activation.	Potassium	95-104	caspase 1	Homo sapiens	136-145
31905258-11	2020	CONCLUSIONS: Cigarette smoke-induced pyroptosis of bladder tissue by activating ROS/NLRP3/caspase-1 signaling pathway.	Reactive Oxygen Species	80-83	caspase 1	Homo sapiens	90-99
31669392-5	2020	Silver and palladium nanoparticles induced autophagy and lysosomal dysfunctions and all metal nanoparticles tested triggered the secretion of IL-1beta through caspase-1 activation.	Metals	88-93	caspase 1	Homo sapiens	159-168
32021639-13	2020	More importantly, we found that instead of cell apoptosis, PA induced significant pyroptosis, evidenced by remarkably increased mRNA and protein expressions of inflammasome marker NLRP3, Caspase-1 and IL-1beta, as well as cell membrane perforation driving protein GSDMD (P &lt; 0.05).	Palmitic Acid	59-61	caspase 1	Homo sapiens	187-196
32001671-0	2020	Lipoxin A4 suppresses angiotensin II type 1 receptor autoantibody in preeclampsia via modulating caspase-1.	lipoxin A4	0-10	caspase 1	Homo sapiens	97-106
32001671-4	2020	Caspase-1, the central enzyme of inflammasome and key target of pyroptosis, may play roles in AT1R exposure and AT1-AA production.	at1-aa	112-118	caspase 1	Homo sapiens	0-9
32001671-6	2020	Lipoxin A4 (LXA4), endogenous dual anti-inflammatory and proresolving lipid mediator, may inhibit AT1-AA production via modulating caspase-1.	lipoxin A4	0-10	caspase 1	Homo sapiens	131-140
32001671-6	2020	Lipoxin A4 (LXA4), endogenous dual anti-inflammatory and proresolving lipid mediator, may inhibit AT1-AA production via modulating caspase-1.	lipoxin A4	12-16	caspase 1	Homo sapiens	131-140
32001671-12	2020	These results suggest that caspase-1 promotes AT1-AA production via inducing trophoblast pyroptosis and AT1R exposure, while LXA4 suppresses AT1-AA production via modulating caspase-1, supporting caspase-1 serving as a therapeutic target for attenuating AT1-AA and LXA4 protecting patients from AT1-AA and PE.	lipoxin A4	125-129	caspase 1	Homo sapiens	174-183
32001671-12	2020	These results suggest that caspase-1 promotes AT1-AA production via inducing trophoblast pyroptosis and AT1R exposure, while LXA4 suppresses AT1-AA production via modulating caspase-1, supporting caspase-1 serving as a therapeutic target for attenuating AT1-AA and LXA4 protecting patients from AT1-AA and PE.	lipoxin A4	125-129	caspase 1	Homo sapiens	174-183
32082152-10	2019	The results of cellular and molecular experiments showed that JSCBR can effectively reduce the protein expression of ASC, caspase-1, IL-1beta, and NRLP3 in monosodium urate-induced THP-1 cells, which indicated that JSCBR mediated inflammation in gouty arthritis by inhibiting the activation of NOD-like receptor signaling pathway.	Uric Acid	156-172	caspase 1	Homo sapiens	122-131
31941010-0	2020	Polyphyllin VI Induces Caspase-1-Mediated Pyroptosis via the Induction of ROS/NF-kappaB/NLRP3/GSDMD Signal Axis in Non-Small Cell Lung Cancer.	polyphyllin H	0-14	caspase 1	Homo sapiens	23-32
31941010-9	2020	In addition, belnacasan (VX-765), an inhibitor of caspase-1, could remarkably decrease the pyroptotic cell death of PPVI-treated A549 and H1299 cells.	polyphyllin H	116-120	caspase 1	Homo sapiens	50-59
31941010-12	2020	Taken together, these data suggested that PPVI-induced, caspase-1-mediated pyroptosis via the induction of the ROS/NF-kappaB/NLRP3/GSDMD signal axis in NSCLC, which further clarified the mechanism of PPVI in the inhibition of NSCLC, and thereby provided a possibility for PPVI to serve as a novel therapeutic agent for NSCLC in the future.	polyphyllin H	42-46	caspase 1	Homo sapiens	56-65
31830726-5	2020	Atorvastatin inhibited pyroptosis by decreasing the expression levels of the canonical inflammasome pathway biomarkers NLRP3, caspase-1, GSDMD, IL-1beta, and IL-18 at both the mRNA and protein levels.	atorvastatin	0-12	caspase 1	Homo sapiens	126-135
31941010-12	2020	Taken together, these data suggested that PPVI-induced, caspase-1-mediated pyroptosis via the induction of the ROS/NF-kappaB/NLRP3/GSDMD signal axis in NSCLC, which further clarified the mechanism of PPVI in the inhibition of NSCLC, and thereby provided a possibility for PPVI to serve as a novel therapeutic agent for NSCLC in the future.	polyphyllin H	200-204	caspase 1	Homo sapiens	56-65
31941010-12	2020	Taken together, these data suggested that PPVI-induced, caspase-1-mediated pyroptosis via the induction of the ROS/NF-kappaB/NLRP3/GSDMD signal axis in NSCLC, which further clarified the mechanism of PPVI in the inhibition of NSCLC, and thereby provided a possibility for PPVI to serve as a novel therapeutic agent for NSCLC in the future.	polyphyllin H	200-204	caspase 1	Homo sapiens	56-65
31938471-10	2020	Moreover, 6-shogaol could inhibit the Akt/ROS signaling and NLRP3/caspase 1/IL-1beta inflammasome and hence attenuated HASMC calcification.	shogaol	10-19	caspase 1	Homo sapiens	66-75
31938742-3	2020	Key findings: Prenatal alcohol exposure induced the generation of ROS, nitrite and lipid peroxide, decreased mitochondrial Complex-I and IV activities, increased Caspase-1 and 3 activities, had no effect on cholinergic neurotransmission, increased expression of PSD-95, decreased LTP and decreased performance on spatial memory tasks.	Ethanol	23-30	caspase 1	Homo sapiens	162-177
32999158-6	2020	Furthermore, the effector molecule caspase-1 (casp1) was revealed to be the downstream target of NLRP1 and propofol repressed the activation of caspase-1 via inhibiting NLRP1 in cortical neurons.	Propofol	107-115	caspase 1	Homo sapiens	46-51
32999158-0	2020	Propofol Attenuates Inflammatory Damage via Inhibiting NLRP1-Casp1-Casp6 Signaling in Ischemic Brain Injury.	Propofol	0-8	caspase 1	Homo sapiens	61-66
32999158-6	2020	Furthermore, the effector molecule caspase-1 (casp1) was revealed to be the downstream target of NLRP1 and propofol repressed the activation of caspase-1 via inhibiting NLRP1 in cortical neurons.	Propofol	107-115	caspase 1	Homo sapiens	35-44
32999158-6	2020	Furthermore, the effector molecule caspase-1 (casp1) was revealed to be the downstream target of NLRP1 and propofol repressed the activation of caspase-1 via inhibiting NLRP1 in cortical neurons.	Propofol	107-115	caspase 1	Homo sapiens	144-153
32999158-7	2020	Moreover, propofol inhibits caspase-6 activation in neurons through the NLRP1-caspase-1 pathway.	Propofol	10-18	caspase 1	Homo sapiens	78-87
32999158-10	2020	In conclusion, our results suggest that propofol plays a neuroprotective role in stroke by inhibiting the inflammatory pathway of NLRP1-caspase-1-caspase-6.	Propofol	40-48	caspase 1	Homo sapiens	136-145
31885713-5	2020	Adipocytes were differentiated from 3T3-L1 cells and treated with low glucose (LG), HG, H2S donor sodium hydrosulfide (NaHS) or N-acetyl-tyrosyl-valyl- alanyl-aspartyl chloromethyl ketone, an inhibitor of the cysteine protease caspase-1.	benzyloxycarbonyl aspartyl-glutamyl-valyl-aspartyl-chloromethyl ketone	128-187	caspase 1	Homo sapiens	227-236
31885713-9	2020	Furthermore, NaHS inhibited the expression of NLRP3, ASC and cleaved caspase-1, and the production of IL-1beta and IL-18 in adipocytes treated with HG.	Sodium	13-17	caspase 1	Homo sapiens	69-78
33012733-9	2020	Additionally, the administration of rCC16 significantly attenuated the increase of pro-IL-1beta, NLRP3 and caspase-1 levels induced by silica particle exposure.	Silicon Dioxide	135-141	caspase 1	Homo sapiens	107-116
31914640-4	2020	Here we show that ginsenoside Rg3 blocks IL-1beta secretion and caspase-1 activation through inhibiting LPS priming and the NLRP3 inflammasome activation in human and mouse macrophages.	ginsenoside Rg3	18-33	caspase 1	Homo sapiens	64-73
33012733-10	2020	Our results suggested that exogenous CC16 could inhibit silica particles-induced inflammation in THP-1 macrophages, mainly through suppressing NF-kappaB pathway and caspase-1 activation.	Silicon Dioxide	56-62	caspase 1	Homo sapiens	165-174
33132241-8	2020	We found that the supernatant from the incubation of gefitinib with FLC-4 cells for 7 days led to increased caspase-1 activity and production of IL-1ss by THP-1 cells.	Gefitinib	53-62	caspase 1	Homo sapiens	108-117
31759040-8	2020	Moreover, C-terminal end of the Gasdermin D molecule is also cleaved by the caspase-1.	Carbon	10-11	caspase 1	Homo sapiens	76-85
31612353-13	2020	Repression of ROS contributes to the inhibition of the expression of NLRP3, caspase-1 and IL-beta proteins as well as of cell migration.	Reactive Oxygen Species	14-17	caspase 1	Homo sapiens	76-85
31705795-6	2020	Under excess glucose conditions, allopurinol significantly inhibited trophoblast secretion of inflammatory IL-1beta; caspase-1 activity; IL-8; RANTES; and GRO-alpha.	Allopurinol	33-44	caspase 1	Homo sapiens	117-126
31680318-3	2020	Findings suggest that neurotoxins, aggregation of alpha-synuclein, mitochondrial reactive oxygen species, and disrupted mitophagy are the key regulators of microglial leucine-rich-repeat- and pyrin-domain-containing 3 inflammasome activation and release of interleukin-1beta and interleukin-18 caspase-1-mediated pyroptotic cell death in the substantia nigra of the brain.	leucylleucine	167-174	caspase 1	Homo sapiens	294-303
31639409-4	2020	It was found that acrolein increased the levels of NLRP3 and cleaved caspase-1, which led to the maturation of interleukin-1beta (IL-1beta).	Acrolein	18-26	caspase 1	Homo sapiens	69-78
33202405-2	2020	The formation of the inflammasome enables activation of an inflammatory protease caspase-1 and pyroptosis initiation with the subsequent cleaving of the pro-inflammatory cytokines interleukin (IL)-1beta and proIL-18 to produce active forms.	proil-18	207-215	caspase 1	Homo sapiens	81-90
30860577-5	2019	Consistent with this result, hydrogen peroxide treatment augmented the cleavage of Gsdmd by caspase-1.	Hydrogen Peroxide	29-46	caspase 1	Homo sapiens	92-101
31905600-6	2019	Low-dose epirubicin at non-cytotoxic doses downregulated NLRP3 inflammasome components and reduced the release of cleaved caspase-1, bioactive IL-1beta, and TNF-alpha following NLRP3 activation in a dose-dependent fashion.	Epirubicin	9-19	caspase 1	Homo sapiens	122-131
31835256-4	2019	RESULTS: Nicotine treatment significantly increased the colocalization of NLRP3 with Asc, caspase-1 activity, IL-beta production, cell permeability in podocytes compared to control cells.	Nicotine	9-17	caspase 1	Homo sapiens	90-99
31835256-5	2019	Pretreatment with caspase-1 inhibitor, WEHD significantly abolished the nicotine-induced colocalization of NLRP3 with Asc, caspase-1 activity, IL-1beta production and cell permeability in podocytes.	Nicotine	72-80	caspase 1	Homo sapiens	18-27
31835256-5	2019	Pretreatment with caspase-1 inhibitor, WEHD significantly abolished the nicotine-induced colocalization of NLRP3 with Asc, caspase-1 activity, IL-1beta production and cell permeability in podocytes.	Nicotine	72-80	caspase 1	Homo sapiens	123-132
31835256-10	2019	Furthermore, prior treatment with ROS scavenger, NAC significantly attenuated the nicotine-induced caspase-1 activity, IL-1beta production, podocin and nephrin reduction in podocytes.	ros	34-37	caspase 1	Homo sapiens	99-108
31835256-10	2019	Furthermore, prior treatment with ROS scavenger, NAC significantly attenuated the nicotine-induced caspase-1 activity, IL-1beta production, podocin and nephrin reduction in podocytes.	Nicotine	82-90	caspase 1	Homo sapiens	99-108
31886288-7	2019	The activity of caspase-1 and production of pyroptotic cytokines were significantly inhibited by Exendin-4 treatment in the diabetic heart and in high glucose-treated cardiomyocytes as well.	Glucose	151-158	caspase 1	Homo sapiens	16-25
31819645-15	2019	Western blot analysis showed that matrine combined with docetaxel treatment led to the expression of caspase1 in both DU145 and PC-3 cells.	matrine	34-41	caspase 1	Homo sapiens	101-109
31866999-7	2019	In the absence of VDR, caspase-1 activation and IL-1beta release are increased in response to LPS-induced inflammation or alum-induced peritoneal inflammation, indicating that VDR is a negative regulator of NLRP3 inflammasome activation in vivo.	aluminum sulfate	122-126	caspase 1	Homo sapiens	23-32
31819645-15	2019	Western blot analysis showed that matrine combined with docetaxel treatment led to the expression of caspase1 in both DU145 and PC-3 cells.	docetaxel	56-65	caspase 1	Homo sapiens	101-109
31638409-3	2019	A high glucose concentration induced HRVEC inflammation metabolic memory by decreasing SIRT1 and increasing Ac-NF-kappaB, NLRP3, caspase 1, interleukin-1beta, inducible nitric oxide synthase, and tumor necrosis factor alpha, whereas exposure of HRVECs to a high glucose medium for 4 days, followed by a normal glucose concentration for an additional 4 days, failed to reverse these changes.	Glucose	7-14	caspase 1	Homo sapiens	129-138
31658511-3	2019	Methods and Results: In this study, we found that the PVC secretome effectively alleviates secretion of both caspase-1 and interleukin-1beta in lipopolysaccharide-primed and activated human and murine macrophages by blocking inflammasome activation and attenuating the production of mitochondrial reactive oxygen species (ROS).	Oxygen	306-312	caspase 1	Homo sapiens	109-118
30877711-7	2019	Gemigliptin-treated kidneys showed a reduction in levels of NLRP3, apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC), caspase-1, and interleukin-1beta, which had all been markedly increased by UUO.	LC15-0444	0-11	caspase 1	Homo sapiens	154-163
31485636-10	2019	It was also observed that curcumin treatment downregulated the expression levels of TXNIP, NLRP3, interleukin (IL)-1beta and IL-18, and downstream caspase-1 compared with PQ treatment alone.	Curcumin	26-34	caspase 1	Homo sapiens	147-156
31086288-4	2019	RESULTS: Activation of THP-1 macrophages with nigericin increased the mRNA expression of NLRP3, IL-1beta, and caspase-1 (P &lt; 0.01).	Nigericin	46-55	caspase 1	Homo sapiens	110-119
31442452-0	2019	Withaferin A modulates AIM2 inflammasome and caspase-1 expression in THP-1 polarized macrophages.	withaferin A	0-12	caspase 1	Homo sapiens	45-54
31775905-8	2019	Furthermore, SAA stimulation induced cleaved caspase-1 (p20) secretion from human neutrophils, and this release was suppressed by HCQ pretreatment.	Hydroxychloroquine	130-133	caspase 1	Homo sapiens	45-54
33693087-7	2019	In macrophages, MSU activates the NLRP3 inflammasome and proteolytic processing mediated by caspase-1 with enhanced interleukin (IL)-1beta and IL-18 secretion.	Uric Acid	16-19	caspase 1	Homo sapiens	92-101
31611962-1	2019	Current studies suggest that the cysteinyl aspartate specific proteinase (caspase/CASP) family may be closely associated with apoptosis.	cysteinyl-aspartate	33-52	caspase 1	Homo sapiens	74-81
31819864-6	2019	Untreated controls were incubated with ATP (1.25 mM) for 1 hr to maximally stimulate NLRP3 inflammasome activity (measured as caspase-1 cleavage of the fluorogenic substrate Ac-YVAD-AFC).	Adenosine Triphosphate	39-42	caspase 1	Homo sapiens	126-135
31819864-6	2019	Untreated controls were incubated with ATP (1.25 mM) for 1 hr to maximally stimulate NLRP3 inflammasome activity (measured as caspase-1 cleavage of the fluorogenic substrate Ac-YVAD-AFC).	N-acetyl-S-farnesylcysteine	174-185	caspase 1	Homo sapiens	126-135
31819864-8	2019	Results: CPPD and MSU activate caspase-1 in urothelial cells in a dose-dependent manner, reaching ~50% and ~25% of the ATP response, respectively.	Uric Acid	18-21	caspase 1	Homo sapiens	31-40
31819864-8	2019	Results: CPPD and MSU activate caspase-1 in urothelial cells in a dose-dependent manner, reaching ~50% and ~25% of the ATP response, respectively.	Adenosine Triphosphate	119-122	caspase 1	Homo sapiens	31-40
31332667-6	2019	In addition, increase in caspase-1/NLRP3 inflammasome activation was blocked by BAY11-7082.	3-(4-methylphenylsulfonyl)-2-propenenitrile	80-90	caspase 1	Homo sapiens	25-34
31332667-9	2019	However, production of IL-1beta, NO/iNOS as well as caspase-1/NLRP3 activity was significantly reduced in the presence of CRID3.	N-(1,2,3,5,6,7-hexahydro-S-indacen-4-ylcarbamoyl)-4-(2-hydroxy-2-propanyl)-2-furansulfonamide	122-127	caspase 1	Homo sapiens	52-61
31597739-1	2019	NLRC4 [nucleotide-binding domain and leucine-rich repeat (NLR) family, caspase recruitment domain (CARD) containing 4] is an innate immune receptor, which, upon detection of certain pathogens or internal distress signals, initiates caspase-1-mediated interleukin-1beta maturation and an inflammatory response.	Leucine	37-44	caspase 1	Homo sapiens	232-241
31302424-3	2019	Nucleotide-binding domain and leucine-rich-repeat-containing family pyrin 3 (NLRP3) inflammasome as a multi-protein complex that activates caspase-1 can give rise to the proinflammatory cytokines such as interleukin-18 (IL-18) and interleukin-1 beta (IL-1beta) maturation.	Leucine	30-37	caspase 1	Homo sapiens	139-148
31649499-14	2019	Conversely, AF-induced LDH release is significantly reduced by MCC950 and Ac-YVAD-cmk (NLRP3 and Caspase-1 inhibitors, respectively), suggesting a pro-inflammatory cell death by pyroptosis.	Actinium	74-76	caspase 1	Homo sapiens	97-106
31586128-5	2019	VU0155069 also significantly blocked IL-1beta production, caspase-1 activation, and pyroptosis caused by several inflammasome-activating signals in the bone marrow-derived macrophages (BMDMs).	N-(1-(4-(5-chloro-2-oxo-2,3-dihydro-1H-benzo(d)imidazol-1-yl)piperidin-1-yl)propan-2-yl)-2-naphthamide	0-9	caspase 1	Homo sapiens	58-67
31586128-8	2019	VU0155069 indirectly inhibited caspase-1 activity caused by LPS + nigericin in BMDMs independent of PLD1 activity.	N-(1-(4-(5-chloro-2-oxo-2,3-dihydro-1H-benzo(d)imidazol-1-yl)piperidin-1-yl)propan-2-yl)-2-naphthamide	0-9	caspase 1	Homo sapiens	31-40
31586128-8	2019	VU0155069 indirectly inhibited caspase-1 activity caused by LPS + nigericin in BMDMs independent of PLD1 activity.	Nigericin	66-75	caspase 1	Homo sapiens	31-40
31381888-7	2019	Pharmacologic inhibition with Ac-YVAD-cmk of caspase 1, a critical component of the NLRP3 inflammasome, prevents DICER1 dysregulation- and dsRNA-induced osteoblast cell death.	ac-yvad	30-37	caspase 1	Homo sapiens	45-54
31315072-7	2019	Suhuang also inhibited NLRP3 inflammasome activation, as evidenced by disrupting the assembly of NLRP3 inflammasome and reducing the expression of cleaved caspase-1, and decreased IL-1beta secretion.	suhuang	0-7	caspase 1	Homo sapiens	155-164
31324698-7	2019	We found that increased caspase-1 activity and production of interleukin-1beta by THP-1 cells were caused by the supernatant from the incubation of carbamazepine with FLC-4 cells.	Carbamazepine	148-161	caspase 1	Homo sapiens	24-33
31429348-9	2019	Ac-YVAD-cmk or increasing extracellular K+ blocked the activation of caspase-1 and attenuated the release of IL-18.	ac-yvad	0-7	caspase 1	Homo sapiens	69-78
31219197-4	2019	At 3 months post-transplant modelling revealed an association between tacrolimus Css and recipient CASP1 rs580523 genotype (P = 0.005), accounting for 52% Css variance.	Tacrolimus	70-80	caspase 1	Homo sapiens	99-104
30978354-4	2019	B19V infection increases the production of tumor necrosis factor-alpha and induces NLRP3-mediated caspase-1 activation in both THP-1 cells differentiated with phorbol 12-myristate 13-acetate and in monocytes from patients with SSc but not from healthy controls.	Tetradecanoylphorbol Acetate	159-190	caspase 1	Homo sapiens	98-107
31276767-5	2019	Results indicate, that consistent with previous finding, DNCB more rapidly (3 h) induces NLRP3, ASC protein expression and caspase-1 activation compared to PPD.	Dinitrochlorobenzene	57-61	caspase 1	Homo sapiens	123-132
31473434-7	2019	We found high glucose could increase Propidium Iodide (PI) positive cells and elevate release of lactate dehydrogenase (LDH), Interleukin 1 beta (IL-1beta) and Interleukin 18 (IL-18); protein levels of GSDMD, GSDMD N-terminal domain (GSDMD-N) and cleaved-caspase-1 were also elevated.	Glucose	14-21	caspase 1	Homo sapiens	255-264
31473434-8	2019	Effect of NaB on LDH release and PI positive cells was further enhanced by inhibiting caspase 1-GSDMD.	nab	10-13	caspase 1	Homo sapiens	86-95
31473434-10	2019	In conclusion, NaB could ameliorate high-glucose induced GECs via caspase1-GSDMD canonical pyroptosis pathway; and NF-kappaB/IkappaB-alpha signaling pathway was involved in it.	nab	15-18	caspase 1	Homo sapiens	66-74
31276767-2	2019	The purpose of this study was to further investigate the effects of DNCB and para-phenylenediamine (PPD) on the expression of the proteins of the inflammasome, namely NLRP3, ASC and caspase 1 by western blot analysis; to define the intracellular localization and co-localization of NLRP3 and NLPR12 by immunoprecipitation and immunohistochemistry; and to define the role of NF-kappaB in Blimp-1 induction by pharmacological inhibition.	Dinitrochlorobenzene	68-72	caspase 1	Homo sapiens	182-191
31276767-2	2019	The purpose of this study was to further investigate the effects of DNCB and para-phenylenediamine (PPD) on the expression of the proteins of the inflammasome, namely NLRP3, ASC and caspase 1 by western blot analysis; to define the intracellular localization and co-localization of NLRP3 and NLPR12 by immunoprecipitation and immunohistochemistry; and to define the role of NF-kappaB in Blimp-1 induction by pharmacological inhibition.	4-phenylenediamine	77-98	caspase 1	Homo sapiens	182-191
31276767-2	2019	The purpose of this study was to further investigate the effects of DNCB and para-phenylenediamine (PPD) on the expression of the proteins of the inflammasome, namely NLRP3, ASC and caspase 1 by western blot analysis; to define the intracellular localization and co-localization of NLRP3 and NLPR12 by immunoprecipitation and immunohistochemistry; and to define the role of NF-kappaB in Blimp-1 induction by pharmacological inhibition.	4-phenylenediamine	100-103	caspase 1	Homo sapiens	182-191
31358323-9	2019	Enhanced expression of NLRP3, caspase-1, and IL-1beta was noted in macrophages treated with LPS (10 ng/ml) and MSU crystals (0.1 mg/ml), which was markedly suppressed by treatment with artemisinin (1, 10, and 100 muM).	Uric Acid	111-114	caspase 1	Homo sapiens	30-39
31400606-5	2019	Our previous study found that pyroptosis was markedly activated in the cardiomyocytes subjected to high-glucose conditions, and miR-214-3p regulated the expression of caspase-1.	Glucose	104-111	caspase 1	Homo sapiens	167-176
31400606-7	2019	Herein, we identified that hsa_circ_0076631, named caspase-1-associated circRNA (CACR), was increased both in high-glucose-treated cardiomyocytes and in the serum of diabetic patients.	Glucose	115-122	caspase 1	Homo sapiens	51-60
31400606-9	2019	CACR knockdown in cardiomyocytes counteracted high-glucose-induced caspase-1 activation.	Glucose	51-58	caspase 1	Homo sapiens	67-76
31551929-9	2019	Exposure to BPA significantly increased CD4+ T cells, IFNgamma, IL-17A, TLR4, caspase-1, and IL-1beta in the heart.	bisphenol A	12-15	caspase 1	Homo sapiens	78-87
31219197-6	2019	As this is the first report of CASP1 genetic variability influencing tacrolimus Css , further validation in larger cohorts is required.	Tacrolimus	69-79	caspase 1	Homo sapiens	31-36
31474553-0	2019	Benzene metabolites trigger pyroptosis and contribute to haematotoxicity via TET2 directly regulating the Aim2/Casp1 pathway.	Benzene	0-7	caspase 1	Homo sapiens	111-116
31474553-3	2019	METHODS: Here, we first found in mRNA microarray that pyroptotic classic genes (Casp1, 4, 5, and IL1beta) were up-regulated and represented dose-dependent differential expression in controls, low-dose benzene-exposed and chronic benzene-poisoned workers, and the expression of Casp1 and IL1beta were confirmed in low-dose benzene-exposed workers and was accompanied with elevated potent proinflammatory IL1beta.	Benzene	201-208	caspase 1	Homo sapiens	80-85
31474553-3	2019	METHODS: Here, we first found in mRNA microarray that pyroptotic classic genes (Casp1, 4, 5, and IL1beta) were up-regulated and represented dose-dependent differential expression in controls, low-dose benzene-exposed and chronic benzene-poisoned workers, and the expression of Casp1 and IL1beta were confirmed in low-dose benzene-exposed workers and was accompanied with elevated potent proinflammatory IL1beta.	Benzene	201-208	caspase 1	Homo sapiens	277-282
31474553-3	2019	METHODS: Here, we first found in mRNA microarray that pyroptotic classic genes (Casp1, 4, 5, and IL1beta) were up-regulated and represented dose-dependent differential expression in controls, low-dose benzene-exposed and chronic benzene-poisoned workers, and the expression of Casp1 and IL1beta were confirmed in low-dose benzene-exposed workers and was accompanied with elevated potent proinflammatory IL1beta.	Benzene	229-236	caspase 1	Homo sapiens	80-85
31474553-3	2019	METHODS: Here, we first found in mRNA microarray that pyroptotic classic genes (Casp1, 4, 5, and IL1beta) were up-regulated and represented dose-dependent differential expression in controls, low-dose benzene-exposed and chronic benzene-poisoned workers, and the expression of Casp1 and IL1beta were confirmed in low-dose benzene-exposed workers and was accompanied with elevated potent proinflammatory IL1beta.	Benzene	229-236	caspase 1	Homo sapiens	277-282
31474553-3	2019	METHODS: Here, we first found in mRNA microarray that pyroptotic classic genes (Casp1, 4, 5, and IL1beta) were up-regulated and represented dose-dependent differential expression in controls, low-dose benzene-exposed and chronic benzene-poisoned workers, and the expression of Casp1 and IL1beta were confirmed in low-dose benzene-exposed workers and was accompanied with elevated potent proinflammatory IL1beta.	Benzene	229-236	caspase 1	Homo sapiens	80-85
31474553-3	2019	METHODS: Here, we first found in mRNA microarray that pyroptotic classic genes (Casp1, 4, 5, and IL1beta) were up-regulated and represented dose-dependent differential expression in controls, low-dose benzene-exposed and chronic benzene-poisoned workers, and the expression of Casp1 and IL1beta were confirmed in low-dose benzene-exposed workers and was accompanied with elevated potent proinflammatory IL1beta.	Benzene	229-236	caspase 1	Homo sapiens	277-282
31474553-4	2019	In vitro studies showed that benzene metabolites induced AHH-1 cell pyroptosis through activating Aim2/Casp1 pathway with the increased expression of GSDMD.	Benzene	29-36	caspase 1	Homo sapiens	103-108
31474553-7	2019	FINDINGS: Exposure to benzene can trigger pyroptosis via TET2 directly regulating the Aim2/Casp1 signaling pathway to cause haematotoxicity.	Benzene	22-29	caspase 1	Homo sapiens	91-96
31474553-8	2019	INTERPRETATION: Benzene metabolites induced pyroptotic cell death through activation of the Aim2/Casp1 pathway which can be regulated by Tet2 overexpression.	Benzene	16-23	caspase 1	Homo sapiens	97-102
31692589-5	2019	Purpose: This article discusses efforts to examine the release of active Caspase-1 from NHEKs activated by various exogenous threats including UVB energy, ATP, Nigericin and Urban Dust.	Adenosine Triphosphate	155-158	caspase 1	Homo sapiens	73-82
31172209-0	2019	Neferine inhibits LPS-ATP-induced endothelial cell pyroptosis via regulation of ROS/NLRP3/Caspase-1 signaling pathway.	neferine	0-8	caspase 1	Homo sapiens	90-99
31364628-1	2019	The hydrogen bond patterns, proton ordering, and phase transitions of monolayer ice in two-dimensional hydrophobic confinement are fundamentally different from those found for bulk ice.	Hydrogen	4-12	caspase 1	Homo sapiens	80-83
31364628-7	2019	For the water-water interaction different water force fields, i.e. SPCE, TIP3P, TIP4P, TIP4P/ICE, and TIP5P, are used.	Water	8-13	caspase 1	Homo sapiens	87-96
31364628-14	2019	For temperatures between 200 K and 400 K we find several second-order phase transitions from one ice structure to another, changing in many cases both the arrangements of the oxygen atoms and the proton ordering.	Oxygen	175-181	caspase 1	Homo sapiens	97-100
31172209-0	2019	Neferine inhibits LPS-ATP-induced endothelial cell pyroptosis via regulation of ROS/NLRP3/Caspase-1 signaling pathway.	Adenosine Triphosphate	22-25	caspase 1	Homo sapiens	90-99
31172209-9	2019	CONCLUSIONS: Our findings indicated neferine may reduce ROS by anti-oxidation and inhibit LPS-ATP-induced endothelial cell pyroptosis via blocking ROS/NLRP3/Caspase-1 signaling pathway, which provides the evidence for therapeutic effect in CKD.	neferine	36-44	caspase 1	Homo sapiens	157-166
31176046-0	2019	The neuroprotection of progesterone against Abeta-induced NLRP3-Caspase-1 inflammasome activation via enhancing autophagy in astrocytes.	Progesterone	23-35	caspase 1	Homo sapiens	64-73
31176046-4	2019	However, the exact role of PG in regulating NLRP3-Caspase-1 inflammasome remains to be elucidated.	Progesterone	27-29	caspase 1	Homo sapiens	50-59
31176046-6	2019	However, pharmacological activation of autophagy by Rapamycin (RAPA) efficiently suppressed Abeta-, lipopolysaccharides (LPS)-induced IL-1beta expression via regulating NLRP3-Caspase-1 inflammasome in astrocytes.	Sirolimus	52-61	caspase 1	Homo sapiens	175-184
31176046-6	2019	However, pharmacological activation of autophagy by Rapamycin (RAPA) efficiently suppressed Abeta-, lipopolysaccharides (LPS)-induced IL-1beta expression via regulating NLRP3-Caspase-1 inflammasome in astrocytes.	Sirolimus	63-67	caspase 1	Homo sapiens	175-184
31176046-7	2019	Remarkably, PG significantly inhibited Abeta-induced NLRP3-Caspase-1 inflammasome activation.	Progesterone	12-14	caspase 1	Homo sapiens	59-68
31176046-9	2019	Taken together, our observations suggest that autophagy-lysosome pathway is one specific molecular mechanism in regulating Abeta-induced NLRP3-Caspase-1 inflammasome activation in astrocytes, particularly uncover the potential neuroprotection of PG in regulating upstream signaling leading to the sequence events of neuroinflammation.	Progesterone	246-248	caspase 1	Homo sapiens	143-152
31176046-10	2019	That neuroprotective mechanism of PG in regulating NLRP3-Caspase-1 inflammasome can be a potential therapeutic target for ameliorating the pathological procession of AD.	Progesterone	34-36	caspase 1	Homo sapiens	57-66
31692589-5	2019	Purpose: This article discusses efforts to examine the release of active Caspase-1 from NHEKs activated by various exogenous threats including UVB energy, ATP, Nigericin and Urban Dust.	Nigericin	160-169	caspase 1	Homo sapiens	73-82
31692589-10	2019	Results: Initial results demonstrate that NHEKs can be activated to release active Caspase-1 by ATP and UVB, but not by Nigericin or Urban Dust.	Adenosine Triphosphate	96-99	caspase 1	Homo sapiens	83-92
31429707-7	2019	The serum caspase-1 levels in ACLF patients showed a negative correlation with total serum bilirubin and a positive correlation with serum total protein and albumin.	Bilirubin	91-100	caspase 1	Homo sapiens	10-19
31485193-7	2019	In addition, levels of ROS, caspase1, and IL-1beta increased in a time- and dose-dependent manner in the high glucose group, even with an increased expression of LC3 (p < 0.01).	Glucose	110-117	caspase 1	Homo sapiens	28-36
31531346-8	2019	Hepatic damage associated with increased ROS and protein expression levels of NOX4, NLRP3, caspase-1, and IL-1beta was attenuated by AVE 0991, an analogue of Ang-(1-7).	AVE 0991	133-141	caspase 1	Homo sapiens	91-100
31412804-9	2019	RESULTS: The expression of IL-1beta, ICAM-1, NLRP3 complexes, and activation of NLRP3 inflammasome could be induced by UA, but the changes induced by UA were partially reversed by siRNA NLRP3 or caspase 1 inhibitor.	Uric Acid	119-121	caspase 1	Homo sapiens	195-204
31315822-4	2019	Exogenous H2S reduced the level of NLRP3, caspase-1, P62, IL-1beta and the ratio of P-mTOR/T-mTOR induced by OA and increased the ratio of LC3 II/I and the protein expression of Beclin1 suppressed by OA.	Hydrogen Sulfide	10-13	caspase 1	Homo sapiens	42-51
31386668-4	2019	We found that NLR markedly increased the release of VEGF from RPE cells and that this effect was attenuated by nintedanib, a multiple receptor tyrosine kinase inhibitor, whereas it was unaffected by inhibitors of NF-kappaB signaling or of caspase-1.	nintedanib	111-121	caspase 1	Homo sapiens	239-248
30940293-5	2019	The mortality of HCC cells was largely reversed by the caspase 1 antagonist, YVAD-cmk, suggesting that E2-induced cell death was associated with caspase 1-dependent pyroptosis.	YVAD	77-81	caspase 1	Homo sapiens	55-64
30940293-5	2019	The mortality of HCC cells was largely reversed by the caspase 1 antagonist, YVAD-cmk, suggesting that E2-induced cell death was associated with caspase 1-dependent pyroptosis.	YVAD	77-81	caspase 1	Homo sapiens	145-154
30940293-8	2019	We observed that E2-induced pyroptosis was dramatically increased by 3-methyladenine (3-MA) treatment, which was abolished by YVAD-cmk treatment, suggesting that caspase 1-dependent pyroptosis was negatively regulated by autophagy.	3-methyladenine	69-84	caspase 1	Homo sapiens	162-171
30940293-8	2019	We observed that E2-induced pyroptosis was dramatically increased by 3-methyladenine (3-MA) treatment, which was abolished by YVAD-cmk treatment, suggesting that caspase 1-dependent pyroptosis was negatively regulated by autophagy.	3-methyladenine	86-90	caspase 1	Homo sapiens	162-171
30940293-8	2019	We observed that E2-induced pyroptosis was dramatically increased by 3-methyladenine (3-MA) treatment, which was abolished by YVAD-cmk treatment, suggesting that caspase 1-dependent pyroptosis was negatively regulated by autophagy.	YVAD	126-130	caspase 1	Homo sapiens	162-171
31360100-5	2019	We found that caffeine significantly reduced NLRP3 expression, ASC speck formation, and caspase 1 cleavage and therefore decreased IL-1beta and IL-18 secretion in THP-1 macrophages.	Caffeine	14-22	caspase 1	Homo sapiens	88-97
31214205-8	2019	We demonstrate that this technique is also able to detect the distribution of active caspase-1 within the ASC aggregates by incubating cells with FAM-FLICATM, a fluorochrome inhibitor of caspase-1.	fam-flicatm	146-157	caspase 1	Homo sapiens	187-196
31272469-8	2019	RESULTS: We show that ethanol increases the number of secreted nanovesicles and their content by raising the levels of both inflammatory-related proteins (TLR4, NFkappaB-p65, IL-1R, caspase-1, NLRP3) and by changing miRNAs (mir-146a, mir-182, and mir-200b) in the EVs from the WT-astrocytes compared with those from the untreated WT cells.	Ethanol	22-29	caspase 1	Homo sapiens	182-191
30917625-10	2019	Caspase 1, which is responsible for IL-1beta production, was similarly induced by LPS and suppressed by TY52156.	1-(4-chlorophenylhydrazono)-1-(4-chlorophenylamino)-3,3-dimethyl-2-butanone	104-111	caspase 1	Homo sapiens	0-9
30976089-8	2019	Lipopolysaccharide from phosphorylcholine (ChoP)-positive bacteria induced NLRP3 and caspase-1 proteins in human alveolar epithelial cells, however antagonism of PAFR prevented NLRP3 activation by ChoP.	Phosphorylcholine	24-41	caspase 1	Homo sapiens	85-94
31217433-11	2019	Finally, we found a negative correlation between DHA content in plasma and the induction of caspase-1 activity in HLA-DR- CD33+ CD15+ MDSC of patients treated with 5-FU-based chemotherapy, strongly suggesting that our data are clinical relevant.	Docosahexaenoic Acids	49-52	caspase 1	Homo sapiens	92-101
31217433-11	2019	Finally, we found a negative correlation between DHA content in plasma and the induction of caspase-1 activity in HLA-DR- CD33+ CD15+ MDSC of patients treated with 5-FU-based chemotherapy, strongly suggesting that our data are clinical relevant.	Fluorouracil	164-168	caspase 1	Homo sapiens	92-101
30977640-0	2019	Polychlorinated Biphenyl Quinone Induces Caspase 1-Mediated Pyroptosis through Induction of Pro-inflammatory HMGB1-TLR4-NLRP3-GSDMD Signal Axis.	polychlorinated biphenyl quinone	0-32	caspase 1	Homo sapiens	41-50
30977640-8	2019	Then we found PCB29-pQ activates NOD-like receptor pyrin domain-containing 3 (NLRP3) inflammasome that mediates caspase 1 activation.	2,3,5-trichloro-6-phenyl-(1,4)benzoquinone	14-22	caspase 1	Homo sapiens	112-121
31244838-3	2019	If tissue damage occurs, danger signals released from necrotic cells, such as ATP, can activate NLRP3-inflammasomes (multiprotein complexes consisting of NLRP3, ASC, and active caspase-1) which cleaves and activates pro-IL-1beta.	Adenosine Triphosphate	78-81	caspase 1	Homo sapiens	177-186
31214205-8	2019	We demonstrate that this technique is also able to detect the distribution of active caspase-1 within the ASC aggregates by incubating cells with FAM-FLICATM, a fluorochrome inhibitor of caspase-1.	fam-flicatm	146-157	caspase 1	Homo sapiens	85-94
31360100-7	2019	Moreover, silencing of the caffeine-antagonized adenosine A2a receptor (A2aR) significantly decreased cleaved caspase 1 expression in THP-1 macrophages by reducing ROS production.	Caffeine	27-35	caspase 1	Homo sapiens	110-119
30901677-7	2019	Moreover, Genistein treatment down-regulated production of caspase-1 and IL-1beta and increased intracellular cAMP level, which were similar to the treatment for INT-777, a semi-synthetic TGR5 agonist, in phorbol myristate acetate (PMA)-differentiated monocytic THP-1 cells and U937 cells.	Genistein	10-19	caspase 1	Homo sapiens	59-68
30958608-8	2019	Moreover, DEX inhibited caspase-1 activation and decreased pyroptosis.	Dexmedetomidine	10-13	caspase 1	Homo sapiens	24-33
30238389-6	2019	Treatment with indole compound NC009-1 (3-((1H-Indole-3-yl)methyl)-4-(2-nitrophenyl)but-3-en-2-one), a potential Abeta aggregation reducer, normalized the Abeta levels and GSK3beta and tau phosphorylation, attenuated caspase 1 activity, and improved neurite outgrowth in AD-iPSC-derived neurons.	Indoles	15-30	caspase 1	Homo sapiens	217-226
30614043-5	2019	Pyroptosis was also determined by lactate dehydrogenase release and active caspase-1-propidium iodide double staining.	Propidium	85-101	caspase 1	Homo sapiens	75-84
30238389-6	2019	Treatment with indole compound NC009-1 (3-((1H-Indole-3-yl)methyl)-4-(2-nitrophenyl)but-3-en-2-one), a potential Abeta aggregation reducer, normalized the Abeta levels and GSK3beta and tau phosphorylation, attenuated caspase 1 activity, and improved neurite outgrowth in AD-iPSC-derived neurons.	nc009-1 (3-((1h-indole-3-yl)methyl)-4-(2-nitrophenyl)but-3-en-2-one	31-98	caspase 1	Homo sapiens	217-226
30796177-6	2019	And ROS scavenger N-acetyl-cysteine attenuated the activation of caspase-1 induced by MST1 and the effect of MST1 in PDAC cell death, proliferation, migration, and invasion.	Reactive Oxygen Species	4-7	caspase 1	Homo sapiens	65-74
31139563-0	2019	Antitumor Effects of Berberine on Gliomas via Inactivation of Caspase-1-Mediated IL-1beta and IL-18 Release.	Berberine	21-30	caspase 1	Homo sapiens	62-71
30796177-6	2019	And ROS scavenger N-acetyl-cysteine attenuated the activation of caspase-1 induced by MST1 and the effect of MST1 in PDAC cell death, proliferation, migration, and invasion.	Acetylcysteine	18-35	caspase 1	Homo sapiens	65-74
30959169-9	2019	Moreover, caspase-1 activity and IL-1beta production were increased in ECs stimulated with oxLDL, ATP or UTP through the modulation of mtROS production and mtDNA expression, in a P2Y2R-dependent manner.	Adenosine Triphosphate	98-101	caspase 1	Homo sapiens	10-19
30959169-9	2019	Moreover, caspase-1 activity and IL-1beta production were increased in ECs stimulated with oxLDL, ATP or UTP through the modulation of mtROS production and mtDNA expression, in a P2Y2R-dependent manner.	Uridine Triphosphate	105-108	caspase 1	Homo sapiens	10-19
30912285-6	2019	Caspase-1 activation increases after ketone salt (Study 1: condition x time interaction, p = 0.012) and monoester supplementation (Study 2: condition x time interaction, p = 0.016) compared to placebo.	ketone salt	37-48	caspase 1	Homo sapiens	0-9
31139563-6	2019	In this study, we demonstrate that berberine significantly inhibits inflammatory cytokine Caspase-1 activation via ERK1/2 signaling and subsequent production of IL-1beta and IL-18 by glioma cells.	Berberine	35-44	caspase 1	Homo sapiens	90-99
31064994-6	2019	Caspase-1-induced apoptosis involves the Bid-caspase-9-caspase-3 axis, which can be followed by GSDME-dependent secondary necrosis/pyroptosis.	gsdme	96-101	caspase 1	Homo sapiens	0-9
31064994-8	2019	Furthermore, cortical neurons and mast cells exhibit little or low GSDMD expression and undergo apoptosis after oxygen glucose deprivation and nigericin stimulation, respectively, in a caspase-1- and Bid-dependent manner.	Nigericin	143-152	caspase 1	Homo sapiens	185-203
30826015-7	2019	Although beta-OHB treatment did not impact markers of apoptosis, it decreased the expression of caspase-1 and proinflammatory cytokines, indicating that beta-OHB blocked pyroptosis.	beta-ohb	9-17	caspase 1	Homo sapiens	96-105
30976816-0	2019	Ursolic acid downregulates thymic stromal lymphopoietin through the blockade of intracellular calcium/caspase-1/NF-kappaB signaling cascade in HMC-1 cells.	ursolic acid	0-12	caspase 1	Homo sapiens	102-111
30976816-8	2019	Caspase-1 activity was increased by exposure to phorbol myristate acetate plus calcium ionophore, whereas it was reduced by UA.	Tetradecanoylphorbol Acetate	48-73	caspase 1	Homo sapiens	0-9
30976816-8	2019	Caspase-1 activity was increased by exposure to phorbol myristate acetate plus calcium ionophore, whereas it was reduced by UA.	Calcium	79-86	caspase 1	Homo sapiens	0-9
30976816-8	2019	Caspase-1 activity was increased by exposure to phorbol myristate acetate plus calcium ionophore, whereas it was reduced by UA.	ursolic acid	124-126	caspase 1	Homo sapiens	0-9
30097848-8	2019	On the other hand, caspases are cysteine endoproteases and mediate neuronal cell death such as apoptosis and pyroptosis, which are programmed cell death.	Cysteine	32-40	caspase 1	Homo sapiens	19-27
30833078-4	2019	RESULTS: U937 macrophages treated with MSU crystals showed increased expression of IL-1beta, IL-18, caspase-1, and TXNIP and activation of NF-kappaB signaling, which were strongly inhibited by addition of antioxidants or transfection with TXNIP siRNA.	Uric Acid	39-42	caspase 1	Homo sapiens	100-109
30873702-7	2019	Then, DHA were first shown to promote AIM2/caspase-1 inflammasome.	artenimol	6-9	caspase 1	Homo sapiens	43-52
30873702-8	2019	Compared with the DHA group, the autophagy inhibitor 3-MA significantly inhibited the expressions of activated Caspase-1, a pyroptotic marker proteins.	3-methyladenine	53-57	caspase 1	Homo sapiens	111-120
30873702-9	2019	Meanwhile, repression of mTOR by rapamycin promoted autophagy and AIM2/caspase-1 activation.	Sirolimus	33-42	caspase 1	Homo sapiens	71-80
30873702-10	2019	The caspase-1 inhibitor Z-YVAD-FMK also notably blocked autophagy cell death characterized by the downexpression of Beclin-1 and LC3-II.	benzyloxycarbonyltyrosyl-valyl-alanyl-aspartic acid fluoromethyl ketone	24-34	caspase 1	Homo sapiens	4-13
30873702-12	2019	Therefore, we first reveal a novel mechanism that DHA promotes AIM2/caspase-1 inflammasome, which contributes to autophagy in HepG2215 cells.	artenimol	50-53	caspase 1	Homo sapiens	68-77
31178664-6	2019	Furthermore, high glucose increased the mRNA expression levels of NLRP3, ACS, and caspase-1.	Glucose	18-25	caspase 1	Homo sapiens	82-91
30782482-8	2019	Additional exposure of IFN-gamma-primed AAA-SMC to CD for 6-24 h, further augmented expression of AIM2, NLRP3, and Caspase-1 protein levels.	Cadmium	51-53	caspase 1	Homo sapiens	115-124
31019507-10	2019	Signaling involves nicotinic acetylcholine receptor subunits alpha7, alpha9, alpha10, and Src kinase activation and results in an inhibition of ATP-induced caspase-1 activation.	Adenosine Triphosphate	144-147	caspase 1	Homo sapiens	156-165
30963625-9	2019	Lidocaine dramatically reduced the protein expression of IL-1alpha, IL-6, THF-alpha, ELAVL1, NLRP3, caspase-1, and IL-1beta in adenovirus-infected thyroid follicular epithelial cells.	Lidocaine	0-9	caspase 1	Homo sapiens	100-109
29475852-13	2019	Consequently, treatment of hepatocytes with ethanol resulted in TXNIP overexpression, activating NLRP3 inflammasome and caspase-1-mediated pyroptosis.	Ethanol	44-51	caspase 1	Homo sapiens	120-129
30796460-2	2019	In this study, we hypothesized that pyroptosis, a caspase-1-dependent inflammatory programmed cell death mechanism, mediates Cd-induced nephrotoxicity.	Cadmium	125-127	caspase 1	Homo sapiens	50-59
30796460-4	2019	These effects were significantly abrogated by inhibiting caspase-1 activity with inhibitor YVAD or silencing NLRP3 with siRNA in vitro, suggesting that Cd induces caspase-1- and NLRP3-inflammasome-dependent pyroptosis.	YVAD	91-95	caspase 1	Homo sapiens	57-66
30796460-4	2019	These effects were significantly abrogated by inhibiting caspase-1 activity with inhibitor YVAD or silencing NLRP3 with siRNA in vitro, suggesting that Cd induces caspase-1- and NLRP3-inflammasome-dependent pyroptosis.	Cadmium	152-154	caspase 1	Homo sapiens	57-66
30796460-4	2019	These effects were significantly abrogated by inhibiting caspase-1 activity with inhibitor YVAD or silencing NLRP3 with siRNA in vitro, suggesting that Cd induces caspase-1- and NLRP3-inflammasome-dependent pyroptosis.	Cadmium	152-154	caspase 1	Homo sapiens	163-172
30471106-7	2019	A higher ROS level is the trigger for activating the caspase-1 and 3 cascade signal pathways.	Reactive Oxygen Species	9-12	caspase 1	Homo sapiens	53-68
30597604-5	2019	Mechanistically, the roles of melatonin in macrophages are related to several cellular signaling pathways, such as NF-kappaB, STATs, and NLRP3/caspase-1.	Melatonin	30-39	caspase 1	Homo sapiens	143-152
30962733-8	2019	Ginsenosides have also been shown to inhibit caspase-1 and to decrease the expression of IL-1beta and IL-18.	Ginsenosides	0-12	caspase 1	Homo sapiens	45-54
30668350-10	2019	Upon administration of caspase-1 inhibitors, anthocyanin-activated pyroptosis was suppressed and cell viability, migration, and invasion rates concomitantly enhanced.	Anthocyanins	45-56	caspase 1	Homo sapiens	23-32
30471106-0	2019	Caspase-1-dependent mechanism mediating the harmful impacts of the quorum-sensing molecule N-(3-oxo-dodecanoyl)-l-homoserine lactone on the intestinal cells.	N-(3-oxododecanoyl)homoserine lactone	91-132	caspase 1	Homo sapiens	0-9
30776150-7	2019	Nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing-3 (NLRP3) was shown to be involved in the IL-1beta response of liver macrophages to HIV-1 infection and NLRP3 blocking experiments in primary CD68+ liver macrophages confirmed the contribution of the NLRP3-caspase 1 inflammatory signaling pathway in the IL-1beta response.	Leucine	27-34	caspase 1	Homo sapiens	289-298
30930781-6	2019	The release of this cytokine was caspase-1- and caspase-4-dependent and correlated to higher levels of 8-OH-dG in COPD compared to non-smoker and smoker-derived PBMCs.	8-ohdg	103-110	caspase 1	Homo sapiens	33-42
30585659-7	2019	Using THP-1 cell in vitro model, we show that IL1beta and CASP-1 are regulated by dapsone independently of NFkappaB activity at transcriptional and post-transcriptional levels, respectively.	Dapsone	82-89	caspase 1	Homo sapiens	58-64
30628671-5	2019	The results of the present study demonstrated that caspase-1 activity, interleukin (IL)-1beta and IL-18 were upregulated in patients with RSA compared with healthy controls.	rabbit sperm membrane autoantigen	138-141	caspase 1	Homo sapiens	51-60
30906223-7	2019	The results showed that high glucose increased the expression of interleukin-18 (IL-18), interleukin-1beta (IL-1beta), NLRP3, caspase-1, and ASC, as well as the protein level of TLR4, nucleus p65, and CaSR.	Glucose	29-36	caspase 1	Homo sapiens	126-135
30611759-9	2019	In addition, western blot and real-time PCR analysis revealed that VPA modulated the protein expression of apoptosis repressor with caspase recruitment domain (ARC), caspase-1 and IL-1beta/IL-18.	Valproic Acid	67-70	caspase 1	Homo sapiens	166-175
30643918-5	2019	In L-02 cells, arsenite caused increases of GSDMD and cleaved caspase-1 levels and decreases of caspase-1 and miR-379-5p levels.	arsenite	15-23	caspase 1	Homo sapiens	62-71
30643918-5	2019	In L-02 cells, arsenite caused increases of GSDMD and cleaved caspase-1 levels and decreases of caspase-1 and miR-379-5p levels.	arsenite	15-23	caspase 1	Homo sapiens	96-105
30906223-9	2019	Meanwhile, NPS2143, BAY 11-7082, and INF39 could significantly abolish the high glucose-enhanced NLRP3, ASC, caspase-1, IL-18, and IL-1beta expression in vitro.	Glucose	80-87	caspase 1	Homo sapiens	109-118
30906223-10	2019	In addition, both NPS2143 and BAY 11-7082 attenuated high glucose-induced upregulation of NLRP3, ASC, caspase-1, IL-18, and IL-1beta expression.	3-(4-methylphenylsulfonyl)-2-propenenitrile	30-41	caspase 1	Homo sapiens	102-111
30906223-10	2019	In addition, both NPS2143 and BAY 11-7082 attenuated high glucose-induced upregulation of NLRP3, ASC, caspase-1, IL-18, and IL-1beta expression.	Glucose	58-65	caspase 1	Homo sapiens	102-111
30842373-5	2019	We observed the activation of caspase-1 and production of IL-1beta after exposure of THP-1 cells to 2,4-dinitrochlorobenzene (DNCB, sensitizer), octanoic acid (OA, non-sensitizer), and salicylic acid (SA, non-sensitizer), implying NLRP3 activation.	Dinitrochlorobenzene	100-124	caspase 1	Homo sapiens	30-39
30447168-6	2019	The disappearance of ethanol"s inhibitory effect on IL-1beta secretion after 48 h was not mediated by the upregulated production of IL-1beta, IL-1alpha, IL-6 or the inflammasome components NLRP3, apoptosis-associated speck-like protein containing a caspase recruitment domain, and caspase 1.	Ethanol	21-28	caspase 1	Homo sapiens	281-290
30612459-3	2019	Gouty arthritis is an inflammatory disease characterized by urate crystal-induced NLRP3 inflammasome activation with up-regulated caspase-1 protease and IL-1 beta in macrophages.	Uric Acid	60-65	caspase 1	Homo sapiens	130-139
30579413-13	2019	Bupivacaine did not alter MNF or THP-1 apoptosis compared with saline control, but reduced caspase-1 activity by 11% (95% CI: 5-17; n=10) in MNF from women in established labour.	Bupivacaine	0-11	caspase 1	Homo sapiens	91-100
30246263-8	2019	Furthermore, upregulation of H 2 S synthesis by treating the cells with NaHS also reduced the protein levels of TXNIP, NLRP3, ASC, caspase-1, and IL-1beta.	Hydrogen Sulfide	29-34	caspase 1	Homo sapiens	131-140
30246263-8	2019	Furthermore, upregulation of H 2 S synthesis by treating the cells with NaHS also reduced the protein levels of TXNIP, NLRP3, ASC, caspase-1, and IL-1beta.	sodium bisulfide	72-76	caspase 1	Homo sapiens	131-140
29601102-7	2019	Similar findings were observed in thioglycolate-elicited peritoneal macrophages, in which RvD2 remarkably reduced ASC oligomerization, inflammasome assembly, and caspase-1 activity.	Thioglycolates	34-47	caspase 1	Homo sapiens	162-171
30944281-4	2019	We tested two inhibitors [the caspase-1 inhibitor acetyl-Tyr-Val-Ala-Asp-chloromethylketone (Ac-YVAD-cmk; hereafter referred to as YVAD), which can mitigate the LPS-induced increases in CD54 expression, and polymyxin B (PMB), which suppresses the effect of LPS by binding to its lipid moiety (i.e., the toxic component of LPS)].	N-acetyl-tyrosyl-valyl-alanyl-aspartyl chloromethyl ketone	50-91	caspase 1	Homo sapiens	30-39
30944281-4	2019	We tested two inhibitors [the caspase-1 inhibitor acetyl-Tyr-Val-Ala-Asp-chloromethylketone (Ac-YVAD-cmk; hereafter referred to as YVAD), which can mitigate the LPS-induced increases in CD54 expression, and polymyxin B (PMB), which suppresses the effect of LPS by binding to its lipid moiety (i.e., the toxic component of LPS)].	ac-yvad	93-100	caspase 1	Homo sapiens	30-39
30944281-4	2019	We tested two inhibitors [the caspase-1 inhibitor acetyl-Tyr-Val-Ala-Asp-chloromethylketone (Ac-YVAD-cmk; hereafter referred to as YVAD), which can mitigate the LPS-induced increases in CD54 expression, and polymyxin B (PMB), which suppresses the effect of LPS by binding to its lipid moiety (i.e., the toxic component of LPS)].	YVAD	96-100	caspase 1	Homo sapiens	30-39
29974310-5	2019	Further mechanistic studies showed that the reduction of pro-inflammatory cytokines by triptolide was mediated by the upregulation of nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing protein 3 (NLRP3) and downregulation of caspase-1.	triptolide	87-97	caspase 1	Homo sapiens	261-270
30579413-4	2019	We examined whether bupivacaine (i) reduces caspase-1 activity and release of the anti-pyrogenic cytokine interleukin (IL)-1 receptor antagonist (IL-1ra), and (ii) is pro-inflammatory through mitochondrial injury/IL-1beta.	Bupivacaine	20-31	caspase 1	Homo sapiens	44-53
30842373-5	2019	We observed the activation of caspase-1 and production of IL-1beta after exposure of THP-1 cells to 2,4-dinitrochlorobenzene (DNCB, sensitizer), octanoic acid (OA, non-sensitizer), and salicylic acid (SA, non-sensitizer), implying NLRP3 activation.	Salicylic Acid	185-199	caspase 1	Homo sapiens	30-39
30842373-5	2019	We observed the activation of caspase-1 and production of IL-1beta after exposure of THP-1 cells to 2,4-dinitrochlorobenzene (DNCB, sensitizer), octanoic acid (OA, non-sensitizer), and salicylic acid (SA, non-sensitizer), implying NLRP3 activation.	Salicylic Acid	201-203	caspase 1	Homo sapiens	30-39
30842373-5	2019	We observed the activation of caspase-1 and production of IL-1beta after exposure of THP-1 cells to 2,4-dinitrochlorobenzene (DNCB, sensitizer), octanoic acid (OA, non-sensitizer), and salicylic acid (SA, non-sensitizer), implying NLRP3 activation.	Dinitrochlorobenzene	126-130	caspase 1	Homo sapiens	30-39
30842373-5	2019	We observed the activation of caspase-1 and production of IL-1beta after exposure of THP-1 cells to 2,4-dinitrochlorobenzene (DNCB, sensitizer), octanoic acid (OA, non-sensitizer), and salicylic acid (SA, non-sensitizer), implying NLRP3 activation.	octanoic acid	145-158	caspase 1	Homo sapiens	30-39
30247270-10	2018	Inhibition of mitochondria, adenosine triphosphate release, or P2 receptors blocked p38 mitogen-activated protein kinase and caspase-1 activation and interleukin-1beta secretion.	Adenosine Triphosphate	28-50	caspase 1	Homo sapiens	125-134
30393145-10	2019	Caspase-1 activity was increased in SiO2- and, on a lesser scale, in TM- exposed cells.	Silicon Dioxide	36-40	caspase 1	Homo sapiens	0-9
30393145-10	2019	Caspase-1 activity was increased in SiO2- and, on a lesser scale, in TM- exposed cells.	Thulium	69-71	caspase 1	Homo sapiens	0-9
30544610-7	2018	Meanwhile, cinnamaldehyde and 2-methoxy cinnamaldehyde prevented the ATP-induced reduction of cytosolic pro-caspase-1 and increase of secreted caspase-1.	cinnamaldehyde	11-25	caspase 1	Homo sapiens	108-117
30544610-7	2018	Meanwhile, cinnamaldehyde and 2-methoxy cinnamaldehyde prevented the ATP-induced reduction of cytosolic pro-caspase-1 and increase of secreted caspase-1.	cinnamaldehyde	11-25	caspase 1	Homo sapiens	143-152
30544610-7	2018	Meanwhile, cinnamaldehyde and 2-methoxy cinnamaldehyde prevented the ATP-induced reduction of cytosolic pro-caspase-1 and increase of secreted caspase-1.	2-methoxycinnamaldehyde	30-54	caspase 1	Homo sapiens	108-117
30378427-4	2018	Using human umbilical vein endothelial cells (HUVEC), we discovered that TCBQ activates caspase 1/4/5 and cleaves gasdermin D (GSDMD) into N-terminal and C-terminal cleavage products.	tetrachlorobenzoquinone	73-77	caspase 1	Homo sapiens	88-101
30544610-7	2018	Meanwhile, cinnamaldehyde and 2-methoxy cinnamaldehyde prevented the ATP-induced reduction of cytosolic pro-caspase-1 and increase of secreted caspase-1.	2-methoxycinnamaldehyde	30-54	caspase 1	Homo sapiens	143-152
30544610-7	2018	Meanwhile, cinnamaldehyde and 2-methoxy cinnamaldehyde prevented the ATP-induced reduction of cytosolic pro-caspase-1 and increase of secreted caspase-1.	Adenosine Triphosphate	69-72	caspase 1	Homo sapiens	108-117
30544610-7	2018	Meanwhile, cinnamaldehyde and 2-methoxy cinnamaldehyde prevented the ATP-induced reduction of cytosolic pro-caspase-1 and increase of secreted caspase-1.	Adenosine Triphosphate	69-72	caspase 1	Homo sapiens	143-152
30343279-8	2018	The intracellular mechanisms of cytotoxicity of As2O3 plus resveratrol were revealed as ROS accumulation and relative decrease of MMP, leading to activation of caspase-3 and -9, but not of caspase-1, -7 and-8.	Arsenic Trioxide	48-53	caspase 1	Homo sapiens	189-208
29034737-4	2018	In PMACI-stimulated cells, treatment with vanillic acid also dramatically inhibited activities of caspase-1 and nuclear factor-kB (p65).	pmaci	3-8	caspase 1	Homo sapiens	98-129
29034737-4	2018	In PMACI-stimulated cells, treatment with vanillic acid also dramatically inhibited activities of caspase-1 and nuclear factor-kB (p65).	Vanillic Acid	42-55	caspase 1	Homo sapiens	98-129
30323145-9	2018	BAPTA-AM pretreatment abolished the H2O2-induced activation of NLRP3 inflammasomes, caspase-1 expression, interleukin-1beta expression and apoptosis in SHSY5Y cells, and had no effect in cells with downregulated STAT3 expression by RNAi.	1,2-bis(2-aminophenoxy)ethane N,N,N',N'-tetraacetic acid acetoxymethyl ester	0-8	caspase 1	Homo sapiens	84-93
30323145-9	2018	BAPTA-AM pretreatment abolished the H2O2-induced activation of NLRP3 inflammasomes, caspase-1 expression, interleukin-1beta expression and apoptosis in SHSY5Y cells, and had no effect in cells with downregulated STAT3 expression by RNAi.	Hydrogen Peroxide	36-40	caspase 1	Homo sapiens	84-93
30205151-4	2018	In addition, exposure to acrolein resulted in NLRP3 inflammasome activation as evidenced by cleavage of caspase-1 and downstream mature interleukin (IL)-1beta and IL-18 secretion.	Acrolein	25-33	caspase 1	Homo sapiens	104-113
30555323-11	2018	In LPS-primed THP-1 cells stimulated by nigericin (a model to study the NLRP3 inflammasome), rifaximin reduced IL-1beta production in a concentration-dependent fashion, this effect being associated with inhibition of the up-stream caspase-1 activation.	Rifaximin	93-102	caspase 1	Homo sapiens	231-240
30320338-10	2018	Although NLR family pyrin domain containing 3 (NLRP3)-inflammasome-caspase-1 activation is required for the maturation of IL-1beta, and DHMEQ reduced the NLRP3 mRNA expression and caspase-1 activity; a caspase-1 inhibitor did not influence the A50-induced IL-1beta production.	dehydroxymethylepoxyquinomicin	136-141	caspase 1	Homo sapiens	180-189
30320338-10	2018	Although NLR family pyrin domain containing 3 (NLRP3)-inflammasome-caspase-1 activation is required for the maturation of IL-1beta, and DHMEQ reduced the NLRP3 mRNA expression and caspase-1 activity; a caspase-1 inhibitor did not influence the A50-induced IL-1beta production.	dehydroxymethylepoxyquinomicin	136-141	caspase 1	Homo sapiens	180-189
30485804-3	2018	Furthermore, BAX/BAK signaling induces a parallel pathway to NLRP3 inflammasome-mediated caspase-1-dependent IL-1beta maturation that requires potassium efflux.	Potassium	143-152	caspase 1	Homo sapiens	89-98
30463629-9	2018	Finally, we found that ATP activates caspase-1 and inhibits phagocytosis, and these effects are blocked by both P2X7R and Cl- channel antagonists.	Adenosine Triphosphate	23-26	caspase 1	Homo sapiens	37-46
30226596-8	2018	The MDA-MB-231 cells exhibited inflammasome activation, as measured by caspase-1 activity and interleukin (IL)-1beta secretion following treatment with TNF-alpha and ATP; these effects were enhanced in the RT-R-MDA-MB-231 cells.	Adenosine Triphosphate	166-169	caspase 1	Homo sapiens	71-80
30138619-9	2018	Treatment of cultured PBMCs with 10 ng of lipopolysaccharide induced NLRP3, caspase-1, ASC, IL-1beta, IL-17A, and IL-23 expression, which was marked suppressed by treatment with ascorbic acid.	Ascorbic Acid	178-191	caspase 1	Homo sapiens	76-85
30226596-9	2018	However, the increased caspase-1 activities and IL-1beta secretion levels induced in response to treatment with TNF-alpha or ATP were significantly reduced by P2Y2R knockdown or the presence of apyrase in both the MDA-MB-231 and RT-R-MDA-MB-231 cells, suggesting the involvement of ATP-activated P2Y2R in inflammasome activation.	Adenosine Triphosphate	125-128	caspase 1	Homo sapiens	23-32
30226596-10	2018	In addition, TNF-alpha and ATP increased the invasive and colony-forming ability of the MDA-MB-231 and RT-R-MDA-MB-231 cells, and these effects were caspase-1-dependent.	Adenosine Triphosphate	27-30	caspase 1	Homo sapiens	149-158
30341337-5	2018	We show that lysophosphatidylcholine (LPC) released following activation of caspase-1 in Salmonella - infected cells and abundant in plasma amplifies production of Sips from this pathogen and promotes its cellular invasion.	Lysophosphatidylcholines	13-36	caspase 1	Homo sapiens	76-85
30076630-5	2018	In addition, PF significantly suppressed PMACI-induced histamine release and caspase-1 activation in HMC-1 cells.	peoniflorin	13-15	caspase 1	Homo sapiens	77-86
30341337-5	2018	We show that lysophosphatidylcholine (LPC) released following activation of caspase-1 in Salmonella - infected cells and abundant in plasma amplifies production of Sips from this pathogen and promotes its cellular invasion.	Lysophosphatidylcholines	38-41	caspase 1	Homo sapiens	76-85
30194878-9	2018	RESULTS: Compared to excess glucose alone, combination excess glucose and low-dose aPL (a) further augmented trophoblast inflammatory IL-1beta, inflammasome-associated uric acid and caspase-1, and pro-angiogenic PlGF; (b) dampened trophoblast inflammatory IL-8, anti-angiogenic sEndoglin, and sFlt-1; and (c) further reduced trophoblast migration.	Glucose	62-69	caspase 1	Homo sapiens	182-191
30270565-2	2018	Our results show that the mRNA levels of IL-1beta, IL-18, NLRP3, ASC, and caspase-1 in the DSS+ZEA-treated group are lower than those in either the DSS or ZEA group, and the protein expression trends are similar.	Dextran Sulfate	91-94	caspase 1	Homo sapiens	74-83
30270565-2	2018	Our results show that the mRNA levels of IL-1beta, IL-18, NLRP3, ASC, and caspase-1 in the DSS+ZEA-treated group are lower than those in either the DSS or ZEA group, and the protein expression trends are similar.	Zearalenone	95-98	caspase 1	Homo sapiens	74-83
30527115-11	2018	Protein expression of caspase-1 was higher in cultures of 100 muM H2O2 compared to controls.	Hydrogen Peroxide	66-70	caspase 1	Homo sapiens	22-31
30006682-12	2018	Our results indicate that CGA exhibits a protective potential via antioxidant and apoptosis caspases and calpains dependent against AMPA-mediated excitotoxicity, and these finding indicate that CGA is able to be a good candidate for preventive approach for neurodegenerative disorders associated with loss and damage in oligodendrocytes and AMPA-mediated excitotoxicity.	alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid	132-136	caspase 1	Homo sapiens	92-100
30054450-7	2018	Accordingly, acute cholesterol depletion in the ER membranes by statins abrogated casp-1 activation and IL-1beta secretion and ablated NLRP3 inflammasome assembly.	Cholesterol	19-30	caspase 1	Homo sapiens	82-88
30527115-13	2018	This concentration reduced protein expression of caspase-1 compared to culture with only H2O2 and control cultures.	Hydrogen Peroxide	89-93	caspase 1	Homo sapiens	49-58
30249062-9	2018	Results showed that treating with methotrexate could alleviate the inflammatory condition, downregulate the activation of NF-kappaB and NLRP3/Caspase-1 inflammatory pathways and reduce the level of related cytokines.	Methotrexate	34-46	caspase 1	Homo sapiens	142-151
30249062-10	2018	Docking interaction between methotrexate and caspase-1 was visualized as six H-bonds indicating a potential inhibitory effect.	Methotrexate	28-40	caspase 1	Homo sapiens	45-54
30249062-12	2018	These findings indicated that methotrexate could inhibit the onset of inflammation in joint tissue by suppressing the activation of NF-kappaB and NLRP3/Caspase-1 pathways and regulating the inflammation related metabolic networks.	Methotrexate	30-42	caspase 1	Homo sapiens	152-161
30100068-4	2018	We report that RILP is directly cleaved by caspase-1 and we have identified a novel caspase-1 recognition site at aspartic acid 75 within the RILP sequence.	Aspartic Acid	114-127	caspase 1	Homo sapiens	43-52
30100068-4	2018	We report that RILP is directly cleaved by caspase-1 and we have identified a novel caspase-1 recognition site at aspartic acid 75 within the RILP sequence.	Aspartic Acid	114-127	caspase 1	Homo sapiens	84-93
30100068-5	2018	Alanine substitution at D75 blocks caspase-1-mediated RILP cleavage.	Alanine	0-7	caspase 1	Homo sapiens	35-44
29803543-10	2018	Interestingly, both NF-kappaB (quinazoline) and caspase-1 (VX-765) inhibitors suppressed the IL-32-related upregulation of pro-inflammatory cytokines (TNFalpha and IL-6).	belnacasan	59-65	caspase 1	Homo sapiens	48-57
30166062-11	2018	In conclusion, HMGB1, regulated by the enzymatic activity of caspase-1, is a crucial mediator in uric acid-induced inflammation.	Uric Acid	97-106	caspase 1	Homo sapiens	61-70
30185776-7	2018	Finally, SARS 3a activates caspase-1 either directly or via an enhanced potassium efflux, which triggers NLRP3 inflammasome assembly.	Potassium	72-81	caspase 1	Homo sapiens	27-36
29857000-9	2018	These results suggest that treatment with Quercetin inhibits the poly (dA:dT)-induced secretion of IL-18 via down-regulation of the expressions of AIM2 and pro-caspase-1 by inhibiting the JAK2/STAT1 pathway in IFN-gamma-primed keratinocytes.	Quercetin	42-51	caspase 1	Homo sapiens	160-169
29857000-9	2018	These results suggest that treatment with Quercetin inhibits the poly (dA:dT)-induced secretion of IL-18 via down-regulation of the expressions of AIM2 and pro-caspase-1 by inhibiting the JAK2/STAT1 pathway in IFN-gamma-primed keratinocytes.	poly	65-69	caspase 1	Homo sapiens	160-169
29857000-9	2018	These results suggest that treatment with Quercetin inhibits the poly (dA:dT)-induced secretion of IL-18 via down-regulation of the expressions of AIM2 and pro-caspase-1 by inhibiting the JAK2/STAT1 pathway in IFN-gamma-primed keratinocytes.	amsonic acid	71-73	caspase 1	Homo sapiens	160-169
29857000-9	2018	These results suggest that treatment with Quercetin inhibits the poly (dA:dT)-induced secretion of IL-18 via down-regulation of the expressions of AIM2 and pro-caspase-1 by inhibiting the JAK2/STAT1 pathway in IFN-gamma-primed keratinocytes.	Thymidine	74-76	caspase 1	Homo sapiens	160-169
30126633-4	2018	We found that the BMDMs (bone marrow-derived macrophages cells) pre-treated with tannic acid blocked caspase-1 cleavage and inhibited IL-1beta secretion in a NLRP3-dependent manner, and suppressed NF-kappaB signaling activation by inhibiting NF-kappaB/P65 nuclear localization, suggesting that tannic acid inhibited NLRP3 inflammasome activation.	Tannins	81-92	caspase 1	Homo sapiens	101-110
29906464-8	2018	NLRP3 siRNA or inhibitors of NF-kappaB, NLRP3 inflammasome oligomerization, or caspase-1 nearly completely inhibited ATP- and S100A12-mediated MUC5AC production.	Adenosine Triphosphate	117-120	caspase 1	Homo sapiens	79-88
29857000-0	2018	Quercetin inhibits the poly(dA:dT)-induced secretion of IL-18 via down-regulation of the expressions of AIM2 and pro-caspase-1 by inhibiting the JAK2/STAT1 pathway in IFN-gamma-primed human keratinocytes.	Quercetin	0-9	caspase 1	Homo sapiens	117-126
29857000-0	2018	Quercetin inhibits the poly(dA:dT)-induced secretion of IL-18 via down-regulation of the expressions of AIM2 and pro-caspase-1 by inhibiting the JAK2/STAT1 pathway in IFN-gamma-primed human keratinocytes.	poly	23-27	caspase 1	Homo sapiens	117-126
29857000-0	2018	Quercetin inhibits the poly(dA:dT)-induced secretion of IL-18 via down-regulation of the expressions of AIM2 and pro-caspase-1 by inhibiting the JAK2/STAT1 pathway in IFN-gamma-primed human keratinocytes.	amsonic acid	28-30	caspase 1	Homo sapiens	117-126
29857000-0	2018	Quercetin inhibits the poly(dA:dT)-induced secretion of IL-18 via down-regulation of the expressions of AIM2 and pro-caspase-1 by inhibiting the JAK2/STAT1 pathway in IFN-gamma-primed human keratinocytes.	Thymidine	31-33	caspase 1	Homo sapiens	117-126
29592872-0	2018	The long non-coding RNA SNHG5 regulates gefitinib resistance in lung adenocarcinoma cells by targetting miR-377/CASP1 axis.	Gefitinib	40-49	caspase 1	Homo sapiens	112-117
29592872-9	2018	In vitro functional assay showed that knockdown of CASP1 in SNHG5-overexpressed PC9GR cells abolished their gefitinib resistance.	Gefitinib	108-117	caspase 1	Homo sapiens	51-56
29592872-10	2018	Overall, the present study demonstrated, for the first time, that the SNHG5/miR-377/CASP1 axis functions as an important role in LAD cells gefitinib resistance and potentially contributes to the improvement of LAD diagnosis and therapy.	Gefitinib	139-148	caspase 1	Homo sapiens	84-89
29856968-4	2018	In the in vitro model, the ABT-737 treatment diminished the levels of several inflammatory cytokines in this case vascular endothelial growth factor (VEGF), thymic stromal lymphopoietin (TSLP), interleukin (IL)-1beta, IL-6, and tumor necrosis factor-alpha (TNF-alpha) by inhibiting caspase-1 and NF-kappaB activation in an activated human mast cell line, here HMC-1 cells.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	27-30	caspase 1	Homo sapiens	282-291
30157949-9	2018	Tofacitinib, which inhibits GM-CSF-induced Janus kinase 2 (Jak2)-mediated signal transduction, completely abrogated GM-CSF-induced IL-1beta and caspase-1 (p20) secretion from neutrophils.	tofacitinib	0-11	caspase 1	Homo sapiens	144-153
29614437-0	2018	Structure-based design, synthesis and evaluation of 2,4-diaminopyrimidine derivatives as novel caspase-1 inhibitors.	2,4-diaminopyrimidine	52-73	caspase 1	Homo sapiens	95-104
30168623-2	2018	The amount of active caspase-1 was determined over 6 h by detecting Ac-YVAD-AMC fluorescence in human neutrophils incubated with S. epidermidis isolates from PJIs (ST2) or normal flora.	Ac-Tyr-Val-Ala-Asp-AMC	68-79	caspase 1	Homo sapiens	21-30
30168624-7	2018	Modified LDL co-stimulated with ATCC33277 exhibited regulatory effects on caspase 1 activity, IL-1beta release and CD36 expression in THP1 cells, whereas W50 induced more modest responses in THP1 cells.	atcc33277	32-41	caspase 1	Homo sapiens	74-83
29614437-3	2018	Here we have reported structure-based design, synthesis and biological evaluation of 2,4-diaminopyrimidine derivatives (6a-6w) as potential caspase-1 inhibitors.	2,4-diaminopyrimidine	85-106	caspase 1	Homo sapiens	140-149
29957081-9	2018	RESULTS: ABT-737 significantly decreased thymic stromal lymphopoietin (TSLP) secretion and caspase-1 activity in activated HaCaT cells.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	9-12	caspase 1	Homo sapiens	91-100
29365280-6	2018	MPs pretreated with caspase 1 inhibitor Y-VAD or pan-caspase inhibitor Z-VAD do not contain cleaved GSDMD.	y-vad	40-45	caspase 1	Homo sapiens	20-29
29345311-7	2018	Exposure to 2 muM cinacalcet elevated mRNA expression of NLRP3, CASP-1, and IL-1beta, as well as an increase in pro-IL-1beta protein.	Cinacalcet	18-28	caspase 1	Homo sapiens	64-70
29752727-6	2018	Caspase-1 GCF levels were significantly higher in pSS group than RA group (p = 0.032).	pss	50-53	caspase 1	Homo sapiens	0-9
30011850-6	2018	PMA plus A23187 stimulation up-regulated caspase-1 activity in HMC-1 cells; however, this up-regulated caspase-1 activity was down-regulated by LA.	Calcimycin	9-15	caspase 1	Homo sapiens	41-50
29941706-0	2018	Mycophenolic Acid Synergizing with Lipopolysaccharide to Induce Interleukin-1beta Release via Activation of Caspase-1.	Mycophenolic Acid	0-17	caspase 1	Homo sapiens	108-117
29941706-9	2018	Ac-YVAD-cmk blocked the activation of caspase-1 and subsequently attenuated IL-1beta secretion (181.00 +- 45.24 pg/ml in LPS + MPA + YVAD group vs. 588.00 +- 41.99 pg/ml in LPS + MPA group, P = 0.014).	ac-yvad	0-7	caspase 1	Homo sapiens	38-47
29941706-9	2018	Ac-YVAD-cmk blocked the activation of caspase-1 and subsequently attenuated IL-1beta secretion (181.00 +- 45.24 pg/ml in LPS + MPA + YVAD group vs. 588.00 +- 41.99 pg/ml in LPS + MPA group, P = 0.014).	YVAD	3-7	caspase 1	Homo sapiens	38-47
29941706-11	2018	These findings suggested that patients immunosuppressed with mycophenolate mofetil may have overly activated caspase-1 during infection, which might contribute to a more sensitive host defense response to invading germs.	Mycophenolic Acid	61-82	caspase 1	Homo sapiens	109-118
29956729-10	2018	When HLECs were cotreated with a caspase-1 inhibitor and 100 microM H2O2, caspase-1 and IL-1beta expression were decreased compared with the 100 microM H2O2-only group.	Hydrogen Peroxide	68-72	caspase 1	Homo sapiens	33-42
29956729-10	2018	When HLECs were cotreated with a caspase-1 inhibitor and 100 microM H2O2, caspase-1 and IL-1beta expression were decreased compared with the 100 microM H2O2-only group.	Hydrogen Peroxide	68-72	caspase 1	Homo sapiens	74-83
29956729-10	2018	When HLECs were cotreated with a caspase-1 inhibitor and 100 microM H2O2, caspase-1 and IL-1beta expression were decreased compared with the 100 microM H2O2-only group.	Hydrogen Peroxide	152-156	caspase 1	Homo sapiens	33-42
29956729-10	2018	When HLECs were cotreated with a caspase-1 inhibitor and 100 microM H2O2, caspase-1 and IL-1beta expression were decreased compared with the 100 microM H2O2-only group.	Hydrogen Peroxide	152-156	caspase 1	Homo sapiens	74-83
30123073-3	2018	Our study clarified that alcohol accumulation could aggravate the progress of esophagitis by inducing pyroptosis; however, Ac-YVAD-CMK, an inhibitor of caspase-1, could effectively suppress the expression of IL-1beta and IL-18 both in vivo and in vitro, reducing the inflammatory response, which is promised to be an agent to inhibit the progression of esophagitis.	Alcohols	25-32	caspase 1	Homo sapiens	152-161
29709093-9	2018	Magnesium sulfate delivered 1- hour post-LPS inhibited LPS-induced caspase-1 activity, and inhibited the augmented IL-1beta response triggered by combination viral dsRNA and LPS.	Magnesium Sulfate	0-17	caspase 1	Homo sapiens	67-76
29891674-6	2018	A GSDMD-derived inhibitor, N-acetyl-Phe-Leu-Thr-Asp-chloromethylketone (Ac-FLTD-CMK), inhibits GSDMD cleavage by caspases-1, -4, -5, and -11 in vitro, suppresses pyroptosis downstream of both canonical and noncanonical inflammasomes, as well as reduces IL-1beta release following activation of the NLRP3 inflammasome in macrophages.	n-acetyl-phe-leu-thr-asp-chloromethylketone	27-70	caspase 1	Homo sapiens	113-140
29709093-10	2018	CONCLUSION: Magnesium sulfate differentially modulates LPS-induced FM inflammation in a time-dependent manner, in part through its modulation of caspase-1 activity.	Magnesium Sulfate	12-29	caspase 1	Homo sapiens	145-154
29895691-5	2018	We observed inflammasome activation and pyroptosis in human microglia and ODCs in vitro after exposure to inflammatory stimuli and demonstrate caspase-1 inhibition by the small-molecule inhibitor VX-765 in both cell types.	belnacasan	196-202	caspase 1	Homo sapiens	143-152
29891674-6	2018	A GSDMD-derived inhibitor, N-acetyl-Phe-Leu-Thr-Asp-chloromethylketone (Ac-FLTD-CMK), inhibits GSDMD cleavage by caspases-1, -4, -5, and -11 in vitro, suppresses pyroptosis downstream of both canonical and noncanonical inflammasomes, as well as reduces IL-1beta release following activation of the NLRP3 inflammasome in macrophages.	ac-fltd	72-79	caspase 1	Homo sapiens	113-140
29891674-8	2018	Crystal structure of caspase-1 in complex with Ac-FLTD-CMK reveals extensive enzyme-inhibitor interactions involving both hydrogen bonds and hydrophobic contacts.	Hydrogen	122-130	caspase 1	Homo sapiens	21-30
29940605-10	2018	Moreover, BK-induced up-regulation of p-p38, NF-kappaB p-p65, NLRP3, ASC, caspase-1, and COX-2 was dose-dependently down-regulated by propofol treatment.	Propofol	134-142	caspase 1	Homo sapiens	74-83
29486619-12	2018	Kaempferol increased the infiltration of peritoneal CD11c+MHCII+ dendritic cells but failed to enhance LPS activated IL-1beta by peritoneal macrophages and suppressed caspase-1 protein expression as compared to that in ovalbumin immunized mice.	kaempferol	0-10	caspase 1	Homo sapiens	167-176
29983861-8	2018	We demonstrate that DAB and VEM activated the NLRC4/Caspase-1 inflammasome.	dabrafenib	20-23	caspase 1	Homo sapiens	52-61
29219210-6	2018	These effects are mediated through CtBP, an NADH-sensitive transcriptional co-repressor; through effects on NLRP3 inflammasome assembly and caspase-1 activation; through formation of advanced glycation end-products; and by less well-defined mechanisms.	ctbp	35-39	caspase 1	Homo sapiens	140-149
29947341-4	2018	METHODS: In this study, N9 microglial cells were treated with hemin, and subsequently used to detect the production of caspase-1 p10 and NLRP3 inflammasome assembly.	Hemin	62-67	caspase 1	Homo sapiens	119-128
29724886-9	2018	We discovered that the expression of the factors was significantly increased in pterygium and that caspase-1-dependent pyroptosis presents in both H2O2-treated HPFs and HConECs during which the expression of these factors was significantly elevated and the elevation of downstream factors IL-18 and IL-1beta was restrained after caspase-1 inhibition.	Hydrogen Peroxide	147-151	caspase 1	Homo sapiens	99-108
29492824-9	2018	Meth treatment potentiated aggregation of inflammasome adaptor apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC), induced activation of the IL-1beta converting enzyme caspase-1 and produced lysosomal and mitochondrial impairment.	Methamphetamine	0-4	caspase 1	Homo sapiens	203-212
29636364-5	2018	In stromal cells of endometriotic lesions, bufalin treatment increased the levels of pyroptosis markers (caspase 1 and the active form of interleukin 1beta) and reduced proliferation.	bufalin	43-50	caspase 1	Homo sapiens	105-114
28437591-9	2018	Interestingly, Fluorofenidone inhibited the activation of NLRP3 inflammasome, downregulated Caspase-1 levels and thereby decreased the cleavage of pro-IL-1beta into IL-1beta in vivo and in vitro.	5-methyl-1-(3-fluorophenyl)-2-(1H)-pyridone	15-29	caspase 1	Homo sapiens	92-101
28437591-10	2018	Fluorofenidone treatment distinctively weakened the interaction between NLRP3 and ASC, as well as ASC and pro-Caspase-1 in vivo.	5-methyl-1-(3-fluorophenyl)-2-(1H)-pyridone	0-14	caspase 1	Homo sapiens	110-119
28437591-11	2018	However, Fluorofenidone treatment only significantly weakened the interaction between ASC and pro-Caspase-1 in co-transfected 293 T cells.	5-methyl-1-(3-fluorophenyl)-2-(1H)-pyridone	9-23	caspase 1	Homo sapiens	98-107
29724886-9	2018	We discovered that the expression of the factors was significantly increased in pterygium and that caspase-1-dependent pyroptosis presents in both H2O2-treated HPFs and HConECs during which the expression of these factors was significantly elevated and the elevation of downstream factors IL-18 and IL-1beta was restrained after caspase-1 inhibition.	Hydrogen Peroxide	147-151	caspase 1	Homo sapiens	329-338
29724886-10	2018	alpha-SMA increase and E-cadherin down-regulation were detected in H2O2-treated HPFs and the changes were reversed by caspase-1 inhibition.	Hydrogen Peroxide	67-71	caspase 1	Homo sapiens	118-127
29648825-3	2018	This report describes the discovery of uracil 20, a potent (38 nM in THP1 cells assay) caspase-1 inhibitor for the topical treatment of inflammatory acne.	Uracil	39-45	caspase 1	Homo sapiens	87-96
29648825-4	2018	The uracil series was designed according to a published caspase-1 pharmacophore model involving a reactive warhead in P1 for covalent reversible inhibition and an aryl moiety in P4 for selectivity against the apoptotic caspases.	Uracil	4-10	caspase 1	Homo sapiens	56-65
29743866-0	2018	Dexmedetomidine inhibits inflammation in microglia cells under stimulation of LPS and ATP by c-Fos/NLRP3/caspase-1 cascades.	Dexmedetomidine	0-15	caspase 1	Homo sapiens	105-114
29313961-7	2018	Sustained monocyte activation, induced by fungal beta-glucan particles upon actin cytoskeleton disruption, relies on Dectin-1 and results in the classical caspase-1 inflammasome formation through NLRP3, generation of an oxidative burst, NF-kappaB activation, and increased inflammatory cytokine release.	beta-Glucans	49-60	caspase 1	Homo sapiens	155-164
29725399-3	2018	Additionally, the human breast cancer MDA-MB-231 cell line was treated with the Caspase-1 small molecule inhibitor Ac-YVAD-CMK, following which the changes to Caspase-1 protein expression were detected via western blotting.	ac-yvad	115-122	caspase 1	Homo sapiens	80-89
29725399-3	2018	Additionally, the human breast cancer MDA-MB-231 cell line was treated with the Caspase-1 small molecule inhibitor Ac-YVAD-CMK, following which the changes to Caspase-1 protein expression were detected via western blotting.	ac-yvad	115-122	caspase 1	Homo sapiens	159-168
29725399-6	2018	Treatment with the Ac-YVAD-CMK markedly decreased the protein expression of Caspase-1 in MDA-MB-231 cells, and the difference was statistically significant (P&lt;0.05).	ac-yvad	19-26	caspase 1	Homo sapiens	76-85
29432801-8	2018	The inhibition assay showed that glybenclamide (a K+ efflux inhibitor that blocks NLRP3 inflammasome activation) and N-benzyloxycarbony-Val-Ala-Asp (O-methyl)-fluoromethylketone (Z-VAD-FMK; a caspase-1 inhibitor) and NLRP3 depletion with siRNAs reduced the levels of IL-1beta and IL-18 release.	n-benzyloxycarbony	117-135	caspase 1	Homo sapiens	192-201
29432801-8	2018	The inhibition assay showed that glybenclamide (a K+ efflux inhibitor that blocks NLRP3 inflammasome activation) and N-benzyloxycarbony-Val-Ala-Asp (O-methyl)-fluoromethylketone (Z-VAD-FMK; a caspase-1 inhibitor) and NLRP3 depletion with siRNAs reduced the levels of IL-1beta and IL-18 release.	Alanine	140-143	caspase 1	Homo sapiens	192-201
29432801-8	2018	The inhibition assay showed that glybenclamide (a K+ efflux inhibitor that blocks NLRP3 inflammasome activation) and N-benzyloxycarbony-Val-Ala-Asp (O-methyl)-fluoromethylketone (Z-VAD-FMK; a caspase-1 inhibitor) and NLRP3 depletion with siRNAs reduced the levels of IL-1beta and IL-18 release.	fluoromethylketone	159-177	caspase 1	Homo sapiens	192-201
29432801-10	2018	This study suggests that L. interrogans infection leads to reactive oxygen species (ROS)- and cathepsin B-dependent NLRP3 inflammasome activation, which subsequently mediates caspase-1 activation and IL-1beta and IL-18 release.	Reactive Oxygen Species	59-82	caspase 1	Homo sapiens	175-184
29432801-10	2018	This study suggests that L. interrogans infection leads to reactive oxygen species (ROS)- and cathepsin B-dependent NLRP3 inflammasome activation, which subsequently mediates caspase-1 activation and IL-1beta and IL-18 release.	Reactive Oxygen Species	84-87	caspase 1	Homo sapiens	175-184
29549805-1	2018	Caspase-1 is a key endoprotease responsible for the post-translational processing of pro-inflammatory cytokines IL-1beta, 18 &amp; 33.	Adenosine Monophosphate	126-129	caspase 1	Homo sapiens	0-9
29323474-0	2018	Caspase-1 Specific Light-Up Probe with Aggregation-Induced Emission Characteristics for Inhibitor Screening of Coumarin-Originated Natural Products.	coumarin	111-119	caspase 1	Homo sapiens	0-9
29323474-3	2018	Coumarin-originated natural products have an anti-inflammation function, but their direct inhibition effect to caspase-1 remains unexplored.	coumarin	0-8	caspase 1	Homo sapiens	111-120
29432801-8	2018	The inhibition assay showed that glybenclamide (a K+ efflux inhibitor that blocks NLRP3 inflammasome activation) and N-benzyloxycarbony-Val-Ala-Asp (O-methyl)-fluoromethylketone (Z-VAD-FMK; a caspase-1 inhibitor) and NLRP3 depletion with siRNAs reduced the levels of IL-1beta and IL-18 release.	Glyburide	33-46	caspase 1	Homo sapiens	192-201
29446486-0	2018	Interleukin-17A participates in podocyte injury by inducing IL-1beta secretion through ROS-NLRP3 inflammasome-caspase-1 pathway.	ros	87-90	caspase 1	Homo sapiens	110-119
29743866-10	2018	The present study revealed that Dex inhibits inflammation in microglia cells under stimulation of LPS and ATP by c-Fos/NLRP3/caspase-1 cascades, which adds new understanding of the anti-inflammatory mechanism of Dex.	Dexmedetomidine	32-35	caspase 1	Homo sapiens	125-134
29743866-10	2018	The present study revealed that Dex inhibits inflammation in microglia cells under stimulation of LPS and ATP by c-Fos/NLRP3/caspase-1 cascades, which adds new understanding of the anti-inflammatory mechanism of Dex.	Adenosine Triphosphate	106-109	caspase 1	Homo sapiens	125-134
29743866-10	2018	The present study revealed that Dex inhibits inflammation in microglia cells under stimulation of LPS and ATP by c-Fos/NLRP3/caspase-1 cascades, which adds new understanding of the anti-inflammatory mechanism of Dex.	Dexmedetomidine	212-215	caspase 1	Homo sapiens	125-134
29743866-0	2018	Dexmedetomidine inhibits inflammation in microglia cells under stimulation of LPS and ATP by c-Fos/NLRP3/caspase-1 cascades.	Adenosine Triphosphate	86-89	caspase 1	Homo sapiens	105-114
29743866-5	2018	Data from ELISA and Western blot assays showed that Dex abrogated the promoting effects of LPS/ATP on the release of pro-inflammatory cytokines including IL-1beta and IL-18 in the cell medium and the expression of NLRP3 and its downstream target caspase-1 in HMC3 cells.	Dexmedetomidine	52-55	caspase 1	Homo sapiens	246-255
29743866-5	2018	Data from ELISA and Western blot assays showed that Dex abrogated the promoting effects of LPS/ATP on the release of pro-inflammatory cytokines including IL-1beta and IL-18 in the cell medium and the expression of NLRP3 and its downstream target caspase-1 in HMC3 cells.	Adenosine Triphosphate	95-98	caspase 1	Homo sapiens	246-255
29545514-5	2018	RESULTS The results of SP showed that NLRP3 and caspase-1 were mainly expressed in the cytoplasm of epithelial cells, mesenchymal cells, and trophoblast cells in fetal membranes, and the cytoplasm of placental syncytiotrophoblasts and vascular endothelial cells in placental tissues.	sp	23-25	caspase 1	Homo sapiens	48-57
29193391-4	2018	In the present study, palmitic acid (PA) treatment led to pyroptosis in human umbilical vein endothelial cells (HUVECs), as evidenced by caspase-1 activation, LDH release, and propidium iodide-positive staining; enhanced the maturation and release of proinflammatory cytokine IL-1beta and activation of the NLRP3 inflammasome; and markedly increased intracellular reactive oxygen species (ROS) and mitochondrial ROS (mtROS) levels.	Palmitic Acid	22-35	caspase 1	Homo sapiens	137-146
29193391-4	2018	In the present study, palmitic acid (PA) treatment led to pyroptosis in human umbilical vein endothelial cells (HUVECs), as evidenced by caspase-1 activation, LDH release, and propidium iodide-positive staining; enhanced the maturation and release of proinflammatory cytokine IL-1beta and activation of the NLRP3 inflammasome; and markedly increased intracellular reactive oxygen species (ROS) and mitochondrial ROS (mtROS) levels.	Palmitic Acid	37-39	caspase 1	Homo sapiens	137-146
29193391-6	2018	However, DHM pretreatment inhibited PA-induced pyroptotic cell death by increasing cell viability, decreasing LDH and IL-1beta release, improving cell membrane integrity, and abolishing caspase-1 cleavage and subsequent IL-1beta maturation.	dihydromyricetin	9-12	caspase 1	Homo sapiens	186-195
29358279-7	2018	In vivo, depletion of bioavailable copper resulted in attenuated caspase-1-dependent inflammation and reduced susceptibility to LPS-induced endotoxic shock.	Copper	35-41	caspase 1	Homo sapiens	65-74
29193391-6	2018	However, DHM pretreatment inhibited PA-induced pyroptotic cell death by increasing cell viability, decreasing LDH and IL-1beta release, improving cell membrane integrity, and abolishing caspase-1 cleavage and subsequent IL-1beta maturation.	Palmitic Acid	36-38	caspase 1	Homo sapiens	186-195
29416034-6	2018	Treatment of human aortic endothelial cells (HAECs) with nicotine resulted in NLRP3-ASC inflammasome activation and pyroptosis, as evidenced by cleavage of caspase-1, production of downstream interleukin (IL)-1beta and IL-18, and elevation of LDH activity and increase of propidium iodide (PI) positive cells, which were all inhibited by caspase-1 inhibitor.	Nicotine	57-65	caspase 1	Homo sapiens	156-165
29479354-7	2018	To further understand the differential expression of cytokines/chemokines, we showed that WFA alters the nigericin-induced co-localization of NLRP3 and ASC proteins, thereby inhibiting caspase-1 activation, which is responsible for the cleavage and maturation of pro-inflammatory cytokines IL-1beta and IL-18.	Nigericin	105-114	caspase 1	Homo sapiens	185-194
29416034-7	2018	Moreover, silencing NLRP3 or ASC by small interfering RNA efficiently suppressed nicotine-induced caspase-1 cleavage, IL-18 and IL-1beta production, and pyroptosis in HAECs.	Nicotine	81-89	caspase 1	Homo sapiens	98-107
29416034-6	2018	Treatment of human aortic endothelial cells (HAECs) with nicotine resulted in NLRP3-ASC inflammasome activation and pyroptosis, as evidenced by cleavage of caspase-1, production of downstream interleukin (IL)-1beta and IL-18, and elevation of LDH activity and increase of propidium iodide (PI) positive cells, which were all inhibited by caspase-1 inhibitor.	Nicotine	57-65	caspase 1	Homo sapiens	338-347
29198726-6	2018	Moreover, a significant inhibition of the inflammasome activation was observed in neopterin pre-conditioned human astrocytes, when challenged with LPS, by reducing IL-1beta, caspase-1 and ASC expression or content, components of the NLRP3 inflammasome.	Neopterin	82-91	caspase 1	Homo sapiens	174-183
29203413-6	2018	Subsequently, MILH induces lipid peroxidation, lysosomal membrane permeabilization and leakage of lysosomal enzymes into the cytosol, including Cathepsin-B which activates Caspase-1 but not apoptotic Caspase-3.	milh	14-18	caspase 1	Homo sapiens	172-181
29274344-7	2018	The SYK inhibitor R406 reduced IL-1beta release and caspase-1 activation in CaP particle-treated VSMCs, indicating that SYK activation occurs upstream of and is required for caspase-1 activation.	R406	18-22	caspase 1	Homo sapiens	52-61
29274344-7	2018	The SYK inhibitor R406 reduced IL-1beta release and caspase-1 activation in CaP particle-treated VSMCs, indicating that SYK activation occurs upstream of and is required for caspase-1 activation.	R406	18-22	caspase 1	Homo sapiens	174-183
29274344-7	2018	The SYK inhibitor R406 reduced IL-1beta release and caspase-1 activation in CaP particle-treated VSMCs, indicating that SYK activation occurs upstream of and is required for caspase-1 activation.	vsmcs	97-102	caspase 1	Homo sapiens	52-61
29274344-7	2018	The SYK inhibitor R406 reduced IL-1beta release and caspase-1 activation in CaP particle-treated VSMCs, indicating that SYK activation occurs upstream of and is required for caspase-1 activation.	vsmcs	97-102	caspase 1	Homo sapiens	174-183
29274344-10	2018	CONCLUSIONS: CaP particles stimulate SYK and caspase-1 activation in VSMCs, leading to the release of IL-1beta, at least in part via exosomes.	calcium phosphate	13-16	caspase 1	Homo sapiens	45-54
29257274-7	2018	In addition, the results demonstrated that miR-33 impaired mitochondrial oxygen consumption rates, resulting in the accumulation of cellular reactive oxygen species, which stimulated NLRP3 expression, caspase-1 activity and IL-1beta secretion.	Oxygen	73-79	caspase 1	Homo sapiens	201-210
29257274-7	2018	In addition, the results demonstrated that miR-33 impaired mitochondrial oxygen consumption rates, resulting in the accumulation of cellular reactive oxygen species, which stimulated NLRP3 expression, caspase-1 activity and IL-1beta secretion.	Reactive Oxygen Species	141-164	caspase 1	Homo sapiens	201-210
29386662-6	2018	DHA-treated breast cancer cells triggered increased caspase-1and gasdermin D activation, enhanced IL-1beta secretion, translocated HMGB1 towards the cytoplasm, and membrane pore formation when compared to untreated cells, suggesting DHA induces pyroptosis programmed cell death in breast cancer cells.	Docosahexaenoic Acids	0-3	caspase 1	Homo sapiens	52-61
29386662-7	2018	Moreover, caspase-1 inhibitor (YVAD) could protect breast cancer cells from DHA-induced pyroptotic cell death.	YVAD	31-35	caspase 1	Homo sapiens	10-19
29386662-7	2018	Moreover, caspase-1 inhibitor (YVAD) could protect breast cancer cells from DHA-induced pyroptotic cell death.	Docosahexaenoic Acids	76-79	caspase 1	Homo sapiens	10-19
29161660-8	2018	In activated HaCaT cells, pretreatment with AST2017-01 or chrysophanol significantly reduced production of TSLP and activation of caspase-1.	chrysophanic acid	58-70	caspase 1	Homo sapiens	130-139
29258746-7	2018	NLRP3 inflammasome inhibition by short hairpin RNA (shRNA)-mediated knockdown of NLRP3, selective inhibitor MCC950, and caspase-1 inhibitor Z-YVAD-FMK attenuated silica-induced EMT.	benzyloxycarbonyltyrosyl-valyl-alanyl-aspartic acid fluoromethyl ketone	140-150	caspase 1	Homo sapiens	120-129
29258746-7	2018	NLRP3 inflammasome inhibition by short hairpin RNA (shRNA)-mediated knockdown of NLRP3, selective inhibitor MCC950, and caspase-1 inhibitor Z-YVAD-FMK attenuated silica-induced EMT.	Silicon Dioxide	162-168	caspase 1	Homo sapiens	120-129
29161660-6	2018	Pretreatment with AST2017-01 or chrysophanol significantly blocked PMACI-induced activation of caspase-1 and nuclear factor-kappaB.	chrysophanic acid	32-44	caspase 1	Homo sapiens	95-104
29161660-6	2018	Pretreatment with AST2017-01 or chrysophanol significantly blocked PMACI-induced activation of caspase-1 and nuclear factor-kappaB.	pmaci	67-72	caspase 1	Homo sapiens	95-104
30277836-0	2018	Sorafenib inhibits caspase-1 expression through suppressing TLR4/stat3/SUMO1 pathway in hepatocellular carcinoma.	Sorafenib	0-9	caspase 1	Homo sapiens	19-28
30277836-3	2018	However, the relationship between caspase-1 and sorafenib has rarely been reported.	Sorafenib	48-57	caspase 1	Homo sapiens	34-43
30277836-5	2018	Moreover, sorafenib treatment could inhibit LPS-stimulated caspase-1 overexpression through restricting the nuclear transport of p65, which contributed to inactivation of NF-kappaB.	Sorafenib	10-19	caspase 1	Homo sapiens	59-68
30277836-7	2018	In conclusion, the results of this study suggest that sorafenib inhibits caspase-1 expression through suppressing the nuclear translocation of p65 and provide new insights into the mechanisms of sorafenib treatment in HCC.	Sorafenib	54-63	caspase 1	Homo sapiens	73-82
30138921-9	2018	RESULTS: Here, we clarified that ethanol treatment could cause cell DNA damage, activate caspase-1, and promote the generation and release of IL-1beta and IL-18.	Ethanol	33-40	caspase 1	Homo sapiens	89-98
30138921-11	2018	Interestingly, a caspase-1 inhibitor could significantly suppress pyroptosis, decrease the release of inflammatory cytokines induced by ethanol, and cause no side effects in vivo and in vitro.	Ethanol	136-143	caspase 1	Homo sapiens	17-26
30138921-12	2018	CONCLUSION: Collectively, our results showed that pyroptosis is involved in the pathogenesis of alcohol-induced gastritis and that caspase-1 inhibitor Ac-yvad-cmk could effectively decrease the damage caused by alcohol, making it a potentially promising agent for the treatment of alcoholic gastritis.	ac-yvad	151-158	caspase 1	Homo sapiens	131-140
30138921-12	2018	CONCLUSION: Collectively, our results showed that pyroptosis is involved in the pathogenesis of alcohol-induced gastritis and that caspase-1 inhibitor Ac-yvad-cmk could effectively decrease the damage caused by alcohol, making it a potentially promising agent for the treatment of alcoholic gastritis.	Alcohols	211-218	caspase 1	Homo sapiens	131-140
29157864-2	2017	Our strategy led to the identification of an original 2-azabicyclo-octane scaffold (2-ABO) that was further elaborated into the potent Caspase-1 inhibitor CD10847 (IC50 = 17 nM).	2-azabicyclo-octane	54-73	caspase 1	Homo sapiens	135-144
29196167-3	2018	Here we demonstrated cathepsin B (CTSB) as a regulator of the activation of NLRP3 inflammasome by H2O2 H2O2 induced IL-1beta secretion in NLRP3 inflammasome-dependent manner H2O2 treatment increased CTSB activity, which in turn activated NLRP3 inflammasome, and subsequently processed pro-caspase-1 cleavage into caspase-1, resulting in IL-1 beta secretion.	Hydrogen Peroxide	98-102	caspase 1	Homo sapiens	289-298
29196167-3	2018	Here we demonstrated cathepsin B (CTSB) as a regulator of the activation of NLRP3 inflammasome by H2O2 H2O2 induced IL-1beta secretion in NLRP3 inflammasome-dependent manner H2O2 treatment increased CTSB activity, which in turn activated NLRP3 inflammasome, and subsequently processed pro-caspase-1 cleavage into caspase-1, resulting in IL-1 beta secretion.	Hydrogen Peroxide	98-102	caspase 1	Homo sapiens	313-322
29196167-3	2018	Here we demonstrated cathepsin B (CTSB) as a regulator of the activation of NLRP3 inflammasome by H2O2 H2O2 induced IL-1beta secretion in NLRP3 inflammasome-dependent manner H2O2 treatment increased CTSB activity, which in turn activated NLRP3 inflammasome, and subsequently processed pro-caspase-1 cleavage into caspase-1, resulting in IL-1 beta secretion.	Hydrogen Peroxide	103-107	caspase 1	Homo sapiens	289-298
29196167-3	2018	Here we demonstrated cathepsin B (CTSB) as a regulator of the activation of NLRP3 inflammasome by H2O2 H2O2 induced IL-1beta secretion in NLRP3 inflammasome-dependent manner H2O2 treatment increased CTSB activity, which in turn activated NLRP3 inflammasome, and subsequently processed pro-caspase-1 cleavage into caspase-1, resulting in IL-1 beta secretion.	Hydrogen Peroxide	103-107	caspase 1	Homo sapiens	313-322
29196167-3	2018	Here we demonstrated cathepsin B (CTSB) as a regulator of the activation of NLRP3 inflammasome by H2O2 H2O2 induced IL-1beta secretion in NLRP3 inflammasome-dependent manner H2O2 treatment increased CTSB activity, which in turn activated NLRP3 inflammasome, and subsequently processed pro-caspase-1 cleavage into caspase-1, resulting in IL-1 beta secretion.	Hydrogen Peroxide	103-107	caspase 1	Homo sapiens	289-298
29196167-3	2018	Here we demonstrated cathepsin B (CTSB) as a regulator of the activation of NLRP3 inflammasome by H2O2 H2O2 induced IL-1beta secretion in NLRP3 inflammasome-dependent manner H2O2 treatment increased CTSB activity, which in turn activated NLRP3 inflammasome, and subsequently processed pro-caspase-1 cleavage into caspase-1, resulting in IL-1 beta secretion.	Hydrogen Peroxide	103-107	caspase 1	Homo sapiens	313-322
29196167-4	2018	Genetic inhibition or pharmacological inhibition of CTSB blocked the cleavage of pro-caspase-1 into caspase-1 and subsequent IL-1 beta secretion induced by H2O2.	Hydrogen Peroxide	156-160	caspase 1	Homo sapiens	85-94
30123891-6	2018	Excessive ROS can then result in activation of the NLRP3 inflammasome and secretion of IL-1 and IL-18 by caspase-1.	Reactive Oxygen Species	10-13	caspase 1	Homo sapiens	105-114
29420995-7	2018	Moreover, cysteine suppressed caspase-1 activation and nuclear factor-kappaB translocation.	Cysteine	10-18	caspase 1	Homo sapiens	30-39
29420995-10	2018	In conclusion, cysteine regulates TSLP production by blocking caspase-1, nuclear factor-kappaB, p38, and c-Jun N-terminal kinase-dependent pathways in activated HMC-1 cells, suggesting its potential as a regulator of allergic inflammatory diseases.	Cysteine	15-23	caspase 1	Homo sapiens	62-71
29031534-13	2017	The expression levels of TXNIP, NLRP3, ASC, and caspase-1 were reduced in the SAL treated cells.	rhodioloside	78-81	caspase 1	Homo sapiens	48-57
29157864-2	2017	Our strategy led to the identification of an original 2-azabicyclo-octane scaffold (2-ABO) that was further elaborated into the potent Caspase-1 inhibitor CD10847 (IC50 = 17 nM).	CD10847	155-162	caspase 1	Homo sapiens	135-144
29030458-6	2017	Additionally, when combined with a priming signal, cGAMP activates the inflammasome through an AIM2, NLRP3, ASC, and caspase-1 dependent process.	cyclic guanosine monophosphate-adenosine monophosphate	51-56	caspase 1	Homo sapiens	117-126
29061850-6	2017	Here, we report that TcpB induces ubiquitination and degradation of the inflammatory caspases 1, 4, and 11.	TCPB	21-25	caspase 1	Homo sapiens	85-106
28990778-8	2017	Compared with the BaP group, the autophagy inhibitor 3-MA significantly (p &lt; 0.01) inhibited the release of LDH by 70.53% +- 0.46 and NO by 50.36% +- 0.80, the increase of electrical conductivity by 12.08% +- 0.55, and the expressions of pyroptotic marker proteins (Caspase-1, Cox-2, IL-1beta, IL-18).	3-methyladenine	53-57	caspase 1	Homo sapiens	269-278
28990231-9	2017	Moreover, IFI16-induced tumour cell death promoted the recruitment of inflammasome complex to enhance tumour inhibition, but the caspase-1 inhibitor Ac-YVAD-CMK (50 mumol/L) could suppress this process in HCC.	ac-yvad	149-156	caspase 1	Homo sapiens	129-138
29250144-6	2017	Further investigations indicated that the effects of formononetin were associated with a reduction of intracellular calcium, suppression of NF-kappaB activation and upstream IkappaKalpha phosphorylation and inhibition of caspase-1 activity.	formononetin	53-65	caspase 1	Homo sapiens	221-230
28940479-10	2017	Application of the ceramide analogue C2 and the sphingosine-1-phosphate-receptor agonist Fingolimod (FTY720) up-regulated levels of IL-1beta and cleaved caspase-1 in wild-type microglia, whereas ASC-/- microglia were unaffected.	Ceramides	19-27	caspase 1	Homo sapiens	153-162
28940479-10	2017	Application of the ceramide analogue C2 and the sphingosine-1-phosphate-receptor agonist Fingolimod (FTY720) up-regulated levels of IL-1beta and cleaved caspase-1 in wild-type microglia, whereas ASC-/- microglia were unaffected.	Fingolimod Hydrochloride	89-99	caspase 1	Homo sapiens	153-162
28755170-0	2017	Identification and validation of uterine stimulant methylergometrine as a potential inhibitor of caspase-1 activation.	Methylergonovine	51-68	caspase 1	Homo sapiens	97-106
28972959-8	2017	RESULTS Pretreatment with paeonol remarkably rescued MPP+-induced cell viability reduction, up-regulation of cell apoptosis, caspase-1 activity, COX-2, iNOS, and Bax/Bcl-2 ratio in primary astrocytes.	paeonol	26-33	caspase 1	Homo sapiens	125-134
29096724-9	2017	RESULTS: Treating HepG2 cells with PA-LPS caused NLRP3 inflammation activation, including overexpression of NLRP3 and caspase-1, and overproduction of IL-1beta and IL-18 as well as TNF-alpha from HepG2 cells.	pa-lps	35-41	caspase 1	Homo sapiens	118-127
28295583-6	2017	Pretreatment with a caspase-1 inhibitor, Z-YVAD-FMK, downregulated the mature IL-1beta expression enhanced by AMBN treatment in LPS-treated U937 cells.	benzyloxycarbonyltyrosyl-valyl-alanyl-aspartic acid fluoromethyl ketone	41-51	caspase 1	Homo sapiens	20-29
28551814-3	2017	This study investigates the role of macrophage-derived, caspase-1-dependent interleukin-1beta (IL-1beta) in an in vitro model of LVI.	lvi	129-132	caspase 1	Homo sapiens	56-65
28266737-6	2017	We transfected polyinosinic:polycytidylic acid (poly I:C), a synthetic viral dsRNA analogue, into cultured primary human keratinocytes at the aid of Lipofectamine 2000, and found that transfected poly I:C activated caspase-1 and induced caspase-1-dependent release of IL-1beta and IL-18, which were suppressed on transfection with NLRP3 siRNA.	polyinosinic:	15-28	caspase 1	Homo sapiens	215-224
28266737-6	2017	We transfected polyinosinic:polycytidylic acid (poly I:C), a synthetic viral dsRNA analogue, into cultured primary human keratinocytes at the aid of Lipofectamine 2000, and found that transfected poly I:C activated caspase-1 and induced caspase-1-dependent release of IL-1beta and IL-18, which were suppressed on transfection with NLRP3 siRNA.	polyinosinic:	15-28	caspase 1	Homo sapiens	237-246
28266737-6	2017	We transfected polyinosinic:polycytidylic acid (poly I:C), a synthetic viral dsRNA analogue, into cultured primary human keratinocytes at the aid of Lipofectamine 2000, and found that transfected poly I:C activated caspase-1 and induced caspase-1-dependent release of IL-1beta and IL-18, which were suppressed on transfection with NLRP3 siRNA.	Poly I-C	48-56	caspase 1	Homo sapiens	215-224
28266737-6	2017	We transfected polyinosinic:polycytidylic acid (poly I:C), a synthetic viral dsRNA analogue, into cultured primary human keratinocytes at the aid of Lipofectamine 2000, and found that transfected poly I:C activated caspase-1 and induced caspase-1-dependent release of IL-1beta and IL-18, which were suppressed on transfection with NLRP3 siRNA.	Poly I-C	48-56	caspase 1	Homo sapiens	237-246
28266737-6	2017	We transfected polyinosinic:polycytidylic acid (poly I:C), a synthetic viral dsRNA analogue, into cultured primary human keratinocytes at the aid of Lipofectamine 2000, and found that transfected poly I:C activated caspase-1 and induced caspase-1-dependent release of IL-1beta and IL-18, which were suppressed on transfection with NLRP3 siRNA.	Poly I-C	196-204	caspase 1	Homo sapiens	215-224
28266737-6	2017	We transfected polyinosinic:polycytidylic acid (poly I:C), a synthetic viral dsRNA analogue, into cultured primary human keratinocytes at the aid of Lipofectamine 2000, and found that transfected poly I:C activated caspase-1 and induced caspase-1-dependent release of IL-1beta and IL-18, which were suppressed on transfection with NLRP3 siRNA.	Poly I-C	196-204	caspase 1	Homo sapiens	237-246
28768565-4	2017	We previously reported that TG-induced macrophage cell death is triggered by caspase-1, and thus investigated the relationship between caspase-2 and caspase-1 in TG-induced macrophage cell death.	Triglycerides	28-30	caspase 1	Homo sapiens	77-86
28768565-4	2017	We previously reported that TG-induced macrophage cell death is triggered by caspase-1, and thus investigated the relationship between caspase-2 and caspase-1 in TG-induced macrophage cell death.	Triglycerides	162-164	caspase 1	Homo sapiens	149-158
28768565-5	2017	Inhibition of caspase-2 activity decreased caspase-1 activity in TG-treated macrophages.	Triglycerides	65-67	caspase 1	Homo sapiens	43-52
28768565-9	2017	Taken together, these results suggest that TG-induced macrophage cell death is mediated via the caspase-2/caspase-1/apoptotic caspases/PARP pathways.	Triglycerides	43-45	caspase 1	Homo sapiens	106-134
29056256-5	2017	Treatment with the potassium ionophore nigericin significantly increased the level of activated caspase-1.	Potassium	19-28	caspase 1	Homo sapiens	96-105
29056256-5	2017	Treatment with the potassium ionophore nigericin significantly increased the level of activated caspase-1.	Nigericin	39-48	caspase 1	Homo sapiens	96-105
29056256-6	2017	Treatment with either LPS or nigericin stimulated IL-1beta secretion, whereas pretreatment with the ATP-sensitive K+ channel inhibitor glibenclamide, the Rho-associated coiled-coil kinase inhibitor Y-27632, or a caspase-1 inhibitor significantly decreased nigericin-induced IL-1beta secretion.	Nigericin	29-38	caspase 1	Homo sapiens	212-221
29056256-7	2017	In addition, dibutyryl-cAMP, which induces trophoblast differentiation, decreased expression of NLRP3, caspase-1, and IL-1beta.	Bucladesine	13-27	caspase 1	Homo sapiens	103-112
29056256-8	2017	These findings suggest that trophoblasts can secrete IL-1beta through the NLRP3/caspase-1 pathway, which is suppressed by glibenclamide, and that the TLR4-mediated NLRP3 inflammasome pathway is more likely to be stimulated in undifferentiated than differentiated trophoblasts.	Glyburide	122-135	caspase 1	Homo sapiens	80-89
28870124-7	2017	Similarly, the expression of NLRP3 and caspase-1 p10 and the release of IL-1beta and IL-18 were significantly increased after ZnO-NPs treatment, which indicated that the NLRP3 inflammasome was activated by ZnO-NPs.	Zinc Oxide	126-129	caspase 1	Homo sapiens	39-48
28645808-5	2017	Under the clinical diagnosis of Ewing-like sarcoma of the abdominal wall with multiple lung metastases, several cycles of ICE (ifosfamide, carboplatin and etoposide) therapy were performed.	Ifosfamide	127-137	caspase 1	Homo sapiens	122-125
28645808-5	2017	Under the clinical diagnosis of Ewing-like sarcoma of the abdominal wall with multiple lung metastases, several cycles of ICE (ifosfamide, carboplatin and etoposide) therapy were performed.	Carboplatin	139-150	caspase 1	Homo sapiens	122-125
28645808-5	2017	Under the clinical diagnosis of Ewing-like sarcoma of the abdominal wall with multiple lung metastases, several cycles of ICE (ifosfamide, carboplatin and etoposide) therapy were performed.	Etoposide	155-164	caspase 1	Homo sapiens	122-125
28870124-7	2017	Similarly, the expression of NLRP3 and caspase-1 p10 and the release of IL-1beta and IL-18 were significantly increased after ZnO-NPs treatment, which indicated that the NLRP3 inflammasome was activated by ZnO-NPs.	Zinc Oxide	206-209	caspase 1	Homo sapiens	39-48
28936177-6	2017	WFA also induced apoptosis of Ca9-22 cells, which was measured by flow cytometry for subG1 percentage, annexin V expression, and pan-caspase activity, as well as western blotting for caspases 1, 8, and 9 activations.	withaferin A	0-3	caspase 1	Homo sapiens	183-203
28778433-0	2017	Lysophosphatidylcholine activates caspase-1 in microglia via a novel pathway involving two inflammasomes.	Lysophosphatidylcholines	0-23	caspase 1	Homo sapiens	34-43
28778433-2	2017	In the present study, we have identified inflammasomes causing caspase-1 activation following stimulation of microglia with lysophosphatidylcholine (LPC), a proinflammatory lipid generated under pathological conditions in the brain.	Lysophosphatidylcholines	124-147	caspase 1	Homo sapiens	63-72
28778433-2	2017	In the present study, we have identified inflammasomes causing caspase-1 activation following stimulation of microglia with lysophosphatidylcholine (LPC), a proinflammatory lipid generated under pathological conditions in the brain.	Lysophosphatidylcholines	149-152	caspase 1	Homo sapiens	63-72
28778433-3	2017	LPC-induced caspase-1 activation in microglia was found to depend on LPS prestimulation, inflammasome NLRP3 and adaptor molecule ASC.	Lysophosphatidylcholines	0-3	caspase 1	Homo sapiens	12-21
29259717-3	2017	Recent studies suggest that cholesterol crystals play a pivotal role in activation of NLRP3 inflammasomes, which regulate caspase-1 activation and the subsequent processing of IL-1beta, in atherosclerotic lesions.	Cholesterol	28-39	caspase 1	Homo sapiens	122-131
28984290-8	2017	The caspase-3 inhibitor z-DEVD-fmk and caspase-1 inhibitor z-YVAD-fmk also reduced the cytotoxicity of RH2.	benzyloxycarbonyltyrosyl-valyl-alanyl-aspartic acid fluoromethyl ketone	59-69	caspase 1	Homo sapiens	39-48
28887507-8	2017	CA inhibited DSS-induced NLRP3 inflammasome activation by reducing caspase 1 activity.	dss	13-16	caspase 1	Homo sapiens	67-76
28651232-7	2017	Silymarin treatment significantly down regulated the inflammatory responses by suppressing NF-kappaB-p65 levels and inflammasome-mediated caspase-1/IL-1beta expressions.	Silymarin	0-9	caspase 1	Homo sapiens	138-147
28726636-6	2017	Here, we demonstrate that these fusion proteins are cleaved by caspases-1 and -11 at Asp-276.	Aspartic Acid	85-88	caspase 1	Homo sapiens	63-81
28694089-7	2017	Moreover, taurine brought a significant inhibition of the activities of NF-kappaB and caspase-1.	Taurine	10-17	caspase 1	Homo sapiens	86-95
28497417-7	2017	The rs3751143 polymorphism was associated with osteoclast apoptosis; ATP-induced caspase-1 activity of osteoclasts with AC and CC genotypes is lower than that of osteoclasts with AA genotype in vitro.	Adenosine Triphosphate	69-72	caspase 1	Homo sapiens	81-90
28668606-3	2017	PDTC (Pyrrolidinedithiocarbamic acid), SB202190 and Z-YVAD-FMK were used to block the MyD88/NF-kappaB, MAPKs/p38 and NLRP3/Caspase-1 pathway, respectively.	pyrrolidine dithiocarbamic acid	6-36	caspase 1	Homo sapiens	123-132
28668606-3	2017	PDTC (Pyrrolidinedithiocarbamic acid), SB202190 and Z-YVAD-FMK were used to block the MyD88/NF-kappaB, MAPKs/p38 and NLRP3/Caspase-1 pathway, respectively.	benzyloxycarbonyltyrosyl-valyl-alanyl-aspartic acid fluoromethyl ketone	52-62	caspase 1	Homo sapiens	123-132
28668606-9	2017	In contrast, when NLRP3/Caspase-1 pathway was blocked with Z-YVAD-FMK, TNF-alpha, IL-6 and IL-1beta levels, LDH enzyme activity, and Caspase-1 and NLRP3 protein levels were significantly declined (P &lt; 0.05) in HMEC-1 cells except IL-8(P &gt; 0.05).	benzyloxycarbonyltyrosyl-valyl-alanyl-aspartic acid fluoromethyl ketone	59-69	caspase 1	Homo sapiens	24-33
28605710-5	2017	DEX (5muMu) exposure for 3d significantly increased the expression of NLRP-1, ASC, caspase-1 and IL-1beta in the hippocampal neurons and the release of IL-1beta and IL-18 in the supernatants.	Dextromethorphan	0-3	caspase 1	Homo sapiens	83-92
28798291-4	2017	RESULTS After six hours, 12 hours, and 24 hours of high glucose stimulation, the secretion of IL-1beta in human glomerular mesangial cells, compared to unstimulated cells, was 1.85-fold, 3.04-fold, and 4.14-fold; the expression of NLRP3 increased by 2.20-fold, 4.62-fold, and 8.32-fold; and the expression of caspase-1 was increased by 1.60-fold, 2.72-fold, and 3.67-fold.	Glucose	56-63	caspase 1	Homo sapiens	309-318
28356568-3	2017	The NLRP3 inflammasome forms an assembly consisting of the ASC (apoptosis-associated speck-like protein containing a C-terminal caspase recruitment domain) adaptor protein and the effector, caspase-1 (cysteine-dependent aspartate-directed protease-1).	Cysteine	201-209	caspase 1	Homo sapiens	190-199
28779175-5	2017	Mitochondrial ROS then induces the translocation of CLICs to the plasma membrane for the induction of chloride efflux to promote NEK7-NLRP3 interaction, inflammasome assembly, caspase-1 activation, and IL-1beta secretion.	Reactive Oxygen Species	14-17	caspase 1	Homo sapiens	176-185
28779175-5	2017	Mitochondrial ROS then induces the translocation of CLICs to the plasma membrane for the induction of chloride efflux to promote NEK7-NLRP3 interaction, inflammasome assembly, caspase-1 activation, and IL-1beta secretion.	Chlorides	102-110	caspase 1	Homo sapiens	176-185
28252317-10	2017	MEASUREMENTS AND MAIN RESULTS: Chlamydia and Haemophilus infections increase NLRP3, caspase-1, IL-1beta responses that drive steroid-resistant neutrophilic inflammation and airway hyperresponsiveness.	Steroids	125-132	caspase 1	Homo sapiens	84-93
28605710-5	2017	DEX (5muMu) exposure for 3d significantly increased the expression of NLRP-1, ASC, caspase-1 and IL-1beta in the hippocampal neurons and the release of IL-1beta and IL-18 in the supernatants.	5mumu	5-10	caspase 1	Homo sapiens	83-92
28732502-11	2017	The mechanistic studies revealed that chronic DEX exposure significantly increased the expression of NLRP1, ASC, caspase-1, IL-1beta, L-18, and BK protein and NLRP1, IL-1beta and BK mRNA levels in hippocampal neurons.	Dexamethasone	46-49	caspase 1	Homo sapiens	113-122
28268194-6	2017	Using this assay system, caspase-1 activation has been determined in THP-1 cells following treatment with alpha-hemolysin, LPS, nigericin, gramicidin, MSU, R848, Pam3CSK4, and flagellin.	Nigericin	128-137	caspase 1	Homo sapiens	25-34
28805975-8	2017	Furthermore, antofine also modulated the activation of AMPK and caspase-1, the key regulator in inflammasome-mediated IL-1beta maturation, in activated macrophage cells.	antofine	13-21	caspase 1	Homo sapiens	64-73
27339879-6	2017	Consistently, we demonstrated that caspase-1 inhibitor suppressed caspase-7/PARP1/AIF-mediated apoptosis pathway by 1-methyl-4-phenylpyridinium ion (MPP+) stimulation in SH-SY5Y cells.	1-Methyl-4-phenylpyridinium	116-147	caspase 1	Homo sapiens	35-44
27339879-6	2017	Consistently, we demonstrated that caspase-1 inhibitor suppressed caspase-7/PARP1/AIF-mediated apoptosis pathway by 1-methyl-4-phenylpyridinium ion (MPP+) stimulation in SH-SY5Y cells.	mangion-purified polysaccharide (Candida albicans)	149-153	caspase 1	Homo sapiens	35-44
28326454-7	2017	Increased production of ROS and expression of IL-1beta, IL-18, and caspase-1 genes and proteins were observed in U937 and THP-1 cells incubated with fructose and were effectively inhibited by quercetin and ascorbic acid.	Fructose	149-157	caspase 1	Homo sapiens	67-76
28454672-4	2017	The data disclosed here also demonstrated that the new alpha-keto amide GSK8999 has a mechanism of action consistent with inhibition of the proteolytic cleavage of CA-SP1.	alpha-keto amide	55-71	caspase 1	Homo sapiens	164-170
28454672-4	2017	The data disclosed here also demonstrated that the new alpha-keto amide GSK8999 has a mechanism of action consistent with inhibition of the proteolytic cleavage of CA-SP1.	gsk8999	72-79	caspase 1	Homo sapiens	164-170
26848183-8	2017	In vitro, TiO2 particles were taken up by IECs and macrophages and triggered NLRP3-ASC-caspase-1 assembly, caspase-1 cleavage and the release of NLRP3-associated interleukin (IL)-1beta and IL-18.	titanium dioxide	10-14	caspase 1	Homo sapiens	87-96
26848183-8	2017	In vitro, TiO2 particles were taken up by IECs and macrophages and triggered NLRP3-ASC-caspase-1 assembly, caspase-1 cleavage and the release of NLRP3-associated interleukin (IL)-1beta and IL-18.	titanium dioxide	10-14	caspase 1	Homo sapiens	107-116
28978034-3	2017	Here, we show that celastrol abolishes the NLRP3 inflammasome activation, inhibits subsequent caspase-1 activation and IL-1beta secretion both in vitro and in vivo.	celastrol	19-28	caspase 1	Homo sapiens	94-103
28592027-5	2017	Results: Compared with the control group, the protein expressions of NLRP3, caspase-1 and IL-1beta in PASMCs were increased to (1.38+-0.09, t=3.998, P&lt;0.001), (1.32+-0.1, t=3.268, P&lt;0.01)and(1.43+-0.19) (t=2.096, P&lt;0.05) folds in the PDGF group.	pasmcs	102-108	caspase 1	Homo sapiens	76-85
28326454-7	2017	Increased production of ROS and expression of IL-1beta, IL-18, and caspase-1 genes and proteins were observed in U937 and THP-1 cells incubated with fructose and were effectively inhibited by quercetin and ascorbic acid.	Quercetin	192-201	caspase 1	Homo sapiens	67-76
28326454-7	2017	Increased production of ROS and expression of IL-1beta, IL-18, and caspase-1 genes and proteins were observed in U937 and THP-1 cells incubated with fructose and were effectively inhibited by quercetin and ascorbic acid.	Ascorbic Acid	206-219	caspase 1	Homo sapiens	67-76
28569730-5	2017	This is followed by signal two, which involves recognition of PAMPs or damage-associated molecular patterns (DAMPs), such as uric acid or ATP, via NLRP3, which leads to caspase-1-dependent cleavage of pro-IL-1beta to active IL-1beta and pyroptosis.	Uric Acid	125-134	caspase 1	Homo sapiens	169-178
28569730-5	2017	This is followed by signal two, which involves recognition of PAMPs or damage-associated molecular patterns (DAMPs), such as uric acid or ATP, via NLRP3, which leads to caspase-1-dependent cleavage of pro-IL-1beta to active IL-1beta and pyroptosis.	Adenosine Triphosphate	138-141	caspase 1	Homo sapiens	169-178
28507328-10	2017	In vitro, HCQ inhibited IL-1beta and caspase 1 activation induced by ATP in a dose-dependent manner.	Hydroxychloroquine	10-13	caspase 1	Homo sapiens	37-46
27726055-9	2017	Treatment with the caspase-1 inhibitor, VX-765, suppressed NLRP3 expression with reduced IL-1beta expression and associated neuroinflammation.	belnacasan	40-46	caspase 1	Homo sapiens	19-28
28507328-10	2017	In vitro, HCQ inhibited IL-1beta and caspase 1 activation induced by ATP in a dose-dependent manner.	Adenosine Triphosphate	69-72	caspase 1	Homo sapiens	37-46
28507328-12	2017	In vivo, HCQ inhibited caspase 1-dependent ATP-induced neutrophil recruitment.	Hydroxychloroquine	9-12	caspase 1	Homo sapiens	23-32
28507328-12	2017	In vivo, HCQ inhibited caspase 1-dependent ATP-induced neutrophil recruitment.	Adenosine Triphosphate	43-46	caspase 1	Homo sapiens	23-32
26983397-7	2017	These findings reveal a general mode of action of TRIMs as autophagic receptor-regulators performing a highly-selective type of autophagy (precision autophagy), with MEFV specializing in the suppression of inflammasome and CASP1 activation engendering IL1B/interleukin-1beta production and implicated in the form of cell death termed pyroptosis, whereas TRIM21 dampens type I interferon responses.	vinyl ethyl methacrylate	50-55	caspase 1	Homo sapiens	223-228
28232172-11	2017	We conclude that alcohol-induced accumulation and crystallization of cholesterol activates NLRP3/caspase-1 in the cerebral vessel that leads to early development of atherosclerosis.	Alcohols	17-24	caspase 1	Homo sapiens	97-106
28232172-11	2017	We conclude that alcohol-induced accumulation and crystallization of cholesterol activates NLRP3/caspase-1 in the cerebral vessel that leads to early development of atherosclerosis.	Cholesterol	69-80	caspase 1	Homo sapiens	97-106
28012441-5	2017	Moreover, UgU elicited mitochondrial superoxide generation in a dose-dependent manner, and a specific scavenger of mitochondrial reactive oxygen species (ROS) diminished UgU-induced IL-1beta and caspase-1 activation.	Reactive Oxygen Species	129-152	caspase 1	Homo sapiens	195-204
28288918-7	2017	Elevations of CO2 cause oligomerization of the inflammasome components ASC, NLRP3, caspase 1, thioredoxin interacting protein, and calreticulin - a protein from endoplasmic reticulum, leading to IL-1beta synthesis.	Carbon Dioxide	14-17	caspase 1	Homo sapiens	83-92
28424426-4	2017	Moreover, circ-0016347 was identified as a sponge of miR-214 that upregulated the expression of caspase-1, which is the functional target of miR-214.	circ	10-14	caspase 1	Homo sapiens	96-105
28012441-5	2017	Moreover, UgU elicited mitochondrial superoxide generation in a dose-dependent manner, and a specific scavenger of mitochondrial reactive oxygen species (ROS) diminished UgU-induced IL-1beta and caspase-1 activation.	Reactive Oxygen Species	154-157	caspase 1	Homo sapiens	195-204
28314590-4	2017	Investigation of the underlying mechanism revealed that upon canonical and non-canonical inflammasome activation, caspase-1 interacted with cyclic GMP-AMP (cGAMP) synthase (cGAS), cleaving it and dampening cGAS-STING-mediated IFN production.	cyclic guanosine monophosphate-adenosine monophosphate	140-154	caspase 1	Homo sapiens	114-123
28356505-1	2017	The NLRP3 inflammasome/caspase-1/IL-1beta axis may be a therapeutic target in severe steroid-resistant asthma.	Steroids	85-92	caspase 1	Homo sapiens	23-32
28266599-6	2017	After stimulation of ORS cells with the double-stranded (ds)RNA mimic polyinosinic:polycytidylic acid (poly[I:C]), the activation of caspase-1 and secretion of IL-1beta were enhanced.	Poly C	83-101	caspase 1	Homo sapiens	133-142
28167279-7	2017	LPS/PA treatment significantly increased NLRP3 expression, decreased SIRT1 expression and promoted caspase-1 activity in MSCs.	Protactinium	4-6	caspase 1	Homo sapiens	99-108
28167279-9	2017	Moreover, inhibition of caspase-1 activity repressed adipogenic differentiation and partially improved osteogenic differentiation of MSCs with LPS/PA treatment.	Protactinium	147-149	caspase 1	Homo sapiens	24-33
28387889-12	2017	Ketamine is more effective in reducing inflammatory factors including IL-1beta, Caspase-1, and NF-kappaB than propofol.	Ketamine	0-8	caspase 1	Homo sapiens	80-89
26961545-7	2017	The presence of ATP during TLR4 activation leads to NLRP3 inflammasome activation and caspase-1-mediated IL-1beta secretion which was inhibited during CD40 activation, accompanied with inhibition of ERK1/2 and reactive oxygen species (ROS), and elevation in p38 MAPK phosphorylation.	Adenosine Triphosphate	16-19	caspase 1	Homo sapiens	86-95
26961545-7	2017	The presence of ATP during TLR4 activation leads to NLRP3 inflammasome activation and caspase-1-mediated IL-1beta secretion which was inhibited during CD40 activation, accompanied with inhibition of ERK1/2 and reactive oxygen species (ROS), and elevation in p38 MAPK phosphorylation.	Reactive Oxygen Species	210-233	caspase 1	Homo sapiens	86-95
26961545-7	2017	The presence of ATP during TLR4 activation leads to NLRP3 inflammasome activation and caspase-1-mediated IL-1beta secretion which was inhibited during CD40 activation, accompanied with inhibition of ERK1/2 and reactive oxygen species (ROS), and elevation in p38 MAPK phosphorylation.	Reactive Oxygen Species	235-238	caspase 1	Homo sapiens	86-95
28253332-3	2017	Stimulation of NOD2 by its ligand (muramyl dipeptide) activates pro-inflammatory pathways such as nuclear factor-kappaB (NF-kappaB), mitogen-activated protein kinases (MAPKs), and Caspase-1.	Acetylmuramyl-Alanyl-Isoglutamine	35-52	caspase 1	Homo sapiens	180-189
27940204-11	2017	Additionally LX-2 cells primed with LPS and subsequently stimulated for 30min with ATP greatly increased mRNA and protein expression of caspase-1, NLRP3 and P2x7R, as well as liver fibrosis markers, alpha-SMA and type I collagen.	Adenosine Triphosphate	83-86	caspase 1	Homo sapiens	136-145
28064010-4	2017	Results show an increment of pro-inflammatory cytokine interleukin (IL) -1beta secretion and caspase-1 activation during the senescence of endothelial cells induced by bleomycin.	Bleomycin	168-177	caspase 1	Homo sapiens	93-102
28052562-5	2017	By using the phorbol 12-myristate 13-acetate-induced cell differentiation model, we found that caspase-1 activation was required for the differentiation of human monocytes to macrophages.	Tetradecanoylphorbol Acetate	13-44	caspase 1	Homo sapiens	95-104
28069553-0	2017	Targeting inflammasome by the inhibition of caspase-1 activity using capped mesoporous silica nanoparticles.	Silicon Dioxide	87-93	caspase 1	Homo sapiens	44-53
28069553-5	2017	Here we describe the design of a smart nanodevice that takes advantage of the passive targeting of nanoparticles to macrophages and enhances the therapeutic effect of caspase-1 inhibitor VX-765 in vivo.	belnacasan	187-193	caspase 1	Homo sapiens	167-176
28057077-7	2017	Ice ingestion with a long rest interval (-0.55 +- 0.07  C; both p &lt; 0.05) allowed for a greater drop in the core temperature than both ice ingestion with a short rest interval (-0.36 +- 0.16  C) and cold water ingestion (-0.11 +- 0.14  C).	Water	207-212	caspase 1	Homo sapiens	0-3
28000894-0	2017	Berberine affects osteosarcoma via downregulating the caspase-1/IL-1beta signaling axis.	Berberine	0-9	caspase 1	Homo sapiens	54-63
28000894-8	2017	Furthermore, administration of berberine is capable of reducing the expression of caspase-1 and IL-1beta in osteosarcoma cells and inhibiting the growth of tumor cells.	Berberine	31-40	caspase 1	Homo sapiens	82-91
28000894-9	2017	Based on the above, for the first time, we propose the hyposis that berberine could gengerate an anti-osteosarcoma property through downregulating caspase-1/IL-1beta inflammatory signaling axis.	Berberine	68-77	caspase 1	Homo sapiens	147-156
27751866-6	2017	Inflammasome activation was initiated by mitochondrial reactive oxygen species production triggered by chromium (VI), as indicated by sensitivity to treatment with the ROS scavenger N-acetyl cysteine and a coinciding failure of K+ efflux, caspase-1, or NLRP3 inhibition to prevent mitochondrial reactive oxygen species accumulation.	Reactive Oxygen Species	55-78	caspase 1	Homo sapiens	239-248
27882694-0	2017	Fused Bicyclic Caspase-1 Inhibitors Assembled by Copper-Free Strain-Promoted Alkyne-Azide Cycloaddition (SPAAC).	Copper	49-55	caspase 1	Homo sapiens	15-24
27882694-0	2017	Fused Bicyclic Caspase-1 Inhibitors Assembled by Copper-Free Strain-Promoted Alkyne-Azide Cycloaddition (SPAAC).	alkyne-azide	77-89	caspase 1	Homo sapiens	15-24
27882694-2	2017	Herein, by making use of the copper-free strain-promoted alkyne-azide cycloaddition (SPAAC) reaction between difluorinated cyclooctynes (DIFOs) and various azide-containing compounds, we showed for the first time that potential caspase-1 inhibitors could be rapidly synthesized.	Copper	29-35	caspase 1	Homo sapiens	228-237
27882694-2	2017	Herein, by making use of the copper-free strain-promoted alkyne-azide cycloaddition (SPAAC) reaction between difluorinated cyclooctynes (DIFOs) and various azide-containing compounds, we showed for the first time that potential caspase-1 inhibitors could be rapidly synthesized.	alkyne-azide	57-69	caspase 1	Homo sapiens	228-237
27882694-2	2017	Herein, by making use of the copper-free strain-promoted alkyne-azide cycloaddition (SPAAC) reaction between difluorinated cyclooctynes (DIFOs) and various azide-containing compounds, we showed for the first time that potential caspase-1 inhibitors could be rapidly synthesized.	difluorinated cyclooctynes	109-135	caspase 1	Homo sapiens	228-237
27882694-2	2017	Herein, by making use of the copper-free strain-promoted alkyne-azide cycloaddition (SPAAC) reaction between difluorinated cyclooctynes (DIFOs) and various azide-containing compounds, we showed for the first time that potential caspase-1 inhibitors could be rapidly synthesized.	Temefos	137-142	caspase 1	Homo sapiens	228-237
27882694-2	2017	Herein, by making use of the copper-free strain-promoted alkyne-azide cycloaddition (SPAAC) reaction between difluorinated cyclooctynes (DIFOs) and various azide-containing compounds, we showed for the first time that potential caspase-1 inhibitors could be rapidly synthesized.	Azides	64-69	caspase 1	Homo sapiens	228-237
27882694-3	2017	The resulting fused bicyclic compounds structurally resembled the central portion (P2 -P3 ) of Pralnacasan (a well-known small molecule caspase-1 inhibitor), with diversity at the P4 -position of the parental inhibitor conveniently installed from the azide component.	pralnacasan	95-106	caspase 1	Homo sapiens	136-145
27882694-4	2017	Since our SPAAC-assembled inhibitor library was synthesized by using a copper-free bioorthogonal chemistry, the resulting 52-membered library (2 DIFOsx26 azides) was immediately ready for subsequent cell-based screening for rapid identification of potential cell-permeable hits capable of effectively inhibiting endogenous caspase-1 activities.	difosx26 azides	145-160	caspase 1	Homo sapiens	323-332
28738323-5	2017	RESULTS: H2S attenuated FFA-induced cell apoptosis, and reduced the expression of NLRP3, ASC, pro-caspase-1, caspase-1, IL- 1beta, IL-18 and caspase-3.	Hydrogen Sulfide	9-12	caspase 1	Homo sapiens	98-107
28738323-5	2017	RESULTS: H2S attenuated FFA-induced cell apoptosis, and reduced the expression of NLRP3, ASC, pro-caspase-1, caspase-1, IL- 1beta, IL-18 and caspase-3.	Hydrogen Sulfide	9-12	caspase 1	Homo sapiens	109-118
28164132-12	2017	The higher expression of NLRP3, caspase1, and secretion of IL-1beta, signaling, and activation might contribute to the hyperinflammation in the human diabetic wound and in high glucose induced macrophages.	Glucose	177-184	caspase 1	Homo sapiens	32-40
27737891-6	2016	Notably, knockdown of NLRP3 or caspase-1, neutralization of S100A9, and pharmacologic inhibition of NLRP3 or NOX suppress pyroptosis, ROS generation, and nuclear beta-catenin in MDSs and are sufficient to restore effective hematopoiesis.	Reactive Oxygen Species	134-137	caspase 1	Homo sapiens	31-40
29911779-7	2017	Deoxyschizandrin (25, 50, 100, and 200 mumol L(-1)) could inhibit the activation of NLRP3 inflammasome caused by nigericin and ATP, and inhibit the secretion of IL-1beta, which was associated with inhibiting the cleavage of pro-caspase-1.	schizandrin A	0-16	caspase 1	Homo sapiens	228-237
29911779-9	2017	Our results confirmed that deoxyschizandrin could suppress the cleavage of pro-caspase-1 and inhibit the activity of NLRP3 inflammasome at 25-200 mumol L-1 to reduce the inflammation response.This study was conducted to investigate the inhibitory effect and the molecular mechanism of deoxyschizandrin on the activity of NLRP3 (NOD-like receptor family,pyrin domain containing 3) inflammasome.Bone marrow-derived macrophages were used to study the effects of deoxyschizandrin on inflammasome activation using inflammasome inducers (ATP and nigericin).	schizandrin A	27-43	caspase 1	Homo sapiens	79-88
27793997-7	2016	Dual activation of newborn DCs via the C-type lectin receptor, macrophage-inducible C-type lectin (trehalose-6,6-dibehenate), and TLR7/8 (R848) greatly enhanced caspase-1 and NF-kappaB activation, Th1 polarizing cytokine production and autologous Th1 polarization.	trehalose 6,6'-dibehenate	99-123	caspase 1	Homo sapiens	161-170
27705930-6	2016	Administration of berberine inhibited the viability, migration and invasion capacity of HepG2 cells through the induction of pyroptosis both in vitro and in vivo, which was attenuated by caspase-1 inhibitor Ac-YVAD-CMK.	Berberine	18-27	caspase 1	Homo sapiens	187-196
27705930-6	2016	Administration of berberine inhibited the viability, migration and invasion capacity of HepG2 cells through the induction of pyroptosis both in vitro and in vivo, which was attenuated by caspase-1 inhibitor Ac-YVAD-CMK.	ac-yvad	207-214	caspase 1	Homo sapiens	187-196
27803035-9	2016	In addition, aldosterone increased the expression of NLRP3, active caspase-1, and mature interleukin-1beta in human peripheral blood mononuclear cells.	Aldosterone	13-24	caspase 1	Homo sapiens	67-76
27373679-3	2016	In this regard, mitochondrial reactive oxygen species are emerging as perfect liaisons that can trigger the assembly and successive activation of large caspase-1- activating complexes known as inflammasomes.	Reactive Oxygen Species	30-53	caspase 1	Homo sapiens	152-161
27894300-0	2016	Pleural inhibition of the caspase-1/IL-1beta pathway diminishes profibrotic lung toxicity of bleomycin.	Bleomycin	93-102	caspase 1	Homo sapiens	26-35
27894300-4	2016	In this work, we explored the role of IL-1beta/caspase-1 signaling in bleomycin lung toxicity and in pleural mesothelial cell transformation.	Bleomycin	70-79	caspase 1	Homo sapiens	47-56
27894300-11	2016	In vitro, caspase-1 inhibition interfered with Met5A cell transformation into the myofibroblast-like phenotype induced by bleomycin or TGF-beta1.	Bleomycin	122-131	caspase 1	Homo sapiens	10-19
27894300-12	2016	Moreover, nigericin, a caspase-1 activator, triggered transformation of Met5A cells and its intra-pleural delivery induced fibrogenesis in mice.	Nigericin	10-19	caspase 1	Homo sapiens	23-32
27731349-3	2016	Here, we identified that HG (30 mM glucose for 48 h) induced the activation of the NLRP3-ASC inflammasome, leading to caspase-1 activation, and IL-1beta and IL-18 secretion in human monocytic cell lines.	Glucose	35-42	caspase 1	Homo sapiens	118-127
26320741-5	2016	LPS and Pam3csk4 also induced IRAK1/4-, ERK- and ROS-dependent activation of activator protein-1 (AP-1), IL-1beta transcription, and IL-1beta processing because significant inhibition in AP-1 activity, IL-1beta transcription, Pro- and mature IL-beta expression, and caspase-1 activity was observed with PD98059, U0126, DPI, NAC, an IRAK1/4 inhibitor, tanshinone IIa, and IRAK1 siRNA treatment.	Reactive Oxygen Species	49-52	caspase 1	Homo sapiens	266-275
27638862-10	2016	Interestingly, pro-IL-1beta and inflammasome components ASC and caspase-1 were released by ATP-activated macrophages through a vesicle-mediated secretion pathway.	Adenosine Triphosphate	91-94	caspase 1	Homo sapiens	64-73
27777559-5	2016	Results: Curcumin significantly reduced the expression of NLRP3 and cleavage of caspase-1 and IL-1beta secretion in PMA-induced macrophages.	Curcumin	9-17	caspase 1	Homo sapiens	80-89
27777559-5	2016	Results: Curcumin significantly reduced the expression of NLRP3 and cleavage of caspase-1 and IL-1beta secretion in PMA-induced macrophages.	Tetradecanoylphorbol Acetate	116-119	caspase 1	Homo sapiens	80-89
27777559-9	2016	Furthermore, curcumin reversed PMA-stimulated P2X7R activation, which further reduced the expression of NLRP3 and cleavage of caspase-1 and IL-1beta secretion.	Curcumin	13-21	caspase 1	Homo sapiens	126-135
27777559-9	2016	Furthermore, curcumin reversed PMA-stimulated P2X7R activation, which further reduced the expression of NLRP3 and cleavage of caspase-1 and IL-1beta secretion.	Tetradecanoylphorbol Acetate	31-34	caspase 1	Homo sapiens	126-135
27452280-5	2016	We found that ZnO delay human eosinophil apoptosis, partially by inhibiting caspases and by preventing caspase-4 and Bcl-xL degradation.	Zinc Oxide	14-17	caspase 1	Homo sapiens	76-84
27636508-6	2016	We found that PMACI induced caspase-1/nuclear factor (NF)-kappaB/mitogen activated protein kinases (MAPKs) activation.	pmaci	14-19	caspase 1	Homo sapiens	28-52
27636508-7	2016	PMACI-caused caspase-1/NF-kappaB/MAPKs activations were attenuated by Atr and KMP6.	pmaci	0-5	caspase 1	Homo sapiens	13-22
27452280-8	2016	Using a pharmacological approach, we demonstrated that inhibition of caspase-1 reversed the ability of ZnO to induce IL-1beta and IL-8 production, whereas inhibition of caspase-4 only reversed that of IL-8.	Zinc Oxide	103-106	caspase 1	Homo sapiens	69-78
28598074-6	2016	The Z-VAD group, the PD98059 group and the SF+H2O2 group resisted the effects of H2O2 on A549 cells by decreasing the mRNA and protein expressions of caspase-1 and NALP3,and the protein expression of p-ERK/ERK, as well as reducing the secretion of IL-1beta(P&lt;0.05),when compared with the H2O2 group.	Hydrogen Peroxide	81-85	caspase 1	Homo sapiens	150-159
27376852-0	2016	A novel compound 2-(4-{2-[(phenylthio)acetyl]carbonohydrazonoyl}phenoxy)acetamide downregulates TSLP through blocking of caspase-1/NF-kappaB pathways.	2-(4-(2-((phenylthio)acetyl)carbonohydrazonoyl)phenoxy)acetamide	17-81	caspase 1	Homo sapiens	121-130
27376852-8	2016	Caspase-1 activation was up-regulated in activated HMC-1 cells, whereas caspase-1 activation was down-regulated by PA.	2-(4-(2-((phenylthio)acetyl)carbonohydrazonoyl)phenoxy)acetamide	115-117	caspase 1	Homo sapiens	72-81
28598074-5	2016	RESULTS: Compared with the control group,H2O2 not only increased the mRNA and protein expression levels of caspase-1 and NALP3 and the protein expression levels of p-ERK/ERK, but also enhanced the secretion of IL-1beta in human lung epithelial cells A549 (P&lt;0.05),while SF group showed no statistic significance of those indicators above (P&gt;0.05).	Hydrogen Peroxide	41-45	caspase 1	Homo sapiens	107-116
28598074-6	2016	The Z-VAD group, the PD98059 group and the SF+H2O2 group resisted the effects of H2O2 on A549 cells by decreasing the mRNA and protein expressions of caspase-1 and NALP3,and the protein expression of p-ERK/ERK, as well as reducing the secretion of IL-1beta(P&lt;0.05),when compared with the H2O2 group.	Hydrogen Peroxide	81-85	caspase 1	Homo sapiens	150-159
28598074-6	2016	The Z-VAD group, the PD98059 group and the SF+H2O2 group resisted the effects of H2O2 on A549 cells by decreasing the mRNA and protein expressions of caspase-1 and NALP3,and the protein expression of p-ERK/ERK, as well as reducing the secretion of IL-1beta(P&lt;0.05),when compared with the H2O2 group.	z-vad	4-9	caspase 1	Homo sapiens	150-159
27470352-7	2016	RESULTS: It was shown that atorvastatin significantly reduced the expression of NLRP3, the cleavage of caspase-1 and IL-1beta in PMA-induced THP-1 cells.	Atorvastatin	27-39	caspase 1	Homo sapiens	103-112
28598074-6	2016	The Z-VAD group, the PD98059 group and the SF+H2O2 group resisted the effects of H2O2 on A549 cells by decreasing the mRNA and protein expressions of caspase-1 and NALP3,and the protein expression of p-ERK/ERK, as well as reducing the secretion of IL-1beta(P&lt;0.05),when compared with the H2O2 group.	Hydrogen Peroxide	46-50	caspase 1	Homo sapiens	150-159
27297387-7	2016	The inhibition assay showed that CA-074 (a cathepsin B inhibitor), glybenclamide (an NLRP3 molecule inhibitor), and N-benzyloxycarbony-Val-Ala-Asp(O-methyl)-fluoromethylketone (Z-VAD-FMK; a caspase-1 inhibitor) reduced the levels of caspase-1 activation and IL-1beta production from THP-1 cells.	n-benzyloxycarbony-val-ala-asp(o-methyl)-fluoromethylketone	116-175	caspase 1	Homo sapiens	233-242
27280600-7	2016	RESULTS: The collected expression and CGH microarray experiment results indicate that the ITGB2, SCL6A7, CASP1 and DUSP genes may comprise a resistance marker for acute leukemia cells correlated with anthracyclines.	Anthracyclines	200-214	caspase 1	Homo sapiens	105-110
27096899-2	2016	Upon lipopolysaccharide (LPS) triggering of toll-like receptor (TLR)-4 and subsequent ATP signaling, the NOD-like receptor containing-pyrin domain 3 (NLRP3) inflammasome is activated to cleave pro-caspase-1 into caspase-1, allowing the secretion of IL-1beta.	Adenosine Triphosphate	86-89	caspase 1	Homo sapiens	197-206
27096899-2	2016	Upon lipopolysaccharide (LPS) triggering of toll-like receptor (TLR)-4 and subsequent ATP signaling, the NOD-like receptor containing-pyrin domain 3 (NLRP3) inflammasome is activated to cleave pro-caspase-1 into caspase-1, allowing the secretion of IL-1beta.	Adenosine Triphosphate	86-89	caspase 1	Homo sapiens	212-221
27300134-7	2016	Palmitic acid stimulated caspase-1 activation and markedly increased interleukin (IL)-1beta secretion in Sw.71 cells.	Palmitic Acid	0-13	caspase 1	Homo sapiens	25-34
27300134-8	2016	Treatment with a caspase-1 inhibitor diminished palmitic acid-induced IL-1beta release.	Palmitic Acid	48-61	caspase 1	Homo sapiens	17-26
27300134-9	2016	In addition, NLRP3 and caspase-1 genome editing using a CRISPR/Cas9 system in Sw.71 cells suppressed IL-1beta secretion, which was stimulated by palmitic acid.	Palmitic Acid	145-158	caspase 1	Homo sapiens	23-32
27154322-9	2016	The expression levels of NLRP3, caspase-1, and AQP4 increased after 6h of OGD, but probenecid treatment attenuated this increase.	Probenecid	83-93	caspase 1	Homo sapiens	32-41
27341352-0	2016	Quantitative Analysis of Caspase-1 Activity in Living Cells Through Dynamic Equilibrium of Chlorophyll-Based Nano-assembly Modulated Photoacoustic Signals.	Chlorophyll	91-102	caspase 1	Homo sapiens	25-34
27341352-3	2016	The dynamic process of self-assembly of chlorophyll-based molecules in complex biological systems can be monitored by photoacoustic signals, which supports a noninvasive way to understand and quantitatively measure the activity of caspase-1.	Chlorophyll	40-51	caspase 1	Homo sapiens	231-240
27219123-1	2016	INTRODUCTION: Gout is considered to be an autoinflammatory disease and the presence of monosodium urate (MSU) crystals stimulates activation of NPRL3 inflammasome and subsequently caspase-1, generating production of active IL-1beta and IL-18.	Uric Acid	87-103	caspase 1	Homo sapiens	180-189
27129183-0	2016	Colchicine therapy in acute coronary syndrome patients acts on caspase-1 to suppress NLRP3 inflammasome monocyte activation.	Colchicine	0-10	caspase 1	Homo sapiens	63-72
27129183-9	2016	Colchicine treatment in ACS patients markedly reduced intracellular and secreted levels of IL-1beta compared with pre-treatment levels (P&lt;0.05 for both), as well as significantly reducing pro-caspase-1 mRNA levels by 57.7% and secreted caspase-1 protein levels by 30.2% compared with untreated patients (P&lt;0.05 for both).	Colchicine	0-10	caspase 1	Homo sapiens	195-204
27129183-9	2016	Colchicine treatment in ACS patients markedly reduced intracellular and secreted levels of IL-1beta compared with pre-treatment levels (P&lt;0.05 for both), as well as significantly reducing pro-caspase-1 mRNA levels by 57.7% and secreted caspase-1 protein levels by 30.2% compared with untreated patients (P&lt;0.05 for both).	Colchicine	0-10	caspase 1	Homo sapiens	239-248
27129183-10	2016	Monocytes from ACS patients are "primed" to secrete inflammasome-related cytokines and short-term colchicine acutely and markedly suppresses monocyte caspase-1 activity, thereby reducing monocyte secretion of IL-1beta.	Colchicine	98-108	caspase 1	Homo sapiens	150-159
27219123-1	2016	INTRODUCTION: Gout is considered to be an autoinflammatory disease and the presence of monosodium urate (MSU) crystals stimulates activation of NPRL3 inflammasome and subsequently caspase-1, generating production of active IL-1beta and IL-18.	Uric Acid	105-108	caspase 1	Homo sapiens	180-189
27006445-0	2016	Caspase-1 Inflammasome Activation Mediates Homocysteine-Induced Pyrop-Apoptosis in Endothelial Cells.	Homocysteine	43-55	caspase 1	Homo sapiens	0-9
27321752-8	2016	These results indicate that in case of HIV infected macrophages exposed to cocaine, increased ROS production and IL-1beta transcription serve as an activators for the formation of NLRP3 and AIM2 mediated inflammasomes that leads to caspase 1 mediated apoptosis.	Cocaine	75-82	caspase 1	Homo sapiens	232-241
27321752-8	2016	These results indicate that in case of HIV infected macrophages exposed to cocaine, increased ROS production and IL-1beta transcription serve as an activators for the formation of NLRP3 and AIM2 mediated inflammasomes that leads to caspase 1 mediated apoptosis.	ros	94-97	caspase 1	Homo sapiens	232-241
27210890-8	2016	In addition, RA significantly inhibited poly(I:C)-induced inflammasome activation, in terms of secretion of active form of IL-1beta and caspase-1.	rosmarinic acid	13-15	caspase 1	Homo sapiens	136-145
27210890-8	2016	In addition, RA significantly inhibited poly(I:C)-induced inflammasome activation, in terms of secretion of active form of IL-1beta and caspase-1.	Poly I-C	40-49	caspase 1	Homo sapiens	136-145
27103438-5	2016	Ro5-4864 efficiently attenuated NLRP3 translocation to mitochondria, inflammasome assembly/oligomerization, activation of caspase-1, and subsequent secretion of the mature forms of interleukin-1beta and -18.	4'-chlorodiazepam	0-8	caspase 1	Homo sapiens	122-131
27076678-4	2016	HIV/TB patients exhibited higher proportions of monocytes expressing activated caspase-1 (casp1) pre-cART, compared with HIV patients without TB, and patients who developed TB-IRIS exhibited the greatest increase in casp1 expression.	Terbium	4-6	caspase 1	Homo sapiens	79-88
27076678-4	2016	HIV/TB patients exhibited higher proportions of monocytes expressing activated caspase-1 (casp1) pre-cART, compared with HIV patients without TB, and patients who developed TB-IRIS exhibited the greatest increase in casp1 expression.	Terbium	4-6	caspase 1	Homo sapiens	90-95
27076678-4	2016	HIV/TB patients exhibited higher proportions of monocytes expressing activated caspase-1 (casp1) pre-cART, compared with HIV patients without TB, and patients who developed TB-IRIS exhibited the greatest increase in casp1 expression.	Terbium	4-6	caspase 1	Homo sapiens	216-221
26959386-12	2016	The NADPH oxidase inhibitor DPI and high extracellular potassium ion suppressed the production of IL-1beta, caspase-1, and the expression of NLRP3 and ASC proteins.	3-aminodiphenyleneiodium	28-31	caspase 1	Homo sapiens	108-117
26959386-12	2016	The NADPH oxidase inhibitor DPI and high extracellular potassium ion suppressed the production of IL-1beta, caspase-1, and the expression of NLRP3 and ASC proteins.	Potassium	55-64	caspase 1	Homo sapiens	108-117
26959386-13	2016	The specific NF-kappaB inhibitor, Bay 11-7082, inhibited IL-1beta production, and also inhibited the production of caspase-1, ASC and NLRP3 proteins.	3-(4-methylphenylsulfonyl)-2-propenenitrile	34-45	caspase 1	Homo sapiens	115-124
27194621-0	2016	Endocytosis of indium-tin-oxide nanoparticles by macrophages provokes pyroptosis requiring NLRP3-ASC-Caspase1 axis that can be prevented by mesenchymal stem cells.	indium tin oxide	15-31	caspase 1	Homo sapiens	101-109
27006445-6	2016	Finally, homocysteine-induced DNA fragmentation was reversed in caspase-1(-/-) EC.	Homocysteine	9-21	caspase 1	Homo sapiens	64-73
26685094-9	2016	In addition, the mRNA expression analyses revealed that HepG2.2.15 cells exposed to 0.8mM sophoridine showed reduced levels of p38 MAPK, TRAF6, ERK1, NLRP10, and caspase-1.	matrine	90-101	caspase 1	Homo sapiens	162-171
27190722-0	2016	Relationship between triterpenoid anticancer drug resistance, autophagy, and caspase-1 in adult T-cell leukemia.	triterpenoid TP-222	21-33	caspase 1	Homo sapiens	77-86
27153094-7	2016	By mutating the potential cleavage sites, we identified aspartic acid (Asp/D) 130 as the ICE cut site in tIL-1beta.	Aspartic Acid	56-69	caspase 1	Homo sapiens	89-92
27153094-7	2016	By mutating the potential cleavage sites, we identified aspartic acid (Asp/D) 130 as the ICE cut site in tIL-1beta.	Aspartic Acid	71-74	caspase 1	Homo sapiens	89-92
27153094-7	2016	By mutating the potential cleavage sites, we identified aspartic acid (Asp/D) 130 as the ICE cut site in tIL-1beta.	Deuterium	75-76	caspase 1	Homo sapiens	89-92
26987291-6	2016	The killing effect of RH2 was reduced by pan-caspase inhibitor z-VAD-fmk and the caspase-1 inhibitor z-YVAD-fmk, suggesting the involvement of apoptosis and pyroptosis.	benzyloxycarbonyltyrosyl-valyl-alanyl-aspartic acid fluoromethyl ketone	101-111	caspase 1	Homo sapiens	81-90
26825457-0	2016	Aluminum-doped zinc oxide nanoparticles attenuate the TSLP levels via suppressing caspase-1 in activated mast cells.	Aluminum	0-8	caspase 1	Homo sapiens	82-91
26865578-3	2016	Baicalin at 50 microg/ml and 100 microg/ml could inhibit the production of ROS, TNF-alpha, IL-1beta and IL-18, and down-regulate mRNA expression of IL-1beta, IL-18, TNF-alpha and NLRP3, as well as expression of cleaved caspase-1 p20.	baicalin	0-8	caspase 1	Homo sapiens	219-228
26825457-0	2016	Aluminum-doped zinc oxide nanoparticles attenuate the TSLP levels via suppressing caspase-1 in activated mast cells.	Zinc Oxide	15-25	caspase 1	Homo sapiens	82-91
26825457-4	2016	Here, we reported the efficacy of aluminum-doped ZO-NP (AZO) on thymic stromal lymphopoietin (TSLP) production and caspase-1 activation in human mast cell line, HMC-1 cells.	aluminum-doped	34-48	caspase 1	Homo sapiens	115-124
26588458-14	2016	ICE (ifosfamide, carboplatin, etoposide) chemotherapy was administered prior to and after RT for a total of 6-8 cycles.	Ifosfamide	5-15	caspase 1	Homo sapiens	0-3
26809137-4	2016	The Cd-induced cell death was identified as pyroptosis, a novel pro-inflammatory form of cell death depending on caspase-1 activation.	Cadmium	4-6	caspase 1	Homo sapiens	113-122
26809137-5	2016	In addition, exposure of HUVECs to Cd resulted in NLRP3 inflammasome activation as evidenced by cleavage of caspase-1 and downstream interleukin (IL)-1beta production.	Cadmium	35-37	caspase 1	Homo sapiens	108-117
26809137-6	2016	Moreover, knockdown of NLRP3 by small interfering RNA efficiently suppressed Cd-induced caspase-1 cleavage, IL-1beta production and pyroptosis in HUVECs.	Cadmium	77-79	caspase 1	Homo sapiens	88-97
27471628-7	2016	The data from current study show sub-chronic arsenic exposure activates AIM2 inflammasome which in turn activates caspase-1 and enhances the secretion of IL-1beta and IL-18 in HaCaT cells and the skin of BALB/c mice.	Arsenic	45-52	caspase 1	Homo sapiens	114-123
26801583-7	2016	Disrupting the autophagy-lysosomal pathway through chloroquine or ATG5-siRNA exacerbated AgNPs-induced caspase-1 activation and lactate dehydrogenase release, suggesting that NLRP3-inflammasome plays an important role in AgNPs-induced cytotoxicity.	Chloroquine	51-62	caspase 1	Homo sapiens	103-112
26718495-7	2016	Furthermore, SAT ceramide concentrations correlated with the expression of CASP1 and IL1B.	Ceramides	17-25	caspase 1	Homo sapiens	75-80
26588458-14	2016	ICE (ifosfamide, carboplatin, etoposide) chemotherapy was administered prior to and after RT for a total of 6-8 cycles.	Carboplatin	17-28	caspase 1	Homo sapiens	0-3
26588458-14	2016	ICE (ifosfamide, carboplatin, etoposide) chemotherapy was administered prior to and after RT for a total of 6-8 cycles.	Etoposide	30-39	caspase 1	Homo sapiens	0-3
26928328-5	2016	Inhibition of caspase-1 blocked VTX-2337-mediated NLRP3 inflammasome activation, but had little impact on production of other TLR8-induced mediators such as TNFalpha.	VTX-2337	32-40	caspase 1	Homo sapiens	14-23
26454448-7	2016	Rebamipide also attenuated enhanced expression of caspase-1 gene by MSU crystals (p &lt; 0.05).	rebamipide	0-10	caspase 1	Homo sapiens	50-59
26929603-7	2016	RESULTS: ANDRO ameliorated the increase in the intracellular calcium, protein, and messenger RNA levels of TSLP induced by phorbol myristate acetate/calcium ionophore A23187, through the blocking of the receptor-interacting protein 2/caspase-1/NF-kappaB pathway in human mast cell line 1 cells.	Tetradecanoylphorbol Acetate	123-148	caspase 1	Homo sapiens	234-243
26929603-7	2016	RESULTS: ANDRO ameliorated the increase in the intracellular calcium, protein, and messenger RNA levels of TSLP induced by phorbol myristate acetate/calcium ionophore A23187, through the blocking of the receptor-interacting protein 2/caspase-1/NF-kappaB pathway in human mast cell line 1 cells.	Calcium	149-156	caspase 1	Homo sapiens	234-243
26929603-7	2016	RESULTS: ANDRO ameliorated the increase in the intracellular calcium, protein, and messenger RNA levels of TSLP induced by phorbol myristate acetate/calcium ionophore A23187, through the blocking of the receptor-interacting protein 2/caspase-1/NF-kappaB pathway in human mast cell line 1 cells.	Calcimycin	167-173	caspase 1	Homo sapiens	234-243
26577567-7	2016	This ferric ammonium citrate-induced interleukin-1beta production is dependent on caspase-1 and is significantly inhibited by an Fe(2+)-specific chelator.	ferric ammonium citrate	5-28	caspase 1	Homo sapiens	82-91
26454448-0	2016	Rebamipide Suppresses Monosodium Urate Crystal-Induced Interleukin-1beta Production Through Regulation of Oxidative Stress and Caspase-1 in THP-1 Cells.	rebamipide	0-10	caspase 1	Homo sapiens	127-136
26454448-0	2016	Rebamipide Suppresses Monosodium Urate Crystal-Induced Interleukin-1beta Production Through Regulation of Oxidative Stress and Caspase-1 in THP-1 Cells.	Uric Acid	22-38	caspase 1	Homo sapiens	127-136
26616294-0	2016	Atrial natriuretic peptide down-regulates LPS/ATP-mediated IL-1beta release by inhibiting NF-kB, NLRP3 inflammasome and caspase-1 activation in THP-1 cells.	Adenosine Triphosphate	46-49	caspase 1	Homo sapiens	120-129
26616294-9	2016	The aim of our study was to evaluate the effect of ANP on IL-1beta/NALP3/caspase-1 expression in LPS/ATP-stimulated human THP1 monocytes.	Adenosine Triphosphate	101-104	caspase 1	Homo sapiens	73-82
26616294-10	2016	We provided new evidence of the direct involvement of ANP/NPR-1/cGMP axis on NF-kB/NALP3/caspase-1-mediated IL-1beta release and NF-kB-mediated pro-IL-1beta production.	Cyclic GMP	64-68	caspase 1	Homo sapiens	89-98
26454448-11	2016	This study demonstrated that rebamipide inhibits IL-1beta activation through suppression of ROS-mediated NF-kappaB signaling pathways and caspase-1 activation in MSU crystal-induced inflammation.	rebamipide	29-39	caspase 1	Homo sapiens	138-147
26555265-4	2016	We observed QS-21 to elicit caspase-1-dependent IL-1beta and IL-18 release in antigen-presenting cells such as macrophages and dendritic cells when co-stimulated with the TLR4-agonist adjuvant monophosphoryl lipid A.	saponin QA-21V1	12-17	caspase 1	Homo sapiens	28-37
26827637-3	2016	The results showed that sulforaphane preferentially inhibited cathepsin B- and caspase-1-dependent NLRP3 inflammasome activation induced by mostly Abeta1-42 monomers, an effect that potently reduced excessive secretion of the proinflammatory cytokine interleukin-1beta (IL-1beta).	sulforaphane	24-36	caspase 1	Homo sapiens	79-88
26707913-0	2016	Methotrexate regulates Th-1 response by suppressing caspase-1 and cytokines in psoriasis patients.	Methotrexate	0-12	caspase 1	Homo sapiens	52-61
26555265-6	2016	At higher concentrations, QS-21 induced macrophage and dendritic cell death in a caspase-1-, ASC-, and NLRP3-independent manner, whereas the presence of cholesterol rescued cell viability.	saponin QA-21V1	26-31	caspase 1	Homo sapiens	81-90
26663311-11	2016	Necrotic-like cell death was also suppressed by this compound and the caspase-1 inhibitor Ac-YVAD-CMK, indicating that histones triggered ECFC pyroptosis.	ac-yvad	90-97	caspase 1	Homo sapiens	70-79
26709853-3	2016	We present DNP-enhanced MAS NMR studies of tubular assemblies of CA and Gag CA-SP1 maturation intermediate and report 20-64-fold sensitivity enhancements due to DNP at 14.1 T. These sensitivity enhancements enabled direct observation of spacer peptide 1 (SP1) resonances in CA-SP1 by dipolar-based correlation experiments, unequivocally indicating that the SP1 peptide is unstructured in assembled CA-SP1 at cryogenic temperatures, corroborating our earlier results.	2,4-Dinitrophenol	11-14	caspase 1	Homo sapiens	76-82
26709853-3	2016	We present DNP-enhanced MAS NMR studies of tubular assemblies of CA and Gag CA-SP1 maturation intermediate and report 20-64-fold sensitivity enhancements due to DNP at 14.1 T. These sensitivity enhancements enabled direct observation of spacer peptide 1 (SP1) resonances in CA-SP1 by dipolar-based correlation experiments, unequivocally indicating that the SP1 peptide is unstructured in assembled CA-SP1 at cryogenic temperatures, corroborating our earlier results.	2,4-Dinitrophenol	11-14	caspase 1	Homo sapiens	274-280
26709853-3	2016	We present DNP-enhanced MAS NMR studies of tubular assemblies of CA and Gag CA-SP1 maturation intermediate and report 20-64-fold sensitivity enhancements due to DNP at 14.1 T. These sensitivity enhancements enabled direct observation of spacer peptide 1 (SP1) resonances in CA-SP1 by dipolar-based correlation experiments, unequivocally indicating that the SP1 peptide is unstructured in assembled CA-SP1 at cryogenic temperatures, corroborating our earlier results.	2,4-Dinitrophenol	11-14	caspase 1	Homo sapiens	274-280
26709853-3	2016	We present DNP-enhanced MAS NMR studies of tubular assemblies of CA and Gag CA-SP1 maturation intermediate and report 20-64-fold sensitivity enhancements due to DNP at 14.1 T. These sensitivity enhancements enabled direct observation of spacer peptide 1 (SP1) resonances in CA-SP1 by dipolar-based correlation experiments, unequivocally indicating that the SP1 peptide is unstructured in assembled CA-SP1 at cryogenic temperatures, corroborating our earlier results.	Glycosaminoglycans	72-75	caspase 1	Homo sapiens	76-82
26709853-3	2016	We present DNP-enhanced MAS NMR studies of tubular assemblies of CA and Gag CA-SP1 maturation intermediate and report 20-64-fold sensitivity enhancements due to DNP at 14.1 T. These sensitivity enhancements enabled direct observation of spacer peptide 1 (SP1) resonances in CA-SP1 by dipolar-based correlation experiments, unequivocally indicating that the SP1 peptide is unstructured in assembled CA-SP1 at cryogenic temperatures, corroborating our earlier results.	2,4-Dinitrophenol	161-164	caspase 1	Homo sapiens	274-280
26709853-3	2016	We present DNP-enhanced MAS NMR studies of tubular assemblies of CA and Gag CA-SP1 maturation intermediate and report 20-64-fold sensitivity enhancements due to DNP at 14.1 T. These sensitivity enhancements enabled direct observation of spacer peptide 1 (SP1) resonances in CA-SP1 by dipolar-based correlation experiments, unequivocally indicating that the SP1 peptide is unstructured in assembled CA-SP1 at cryogenic temperatures, corroborating our earlier results.	2,4-Dinitrophenol	161-164	caspase 1	Homo sapiens	274-280
26555265-4	2016	We observed QS-21 to elicit caspase-1-dependent IL-1beta and IL-18 release in antigen-presenting cells such as macrophages and dendritic cells when co-stimulated with the TLR4-agonist adjuvant monophosphoryl lipid A.	monophosphoryl	193-207	caspase 1	Homo sapiens	28-37
26555265-4	2016	We observed QS-21 to elicit caspase-1-dependent IL-1beta and IL-18 release in antigen-presenting cells such as macrophages and dendritic cells when co-stimulated with the TLR4-agonist adjuvant monophosphoryl lipid A.	Lipid A	208-215	caspase 1	Homo sapiens	28-37
26612442-8	2016	Elevated levels of calcium acting via the CaSR can function as a danger signal that stimulates assembly of myeloid cell cytosolic multiprotein inflammasomes resulting in maturation of the proinflammatory cytokine IL-1beta by caspase-1.	Calcium	19-26	caspase 1	Homo sapiens	225-234
26725432-0	2016	Cordycepin Suppresses Thymic Stromal Lymphopoietin Expression via Blocking Caspase-1 and Receptor-Interacting Protein 2 Signaling Pathways in Mast Cells.	cordycepin	0-10	caspase 1	Homo sapiens	75-119
26187854-3	2016	The stimulatory effect of sphingosine or 77-6 on LPS-stimulated IL-1beta release was reduced by pretreatment of cells with the caspase-1 inhibitor, Ac-YVAD-CHO, thereby indicating a role for the inflammasome.	Sphingosine	26-37	caspase 1	Homo sapiens	127-136
26187854-3	2016	The stimulatory effect of sphingosine or 77-6 on LPS-stimulated IL-1beta release was reduced by pretreatment of cells with the caspase-1 inhibitor, Ac-YVAD-CHO, thereby indicating a role for the inflammasome.	L 709049	148-159	caspase 1	Homo sapiens	127-136
26355761-7	2016	Also, we found that homoplantaginin tightly controlled PA-induced reactive oxygen species to prevent nucleotide-binding domain-like receptor 3 (NLRP3) inflammasome activation by suppressing reactive oxygen species-sensitive thioredoxin-interacting protein, NLRP3, and caspase-1.	Palmitic Acid	55-57	caspase 1	Homo sapiens	268-277
26355761-7	2016	Also, we found that homoplantaginin tightly controlled PA-induced reactive oxygen species to prevent nucleotide-binding domain-like receptor 3 (NLRP3) inflammasome activation by suppressing reactive oxygen species-sensitive thioredoxin-interacting protein, NLRP3, and caspase-1.	Reactive Oxygen Species	66-89	caspase 1	Homo sapiens	268-277
26355761-7	2016	Also, we found that homoplantaginin tightly controlled PA-induced reactive oxygen species to prevent nucleotide-binding domain-like receptor 3 (NLRP3) inflammasome activation by suppressing reactive oxygen species-sensitive thioredoxin-interacting protein, NLRP3, and caspase-1.	Reactive Oxygen Species	190-213	caspase 1	Homo sapiens	268-277
26546608-2	2015	The NLRP3 inflammasome mediates caspase-1 activation and subsequent IL-1beta processing in response to various stimuli, including extracellular ATP, although the roles of intracellular ATP (iATP) in NLRP3 activation remain unclear.	Adenosine Triphosphate	144-147	caspase 1	Homo sapiens	32-41
26593037-5	2015	We studied the inhibitory effects of chicoric acid on the nuclear translocation of nuclear factor kappa B (NF-kappaB) and activation of caspase-1.	chicoric acid	37-50	caspase 1	Homo sapiens	136-145
26689911-5	2015	Based on our preliminary findings we hypothesized that treatment of MMs with chemotherapeutic drugs may elevate the levels of NLRP3 and caspase-1 resulting in increased cell death by pyroptosis while increasing the levels of IL-1beta and other pro-inflammatory molecules.	Methyl Methanesulfonate	68-71	caspase 1	Homo sapiens	136-145
26546608-3	2015	In this study, we found that in activated macrophages artificial reduction of iATP by 2-deoxyglucose, a glycolysis inhibitor, caused mitochondrial membrane depolarization, leading to IL-1beta secretion via NLRP3 and caspase-1 activation.	Deoxyglucose	86-100	caspase 1	Homo sapiens	216-225
26668503-7	2015	In HepG2 cells, PA and LPS treatment markedly increased mRNA of several nucleotide-binding and oligomerization domain-like receptor family members (NLRP3, NLRP6, and NLRP10), caspase-1 and IL-1beta.	Palmitic Acid	16-18	caspase 1	Homo sapiens	175-184
26400108-0	2015	Methylene Blue Inhibits Caspases by Oxidation of the Catalytic Cysteine.	Methylene Blue	0-14	caspase 1	Homo sapiens	24-32
26384528-6	2015	In addition, high glucose concentration and fatty acids independently activate inflammasome, an intracellular multi-protein complex that promotes the proteolytic activation of caspase 1, leading to the processing and secretion of IL-1beta.	Glucose	18-25	caspase 1	Homo sapiens	176-185
26384528-6	2015	In addition, high glucose concentration and fatty acids independently activate inflammasome, an intracellular multi-protein complex that promotes the proteolytic activation of caspase 1, leading to the processing and secretion of IL-1beta.	Fatty Acids	44-55	caspase 1	Homo sapiens	176-185
26116704-4	2015	Moreover, the caspase 1 inhibitor Z-YVAD-FMK and the cathepsin B inhibitor CA-074Me reduced production of IL-1beta in a dose-dependent manner after LPS + MSU treatment.	benzyloxycarbonyltyrosyl-valyl-alanyl-aspartic acid fluoromethyl ketone	34-44	caspase 1	Homo sapiens	14-23
25903262-8	2015	Pathologically activated caspase-1 and caspase-3 decreased their activities in the presence of hepatoprotectors with melaxen showing the highest effect.	Melatonin	117-124	caspase 1	Homo sapiens	25-34
26168332-5	2015	Subordination of the Th1 response to caspase-1, effector of the inflammasome, was determined in explant cultures subjected to pharmacological inhibition of caspase-1 by YVAD.	YVAD	169-173	caspase 1	Homo sapiens	37-46
26168332-5	2015	Subordination of the Th1 response to caspase-1, effector of the inflammasome, was determined in explant cultures subjected to pharmacological inhibition of caspase-1 by YVAD.	YVAD	169-173	caspase 1	Homo sapiens	156-165
26168332-7	2015	Inhibition of caspase-1 activation using the specific inhibitor YVAD identified a homogenous non responder group featuring a caspase-1-independent IL-18/IFN-gamma response, and a heterogenous responder group, in which both IL-18 and IFN-gamma responses were caspase-1-dependent, with a 40-70% range of inhibition by YVAD.	YVAD	64-68	caspase 1	Homo sapiens	14-23
26168332-7	2015	Inhibition of caspase-1 activation using the specific inhibitor YVAD identified a homogenous non responder group featuring a caspase-1-independent IL-18/IFN-gamma response, and a heterogenous responder group, in which both IL-18 and IFN-gamma responses were caspase-1-dependent, with a 40-70% range of inhibition by YVAD.	YVAD	316-320	caspase 1	Homo sapiens	14-23
26453510-0	2015	Attenuation of IL-32-induced caspase-1 and nuclear factor-kappaB activations by acteoside.	acteoside	80-89	caspase 1	Homo sapiens	29-38
26453510-6	2015	Acteoside attenuated IL-32-induced caspase-1 and nuclear factor-kappaB activations in THP-1 cells.	acteoside	0-9	caspase 1	Homo sapiens	35-44
26494301-9	2015	Furthermore, treatment with EGCG attenuated poly(dA:dT)-induced ASC oligomerization and caspase-1 activation in IFN-gamma-primed HEKn cells.	epigallocatechin gallate	28-32	caspase 1	Homo sapiens	88-97
26494301-9	2015	Furthermore, treatment with EGCG attenuated poly(dA:dT)-induced ASC oligomerization and caspase-1 activation in IFN-gamma-primed HEKn cells.	poly	44-48	caspase 1	Homo sapiens	88-97
26494301-9	2015	Furthermore, treatment with EGCG attenuated poly(dA:dT)-induced ASC oligomerization and caspase-1 activation in IFN-gamma-primed HEKn cells.	amsonic acid	49-51	caspase 1	Homo sapiens	88-97
26494301-9	2015	Furthermore, treatment with EGCG attenuated poly(dA:dT)-induced ASC oligomerization and caspase-1 activation in IFN-gamma-primed HEKn cells.	Thymidine	52-54	caspase 1	Homo sapiens	88-97
26416893-4	2015	Rotenone-induced priming of NLRP3 in the presence of ATP triggered the formation of specklike NLRP3 or ASC aggregates and the association of NLRP3 with ASC, resulting in NLRP3-dependent caspase-1 activation.	Rotenone	0-8	caspase 1	Homo sapiens	186-195
26416893-4	2015	Rotenone-induced priming of NLRP3 in the presence of ATP triggered the formation of specklike NLRP3 or ASC aggregates and the association of NLRP3 with ASC, resulting in NLRP3-dependent caspase-1 activation.	Adenosine Triphosphate	53-56	caspase 1	Homo sapiens	186-195
26417837-1	2015	A general synthetic strategy to cis-fused bicyclic gamma-butyrolactones via the retro-Diels-Alder reaction/intramolecular conjugate ene cascade (RDA/ICE) reaction under the flash-vacuum pyrolysis of maleic anhydride adducts is developed.	4-Butyrolactone	51-71	caspase 1	Homo sapiens	149-152
26327597-12	2015	LDL(-) triggered 2-fold caspase-1 activation compared to native LDL and IL-1beta release was strongly diminished in the presence of the caspase-1 inhibitor Z-YVAD.	z-yvad	156-162	caspase 1	Homo sapiens	24-33
26327597-12	2015	LDL(-) triggered 2-fold caspase-1 activation compared to native LDL and IL-1beta release was strongly diminished in the presence of the caspase-1 inhibitor Z-YVAD.	z-yvad	156-162	caspase 1	Homo sapiens	136-145
25871734-0	2015	Lazaroids U83836E and U74389G are potent, time-dependent inhibitors of caspase-1.	lazaroids	0-9	caspase 1	Homo sapiens	71-80
25871734-0	2015	Lazaroids U83836E and U74389G are potent, time-dependent inhibitors of caspase-1.	U 78517F	10-17	caspase 1	Homo sapiens	71-80
25871734-0	2015	Lazaroids U83836E and U74389G are potent, time-dependent inhibitors of caspase-1.	U 74389F	22-28	caspase 1	Homo sapiens	71-80
26502906-4	2016	The treatment of cells with a chemical inhibitor of glycosphingolipid biosynthesis, which suppresses the expression of the Stx receptor globotriaosylceramide and subsequent endocytosis of the toxin, substantially blocked activation of the NLRP3 inflammasome and processing of caspase-1 and IL-1beta.	Glycosphingolipids	52-69	caspase 1	Homo sapiens	276-285
26277554-7	2015	ATP-induced microvesicle formation, exosome release, and K(+) efflux followed by caspase-1 activation are likely involved in the GAPDH release, but ATP-induced dilatation of membrane pores and lysosome exocytosis are not.	Adenosine Triphosphate	0-3	caspase 1	Homo sapiens	81-90
26605247-14	2015	CONCLUSIONS: We show here that chronic inflammation decrease caspase-1 expression and exposure of human lymphocytes to TCDD promote caspase-1 expression.	Polychlorinated Dibenzodioxins	119-123	caspase 1	Homo sapiens	132-141
26400108-0	2015	Methylene Blue Inhibits Caspases by Oxidation of the Catalytic Cysteine.	Cysteine	63-71	caspase 1	Homo sapiens	24-32
26400108-2	2015	Here, we investigated if methylene blue can inhibit caspases via the oxidation of their active site cysteine.	Methylene Blue	25-39	caspase 1	Homo sapiens	52-60
26400108-2	2015	Here, we investigated if methylene blue can inhibit caspases via the oxidation of their active site cysteine.	Cysteine	100-108	caspase 1	Homo sapiens	52-60
26400108-4	2015	Methylene blue also inhibited recombinant Casp1 and Casp3.	Methylene Blue	0-14	caspase 1	Homo sapiens	42-47
26400108-7	2015	Together, these results show a novel inhibitory mechanism of caspases via sulfenation of the active site cysteine.	Cysteine	105-113	caspase 1	Homo sapiens	61-69
26400108-8	2015	These results indicate that methylene blue or its derivatives could (1) have an additional effect against Alzheimer Disease by inhibiting brain caspase activity, (2) be used as a drug to prevent caspase activation in other conditions, and (3) predispose chronically treated individuals to cancer via the inhibition of caspases.	Methylene Blue	28-42	caspase 1	Homo sapiens	144-151
26400108-8	2015	These results indicate that methylene blue or its derivatives could (1) have an additional effect against Alzheimer Disease by inhibiting brain caspase activity, (2) be used as a drug to prevent caspase activation in other conditions, and (3) predispose chronically treated individuals to cancer via the inhibition of caspases.	Methylene Blue	28-42	caspase 1	Homo sapiens	195-202
26400108-8	2015	These results indicate that methylene blue or its derivatives could (1) have an additional effect against Alzheimer Disease by inhibiting brain caspase activity, (2) be used as a drug to prevent caspase activation in other conditions, and (3) predispose chronically treated individuals to cancer via the inhibition of caspases.	Methylene Blue	28-42	caspase 1	Homo sapiens	318-326
26158519-4	2015	We observed caspase-1 dimerization induced by the coexpression of a range of inflammasome proteins and by lipospolysaccharide (LPS) treatment in primary macrophages.	lipospolysaccharide	106-125	caspase 1	Homo sapiens	12-21
26385789-10	2015	Upon priming with TLR4 (LPS) and ATP, RA-derived cell extracts (n = 7) displayed increased expression of NLRP3 (p &lt; 0.01) and active caspase-1 (p &lt; 0.001).	Adenosine Triphosphate	33-36	caspase 1	Homo sapiens	136-145
26307448-4	2015	A 4-h priming of peritoneal macrophages with LPS followed by a 30-min incubation with ATP caused the activation of caspase 1 and the release of IL-1beta, indicative of inflammasome activation.	Adenosine Triphosphate	86-89	caspase 1	Homo sapiens	115-124
26307448-6	2015	(-)Sch B suppressed the LPS/ATP-induced activation of caspase 1 and release of IL-1beta in peritoneal macrophages.	Adenosine Triphosphate	28-31	caspase 1	Homo sapiens	54-63
26241783-0	2015	Silver nanoparticles rapidly induce atypical human neutrophil cell death by a process involving inflammatory caspases and reactive oxygen species and induce neutrophil extracellular traps release upon cell adhesion.	Silver	0-6	caspase 1	Homo sapiens	109-117
26241783-7	2015	The AgNP-induced atypical cell death is distinct from necrosis and reversed by a pancaspase inhibitor or by inhibitors of the inflammatory caspase-1 and caspase-4.	agnp	4-8	caspase 1	Homo sapiens	139-148
26202987-4	2015	LPS from Gram-negative bacteria is a prototypical first signal inducing pro-IL-1beta synthesis, whereas extracellular ATP is a typical second signal sensed by the ATP receptor P2X7 that triggers activation of the NLRP3-containing inflammasome, proteolytic cleavage of pro-IL-1beta by caspase-1, and release of mature IL-1beta.	Adenosine Triphosphate	118-121	caspase 1	Homo sapiens	284-293
26079697-8	2015	In addition, z-YVAD-fmk, an inhibitor of caspase-1, decreased the ethanol-induced HMGB1 release.	benzyloxycarbonyltyrosyl-valyl-alanyl-aspartic acid fluoromethyl ketone	13-23	caspase 1	Homo sapiens	41-50
26079697-8	2015	In addition, z-YVAD-fmk, an inhibitor of caspase-1, decreased the ethanol-induced HMGB1 release.	Ethanol	66-73	caspase 1	Homo sapiens	41-50
25684031-5	2015	Additionally, we investigate the role of the NLRP3/caspase-1 inflammasome pathway in human dental pulp fibroblasts and show that ATP activates the P2X7 receptor on the cell membrane triggering K(+) efflux and inducing the gradual recruitment of the membrane pore pannexin-1.	Adenosine Triphosphate	129-132	caspase 1	Homo sapiens	51-60
25575547-6	2015	AAP (0.5-1.0 mM) and NAC (0.5-1.0 mM) used individually or in combination could down-regulate protein expression of cleaved caspase-1 and mRNA expression of IL-1beta, IL-18 and NLRP3.	Acetaminophen	0-3	caspase 1	Homo sapiens	124-133
25575547-6	2015	AAP (0.5-1.0 mM) and NAC (0.5-1.0 mM) used individually or in combination could down-regulate protein expression of cleaved caspase-1 and mRNA expression of IL-1beta, IL-18 and NLRP3.	Acetylcysteine	21-24	caspase 1	Homo sapiens	124-133
25575547-9	2015	These results indicate that the anti-inflammatory effects of AAP and NAC occur via the regulation on mRNA expression of NLRP3 and activation of caspase-1.	Acetylcysteine	69-72	caspase 1	Homo sapiens	144-153
25783493-5	2015	Interleukin secretion was dependent on the activity of NLRP3, caspase-1, and lysosomal proteases cathepsin B and L. These results demonstrate that accumulation of lipofuscin-like material in vitro renders RPE cells susceptible to phototoxic destabilization of lysosomes, resulting in NLRP3 inflammasome activation and secretion of inflammatory cytokines.	Lipofuscin	163-173	caspase 1	Homo sapiens	62-71
26355342-10	2015	In contrast, the LPS challenge is blocked by the ER stress inhibitor TUDCA, resulting in: CHOP downregulation, reduced caspase-1, caspase-11, caspase-3 activities, lowered interleukin-1beta secretion and rescue from cell death.	ursodoxicoltaurine	69-74	caspase 1	Homo sapiens	119-128
26123077-7	2015	In addition, genipin altered adenosine triphosphate (ATP)- and hydrogen peroxide (H2O2)-mediated interleukin-1 beta (IL-1beta) secretion and significantly suppressed caspase-1 activity in inflammasome-activated human macrophages.	genipin	13-20	caspase 1	Homo sapiens	166-175
26096886-9	2015	These effects were accompanied by a decreased intracellular activation of caspase-1 and interleukin-1beta release from ATP-treated cells, thus suggesting that FAEs antagonise the effects of ATP by preventing the activation of the pyroptotic molecular cascade leading to cell death.	Fumarates	159-163	caspase 1	Homo sapiens	74-83
26096886-9	2015	These effects were accompanied by a decreased intracellular activation of caspase-1 and interleukin-1beta release from ATP-treated cells, thus suggesting that FAEs antagonise the effects of ATP by preventing the activation of the pyroptotic molecular cascade leading to cell death.	Adenosine Triphosphate	190-193	caspase 1	Homo sapiens	74-83
25863775-9	2015	RESULTS: LPS up-regulated NLRP3 and IL-1beta expression while ATP induced the activation of caspase-1 and the release of IL-1beta in LPS-primed HDPFs.	Adenosine Triphosphate	62-65	caspase 1	Homo sapiens	92-101
25863775-12	2015	ATP potently promoted ROS generation in HDPFs; N-acetyl cysteine inhibited ROS production, caspase-1 activation and IL-1beta secretion induced by ATP.	Acetylcysteine	47-64	caspase 1	Homo sapiens	91-100
25863775-12	2015	ATP potently promoted ROS generation in HDPFs; N-acetyl cysteine inhibited ROS production, caspase-1 activation and IL-1beta secretion induced by ATP.	Adenosine Triphosphate	146-149	caspase 1	Homo sapiens	91-100
26119735-5	2015	Downregulation of glycolysis by inhibition of Raptor/mTORC1 or HK1 suppressed both pro-IL-1beta maturation and caspase-1 activation in macrophages in response to LPS and ATP.	Adenosine Triphosphate	170-173	caspase 1	Homo sapiens	111-120
26005910-8	2015	Moreover, Ang II-induced increases in the expression of NLRP3, ASC, caspase-1, IL-1beta, and IL-18 were significantly inhibited by pretreatment with the ERS inhibitor 4-PBA (5 mmol/L).	4-phenylbutylamine	167-172	caspase 1	Homo sapiens	68-77
26136643-6	2015	Compatible with this, secretion of IL-1beta by PBMCs stimulated with LPS alone or LPS plus ATP was increased in BD compared to healthy controls, which was suppressed by caspase-1 inhibitor.	Adenosine Triphosphate	91-94	caspase 1	Homo sapiens	169-178
25938942-2	2015	To elucidate mechanisms of glucocorticoid resistance, we determined the prednisolone sensitivity of primary leukemia cells from 444 patients newly diagnosed with ALL and found significantly higher expression of CASP1 (encoding caspase 1) and its activator NLRP3 in glucocorticoid-resistant leukemia cells, resulting from significantly lower somatic methylation of the CASP1 and NLRP3 promoters.	Prednisolone	72-84	caspase 1	Homo sapiens	211-216
26091108-13	2015	MWCNT exposure after HDM sensitization increased total cell numbers in BALF, but decreased numbers of neutrophils and IL-1beta in BALF as well as reduced pro-caspase-1 in lung tissue.	mwcnt	0-5	caspase 1	Homo sapiens	158-167
26091108-15	2015	CONCLUSIONS: These data indicate that Th2 cytokines suppress MWCNT-induced inflammasome activation via STAT6-dependent down-regulation of pro-caspase-1 and suggest that suppression of inflammasome activation and IL-1beta by an allergic lung microenvironment is a mechanism through which MWCNTs exacerbate allergen-induced airway fibrosis.	mwcnt	61-66	caspase 1	Homo sapiens	142-151
25975581-7	2015	It was found that anti-inflammatory effects of isoacteoside are mediated by action on caspase-1, mitogen-activated protein kinases (c-Jun N-terminal kinase, p38, extracellular signal-regulated protein kinase) and nuclear factor-kappa B pathways.	isoacteoside	47-59	caspase 1	Homo sapiens	86-95
26074413-8	2015	Likewise, LPS/ATP induced caspase-1-dependent IL-1beta release at significantly lower amounts in the FMF group (1182+-192 versus 2134+-245pg/mL in controls, p=0.004).	Adenosine Triphosphate	14-17	caspase 1	Homo sapiens	26-35
25938942-2	2015	To elucidate mechanisms of glucocorticoid resistance, we determined the prednisolone sensitivity of primary leukemia cells from 444 patients newly diagnosed with ALL and found significantly higher expression of CASP1 (encoding caspase 1) and its activator NLRP3 in glucocorticoid-resistant leukemia cells, resulting from significantly lower somatic methylation of the CASP1 and NLRP3 promoters.	Prednisolone	72-84	caspase 1	Homo sapiens	227-236
25938942-2	2015	To elucidate mechanisms of glucocorticoid resistance, we determined the prednisolone sensitivity of primary leukemia cells from 444 patients newly diagnosed with ALL and found significantly higher expression of CASP1 (encoding caspase 1) and its activator NLRP3 in glucocorticoid-resistant leukemia cells, resulting from significantly lower somatic methylation of the CASP1 and NLRP3 promoters.	Prednisolone	72-84	caspase 1	Homo sapiens	368-373
25770182-5	2015	Here, we demonstrated that CO inhibited caspase-1 activation and the secretion of IL-1beta and IL-18 in response to lipopolysaccharide (LPS) and ATP treatment in bone marrow-derived macrophages.	Adenosine Triphosphate	145-148	caspase 1	Homo sapiens	40-49
25834143-9	2015	Furthermore, NAC treatment could inhibit NLRP3 inflammasome formation and caspase-1 activation and suppress the release of IL-1beta and IL-18 from H. pylori-infected THP-1 cells.	Acetylcysteine	13-16	caspase 1	Homo sapiens	74-83
25770182-8	2015	LPS and ATP stimulation induced the formation of complexes between NLRP3 and apoptosis-associated speck-like protein, or NLRP3 and caspase-1.	Adenosine Triphosphate	8-11	caspase 1	Homo sapiens	131-140
25379992-7	2015	Furthermore, procyanidin B2 decreases NLRP3 and pro-IL-1beta cytoplasmic pools, limiting components of inflammasome activation and impeding inflammasome assembly and caspase-1 activation, and finally secretion of active IL-1beta.	procyanidin B2	13-27	caspase 1	Homo sapiens	166-175
25933603-14	2015	Her disease continued to progress despite second and third line chemotherapy with DHAP (dexamethasone, cisplatin and cytarabine) and ICE (ifosfamide, carboplatin and etoposide) respectively.	Ifosfamide	138-148	caspase 1	Homo sapiens	133-136
25589411-5	2015	While endosomal superoxide production induces caspase-1 and NLRP3 transcription, it does not affect prae-IL-1beta transcription.	Superoxides	16-26	caspase 1	Homo sapiens	46-55
25786687-7	2015	Furthermore, CT, mmCT, and dmLT induced IL-1beta production and caspase-1 activation in monocytes, which was associated with increased expression of key proinflammatory and inflammasome-related genes, including NLRP1, NLRP3, and NLRC4.	dmlt	27-31	caspase 1	Homo sapiens	64-73
25786687-9	2015	We conclude that CT, mmCT, and dmLT promote human Th17 responses via cAMP-dependent protein kinase A and caspase-1/inflammasome-dependent IL-1 signaling.	mmct	21-25	caspase 1	Homo sapiens	105-114
25786687-9	2015	We conclude that CT, mmCT, and dmLT promote human Th17 responses via cAMP-dependent protein kinase A and caspase-1/inflammasome-dependent IL-1 signaling.	dmlt	31-35	caspase 1	Homo sapiens	105-114
25798846-5	2015	Additionally, elevated mitochondrial ROS level, colocalization of NLRP3/ASC/mitochondria in peripheral blood mononuclear cells from CKD-HD patients and down-regulation of CASP-1, IL1-beta and IL-18 protein levels in immune-cells of CKD-HD patients stimulated with LPS/ATP in presence of mitoTEMPO, inhibitor of mitochondrial ROS production, suggested a possible role of this organelle in the aforementioned CKD-associated inflammasome activation.	Adenosine Triphosphate	268-271	caspase 1	Homo sapiens	171-177
25798846-5	2015	Additionally, elevated mitochondrial ROS level, colocalization of NLRP3/ASC/mitochondria in peripheral blood mononuclear cells from CKD-HD patients and down-regulation of CASP-1, IL1-beta and IL-18 protein levels in immune-cells of CKD-HD patients stimulated with LPS/ATP in presence of mitoTEMPO, inhibitor of mitochondrial ROS production, suggested a possible role of this organelle in the aforementioned CKD-associated inflammasome activation.	ros	325-328	caspase 1	Homo sapiens	171-177
25817825-3	2015	Consistent with this aim, we show that exposure of human epithelial cells (EC), both RPMI 2650 and FaDu, to NE results in the activation of caspases (1, 3/7, 6, 8, and 9) and the expression of genes involved in apoptotic as well as authophagy and necrosis pathways.	rpmi	85-89	caspase 1	Homo sapiens	140-169
25701684-11	2015	NAC suppressed hyperosmolarity-induced rises in ROS levels, NLRP3 inflammasome formation and activation, caspase-1 activity and IL-1beta release.	Acetylcysteine	0-3	caspase 1	Homo sapiens	105-114
25813103-1	2015	Urate crystals activate innate immunity through Toll like receptor 4 (TLR4) activation, leading to the formation of the NACHT, LRR and PYD domains-containing protein 3 [NALP3; also known as NOD-like receptor family, pyrin domain containing 3 (NALP3) and cryopyrin] inflammasome, caspase-1 activation and interleukin (IL)-1beta expression in gout.	Uric Acid	0-5	caspase 1	Homo sapiens	279-288
25813103-5	2015	Soluble UA significantly enhanced TLR4, NALP3, caspase-1, IL-1beta and ICAM-1 expression in the human primary renal proximal tubule epithelial cells.	Uric Acid	8-10	caspase 1	Homo sapiens	47-56
25813103-6	2015	The TLR4 inhibitor, TAK242 effectively blocked the soluble UA-induced upregulation of TLR4, NALP3, caspase-1, IL-1beta and ICAM-1 expression in the human primary renal proximal tubule epithelial cells.	ethyl 6-(N-(2-chloro-4-fluorophenyl)sulfamoyl)cyclohex-1-ene-1-carboxylate	20-26	caspase 1	Homo sapiens	99-108
25813103-6	2015	The TLR4 inhibitor, TAK242 effectively blocked the soluble UA-induced upregulation of TLR4, NALP3, caspase-1, IL-1beta and ICAM-1 expression in the human primary renal proximal tubule epithelial cells.	Uric Acid	59-61	caspase 1	Homo sapiens	99-108
25813103-7	2015	Our findings indicate that soluble UA enhances NALP3 expression, caspase-1 activation, IL-1beta and ICAM-1 production in renal proximal tubule epithelial cells in a TLR4-dependent manner, suggesting the activation of innate immunity in human primary renal proximal tubule epithelial cells by soluble UA.	Uric Acid	35-37	caspase 1	Homo sapiens	65-74
25639477-6	2015	Both 1,25(OH)2D3 - and 25(OH)D3 induced IL-1beta release from THP-1 cells, and these effects were blocked with application of the caspase-1 inhibitor YVAD and the NLRP3 inhibitors glyburide and Bay 11-7082.	Calcitriol	5-16	caspase 1	Homo sapiens	130-139
25639477-6	2015	Both 1,25(OH)2D3 - and 25(OH)D3 induced IL-1beta release from THP-1 cells, and these effects were blocked with application of the caspase-1 inhibitor YVAD and the NLRP3 inhibitors glyburide and Bay 11-7082.	Calcifediol	23-31	caspase 1	Homo sapiens	130-139
25639477-6	2015	Both 1,25(OH)2D3 - and 25(OH)D3 induced IL-1beta release from THP-1 cells, and these effects were blocked with application of the caspase-1 inhibitor YVAD and the NLRP3 inhibitors glyburide and Bay 11-7082.	YVAD	150-154	caspase 1	Homo sapiens	130-139
25639477-6	2015	Both 1,25(OH)2D3 - and 25(OH)D3 induced IL-1beta release from THP-1 cells, and these effects were blocked with application of the caspase-1 inhibitor YVAD and the NLRP3 inhibitors glyburide and Bay 11-7082.	3-(4-methylphenylsulfonyl)-2-propenenitrile	194-205	caspase 1	Homo sapiens	130-139
25914711-3	2015	Although there is limited sequence identity between VPE and caspase 1, their predicted three-dimensional structures revealed that the essential amino-acid residues for these enzymes form similar pockets for the substrate peptide YVAD.	Amino Acids, Essential	134-154	caspase 1	Homo sapiens	60-69
25593314-5	2015	Also, AgNP15 induced pyroptosis and activation of the NLRP-3 inflammasome as demonstrated by the processing and increased activity of caspase-1 and secretion of IL-1beta and ASC (apoptosis-associated speck-like protein containing a CARD domain) pyroptosome formation.	agnp15	6-12	caspase 1	Homo sapiens	134-143
25445379-6	2015	Next, using a caspase-1 inhibitor (Ac-YVAD-CMK) to block caspase-1 activation in vitro and in vivo, we further demonstrated that X-ray irradiation may inhibit proliferation, induce senescence of NSPCs through caspase-1 activation.	ac-yvad	35-42	caspase 1	Homo sapiens	14-23
25451941-2	2015	ITF2357 inhibits both Class I and II HDACs and reduces caspase-1 activity in human peripheral blood mononuclear cells and the secretion of IL-1beta and other cytokines at 25-100 nm; at concentrations &gt;200 nm, ITF2357 is toxic in vitro.	givinostat hydrochloride	0-7	caspase 1	Homo sapiens	55-64
25310769-12	2015	Caspase-1 activity and active caspase-1 protein (10 kDa) were significantly increased in Cisplatin-treated PTs.	Cisplatin	89-98	caspase 1	Homo sapiens	0-9
25310769-12	2015	Caspase-1 activity and active caspase-1 protein (10 kDa) were significantly increased in Cisplatin-treated PTs.	Cisplatin	89-98	caspase 1	Homo sapiens	30-39
25378535-4	2015	Subsequent gene set enrichment analysis showed that many genes associated with the high iron cluster were involved in the toll-like receptor system (TLR4, TLR7, and TLR8) and inflammasome complex pathway (NLRP3, NLRC4, and CASP1).	Iron	88-92	caspase 1	Homo sapiens	223-228
25445379-6	2015	Next, using a caspase-1 inhibitor (Ac-YVAD-CMK) to block caspase-1 activation in vitro and in vivo, we further demonstrated that X-ray irradiation may inhibit proliferation, induce senescence of NSPCs through caspase-1 activation.	ac-yvad	35-42	caspase 1	Homo sapiens	57-66
25445379-6	2015	Next, using a caspase-1 inhibitor (Ac-YVAD-CMK) to block caspase-1 activation in vitro and in vivo, we further demonstrated that X-ray irradiation may inhibit proliferation, induce senescence of NSPCs through caspase-1 activation.	ac-yvad	35-42	caspase 1	Homo sapiens	57-66
26160272-6	2015	RESULTS: RT-PCR analyses demonstrated that the mRNA levels of NLRP3 and caspase-1 genes were elevated significantly in renal tissues of PGN patients compared to those from normal pericarcinoma tissues.	pgn	136-139	caspase 1	Homo sapiens	72-81
25311115-7	2015	Our analyses also reveal a strong inhibitory effect of placental infection on LPS/ATP-induced caspase-1 activity in cord blood monocytes.	Adenosine Triphosphate	82-85	caspase 1	Homo sapiens	94-103
26557856-6	2015	The study suggested that CASP1 gene and its transcript variant may play a critical role in the inflammatory response of patients with PG in different phases and TCM syndromes.	pg	134-136	caspase 1	Homo sapiens	25-30
25327779-9	2015	The depletion of Kupffer cells with gadolinium chloride markedly decreased NLRP3 and AIM2 inflammasome expression and activation of their signaling pathways, and also reduced the level of caspase-1 protein in F4/80-positive cells.	gadolinium chloride	36-55	caspase 1	Homo sapiens	188-197
24760326-9	2015	Moreover, Y27632 suppressed pro-IL-1beta protein levels and the release of activated-cathepsin B and activated-caspase-1 induced by MWCNTs or asbestos.	Y 27632	10-16	caspase 1	Homo sapiens	111-120
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 1	Homo sapiens	127-162
25394311-4	2015	ANCA-induced reactive oxygen species generation plays an important role in downregulating inflammation by inhibition of the inflammasome-dependent caspase-1 activation and subsequent IL-1beta generation.	Reactive Oxygen Species	13-36	caspase 1	Homo sapiens	147-156
26435646-8	2015	RESULTS: Urate induced caspase-1 activation and IL-1beta release by T-cells.	Uric Acid	9-14	caspase 1	Homo sapiens	23-32
26435646-10	2015	Glyburide inhibited urate-induced caspase-1 activation, IL-1beta secretion and proliferation.	Glyburide	0-9	caspase 1	Homo sapiens	34-43
26435646-10	2015	Glyburide inhibited urate-induced caspase-1 activation, IL-1beta secretion and proliferation.	Uric Acid	20-25	caspase 1	Homo sapiens	34-43
26160272-8	2015	Immunofluorescence analysis also showed the protein expressions of NLRP3 and caspase-1 were increased in the glomeruli of PGN patients.	pgn	122-125	caspase 1	Homo sapiens	77-86
26075098-4	2015	Upon sensing mitochondrial release of ROS, NLRP3 assembles the NLRP3 inflammasome, which releases caspase 1 to begin the inflammatory cascade.	Reactive Oxygen Species	38-41	caspase 1	Homo sapiens	98-107
25445147-4	2014	Silica and monosodium urate crystal-treated macrophages with undisturbed lysosomes demonstrated strong co-localization of ASC and Caspase-1, indicative of NLRP3 inflammasome activation.	Silicon Dioxide	0-6	caspase 1	Homo sapiens	130-139
25501827-5	2014	We show that caspase-1 is rapidly activated in cardiomyocyte nuclei treated with the cell death inducing drug Doxorubicin.	Doxorubicin	110-121	caspase 1	Homo sapiens	13-22
25445147-4	2014	Silica and monosodium urate crystal-treated macrophages with undisturbed lysosomes demonstrated strong co-localization of ASC and Caspase-1, indicative of NLRP3 inflammasome activation.	Uric Acid	11-27	caspase 1	Homo sapiens	130-139
25281528-6	2014	Moreover, the silencing of the Nlrp3 gene or the use of the caspase-1 inhibitor Z-VAD-fmk significantly attenuated the albumin-induced increase in IL-1beta and IL-18 expression in HK2 cells.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	80-89	caspase 1	Homo sapiens	60-69
25117218-4	2014	These pattern recognition receptors detect host-derived danger-associated molecular patterns (DAMPs), such as microcrystals and reactive oxygen species, and respond by inducing activation of caspase-1.	Reactive Oxygen Species	128-151	caspase 1	Homo sapiens	191-200
25135357-2	2014	At molecular level, GSNO effects have been shown to modulate the activity of a series of transcription factors (notably NF-kappaB, AP-1, CREB and others) as well as other components of signal transduction chains (e.g. IKK-beta, caspase 1, calpain and others), resulting in the modulation of several cytokines and chemokines expression (TNFalpha, IL-1beta, IFN-gamma, IL-4, IL-8, RANTES, MCP-1 and others).	S-Nitrosoglutathione	20-24	caspase 1	Homo sapiens	228-237
25313054-3	2014	Caspase-1 activates multiple pathways to precipitate mitochondrial disassembly, resulting in mitochondrial reactive oxygen species (ROS) production, dissipation of mitochondrial membrane potential, mitochondrial permeabilization, and fragmentation of the mitochondrial network.	Reactive Oxygen Species	107-130	caspase 1	Homo sapiens	0-9
24954757-9	2014	The caspase-1 expression was positively correlated with total cholesterol, low density lipoprotein cholesterol, and lipoprotein(a) (P &lt; 0.05); but negatively correlated with high density lipoprotein cholesterol (P &lt; 0.05).	Cholesterol	62-73	caspase 1	Homo sapiens	4-13
25389767-5	2014	Incubating the cells with 5-FU increased the expression of nucleotide-binding domain and leucine-rich repeat containing PYD-3 (NLRP3) and caspase-1.	Fluorouracil	26-30	caspase 1	Homo sapiens	138-147
25389767-6	2014	The cleavage of caspase-1 was observed in 5-FU-treated cells, which was followed by an increased secretion of interleukin (IL)-1beta.	Fluorouracil	42-46	caspase 1	Homo sapiens	16-25
25313054-3	2014	Caspase-1 activates multiple pathways to precipitate mitochondrial disassembly, resulting in mitochondrial reactive oxygen species (ROS) production, dissipation of mitochondrial membrane potential, mitochondrial permeabilization, and fragmentation of the mitochondrial network.	Reactive Oxygen Species	132-135	caspase 1	Homo sapiens	0-9
24149798-5	2014	We examined the possibility that cis- and trans-resveratrol may affect cytokine secretion by modulating inflammasomes, intracellular multi-protein complexes, the assembly of which leads to caspase-1 activation and secretion of active IL-1beta by macrophages.	cis- and trans-resveratrol	33-59	caspase 1	Homo sapiens	189-198
25281537-3	2014	Interestingly, doxorubicin upregulated caspase-1 in a concentration-dependent manner, and z-YAVD-fmk, a specific inhibitor of caspase-1, reversed the doxorubicin-induced decrease in cyclin A1 in A549 lung cancer and MCF7 breast cancer cells.	Doxorubicin	15-26	caspase 1	Homo sapiens	39-48
25281537-3	2014	Interestingly, doxorubicin upregulated caspase-1 in a concentration-dependent manner, and z-YAVD-fmk, a specific inhibitor of caspase-1, reversed the doxorubicin-induced decrease in cyclin A1 in A549 lung cancer and MCF7 breast cancer cells.	Doxorubicin	15-26	caspase 1	Homo sapiens	126-135
25281537-3	2014	Interestingly, doxorubicin upregulated caspase-1 in a concentration-dependent manner, and z-YAVD-fmk, a specific inhibitor of caspase-1, reversed the doxorubicin-induced decrease in cyclin A1 in A549 lung cancer and MCF7 breast cancer cells.	z-yavd-fmk	90-100	caspase 1	Homo sapiens	126-135
25281537-3	2014	Interestingly, doxorubicin upregulated caspase-1 in a concentration-dependent manner, and z-YAVD-fmk, a specific inhibitor of caspase-1, reversed the doxorubicin-induced decrease in cyclin A1 in A549 lung cancer and MCF7 breast cancer cells.	Doxorubicin	150-161	caspase 1	Homo sapiens	39-48
25281537-3	2014	Interestingly, doxorubicin upregulated caspase-1 in a concentration-dependent manner, and z-YAVD-fmk, a specific inhibitor of caspase-1, reversed the doxorubicin-induced decrease in cyclin A1 in A549 lung cancer and MCF7 breast cancer cells.	Doxorubicin	150-161	caspase 1	Homo sapiens	126-135
25330190-0	2014	Transcriptomic analysis unveils correlations between regulative apoptotic caspases and genes of cholesterol homeostasis in human brain.	Cholesterol	96-107	caspase 1	Homo sapiens	74-82
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 1	Homo sapiens	125-130
25225670-3	2014	In this study, we found that cytosolic poly(I:C), but not total RNA from healthy macrophages, macrophages undergoing pyroptosis, or mitochondrial RNA, induces caspase-1 activation and IL-1beta release through the Nlrp3 inflammasome.	poly	39-43	caspase 1	Homo sapiens	159-168
24149798-6	2014	Our results show that pre-treatment of macrophages with cis-resveratrol not only reduces pro-IL-1beta production and IL-1beta secretion, but also suppresses ATP-induced transcription and activation of caspase-1 and caspase-4.	Resveratrol	56-71	caspase 1	Homo sapiens	201-210
24149798-6	2014	Our results show that pre-treatment of macrophages with cis-resveratrol not only reduces pro-IL-1beta production and IL-1beta secretion, but also suppresses ATP-induced transcription and activation of caspase-1 and caspase-4.	Adenosine Triphosphate	157-160	caspase 1	Homo sapiens	201-210
25202950-6	2014	RESULTS: Compared with the THP-1 macrophages without palmitic acid, the level of ROS, NALP3 protein and caspase-1 protein, and the expression of IL-1beta were increased after palmitic acid treatment in a dose dependent manner (P&lt;0.05).	Palmitic Acid	175-188	caspase 1	Homo sapiens	104-113
25261974-8	2014	Induction of IL-1beta by MSU was fully inhibited by a caspase-1 inhibitor confirming inflammasome activation as the mechanism for generating this cytokine.	Uric Acid	25-28	caspase 1	Homo sapiens	54-63
25234616-14	2014	Further dose- and time-dependent suppression of the activated caspase 1 and pPKCepsilon was detected in macrophages when treated with BAP.	benzylaminopurine	134-137	caspase 1	Homo sapiens	62-71
24919149-5	2014	Here we show that Pyrin mediates caspase 1 inflammasome activation in response to Rho-glucosylation activity of cytotoxin TcdB, a major virulence factor of Clostridium difficile, which causes most cases of nosocomial diarrhoea.	trimethylaminocarboxyldihydroboran	122-126	caspase 1	Homo sapiens	33-42
25048991-13	2014	Calcium removal blocks caspase-1 activation.	Calcium	0-7	caspase 1	Homo sapiens	23-32
24925806-6	2014	While several inhibitors are available for caspase-1 blocking experiments, in this study we show effects of two commonly used caspase inhibitors: z-VAD-fmk and ac-YVAD-cmk on secretion of pro-inflammatory cytokines: IL-1beta, TNFalpha, IL-8 and IL-6 in whole blood stimulated with LPS.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	146-155	caspase 1	Homo sapiens	43-52
24925806-7	2014	We demonstrate ac-YVAD-cmk is a specific caspase-1 inhibitor resulting in pronounced decreases in IL-1beta and less suppression of TNFalpha, IL-6 and IL-8, while pan-caspase inhibitor, z-VAD-fmk, only weakly suppressed Il-1beta while acting strongly on the other three cytokines.	ac-yvad	15-22	caspase 1	Homo sapiens	41-50
24925806-7	2014	We demonstrate ac-YVAD-cmk is a specific caspase-1 inhibitor resulting in pronounced decreases in IL-1beta and less suppression of TNFalpha, IL-6 and IL-8, while pan-caspase inhibitor, z-VAD-fmk, only weakly suppressed Il-1beta while acting strongly on the other three cytokines.	ac-yvad	15-22	caspase 1	Homo sapiens	41-48
24894535-9	2014	Caspase-1-dependent IL-1beta secretion was impaired in monocytes from patients with AD compared to patients with psoriasis and healthy controls by alpha-toxin stimulation following priming with lipoteichoic acid.	lipoteichoic acid	194-211	caspase 1	Homo sapiens	0-9
24842757-7	2014	IL-18RAP responded to NOD2-initiated early, caspase-1-dependent autocrine IL-18, which dramatically enhanced MAPK, NF-kappaB, PI3K, and calcium signaling.	Calcium	136-143	caspase 1	Homo sapiens	44-53
25184735-11	2014	Intriguingly, stimulation with low ATP concentrations augmented the production of IL-1beta in LPS-primed MCs in a P2X7-independent but caspase-1-dependent manner.	Adenosine Triphosphate	35-38	caspase 1	Homo sapiens	135-144
24657787-7	2014	Conversely, another caspase 1 inhibitor, glyburide, significantly inhibited virus infection suggesting it had off-target effects on related enzymes or interfered with infection via non-enzymatic mechanisms.	Glyburide	41-50	caspase 1	Homo sapiens	20-29
24721152-6	2014	But in the meantime, rhein enhances the activity of caspase-1 by inhibiting intracellular (in situ) IKKbeta, in turn increasing the IL-1beta and high-mobility-group box 1 release, which can be amplified by rhein s reductive effect on intracellular superoxide anion.	Superoxides	248-264	caspase 1	Homo sapiens	52-61
24915862-8	2014	Cell death and cytokine production were significantly reduced by antioxidants, siRNA to NLRP3, a caspase-1 inhibitor (z-WEHD-FMK) or a cathepsin B inhibitor (CA-074Me).	Z-WEHD-FMK	118-128	caspase 1	Homo sapiens	97-106
24525029-5	2014	Similarly to IL-1beta secretion induced by other crystalline inflammasome activators, cystine crystal-induced IL-1beta secretion required activation of caspase-1.	Cystine	86-93	caspase 1	Homo sapiens	152-161
24884459-6	2014	YVAD is a tetrapeptide (tyrosine-valine-alanine-aspartic acid) that specifically inhibits caspase-1, which catalyzes the production of interleukin (IL)-1beta, an inflammatory cytokine, from its inactive precursor.	YVAD	0-4	caspase 1	Homo sapiens	90-99
24587486-0	2014	Enhanced p62 expression through impaired  proteasomal degradation is involved in caspase-1  activation in monosodium urate crystal-induced  interleukin-1b expression.	monosodium urate crystal	106-130	caspase 1	Homo sapiens	81-90
24884459-6	2014	YVAD is a tetrapeptide (tyrosine-valine-alanine-aspartic acid) that specifically inhibits caspase-1, which catalyzes the production of interleukin (IL)-1beta, an inflammatory cytokine, from its inactive precursor.	Tyrosine	24-33	caspase 1	Homo sapiens	90-99
24884459-6	2014	YVAD is a tetrapeptide (tyrosine-valine-alanine-aspartic acid) that specifically inhibits caspase-1, which catalyzes the production of interleukin (IL)-1beta, an inflammatory cytokine, from its inactive precursor.	valine-alanine-	33-48	caspase 1	Homo sapiens	90-99
24884459-6	2014	YVAD is a tetrapeptide (tyrosine-valine-alanine-aspartic acid) that specifically inhibits caspase-1, which catalyzes the production of interleukin (IL)-1beta, an inflammatory cytokine, from its inactive precursor.	Aspartic Acid	48-61	caspase 1	Homo sapiens	90-99
24574398-7	2014	That and the pattern of viral determinants maintained in gemcitabine-treated cells suggested the activation of an inflammasome/caspase 1 (CASP1) platform alongside DNA detachment and/or nuclear exclusion of HMGB1 during early stages of the viral life cycle.	gemcitabine	57-68	caspase 1	Homo sapiens	127-136
24613657-11	2014	Finally, MK128 reduced the quantity of p20 caspase-1 produced in the culture medium.	mk128	9-14	caspase 1	Homo sapiens	43-52
24252030-6	2014	RESULTS: DHMEQ inhibited expression of proIL-1beta and NLRP3 by normal PBMCs primed with LPS, resulting in inhibition of caspase-1 activation and IL-1beta secretion by the cells after subsequent stimulation with ATP.	dehydroxymethylepoxyquinomicin	9-14	caspase 1	Homo sapiens	121-130
24574398-7	2014	That and the pattern of viral determinants maintained in gemcitabine-treated cells suggested the activation of an inflammasome/caspase 1 (CASP1) platform alongside DNA detachment and/or nuclear exclusion of HMGB1 during early stages of the viral life cycle.	gemcitabine	57-68	caspase 1	Homo sapiens	138-143
24380723-3	2014	Based on the anti-inflammatory characteristics of DMSO, we elucidated the effects of DMSO on activation of inflammasomes, which are cytoplasmic multi-protein complexes that mediate the maturation of interleukin (IL)-1beta by activating caspase-1 (Casp1).	Dimethyl Sulfoxide	85-89	caspase 1	Homo sapiens	236-245
24623131-6	2014	Within minutes of endotoxin priming, the NLRP3 inflammasome is licensed for ATP-induced release of processed IL-18, apoptosis-associated speck-forming complex containing CARD, and active caspase-1, independent of new mRNA or protein synthesis.	Adenosine Triphosphate	76-79	caspase 1	Homo sapiens	187-196
24585381-3	2014	Caspase-1 is a cysteine protease that uses cysteine as a nucleophile and has a CARD domain for protein interaction.	Cysteine	15-23	caspase 1	Homo sapiens	0-9
24380723-3	2014	Based on the anti-inflammatory characteristics of DMSO, we elucidated the effects of DMSO on activation of inflammasomes, which are cytoplasmic multi-protein complexes that mediate the maturation of interleukin (IL)-1beta by activating caspase-1 (Casp1).	Dimethyl Sulfoxide	85-89	caspase 1	Homo sapiens	247-252
24380723-4	2014	In the present study, we prove that DMSO attenuated IL-1beta maturation, Casp1 activity, and ASC pyroptosome formation via NLRP3 inflammasome activators.	Dimethyl Sulfoxide	36-40	caspase 1	Homo sapiens	73-78
24158569-6	2014	Together, these results identified a novel innate immune signaling pathway (NLRP3-ASC-caspase-1-IL-1beta) activated by Ni(2+) and provided a mechanistic basis for optimizing the therapeutic intervention against Ni(2+)-induced allergy in patients.	Nickel(2+)	211-217	caspase 1	Homo sapiens	86-95
24158569-0	2014	Nickel induces interleukin-1beta secretion via the NLRP3-ASC-caspase-1 pathway.	Nickel	0-6	caspase 1	Homo sapiens	61-70
24158569-3	2014	Here we report that Ni(2+) activates the NLRP3-ASC-caspase-1 immune signaling pathway in antigen-presenting cells, leading to the proteolytic processing and secretion of a proinflammatory cytokine, interleukin-1beta (IL-1beta).	Nickel(2+)	20-26	caspase 1	Homo sapiens	51-60
23792296-7	2014	Likewise, an ethidium bromide uptake test showed that the P2X7-K(+) efflux-caspase-1 signaling pathway triggered by HNP-1 contributed to pyroptotic pore formation.	Ethidium	13-29	caspase 1	Homo sapiens	75-84
24431405-5	2014	Using in vitro models with mouse and human malignant mesothelioma cells, curcumin is shown to induce pyroptosis through activation of caspase-1 and increased release of high-mobility group box 1 (HMGB1) without processing of IL-1beta and IL-18.	Curcumin	73-81	caspase 1	Homo sapiens	134-143
24158569-5	2014	Instead, Ni(2+) induces mitochondrial reactive oxygen species accumulation and cation fluxes, both of which are required for activating the NLRP3-ASC-caspase-1 pathway.	Nickel(2+)	9-15	caspase 1	Homo sapiens	150-159
24158569-6	2014	Together, these results identified a novel innate immune signaling pathway (NLRP3-ASC-caspase-1-IL-1beta) activated by Ni(2+) and provided a mechanistic basis for optimizing the therapeutic intervention against Ni(2+)-induced allergy in patients.	Nickel(2+)	119-125	caspase 1	Homo sapiens	86-95
24431405-8	2014	We also demonstrate that curcumin-mediated caspase-1 activation is oxidant dependent by using N-acetyl-L-cysteine (NAC) to inhibit pyroptosis.	Acetylcysteine	94-113	caspase 1	Homo sapiens	43-52
24431405-6	2014	Absence of IL-1beta processing in response to curcumin-mediated caspase-1 activation is attributed to blockade of pro-IL-1beta priming through inhibition of the NF-kappaB pathway.	Curcumin	46-54	caspase 1	Homo sapiens	64-73
24431405-7	2014	Furthermore, curcumin"s cytotoxicity in malignant mesothelioma cells is demonstrated to be dependent on pyroptosis as inhibition of caspase-1 resulted in protection against curcumin-induced cell death.	Curcumin	13-21	caspase 1	Homo sapiens	132-141
24431405-7	2014	Furthermore, curcumin"s cytotoxicity in malignant mesothelioma cells is demonstrated to be dependent on pyroptosis as inhibition of caspase-1 resulted in protection against curcumin-induced cell death.	Curcumin	173-181	caspase 1	Homo sapiens	132-141
24431405-8	2014	We also demonstrate that curcumin-mediated caspase-1 activation is oxidant dependent by using N-acetyl-L-cysteine (NAC) to inhibit pyroptosis.	Curcumin	25-33	caspase 1	Homo sapiens	43-52
24516390-10	2014	siRNA-mediated knockdown of Naip2, but not Naip5, inhibited Shigella-induced caspase-1 activation, IL-1beta maturation and Asc pyroptosome formation.	naip2	28-33	caspase 1	Homo sapiens	77-86
24138091-7	2014	HS could also activate MaxiK channels to promote the efflux of potassium ions from cells, as measured by the elevated activity of caspase-1, whereas this was significantly abolished by treatment with paxilline, a specific blocker of the MaxiK channel.	Heparitin Sulfate	0-2	caspase 1	Homo sapiens	130-139
24138091-7	2014	HS could also activate MaxiK channels to promote the efflux of potassium ions from cells, as measured by the elevated activity of caspase-1, whereas this was significantly abolished by treatment with paxilline, a specific blocker of the MaxiK channel.	Potassium	63-72	caspase 1	Homo sapiens	130-139
24138091-7	2014	HS could also activate MaxiK channels to promote the efflux of potassium ions from cells, as measured by the elevated activity of caspase-1, whereas this was significantly abolished by treatment with paxilline, a specific blocker of the MaxiK channel.	paxilline	200-209	caspase 1	Homo sapiens	130-139
24516390-12	2014	These results indicate that activation of caspase-1 by Shigella is triggered by the rod protein MxiI that interacts with Naip2 to induce activation of the Nlrc4 inflammasome independently of the Pkcdelta kinase.	naip2	121-126	caspase 1	Homo sapiens	42-51
24285499-8	2014	Glyburide completely blocked CP-induced activation of caspase-1 and the production of IL-1beta at 4 h. At 24 h, glyburide reduced two markers of inflammation by 30-50% and reversed much of the inflammatory morphology.	Glyburide	0-9	caspase 1	Homo sapiens	54-63
24495380-9	2014	Caspase-1 and Caspase-3 activities were blocked using specific inhibitors YVAD and DEVD, respectively.	YVAD	74-78	caspase 1	Homo sapiens	0-9
24495380-9	2014	Caspase-1 and Caspase-3 activities were blocked using specific inhibitors YVAD and DEVD, respectively.	DEVD	83-87	caspase 1	Homo sapiens	0-9
24495380-15	2014	CONCLUSIONS: In the LPAC model, HIV-1 induced Caspase-1 mediated pyroptosis in bystander CD4+ T cells, but microbial exposure shifted the PCD mechanism toward apoptosis of productively infected T cells.	lpac	20-24	caspase 1	Homo sapiens	46-55
24238269-7	2014	However, levels of extracellular IL-1beta were greatly increased by subsequent treatment with the potassium-proton ionophore Adenosine triphosphate (ATP) or nigericin; an effect that was dependent on active caspase-1.	Potassium	98-107	caspase 1	Homo sapiens	207-216
24238269-7	2014	However, levels of extracellular IL-1beta were greatly increased by subsequent treatment with the potassium-proton ionophore Adenosine triphosphate (ATP) or nigericin; an effect that was dependent on active caspase-1.	Adenosine Triphosphate	125-147	caspase 1	Homo sapiens	207-216
24238269-7	2014	However, levels of extracellular IL-1beta were greatly increased by subsequent treatment with the potassium-proton ionophore Adenosine triphosphate (ATP) or nigericin; an effect that was dependent on active caspase-1.	Adenosine Triphosphate	149-152	caspase 1	Homo sapiens	207-216
24238269-7	2014	However, levels of extracellular IL-1beta were greatly increased by subsequent treatment with the potassium-proton ionophore Adenosine triphosphate (ATP) or nigericin; an effect that was dependent on active caspase-1.	Nigericin	157-166	caspase 1	Homo sapiens	207-216
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 1	Homo sapiens	92-97
24231507-6	2014	Using a PCR array for 84 apoptosis genes, cantharidin treatment upregulated gene expression of caspase-1 and nerve growth factor receptor, but downregulated mRNA expression of Bcl-2 like protein 10, Fas ligand, and tumor necrosis factor-alpha.	Cantharidin	42-53	caspase 1	Homo sapiens	95-104
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 1	Homo sapiens	92-97
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 1	Homo sapiens	92-97
24275551-11	2014	Analysis of the action of caspase-1 revealed that leptin up regulates caspase-1 activity and the effect of leptin on IL-18 release is prevented by caspase-1 inhibitor (Ac-YVAD-cmk).	ac-yvad	168-175	caspase 1	Homo sapiens	26-35
24513871-9	2014	Interestingly, amitriptyline treatment reduced NLRP3 and caspase-1 gene expression, and IL-1beta and IL-18 serum levels.	Amitriptyline	15-28	caspase 1	Homo sapiens	57-66
24275551-11	2014	Analysis of the action of caspase-1 revealed that leptin up regulates caspase-1 activity and the effect of leptin on IL-18 release is prevented by caspase-1 inhibitor (Ac-YVAD-cmk).	ac-yvad	168-175	caspase 1	Homo sapiens	70-79
24275551-11	2014	Analysis of the action of caspase-1 revealed that leptin up regulates caspase-1 activity and the effect of leptin on IL-18 release is prevented by caspase-1 inhibitor (Ac-YVAD-cmk).	ac-yvad	168-175	caspase 1	Homo sapiens	70-79
23963575-7	2013	Strikingly, ROS exerted opposite effects on the processing and secretion of IL-1beta; whereas ROS negatively controlled caspase-1 activity, as reported in mononuclear phagocytes, ROS were found to be necessary for the exportation of mature IL-1beta out of the cell, a role never previously described.	Reactive Oxygen Species	12-15	caspase 1	Homo sapiens	120-129
24330827-8	2013	Cultured human microglia displayed expression of inflammasome-associated genes and responded to inflammasome activators by releasing IL-1beta, which was inhibited by the caspase inhibitor, zVAD-fmk.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	189-197	caspase 1	Homo sapiens	170-177
23963575-7	2013	Strikingly, ROS exerted opposite effects on the processing and secretion of IL-1beta; whereas ROS negatively controlled caspase-1 activity, as reported in mononuclear phagocytes, ROS were found to be necessary for the exportation of mature IL-1beta out of the cell, a role never previously described.	Reactive Oxygen Species	94-97	caspase 1	Homo sapiens	120-129
24296756-7	2014	Furthermore, PPP inhibition with 6-aminonicotinamide (6-AN) in combination with autophagy inhibition suppressed proliferation and prompted the activation of NF-kappaB and CASP1 in TSC2-deficient, but not TSC2-proficient cells.	6-Aminonicotinamide	33-52	caspase 1	Homo sapiens	171-176
24296756-7	2014	Furthermore, PPP inhibition with 6-aminonicotinamide (6-AN) in combination with autophagy inhibition suppressed proliferation and prompted the activation of NF-kappaB and CASP1 in TSC2-deficient, but not TSC2-proficient cells.	6-Aminonicotinamide	54-58	caspase 1	Homo sapiens	171-176
24357806-5	2013	The processing is induced by an increase in activity of caspase-1 and NOD-like receptor family, pyrin domain containing 3 (NLRP3) via mitochondrial reactive oxygen species (ROS) and partially via NADPH oxidase-induced ROS.	Reactive Oxygen Species	148-171	caspase 1	Homo sapiens	56-65
24357806-5	2013	The processing is induced by an increase in activity of caspase-1 and NOD-like receptor family, pyrin domain containing 3 (NLRP3) via mitochondrial reactive oxygen species (ROS) and partially via NADPH oxidase-induced ROS.	Reactive Oxygen Species	173-176	caspase 1	Homo sapiens	56-65
24357806-5	2013	The processing is induced by an increase in activity of caspase-1 and NOD-like receptor family, pyrin domain containing 3 (NLRP3) via mitochondrial reactive oxygen species (ROS) and partially via NADPH oxidase-induced ROS.	Reactive Oxygen Species	218-221	caspase 1	Homo sapiens	56-65
24357806-6	2013	The caspase-1 inhibitor Z-YVAD-FMK inhibits the processing of IL-1beta, and attenuates microglial neurotoxicity.	benzyloxycarbonyltyrosyl-valyl-alanyl-aspartic acid fluoromethyl ketone	24-34	caspase 1	Homo sapiens	4-13
23963575-7	2013	Strikingly, ROS exerted opposite effects on the processing and secretion of IL-1beta; whereas ROS negatively controlled caspase-1 activity, as reported in mononuclear phagocytes, ROS were found to be necessary for the exportation of mature IL-1beta out of the cell, a role never previously described.	Reactive Oxygen Species	94-97	caspase 1	Homo sapiens	120-129
23916847-10	2013	Methylation at fibroblast growth factor receptor 2, methionine adenosyl methyltransferase 1A, and caspase 1 was validated by bisulfite pyrosequencing and the findings were reproduced in the replication cohort.	hydrogen sulfite	125-134	caspase 1	Homo sapiens	98-107
24140411-6	2013	At the posttranscriptional level, the activation of caspase-1 induced by cucurbitacin D has also been demonstrated following treatment with a caspase-1 inhibitor and siRNA.	cucurbitacin D	73-87	caspase 1	Homo sapiens	52-61
24140411-6	2013	At the posttranscriptional level, the activation of caspase-1 induced by cucurbitacin D has also been demonstrated following treatment with a caspase-1 inhibitor and siRNA.	cucurbitacin D	73-87	caspase 1	Homo sapiens	142-151
24107183-2	2013	Here we describe a nanosensor for caspase-1 ratiometric measurements, consisting of a rhodamine-labeled, caspase-1 cleavable peptide linked to quantum dots (QDs).	Rhodamines	86-95	caspase 1	Homo sapiens	34-43
24107183-2	2013	Here we describe a nanosensor for caspase-1 ratiometric measurements, consisting of a rhodamine-labeled, caspase-1 cleavable peptide linked to quantum dots (QDs).	Rhodamines	86-95	caspase 1	Homo sapiens	105-114
24235127-6	2013	Release of ATP is a rate-limiting step for activating caspase-1, as extracellular ATP triggers the P2X7 purinergic receptor to initiate oligomerization of NLRP3.	Adenosine Triphosphate	11-14	caspase 1	Homo sapiens	54-63
24235127-6	2013	Release of ATP is a rate-limiting step for activating caspase-1, as extracellular ATP triggers the P2X7 purinergic receptor to initiate oligomerization of NLRP3.	Adenosine Triphosphate	82-85	caspase 1	Homo sapiens	54-63
24244322-6	2013	Moreover, secretion of IL-1beta was decreased in parallel with reduction of caspase-1 activation, demonstrating that ethanol inhibits inflammasome activation instead of synthesis of pro-IL-1beta.	Ethanol	117-124	caspase 1	Homo sapiens	76-85
23839215-4	2013	Treating monocytes with the caspase-1 inhibitor Ac-YVAD-CMK reduced IL-1beta release, suggesting a role for the inflammasome in T. gondii-induced IL-1beta production.	ac-yvad	48-55	caspase 1	Homo sapiens	28-37
23943306-8	2013	At low dose (12.5 muM), TQ was found to induce expression of four pro-apoptotic genes: BIK (~22.7-fold), FASL (~2.9-fold), BCL2L10 (~2.1-fold), and CASP1 (~2-fold).	thymoquinone	24-26	caspase 1	Homo sapiens	148-153
23919525-7	2013	CLN3(Deltaex7/8) microglia displayed constitutive caspase-1 activity that when blocked led to increased glutamate release that coincided with hemichannel opening.	Glutamic Acid	104-113	caspase 1	Homo sapiens	50-59
23940760-5	2013	We show here that exposure of a human neuroblastoma cell line (SK-N-MC cells) to TNF-alpha promotes ROS-mediated caspase-1 activation and IL-1beta secretion.	ros	100-103	caspase 1	Homo sapiens	113-122
23607494-8	2013	Furthermore, poly(I:C) and proinflammatory cytokines [(IL-1beta, interferon (IFN)-gamma and tumour necrosis factor (TNF)-alpha] induced IL-32 expression strongly in cultured BECs, accompanying the constant expression of TLR-3 and caspase 1.	poly	13-17	caspase 1	Homo sapiens	230-239
23607494-8	2013	Furthermore, poly(I:C) and proinflammatory cytokines [(IL-1beta, interferon (IFN)-gamma and tumour necrosis factor (TNF)-alpha] induced IL-32 expression strongly in cultured BECs, accompanying the constant expression of TLR-3 and caspase 1.	Iodine	18-19	caspase 1	Homo sapiens	230-239
23607494-8	2013	Furthermore, poly(I:C) and proinflammatory cytokines [(IL-1beta, interferon (IFN)-gamma and tumour necrosis factor (TNF)-alpha] induced IL-32 expression strongly in cultured BECs, accompanying the constant expression of TLR-3 and caspase 1.	Carbon	20-21	caspase 1	Homo sapiens	230-239
23794630-5	2013	We report in this article that downstream depletion of geranylgeranyl pyrophosphate (GGPP), which is required for protein prenylation, caused cell stress in monocytes, followed by caspase-1-mediated maturation and release of IL-18, which, in turn, induced gammadelta T cell CCL2.	geranylgeranyl pyrophosphate	55-83	caspase 1	Homo sapiens	180-189
23794630-5	2013	We report in this article that downstream depletion of geranylgeranyl pyrophosphate (GGPP), which is required for protein prenylation, caused cell stress in monocytes, followed by caspase-1-mediated maturation and release of IL-18, which, in turn, induced gammadelta T cell CCL2.	geranylgeranyl pyrophosphate	85-89	caspase 1	Homo sapiens	180-189
24006511-4	2013	Palmitate and stearate, both SFAs, triggered IL-1beta secretion in a caspase-1/ASC/NLRP3-dependent pathway.	Palmitates	0-9	caspase 1	Homo sapiens	69-78
24006511-4	2013	Palmitate and stearate, both SFAs, triggered IL-1beta secretion in a caspase-1/ASC/NLRP3-dependent pathway.	Stearates	14-22	caspase 1	Homo sapiens	69-78
24043885-5	2013	Activation of TLR2 by palmitic acid leads to expression of pro-IL-1beta that is cleaved by caspase-1, which is constitutively present in monocytes, to release mature IL-1beta.	Palmitic Acid	22-35	caspase 1	Homo sapiens	91-100
23830798-10	2013	Gene expression arrays showed that ATRA-induced apoptosis in RARA-amplified cell lines was related to an increase in CASP1 and IRF1.	Tretinoin	35-39	caspase 1	Homo sapiens	117-122
23625868-7	2013	Stimulation of human astrocytes with ATP resulted in activation of the NLRP2 inflammasome leading to the processing of inflammatory caspase-1 and interleukin-1beta (IL-1beta).	Adenosine Triphosphate	37-40	caspase 1	Homo sapiens	132-141
23625868-9	2013	siRNA knockdown of NLRP2 significantly decreased NLRP2 levels and caspase-1 processing in human astrocytes in response to ATP.	Adenosine Triphosphate	122-125	caspase 1	Homo sapiens	66-75
23840534-8	2013	Inhibition of caspase-1 in human lung tissue led to a significant reduction of IL-1beta and IL-18 levels (IL-1beta: NTHi 24 h 17423+-3198pg/ml vs. NTHi+Z-YVAD-FMK 6961+-1751pg/ml, p&lt;0.01).	nthi	116-120	caspase 1	Homo sapiens	14-23
23809162-2	2013	Here we show that stimulation of macrophages with omega-3 FAs, including eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), and other family members, abolished NLRP3 inflammasome activation and inhibited subsequent caspase-1 activation and IL-1beta secretion.	Fatty Acids, Omega-3	50-61	caspase 1	Homo sapiens	221-230
23809162-2	2013	Here we show that stimulation of macrophages with omega-3 FAs, including eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), and other family members, abolished NLRP3 inflammasome activation and inhibited subsequent caspase-1 activation and IL-1beta secretion.	Eicosapentaenoic Acid	73-94	caspase 1	Homo sapiens	221-230
23809162-2	2013	Here we show that stimulation of macrophages with omega-3 FAs, including eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), and other family members, abolished NLRP3 inflammasome activation and inhibited subsequent caspase-1 activation and IL-1beta secretion.	Eicosapentaenoic Acid	96-99	caspase 1	Homo sapiens	221-230
23809162-2	2013	Here we show that stimulation of macrophages with omega-3 FAs, including eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), and other family members, abolished NLRP3 inflammasome activation and inhibited subsequent caspase-1 activation and IL-1beta secretion.	Docosahexaenoic Acids	102-122	caspase 1	Homo sapiens	221-230
23840534-8	2013	Inhibition of caspase-1 in human lung tissue led to a significant reduction of IL-1beta and IL-18 levels (IL-1beta: NTHi 24 h 17423+-3198pg/ml vs. NTHi+Z-YVAD-FMK 6961+-1751pg/ml, p&lt;0.01).	benzyloxycarbonyltyrosyl-valyl-alanyl-aspartic acid fluoromethyl ketone	152-162	caspase 1	Homo sapiens	14-23
23710297-10	2013	We found that both ATP and Nig stimulation could activate and release cleaved caspase-1 from the monocytes.	Adenosine Triphosphate	19-22	caspase 1	Homo sapiens	78-87
23701470-4	2013	To accomplish this, we have identified a non-conserved residue on the small subunit of all caspases that is near the substrate-binding pocket and that can be mutated to a non-catalytic cysteine residue.	Cysteine	185-193	caspase 1	Homo sapiens	91-99
23386603-1	2013	Caspases are intracellular cysteine-class proteases with aspartate specificity that is critical for driving processes as diverse as the innate immune response and apoptosis, exemplified by caspase-1 and caspase-3, respectively.	Aspartic Acid	57-66	caspase 1	Homo sapiens	0-8
23530046-10	2013	Acidic medium triggered pH-dependent secretion of IL-1beta and activation of caspase-1 via a mechanism involving potassium efflux from the cells.	Potassium	113-122	caspase 1	Homo sapiens	77-86
23434541-8	2013	In vitro culture experiments showed NLRP3 protein expression, cleavage of caspase-1 and IL-1beta, and release of IL-1beta, IL-18 and ATP in HK-2 cells significantly increased after high glucose stimulation.	Glucose	186-193	caspase 1	Homo sapiens	74-83
23434541-10	2013	The P2 receptor antagonist suramin, P2X receptor antagonist TNP-ATP, P2X4 selective antagonist 5-BDBD, and P2X4 gene silencing attenuated NLRP3 expression, cleavage of caspase-1 and IL-1beta, and release of IL-1beta and IL-18 induced by high glucose.	Suramin	27-34	caspase 1	Homo sapiens	168-177
23386603-1	2013	Caspases are intracellular cysteine-class proteases with aspartate specificity that is critical for driving processes as diverse as the innate immune response and apoptosis, exemplified by caspase-1 and caspase-3, respectively.	Aspartic Acid	57-66	caspase 1	Homo sapiens	189-198
23386603-5	2013	We have created a hemi-active site-labeled dimer of caspase-1, where one site is blocked with the covalent active site inhibitor, benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone.	Caspase Inhibitor VI	130-178	caspase 1	Homo sapiens	52-61
23386603-6	2013	This hemi-labeled enzyme is about 9-fold more active than the apo-dimer of caspase-1.	1-(2-Hydroxyethyl)-1H-pyrrole-2,5-dione	5-9	caspase 1	Homo sapiens	75-84
23590971-6	2013	Treatments with inhibitors of caspase-1 and Stat3 reduce the Fas-signal-associated induction of RORgammat, IL-17A, and IL-17F, as well as the phosphorylation of Stat3.	ammonium ferrous sulfate	61-64	caspase 1	Homo sapiens	30-39
23399723-0	2013	Synthesis and biological evaluation of a new derivative of bevirimat that targets the Gag CA-SP1 cleavage site.	bevirimat	59-68	caspase 1	Homo sapiens	90-96
23399723-1	2013	Bevirimat (2), the first-in-class HIV-1 maturation inhibitor, shows a low efficacy due essentially to the natural polymorphism of its target, the CA-SP1 junction.	bevirimat	0-9	caspase 1	Homo sapiens	146-152
23399723-7	2013	Moreover, for the first time a direct interaction between a derivative of bevirimat (16) and the domain CA-SP1-NC is shown by NMR.	bevirimat	74-83	caspase 1	Homo sapiens	104-110
24376319-0	2013	Uric acid induces caspase-1 activation, IL-1beta secretion and P2X7 receptor dependent proliferation in primary human lymphocytes.	Uric Acid	0-9	caspase 1	Homo sapiens	18-27
24376319-1	2013	BACKGROUND: Urate through Nacht Domain, Leucine-Rich Repeat, and pyrin domain-containing protein 3 (NALP3) dependent caspase-1 activation stimulates macrophages to secrete inteleukin-1beta (IL-1beta).	Uric Acid	12-17	caspase 1	Homo sapiens	117-126
24376319-8	2013	RESULTS: Urate induced caspase-1 activation and IL-1beta release by lymphocytes.	Uric Acid	9-14	caspase 1	Homo sapiens	23-32
23654106-5	2013	RESULTS: At 8h exposure to ZnO-NPs, there was no significant difference in the activity of LDH in the cell culture media among the ZnO-NPs-treated and control groups, but the activity of caspase-1 and the levels of IL-1beta in A549 cells were significantly increased in 20 microg/ml ZnO-NPs group compared to that in the control group (P &lt; 0.05).	Zinc Oxide	27-30	caspase 1	Homo sapiens	187-196
23654106-6	2013	Levels of IL-1beta and activity of LDH in the groups treated with ZnO-NPs (10 or 20 microg/ml) were significantly higher than that in the control group after 24 h exposure to ZnO-NPs, but there was no significant difference in the activity of caspase-1 among ZnO-NPs and control group.	Zinc Oxide	66-69	caspase 1	Homo sapiens	243-252
23412688-5	2013	Cholesterol crystals can activate the NLRP3 inflammasome, a multimolecular signaling complex of the innate immune system, resulting in caspase-1 mediated activation and secretion of proinflammatory interleukin-1 family cytokines.	Cholesterol	0-11	caspase 1	Homo sapiens	135-144
23266381-8	2013	Interestingly, DPC-333 was found to up-regulate mRNA expression of caspase-1 in hPBMC in a dose dependent fashion and selective caspase-1 inhibitor completely restored DPC-333 induced IL-1beta and IFN-gamma.	BMS561392	15-22	caspase 1	Homo sapiens	67-76
23590971-8	2013	The results suggest that the Fas signal favors the Th17-phenotypic features of human T cells through the caspase-1/Stat3 signaling pathway.	ammonium ferrous sulfate	29-32	caspase 1	Homo sapiens	105-114
23221073-6	2013	Active caspase-1 was detected using FAM-YVAD-FMK, a fluorescent-labeled inhibitor of caspases (FLICA) specific for caspase-1.	fam-yvad-fmk	36-48	caspase 1	Homo sapiens	7-16
23159926-0	2013	HMG-CoA reductase inhibitors activate caspase-1 in human monocytes depending on ATP release and P2X7 activation.	Adenosine Triphosphate	80-83	caspase 1	Homo sapiens	38-47
23221073-6	2013	Active caspase-1 was detected using FAM-YVAD-FMK, a fluorescent-labeled inhibitor of caspases (FLICA) specific for caspase-1.	fam-yvad-fmk	36-48	caspase 1	Homo sapiens	115-124
23221073-11	2013	Lysosomal destabilization induced by Leu-Leu-OMe triggered caspase-1 activation, IL-1beta secretion, and ARPE-19 cell death.	leucyl-leucine-methyl ester	37-48	caspase 1	Homo sapiens	59-68
23221073-12	2013	Blocking Leu-Leu-OMe-induced lysosomal disruption with the compound Gly-Phe-CHN(2) or inhibiting caspase-1 with Z-YVAD-FMK abrogated IL-1beta release and ARPE-19 cytotoxicity.	benzyloxycarbonyltyrosyl-valyl-alanyl-aspartic acid fluoromethyl ketone	112-122	caspase 1	Homo sapiens	97-106
23852607-1	2013	Sterile particulates such as monosodium urate crystals induce inflammasome activation resulting in activation of caspase-1, secretion of IL-1alpha, and processing of IL-1beta.	Uric Acid	29-45	caspase 1	Homo sapiens	113-122
23302643-10	2013	This is the first report implicating the activation of caspase-1 and the triggering of the pyroptosis pathway in TG-induced macrophage cell death.	Triglycerides	113-115	caspase 1	Homo sapiens	55-64
23295863-6	2013	First, CsA could upregulate Fas/Fas ligand, downregulate Bcl-2/Bcl-XL, and increase caspase-1 and caspase-3.	Cyclosporine	7-10	caspase 1	Homo sapiens	84-93
23295863-12	2013	CsA can induce renal cell apoptosis using five pathways in vivo and activated caspases might be the ultimate intersection of these pathways and the common intracellular pathway mediating apoptosis.	Cyclosporine	0-3	caspase 1	Homo sapiens	78-86
23302643-0	2013	Triglyceride-induced macrophage cell death is triggered by caspase-1.	Triglycerides	0-12	caspase 1	Homo sapiens	59-68
23302643-7	2013	Since caspase-1 is known to be involved in activation and secretion of IL-1beta protein and pyroptotic cell death, next we determined whether caspase-1 is associated with TG-induced macrophage cell death.	Triglycerides	171-173	caspase 1	Homo sapiens	142-151
23302643-8	2013	We found an increase in caspase-1 activity in TG-treated THP-1 macrophages and inhibition of caspase-1 activity using a specific inhibitor partially rescued cell death.	Triglycerides	46-48	caspase 1	Homo sapiens	24-33
24073415-2	2013	The consequent shortage of mevalonate-derived isoprenoid compounds results in an inflammatory phenotype, caused by the activation of the NALP3 inflammasome that determines an increased caspase-1 activation and IL-1 beta release.	Mevalonic Acid	27-37	caspase 1	Homo sapiens	185-194
24073415-2	2013	The consequent shortage of mevalonate-derived isoprenoid compounds results in an inflammatory phenotype, caused by the activation of the NALP3 inflammasome that determines an increased caspase-1 activation and IL-1 beta release.	Terpenes	46-56	caspase 1	Homo sapiens	185-194
23744438-8	2013	In the activated HMC-1 cells, caspase-1 activity was increased, whereas caspase-1 activity was decreased by pretreatment with curcumin.	Curcumin	126-134	caspase 1	Homo sapiens	72-81
22895087-7	2012	Both GG and LC705 induced interleukin-1beta production in macrophages that required caspase-1 activity.	lc705	12-17	caspase 1	Homo sapiens	84-93
23433161-5	2013	RESULTS: The activity of caspase-1 in 1 and 3 microg/ml CTP groups were (9.29 +- 0.30) and (8.67 +- 0.59) micromol/ml respectively which were both significantly increased compared to that (7.42 +- 0.59) micromol/ml in the control group (P &lt; 0.05) after 8 h exposure, but there was no significant difference in the activity of LDH and levels of IL-1beta in the cell culture media among the CTP and control groups.	Cytidine Triphosphate	56-59	caspase 1	Homo sapiens	25-34
23433161-5	2013	RESULTS: The activity of caspase-1 in 1 and 3 microg/ml CTP groups were (9.29 +- 0.30) and (8.67 +- 0.59) micromol/ml respectively which were both significantly increased compared to that (7.42 +- 0.59) micromol/ml in the control group (P &lt; 0.05) after 8 h exposure, but there was no significant difference in the activity of LDH and levels of IL-1beta in the cell culture media among the CTP and control groups.	Cytidine Triphosphate	392-395	caspase 1	Homo sapiens	25-34
23433161-7	2013	CONCLUSION: CTP treatment induced early increase in caspase-1 activity followed by the increase in LDH activity and IL-1 levels, indicative of pyroptosis in human bronchial epithelial cells.	Cytidine Triphosphate	12-15	caspase 1	Homo sapiens	52-61
22578178-11	2012	Furthermore, CCG suppressed the activation of caspase-1.	cationic colloidal gold	13-16	caspase 1	Homo sapiens	46-55
23190696-8	2012	Chondroprotective drugs such as chondroitin sulfate (CS) and the traditional Korean medicine, BaekJeol-Tang (BT) decrease production of TSLP and activation of caspase-1 and nuclear factor-kappaB.	Chondroitin Sulfates	32-51	caspase 1	Homo sapiens	159-168
23190696-8	2012	Chondroprotective drugs such as chondroitin sulfate (CS) and the traditional Korean medicine, BaekJeol-Tang (BT) decrease production of TSLP and activation of caspase-1 and nuclear factor-kappaB.	Chondroitin Sulfates	53-55	caspase 1	Homo sapiens	159-168
23190696-11	2012	The effects of CS and BT were associated with the downregulation of TSLP and caspase-1 through negative regulation of IL-32 pathways in RA.	Chondroitin Sulfates	15-17	caspase 1	Homo sapiens	77-86
23190696-11	2012	The effects of CS and BT were associated with the downregulation of TSLP and caspase-1 through negative regulation of IL-32 pathways in RA.	benzothiazole	22-24	caspase 1	Homo sapiens	77-86
23017228-2	2012	Direct treatment of THP-1 cells with Chry caused cell death, activation of caspase-1 and release of IL-1beta, while the addition of caspase-1 inhibitor, Z-YVAD-FMK, reduced IL-1beta, suggesting that Chry activated the caspase-1 mediated Nod-like receptor protein 3 (NLRP3) inflammasome; by comparison, LIB had less effects on all of these parameters.	benzyloxycarbonyltyrosyl-valyl-alanyl-aspartic acid fluoromethyl ketone	153-163	caspase 1	Homo sapiens	132-141
23017228-2	2012	Direct treatment of THP-1 cells with Chry caused cell death, activation of caspase-1 and release of IL-1beta, while the addition of caspase-1 inhibitor, Z-YVAD-FMK, reduced IL-1beta, suggesting that Chry activated the caspase-1 mediated Nod-like receptor protein 3 (NLRP3) inflammasome; by comparison, LIB had less effects on all of these parameters.	benzyloxycarbonyltyrosyl-valyl-alanyl-aspartic acid fluoromethyl ketone	153-163	caspase 1	Homo sapiens	132-141
22770526-5	2012	5 nm and 28 nm silver nanoparticles induced inflammasome formation and subsequent caspase-1 activation.	Silver	15-21	caspase 1	Homo sapiens	82-91
22906632-9	2012	In the activated HMC-1 cells, the activation of caspase-1 was increased, whereas the activation of caspase-1 was decreased by pretreatment with schizandrin.	schizandrin	144-155	caspase 1	Homo sapiens	99-108
22632542-1	2012	BACKGROUND: Colchicine, a first-line drug for the treatment of Behcet disease (BD), inhibits caspase-1 activation and inflammatory cytokine production.	Colchicine	12-22	caspase 1	Homo sapiens	93-102
22578802-5	2012	BAPTA-AM also inhibited the nuclear factor-kappaB activation, IkappaBalpha phosphorylation, receptor interacting protein2 (RIP2) expression, and caspase-1 activation in HMC-1 cells.	1,2-bis(2-aminophenoxy)ethane N,N,N',N'-tetraacetic acid acetoxymethyl ester	0-8	caspase 1	Homo sapiens	145-154
22837397-4	2012	A common SNP associated with reduced expression of a putative methionine salvage pathway dehydratase, apoptotic protease activating factor 1 (APAF1)-interacting protein (APIP), was associated with increased caspase-1-mediated cell death in response to Salmonella.	Methionine	62-72	caspase 1	Homo sapiens	207-216
22842458-2	2012	Because the tyrosine kinase inhibitor AG126 can prevent DAMP/PAMP induced activation of caspase-1, we hypothesized that tipping the tyrosine kinase/phosphatase balance toward phosphorylation would promote caspase-1 activation and cell death.	AG 127	38-43	caspase 1	Homo sapiens	88-97
22842458-2	2012	Because the tyrosine kinase inhibitor AG126 can prevent DAMP/PAMP induced activation of caspase-1, we hypothesized that tipping the tyrosine kinase/phosphatase balance toward phosphorylation would promote caspase-1 activation and cell death.	AG 127	38-43	caspase 1	Homo sapiens	205-214
22086213-8	2012	In the activated HMC-1 cells, the activation of caspase-1 was increased; whereas the activation of caspase-1 was decreased by pretreatment with Se.	Selenium	144-146	caspase 1	Homo sapiens	99-108
22578802-6	2012	These results provide evidence that calcium regulates the level of TSLP through RIP2/caspase-1/NF-kappaB/IkappaBalpha signal.	Calcium	36-43	caspase 1	Homo sapiens	85-94
21833768-0	2012	Epigallocatechin-3-O-gallate inhibits the production of thymic stromal lymphopoietin by the blockade of caspase-1/NF-kappaB pathway in mast cells.	epigallocatechin gallate	0-28	caspase 1	Homo sapiens	104-113
22583561-7	2012	Diacerein reduces association of the IL-1 receptor to form heterodimer complexes, repressing IL-1 and its related downstream events and impairing active IL-1 release due to the inhibition of the IL-1-converting enzyme (ICE).	diacerein	0-9	caspase 1	Homo sapiens	195-217
22583561-7	2012	Diacerein reduces association of the IL-1 receptor to form heterodimer complexes, repressing IL-1 and its related downstream events and impairing active IL-1 release due to the inhibition of the IL-1-converting enzyme (ICE).	diacerein	0-9	caspase 1	Homo sapiens	219-222
22404322-4	2012	In vitro studies of human keratinocytes were conducted to establish effects of finasteride, dihydrotestosterone (DHT), and testosterone on caspase-1 levels using immunoblot analysis.	Finasteride	79-90	caspase 1	Homo sapiens	139-148
22404322-4	2012	In vitro studies of human keratinocytes were conducted to establish effects of finasteride, dihydrotestosterone (DHT), and testosterone on caspase-1 levels using immunoblot analysis.	Dihydrotestosterone	92-111	caspase 1	Homo sapiens	139-148
22404322-4	2012	In vitro studies of human keratinocytes were conducted to establish effects of finasteride, dihydrotestosterone (DHT), and testosterone on caspase-1 levels using immunoblot analysis.	Dihydrotestosterone	113-116	caspase 1	Homo sapiens	139-148
22404322-4	2012	In vitro studies of human keratinocytes were conducted to establish effects of finasteride, dihydrotestosterone (DHT), and testosterone on caspase-1 levels using immunoblot analysis.	Testosterone	99-111	caspase 1	Homo sapiens	139-148
22404322-7	2012	In contrast, in men taking finasteride, caspase-1 levels were lower and were similar to those in normal controls.	Finasteride	27-38	caspase 1	Homo sapiens	40-49
22404322-8	2012	In vitro studies showed that keratinocytes treated with finasteride in combination with testosterone or DHT resulted in a significant decrease in caspase-1 expression.	Finasteride	56-67	caspase 1	Homo sapiens	146-155
22404322-8	2012	In vitro studies showed that keratinocytes treated with finasteride in combination with testosterone or DHT resulted in a significant decrease in caspase-1 expression.	Testosterone	88-100	caspase 1	Homo sapiens	146-155
22404322-8	2012	In vitro studies showed that keratinocytes treated with finasteride in combination with testosterone or DHT resulted in a significant decrease in caspase-1 expression.	Dihydrotestosterone	104-107	caspase 1	Homo sapiens	146-155
22404322-9	2012	CONCLUSION: In vivo and in vitro finasteride treatment resulted in lower caspase-1 expression, supporting the idea that androgens influence innate immunity involved in the hair cycle in AGA.	Finasteride	33-44	caspase 1	Homo sapiens	73-82
22100755-5	2012	We show that DWCNTs-induced IL-1beta secretion is exclusively linked to caspase-1 and to Nlrp3 inflammasome activation in human monocytes.	dwcnts	13-19	caspase 1	Homo sapiens	72-81
22521247-0	2012	Imidazoquinoline Toll-like receptor 8 agonists activate human newborn monocytes and dendritic cells through adenosine-refractory and caspase-1-dependent pathways.	THOS Streptonigrin	0-16	caspase 1	Homo sapiens	133-142
22521247-11	2012	Newborn MoDCs displayed impaired LPS/ATP-induced caspase-1-mediated IL-1beta production but robust 3M-002-induced caspase-1-mediated inflammasome activation independent of exogenous ATP.	Adenosine Triphosphate	37-40	caspase 1	Homo sapiens	49-58
21833768-7	2012	Furthermore, EGCG inhibited the activation of caspase-1 in HMC-1 cells.	epigallocatechin gallate	13-17	caspase 1	Homo sapiens	46-55
21933296-3	2012	We show that a novel specific P2X(7)  receptor antagonist, GSK1370319A, inhibits ATP-induced increase in IL-1beta release and caspase 1 activation in lipopolysaccharide (LPS)-primed mixed glia by blocking assembly of the inflammasome in a pannexin 1-dependent manner.	GSK 1370319A	59-70	caspase 1	Homo sapiens	126-135
22402362-10	2012	CONCLUSIONS: Alcohol-induced MMPs activation is a key mechanism for dysfunction of BBB via degradation of VEGFR-2 protein and activation of caspase-1 or IL-1beta release.	Alcohols	13-20	caspase 1	Homo sapiens	140-149
21933296-5	2012	Significantly, GSK1370319A attenuates age-related deficits in long-term potentiation (LTP) and inhibits the accompanying age-related caspase 1 activity.	GSK 1370319A	15-26	caspase 1	Homo sapiens	133-142
21344174-9	2012	Furthermore, theanine suppressed the activation of caspase-1 and the expression of receptor interacting protein-2.	theanine	13-21	caspase 1	Homo sapiens	51-60
21933296-3	2012	We show that a novel specific P2X(7)  receptor antagonist, GSK1370319A, inhibits ATP-induced increase in IL-1beta release and caspase 1 activation in lipopolysaccharide (LPS)-primed mixed glia by blocking assembly of the inflammasome in a pannexin 1-dependent manner.	Adenosine Triphosphate	81-84	caspase 1	Homo sapiens	126-135
22075093-0	2012	The cationic lipid, diC14 amidine, extends the adjuvant properties of aluminum salts through a TLR-4- and caspase-1-independent mechanism.	N-t-butyl-n'-tetradecyl-3-tetradecylaminopropionamidine	20-33	caspase 1	Homo sapiens	106-115
22323498-6	2012	In microarray analyses of HeLa cells, a set of 19 genes related to interferon signaling was significantly over-represented among genes regulated by doxorubicin exposure, including signal transducer and activator of transcription (STAT) 1 and 2, interferon regulatory factor 9, N-myc and STAT interactor, and caspase 1.	Doxorubicin	148-159	caspase 1	Homo sapiens	308-317
22515414-10	2012	Furthermore, PA induced caspase-1 activation in a dose-dependent manner, resulting in exacerbating of procaspase-1 and pro-IL-1beta processing.	Palmitates	13-15	caspase 1	Homo sapiens	24-33
22515414-11	2012	Knockdown of NLRC4 partially abrogated PA-induced caspase-1 activation and IL-1beta maturation and completely abolished these events in the presence of DHA.	Palmitates	39-41	caspase 1	Homo sapiens	50-59
22515414-12	2012	CONCLUSIONS: Our findings indicate DHA attenuates PA-induced lipid accumulation and inflammation through suppressing NLRC4 inflammasome activation, caspase-1 activation and IL-1beta cleavage.	Docosahexaenoic Acids	35-38	caspase 1	Homo sapiens	148-157
22515414-12	2012	CONCLUSIONS: Our findings indicate DHA attenuates PA-induced lipid accumulation and inflammation through suppressing NLRC4 inflammasome activation, caspase-1 activation and IL-1beta cleavage.	Palmitates	50-52	caspase 1	Homo sapiens	148-157
22140296-0	2012	Some natural flavonoids are competitive inhibitors of Caspase-1, -3 and -7 despite their cellular toxicity.	Flavonoids	13-23	caspase 1	Homo sapiens	54-74
22140296-3	2012	It has been discovered that several flavonoids are inhibitors of caspases.	Flavonoids	36-46	caspase 1	Homo sapiens	65-73
22322153-8	2012	The inducing effect of PFOA on the pro-inflammatory cytokines was nuclear factor-kappaB, p38 mitogen-activated protein kinase, and caspase-1 dependent.	perfluorooctanoic acid	23-27	caspase 1	Homo sapiens	131-140
22568037-0	2012	Identification of curcumin targets in neuroinflammatory pathways: molecular docking scores with GSK-3beta, p38 MAPK, COX, ICE and TACE enzymes.	Curcumin	18-26	caspase 1	Homo sapiens	122-125
22568037-2	2012	The anti-inflammatory pathway of curcumin was identified through docking with of curcumin with various inflammation inducing enzymes like glycogen synthase kinase (GSK-3beta), p38 mitogen activated protein kinase (MAPK), COX, interleukin-1beta converting enzyme (ICE) and tumor necrosis factor-alpha converting enzyme (TACE).	Curcumin	33-41	caspase 1	Homo sapiens	226-261
22568037-2	2012	The anti-inflammatory pathway of curcumin was identified through docking with of curcumin with various inflammation inducing enzymes like glycogen synthase kinase (GSK-3beta), p38 mitogen activated protein kinase (MAPK), COX, interleukin-1beta converting enzyme (ICE) and tumor necrosis factor-alpha converting enzyme (TACE).	Curcumin	33-41	caspase 1	Homo sapiens	263-266
22568037-2	2012	The anti-inflammatory pathway of curcumin was identified through docking with of curcumin with various inflammation inducing enzymes like glycogen synthase kinase (GSK-3beta), p38 mitogen activated protein kinase (MAPK), COX, interleukin-1beta converting enzyme (ICE) and tumor necrosis factor-alpha converting enzyme (TACE).	Curcumin	81-89	caspase 1	Homo sapiens	226-261
22568037-2	2012	The anti-inflammatory pathway of curcumin was identified through docking with of curcumin with various inflammation inducing enzymes like glycogen synthase kinase (GSK-3beta), p38 mitogen activated protein kinase (MAPK), COX, interleukin-1beta converting enzyme (ICE) and tumor necrosis factor-alpha converting enzyme (TACE).	Curcumin	81-89	caspase 1	Homo sapiens	263-266
22014003-4	2012	Among the 62 hits of a screen of ~15 000 thiol-containing fragments, a naphthyl-thiazole-containing molecule was identified that selectively inhibited and labeled the allosteric cysteine in the p10 subunit of caspase-5, but caused very little inhibition or labeling of caspase-1.	Sulfhydryl Compounds	41-46	caspase 1	Homo sapiens	269-278
22014003-4	2012	Among the 62 hits of a screen of ~15 000 thiol-containing fragments, a naphthyl-thiazole-containing molecule was identified that selectively inhibited and labeled the allosteric cysteine in the p10 subunit of caspase-5, but caused very little inhibition or labeling of caspase-1.	naphthyl-thiazole	71-88	caspase 1	Homo sapiens	269-278
22014003-4	2012	Among the 62 hits of a screen of ~15 000 thiol-containing fragments, a naphthyl-thiazole-containing molecule was identified that selectively inhibited and labeled the allosteric cysteine in the p10 subunit of caspase-5, but caused very little inhibition or labeling of caspase-1.	Cysteine	178-186	caspase 1	Homo sapiens	269-278
22832107-2	2012	Here we show that age-related increase in "lipotoxic danger signals" such as free cholesterol (FC) and ceramides, leads to thymic caspase-1 activation via the Nlrp3 inflammasome.	Cholesterol	82-93	caspase 1	Homo sapiens	130-139
22832107-2	2012	Here we show that age-related increase in "lipotoxic danger signals" such as free cholesterol (FC) and ceramides, leads to thymic caspase-1 activation via the Nlrp3 inflammasome.	Fc(alpha) receptor	95-97	caspase 1	Homo sapiens	130-139
22832107-2	2012	Here we show that age-related increase in "lipotoxic danger signals" such as free cholesterol (FC) and ceramides, leads to thymic caspase-1 activation via the Nlrp3 inflammasome.	Ceramides	103-112	caspase 1	Homo sapiens	130-139
22318382-9	2012	Furthermore, caspase-1 inhibition prevented poly(I:C)-induced caspase-3/7 activation.	Poly I-C	44-53	caspase 1	Homo sapiens	13-22
22166834-0	2012	Methallyl isothiocyanate inhibits the caspase-1 activity through the inhibition of intracellular calcium levels.	Methallyl isothiocyanate	0-24	caspase 1	Homo sapiens	38-47
22166834-0	2012	Methallyl isothiocyanate inhibits the caspase-1 activity through the inhibition of intracellular calcium levels.	Calcium	97-104	caspase 1	Homo sapiens	38-47
22276851-0	2012	Caspase-1 and -3 inhibiting drimane sesquiterpenoids from the extremophilic fungus Penicillium solitum.	sesquiterpenoids	36-52	caspase 1	Homo sapiens	0-9
22155150-5	2012	Moreover, inhibition of extracellular signal-related kinase (ERK), nuclear factor-kappaB (NF-kappaB) and caspase-1 significantly suppressed oridonin-induced phagocytosis and autophagy.	oridonin	140-148	caspase 1	Homo sapiens	105-114
22155150-6	2012	In addition, oridonin increased the protein levels of p-ERK, NF-kappaB, caspase-1 and pro IL-1beta.	oridonin	13-21	caspase 1	Homo sapiens	72-81
22155150-7	2012	Autophagic inhibitor 3-methyladenine (3-MA) decreased phagocytosis and the expression of ERK whereas increased the expression of NF-kappaB- and caspase-1-mediated IL-1beta release.	3-methyladenine	21-36	caspase 1	Homo sapiens	144-153
22155150-7	2012	Autophagic inhibitor 3-methyladenine (3-MA) decreased phagocytosis and the expression of ERK whereas increased the expression of NF-kappaB- and caspase-1-mediated IL-1beta release.	3-methyladenine	38-42	caspase 1	Homo sapiens	144-153
22155150-11	2012	These results demonstrated that autophagy enhanced oridonin-induced phagocytosis through feedback regulation of ERK, NF-kappaB- and caspase-1-mediated IL-1beta release.	oridonin	51-59	caspase 1	Homo sapiens	132-141
22075093-0	2012	The cationic lipid, diC14 amidine, extends the adjuvant properties of aluminum salts through a TLR-4- and caspase-1-independent mechanism.	aluminum salts	70-84	caspase 1	Homo sapiens	106-115
22247602-7	2012	As for the phosphorylation pathway, PD98059 (ERK1/2 inhibitor), SB203580 (p38 MAPK inhibitor), SP600125 (JNK1/2 inhibitor) decreased caspase-1 activity and interleukin-1beta production to approximately 50% of the controls.	pyrazolanthrone	95-103	caspase 1	Homo sapiens	133-142
23295692-8	2012	We found that macrophage-like cells readily take up TiO(2) after 6 h. Incubation of cells with TiO(2) resulted in the assembly of NLRP3 with caspase-1.	titanium dioxide	52-58	caspase 1	Homo sapiens	141-150
23295692-8	2012	We found that macrophage-like cells readily take up TiO(2) after 6 h. Incubation of cells with TiO(2) resulted in the assembly of NLRP3 with caspase-1.	titanium dioxide	95-101	caspase 1	Homo sapiens	141-150
22247602-6	2012	Butyrate with lipopolysaccharide increased caspase-1 activity more than lipopolysaccharide alone.	Butyrates	0-8	caspase 1	Homo sapiens	43-52
22247602-7	2012	As for the phosphorylation pathway, PD98059 (ERK1/2 inhibitor), SB203580 (p38 MAPK inhibitor), SP600125 (JNK1/2 inhibitor) decreased caspase-1 activity and interleukin-1beta production to approximately 50% of the controls.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	36-43	caspase 1	Homo sapiens	133-142
22247602-12	2012	In conclusions, butyrate enhances interleukin-1beta production by activating caspase-1, via reactive oxygen species, the phosphorylation of MAPK, and G protein mediated pathways in lipopolysaccharide stimulated THP-1 cells.	Butyrates	16-24	caspase 1	Homo sapiens	77-86
22247602-7	2012	As for the phosphorylation pathway, PD98059 (ERK1/2 inhibitor), SB203580 (p38 MAPK inhibitor), SP600125 (JNK1/2 inhibitor) decreased caspase-1 activity and interleukin-1beta production to approximately 50% of the controls.	SB 203580	64-72	caspase 1	Homo sapiens	133-142
22247602-12	2012	In conclusions, butyrate enhances interleukin-1beta production by activating caspase-1, via reactive oxygen species, the phosphorylation of MAPK, and G protein mediated pathways in lipopolysaccharide stimulated THP-1 cells.	Reactive Oxygen Species	92-115	caspase 1	Homo sapiens	77-86
23226468-13	2012	A1PI-M co-localized with caspase-1 in gel-filtered cytoplasmic THP-1 preparations, and was co-immunoprecipitated with caspase 1 from nigericin-stimulated THP-1 cell lysate.	Nigericin	133-142	caspase 1	Homo sapiens	118-127
23226286-8	2012	Finally, it is shown that sea bass and avian IL-1beta are specifically cleaved by caspase-1 at different but phylogenetically conserved aspartates, distinct from the cleavage site of mammalian IL-1beta.	Aspartic Acid	136-146	caspase 1	Homo sapiens	82-91
22111911-10	2011	The PS-NH(2)-mediated proinflammatory macrophage activation could be antagonized by the radical scavenger N-acetyl-L-cysteine, which prevented mitochondrial damage, caspase-1 activation, and the subsequent release of IL-1beta.	ps-nh(2)	4-12	caspase 1	Homo sapiens	165-174
25191407-2	2012	Recent studies show that binding of ATP to the ionotropic P2X7 receptor of inflammatory cells (macrophages and monocytes) will induce caspase 1 activation.	Adenosine Triphosphate	36-39	caspase 1	Homo sapiens	134-143
23028481-0	2012	(-)-Epigallocatechin-3-gallate protects against NO-induced ototoxicity through the regulation of caspase- 1, caspase-3, and NF-kappaB activation.	epigallocatechin gallate	0-30	caspase 1	Homo sapiens	97-107
22844468-9	2012	In addition, caspase-1 was activated and involved in proteolytic cleavage and secretion of IL-1beta in AbM-treated macrophages.	abm	103-106	caspase 1	Homo sapiens	13-22
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 1	Homo sapiens	256-261
22393394-7	2012	CONCLUSION/SIGNIFICANCE: Our results identify a mechanism mediated by Reactive Oxygen Species (ROS) production and potassium efflux as the two danger signals that link JEV infection to caspase-1 activation resulting in subsequent IL-1beta and IL-18 maturation.	Reactive Oxygen Species	70-93	caspase 1	Homo sapiens	185-194
22393394-7	2012	CONCLUSION/SIGNIFICANCE: Our results identify a mechanism mediated by Reactive Oxygen Species (ROS) production and potassium efflux as the two danger signals that link JEV infection to caspase-1 activation resulting in subsequent IL-1beta and IL-18 maturation.	Reactive Oxygen Species	95-98	caspase 1	Homo sapiens	185-194
22393394-7	2012	CONCLUSION/SIGNIFICANCE: Our results identify a mechanism mediated by Reactive Oxygen Species (ROS) production and potassium efflux as the two danger signals that link JEV infection to caspase-1 activation resulting in subsequent IL-1beta and IL-18 maturation.	Potassium	115-124	caspase 1	Homo sapiens	185-194
22111911-10	2011	The PS-NH(2)-mediated proinflammatory macrophage activation could be antagonized by the radical scavenger N-acetyl-L-cysteine, which prevented mitochondrial damage, caspase-1 activation, and the subsequent release of IL-1beta.	Acetylcysteine	106-125	caspase 1	Homo sapiens	165-174
21673342-5	2011	gammadelta T cell-independent NK cell activation in response to zoledronate was because of downstream depletion of endogenous prenyl pyrophosphates and subsequent caspase-1 activation in DC-like cells, which then provide mature IL-18 and IL-1beta for the activation of IL-2-primed NK cells.	Zoledronic Acid	64-75	caspase 1	Homo sapiens	163-172
22151792-2	2011	In contrast to inhibitors that target the active site of the viral protease, bevirimat specifically inhibits a single cleavage event, the final processing step for the Gag precursor where p25 (CA-SP1) is cleaved to p24 (CA) and SP1.	bevirimat	77-86	caspase 1	Homo sapiens	193-199
21320026-0	2011	Inhibitory effects of chelidonic acid on IL-6 production by blocking NF-kappaB and caspase-1 in HMC-1 cells.	chelidonic acid	22-37	caspase 1	Homo sapiens	83-92
21856447-0	2011	Berberine inhibits the production of thymic stromal lymphopoietin by the blockade of caspase-1/NF-kappaB pathway in mast cells.	Berberine	0-9	caspase 1	Homo sapiens	85-94
21982776-5	2011	Since inflammasomes are involved in IL-1beta secretion, we investigated whether IL-1beta suppression was mediated by inflammasomes, and found that EGCG treatment led to downregulation of the inflammasome component, NLRP1, and reduced caspase-1 activation.	epigallocatechin gallate	147-151	caspase 1	Homo sapiens	234-243
21963452-0	2011	Naringenin suppresses the production of thymic stromal lymphopoietin through the blockade of RIP2 and caspase-1 signal cascade in mast cells.	naringenin	0-10	caspase 1	Homo sapiens	102-111
21963452-8	2011	In the activated HMC-1 cells, the activations of receptor-interacting protein (RIP)2 and caspase-1 were increased, whereas the activations of RIP2 and caspase-1 were decreased by pretreatment with naringenin.	naringenin	197-207	caspase 1	Homo sapiens	89-98
21963452-8	2011	In the activated HMC-1 cells, the activations of receptor-interacting protein (RIP)2 and caspase-1 were increased, whereas the activations of RIP2 and caspase-1 were decreased by pretreatment with naringenin.	naringenin	197-207	caspase 1	Homo sapiens	151-160
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 1	Homo sapiens	45-66
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 1	Homo sapiens	208-229
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.	cholix	275-281	caspase 1	Homo sapiens	45-66
21673342-6	2011	Pharmacologic inhibition of caspase-1 almost abolished IFN-gamma production in NK cells and gammadelta T lymphocytes, indicating that caspase-1-mediated cytokine maturation is the crucial mechanism underlying innate lymphocyte activation in response to zoledronate.	Zoledronic Acid	253-264	caspase 1	Homo sapiens	28-37
21673342-6	2011	Pharmacologic inhibition of caspase-1 almost abolished IFN-gamma production in NK cells and gammadelta T lymphocytes, indicating that caspase-1-mediated cytokine maturation is the crucial mechanism underlying innate lymphocyte activation in response to zoledronate.	Zoledronic Acid	253-264	caspase 1	Homo sapiens	134-143
21270263-9	2011	CONCLUSIONS: High glucose activates caspase-1 in human and murine adipose tissue.	Glucose	18-25	caspase 1	Homo sapiens	36-45
21684332-11	2011	Interestingly, the inflammasome activator monosodium urate crystals (MSU) induced the release of CXCL-8 and IL-1beta and the caspase-1 inhibitor Z-VADDCB suppressed the CS-induced release of CXCL-8.	z-VAD-DCB	145-153	caspase 1	Homo sapiens	125-134
21684332-11	2011	Interestingly, the inflammasome activator monosodium urate crystals (MSU) induced the release of CXCL-8 and IL-1beta and the caspase-1 inhibitor Z-VADDCB suppressed the CS-induced release of CXCL-8.	Cesium	169-171	caspase 1	Homo sapiens	125-134
21684332-12	2011	In addition, CS, CpGODN, lipopolysaccharide and MSU all increased the expression of caspase-1 and IL-1beta.	Cesium	13-15	caspase 1	Homo sapiens	84-93
21684332-12	2011	In addition, CS, CpGODN, lipopolysaccharide and MSU all increased the expression of caspase-1 and IL-1beta.	CPG-oligonucleotide	17-23	caspase 1	Homo sapiens	84-93
21684332-12	2011	In addition, CS, CpGODN, lipopolysaccharide and MSU all increased the expression of caspase-1 and IL-1beta.	msu	48-51	caspase 1	Homo sapiens	84-93
21804020-3	2011	Active caspase-1 increased cellular membrane permeability and intracellular calcium levels, which facilitated lysosome exocytosis and release of host antimicrobial factors and microbial products.	Calcium	76-83	caspase 1	Homo sapiens	7-16
21525001-6	2011	The cell death that occurred with carbon black nanoparticle exposure was identified as pyroptosis by the protective effect of a caspase 1 inhibitor and a pyroptosis inhibitor.	Carbon	34-40	caspase 1	Homo sapiens	128-137
21463955-7	2011	Furthermore, caspase-1 inhibitor decreased the expression of TSLP mRNA induced by PMA plus A23187.	Calcimycin	91-97	caspase 1	Homo sapiens	13-22
21593871-9	2011	CASP1 displays numerous features required for a constituent of a plant junctional complex: it forms complexes with other CASPs; it becomes immobile upon localization; and it sediments like a large polymer.	Polymers	197-204	caspase 1	Homo sapiens	0-5
21478880-3	2011	We show that the saturated fatty acid palmitate, but not unsaturated oleate, induces the activation of the NLRP3-ASC inflammasome, causing caspase-1, IL-1beta and IL-18 production.	saturated fatty acid palmitate	17-47	caspase 1	Homo sapiens	139-148
21526214-0	2011	Rosmarinic acid, active component of Dansam-Eum attenuates ototoxicity of cochlear hair cells through blockage of caspase-1 activity.	rosmarinic acid	0-15	caspase 1	Homo sapiens	114-123
21526214-7	2011	A molecular docking simulation and a kinetic assay show that RA controls the activity of caspase-1 by interaction with the active site of caspase-1.	rosmarinic acid	61-63	caspase 1	Homo sapiens	89-98
21526214-7	2011	A molecular docking simulation and a kinetic assay show that RA controls the activity of caspase-1 by interaction with the active site of caspase-1.	rosmarinic acid	61-63	caspase 1	Homo sapiens	138-147
21526214-8	2011	Pretreatment of RA inhibited caspase-1 downstream signal pathway, such as the activation of caspase-3 and 9, release of cytochrome c, translocation of apoptosis-inducing factor, up-regulation of Bax, down-regulation of Bcl-2, generation of reactive oxygen species, and activation of nuclear factor-kappaB.	rosmarinic acid	16-18	caspase 1	Homo sapiens	29-38
21526214-8	2011	Pretreatment of RA inhibited caspase-1 downstream signal pathway, such as the activation of caspase-3 and 9, release of cytochrome c, translocation of apoptosis-inducing factor, up-regulation of Bax, down-regulation of Bcl-2, generation of reactive oxygen species, and activation of nuclear factor-kappaB.	Reactive Oxygen Species	240-263	caspase 1	Homo sapiens	29-38
20604677-0	2011	The regulatory mechanism of beta-eudesmol is through the suppression of caspase-1 activation in mast cell-mediated inflammatory response.	beta-eudesmol	28-41	caspase 1	Homo sapiens	72-81
20604677-6	2011	In addition, beta-eudesmol suppressed the activation of caspase-1 and expression of receptor-interacting protein-2.	beta-eudesmol	13-26	caspase 1	Homo sapiens	56-65
21052690-0	2011	The 5352 A allele of the pro-inflammatory caspase-1 gene predicts late-acquired stent malapposition in STEMI patients treated with sirolimus stents.	Sirolimus	131-140	caspase 1	Homo sapiens	42-51
21052690-8	2011	We found a significantly higher risk for LASM in patients carrying the caspase-1 (CASP1) 5352 A allele (RR = 2.32; 95% CI 1.22-4.42).	lasm	41-45	caspase 1	Homo sapiens	71-80
21052690-8	2011	We found a significantly higher risk for LASM in patients carrying the caspase-1 (CASP1) 5352 A allele (RR = 2.32; 95% CI 1.22-4.42).	lasm	41-45	caspase 1	Homo sapiens	82-87
21052690-11	2011	In conclusion, carriers of the 5352 A allele in the caspase-1 gene are at increased risk of developing LASM after SES implantation.	lasm	103-107	caspase 1	Homo sapiens	52-61
21052690-11	2011	In conclusion, carriers of the 5352 A allele in the caspase-1 gene are at increased risk of developing LASM after SES implantation.	ses	114-117	caspase 1	Homo sapiens	52-61
21184820-7	2011	Additionally, IHT inhibited the production of interleukin (IL)-6, IL-8, and TNF-alpha, as well as the activation of nuclear factor-kappaB and caspase-1 in PMACI-stimulated HMC-1.	pmaci	155-160	caspase 1	Homo sapiens	142-151
21270263-7	2011	In human adipose tissue, high glucose resulted in a 10-fold upregulation of TXNIP gene expression levels (P &lt; 0.01) and a 10% elevation of caspase-1 activity (P &lt; 0.05), together with induction of IL-1beta transcription (twofold, P &lt; 0.01) and a significant increase in IL-1beta secretion.	Glucose	30-37	caspase 1	Homo sapiens	142-151
21915284-10	2011	These results advocate the critical role of the P2X7/caspase 1 axis in CS-induced inflammation, highlighting this as a possible therapeutic target in combating COPD.	Cesium	71-73	caspase 1	Homo sapiens	53-62
20632067-4	2011	XOD produces uric acid and reactive oxygen species, which could activate Nalp3 and therefore induce activation of caspase 1, known to convert inactive pro-IL-1beta into active IL-1beta.	Uric Acid	13-22	caspase 1	Homo sapiens	114-123
20632067-4	2011	XOD produces uric acid and reactive oxygen species, which could activate Nalp3 and therefore induce activation of caspase 1, known to convert inactive pro-IL-1beta into active IL-1beta.	Reactive Oxygen Species	27-50	caspase 1	Homo sapiens	114-123
20655126-4	2011	Here we demonstrate that the proinflammatory lipid lysophosphatidylcholine (LPC) initiates microglial caspase-1 activation in a Na(+)-dependent manner.	Lysophosphatidylcholines	76-79	caspase 1	Homo sapiens	102-111
20655126-5	2011	LPC-induced caspase-1 activity was almost completely inhibited upon omission of extracellular Na(+), but was unaffected by inhibition of Na(+)/K(+)-ATPase with ouabain or by inhibition of Na(+)/H(+) antiport with amiloride.	Lysophosphatidylcholines	0-3	caspase 1	Homo sapiens	12-21
20655126-5	2011	LPC-induced caspase-1 activity was almost completely inhibited upon omission of extracellular Na(+), but was unaffected by inhibition of Na(+)/K(+)-ATPase with ouabain or by inhibition of Na(+)/H(+) antiport with amiloride.	Amiloride	213-222	caspase 1	Homo sapiens	12-21
20655126-8	2011	Since ROS production was found to be crucial to caspase-1 activation in LPC-stimulated microglia, the Na(+) dependence of caspase-1 can be related to the Na(+) dependence of NADPH oxidase.	Reactive Oxygen Species	6-9	caspase 1	Homo sapiens	48-57
20655126-8	2011	Since ROS production was found to be crucial to caspase-1 activation in LPC-stimulated microglia, the Na(+) dependence of caspase-1 can be related to the Na(+) dependence of NADPH oxidase.	Lysophosphatidylcholines	72-75	caspase 1	Homo sapiens	48-57
20655126-8	2011	Since ROS production was found to be crucial to caspase-1 activation in LPC-stimulated microglia, the Na(+) dependence of caspase-1 can be related to the Na(+) dependence of NADPH oxidase.	Lysophosphatidylcholines	72-75	caspase 1	Homo sapiens	122-131
20655126-9	2011	In summary, it is suggested that in LPC-activated microglia, Na(+) influx is required for the production of NADPH oxidase-mediated ROS, which subsequently stimulate caspase-1 activity.	Reactive Oxygen Species	131-134	caspase 1	Homo sapiens	165-174
20940146-5	2011	NOMID tumor cells showed high PKA activity, and an increase in their cAMP signaling led to PKA-specific activation of caspase-1.	Cyclic AMP	69-73	caspase 1	Homo sapiens	118-127
20940146-9	2011	These data reveal a previously unsuspected link between abnormal cAMP signaling and defective regulation of the inflammasome and suggest that caspase-1 and PGE2 inhibition may be therapeutic targets in bone lesions associated with defects of these two pathways.	Cyclic AMP	65-69	caspase 1	Homo sapiens	142-151
21128834-0	2011	Specific blockage of caspase-1 activation by purple bamboo-salt prevents apoptosis of auditory cell line, HEI-OC1.	Salts	59-63	caspase 1	Homo sapiens	21-30
21128834-9	2011	Lastly, BS suppressed cisplatin-induced caspase-1 activation.	Cisplatin	22-31	caspase 1	Homo sapiens	40-49
21628878-8	2011	The underlying mechanism involves, at least in part, inactivation of caspase-1, which provides new evidence for therapeutic application of SA to target inflammatory processes.	saikosaponin D	139-141	caspase 1	Homo sapiens	69-78
20655126-0	2011	Sodium dependence of lysophosphatidylcholine-induced caspase-1 activity and reactive oxygen species generation.	Sodium	0-6	caspase 1	Homo sapiens	53-62
20655126-0	2011	Sodium dependence of lysophosphatidylcholine-induced caspase-1 activity and reactive oxygen species generation.	Lysophosphatidylcholines	21-44	caspase 1	Homo sapiens	53-62
20655126-4	2011	Here we demonstrate that the proinflammatory lipid lysophosphatidylcholine (LPC) initiates microglial caspase-1 activation in a Na(+)-dependent manner.	Lysophosphatidylcholines	51-74	caspase 1	Homo sapiens	102-111
22046441-11	2011	Moreover, the constitutive knockdown of the IFI16 expression in THP-1 cells increased the basal and induced [induced by poly(dA:dT) or alum] activation of the caspase-1 by the AIM2 and NLRP3 inflammasomes.	poly(	120-125	caspase 1	Homo sapiens	159-168
22046441-11	2011	Moreover, the constitutive knockdown of the IFI16 expression in THP-1 cells increased the basal and induced [induced by poly(dA:dT) or alum] activation of the caspase-1 by the AIM2 and NLRP3 inflammasomes.	amsonic acid	125-128	caspase 1	Homo sapiens	159-168
22046441-11	2011	Moreover, the constitutive knockdown of the IFI16 expression in THP-1 cells increased the basal and induced [induced by poly(dA:dT) or alum] activation of the caspase-1 by the AIM2 and NLRP3 inflammasomes.	Thymidine	128-131	caspase 1	Homo sapiens	159-168
22046441-11	2011	Moreover, the constitutive knockdown of the IFI16 expression in THP-1 cells increased the basal and induced [induced by poly(dA:dT) or alum] activation of the caspase-1 by the AIM2 and NLRP3 inflammasomes.	aluminum sulfate	135-139	caspase 1	Homo sapiens	159-168
21915284-4	2011	The aim of this study was to determine whether activation of the P2X7/caspase 1 pathway has a functional role in CS-induced airway inflammation.	Cesium	113-115	caspase 1	Homo sapiens	70-79
21915284-6	2011	We have demonstrated that CS-induced neutrophilia in a pre-clinical model is temporally associated with markers of inflammasome activation, (increased caspase 1 activity and release of IL-1beta/IL-18) in the lungs.	Cesium	26-28	caspase 1	Homo sapiens	151-160
21915284-8	2011	Furthermore, we demonstrated that the role of this pathway was not restricted to early stages of disease development by showing increased caspase 1 activation in lungs from a more chronic exposure to CS and from patients with COPD.	Cesium	200-202	caspase 1	Homo sapiens	138-147
20955686-1	2010	A series of substrate-based alpha-keto-beta-aldehyde (glyoxal) sequences have been synthesised and evaluated as inhibitors of the caspase family of cysteine proteases.	Glyoxal	54-61	caspase 1	Homo sapiens	130-137
21151640-9	2010	Initiation of disassembly of the immature Gag lattice requires cleavage to occur on both sides of CA-SP1, while assembly of the mature core also requires cleavage of SP1 from CA.	Glycosaminoglycans	42-45	caspase 1	Homo sapiens	98-104
21108840-9	2010	In addition, CYT and quercetin inhibited LPS-induced IL-32 expression and caspase-1 activation.	Quercetin	21-30	caspase 1	Homo sapiens	74-83
20955686-3	2010	For example, a palmitic acid containing sequence pal-Tyr-Val-Ala-Asp-glyoxal was demonstrated to be an extremely effective inhibitor of caspase-1, inhibiting not only the action of the protease against synthetic fluorogenic substrates (K(i)=0.3 nM) but also blocking its processing of pro-interleukin-1beta (pro-IL-1beta).	Palmitic Acid	15-28	caspase 1	Homo sapiens	136-145
20955686-3	2010	For example, a palmitic acid containing sequence pal-Tyr-Val-Ala-Asp-glyoxal was demonstrated to be an extremely effective inhibitor of caspase-1, inhibiting not only the action of the protease against synthetic fluorogenic substrates (K(i)=0.3 nM) but also blocking its processing of pro-interleukin-1beta (pro-IL-1beta).	pal-tyr-val-ala-asp-glyoxal	49-76	caspase 1	Homo sapiens	136-145
20955686-4	2010	In addition, the peptide Ac-Asp-Glu-Val-Asp-glyoxal, which is based on the consensus cleavage sequence for caspase-3, is a potent inhibitor of this protease (K(i)=0.26 nM) yet only functions as a comparatively modest inhibitor of caspase-1 (K(i)=451 nM).	ac-asp-glu-val-asp-glyoxal	25-51	caspase 1	Homo sapiens	230-239
20674352-0	2010	Inhibition of interleukin-1beta converting enzyme (ICE or caspase 1) by aspartyl acyloxyalkyl ketones and aspartyl amidooxyalkyl ketones.	aspartyl acyloxyalkyl ketones	72-101	caspase 1	Homo sapiens	14-49
20656488-0	2010	Succinic acid amides as P2-P3 replacements for inhibitors of interleukin-1beta converting enzyme (ICE or caspase 1).	succinic acid amides	0-20	caspase 1	Homo sapiens	98-101
20656488-0	2010	Succinic acid amides as P2-P3 replacements for inhibitors of interleukin-1beta converting enzyme (ICE or caspase 1).	succinic acid amides	0-20	caspase 1	Homo sapiens	105-114
20635349-8	2010	We found the EGR-1, caspase-1 and TSP-1 genes to be markedly up-regulated when NPC-pBIG2i-IGFBP-6 was treated with doxycycline.	Doxycycline	115-126	caspase 1	Homo sapiens	20-29
20674352-0	2010	Inhibition of interleukin-1beta converting enzyme (ICE or caspase 1) by aspartyl acyloxyalkyl ketones and aspartyl amidooxyalkyl ketones.	aspartyl acyloxyalkyl ketones	72-101	caspase 1	Homo sapiens	51-54
20674352-0	2010	Inhibition of interleukin-1beta converting enzyme (ICE or caspase 1) by aspartyl acyloxyalkyl ketones and aspartyl amidooxyalkyl ketones.	aspartyl acyloxyalkyl ketones	72-101	caspase 1	Homo sapiens	58-67
20656488-0	2010	Succinic acid amides as P2-P3 replacements for inhibitors of interleukin-1beta converting enzyme (ICE or caspase 1).	p2-p3	24-29	caspase 1	Homo sapiens	105-114
20674352-0	2010	Inhibition of interleukin-1beta converting enzyme (ICE or caspase 1) by aspartyl acyloxyalkyl ketones and aspartyl amidooxyalkyl ketones.	aspartyl amidooxyalkyl ketones	106-136	caspase 1	Homo sapiens	14-49
20656488-1	2010	Succinic acid amides have been found to be effective P2-P3 scaffold replacements for peptidic ICE inhibitors.	succinic acid amides	0-20	caspase 1	Homo sapiens	94-97
20656488-1	2010	Succinic acid amides have been found to be effective P2-P3 scaffold replacements for peptidic ICE inhibitors.	p2-p3	53-58	caspase 1	Homo sapiens	94-97
20674352-0	2010	Inhibition of interleukin-1beta converting enzyme (ICE or caspase 1) by aspartyl acyloxyalkyl ketones and aspartyl amidooxyalkyl ketones.	aspartyl amidooxyalkyl ketones	106-136	caspase 1	Homo sapiens	51-54
20674352-0	2010	Inhibition of interleukin-1beta converting enzyme (ICE or caspase 1) by aspartyl acyloxyalkyl ketones and aspartyl amidooxyalkyl ketones.	aspartyl amidooxyalkyl ketones	106-136	caspase 1	Homo sapiens	58-67
20462856-5	2010	MTT assay revealed that 1.0% PectaSol exerted cytotoxicity on LNCaP, PC3, CASP2.1, CASP1.1, and BPH-1 cells for 4-day treatment by 48.0% +/- 2.1%, 54.4% +/- 0.3%, 15.4% +/- 0.8%, 46.1% +/- 1.7%, and 27.4% +/- 1.6%, respectively; whereas 1.0% PectaSol-C showed cytotoxity by 52.2% +/- 1.8%, 48.2% +/- 2.9%, 23.0% +/- 2.6%, 49.0% +/- 1.3%, and 26.8% +/- 2.6%, respectively.	pectasol	29-37	caspase 1	Homo sapiens	83-88
20936723-2	2010	The inflammasome can activate caspase-1, and later makes the pro-IL-1beta, proIL-18 precursor mature by cleavaging, thereby mediates the innate immunity.	proil	75-80	caspase 1	Homo sapiens	30-39
20588114-5	2010	Caspase-1 is required for IL-1beta activity and the release of free fatty acids from the adipocyte.	Fatty Acids, Nonesterified	63-79	caspase 1	Homo sapiens	0-9
20434582-5	2010	As for other infections causing NRLP3 inflammasome assembly, caspase-1 activation in monocytes is triggered by potassium efflux and reactive oxygen species production.	Potassium	111-120	caspase 1	Homo sapiens	61-70
20434582-5	2010	As for other infections causing NRLP3 inflammasome assembly, caspase-1 activation in monocytes is triggered by potassium efflux and reactive oxygen species production.	Reactive Oxygen Species	132-155	caspase 1	Homo sapiens	61-70
20668705-7	2010	The cholesterol crystal-induced secretion of IL-1beta was caspase-1-dependent, suggesting the involvement of an inflammasome-mediated pathway.	Cholesterol	4-15	caspase 1	Homo sapiens	58-67
20179743-2	2010	The shortage of mevalonate-derived intermediates, and in particular of geranylgeranyl pyrophosphate (GGPP), has been linked with the activation of caspase-1 and thereby with the production of IL-1beta, but the true concatenation of these two events has not been clarified yet.	Mevalonic Acid	16-26	caspase 1	Homo sapiens	147-156
20179743-2	2010	The shortage of mevalonate-derived intermediates, and in particular of geranylgeranyl pyrophosphate (GGPP), has been linked with the activation of caspase-1 and thereby with the production of IL-1beta, but the true concatenation of these two events has not been clarified yet.	geranylgeranyl pyrophosphate	71-99	caspase 1	Homo sapiens	147-156
20179743-2	2010	The shortage of mevalonate-derived intermediates, and in particular of geranylgeranyl pyrophosphate (GGPP), has been linked with the activation of caspase-1 and thereby with the production of IL-1beta, but the true concatenation of these two events has not been clarified yet.	geranylgeranyl pyrophosphate	101-105	caspase 1	Homo sapiens	147-156
20179743-3	2010	We hypothesized that inflammasomes could mediate the activation of caspase-1 due to the shortage of GGPP.	geranylgeranyl pyrophosphate	100-104	caspase 1	Homo sapiens	67-76
20232307-1	2010	Caspases are a conserved family of cell death proteases that cleave intracellular substrates at Asp residues to modify their function and promote apoptosis.	Aspartic Acid	96-99	caspase 1	Homo sapiens	0-8
20304105-1	2010	The inhibition of mevalonate pathway through genetic defects (mevalonate kinase deficiency, MKD) or pharmacologic drugs (aminobisphosphonates) causes a shortage of intermediate compounds and, in particular, of geranylgeranyl-pyrophosphate (GGPP) associated to the activation of caspase-1 and IL-1beta release.	Mevalonic Acid	18-28	caspase 1	Homo sapiens	278-287
20304105-1	2010	The inhibition of mevalonate pathway through genetic defects (mevalonate kinase deficiency, MKD) or pharmacologic drugs (aminobisphosphonates) causes a shortage of intermediate compounds and, in particular, of geranylgeranyl-pyrophosphate (GGPP) associated to the activation of caspase-1 and IL-1beta release.	aminobisphosphonates	121-141	caspase 1	Homo sapiens	278-287
20304105-1	2010	The inhibition of mevalonate pathway through genetic defects (mevalonate kinase deficiency, MKD) or pharmacologic drugs (aminobisphosphonates) causes a shortage of intermediate compounds and, in particular, of geranylgeranyl-pyrophosphate (GGPP) associated to the activation of caspase-1 and IL-1beta release.	geranylgeranyl pyrophosphate	210-238	caspase 1	Homo sapiens	278-287
20621450-6	2010	However, caspase-1 is absent in non-hematopoietic cells, suggesting that there is another candidate to cleave proIL-18 except for caspase-1.	proil	110-115	caspase 1	Homo sapiens	9-18
20179743-7	2010	Our results, although preliminary, showed that the inhibition of the mevalonate pathway led to a hyper-expression of NALP3, suggesting a possible involvement of NALP3-inflammasome in the activation of caspase-1 consequent to GGPP decrement.	Mevalonic Acid	69-79	caspase 1	Homo sapiens	201-210
20349422-9	2010	RESULTS: We observed a significant increase in caspase-1 activity and decrease in caspase-3 activity in neutrophils after HD with cuprophane, but not with polysulphone.	cuprammonium cellulose	130-140	caspase 1	Homo sapiens	47-56
20349422-13	2010	CONCLUSIONS: The results suggest that HD with bioincompatible cuprophane may prolong the life span of neutrophils due to the intense inflammatory reaction and high activity of caspase-1.	cuprammonium cellulose	62-72	caspase 1	Homo sapiens	176-185
20060974-4	2010	RESULTS: This study has made the following findings: first, we verified that caspase-1 and caspase-9 shared 100% aspartic acid in the P1 position.	Aspartic Acid	113-126	caspase 1	Homo sapiens	77-86
20093358-4	2010	Here, we show that the herbal NF-kappaB inhibitory compound parthenolide inhibits the activity of multiple inflammasomes in macrophages by directly inhibiting the protease activity of caspase-1.	parthenolide	60-72	caspase 1	Homo sapiens	184-193
20229566-0	2010	A highly potent and selective caspase 1 inhibitor that utilizes a key 3-cyanopropanoic acid moiety.	3-Cyanopropanoic acid	70-91	caspase 1	Homo sapiens	30-39
20229566-1	2010	Herein, we examine the potential of a nitrile-containing propionic acid moiety as an electrophile for covalent attack by the active-site cysteine residue of caspase 1.	Nitriles	38-45	caspase 1	Homo sapiens	157-166
20229566-1	2010	Herein, we examine the potential of a nitrile-containing propionic acid moiety as an electrophile for covalent attack by the active-site cysteine residue of caspase 1.	propionic acid	57-71	caspase 1	Homo sapiens	157-166
20229566-1	2010	Herein, we examine the potential of a nitrile-containing propionic acid moiety as an electrophile for covalent attack by the active-site cysteine residue of caspase 1.	Cysteine	137-145	caspase 1	Homo sapiens	157-166
20356061-0	2010	Asymmetric total synthesis of the caspase-1 inhibitor (-)-berkeleyamide A.	berkeleyamide A	54-73	caspase 1	Homo sapiens	34-43
20356061-1	2010	The asymmetric total synthesis of (-)-berkeleyamide A (1), a naturally occurring caspase-1 inhibitor, has been achieved by employing Evans" syn-aldol reaction of N-acyl-(4R)-benzyl oxazolidin-2-one 3 as the key step.	berkeleyamide A	34-53	caspase 1	Homo sapiens	81-90
19960512-4	2010	Purified caspase-14 revealed the highest activity on WEHD-methylcoumaryl-amide (MCA), although YVAD-MCA, another caspase-1 substrate, was poorly hydrolyzed.	wehd-methylcoumaryl-amide	53-78	caspase 1	Homo sapiens	9-18
20170165-0	2010	Noncovalent tripeptidyl benzyl- and cyclohexyl-amine inhibitors of the cysteine protease caspase-1.	tripeptidyl benzyl- and cyclohexyl-amine	12-52	caspase 1	Homo sapiens	89-98
20170165-1	2010	Potent and noncovalent inhibitors of caspase-1 were produced by incorporating a secondary amine (reduced amide) isostere in place of the conventional electrophile (e.g., aldehyde) that normally confers high potency to cysteine protease inhibitors.	amine (reduced amide	90-110	caspase 1	Homo sapiens	37-46
20170165-1	2010	Potent and noncovalent inhibitors of caspase-1 were produced by incorporating a secondary amine (reduced amide) isostere in place of the conventional electrophile (e.g., aldehyde) that normally confers high potency to cysteine protease inhibitors.	Aldehydes	170-178	caspase 1	Homo sapiens	37-46
20170165-2	2010	Benzyl- or cyclohexylamines produced potent, reversible, and competitive inhibitors that were selective for caspase-1 (e.g., K(i) = 47 nM) over caspases 3 and 8 with minimal cytotoxicity.	benzyl- or cyclohexylamines	0-27	caspase 1	Homo sapiens	108-117
20170165-2	2010	Benzyl- or cyclohexylamines produced potent, reversible, and competitive inhibitors that were selective for caspase-1 (e.g., K(i) = 47 nM) over caspases 3 and 8 with minimal cytotoxicity.	benzyl- or cyclohexylamines	0-27	caspase 1	Homo sapiens	144-152
19960512-4	2010	Purified caspase-14 revealed the highest activity on WEHD-methylcoumaryl-amide (MCA), although YVAD-MCA, another caspase-1 substrate, was poorly hydrolyzed.	mca	80-83	caspase 1	Homo sapiens	9-18
19915007-6	2010	Activity of Blastocystis legumain was greatly inhibited by the legumain-specific inhibitor carbobenzyloxy-Ala-Ala-AAsn-epoxycarboxylate ethyl ester (APE-RR) (where AAsn is aza-asparagine) and moderately inhibited by mAb 1D5, cystatin, and caspase-1 inhibitor.	aasn	114-118	caspase 1	Homo sapiens	239-248
20086177-5	2010	ATP activates purinergic P2RX7 receptors on DC, thus activating the NLRP3/ASC/caspase-1 inflammasome and driving the secretion of interleukin-1beta (IL-1beta).	Adenosine Triphosphate	0-3	caspase 1	Homo sapiens	78-87
20059972-0	2010	Titanium dioxide induces different levels of IL-1beta production dependent on its particle characteristics through caspase-1 activation mediated by reactive oxygen species and cathepsin B.	titanium dioxide	0-16	caspase 1	Homo sapiens	115-124
20059972-0	2010	Titanium dioxide induces different levels of IL-1beta production dependent on its particle characteristics through caspase-1 activation mediated by reactive oxygen species and cathepsin B.	Reactive Oxygen Species	148-171	caspase 1	Homo sapiens	115-124
20044024-1	2010	HL-60 cells treated by prostaglandin (PG) A(2) showed characteristics of apoptosis such as accumulation of hypodiploid and annexin V positive cells, condensed and fragmented nuclei, cytochrome c (Cyt C) release from mitochondria and activation of caspase-1, -2, -3, -7 and -9.	Prostaglandins A	23-43	caspase 1	Homo sapiens	247-275
19737897-9	2010	The extracellular release of IL-1beta in response to PGA was ICE dependent, since the administration of an ICE inhibitor prior to PGA treatment blocked induction of IL-1beta.	Folic Acid	53-56	caspase 1	Homo sapiens	61-64
20832779-0	2010	Importance of lipid rafts for lysophosphatidylcholine-induced caspase-1 activation and reactive oxygen species generation.	Lysophosphatidylcholines	30-53	caspase 1	Homo sapiens	62-71
20832779-2	2010	Here, we demonstrate that in microglia stimulated with the pro-inflammatory lipid lysophosphatidylcholine (LPC), caspase-1 activation and NADPH oxidase activity depend on intact lipid rafts.	Lysophosphatidylcholines	82-105	caspase 1	Homo sapiens	113-122
20832779-3	2010	Disruption of lipid rafts with methyl-beta-cyclodextrin, fumonisin B1 or nystatin prevented LPC-stimulated caspase-1 activation and reactive oxygen species (ROS) production, whereas LPC-induced Na(+) influx remained unaffected.	methyl-beta-cyclodextrin	31-55	caspase 1	Homo sapiens	107-116
20832779-3	2010	Disruption of lipid rafts with methyl-beta-cyclodextrin, fumonisin B1 or nystatin prevented LPC-stimulated caspase-1 activation and reactive oxygen species (ROS) production, whereas LPC-induced Na(+) influx remained unaffected.	fumonisin B1	57-69	caspase 1	Homo sapiens	107-116
20832779-3	2010	Disruption of lipid rafts with methyl-beta-cyclodextrin, fumonisin B1 or nystatin prevented LPC-stimulated caspase-1 activation and reactive oxygen species (ROS) production, whereas LPC-induced Na(+) influx remained unaffected.	Nystatin	73-81	caspase 1	Homo sapiens	107-116
20832779-3	2010	Disruption of lipid rafts with methyl-beta-cyclodextrin, fumonisin B1 or nystatin prevented LPC-stimulated caspase-1 activation and reactive oxygen species (ROS) production, whereas LPC-induced Na(+) influx remained unaffected.	Lysophosphatidylcholines	92-95	caspase 1	Homo sapiens	107-116
20832779-4	2010	Since ROS regulate caspase-1 activity in LPC-stimulated microglia, the effects of lipid raft-disrupting agents on caspase-1 activation can be related to their inhibition of NADPH oxidase-mediated ROS production.	Reactive Oxygen Species	6-9	caspase 1	Homo sapiens	19-28
20832779-4	2010	Since ROS regulate caspase-1 activity in LPC-stimulated microglia, the effects of lipid raft-disrupting agents on caspase-1 activation can be related to their inhibition of NADPH oxidase-mediated ROS production.	Reactive Oxygen Species	196-199	caspase 1	Homo sapiens	114-123
19737897-9	2010	The extracellular release of IL-1beta in response to PGA was ICE dependent, since the administration of an ICE inhibitor prior to PGA treatment blocked induction of IL-1beta.	Folic Acid	53-56	caspase 1	Homo sapiens	107-110
19737897-9	2010	The extracellular release of IL-1beta in response to PGA was ICE dependent, since the administration of an ICE inhibitor prior to PGA treatment blocked induction of IL-1beta.	Folic Acid	130-133	caspase 1	Homo sapiens	61-64
19737897-11	2010	anthracis PGA elicits IL-1beta production through activation of ICE in PMA-differentiated THP-1 cells and hMoDCs, suggesting the potential for PGA as a therapeutic target for anthrax.	anthracis pga	0-13	caspase 1	Homo sapiens	64-67
19737897-11	2010	anthracis PGA elicits IL-1beta production through activation of ICE in PMA-differentiated THP-1 cells and hMoDCs, suggesting the potential for PGA as a therapeutic target for anthrax.	Folic Acid	10-13	caspase 1	Homo sapiens	64-67
19805571-4	2009	Viral variants resistant to PF-46396 contain a single amino acid substitution in HIV-1 CA sequences (CAI201V), distal to the CA/SP1 cleavage site in the primary structure, which we demonstrate is sufficient to confer significant resistance to PF-46396 and 3-O-(3",3"-dimethylsuccinyl) betulinic acid (DSB), a previously described maturation inhibitor.	pyrazofurin	28-30	caspase 1	Homo sapiens	87-89
19805571-4	2009	Viral variants resistant to PF-46396 contain a single amino acid substitution in HIV-1 CA sequences (CAI201V), distal to the CA/SP1 cleavage site in the primary structure, which we demonstrate is sufficient to confer significant resistance to PF-46396 and 3-O-(3",3"-dimethylsuccinyl) betulinic acid (DSB), a previously described maturation inhibitor.	pyrazofurin	28-30	caspase 1	Homo sapiens	101-103
19805571-4	2009	Viral variants resistant to PF-46396 contain a single amino acid substitution in HIV-1 CA sequences (CAI201V), distal to the CA/SP1 cleavage site in the primary structure, which we demonstrate is sufficient to confer significant resistance to PF-46396 and 3-O-(3",3"-dimethylsuccinyl) betulinic acid (DSB), a previously described maturation inhibitor.	PF-46396	28-36	caspase 1	Homo sapiens	87-89
19805571-4	2009	Viral variants resistant to PF-46396 contain a single amino acid substitution in HIV-1 CA sequences (CAI201V), distal to the CA/SP1 cleavage site in the primary structure, which we demonstrate is sufficient to confer significant resistance to PF-46396 and 3-O-(3",3"-dimethylsuccinyl) betulinic acid (DSB), a previously described maturation inhibitor.	PF-46396	28-36	caspase 1	Homo sapiens	101-103
19805571-4	2009	Viral variants resistant to PF-46396 contain a single amino acid substitution in HIV-1 CA sequences (CAI201V), distal to the CA/SP1 cleavage site in the primary structure, which we demonstrate is sufficient to confer significant resistance to PF-46396 and 3-O-(3",3"-dimethylsuccinyl) betulinic acid (DSB), a previously described maturation inhibitor.	bevirimat	256-299	caspase 1	Homo sapiens	87-89
19805571-4	2009	Viral variants resistant to PF-46396 contain a single amino acid substitution in HIV-1 CA sequences (CAI201V), distal to the CA/SP1 cleavage site in the primary structure, which we demonstrate is sufficient to confer significant resistance to PF-46396 and 3-O-(3",3"-dimethylsuccinyl) betulinic acid (DSB), a previously described maturation inhibitor.	bevirimat	256-299	caspase 1	Homo sapiens	101-103
19805571-4	2009	Viral variants resistant to PF-46396 contain a single amino acid substitution in HIV-1 CA sequences (CAI201V), distal to the CA/SP1 cleavage site in the primary structure, which we demonstrate is sufficient to confer significant resistance to PF-46396 and 3-O-(3",3"-dimethylsuccinyl) betulinic acid (DSB), a previously described maturation inhibitor.	bevirimat	301-304	caspase 1	Homo sapiens	87-89
19805571-4	2009	Viral variants resistant to PF-46396 contain a single amino acid substitution in HIV-1 CA sequences (CAI201V), distal to the CA/SP1 cleavage site in the primary structure, which we demonstrate is sufficient to confer significant resistance to PF-46396 and 3-O-(3",3"-dimethylsuccinyl) betulinic acid (DSB), a previously described maturation inhibitor.	bevirimat	301-304	caspase 1	Homo sapiens	101-103
19779610-4	2009	This activity is not a direct effect of endotoxin, and is inhibited by the caspase-1 inhibitor YVADcmk but not by inhibitors of Fas-L, IL-1beta and IL-18.	N-acetyl-tyrosyl-valyl-alanyl-aspartyl chloromethyl ketone	95-102	caspase 1	Homo sapiens	75-84
19643964-9	2009	Although caspase-4 inhibitor Z-LEVD-fmk and caspase-1 and -4 inhibitor Z-YVAD-fmk reduced tunicamycin-induced hRPE apoptotic cell death by 59% and 86%, respectively, pan-caspase inhibitor Z-VAD-fmk completely abolished the induced apoptosis.	benzyloxycarbonyltyrosyl-valyl-alanyl-aspartic acid fluoromethyl ketone	71-81	caspase 1	Homo sapiens	44-60
19643964-9	2009	Although caspase-4 inhibitor Z-LEVD-fmk and caspase-1 and -4 inhibitor Z-YVAD-fmk reduced tunicamycin-induced hRPE apoptotic cell death by 59% and 86%, respectively, pan-caspase inhibitor Z-VAD-fmk completely abolished the induced apoptosis.	Tunicamycin	90-101	caspase 1	Homo sapiens	44-60
19633559-4	2009	In particular, nalp3 mediated inflammasome activation of caspase-1 and conversion of pro-IL-1 to IL-1 play a key role in silica-mediated and bleomycin-mediated pulmonary fibrosis.	Silicon Dioxide	121-127	caspase 1	Homo sapiens	57-66
19633559-4	2009	In particular, nalp3 mediated inflammasome activation of caspase-1 and conversion of pro-IL-1 to IL-1 play a key role in silica-mediated and bleomycin-mediated pulmonary fibrosis.	Bleomycin	141-150	caspase 1	Homo sapiens	57-66
19690144-2	2009	Activation of all intracellular caspases, except caspase-1, was detected in I-Trp-treated cells.	i-trp	76-81	caspase 1	Homo sapiens	32-40
19690144-2	2009	Activation of all intracellular caspases, except caspase-1, was detected in I-Trp-treated cells.	i-trp	76-81	caspase 1	Homo sapiens	49-58
19621082-3	2009	RESULTS: Cells treated with H35N (a mutant of alpha-HL that remains as membrane bound monomer), have been shown to accumulate hypodiploid nuclei, activate caspases and induce intrinsic mitochondrial apoptotic pathway.	h35n	28-32	caspase 1	Homo sapiens	155-163
19596994-3	2009	We identify 7-bromoindirubin-3"-oxime, an indirubin oxime derivative that induces necrosis, as a potent inducer of caspase-1 activation and release of mature IL-1beta and IL-18.	7-bromoindirubin-3'-oxime	12-37	caspase 1	Homo sapiens	115-124
19596994-3	2009	We identify 7-bromoindirubin-3"-oxime, an indirubin oxime derivative that induces necrosis, as a potent inducer of caspase-1 activation and release of mature IL-1beta and IL-18.	indirubin oxime	42-57	caspase 1	Homo sapiens	115-124
19825518-6	2009	In this review, we discuss recent reports demonstrating that in vitro inhibition of the mevalonate pathway by statins specifically increases the production, by activated monocytes, of cytokines of the IL-1 family, by enhancing caspase-1 activity, the enzyme responsible for IL-1beta and IL-18 maturation.	Mevalonic Acid	88-98	caspase 1	Homo sapiens	227-236
19825520-8	2009	Simvastatin did not modify pro-IL-1beta expression, but enhanced caspase-1 activity, the enzyme responsible for IL-1beta and IL-18 maturation.	Simvastatin	0-11	caspase 1	Homo sapiens	65-74
19825520-11	2009	CONCLUSION: Pharmacological inhibition of the mevalonate pathway by statins highlighted the specific induction of the proinflammatory cytokines of the IL-1 family whose maturation is either directly (i.e. IL-1beta and IL-18), or indirectly (i.e. IL-1alpha) dependant on caspase-1.	Mevalonic Acid	46-56	caspase 1	Homo sapiens	270-279
19621082-6	2009	The cells treated with H35N were unable to recover despite activation of membrane repair mechanism involving caspase-1 dependent activation of sterol regulatory element binding protein-1.	h35n	23-27	caspase 1	Homo sapiens	109-118
19542372-3	2009	We show here that exposure of macrophages and dendritic cells to TNF-alpha promotes ATP- or silica-mediated caspase-1 activation and IL-1beta secretion in the absence of microbial stimulation.	Adenosine Triphosphate	84-87	caspase 1	Homo sapiens	108-117
19542372-3	2009	We show here that exposure of macrophages and dendritic cells to TNF-alpha promotes ATP- or silica-mediated caspase-1 activation and IL-1beta secretion in the absence of microbial stimulation.	Silicon Dioxide	92-98	caspase 1	Homo sapiens	108-117
19542372-5	2009	In addition to TNF-alpha, IL-1alpha and IL-1beta promoted caspase-1 activation via Nlrp3 in response to ATP.	Adenosine Triphosphate	104-107	caspase 1	Homo sapiens	58-67
19655264-5	2009	We observed that caspases-3, -8, -9 and pan caspase inhibitors resulted in significant inhibition of etoposide-induced DNA fragmentation.	Etoposide	101-110	caspase 1	Homo sapiens	17-24
19416975-5	2009	Here we show that high extracellular potassium opens pannexin channels leading to caspase-1 activation in primary neurons and astrocytes.	Potassium	37-46	caspase 1	Homo sapiens	82-91
19105226-4	2009	We hypothesized that metal implant debris can activate the inflammasome pathway in macrophages that causes caspase-1-induced cleavage of intracellular pro-IL-1beta into its mature form, resulting in IL-1beta secretion and induction of a broader proinflammatory response.	Metals	21-26	caspase 1	Homo sapiens	107-116
19414795-10	2009	In conclusion, our results indicate that human macrophages sense trichothecene mycotoxins as a danger signal, which activates caspase-1, and further enables the secretion of IL-1beta and IL-18 from the LPS-primed cells.	trichothecene mycotoxins	65-89	caspase 1	Homo sapiens	126-135
19439663-5	2009	We show that full-length IL-33(1-270) binds and activates ST2, similarly to IL-33(112-270), and that cleavage by caspase-1 does not occur at the site initially proposed (Ser(111)), but rather after residue Asp(178) between the fourth and fifth predicted beta-strands of the IL-1-like domain.	Aspartic Acid	206-209	caspase 1	Homo sapiens	113-122
19414795-6	2009	As a result, satratoxin-positive S. chartarum activated inflammasome-associated caspase-1, which is needed for proteolytic processing of IL-1beta and IL-18.	satratoxin	13-23	caspase 1	Homo sapiens	80-89
19439372-4	2009	Aluminum adjuvants activate the nucleotide-binding domain and leucine-rich-repeat-containing gene family pyrin-domain-containing 3 (known as NLRP3 or NALP3) inflammasome to activate caspase-1 and to induce proinflammatory cytokines interleukin (IL)-1beta and IL-18 by innate cells.	Aluminum	0-8	caspase 1	Homo sapiens	182-191
19208804-6	2009	Bivalent IgG forms of the Fabs were used to localize the different states in cells and revealed the activated caspase-1 is concentrated in a central structure in the cytosol, similar to what has been described as the pyroptosome.	fabs	26-30	caspase 1	Homo sapiens	110-119
19414795-7	2009	Furthermore, purified trichothecene mycotoxins, roridin A, verrucarin A, and T-2 toxin activated caspase-1, and these mycotoxins also strongly enhanced LPS-dependent secretion of IL-1beta and IL-18.	trichothecene mycotoxins	22-46	caspase 1	Homo sapiens	97-106
19414795-7	2009	Furthermore, purified trichothecene mycotoxins, roridin A, verrucarin A, and T-2 toxin activated caspase-1, and these mycotoxins also strongly enhanced LPS-dependent secretion of IL-1beta and IL-18.	roridin A	48-57	caspase 1	Homo sapiens	97-106
19414795-7	2009	Furthermore, purified trichothecene mycotoxins, roridin A, verrucarin A, and T-2 toxin activated caspase-1, and these mycotoxins also strongly enhanced LPS-dependent secretion of IL-1beta and IL-18.	muconomycin A	59-71	caspase 1	Homo sapiens	97-106
26609711-11	2009	The method is validated for a series of small molecules and further applied to alanine dipeptide as a prototype to describe vibrational interactions between two peptide units; to crambin, a small protein with 46 amino acid residues; and to ICE/caspase-1, which contains 518 amino acid residues.	alanylalanine	79-96	caspase 1	Homo sapiens	240-243
26609711-11	2009	The method is validated for a series of small molecules and further applied to alanine dipeptide as a prototype to describe vibrational interactions between two peptide units; to crambin, a small protein with 46 amino acid residues; and to ICE/caspase-1, which contains 518 amino acid residues.	alanylalanine	79-96	caspase 1	Homo sapiens	244-253
19067254-1	2009	The polycation poly(ethylenimine) (PEI) was used to deliver the plasmids coding for various combinations of caspases to Cox-2 overexpressing cancer cell lines.	Polyethyleneimine	15-33	caspase 1	Homo sapiens	108-116
19067254-1	2009	The polycation poly(ethylenimine) (PEI) was used to deliver the plasmids coding for various combinations of caspases to Cox-2 overexpressing cancer cell lines.	Polyethyleneimine	35-38	caspase 1	Homo sapiens	108-116
19130485-5	2009	One of the endogenous mediators of IL-1beta secretion is adenosine triphosphate, acting via the P2X7-receptor and caspase-1 activation in cells primed with an inflammatory stimulus such as LPS.	Adenosine Triphosphate	57-79	caspase 1	Homo sapiens	114-123
20548851-5	2009	RESULTS: The caspase-1 and STAT-6 mRNA expression levels from the SP lesional skin of the patients were increased compared with the caspase-1 and STAT-6 mRNA expression levels from SP non-lesional skin or normal skin, but these expression levels from the SP non-lesional skin were not significantly different from those of the LP non-lesional skin.	leucylproline	327-329	caspase 1	Homo sapiens	13-22
18390571-0	2009	Crystals of monosodium urate monohydrate enhance lipopolysaccharide-induced release of interleukin 1 beta by mononuclear cells through a caspase 1-mediated process.	Uric Acid	12-40	caspase 1	Homo sapiens	137-146
18390571-11	2009	The synergy between LPS and MSU crystals ceased to exist in the presence of a caspase 1 inhibitor.	Uric Acid	28-31	caspase 1	Homo sapiens	78-87
18977395-9	2009	Although its precise primary target is not clear, the action mechanisms of minocycline for neuroprotection reported so far are; via; the inhibition of mitochondrial permeability-transition mediated cytochrome c release from mitochondria, the inhibition of caspase-1 and -3 expressions, and the suppression of microglial activation, involvement in some signaling pathways, metalloprotease activity inhibition.	Minocycline	75-86	caspase 1	Homo sapiens	256-272
19004566-0	2009	Ritonavir and disulfiram have potential to inhibit caspase-1 mediated inflammation and reduce neurological sequelae after minor blast exposure.	Ritonavir	0-9	caspase 1	Homo sapiens	51-60
19004566-0	2009	Ritonavir and disulfiram have potential to inhibit caspase-1 mediated inflammation and reduce neurological sequelae after minor blast exposure.	Disulfiram	14-24	caspase 1	Homo sapiens	51-60
19004566-3	2009	Ritonavir, a generically available protease inhibitor with a benign short-term side-effect profile, has been shown to inhibit expression of caspase-1.	Ritonavir	0-9	caspase 1	Homo sapiens	140-149
18799371-0	2009	Frameshift mutation at a mononucleotide repeat in CASP1 is rare in gastric and colorectal carcinomas with microsatellite instability.	mononucleotide	25-39	caspase 1	Homo sapiens	50-55
18662322-0	2008	Enzastaurin-induced apoptosis in glioma cells is caspase-dependent and inhibited by BCL-XL.	enzastaurin	0-11	caspase 1	Homo sapiens	49-56
21783928-4	2009	By microarray, we found that apoptosis-related genes such as apoptosis-associated tyrosine kinase, interleukin 10 receptor beta, caspase 1 and DNA fragmentation factor beta subunit (40kDa) were down-regulated in TC-treated A549 cells.	Technetium	212-214	caspase 1	Homo sapiens	129-138
18667412-3	2008	Of the 1022 proteins that were identified, 20 were found to be specifically cleaved after Asp in the setup incubated with recombinant caspase-1.	Aspartic Acid	90-93	caspase 1	Homo sapiens	134-143
18667412-6	2008	Consistently recombinant caspase-1 cleaved caspase-7 at the canonical activation sites Asp(23) and Asp(198), and recombinant caspase-7 processed a subset of the identified substrates.	Aspartic Acid	87-90	caspase 1	Homo sapiens	25-34
18667412-6	2008	Consistently recombinant caspase-1 cleaved caspase-7 at the canonical activation sites Asp(23) and Asp(198), and recombinant caspase-7 processed a subset of the identified substrates.	Aspartic Acid	99-102	caspase 1	Homo sapiens	25-34
18667412-7	2008	In vivo, caspase-7 activation was observed in conditions known to induce activation of caspase-1, including Salmonella infection and microbial stimuli combined with ATP.	Adenosine Triphosphate	165-168	caspase 1	Homo sapiens	87-96
18667412-8	2008	Interestingly Salmonella- and lipopolysaccharide + ATP-induced activation of caspase-7 was abolished in macrophages deficient in caspase-1, the pattern recognition receptors Ipaf and Cryopyrin, and the inflammasome adaptor ASC, demonstrating an upstream role for the caspase-1 inflammasomes in caspase-7 activation in vivo.	Adenosine Triphosphate	51-54	caspase 1	Homo sapiens	129-138
18667412-8	2008	Interestingly Salmonella- and lipopolysaccharide + ATP-induced activation of caspase-7 was abolished in macrophages deficient in caspase-1, the pattern recognition receptors Ipaf and Cryopyrin, and the inflammasome adaptor ASC, demonstrating an upstream role for the caspase-1 inflammasomes in caspase-7 activation in vivo.	Adenosine Triphosphate	51-54	caspase 1	Homo sapiens	267-276
18981155-2	2008	We observed that cellular levels of retinoic acid-inducible gene-I (RIG-I) were enhanced when the pan-caspase inhibitor Z-VAD-fmk or caspase-1-specific inhibitor Z-WEHD-fmk blocked caspase activity.	Z-WEHD-FMK	162-172	caspase 1	Homo sapiens	133-142
18684863-6	2008	IL-1beta release is mediated by caspase-1, and simvastatin treatment resulted in increased caspase-1 activity in a Rac1/PI3K-dependent manner.	Simvastatin	47-58	caspase 1	Homo sapiens	91-100
18684863-7	2008	These data suggest that, in MKD, dysregulated isoprenoid biosynthesis activates Rac1/PI3K/PKB, resulting in caspase-1 activation with increased IL-1beta release.	Terpenes	46-56	caspase 1	Homo sapiens	108-117
19069247-8	2008	The cell death was completely prevented by the pan caspase inhibitor benzyloxy carbonyl-Val-Ala-Asp- fluoromethyl-ketone (Z-VAD-FMK).	benzyloxy carbonyl-val-ala-asp- fluoromethyl-ketone	69-120	caspase 1	Homo sapiens	51-58
19069247-8	2008	The cell death was completely prevented by the pan caspase inhibitor benzyloxy carbonyl-Val-Ala-Asp- fluoromethyl-ketone (Z-VAD-FMK).	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	122-131	caspase 1	Homo sapiens	51-58
18725521-6	2008	Surprisingly, poly(I:C)- and LPS-induced pro-IL-1beta processing still occurred in caspase-1-deficient cells.	Poly I-C	14-23	caspase 1	Homo sapiens	83-92
20160900-3	2009	Bromoenol lactone (BEL), an inhibitor that was originally used to support a role for iPLA2 in the secretion of IL-1 beta, prevented caspase-1 activation induced by LPS and ATP as described, and also activation triggered by Salmonella infection and cytosolic flagellin, which rely on the Nlrc4 inflammasome.	6-(bromomethylene)tetrahydro-3-(1-naphthaleneyl)-2H-pyran-2-one	0-17	caspase 1	Homo sapiens	132-141
20160900-3	2009	Bromoenol lactone (BEL), an inhibitor that was originally used to support a role for iPLA2 in the secretion of IL-1 beta, prevented caspase-1 activation induced by LPS and ATP as described, and also activation triggered by Salmonella infection and cytosolic flagellin, which rely on the Nlrc4 inflammasome.	6-(bromomethylene)tetrahydro-3-(1-naphthaleneyl)-2H-pyran-2-one	19-22	caspase 1	Homo sapiens	132-141
20160900-3	2009	Bromoenol lactone (BEL), an inhibitor that was originally used to support a role for iPLA2 in the secretion of IL-1 beta, prevented caspase-1 activation induced by LPS and ATP as described, and also activation triggered by Salmonella infection and cytosolic flagellin, which rely on the Nlrc4 inflammasome.	Adenosine Triphosphate	172-175	caspase 1	Homo sapiens	132-141
18976637-5	2008	Ac-YVAD-pNA, the designated substrate for caspase-1, is found to be the most specific substrate.	acetyl-tyrosyl-valyl-alanyl-aspartic acid p-nitroanilide	0-11	caspase 1	Homo sapiens	42-51
18662322-3	2008	ENZA-induced apoptosis involved cleavage of caspases 3, 8, and 9 and led to mitochondrial cytochrome c release and was strongly suppressed by the broad spectrum caspase inhibitor zVAD-fmk but only slightly by the expression of the viral caspase 1/8 inhibitor cytokine response modifier-A.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	179-187	caspase 1	Homo sapiens	44-51
18638431-3	2008	At micromolar concentrations, it suppresses monosodium urate crystal-induced NACHT-LRR-PYD-containing protein-3 (NALP3) inflammasome-driven caspase-1 activation, IL-1beta processing and release, and L-selectin expression on neutrophils.	Uric Acid	44-60	caspase 1	Homo sapiens	140-149
18523309-1	2008	P2X(7) receptors (P2X(7)Rs) are ATP-gated ion channels that trigger caspase-1 activation in the presence of TLR ligands.	Adenosine Triphosphate	32-35	caspase 1	Homo sapiens	68-77
18577586-4	2008	Stimulation of macrophages with silica results in the activation of caspase-1 in a Nalp3-dependent manner.	Silicon Dioxide	32-38	caspase 1	Homo sapiens	68-77
18523309-4	2008	In this study we demonstrate that ATP-induced cellular oxidation is critical for caspase-1 activation and subsequent IL-1beta processing.	Adenosine Triphosphate	34-37	caspase 1	Homo sapiens	81-90
18523309-7	2008	Nigericin, a K(+)/H(+) antiporter, also increases NADPH oxidase activity, leading to IL-1beta and caspase-1 processing that is blocked by a peroxynitrite scavenger or inhibition of NADPH oxidase.	Nigericin	0-9	caspase 1	Homo sapiens	98-107
18523309-7	2008	Nigericin, a K(+)/H(+) antiporter, also increases NADPH oxidase activity, leading to IL-1beta and caspase-1 processing that is blocked by a peroxynitrite scavenger or inhibition of NADPH oxidase.	Peroxynitrous Acid	140-153	caspase 1	Homo sapiens	98-107
18469453-4	2008	The anti-retroviral drug ritonavir inhibits conversion of inactive pro-caspase-1 to active caspase-1.	Ritonavir	25-34	caspase 1	Homo sapiens	71-80
18263705-8	2008	Similarly, cultured human islets exposed to high glucose- and leptin-induced caspase 1 and JNK inhibition prevented this up-regulation.	Glucose	49-56	caspase 1	Homo sapiens	77-86
18311838-3	2008	Here we have shown that addition of C2-ceramide is able to produce extensive death of cultured CGC, which is associated with chromatin condensation, ladder-like DNA fragmentation, and activation of caspases.	N-acetylsphingosine	36-47	caspase 1	Homo sapiens	198-206
18497968-6	2008	35S-labeled full-length AKAP149 was completely cleaved in vitro by active caspase-3, -8 and -10 into two fragments of approximately 105 and 45 kDa, while caspase-2 cleaved it partially and caspase-1 did not cleave it at all.	Sulfur-35	0-3	caspase 1	Homo sapiens	189-198
18497968-7	2008	AKAP149 was also cleaved by caspases during Fas- and staurosporine-induced apoptosis in Jurkat T and HeLa cells, which were blocked by specific inhibitors of caspase-3 and -8.	ammonium ferrous sulfate	44-47	caspase 1	Homo sapiens	28-36
18497968-7	2008	AKAP149 was also cleaved by caspases during Fas- and staurosporine-induced apoptosis in Jurkat T and HeLa cells, which were blocked by specific inhibitors of caspase-3 and -8.	Staurosporine	53-66	caspase 1	Homo sapiens	28-36
18469453-4	2008	The anti-retroviral drug ritonavir inhibits conversion of inactive pro-caspase-1 to active caspase-1.	Ritonavir	25-34	caspase 1	Homo sapiens	91-100
18469453-5	2008	Since ritonavir is well tolerated in short-term use it may therefore prove useful in treating acute pancreatitis by lowering caspase-1 mediated IL-18 formation and the many inflammatory mediators downstream from that.	Ritonavir	6-15	caspase 1	Homo sapiens	125-134
18469453-8	2008	Disulfiram inhibits several human proteases, among them caspase-1.	Disulfiram	0-10	caspase 1	Homo sapiens	56-65
18469453-10	2008	The first clinically used angiotensin converting enzyme inhibitor, captopril, has shown potent caspase-1 inhibiting activity as well and should be investigated in rodent models of human pancreatitis.	Captopril	67-76	caspase 1	Homo sapiens	95-104
19145821-7	2008	The combined effects of glutargin and erbisol in patients of this group are characterized by a decrease (but not normalization) of the blood content of sCD 117 by 47% and more than twofold decrease of the activity of caspases-1,-3 and -8.	arginine glutamate	24-33	caspase 1	Homo sapiens	217-237
17429439-6	2007	We show here that key components of the inflammasome are present in human keratinocytes and that CS like trinitro-chlorobenzene induce caspase-1/ASC dependent IL-1beta and IL-18 processing and secretion.	Cesium	97-99	caspase 1	Homo sapiens	135-144
18242710-6	2008	Our study revealed that LPS-stimulated THP-1 cells treated with simvastatin had an increased caspase-1 mediated processing of proIL-1beta.	Simvastatin	64-75	caspase 1	Homo sapiens	93-102
18242710-8	2008	Simvastatin-induced activation of caspase-1 was caused by an impairment of non-sterol isoprenoid biosynthesis, as the isoprenyl intermediate GGPP could block activation of caspase-1 and mIL-1beta release.	Simvastatin	0-11	caspase 1	Homo sapiens	34-43
18242710-8	2008	Simvastatin-induced activation of caspase-1 was caused by an impairment of non-sterol isoprenoid biosynthesis, as the isoprenyl intermediate GGPP could block activation of caspase-1 and mIL-1beta release.	Simvastatin	0-11	caspase 1	Homo sapiens	172-181
18242710-8	2008	Simvastatin-induced activation of caspase-1 was caused by an impairment of non-sterol isoprenoid biosynthesis, as the isoprenyl intermediate GGPP could block activation of caspase-1 and mIL-1beta release.	sterol isoprenoid	79-96	caspase 1	Homo sapiens	34-43
18242710-8	2008	Simvastatin-induced activation of caspase-1 was caused by an impairment of non-sterol isoprenoid biosynthesis, as the isoprenyl intermediate GGPP could block activation of caspase-1 and mIL-1beta release.	mil-1beta	186-195	caspase 1	Homo sapiens	34-43
18242710-10	2008	Taken together, these results demonstrate that simvastatin augments LPS-induced IL-1beta release post-translationally, by inducing caspase-1 activity.	Simvastatin	47-58	caspase 1	Homo sapiens	131-140
18322214-0	2008	Pannexin-1-mediated intracellular delivery of muramyl dipeptide induces caspase-1 activation via cryopyrin/NLRP3 independently of Nod2.	Acetylmuramyl-Alanyl-Isoglutamine	46-63	caspase 1	Homo sapiens	72-81
18322214-7	2008	Caspase-1 activation induced by MDP and ATP required pannexin-1 and Cryopyrin but was independent of Nod2.	Adenosine Triphosphate	40-43	caspase 1	Homo sapiens	0-9
19024627-3	2008	Specific inhibition of the final rate-limiting step in Gag processing by bevirimat prevents release of mature capsid protein from its precursor (CA-SP1), resulting in the production of immature, non-infectious virus particles.	Glycosaminoglycans	55-58	caspase 1	Homo sapiens	145-151
17610954-9	2008	It was also demonstrated that the recombinant seabream caspase-1 ectopically expressed in HEK293 cells was able to cleave a caspase-1 specific substrate, this activity being enhanced upon activation of the rat P2X7 receptor with BzATP.	3'-O-(4-benzoyl)benzoyladenosine 5'-triphosphate	229-234	caspase 1	Homo sapiens	55-64
17610954-9	2008	It was also demonstrated that the recombinant seabream caspase-1 ectopically expressed in HEK293 cells was able to cleave a caspase-1 specific substrate, this activity being enhanced upon activation of the rat P2X7 receptor with BzATP.	3'-O-(4-benzoyl)benzoyladenosine 5'-triphosphate	229-234	caspase 1	Homo sapiens	124-133
18383921-5	2008	The effects of stobadine, theophylline and adenine derivatives on the activity of caspase 1 was investigated with the use of spectrophotometry.	dicarbine	15-24	caspase 1	Homo sapiens	82-91
18383921-5	2008	The effects of stobadine, theophylline and adenine derivatives on the activity of caspase 1 was investigated with the use of spectrophotometry.	Theophylline	26-38	caspase 1	Homo sapiens	82-91
18383921-5	2008	The effects of stobadine, theophylline and adenine derivatives on the activity of caspase 1 was investigated with the use of spectrophotometry.	Adenine	43-50	caspase 1	Homo sapiens	82-91
17597823-4	2007	In vitro experiments in cultured human keratinocytes demonstrated anisomycin-induced, p38 mitogen-activated protein kinase (p38 MAPK)-dependent increased secretion of procaspase-1 and active caspase-1.	Anisomycin	66-76	caspase 1	Homo sapiens	170-179
17597823-5	2007	Furthermore, anisomycin increased the mRNA expression of IL-18 through a p38 MAPK-dependent but caspase-1-independent mechanism, reaching a maximum level after 12 hours of stimulation.	Anisomycin	13-23	caspase 1	Homo sapiens	96-105
17692289-2	2007	The cleavage of the BH4 domain in Bcl-x(L) and Bcl-2 by caspase 1 or 3 converts the anti-apoptotic Bcl-x(L) and Bcl-2 into pro-apoptotic proteins that potently induce apoptosis.	sapropterin	20-23	caspase 1	Homo sapiens	56-65
17429439-6	2007	We show here that key components of the inflammasome are present in human keratinocytes and that CS like trinitro-chlorobenzene induce caspase-1/ASC dependent IL-1beta and IL-18 processing and secretion.	Picryl Chloride	105-127	caspase 1	Homo sapiens	135-144
17442855-4	2007	Cryopyrin/NALP3 mediates caspase-1 activation in response to a wide variety of bacterial ligands, imidazoquinolines, dsRNA, and the endogenous danger signal uric acid.	imidazoquinolines	98-115	caspase 1	Homo sapiens	25-34
17442855-4	2007	Cryopyrin/NALP3 mediates caspase-1 activation in response to a wide variety of bacterial ligands, imidazoquinolines, dsRNA, and the endogenous danger signal uric acid.	Uric Acid	157-166	caspase 1	Homo sapiens	25-34
17572009-0	2007	The synthetic tellurium compound, AS101, is a novel inhibitor of IL-1beta converting enzyme.	Tellurium	14-23	caspase 1	Homo sapiens	65-91
17314138-5	2007	These were mainly due to the peculiar Tellur(IV)-thiol chemistry of the compound, which enabled the compound to interact with cysteine residues on both inflammatory and apoptotic caspases, resulting in their inactivation.	Sulfhydryl Compounds	49-54	caspase 1	Homo sapiens	179-187
17314138-5	2007	These were mainly due to the peculiar Tellur(IV)-thiol chemistry of the compound, which enabled the compound to interact with cysteine residues on both inflammatory and apoptotic caspases, resulting in their inactivation.	Cysteine	126-134	caspase 1	Homo sapiens	179-187
17585855-1	2007	A series of isatin sulfonamide analogs having a Michael acceptor were prepared and their potencies for inhibiting caspase-1, -3, -6, -7, and -8 were evaluated.	isatin sulfonamide	12-30	caspase 1	Homo sapiens	114-143
17558311-5	2007	In-vitro ATP-induced caspase-1 determinations were performed on osteoclasts from the different genotypes.	Adenosine Triphosphate	9-12	caspase 1	Homo sapiens	21-30
17485153-7	2007	Aluminum-containing adjuvants stimulated the release of IL-1beta and IL-18 from DCs via caspase-1 activation.	Aluminum	0-8	caspase 1	Homo sapiens	88-97
17572009-0	2007	The synthetic tellurium compound, AS101, is a novel inhibitor of IL-1beta converting enzyme.	ammonium trichloro(dioxoethylene-O,O'-)tellurate	34-39	caspase 1	Homo sapiens	65-91
17572009-4	2007	In the present study, using a substrate-specific enzymatic assay, we show that treatment of caspase-1 (interleukin-1beta [IL-1beta] converting enzyme [ICE]) with AS101 inhibits its enzymatic activity in a dose-dependent manner.	ammonium trichloro(dioxoethylene-O,O'-)tellurate	162-167	caspase 1	Homo sapiens	92-101
17404311-0	2007	Aluminum hydroxide adjuvants activate caspase-1 and induce IL-1beta and IL-18 release.	Aluminum Hydroxide	0-18	caspase 1	Homo sapiens	38-47
17418785-3	2007	We have identified a mammalian analog of this caspase-regulatory system in the NLR-family protein NALP1, a nucleotide-dependent activator of cytokine-processing protease caspase-1, which responds to bacterial ligand muramyl-dipeptide (MDP).	Acetylmuramyl-Alanyl-Isoglutamine	216-233	caspase 1	Homo sapiens	46-53
17418785-3	2007	We have identified a mammalian analog of this caspase-regulatory system in the NLR-family protein NALP1, a nucleotide-dependent activator of cytokine-processing protease caspase-1, which responds to bacterial ligand muramyl-dipeptide (MDP).	Acetylmuramyl-Alanyl-Isoglutamine	216-233	caspase 1	Homo sapiens	170-179
17418785-3	2007	We have identified a mammalian analog of this caspase-regulatory system in the NLR-family protein NALP1, a nucleotide-dependent activator of cytokine-processing protease caspase-1, which responds to bacterial ligand muramyl-dipeptide (MDP).	Acetylmuramyl-Alanyl-Isoglutamine	235-238	caspase 1	Homo sapiens	46-53
17418785-3	2007	We have identified a mammalian analog of this caspase-regulatory system in the NLR-family protein NALP1, a nucleotide-dependent activator of cytokine-processing protease caspase-1, which responds to bacterial ligand muramyl-dipeptide (MDP).	Acetylmuramyl-Alanyl-Isoglutamine	235-238	caspase 1	Homo sapiens	170-179
17349957-4	2007	Oligomerization of NALP1 and activation of caspase-1 occur via a two-step mechanism, requiring microbial product, muramyl-dipeptide, a component of peptidoglycan, followed by ribonucleoside triphosphates.	Acetylmuramyl-Alanyl-Isoglutamine	114-131	caspase 1	Homo sapiens	43-52
17433728-1	2007	Cryopyrin is essential for caspase-1 activation triggered by Toll-like receptor (TLR) ligands in the presence of adenosine triphosphate (ATP).	Adenosine Triphosphate	113-135	caspase 1	Homo sapiens	27-36
17433728-1	2007	Cryopyrin is essential for caspase-1 activation triggered by Toll-like receptor (TLR) ligands in the presence of adenosine triphosphate (ATP).	Adenosine Triphosphate	137-140	caspase 1	Homo sapiens	27-36
17349957-4	2007	Oligomerization of NALP1 and activation of caspase-1 occur via a two-step mechanism, requiring microbial product, muramyl-dipeptide, a component of peptidoglycan, followed by ribonucleoside triphosphates.	ribonucleoside triphosphates	175-203	caspase 1	Homo sapiens	43-52
17132626-3	2007	Cleavage and secretion of the cytokines is mediated by caspase-1, in association with an inflammasome containing Nalp3, which can be activated by binding of extracellular ATP to purinergic receptors.	Adenosine Triphosphate	171-174	caspase 1	Homo sapiens	55-64
17132626-7	2007	In parallel, ATP-mediated ROS-dependent PI3K is required for activation of caspase-1 and secretion of IL-1beta and IL-18.	Adenosine Triphosphate	13-16	caspase 1	Homo sapiens	75-84
17132626-7	2007	In parallel, ATP-mediated ROS-dependent PI3K is required for activation of caspase-1 and secretion of IL-1beta and IL-18.	Reactive Oxygen Species	26-29	caspase 1	Homo sapiens	75-84
17127070-3	2007	This strategy proved to be effective for the synthesis of ICE inhibitors, maintaining key hydrogen bond interactions with the enzyme and invoking a preferred conformation for binding.	Hydrogen	90-98	caspase 1	Homo sapiens	58-61
17464345-3	2007	Here we report a novel derivative of isoquinoline-1,3,4-trione that is highly potent in inhibiting caspase-1 activity in an irreversible and slow-binding manner, thus inhibiting cellular caspase-1 activity and the maturation of interleukin 1beta in U-937 cells.	isoquinoline-1,3,4-trione	37-62	caspase 1	Homo sapiens	99-108
17464345-3	2007	Here we report a novel derivative of isoquinoline-1,3,4-trione that is highly potent in inhibiting caspase-1 activity in an irreversible and slow-binding manner, thus inhibiting cellular caspase-1 activity and the maturation of interleukin 1beta in U-937 cells.	isoquinoline-1,3,4-trione	37-62	caspase 1	Homo sapiens	187-196
16782334-0	2006	Synthesis and evaluation of novel 1-(2-acylhydrazinocarbonyl)-cycloalkyl carboxamides as interleukin-1beta converting enzyme (ICE) inhibitors.	1-(2-acylhydrazinocarbonyl)-cycloalkyl carboxamides	34-85	caspase 1	Homo sapiens	89-124
16837047-1	2007	Mammalian interleukin-1beta (IL-1beta) is produced as a biologically inactive precursor molecule, which is proteolytically cleaved to an active form by IL-1beta-converting enzyme (ICE) after the activation of P2X(7) receptor by extracellular ATP.	Adenosine Triphosphate	242-245	caspase 1	Homo sapiens	152-178
16837047-1	2007	Mammalian interleukin-1beta (IL-1beta) is produced as a biologically inactive precursor molecule, which is proteolytically cleaved to an active form by IL-1beta-converting enzyme (ICE) after the activation of P2X(7) receptor by extracellular ATP.	Adenosine Triphosphate	242-245	caspase 1	Homo sapiens	180-183
16927020-8	2006	Finally, we show by different approaches that the inhibition of cell death by nicotine through NO release is related to modulation of caspase-1 activation.	Nicotine	78-86	caspase 1	Homo sapiens	134-143
17036048-3	2006	Here, we identify pannexin-1, a recently described mammalian protein that functions as a hemichannel when ectopically expressed, as this dye-uptake pathway and show that signalling through pannexin-1 is required for processing of caspase-1 and release of mature IL-1beta induced by P2X(7) receptor activation.	hemichannel	89-100	caspase 1	Homo sapiens	230-239
17138058-6	2006	RESULTS: sCD30 and caspase-1 concentrations were non-significantly up-regulated in all analysed groups--with or without rejection signs or immunosuppressed with cyclosporine or especially tacrolimus.	Cyclosporine	161-173	caspase 1	Homo sapiens	19-28
17138058-6	2006	RESULTS: sCD30 and caspase-1 concentrations were non-significantly up-regulated in all analysed groups--with or without rejection signs or immunosuppressed with cyclosporine or especially tacrolimus.	Tacrolimus	188-198	caspase 1	Homo sapiens	19-28
16984172-4	2006	This new approach resulted in potent, reversible, competitive inhibitors of caspase-1 (IC50 &lt; 10 nM), with significant advantages over aldehydes such as high stability in vitro to thiols (10 mM dithiothreitol (pH 7.2), 20 mM glutathione (pH 7.2, 9, 11)) and aqueous media, as well as some highly desirable druglike features.	Aldehydes	138-147	caspase 1	Homo sapiens	76-85
16984172-4	2006	This new approach resulted in potent, reversible, competitive inhibitors of caspase-1 (IC50 &lt; 10 nM), with significant advantages over aldehydes such as high stability in vitro to thiols (10 mM dithiothreitol (pH 7.2), 20 mM glutathione (pH 7.2, 9, 11)) and aqueous media, as well as some highly desirable druglike features.	Sulfhydryl Compounds	183-189	caspase 1	Homo sapiens	76-85
16984172-4	2006	This new approach resulted in potent, reversible, competitive inhibitors of caspase-1 (IC50 &lt; 10 nM), with significant advantages over aldehydes such as high stability in vitro to thiols (10 mM dithiothreitol (pH 7.2), 20 mM glutathione (pH 7.2, 9, 11)) and aqueous media, as well as some highly desirable druglike features.	Dithiothreitol	197-211	caspase 1	Homo sapiens	76-85
16984172-4	2006	This new approach resulted in potent, reversible, competitive inhibitors of caspase-1 (IC50 &lt; 10 nM), with significant advantages over aldehydes such as high stability in vitro to thiols (10 mM dithiothreitol (pH 7.2), 20 mM glutathione (pH 7.2, 9, 11)) and aqueous media, as well as some highly desirable druglike features.	Glutathione	228-239	caspase 1	Homo sapiens	76-85
16984172-5	2006	It was also demonstrated that azides can be incorporated into inhibitors of other caspases (e.g. 3, 8) and cathepsins (e.g. K, S, B), indicating the versatility of this valuable new approach to cysteine protease inhibition.	Azides	30-36	caspase 1	Homo sapiens	82-90
16870441-0	2006	Synthesis and evaluation of thiazepines as interleukin-1beta converting enzyme (ICE) inhibitors.	Thiazepines	28-39	caspase 1	Homo sapiens	43-78
16870441-0	2006	Synthesis and evaluation of thiazepines as interleukin-1beta converting enzyme (ICE) inhibitors.	Thiazepines	28-39	caspase 1	Homo sapiens	80-83
16870441-1	2006	A series of monocyclic thiazepine inhibitors of interleukin-1beta converting enzyme (ICE) were synthesized in eight steps from commercially available intermediates.	Thiazepines	23-33	caspase 1	Homo sapiens	48-83
16870441-1	2006	A series of monocyclic thiazepine inhibitors of interleukin-1beta converting enzyme (ICE) were synthesized in eight steps from commercially available intermediates.	Thiazepines	23-33	caspase 1	Homo sapiens	85-88
16870441-2	2006	In vitro biological evaluation showed the thiazepines to be moderately potent ICE inhibitors, with the most active compound exhibiting an IC50 value of 30 nM in an enzyme inhibition assay.	Thiazepines	42-53	caspase 1	Homo sapiens	78-81
17164758-3	2007	Preliminary microarray comparisons on DCIS and invasive carcinoma samples dissected from formalin-fixed paraffin sections showed a consistent downregulation of two previously identified FHIT-related genes, caspase 1 and BRCA1 in lesions underexpressing FHIT.	Formaldehyde	89-97	caspase 1	Homo sapiens	206-215
17164758-3	2007	Preliminary microarray comparisons on DCIS and invasive carcinoma samples dissected from formalin-fixed paraffin sections showed a consistent downregulation of two previously identified FHIT-related genes, caspase 1 and BRCA1 in lesions underexpressing FHIT.	Paraffin	104-112	caspase 1	Homo sapiens	206-215
16995876-5	2006	Furthermore, amrubicin- and amrubicinol-induced apoptosis was mediated by the activation of caspase-3/7, but not caspase-1, preceding a loss of mitochondrial membrane potential.	amrubicin	13-22	caspase 1	Homo sapiens	113-122
16995876-5	2006	Furthermore, amrubicin- and amrubicinol-induced apoptosis was mediated by the activation of caspase-3/7, but not caspase-1, preceding a loss of mitochondrial membrane potential.	amrubicinol	28-39	caspase 1	Homo sapiens	113-122
16990137-3	2006	Here we show that toxin-induced membrane permeabilization leads to a decrease in cytoplasmic potassium, which promotes the formation of a multiprotein oligomeric innate immune complex, called the inflammasome, and the activation of caspase-1.	Potassium	93-102	caspase 1	Homo sapiens	232-241
16782334-0	2006	Synthesis and evaluation of novel 1-(2-acylhydrazinocarbonyl)-cycloalkyl carboxamides as interleukin-1beta converting enzyme (ICE) inhibitors.	1-(2-acylhydrazinocarbonyl)-cycloalkyl carboxamides	34-85	caspase 1	Homo sapiens	126-129
16782334-1	2006	Novel 1-(2-acylhydrazinocarbonyl)cycloalkyl carboxamides were designed as peptidomimetic inhibitors of interleukin-1beta converting enzyme (ICE).	1-(2-acylhydrazinocarbonyl)cycloalkyl carboxamides	6-56	caspase 1	Homo sapiens	103-138
16782334-1	2006	Novel 1-(2-acylhydrazinocarbonyl)cycloalkyl carboxamides were designed as peptidomimetic inhibitors of interleukin-1beta converting enzyme (ICE).	1-(2-acylhydrazinocarbonyl)cycloalkyl carboxamides	6-56	caspase 1	Homo sapiens	140-143
16774272-1	2006	[reaction: see text] The total synthesis of the interleukin-1beta converting enzyme inhibitor EI-1941-2 was achieved utilizing tandem oxidation/oxa-electrocyclization/oxidation to access a key alpha-pyrone intermediate.	Pyrones	193-205	caspase 1	Homo sapiens	48-83
16723495-4	2006	Cimetidine induced the activation of caspase-1, which is reported to modify immature IL-18 to mature/active IL-18, and the elevation of intracellular cAMP, leading to the activation of protein kinase A (PKA).	Cimetidine	0-10	caspase 1	Homo sapiens	37-46
16682620-2	2006	Highly specific thiol-containing inhibitors of the human inflammatory caspase-1 were identified by using disulfide trapping, a method for site-directed small-molecule discovery.	Sulfhydryl Compounds	16-21	caspase 1	Homo sapiens	70-79
16864444-2	2006	Caspase -1, -3, -8, -9, and -10 inhibitors partially reversed the cell death induced by dracorhodin perchlorate.	dracorhodin	88-111	caspase 1	Homo sapiens	0-31
16864444-6	2006	Taken together, dracorhodin perchlorate-induced apoptosis in HL-60 cells via up-regulation of Bax, activation of caspases and ERK/p38/JNK MAPKs.	dracorhodin	16-39	caspase 1	Homo sapiens	113-121
16547592-5	2006	VPE and caspase-1 share several structural properties: the catalytic dyads and three amino acids forming the substrate pockets (Asp pocket) are conserved between VPE and caspase-1.	Aspartic Acid	128-131	caspase 1	Homo sapiens	8-17
16547592-5	2006	VPE and caspase-1 share several structural properties: the catalytic dyads and three amino acids forming the substrate pockets (Asp pocket) are conserved between VPE and caspase-1.	Aspartic Acid	128-131	caspase 1	Homo sapiens	170-179
16817903-6	2006	Doxorubicin-induced apoptosis was potentiated by the expression of caspase 1 (but not by a catalytic mutant of caspase 1) and required endogenous Ipaf.	Doxorubicin	0-11	caspase 1	Homo sapiens	67-76
16817903-6	2006	Doxorubicin-induced apoptosis was potentiated by the expression of caspase 1 (but not by a catalytic mutant of caspase 1) and required endogenous Ipaf.	Doxorubicin	0-11	caspase 1	Homo sapiens	111-120
16817903-7	2006	Doxorubicin treatment of MCF-7 cells resulted in activation of exogenous caspase 1, which was partly dependent on endogenous Ipaf.	Doxorubicin	0-11	caspase 1	Homo sapiens	73-82
16817903-9	2006	Caspase 1-dependent apoptosis induced by doxorubicin was also inhibited by Bcl2 and caspase 9s, but caspase 1 activation by activated Ipaf was not inhibited by Bcl2.	Doxorubicin	41-52	caspase 1	Homo sapiens	0-9
16682620-2	2006	Highly specific thiol-containing inhibitors of the human inflammatory caspase-1 were identified by using disulfide trapping, a method for site-directed small-molecule discovery.	Disulfides	105-114	caspase 1	Homo sapiens	70-79
16682620-6	2006	Recently, disulfide trapping identified a similar small-molecule site and allosteric transition in the apoptotic caspase-7 that shares only a 23% sequence identity with caspase-1.	Disulfides	10-19	caspase 1	Homo sapiens	169-178
16621994-10	2006	Active caspase-1, which is required for the processing and secretion of IL-18 and IL-1beta, was activated in simvastatin-treated monocytes.	Simvastatin	109-120	caspase 1	Homo sapiens	7-16
16596269-8	2006	Caspase-1 expression mediated by an adenoviral vector was able to kill directly cells and to sensitise the remaining cells to cisplatin or gamma-radiation in vitro.	Cisplatin	126-135	caspase 1	Homo sapiens	0-9
16596269-9	2006	In HeLa cells stably transfected with caspase-1, sensitisation to cisplatin was due to an amplification of the cisplatin-induced mitochondrial apoptotic pathway activation.	Cisplatin	66-75	caspase 1	Homo sapiens	38-47
16596269-9	2006	In HeLa cells stably transfected with caspase-1, sensitisation to cisplatin was due to an amplification of the cisplatin-induced mitochondrial apoptotic pathway activation.	Cisplatin	111-120	caspase 1	Homo sapiens	38-47
16596269-10	2006	Caspase-1 mediated sensitisation to cisplatin and gamma-radiation was also observed in vivo.	Cisplatin	36-45	caspase 1	Homo sapiens	0-9
16732410-4	2006	The caspases were detected by immunoblots with polyclonal rabbit-anti-caspases-antibodies after 15% sodium dodecyl sulfate-polyacrylgel electrophoresis (SDS-PAGE) under reducing conditions.	Sodium Dodecyl Sulfate	100-122	caspase 1	Homo sapiens	4-12
16573645-2	2006	Caspases are present in synapses and dendrites of neurons where they can be activated in response to glutamate receptor stimulation and calcium influx.	Calcium	136-143	caspase 1	Homo sapiens	0-8
16573645-4	2006	We provide evidence that caspase-1 plays a role in regulating alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor-mediated calcium influx and synaptic plasticity in the hippocampus.	Calcium	144-151	caspase 1	Homo sapiens	25-34
16573645-7	2006	Calcium responses to AMPA were enhanced in hippocampal neurons treated with a caspase-1 inhibitor suggesting that caspase-1 normally functions to reduce AMPA receptor-mediated calcium influx.	Calcium	0-7	caspase 1	Homo sapiens	78-87
16573645-7	2006	Calcium responses to AMPA were enhanced in hippocampal neurons treated with a caspase-1 inhibitor suggesting that caspase-1 normally functions to reduce AMPA receptor-mediated calcium influx.	Calcium	0-7	caspase 1	Homo sapiens	114-123
16573645-7	2006	Calcium responses to AMPA were enhanced in hippocampal neurons treated with a caspase-1 inhibitor suggesting that caspase-1 normally functions to reduce AMPA receptor-mediated calcium influx.	Calcium	176-183	caspase 1	Homo sapiens	78-87
16573645-7	2006	Calcium responses to AMPA were enhanced in hippocampal neurons treated with a caspase-1 inhibitor suggesting that caspase-1 normally functions to reduce AMPA receptor-mediated calcium influx.	Calcium	176-183	caspase 1	Homo sapiens	114-123
16573645-8	2006	These findings suggest that, by selectively reducing AMPA currents and calcium influx, caspase-1 functions as a negative regulator of LTP at hippocampal synapses.	alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid	53-57	caspase 1	Homo sapiens	87-96
16573645-8	2006	These findings suggest that, by selectively reducing AMPA currents and calcium influx, caspase-1 functions as a negative regulator of LTP at hippocampal synapses.	Calcium	71-78	caspase 1	Homo sapiens	87-96
16609959-7	2006	Moreover, the pro-apoptotic effect of 10 microM WIN55,212-2 could be reduced by the addition to the incubation medium of a cell-permeant inhibitor of caspase-1 (50 nM).	win55	48-53	caspase 1	Homo sapiens	150-159
16613759-12	2006	The cleavage product was active in the bioassay for IL-1 activity, and the caspase-1 inhibitor YVAD blocked processing.	YVAD	95-99	caspase 1	Homo sapiens	75-84
16274992-1	2006	Disulfide Tethering was applied to the active site of human caspase-1, resulting in the discovery of a novel, tricyclic molecular fragment that selectively binds in S4.	Disulfides	0-9	caspase 1	Homo sapiens	60-69
16732410-4	2006	The caspases were detected by immunoblots with polyclonal rabbit-anti-caspases-antibodies after 15% sodium dodecyl sulfate-polyacrylgel electrophoresis (SDS-PAGE) under reducing conditions.	polyacrylgel	123-135	caspase 1	Homo sapiens	4-12
16732410-4	2006	The caspases were detected by immunoblots with polyclonal rabbit-anti-caspases-antibodies after 15% sodium dodecyl sulfate-polyacrylgel electrophoresis (SDS-PAGE) under reducing conditions.	Sodium Dodecyl Sulfate	153-156	caspase 1	Homo sapiens	4-12
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 1	Homo sapiens	36-45
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 1	Homo sapiens	36-43
16732410-7	2006	Possibly, glycerol may also contribute to activation of caspases via direct toxic effects to mitochondria during cryopreservation of spermatozoa.	Glycerol	10-18	caspase 1	Homo sapiens	56-64
16137654-0	2005	Synthesis and evaluation of novel dipeptidyl benzoyloxymethyl ketones as caspase inhibitors.	dipeptidyl benzoyloxymethyl ketones	34-69	caspase 1	Homo sapiens	73-80
16302804-1	2005	A number of isatin sulfonamide analogues were prepared and their potencies for inhibiting caspase-1, -3, -6, -7, and -8 were evaluated in vitro.	isatin sulfonamide	12-30	caspase 1	Homo sapiens	90-119
16135520-0	2005	Role of p73 in regulating human caspase-1 gene transcription induced by interferon-{gamma} and cisplatin.	Cisplatin	95-104	caspase 1	Homo sapiens	32-41
16135520-6	2005	Treatment of cells with cisplatin (which increases p73 protein level) resulted in increased caspase-1 promoter activity and its mRNA level.	Cisplatin	24-33	caspase 1	Homo sapiens	92-101
16135520-7	2005	Blocking of p73 function by a dominant negative mutant reduced basal as well as cisplatin-induced caspase-1 promoter activity.	Cisplatin	80-89	caspase 1	Homo sapiens	98-107
16135520-13	2005	IRF-1 cooperated with p73 and cisplatin cooperated with interferon-gamma in the activation of the caspase-1 promoter.	Cisplatin	30-39	caspase 1	Homo sapiens	98-107
16137654-4	2005	The benzyloxycarbonyl-phenylglycyl-aspartyl benzoyloxymethyl ketone (Z-Phg-Asp-CH2OCO-Ph, coded as HU44) was the most potent inhibitor of caspase-1 and caspase-3.	benzyloxycarbonyl-phenylglycyl-aspartyl benzoyloxymethyl ketone	4-67	caspase 1	Homo sapiens	138-147
16137654-4	2005	The benzyloxycarbonyl-phenylglycyl-aspartyl benzoyloxymethyl ketone (Z-Phg-Asp-CH2OCO-Ph, coded as HU44) was the most potent inhibitor of caspase-1 and caspase-3.	z-phg-asp	69-78	caspase 1	Homo sapiens	138-147
16137654-4	2005	The benzyloxycarbonyl-phenylglycyl-aspartyl benzoyloxymethyl ketone (Z-Phg-Asp-CH2OCO-Ph, coded as HU44) was the most potent inhibitor of caspase-1 and caspase-3.	ch2oco	79-85	caspase 1	Homo sapiens	138-147
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 1	Homo sapiens	159-168
16204022-11	2005	Immunohistochemically, caspase-1 was lower in ovarian serous carcinomas than in OSE.	serine O-sulfate	80-83	caspase 1	Homo sapiens	23-32
16046125-1	2005	A novel diazocan containing dipeptide mimetic was synthesized via reductive N-N bond cleavage of a pyrazolidino-pyrazolidine using Raney-Ni and evaluated as an ICE inhibitor.	diazocan	8-16	caspase 1	Homo sapiens	160-163
16046125-1	2005	A novel diazocan containing dipeptide mimetic was synthesized via reductive N-N bond cleavage of a pyrazolidino-pyrazolidine using Raney-Ni and evaluated as an ICE inhibitor.	Dipeptides	28-37	caspase 1	Homo sapiens	160-163
16046129-0	2005	Synthesis and evaluation of tricyclic pyrrolopyrimidinones as dipeptide mimetics: inhibition of interleukin-1beta-converting enzyme.	tricyclic pyrrolopyrimidinones	28-58	caspase 1	Homo sapiens	96-131
16046129-0	2005	Synthesis and evaluation of tricyclic pyrrolopyrimidinones as dipeptide mimetics: inhibition of interleukin-1beta-converting enzyme.	Dipeptides	62-71	caspase 1	Homo sapiens	96-131
16046129-1	2005	The application of a tricyclic pyrrolopyrimidinone scaffold for the synthesis of peptidomimetic inhibitors of interleukin-1beta-converting enzyme (ICE) is reported.	tricyclic pyrrolopyrimidinone	21-50	caspase 1	Homo sapiens	110-145
16046129-1	2005	The application of a tricyclic pyrrolopyrimidinone scaffold for the synthesis of peptidomimetic inhibitors of interleukin-1beta-converting enzyme (ICE) is reported.	tricyclic pyrrolopyrimidinone	21-50	caspase 1	Homo sapiens	147-150
16046129-3	2005	In vitro biological evaluation of the tricyclic pyrrolopyrimidinones revealed fair to good ICE inhibitors, with the most active compound exhibiting an IC50 of 14 nM in a caspase-1 enzyme binding assay.	tricyclic pyrrolopyrimidinones	38-68	caspase 1	Homo sapiens	91-94
16046129-3	2005	In vitro biological evaluation of the tricyclic pyrrolopyrimidinones revealed fair to good ICE inhibitors, with the most active compound exhibiting an IC50 of 14 nM in a caspase-1 enzyme binding assay.	tricyclic pyrrolopyrimidinones	38-68	caspase 1	Homo sapiens	170-179
16005468-4	2005	Microarray profiling of fas-resistant versus sensitive cells identified a set of genes including STATs, caspase 1, cyclin D1, Bcl-xL, VDAC2, and BAD.	ammonium ferrous sulfate	24-27	caspase 1	Homo sapiens	104-113
16001973-13	2005	Caspase-1, -3, -6, -8, and -9 were increased indicating that these proteases are key factors in the execution of doxorubicin mediated apoptosis.	Doxorubicin	113-124	caspase 1	Homo sapiens	0-29
16103071-4	2005	In support of the hypothesis that caspase-1 might be a target involved in the sensitization of DLD-1 cells to Fas-induced apoptosis by ETS1, overexpression of caspase-1 bypasses Fas-induced apoptosis in these cells as well.	ammonium ferrous sulfate	110-113	caspase 1	Homo sapiens	34-43
16103071-4	2005	In support of the hypothesis that caspase-1 might be a target involved in the sensitization of DLD-1 cells to Fas-induced apoptosis by ETS1, overexpression of caspase-1 bypasses Fas-induced apoptosis in these cells as well.	ammonium ferrous sulfate	110-113	caspase 1	Homo sapiens	159-168
16103071-4	2005	In support of the hypothesis that caspase-1 might be a target involved in the sensitization of DLD-1 cells to Fas-induced apoptosis by ETS1, overexpression of caspase-1 bypasses Fas-induced apoptosis in these cells as well.	ammonium ferrous sulfate	178-181	caspase 1	Homo sapiens	34-43
16103071-4	2005	In support of the hypothesis that caspase-1 might be a target involved in the sensitization of DLD-1 cells to Fas-induced apoptosis by ETS1, overexpression of caspase-1 bypasses Fas-induced apoptosis in these cells as well.	ammonium ferrous sulfate	178-181	caspase 1	Homo sapiens	159-168
16081838-4	2005	VX-765, an orally active IL-converting enzyme/caspase-1 inhibitor, blocked IL-1beta secretion with equal potency in LPS-stimulated cells from FCAS and control subjects.	belnacasan	0-6	caspase 1	Homo sapiens	46-55
16081838-5	2005	These results further link mutations in cryopyrin with abnormal caspase-1 activation, and support the clinical testing of caspase-1 inhibitors such as VX-765 in autoinflammatory disorders.	belnacasan	151-157	caspase 1	Homo sapiens	122-131
15846371-0	2005	Neuroprotection by the caspase-1 inhibitor Ac-YVAD-(acyloxy)mk in experimental neuroAIDS is independent from IL-1beta generation.	ac-yvad-(acyloxy)mk	43-62	caspase 1	Homo sapiens	23-32
16081838-0	2005	IL-converting enzyme/caspase-1 inhibitor VX-765 blocks the hypersensitive response to an inflammatory stimulus in monocytes from familial cold autoinflammatory syndrome patients.	belnacasan	41-47	caspase 1	Homo sapiens	21-30
15980455-1	2005	Caspases and granzyme B are proteases that share the primary specificity to cleave at the carboxyl terminal of aspartate residues in their substrates.	Aspartic Acid	111-120	caspase 1	Homo sapiens	0-8
15909122-4	2005	Flavone induces the activation of caspases 2, 3, 8, 9 and 10 and a decrease of mitochondrial anti-apoptotic Bcl(2) protein expression.	flavone	0-7	caspase 1	Homo sapiens	34-42
15809717-2	2005	Caspase-1 (interleukin-1beta-converting enzyme) is a member of the cysteine protease family, which cleaves target proteins following aspartic acid residues.	Aspartic Acid	133-146	caspase 1	Homo sapiens	11-46
15809717-8	2005	On treatment with 5-aza-2"-deoxycytidine (5-aza-C), and/or trichostatin A (TSA), all three cell lines re-expressed caspase-1 mRNA.	Decitabine	18-40	caspase 1	Homo sapiens	115-124
15809717-2	2005	Caspase-1 (interleukin-1beta-converting enzyme) is a member of the cysteine protease family, which cleaves target proteins following aspartic acid residues.	Aspartic Acid	133-146	caspase 1	Homo sapiens	0-9
15809717-8	2005	On treatment with 5-aza-2"-deoxycytidine (5-aza-C), and/or trichostatin A (TSA), all three cell lines re-expressed caspase-1 mRNA.	Decitabine	42-49	caspase 1	Homo sapiens	115-124
15809717-8	2005	On treatment with 5-aza-2"-deoxycytidine (5-aza-C), and/or trichostatin A (TSA), all three cell lines re-expressed caspase-1 mRNA.	trichostatin A	59-73	caspase 1	Homo sapiens	115-124
15809717-8	2005	On treatment with 5-aza-2"-deoxycytidine (5-aza-C), and/or trichostatin A (TSA), all three cell lines re-expressed caspase-1 mRNA.	trichostatin A	75-78	caspase 1	Homo sapiens	115-124
15831282-6	2005	MAIN OUTCOME MEASURE(S): Active caspases-1, -3, -8, and -9 were examined in human spermatozoa by flow cytometry using carboxyfluorescein derivatives.	6-carboxyfluorescein	118-136	caspase 1	Homo sapiens	32-58
15686411-0	2005	Acacetin induces apoptosis in human gastric carcinoma cells accompanied by activation of caspase cascades and production of reactive oxygen species.	acacetin	0-8	caspase 1	Homo sapiens	89-96
15827328-5	2005	Resveratrol induces activation of caspase-3 and increases the cleavage of the downstream caspase substrate, poly(ADP-ribose) polymerase.	Resveratrol	0-11	caspase 1	Homo sapiens	34-41
15827328-6	2005	Resveratrol-induced DNA fragmentation can be completely blocked by either a general caspase inhibitor (Z-VAD-FMK) or a selective caspase-3 inhibitor (Z-DEVD-FMK), but not by a selective caspase-1 inhibitor.	Resveratrol	0-11	caspase 1	Homo sapiens	84-91
15827328-6	2005	Resveratrol-induced DNA fragmentation can be completely blocked by either a general caspase inhibitor (Z-VAD-FMK) or a selective caspase-3 inhibitor (Z-DEVD-FMK), but not by a selective caspase-1 inhibitor.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	103-112	caspase 1	Homo sapiens	84-91
15635642-1	2005	Peptide aldehydes are of interest due to their inhibitory properties toward numerous classes of proteolytic enzymes such as caspases or the proteasome.	Aldehydes	8-17	caspase 1	Homo sapiens	124-132
15635642-8	2005	A small collection of new and known peptide aldehydes has been tested for inhibitory activity against caspases 1 and 3.	Aldehydes	44-53	caspase 1	Homo sapiens	102-118
15614043-7	2005	Although caspase-1 inhibitor completely abolished the production of IL-18, anti-IL-18 mAb and caspase-1 inhibitor partially inhibited the increase in ICAM-1 and CD40 expression induced by doxazosin, prazosin, and terazosin.	Doxazosin	188-197	caspase 1	Homo sapiens	9-18
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 1	Homo sapiens	191-200
15684607-7	2005	However, the chemotherapeutic agent 5-FU, by inducing Caspase-1 and Caspase-3 activation, induced secretion of proteolytically processed mature and degraded IL-18 species, respectively, in Capan-2 cells.	Fluorouracil	36-40	caspase 1	Homo sapiens	54-63
15622543-3	2005	We hypothesized that two caspase-1-processed cytokines, interleukin (IL)-1beta and IL-18, are involved in oxygen-induced neuronal cell death.	Oxygen	106-112	caspase 1	Homo sapiens	25-34
15614043-7	2005	Although caspase-1 inhibitor completely abolished the production of IL-18, anti-IL-18 mAb and caspase-1 inhibitor partially inhibited the increase in ICAM-1 and CD40 expression induced by doxazosin, prazosin, and terazosin.	Doxazosin	188-197	caspase 1	Homo sapiens	94-103
15614043-7	2005	Although caspase-1 inhibitor completely abolished the production of IL-18, anti-IL-18 mAb and caspase-1 inhibitor partially inhibited the increase in ICAM-1 and CD40 expression induced by doxazosin, prazosin, and terazosin.	Prazosin	199-207	caspase 1	Homo sapiens	9-18
15614043-7	2005	Although caspase-1 inhibitor completely abolished the production of IL-18, anti-IL-18 mAb and caspase-1 inhibitor partially inhibited the increase in ICAM-1 and CD40 expression induced by doxazosin, prazosin, and terazosin.	Prazosin	199-207	caspase 1	Homo sapiens	94-103
15614043-7	2005	Although caspase-1 inhibitor completely abolished the production of IL-18, anti-IL-18 mAb and caspase-1 inhibitor partially inhibited the increase in ICAM-1 and CD40 expression induced by doxazosin, prazosin, and terazosin.	Terazosin	213-222	caspase 1	Homo sapiens	94-103
15326478-6	2004	The 12 bp exon-3 encodes for the AEDD amino-acid sequence, which is N-terminal with respect to the cleavage site of caspase-1.	aedd amino-acid	33-48	caspase 1	Homo sapiens	116-125
15813022-9	2004	CONCLUSION: Dracorhodin perchlorate induced Hela cell death via alteration of Bax/Bcl-XL ratio and activation of caspases.	dracorhodin	12-35	caspase 1	Homo sapiens	113-121
15467738-4	2004	Here we show that 1.0 microM Tam promotes apoptosis in acutely damaged ER-poor HMECs through IRF-1 induction and caspase-1/3 activation.	Tamoxifen	29-32	caspase 1	Homo sapiens	113-122
15467738-5	2004	Treatment of acutely damaged HMEC-E6 cells with 1.0 microM Tam resulted in recruitment of CBP to the gamma-IFN-activated sequence element of the IRF-1 promoter, induction of IRF-1, and sequential activation of caspase-1 and -3.	Tamoxifen	59-62	caspase 1	Homo sapiens	210-226
15467738-6	2004	The effects of Tam were blocked by expression of siRNA directed against IRF-1 and caspase-1 inhibitors.	Tamoxifen	15-18	caspase 1	Homo sapiens	82-91
15467738-7	2004	These data indicate that Tam induces apoptosis in HMEC-E6 cells through a novel IRF-1-mediated signaling pathway that results in activated caspase-1 and -3.	Tamoxifen	25-28	caspase 1	Homo sapiens	139-155
15477863-8	2004	The cell death was blocked by the pan-caspase inhibitor Z-VAD-fmk, and also by submicromolar concentrations of Z-YVAD-fmk and Z-IETD-fmk, inhibitors of caspase-1 and -8, respectively.	benzyloxycarbonyltyrosyl-valyl-alanyl-aspartic acid fluoromethyl ketone	111-121	caspase 1	Homo sapiens	152-168
15477863-8	2004	The cell death was blocked by the pan-caspase inhibitor Z-VAD-fmk, and also by submicromolar concentrations of Z-YVAD-fmk and Z-IETD-fmk, inhibitors of caspase-1 and -8, respectively.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	126-136	caspase 1	Homo sapiens	152-168
15475455-8	2004	Death signaling by TRAIL in these cells was Fas-associated death domain and caspase dependent because dominant negative Fas-associated death domain or the cowpox interleukin 1beta-converting enzyme inhibitor protein cytokine response modifier A prevented apoptosis in the presence of DRB.	5,6-dichlorobenzimidazole	284-287	caspase 1	Homo sapiens	162-197
15379993-0	2004	Caspase-1 and poly (ADP-ribose) polymerase inhibitors may protect against peroxynitrite-induced neurotoxicity independent of their enzyme inhibitor activity.	Peroxynitrous Acid	74-87	caspase 1	Homo sapiens	0-9
15379993-6	2004	Ac-Tyr-Val-Ala-Asp-chloromethyl ketone (Ac-YVAD-cmk), a specific caspase-1 inhibitor, completely blocked neurotoxicity as well as ATP depletion induced by SIN-1.	N-acetyl-tyrosyl-valyl-alanyl-aspartyl chloromethyl ketone	0-38	caspase 1	Homo sapiens	65-74
15379993-6	2004	Ac-Tyr-Val-Ala-Asp-chloromethyl ketone (Ac-YVAD-cmk), a specific caspase-1 inhibitor, completely blocked neurotoxicity as well as ATP depletion induced by SIN-1.	Adenosine Triphosphate	130-133	caspase 1	Homo sapiens	65-74
15289867-6	2004	Activation of caspase 3 protein procession and enzyme activity with inducing cleavage of caspase 3 substrates PARP was identified in flavone-treated cells, and an inhibitory peptide Ac-DEVD-FMK for caspase 3, but not Ac-YVAD-FMK for caspase 1, attenuates the cytotoxic effect of flavone in COLO205 and HT29 cells.	flavone	133-140	caspase 1	Homo sapiens	233-242
15498465-7	2004	However, mutational change at the caspase-1 active center of the Cys 246 of caspase-1zeta, as well as Cys 285 of caspase-1alpha, completely abolished their apoptotic activity.	Cysteine	65-68	caspase 1	Homo sapiens	34-43
15304288-1	2004	The primary objective of this study was to test the hypothesis that inhibition of mitochondrial permeability transition and/or inhibition of caspase family enzymes can block chondrocyte apoptosis induced by H2O2.	Hydrogen Peroxide	207-211	caspase 1	Homo sapiens	141-148
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 1	Homo sapiens	161-170
15304288-11	2004	A non-selective caspase inhibitor, a caspase 3-selective inhibitor, and a caspase 1-selective inhibitor, all blocked chondrocyte apoptosis induced by H2O2.	Hydrogen Peroxide	150-154	caspase 1	Homo sapiens	74-83
15205454-4	2004	ETA-induced ssDNA formation was completely inhibited by Z-VAD (where Z is benzyloxycarbonyl), which blocks multiple caspases, suggesting a role for caspases in this process.	z-vad	56-61	caspase 1	Homo sapiens	116-124
15294346-0	2004	Production of macrophage IL-1beta was inhibited both at the levels of transcription and maturation by caspase-1 following inhalation exposure to isobutyl nitrite.	isobutyl nitrite	145-161	caspase 1	Homo sapiens	102-111
15294346-7	2004	Nitrite inhalant exposure blocked activation-induced increases in caspase-1 activity, consistent with a 50% reduction in 17 kDa IL-1beta shown in Western blots.	Nitrites	0-7	caspase 1	Homo sapiens	66-75
15294346-8	2004	Thus, exposure to nitrite inhalants reduced macrophage production of IL-1beta by reducing transcription, as well as post-translational processing mediated by caspase-1.	Nitrites	18-25	caspase 1	Homo sapiens	158-167
15205454-4	2004	ETA-induced ssDNA formation was completely inhibited by Z-VAD (where Z is benzyloxycarbonyl), which blocks multiple caspases, suggesting a role for caspases in this process.	z-vad	56-61	caspase 1	Homo sapiens	148-156
15296730-0	2004	Crystal structures of a ligand-free and malonate-bound human caspase-1: implications for the mechanism of substrate binding.	malonic acid	40-48	caspase 1	Homo sapiens	61-70
15460444-1	2004	In human neuroblastoma SK-N-BE(2) cells undergoing apoptotic death induced by ginsenoside Rh2, a dammarane glycoside that was isolated from Panax ginseng C. A. Meyer, caspase-1 and caspase-3 were activated.	dammarane glycoside	97-116	caspase 1	Homo sapiens	167-176
15460444-5	2004	These results suggest that activation of caspase-1 and -3 and the up-regulation of Bax are required in order for apoptotic death of SK-N-BE(2) cells to be induced by ginsenoside Rh2, and p53 plays an important role in the pathways to promote apoptosis.	sk-n-be	132-139	caspase 1	Homo sapiens	41-57
15296730-1	2004	Caspase-1, a mediator of the posttranslational processing of IL-1beta and IL-18, requires an aspartic acid in the P1 position of its substrates.	Aspartic Acid	93-106	caspase 1	Homo sapiens	0-9
15296730-2	2004	The mechanisms of caspase-1 activation remain poorly understood despite numerous structures of the enzyme complexed with aspartate-based inhibitors.	Aspartic Acid	121-130	caspase 1	Homo sapiens	18-27
15296730-5	2004	These results illustrate the essential function of the obligatory aspartate recognition element that opens the active site of caspase-1 to substrates and may be the determinant responsible for the conformational changes between ligand-free and -bound forms of the enzyme, and suggest a new approach for identifying novel aspartic acid mimetics.	Aspartic Acid	66-75	caspase 1	Homo sapiens	126-135
15296730-5	2004	These results illustrate the essential function of the obligatory aspartate recognition element that opens the active site of caspase-1 to substrates and may be the determinant responsible for the conformational changes between ligand-free and -bound forms of the enzyme, and suggest a new approach for identifying novel aspartic acid mimetics.	Aspartic Acid	321-334	caspase 1	Homo sapiens	126-135
15140190-6	2004	Site-directed mutagenesis experiments eliminating three, six or nine potential caspase cleavage sites in the protein suggest redundancy in the site(s) at which cleavage can occur, as previously described for other disease proteins; but also map a major cleavage event to a cluster of aspartate residues within the ubiquitin-binding domain of ataxin-3 near the polyglutamine tract.	Aspartic Acid	284-293	caspase 1	Homo sapiens	79-86
15225375-0	2004	The sequence of the CA-SP1 junction accounts for the differential sensitivity of HIV-1 and SIV to the small molecule maturation inhibitor 3-O-{3",3"-dimethylsuccinyl}-betulinic acid.	bevirimat	138-181	caspase 1	Homo sapiens	20-26
15225375-2	2004	We previously reported that the small molecule 3-O-{3",3"-dimethylsuccinyl}-betulinic acid (DSB) specifically inhibits HIV-1 replication by delaying the processing of the CA-SP1 junction in Pr55Gag.	bevirimat	47-90	caspase 1	Homo sapiens	171-177
15225375-2	2004	We previously reported that the small molecule 3-O-{3",3"-dimethylsuccinyl}-betulinic acid (DSB) specifically inhibits HIV-1 replication by delaying the processing of the CA-SP1 junction in Pr55Gag.	bevirimat	92-95	caspase 1	Homo sapiens	171-177
15215653-3	2004	It also increased caspase-1 activity and a caspase-1 inhibitor, Ac-YVAD-cmk, and a caspase-10 inhibitor z-AEVD-fmk, also reduced dracorhodin-perchlorate-induced HeLa cell death.	dracorhodin	129-152	caspase 1	Homo sapiens	43-52
15215653-5	2004	Dracorhodin perchlorate induced a sustained generation of reactive oxygen species (ROS) in HeLa cells; caspase-1 inhibitor, Ac-YVAD-cmk, and caspase-3 inhibitor, z-DEVD-fmk, attenuated the generation of ROS.	dracorhodin	0-23	caspase 1	Homo sapiens	103-112
15215653-6	2004	Taken together, our results indicate that dracorhodin perchlorate alters the intracellular redox status, changed the balance of Bcl-X(L) and Bax protein expression, and induces apoptosis through caspase pathways in HeLa cells.	dracorhodin	42-65	caspase 1	Homo sapiens	195-202
15140190-6	2004	Site-directed mutagenesis experiments eliminating three, six or nine potential caspase cleavage sites in the protein suggest redundancy in the site(s) at which cleavage can occur, as previously described for other disease proteins; but also map a major cleavage event to a cluster of aspartate residues within the ubiquitin-binding domain of ataxin-3 near the polyglutamine tract.	polyglutamine	360-373	caspase 1	Homo sapiens	79-86
15192144-6	2004	Externalization of mature IL-1 beta and caspase-1 together with lysosomal proteins is then facilitated by extracellular ATP.	Adenosine Triphosphate	120-123	caspase 1	Homo sapiens	40-49
15215653-0	2004	Dracorhodin perchlorate induces apoptosis via activation of caspases and generation of reactive oxygen species.	dracorhodin	0-23	caspase 1	Homo sapiens	60-68
15215653-3	2004	It also increased caspase-1 activity and a caspase-1 inhibitor, Ac-YVAD-cmk, and a caspase-10 inhibitor z-AEVD-fmk, also reduced dracorhodin-perchlorate-induced HeLa cell death.	dracorhodin	129-152	caspase 1	Homo sapiens	18-27
15274298-5	2004	Caspase-1 overexpressing clones were characterized for their apoptotic response to ionizing irradiation (0-9 Gy) on the basis of cell viability and Hoechst staining assays and profiling of expression of key apoptosis regulators, such as caspase -3 and -9.	hoechst	148-155	caspase 1	Homo sapiens	0-9
15274298-6	2004	RESULTS: Caspase-1 transfectants exhibited a greater sensitivity in response to ionizing radiation than the neomycin control transfectants, as demonstrated by a dramatic loss in cell viability, that temporally correlated with apoptosis induction.	Neomycin	108-116	caspase 1	Homo sapiens	9-18
15274298-7	2004	Furthermore, caspase-1 overexpression resulted in a significant decrease in clonogenic survival following treatment with ionizing radiation, while the caspase-1 inhibitor, Z-YVAD.fmk, suppressed apoptosis induction in caspase-1 transfectants (p&lt;0.008).	z-yvad	172-178	caspase 1	Homo sapiens	151-160
15274298-7	2004	Furthermore, caspase-1 overexpression resulted in a significant decrease in clonogenic survival following treatment with ionizing radiation, while the caspase-1 inhibitor, Z-YVAD.fmk, suppressed apoptosis induction in caspase-1 transfectants (p&lt;0.008).	z-yvad	172-178	caspase 1	Homo sapiens	151-160
14741295-0	2004	The design and synthesis of sulfonamides as caspase-1 inhibitors.	Sulfonamides	28-40	caspase 1	Homo sapiens	44-53
14634045-7	2004	Two caspase inhibitors, YVAD (caspase 1) and DEVD (caspase 3), attenuated both BzATP-induced pore formation and IL-1beta release in a concentration-dependent fashion.	YVAD	24-28	caspase 1	Homo sapiens	4-11
14634045-7	2004	Two caspase inhibitors, YVAD (caspase 1) and DEVD (caspase 3), attenuated both BzATP-induced pore formation and IL-1beta release in a concentration-dependent fashion.	YVAD	24-28	caspase 1	Homo sapiens	30-39
14634045-7	2004	Two caspase inhibitors, YVAD (caspase 1) and DEVD (caspase 3), attenuated both BzATP-induced pore formation and IL-1beta release in a concentration-dependent fashion.	DEVD	45-49	caspase 1	Homo sapiens	4-11
14634045-7	2004	Two caspase inhibitors, YVAD (caspase 1) and DEVD (caspase 3), attenuated both BzATP-induced pore formation and IL-1beta release in a concentration-dependent fashion.	BzATP	79-84	caspase 1	Homo sapiens	4-11
14634045-7	2004	Two caspase inhibitors, YVAD (caspase 1) and DEVD (caspase 3), attenuated both BzATP-induced pore formation and IL-1beta release in a concentration-dependent fashion.	BzATP	79-84	caspase 1	Homo sapiens	30-39
14998341-0	2004	Design, synthesis, and evaluation of aza-peptide epoxides as selective and potent inhibitors of caspases-1, -3, -6, and -8.	aza-peptide epoxides	37-57	caspase 1	Homo sapiens	96-122
14998341-2	2004	Aza-peptide epoxides with an aza-Asp residue at P1 are excellent irreversible inhibitors of caspases-1, -3, -6, and -8 with second-order inhibition rates up to 1 910 000 M(-1) s(-1).	aza-peptide epoxides	0-20	caspase 1	Homo sapiens	92-118
14998341-2	2004	Aza-peptide epoxides with an aza-Asp residue at P1 are excellent irreversible inhibitors of caspases-1, -3, -6, and -8 with second-order inhibition rates up to 1 910 000 M(-1) s(-1).	aza-asp	29-36	caspase 1	Homo sapiens	92-118
15072464-0	2004	Caspase-1 mediates Fas-induced apoptosis and is up-regulated by interferon-gamma in human astrocytoma cells.	ammonium ferrous sulfate	19-22	caspase 1	Homo sapiens	0-9
15072464-6	2004	Studies using specific caspase inhibitors showed that Fas-induced cell death was mediated by caspases-1, -3 and 8 in the Fas-sensitive human astrocytoma cell lines, CRT-J and U87-MG. We further demonstrated that these caspases were proteolytically cleaved upon Fas ligation in these cells.	ammonium ferrous sulfate	54-57	caspase 1	Homo sapiens	23-30
15072464-6	2004	Studies using specific caspase inhibitors showed that Fas-induced cell death was mediated by caspases-1, -3 and 8 in the Fas-sensitive human astrocytoma cell lines, CRT-J and U87-MG. We further demonstrated that these caspases were proteolytically cleaved upon Fas ligation in these cells.	ammonium ferrous sulfate	54-57	caspase 1	Homo sapiens	93-113
15072464-6	2004	Studies using specific caspase inhibitors showed that Fas-induced cell death was mediated by caspases-1, -3 and 8 in the Fas-sensitive human astrocytoma cell lines, CRT-J and U87-MG. We further demonstrated that these caspases were proteolytically cleaved upon Fas ligation in these cells.	ammonium ferrous sulfate	54-57	caspase 1	Homo sapiens	93-101
15072464-6	2004	Studies using specific caspase inhibitors showed that Fas-induced cell death was mediated by caspases-1, -3 and 8 in the Fas-sensitive human astrocytoma cell lines, CRT-J and U87-MG. We further demonstrated that these caspases were proteolytically cleaved upon Fas ligation in these cells.	ammonium ferrous sulfate	121-124	caspase 1	Homo sapiens	23-30
15072464-6	2004	Studies using specific caspase inhibitors showed that Fas-induced cell death was mediated by caspases-1, -3 and 8 in the Fas-sensitive human astrocytoma cell lines, CRT-J and U87-MG. We further demonstrated that these caspases were proteolytically cleaved upon Fas ligation in these cells.	ammonium ferrous sulfate	121-124	caspase 1	Homo sapiens	93-113
15072464-6	2004	Studies using specific caspase inhibitors showed that Fas-induced cell death was mediated by caspases-1, -3 and 8 in the Fas-sensitive human astrocytoma cell lines, CRT-J and U87-MG. We further demonstrated that these caspases were proteolytically cleaved upon Fas ligation in these cells.	ammonium ferrous sulfate	121-124	caspase 1	Homo sapiens	93-101
15072464-7	2004	Interestingly, caspase-1 protein expression but not that of caspase-3 nor -8 was up-regulated by IFN-gamma only in Fas-sensitive CRT-J cells but not in Fas-resistant U373-MG cells.	ammonium ferrous sulfate	115-118	caspase 1	Homo sapiens	15-24
15072464-7	2004	Interestingly, caspase-1 protein expression but not that of caspase-3 nor -8 was up-regulated by IFN-gamma only in Fas-sensitive CRT-J cells but not in Fas-resistant U373-MG cells.	ammonium ferrous sulfate	152-155	caspase 1	Homo sapiens	15-24
15072464-8	2004	These results collectively suggest that caspase-1, along with caspases-3 and -8, mediate Fas-induced cell death in human astrocytoma cells, and post-transcriptional regulation of caspase-1 may determine the responsiveness to IFN-gamma-induced sensitization to Fas-mediated apoptosis.	ammonium ferrous sulfate	89-92	caspase 1	Homo sapiens	40-79
15072464-8	2004	These results collectively suggest that caspase-1, along with caspases-3 and -8, mediate Fas-induced cell death in human astrocytoma cells, and post-transcriptional regulation of caspase-1 may determine the responsiveness to IFN-gamma-induced sensitization to Fas-mediated apoptosis.	ammonium ferrous sulfate	89-92	caspase 1	Homo sapiens	40-49
14751267-5	2004	By selecting suitable lanthanide chelates and substrates we developed a multiparametric homogeneous time-resolved fluorescence quenching-based assay for caspases 1, 3, and 6.	Lanthanoid Series Elements	22-32	caspase 1	Homo sapiens	153-173
14741295-1	2004	A series of sulfonamides (1) has been prepared as inhibitors of interleukin-1beta converting enzyme (ICE), also known as caspase 1.	Sulfonamides	12-24	caspase 1	Homo sapiens	64-99
14741295-1	2004	A series of sulfonamides (1) has been prepared as inhibitors of interleukin-1beta converting enzyme (ICE), also known as caspase 1.	Sulfonamides	12-24	caspase 1	Homo sapiens	101-104
14741295-1	2004	A series of sulfonamides (1) has been prepared as inhibitors of interleukin-1beta converting enzyme (ICE), also known as caspase 1.	Sulfonamides	12-24	caspase 1	Homo sapiens	121-130
14741295-3	2004	An X-ray crystal structure of a representative member of this series bound to the active site of ICE, confirms the presence of the hydrogen bonding interaction.	Hydrogen	131-139	caspase 1	Homo sapiens	97-100
12877678-3	2003	As cytoplasmatic adaptor molecules of FAS, e.g. FLIP [Fas-associated death domain protein (FADD)-like interleukin 1 beta-converting enzyme [FLICE (caspase-8)-inhibitory protein]], also modulate TRAIL signals, we determined whether chelerythrin affected TRAIL-mediated apoptosis.	chelerythrin	231-243	caspase 1	Homo sapiens	102-138
14532296-6	2003	Studies of the interplay between the caspase cascade and the JNK pathway showed that both apoptosis and caspase-3 activation were suppressed by treatment with a JNK inhibitor and by transfection of antisense jnk1 oligonucleotides or antisense-c-jun, whereas a selective inhibitor of caspases-1 and -3 prevented apoptosis but not c-Jun activation.	Oligonucleotides	213-229	caspase 1	Homo sapiens	37-44
15015724-3	2003	EI-2346, a novel interleukin-1beta converting enzyme (ICE) inhibitor, was isolated from the culture broths of Streptomyces sp.	EI-2346	0-7	caspase 1	Homo sapiens	54-57
15015724-5	2003	EI-2346 selectively inhibited the human recombinant ICE activity with an IC50 value of 3.9 microM, without inhibiting elastase and cathepsin B.	EI-2346	0-7	caspase 1	Homo sapiens	52-55
12949795-1	2003	ASC/TMS1 is an adaptor protein activating caspase-1 that stimulates processing of proIL-1beta and proIL-18.	proil	82-87	caspase 1	Homo sapiens	42-51
14583501-10	2003	In contrast, caspase-9 was activated only by VES, whereas caspases-1 and -12 were activated only by MSA.	methylselenic acid	100-103	caspase 1	Homo sapiens	58-76
14507655-6	2003	In in vitro studies using primary cultured mouse salivary gland cells and human salivary gland cells, we found a cleavage product of 120-kd alpha-fodrin in cells that had undergone tamoxifen (Tam)-induced apoptosis through caspase activation, especially caspase-1.	Tamoxifen	181-190	caspase 1	Homo sapiens	254-263
14507655-6	2003	In in vitro studies using primary cultured mouse salivary gland cells and human salivary gland cells, we found a cleavage product of 120-kd alpha-fodrin in cells that had undergone tamoxifen (Tam)-induced apoptosis through caspase activation, especially caspase-1.	Tamoxifen	192-195	caspase 1	Homo sapiens	254-263
12934070-0	2003	Critical role for cathepsin B in mediating caspase-1-dependent interleukin-18 maturation and caspase-1-independent necrosis triggered by the microbial toxin nigericin.	Nigericin	157-166	caspase 1	Homo sapiens	93-102
12934070-1	2003	The potassium ionophore nigericin induces cell death and promotes the maturation and release of IL-1beta in lipopolysaccharide (LPS)-primed monocytes and macrophages, the latter depending on caspase-1 activation by an unknown mechanism.	Potassium	4-13	caspase 1	Homo sapiens	191-200
12934070-1	2003	The potassium ionophore nigericin induces cell death and promotes the maturation and release of IL-1beta in lipopolysaccharide (LPS)-primed monocytes and macrophages, the latter depending on caspase-1 activation by an unknown mechanism.	Nigericin	24-33	caspase 1	Homo sapiens	191-200
14667927-5	2004	Mahanine activated various caspases such as caspase-3, -6, -8 and -9 (like) activities but not caspase-1 like activity.	mahanine	0-8	caspase 1	Homo sapiens	27-35
14656672-7	2004	The caspase-1 selective inhibitor Z-YVAD also blocked chondrocyte apoptosis under these conditions, in contrast to previous studies where caspase-1 inhibition failed to block apoptosis induced by agents such as the topoisomerase inhibitor camptothecin.	z-yvad	34-40	caspase 1	Homo sapiens	4-13
14598973-4	2003	ICE activity was significantly lower in TB patients (65.3 +/- 34.4 vs. 142.2 +/- 75.6 U/mg) (P &lt; 0.05).	Terbium	40-42	caspase 1	Homo sapiens	0-3
12918059-4	2003	IFN-gamma produced in prostate cancers induced caspase-1 mRNA and IL-18 secretion of tumor cell lines, which was inhibited by the cell-permeable Tyr-Val-Ala-Asp-aldehyde caspase-1 inhibitor (YVAD-CHO).	tyrosyl-valyl-alanyl-aspartal	145-169	caspase 1	Homo sapiens	47-56
12918059-4	2003	IFN-gamma produced in prostate cancers induced caspase-1 mRNA and IL-18 secretion of tumor cell lines, which was inhibited by the cell-permeable Tyr-Val-Ala-Asp-aldehyde caspase-1 inhibitor (YVAD-CHO).	tyrosyl-valyl-alanyl-aspartal	145-169	caspase 1	Homo sapiens	170-179
12918059-4	2003	IFN-gamma produced in prostate cancers induced caspase-1 mRNA and IL-18 secretion of tumor cell lines, which was inhibited by the cell-permeable Tyr-Val-Ala-Asp-aldehyde caspase-1 inhibitor (YVAD-CHO).	tyrosyl-valyl-alanyl-aspartal	191-199	caspase 1	Homo sapiens	47-56
12918059-4	2003	IFN-gamma produced in prostate cancers induced caspase-1 mRNA and IL-18 secretion of tumor cell lines, which was inhibited by the cell-permeable Tyr-Val-Ala-Asp-aldehyde caspase-1 inhibitor (YVAD-CHO).	tyrosyl-valyl-alanyl-aspartal	191-199	caspase 1	Homo sapiens	170-179
12934070-3	2003	We show that without LPS priming, nigericin alone triggered caspase-1 activation and IL-18 generation in THP-1 monocytic cells.	Nigericin	34-43	caspase 1	Homo sapiens	60-69
12934070-4	2003	Simultaneously, nigericin induced caspase-1-independent necrotic cell death, which was blocked by the cathepsin B inhibitor CA-074-Me and other cathepsin inhibitors.	Nigericin	16-25	caspase 1	Homo sapiens	34-43
12934070-4	2003	Simultaneously, nigericin induced caspase-1-independent necrotic cell death, which was blocked by the cathepsin B inhibitor CA-074-Me and other cathepsin inhibitors.	CA 074 methyl ester	124-133	caspase 1	Homo sapiens	34-43
12934070-8	2003	Collectively, our study establishes a critical role for cathepsin B in nigericin-induced caspase-1-dependent IL-18 maturation and caspase-1-independent necrosis.	Nigericin	71-80	caspase 1	Homo sapiens	89-98
12934070-8	2003	Collectively, our study establishes a critical role for cathepsin B in nigericin-induced caspase-1-dependent IL-18 maturation and caspase-1-independent necrosis.	Nigericin	71-80	caspase 1	Homo sapiens	130-139
12832055-6	2003	Caspase 1 cleaved LPKH between the PK and H regions.	lpkh	18-22	caspase 1	Homo sapiens	0-9
12851674-1	2003	We demonstrate here that selective activation of endogenous members of the caspase family and cleavage of substrates responsible for the maintenance of nuclear functional and structural integrity are major effectors of antigen receptor (AgR)- and ionomycin-triggered apoptosis in Ramos-Burkitt lymphoma (Ramos-BL) B cells.	Ionomycin	247-256	caspase 1	Homo sapiens	75-82
12874316-8	2003	The specific caspase-1 inhibitor Ac-YVAD-CMK blocked the early IL-18 release in AM infected with the virulent strain.	ac-yvad	33-40	caspase 1	Homo sapiens	13-22
12874324-8	2003	Presence of the caspase 1 inhibitor Ac-YVAD-CMK significantly blocked the leukotoxin-induced lysis of monocytes only.	ac-yvad	36-43	caspase 1	Homo sapiens	16-25
12719786-5	2003	AEA also showed a marked increase of interleukin Ibeta- converting enzyme (ICE)CED-3 family protease (caspase-3) activity.	anandamide	0-3	caspase 1	Homo sapiens	75-78
12794166-8	2003	Functional studies demonstrated that both caspase-1 and ICSBP were involved in Fas-mediated apoptosis following IFN-gamma sensitization, but proceeded via two distinct pathways.	ammonium ferrous sulfate	79-82	caspase 1	Homo sapiens	42-51
12551850-0	2003	Two caspase-mediated apoptotic pathways induced by rotenone toxicity in cortical neuronal cells.	Rotenone	51-59	caspase 1	Homo sapiens	4-11
12603604-7	2003	We examined the inhibitory effects of various caspase inhibitors on the expression of CD86 in cells treated with NaB, because NaB also induced apoptosis with slow kinetics.	nab	113-116	caspase 1	Homo sapiens	46-53
12603604-8	2003	Intriguingly, our results demonstrated that inhibitors of the interleukin-1beta converting enzyme subfamily (caspase-1, -4, -5 and -13) blocked the butyrate-induced increase in level of CD86.	Butyrates	148-156	caspase 1	Homo sapiens	109-134
12603604-10	2003	These results suggested that butyrate not only acetylates histones on the CD86 promoter through the suppression of HDAC activity, but that butyrate also regulates CREB-mediated transcription, possibly through the caspase activities triggered by NaB.	Butyrates	29-37	caspase 1	Homo sapiens	213-220
12603604-10	2003	These results suggested that butyrate not only acetylates histones on the CD86 promoter through the suppression of HDAC activity, but that butyrate also regulates CREB-mediated transcription, possibly through the caspase activities triggered by NaB.	nab	245-248	caspase 1	Homo sapiens	213-220
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 1	Homo sapiens	100-109
12628757-3	2003	In fact, here we show that acetyl-Tyr-Val-Ala-Asp-chloromethylketone (Ac-YVAD-CMK) and t-butoxycarbonyl-L-aspartic acid benzyl ester-chloromethylketone (Boc-Asp-(OBzl)-CMK), two inhibitors of Interleukin-1 Converting Enzyme (ICE; also referred to as caspase-1), abolish COX-2 expression enhanced by gp120 and consequent cell death.	N-acetyl-tyrosyl-valyl-alanyl-aspartyl chloromethyl ketone	27-68	caspase 1	Homo sapiens	192-223
12628757-3	2003	In fact, here we show that acetyl-Tyr-Val-Ala-Asp-chloromethylketone (Ac-YVAD-CMK) and t-butoxycarbonyl-L-aspartic acid benzyl ester-chloromethylketone (Boc-Asp-(OBzl)-CMK), two inhibitors of Interleukin-1 Converting Enzyme (ICE; also referred to as caspase-1), abolish COX-2 expression enhanced by gp120 and consequent cell death.	N-acetyl-tyrosyl-valyl-alanyl-aspartyl chloromethyl ketone	27-68	caspase 1	Homo sapiens	225-228
12628757-3	2003	In fact, here we show that acetyl-Tyr-Val-Ala-Asp-chloromethylketone (Ac-YVAD-CMK) and t-butoxycarbonyl-L-aspartic acid benzyl ester-chloromethylketone (Boc-Asp-(OBzl)-CMK), two inhibitors of Interleukin-1 Converting Enzyme (ICE; also referred to as caspase-1), abolish COX-2 expression enhanced by gp120 and consequent cell death.	N-acetyl-tyrosyl-valyl-alanyl-aspartyl chloromethyl ketone	27-68	caspase 1	Homo sapiens	250-259
12628757-3	2003	In fact, here we show that acetyl-Tyr-Val-Ala-Asp-chloromethylketone (Ac-YVAD-CMK) and t-butoxycarbonyl-L-aspartic acid benzyl ester-chloromethylketone (Boc-Asp-(OBzl)-CMK), two inhibitors of Interleukin-1 Converting Enzyme (ICE; also referred to as caspase-1), abolish COX-2 expression enhanced by gp120 and consequent cell death.	t-butoxycarbonyl-l-aspartic acid benzyl ester	87-132	caspase 1	Homo sapiens	192-223
12628757-3	2003	In fact, here we show that acetyl-Tyr-Val-Ala-Asp-chloromethylketone (Ac-YVAD-CMK) and t-butoxycarbonyl-L-aspartic acid benzyl ester-chloromethylketone (Boc-Asp-(OBzl)-CMK), two inhibitors of Interleukin-1 Converting Enzyme (ICE; also referred to as caspase-1), abolish COX-2 expression enhanced by gp120 and consequent cell death.	t-butoxycarbonyl-l-aspartic acid benzyl ester	87-132	caspase 1	Homo sapiens	225-228
12628757-3	2003	In fact, here we show that acetyl-Tyr-Val-Ala-Asp-chloromethylketone (Ac-YVAD-CMK) and t-butoxycarbonyl-L-aspartic acid benzyl ester-chloromethylketone (Boc-Asp-(OBzl)-CMK), two inhibitors of Interleukin-1 Converting Enzyme (ICE; also referred to as caspase-1), abolish COX-2 expression enhanced by gp120 and consequent cell death.	t-butoxycarbonyl-l-aspartic acid benzyl ester	87-132	caspase 1	Homo sapiens	250-259
12628757-3	2003	In fact, here we show that acetyl-Tyr-Val-Ala-Asp-chloromethylketone (Ac-YVAD-CMK) and t-butoxycarbonyl-L-aspartic acid benzyl ester-chloromethylketone (Boc-Asp-(OBzl)-CMK), two inhibitors of Interleukin-1 Converting Enzyme (ICE; also referred to as caspase-1), abolish COX-2 expression enhanced by gp120 and consequent cell death.	chloromethylketone	50-68	caspase 1	Homo sapiens	192-223
12628757-3	2003	In fact, here we show that acetyl-Tyr-Val-Ala-Asp-chloromethylketone (Ac-YVAD-CMK) and t-butoxycarbonyl-L-aspartic acid benzyl ester-chloromethylketone (Boc-Asp-(OBzl)-CMK), two inhibitors of Interleukin-1 Converting Enzyme (ICE; also referred to as caspase-1), abolish COX-2 expression enhanced by gp120 and consequent cell death.	chloromethylketone	50-68	caspase 1	Homo sapiens	225-228
12628757-3	2003	In fact, here we show that acetyl-Tyr-Val-Ala-Asp-chloromethylketone (Ac-YVAD-CMK) and t-butoxycarbonyl-L-aspartic acid benzyl ester-chloromethylketone (Boc-Asp-(OBzl)-CMK), two inhibitors of Interleukin-1 Converting Enzyme (ICE; also referred to as caspase-1), abolish COX-2 expression enhanced by gp120 and consequent cell death.	chloromethylketone	50-68	caspase 1	Homo sapiens	250-259
12646627-7	2003	Furthermore, a caspase-1 inhibitor (Z-YVAD-FMK), but not others such as Z-IETD-FMK (caspase-8 inhibitor), Z-LEHD-FMK (caspase-9 inhibitor), and Z-AEVD-FMK (caspase-10 inhibitor), inhibited Gal-9-induced apoptosis.	benzyloxycarbonyltyrosyl-valyl-alanyl-aspartic acid fluoromethyl ketone	36-46	caspase 1	Homo sapiens	15-24
12551850-1	2003	Our results presented here suggest that cortical neurons degenerate via two caspase-mediated apoptotic pathways when challenged with 0.5 microM rotenone.	Rotenone	144-152	caspase 1	Homo sapiens	76-83
12573542-2	2003	Here we demonstrate that glutamate-induced excitotoxicity of cerebellar granule neurons was accompanied by apoptosis-like nuclear shrinkage, chromatin condensation, and disintegration of nuclear DNA into high molecular weight DNA fragments, but was neither associated with activation of caspase 1, -2, -3, -9, nor was protected by a pan-caspase inhibitor, zVAD-fmk.	Glutamic Acid	25-34	caspase 1	Homo sapiens	287-308
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 1	Homo sapiens	148-183
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 1	Homo sapiens	148-183
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 1	Homo sapiens	148-183
12604404-10	2003	Caspases 1 and 6</protein-id> were the major caspases involved in fludarabine apoptosis induction in resting B cells, while only anti-TNFalpha/-IFNgamma monoclonal antibodies reduced apoptosis in activated cells.	fludarabine	66-77	caspase 1	Homo sapiens	45-53
12789619-1	2003	Vertex is collaborating with Aventis Pharma AG (formerly Hoechst Marion Roussel Inc) in the development of pralnacasan, an interleukin (IL)-1b converting enzyme (ICE) inhibitor, for the potential treatment of inflammatory diseases [170247], [188293], [453094].	pralnacasan	107-118	caspase 1	Homo sapiens	162-165
12675482-11	2003	Caspase-1 gene expression is distinctly upregulated after light exposure and there are several factors which completely protect against light-induced cell death, such as the anesthetic halothane, dexamethasone and the absence of bleachable rhodopsin during light exposure.	Halothane	185-194	caspase 1	Homo sapiens	0-9
12471614-0	2003	Beta2-microglobulin induces caspase-dependent apoptosis in the CCRF-HSB-2 human leukemia cell line independently of the caspase-3, -8 and -9 pathways but through increased reactive oxygen species.	Reactive Oxygen Species	172-195	caspase 1	Homo sapiens	28-35
12527914-0	2003	Thiol alkylation inhibits the mitogenic effects of platelet-derived growth factor and renders it proapoptotic via activation of STATs and p53 and induction of expression of caspase1 and p21(waf1/cip1).	Sulfhydryl Compounds	0-5	caspase 1	Homo sapiens	173-181
12527914-7	2003	The inhibition of AP-1 and activation of STATs, particularly STAT1, by thiol alkylation correlated with increased production of active caspase 1 and apoptosis in VSMC.	Sulfhydryl Compounds	71-76	caspase 1	Homo sapiens	135-144
12680251-0	2003	All-trans-retinoic acid activates caspase-1 in a dose-dependent manner in cervical squamous carcinoma cells.	Tretinoin	0-23	caspase 1	Homo sapiens	34-43
12680251-4	2003	We found that high-dose, but not low-dose, ATRA treatment activated caspase-1 in those cervical carcinoma cells.	Tretinoin	43-47	caspase 1	Homo sapiens	68-77
12680251-5	2003	Transient transfection of an antisense-IRF-1 construct diminished high-dose ATRA-mediated caspase-1 activation.	Tretinoin	76-80	caspase 1	Homo sapiens	90-99
12680251-7	2003	These results suggested the importance of both IRF-1 and STAT1 in high-dose ATRA-induced activation of caspase-1.	Tretinoin	76-80	caspase 1	Homo sapiens	103-112
12708481-6	2003	Taken together, our data indicated that evodiamine alters the balance of Bcl-2 and Bax gene expression and induces apoptosis through the caspase pathway in HeLa cells.	evodiamine	40-50	caspase 1	Homo sapiens	137-144
12675482-11	2003	Caspase-1 gene expression is distinctly upregulated after light exposure and there are several factors which completely protect against light-induced cell death, such as the anesthetic halothane, dexamethasone and the absence of bleachable rhodopsin during light exposure.	Dexamethasone	196-209	caspase 1	Homo sapiens	0-9
14502257-0	2003	Downregulation of Bcl-xL and activation of caspases during retinoic acid-induced apoptosis in an adult T-cell leukemia cell line.	Tretinoin	59-72	caspase 1	Homo sapiens	43-51
12477768-4	2003	METHODS: Using Caco-2 cells we focused on the bcl family of proteins, mitochondrial pathway, and caspase signalling cascade involved in butyrate induced apoptosis.	Butyrates	136-144	caspase 1	Homo sapiens	97-104
12477768-11	2003	Upregulation of bak and translocation of cytochrome-c were upstream of the caspase cascade.	bakuchiol	16-19	caspase 1	Homo sapiens	75-82
14502257-12	2003	Broad range caspase inhibitors, Z-Asp and Z-VAD, prevented DNA fragmentation.	benzyloxycarbonyl-asparagine	32-37	caspase 1	Homo sapiens	12-19
14502257-12	2003	Broad range caspase inhibitors, Z-Asp and Z-VAD, prevented DNA fragmentation.	z-vad	42-47	caspase 1	Homo sapiens	12-19
12065092-7	2002	Furthermore, the Gyp-induced apoptosis was markedly blocked by the broad-spectrum caspase inhibitor, z-VAD-fmk.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	101-110	caspase 1	Homo sapiens	82-89
12459463-5	2002	Mutant procaspase-1 also inhibited apoptosis induced by p53 overexpression or doxorubicin treatment, which induce caspase-1 gene expression.	Doxorubicin	78-89	caspase 1	Homo sapiens	10-19
12242728-5	2002	Furthermore, molecular analysis indicated that this antagonistic effect of bcl-2 on apoptosis was due to partial suppression of TGF-beta and DHT-mediated induction of caspase-1 expression and activation in LNCaP TbetaRII-hygro/bcl-2 transfectants.	Dihydrotestosterone	141-144	caspase 1	Homo sapiens	167-176
12529972-4	2002	Treatment with the general caspase inhibitor Z-VAD-fmk, as well as the caspase-1 inhibitor YVAD-CHO, significantly blocked beta 2m-induced apoptosis.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	45-54	caspase 1	Homo sapiens	27-34
12529972-4	2002	Treatment with the general caspase inhibitor Z-VAD-fmk, as well as the caspase-1 inhibitor YVAD-CHO, significantly blocked beta 2m-induced apoptosis.	tyrosyl-valyl-alanyl-aspartal	91-99	caspase 1	Homo sapiens	71-80
11934593-0	2002	A practical synthesis of (S) 3-tert-butoxycarbonylamino-2-oxo-2,3,4,5-tetrahydro-1,5-benzodiazepine-1-acetic acid methyl ester as a conformationally restricted dipeptido-mimetic for caspase-1 (ICE) inhibitors.	(s) 3-tert-butoxycarbonylamino-2-oxo-2,3,4,5-tetrahydro-1,5-benzodiazepine	25-99	caspase 1	Homo sapiens	182-191
12097652-2	2002	Caco-2 and RSB cells were exposed to 2, 5 and 10 mmol/L butyrate for 48 h. Caspase-1 was cleaved in Caco-2-cells at all butyrate concentrations, whereas in RSB-cells caspase-1 expression was undetectable.	(1S,5S,6R)-10-(benzo[d]thiazol-6-ylsulfonyl)-5-(methoxymethyl)-3-(pyridin-2-ylethyl)-3,10-diazabicyclo[4.3.1]decan-2-one	11-14	caspase 1	Homo sapiens	75-84
12097652-2	2002	Caco-2 and RSB cells were exposed to 2, 5 and 10 mmol/L butyrate for 48 h. Caspase-1 was cleaved in Caco-2-cells at all butyrate concentrations, whereas in RSB-cells caspase-1 expression was undetectable.	Butyrates	56-64	caspase 1	Homo sapiens	75-84
12097652-2	2002	Caco-2 and RSB cells were exposed to 2, 5 and 10 mmol/L butyrate for 48 h. Caspase-1 was cleaved in Caco-2-cells at all butyrate concentrations, whereas in RSB-cells caspase-1 expression was undetectable.	Butyrates	120-128	caspase 1	Homo sapiens	75-84
12097652-10	2002	Inactivation of caspase-1 with Z-YVAD-FMK abrogated butyrate-induced apoptosis in Caco-2 but not in RSB cells.	benzyloxycarbonyltyrosyl-valyl-alanyl-aspartic acid fluoromethyl ketone	31-41	caspase 1	Homo sapiens	16-25
12097652-10	2002	Inactivation of caspase-1 with Z-YVAD-FMK abrogated butyrate-induced apoptosis in Caco-2 but not in RSB cells.	Butyrates	52-60	caspase 1	Homo sapiens	16-25
12215207-8	2002	Fas and caspase-1 were down-expressed and p35 over-expressed in lymphocytes from patients of the L-carnitine group.	Carnitine	97-108	caspase 1	Homo sapiens	8-17
11992539-6	2002	The inhibitory effect of [D-Trp(6)]LHRH on A431 cell proliferation was associated with apoptosis as evidenced by the cell morphology and DNA integrity (ladder pattern), the expression of interleukin 1beta-converting enzyme (ICE) and activation of caspase.	[d-trp	25-31	caspase 1	Homo sapiens	187-222
11992539-6	2002	The inhibitory effect of [D-Trp(6)]LHRH on A431 cell proliferation was associated with apoptosis as evidenced by the cell morphology and DNA integrity (ladder pattern), the expression of interleukin 1beta-converting enzyme (ICE) and activation of caspase.	[d-trp	25-31	caspase 1	Homo sapiens	224-227
11992539-6	2002	The inhibitory effect of [D-Trp(6)]LHRH on A431 cell proliferation was associated with apoptosis as evidenced by the cell morphology and DNA integrity (ladder pattern), the expression of interleukin 1beta-converting enzyme (ICE) and activation of caspase.	[d-trp	25-31	caspase 1	Homo sapiens	247-254
12322783-7	2002	Therefore, we applied N-benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone (zVAD x fmk), an ICE blocker 3 or 6 h after pMCAO.	Caspase Inhibitor VI	22-72	caspase 1	Homo sapiens	90-93
12322783-7	2002	Therefore, we applied N-benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone (zVAD x fmk), an ICE blocker 3 or 6 h after pMCAO.	zvad x fmk	74-84	caspase 1	Homo sapiens	90-93
12567888-7	2002	However, caspase-1 inhibitor, Ac-Tyr-Val-Ala-Asp-chloromethyl-ketone (Ac-YVAD-cmk), did not antagonize evodiamine induced cell death.	N-acetyl-tyrosyl-valyl-alanyl-aspartyl chloromethyl ketone	30-68	caspase 1	Homo sapiens	9-18
12105852-12	2002	CONCLUSIONS: Our results indicate that GTN (1) activates an unusual caspase cascade to induce apoptosis in colon cancer cells and (2) sensitizes these cells to Fas-mediated cell death by increasing the expression of Fas and decreasing the expression of several IAPs.	Nitroglycerin	39-42	caspase 1	Homo sapiens	68-75
12115655-4	2002	Since the release of IL-1beta in LPS-stimulated whole blood was blocked by the caspase-1 inhibitor YVAD-cmk, processing of proIL-1beta appears to depend on caspase-1 activity.	YVAD	99-103	caspase 1	Homo sapiens	79-88
12115655-4	2002	Since the release of IL-1beta in LPS-stimulated whole blood was blocked by the caspase-1 inhibitor YVAD-cmk, processing of proIL-1beta appears to depend on caspase-1 activity.	YVAD	99-103	caspase 1	Homo sapiens	156-165
12115655-6	2002	Intracellular caspase-1 activity in monocytes was measured by flow cytometry with the cell-permeablecaspase substrate Asp(2)-rhodamine.	asp(2)-rhodamine	118-134	caspase 1	Homo sapiens	14-23
11997061-6	2002	Studies using an immortalized human oligodendroglial hybrid cell line exposed to cytokine challenge showed that death induction was blocked by the caspase-1-like inhibitor Z-YVAD-fmk, while the caspase-3-like inhibitor Z-DEVD-fmk was less effective.	benzyloxycarbonyltyrosyl-valyl-alanyl-aspartic acid fluoromethyl ketone	172-182	caspase 1	Homo sapiens	147-156
11934593-0	2002	A practical synthesis of (S) 3-tert-butoxycarbonylamino-2-oxo-2,3,4,5-tetrahydro-1,5-benzodiazepine-1-acetic acid methyl ester as a conformationally restricted dipeptido-mimetic for caspase-1 (ICE) inhibitors.	(s) 3-tert-butoxycarbonylamino-2-oxo-2,3,4,5-tetrahydro-1,5-benzodiazepine	25-99	caspase 1	Homo sapiens	193-196
11934593-0	2002	A practical synthesis of (S) 3-tert-butoxycarbonylamino-2-oxo-2,3,4,5-tetrahydro-1,5-benzodiazepine-1-acetic acid methyl ester as a conformationally restricted dipeptido-mimetic for caspase-1 (ICE) inhibitors.	methyl acetate	101-126	caspase 1	Homo sapiens	182-191
11934593-0	2002	A practical synthesis of (S) 3-tert-butoxycarbonylamino-2-oxo-2,3,4,5-tetrahydro-1,5-benzodiazepine-1-acetic acid methyl ester as a conformationally restricted dipeptido-mimetic for caspase-1 (ICE) inhibitors.	methyl acetate	101-126	caspase 1	Homo sapiens	193-196
11953454-2	2002	To study the specific role of caspase-3 activation in neuronal cells, we generated a stable tetracycline-regulated SK-N-MC neuroblastoma cell line, which expressed a highly efficient self-activating chimeric caspase-3, consisting of the caspase-1 prodomain fused to the caspase-3 catalytic domain.	Tetracycline	92-104	caspase 1	Homo sapiens	237-246
11922616-6	2002	Cells on oxidized matrix demonstrated enhanced expression of Bax, increased fragmentation of PARP, and diminished apoptosis in the presence of the interleukin-1 beta converting enzyme inhibitor Ac-Tyr-Val-Ala-Asp-aldehyde.	L 709049	194-221	caspase 1	Homo sapiens	147-183
11960374-2	2002	Pretreatment with caspase inhibitors blocks cell death, suggesting that a set of caspase activities including caspase 1, as well as caspase 3, are involved in ceramide-induced apoptosis in SKN-SH cells.	Ceramides	159-167	caspase 1	Homo sapiens	110-119
11960374-7	2002	These results suggest that p53 regulates the ratio Bcl-2/Bax and the expression/activation of caspases during ceramide-induced apoptosis in SKN-SH cells.	Ceramides	110-118	caspase 1	Homo sapiens	94-102
11953454-5	2002	In contrast, staurosporine treatment of the same cells resulted in activation of multiple caspases and profound apoptotic morphology.	Staurosporine	13-26	caspase 1	Homo sapiens	90-98
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 1	Homo sapiens	160-189
11841926-5	2002	In the present study we have demonstrated that H(2)O(2) and the lipid derived aldehydes, HNE and 4-hydroxyhexenal (HHE), can induce dose- and time-dependent loss of cell viability and a simultaneous increase in apoptosis involving activation of caspases such as caspase-1, -2, -3, and -8 in the cultured human lens epithelial cells.	Hydrogen Peroxide	47-55	caspase 1	Homo sapiens	245-253
11841926-5	2002	In the present study we have demonstrated that H(2)O(2) and the lipid derived aldehydes, HNE and 4-hydroxyhexenal (HHE), can induce dose- and time-dependent loss of cell viability and a simultaneous increase in apoptosis involving activation of caspases such as caspase-1, -2, -3, and -8 in the cultured human lens epithelial cells.	Hydrogen Peroxide	47-55	caspase 1	Homo sapiens	262-287
11841926-5	2002	In the present study we have demonstrated that H(2)O(2) and the lipid derived aldehydes, HNE and 4-hydroxyhexenal (HHE), can induce dose- and time-dependent loss of cell viability and a simultaneous increase in apoptosis involving activation of caspases such as caspase-1, -2, -3, and -8 in the cultured human lens epithelial cells.	Aldehydes	78-87	caspase 1	Homo sapiens	245-253
11841926-5	2002	In the present study we have demonstrated that H(2)O(2) and the lipid derived aldehydes, HNE and 4-hydroxyhexenal (HHE), can induce dose- and time-dependent loss of cell viability and a simultaneous increase in apoptosis involving activation of caspases such as caspase-1, -2, -3, and -8 in the cultured human lens epithelial cells.	Aldehydes	78-87	caspase 1	Homo sapiens	262-287
11841926-5	2002	In the present study we have demonstrated that H(2)O(2) and the lipid derived aldehydes, HNE and 4-hydroxyhexenal (HHE), can induce dose- and time-dependent loss of cell viability and a simultaneous increase in apoptosis involving activation of caspases such as caspase-1, -2, -3, and -8 in the cultured human lens epithelial cells.	4-hydroxyhexenal	97-113	caspase 1	Homo sapiens	245-253
11841926-5	2002	In the present study we have demonstrated that H(2)O(2) and the lipid derived aldehydes, HNE and 4-hydroxyhexenal (HHE), can induce dose- and time-dependent loss of cell viability and a simultaneous increase in apoptosis involving activation of caspases such as caspase-1, -2, -3, and -8 in the cultured human lens epithelial cells.	4-hydroxyhexenal	97-113	caspase 1	Homo sapiens	262-287
11841926-6	2002	Interestingly, we observed that Z-VAD, a broad range inhibitor of caspases, conferred protection against H(2)O(2)- and HNE-induced apoptosis, suggesting the involvement of caspases in this apoptotic system.	z-vad	32-37	caspase 1	Homo sapiens	66-74
11841926-6	2002	Interestingly, we observed that Z-VAD, a broad range inhibitor of caspases, conferred protection against H(2)O(2)- and HNE-induced apoptosis, suggesting the involvement of caspases in this apoptotic system.	z-vad	32-37	caspase 1	Homo sapiens	172-180
11841926-6	2002	Interestingly, we observed that Z-VAD, a broad range inhibitor of caspases, conferred protection against H(2)O(2)- and HNE-induced apoptosis, suggesting the involvement of caspases in this apoptotic system.	Hydrogen Peroxide	105-113	caspase 1	Homo sapiens	66-74
11841926-6	2002	Interestingly, we observed that Z-VAD, a broad range inhibitor of caspases, conferred protection against H(2)O(2)- and HNE-induced apoptosis, suggesting the involvement of caspases in this apoptotic system.	Hydrogen Peroxide	105-113	caspase 1	Homo sapiens	172-180
11896416-6	2002	After 6 months of finasteride treatment, both caspases and XIAP were similar to levels exhibited by normal subjects.	Finasteride	18-29	caspase 1	Homo sapiens	46-54
11720765-0	2001	Manganese induces endoplasmic reticulum (ER) stress and activates multiple caspases in nigral dopaminergic neuronal cells, SN4741.	Manganese	0-9	caspase 1	Homo sapiens	75-83
11591724-12	2001	Caspase-1 inhibitor, Ac-YVAD-CHO, did not protect ECV 304 cells from apoptosis.	L 709049	21-32	caspase 1	Homo sapiens	0-9
12903195-3	2002	General caspases inhibitor, Z-Asp-CH2-DCB inhibited cell death.	benzyloxycarbonyl-Asp-CH2OC(O)-2,6-dichlorobenzene	28-41	caspase 1	Homo sapiens	8-16
12903195-7	2002	ECyd-induced rRNA fragmentation was inhibited by general caspases inhibitor (Z-Asp-CH2-DCB) and caspase-5 inhibitor (Z-WEHD-fmk).	benzyloxycarbonyl-Asp-CH2OC(O)-2,6-dichlorobenzene	77-90	caspase 1	Homo sapiens	57-65
11720765-7	2001	Manganese treatment elicited endoplasmic reticulum (ER) stress responses, such as an increased level of the ER chaperone BiP, and simultaneously activated the ER resident caspase-12.	Manganese	0-9	caspase 1	Homo sapiens	171-178
11720765-8	2001	Peak activation of other major initiator caspases-like activities, such as caspase-1, -8 and -9, ensued, resulting in activation of caspase-3-like activity during manganese-induced DA cell death.	Manganese	163-172	caspase 1	Homo sapiens	75-95
11704656-6	2001	ELISA experiments have established that gp120 enhances immunoreactive IL-1beta levels in the culture medium and this is prevented by exposure to the IL-1 converting enzyme (ICE) inhibitor t-butoxycarbonyl-L-aspartic acid benzyl ester-chloromethylketone [Boc-Asp(OBzl)-CMK] used at a concentration (2.5 microM) which significantly (P&lt;0.001) reduces cell death.	-l-aspartic acid benzyl ester	204-233	caspase 1	Homo sapiens	149-171
11746831-7	2001	Moreover, a permeable ceramide was effective in inducing apoptosis in both HL-60 and HL-525 cells, and this induction was caspase-1 and/or -4 dependent because an inhibitor of these caspases abrogated the induced apoptosis.	Ceramides	22-30	caspase 1	Homo sapiens	122-141
11746831-7	2001	Moreover, a permeable ceramide was effective in inducing apoptosis in both HL-60 and HL-525 cells, and this induction was caspase-1 and/or -4 dependent because an inhibitor of these caspases abrogated the induced apoptosis.	Ceramides	22-30	caspase 1	Homo sapiens	182-190
11704656-6	2001	ELISA experiments have established that gp120 enhances immunoreactive IL-1beta levels in the culture medium and this is prevented by exposure to the IL-1 converting enzyme (ICE) inhibitor t-butoxycarbonyl-L-aspartic acid benzyl ester-chloromethylketone [Boc-Asp(OBzl)-CMK] used at a concentration (2.5 microM) which significantly (P&lt;0.001) reduces cell death.	-l-aspartic acid benzyl ester	204-233	caspase 1	Homo sapiens	173-176
11704656-6	2001	ELISA experiments have established that gp120 enhances immunoreactive IL-1beta levels in the culture medium and this is prevented by exposure to the IL-1 converting enzyme (ICE) inhibitor t-butoxycarbonyl-L-aspartic acid benzyl ester-chloromethylketone [Boc-Asp(OBzl)-CMK] used at a concentration (2.5 microM) which significantly (P&lt;0.001) reduces cell death.	chloromethylketone	234-252	caspase 1	Homo sapiens	149-171
11704656-6	2001	ELISA experiments have established that gp120 enhances immunoreactive IL-1beta levels in the culture medium and this is prevented by exposure to the IL-1 converting enzyme (ICE) inhibitor t-butoxycarbonyl-L-aspartic acid benzyl ester-chloromethylketone [Boc-Asp(OBzl)-CMK] used at a concentration (2.5 microM) which significantly (P&lt;0.001) reduces cell death.	chloromethylketone	234-252	caspase 1	Homo sapiens	173-176
11704656-6	2001	ELISA experiments have established that gp120 enhances immunoreactive IL-1beta levels in the culture medium and this is prevented by exposure to the IL-1 converting enzyme (ICE) inhibitor t-butoxycarbonyl-L-aspartic acid benzyl ester-chloromethylketone [Boc-Asp(OBzl)-CMK] used at a concentration (2.5 microM) which significantly (P&lt;0.001) reduces cell death.	boc-asp	254-261	caspase 1	Homo sapiens	149-171
11704656-6	2001	ELISA experiments have established that gp120 enhances immunoreactive IL-1beta levels in the culture medium and this is prevented by exposure to the IL-1 converting enzyme (ICE) inhibitor t-butoxycarbonyl-L-aspartic acid benzyl ester-chloromethylketone [Boc-Asp(OBzl)-CMK] used at a concentration (2.5 microM) which significantly (P&lt;0.001) reduces cell death.	boc-asp	254-261	caspase 1	Homo sapiens	173-176
11704656-8	2001	Death of CHP100 cells induced by gp120 is also prevented by acetyl-Tyr-Val-Ala-Asp-chloromethylketone (Ac-YVAD-CMK; 10-100 microM), a second inhibitor of ICE, supporting the concept that the viral protein stimulates the conversion of the 31 kDa pro-IL-1beta in to the 17 kDa mature cytokine which is then secreted to cause death.	N-acetyl-tyrosyl-valyl-alanyl-aspartyl chloromethyl ketone	60-101	caspase 1	Homo sapiens	154-157
11704656-8	2001	Death of CHP100 cells induced by gp120 is also prevented by acetyl-Tyr-Val-Ala-Asp-chloromethylketone (Ac-YVAD-CMK; 10-100 microM), a second inhibitor of ICE, supporting the concept that the viral protein stimulates the conversion of the 31 kDa pro-IL-1beta in to the 17 kDa mature cytokine which is then secreted to cause death.	ac-yvad	103-110	caspase 1	Homo sapiens	154-157
11703590-0	2001	Role and regulation of activation of caspases in cisplatin-induced injury to renal tubular epithelial cells.	Cisplatin	49-58	caspase 1	Homo sapiens	37-45
11703590-3	2001	METHODS: The role of caspases in cisplatin-induced injury was determined using caspase inhibitors and p35 transfected LLC-PK1 cells.	Cisplatin	33-42	caspase 1	Homo sapiens	21-29
11703590-13	2001	CONCLUSIONS: These studies demonstrate differential activation and role of caspases in cisplatin injury, and provide the first evidence of cisplatin-induced induction of the Akt/PKB phosphorylation pathway, inhibition of which enhances activation of caspase-3 and caspase-9.	Cisplatin	139-148	caspase 1	Homo sapiens	75-83
11703590-3	2001	METHODS: The role of caspases in cisplatin-induced injury was determined using caspase inhibitors and p35 transfected LLC-PK1 cells.	Cisplatin	33-42	caspase 1	Homo sapiens	21-28
11703590-8	2001	We then examined the role of the Akt/PKB phosphorylation pathway in regulation of cisplatin-induced caspase activation.	Cisplatin	82-91	caspase 1	Homo sapiens	100-107
11703590-12	2001	The impact of enhanced activation of caspases by wortmannin or LY294002 was reflected on accelerated cisplatin-induced cell death.	Wortmannin	49-59	caspase 1	Homo sapiens	37-45
11703590-12	2001	The impact of enhanced activation of caspases by wortmannin or LY294002 was reflected on accelerated cisplatin-induced cell death.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	63-71	caspase 1	Homo sapiens	37-45
11703590-12	2001	The impact of enhanced activation of caspases by wortmannin or LY294002 was reflected on accelerated cisplatin-induced cell death.	Cisplatin	101-110	caspase 1	Homo sapiens	37-45
11703590-13	2001	CONCLUSIONS: These studies demonstrate differential activation and role of caspases in cisplatin injury, and provide the first evidence of cisplatin-induced induction of the Akt/PKB phosphorylation pathway, inhibition of which enhances activation of caspase-3 and caspase-9.	Cisplatin	87-96	caspase 1	Homo sapiens	75-83
11704825-7	2001	Additionally, Z-VAD-fmk, a general inhibitor of caspases which inhibited cytochrome c release in HL-60 and HL-60/VCR cells, had no effect on AIF release in any of these cell lines, but inhibited beta(2)m-induced apoptosis in all three cell lines.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	14-23	caspase 1	Homo sapiens	48-56
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 1	Homo sapiens	146-153
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 1	Homo sapiens	196-203
11673515-4	2001	When examined by confocal microscopy, anti-Fas-treated CTL showed the early appearance of IETDase-containing plasma membrane vesicles and their release from the CTL surface, followed by activation of other caspase activities in the cell interior.	ammonium ferrous sulfate	43-46	caspase 1	Homo sapiens	206-213
11399535-5	2001	In this study we have analyzed the family of caspases, 1-10 along with usurpin, and XIAP, in men with normal scalp and in men with androgenetic alopecia before and after 6 months treatment with 1 mg oral finasteride treatment.	Finasteride	204-215	caspase 1	Homo sapiens	45-53
11591522-0	2001	Structure-based design of caspase-1 inhibitor containing a diphenyl ether sulfonamide.	diphenyl ether sulfonamide	59-85	caspase 1	Homo sapiens	26-35
11591522-3	2001	An X-ray crystal structure of a representative member of the diphenyl ether sulfonamide series bound to the active site of caspase-1 was obtained.	diphenyl ether sulfonamide	61-87	caspase 1	Homo sapiens	123-132
11438643-8	2001	All three caspases cleaved AP-2alpha at asp(19) of the sequence asp-arg-his-asp (DRHD(19)).	Asp-Arg-His	64-75	caspase 1	Homo sapiens	10-18
11438643-8	2001	All three caspases cleaved AP-2alpha at asp(19) of the sequence asp-arg-his-asp (DRHD(19)).	Aspartic Acid	40-43	caspase 1	Homo sapiens	10-18
11399535-9	2001	Results from our study indicate caspase 3 to be of primary importance in normal hair homeostasis and that DHT may be signaling greater expression of caspases, inducing apoptosis in androgenetic alopecia.	Dihydrotestosterone	106-109	caspase 1	Homo sapiens	149-157
11399535-10	2001	In conclusion, DHT may selectively regulate the caspase genes which play an important role in signaling programmed cell death, affecting the hair growth cycle.	Dihydrotestosterone	15-18	caspase 1	Homo sapiens	48-55
11408612-7	2001	The use of the antioxidant N-acetyl cysteine and caspase inhibitors prevents CDDP-induced apoptosis in c-Myc low-expressing clones, demonstrating that ROS, caspase-1, and caspase-3 are required for apoptotic cell death.	Acetylcysteine	27-44	caspase 1	Homo sapiens	156-165
11772244-5	2001	Pralnacasan, the first orally available, potent and selective ICE inhibitor to enter clinical trials, is currently under investigation in rheumatoid arthritis.	pralnacasan	0-11	caspase 1	Homo sapiens	62-65
11408612-7	2001	The use of the antioxidant N-acetyl cysteine and caspase inhibitors prevents CDDP-induced apoptosis in c-Myc low-expressing clones, demonstrating that ROS, caspase-1, and caspase-3 are required for apoptotic cell death.	Cisplatin	77-81	caspase 1	Homo sapiens	49-56
11408612-7	2001	The use of the antioxidant N-acetyl cysteine and caspase inhibitors prevents CDDP-induced apoptosis in c-Myc low-expressing clones, demonstrating that ROS, caspase-1, and caspase-3 are required for apoptotic cell death.	Reactive Oxygen Species	151-154	caspase 1	Homo sapiens	49-56
11408612-8	2001	Moreover, ROS generation depends on caspase-1-like activation because the Ac-YVAD-cho inhibitor abrogates CDDP-induced ROS in the c-Myc low-expressing clones.	Reactive Oxygen Species	10-13	caspase 1	Homo sapiens	36-45
11408612-8	2001	Moreover, ROS generation depends on caspase-1-like activation because the Ac-YVAD-cho inhibitor abrogates CDDP-induced ROS in the c-Myc low-expressing clones.	ac-yvad	74-81	caspase 1	Homo sapiens	36-45
11408612-8	2001	Moreover, ROS generation depends on caspase-1-like activation because the Ac-YVAD-cho inhibitor abrogates CDDP-induced ROS in the c-Myc low-expressing clones.	Cisplatin	106-110	caspase 1	Homo sapiens	36-45
11408612-8	2001	Moreover, ROS generation depends on caspase-1-like activation because the Ac-YVAD-cho inhibitor abrogates CDDP-induced ROS in the c-Myc low-expressing clones.	Reactive Oxygen Species	119-122	caspase 1	Homo sapiens	36-45
11496824-7	2001	All effects of histamine were abolished by the presence of anti-IL-18 antibody or IL-1b-converting enzyme/caspase-1 inhibitor, indicating that histamine action is dependent on mature IL-18 secretion and that IL-18 production was present most upstream of the cytokine cascade triggered by histamine.	Histamine	15-24	caspase 1	Homo sapiens	106-115
11356690-5	2001	Furthermore, apoptosis induction was suppressed by the caspase-1 inhibitor, z-YVAD, but not the caspase-3 inhibitor, z-DQMD, thus demonstrating the functional significance of increased procaspase-1 expression in TGF-beta-mediated apoptosis in prostate cancer cells.	z-yvad	76-82	caspase 1	Homo sapiens	55-64
11496824-7	2001	All effects of histamine were abolished by the presence of anti-IL-18 antibody or IL-1b-converting enzyme/caspase-1 inhibitor, indicating that histamine action is dependent on mature IL-18 secretion and that IL-18 production was present most upstream of the cytokine cascade triggered by histamine.	Histamine	143-152	caspase 1	Homo sapiens	106-115
11496824-7	2001	All effects of histamine were abolished by the presence of anti-IL-18 antibody or IL-1b-converting enzyme/caspase-1 inhibitor, indicating that histamine action is dependent on mature IL-18 secretion and that IL-18 production was present most upstream of the cytokine cascade triggered by histamine.	Histamine	143-152	caspase 1	Homo sapiens	106-115
11319773-7	2001	Caspase activation, PS translocation and chromatin condensation were downstream of ROS production.	Reactive Oxygen Species	83-86	caspase 1	Homo sapiens	0-7
11351255-4	2001	In contrast, cotreatment with N-acetyl-Tyr-Val-Ala-Asp aldehyde (AC-YVAD-CHO), a caspase 1 inhibitor did not prevent any cytotoxic effect of these drugs.	L 709049	30-63	caspase 1	Homo sapiens	81-90
11351255-4	2001	In contrast, cotreatment with N-acetyl-Tyr-Val-Ala-Asp aldehyde (AC-YVAD-CHO), a caspase 1 inhibitor did not prevent any cytotoxic effect of these drugs.	L 709049	65-76	caspase 1	Homo sapiens	81-90
11397893-7	2001	Dex inhibited TNFalpha-induced messenger ribonucleic acid expression of ICE, TNF alpha, and IL-1 beta (P &lt; 0.01), but not that of bcl-2 and NF kappa B.	Dexamethasone	0-3	caspase 1	Homo sapiens	72-75
11517925-4	2001	Clan CD contains the families of clostripain (C11), gingipain R (C25), legumain (C13), caspase-1 (C14) and separin (C50).	clan cd	0-7	caspase 1	Homo sapiens	87-96
11319773-8	2001	In contrast to H(2)O(2), ROS produced by a xanthine/xanthine oxidase system in CGN cultured in K25 were able to directly induce caspase-3 activation and death that resulted sensitive to z-VAD, a caspase inhibitor.	z-vad	186-191	caspase 1	Homo sapiens	128-135
11319773-9	2001	These findings indicate that a reduction in [Ca(2+)](i) triggers CGN death by inducing a generation of ROS after 3--4 hr, which could play a critical role in the initial phases of the apoptotic process including PS translocation, chromatin condensation and the activation of initiator and executor caspases.	Reactive Oxygen Species	103-106	caspase 1	Homo sapiens	298-306
11319773-8	2001	In contrast to H(2)O(2), ROS produced by a xanthine/xanthine oxidase system in CGN cultured in K25 were able to directly induce caspase-3 activation and death that resulted sensitive to z-VAD, a caspase inhibitor.	Reactive Oxygen Species	25-28	caspase 1	Homo sapiens	128-135
11295216-0	2001	Preliminary evaluation of caspases-dependent apoptosis signaling pathways of free and HPMA copolymer-bound doxorubicin in human ovarian carcinoma cells.	copolymer	91-100	caspase 1	Homo sapiens	26-34
11295216-0	2001	Preliminary evaluation of caspases-dependent apoptosis signaling pathways of free and HPMA copolymer-bound doxorubicin in human ovarian carcinoma cells.	Doxorubicin	107-118	caspase 1	Homo sapiens	26-34
11295216-1	2001	The purpose of the study was to examine the role of caspases in signaling pathways of apoptosis induced by free doxorubicin (DOX) and HPMA copolymer-bound DOX (P(GFLG)-DOX) in human ovarian carcinoma cells.	Doxorubicin	112-123	caspase 1	Homo sapiens	52-60
11295216-1	2001	The purpose of the study was to examine the role of caspases in signaling pathways of apoptosis induced by free doxorubicin (DOX) and HPMA copolymer-bound DOX (P(GFLG)-DOX) in human ovarian carcinoma cells.	Doxorubicin	125-128	caspase 1	Homo sapiens	52-60
11295216-1	2001	The purpose of the study was to examine the role of caspases in signaling pathways of apoptosis induced by free doxorubicin (DOX) and HPMA copolymer-bound DOX (P(GFLG)-DOX) in human ovarian carcinoma cells.	hpma copolymer	134-148	caspase 1	Homo sapiens	52-60
11295216-1	2001	The purpose of the study was to examine the role of caspases in signaling pathways of apoptosis induced by free doxorubicin (DOX) and HPMA copolymer-bound DOX (P(GFLG)-DOX) in human ovarian carcinoma cells.	Doxorubicin	155-158	caspase 1	Homo sapiens	52-60
11295216-1	2001	The purpose of the study was to examine the role of caspases in signaling pathways of apoptosis induced by free doxorubicin (DOX) and HPMA copolymer-bound DOX (P(GFLG)-DOX) in human ovarian carcinoma cells.	Doxorubicin	155-158	caspase 1	Homo sapiens	52-60
11278253-8	2001	Treatment of p53-positive MCF-7 cells with the DNA-damaging drug, doxorubicin, which increases p53 levels, enhanced caspase-1 promoter activity 4-5-fold, but similar treatment of MCF-7-mp53 (a clone of MCF-7 cells expressing mutant p53) and p53-negative HeLa cells with doxorubicin did not increase caspase-1 promoter activity.	Doxorubicin	66-77	caspase 1	Homo sapiens	116-125
11278253-9	2001	Doxorubicin treatment increased caspase-1 mRNA levels in MCF-7 cells but not in MCF-7-mp53 or HeLa cells.	Doxorubicin	0-11	caspase 1	Homo sapiens	32-41
11108714-11	2001	The viral replicative intermediate dsRNA stimulates beta-cell production of pro-IL-1beta, and following cleavage to its mature form by IFN-gamma-activated ICE, IL-1 then initiates beta-cell damage in a nitric oxide-dependent fashion.	Nitric Oxide	202-214	caspase 1	Homo sapiens	155-158
11278253-8	2001	Treatment of p53-positive MCF-7 cells with the DNA-damaging drug, doxorubicin, which increases p53 levels, enhanced caspase-1 promoter activity 4-5-fold, but similar treatment of MCF-7-mp53 (a clone of MCF-7 cells expressing mutant p53) and p53-negative HeLa cells with doxorubicin did not increase caspase-1 promoter activity.	Doxorubicin	66-77	caspase 1	Homo sapiens	299-308
11282563-7	2001	It is hypothesized that in Fas-induced PMN apoptosis caspase-1 has a double role: it can protect from apoptosis through generation of protective IL-1beta, as in spontaneous apoptosis, and it can also exert pro-apoptotic activity which counterbalances the protective effect and allows accelerated apoptosis.	ammonium ferrous sulfate	27-30	caspase 1	Homo sapiens	53-62
11312881-0	2001	Induction of apoptosis by garcinol and curcumin through cytochrome c release and activation of caspases in human leukemia HL-60 cells.	Curcumin	39-47	caspase 1	Homo sapiens	95-103
11267979-7	2001	Furthermore, treatment of a human renal cancer cell line, ACHN, with 5-aza-2"-deoxycytidine also caused recovery of caspase-1 expression, which was not detected before treatment.	1,1'-Azobis(cyanocyclohexane)	58-62	caspase 1	Homo sapiens	116-125
11267979-7	2001	Furthermore, treatment of a human renal cancer cell line, ACHN, with 5-aza-2"-deoxycytidine also caused recovery of caspase-1 expression, which was not detected before treatment.	Decitabine	69-91	caspase 1	Homo sapiens	116-125
11312881-0	2001	Induction of apoptosis by garcinol and curcumin through cytochrome c release and activation of caspases in human leukemia HL-60 cells.	garcinol	26-34	caspase 1	Homo sapiens	95-103
11056157-0	2001	ATP-stimulated release of interleukin (IL)-1beta and IL-18 requires priming by lipopolysaccharide and is independent of caspase-1 cleavage.	Adenosine Triphosphate	0-3	caspase 1	Homo sapiens	120-129
11179455-9	2001	Furthermore, paclitaxel-induced apoptosis and cleavage of beta-catenin and gamma-catenin were inhibited by the pan-caspase inhibitor Z-VAD-FMK and partially inhibited by the caspase-3 inhibitor Z-DEVD-FMK but were not affected by the caspase-1 inhibitor AC-YVAD-CMK.	Paclitaxel	13-23	caspase 1	Homo sapiens	234-243
11179455-9	2001	Furthermore, paclitaxel-induced apoptosis and cleavage of beta-catenin and gamma-catenin were inhibited by the pan-caspase inhibitor Z-VAD-FMK and partially inhibited by the caspase-3 inhibitor Z-DEVD-FMK but were not affected by the caspase-1 inhibitor AC-YVAD-CMK.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	133-142	caspase 1	Homo sapiens	234-243
11181049-3	2001	Cytotoxic drug-induced apoptosisinvolves delayed activation of caspases 2, 7, and 9, but not 8 and 3, and is blocked by a broad spectrum caspase inhibitor, zVAD-fmk.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	156-164	caspase 1	Homo sapiens	63-71
11056157-8	2001	In evaluating the signaling components involved in the ATP effect, we identified that the protein-tyrosine kinase inhibitor, AG126, produced a profound inhibition of both ICE activation as well as release of IL-1beta/IL-18.	Adenosine Triphosphate	55-58	caspase 1	Homo sapiens	171-174
11056157-8	2001	In evaluating the signaling components involved in the ATP effect, we identified that the protein-tyrosine kinase inhibitor, AG126, produced a profound inhibition of both ICE activation as well as release of IL-1beta/IL-18.	AG 127	125-130	caspase 1	Homo sapiens	171-174
11162250-4	2001	Staurosporine-induced Tau cleavage was blocked by 20 microM z-Asp-Glu-Val-Asp-chloromethylketone, a caspase-3 inhibitor, and in vitro, Tau was selectively cleaved by caspase-3 or calpain, a calcium-activated protease, but not by caspases-1, -8, or -9.	Staurosporine	0-13	caspase 1	Homo sapiens	229-250
11334117-8	2001	Fas-ligation induced upregulation of caspase-1 and -3 expression in the nucleus and cytoplasm in A549 cells.	ammonium ferrous sulfate	0-3	caspase 1	Homo sapiens	37-53
11162250-4	2001	Staurosporine-induced Tau cleavage was blocked by 20 microM z-Asp-Glu-Val-Asp-chloromethylketone, a caspase-3 inhibitor, and in vitro, Tau was selectively cleaved by caspase-3 or calpain, a calcium-activated protease, but not by caspases-1, -8, or -9.	benzyloxycarbonyl aspartyl-glutamyl-valyl-aspartyl-chloromethyl ketone	60-96	caspase 1	Homo sapiens	229-250
11029523-0	2000	Caspase-1 activity as a possible predictor of apoptosis induced by cisplatin in gastric cancer cells.	Cisplatin	67-76	caspase 1	Homo sapiens	0-9
11154867-2	2001	It has been demonstrated that the protease caspase-3, a downstream molecule of the CD95 pathway, is activated in UV-exposed HaCaT cells, and that the DNA-dependent protein kinase catalytic subunit (DNA-PKcs) is cleaved by interleukin-1beta converting enzyme (ICE)-like protease during apoptosis induced by X-rays, staurosporine and etoposide.	Staurosporine	314-327	caspase 1	Homo sapiens	222-257
11154867-2	2001	It has been demonstrated that the protease caspase-3, a downstream molecule of the CD95 pathway, is activated in UV-exposed HaCaT cells, and that the DNA-dependent protein kinase catalytic subunit (DNA-PKcs) is cleaved by interleukin-1beta converting enzyme (ICE)-like protease during apoptosis induced by X-rays, staurosporine and etoposide.	Etoposide	332-341	caspase 1	Homo sapiens	222-257
11110692-3	2000	Because fas-mediated programmed cell death in many cells involves sequential activation of specific caspases, we tested the hypothesis that programmed cell death in FA HPC involves the ordered activation of specific caspase molecules.	ammonium ferrous sulfate	8-11	caspase 1	Homo sapiens	100-108
11110692-6	2000	Inhibitors (ac-YVAD-cho, CP-YVAD-cho, Z-YVAD-FMK) of caspase 1 did not block apoptosis or caspase 3 activation.	benzyloxycarbonyltyrosyl-valyl-alanyl-aspartic acid fluoromethyl ketone	38-48	caspase 1	Homo sapiens	53-62
11164419-4	2000	Fluvastatin treatment resulted in the activation of caspase-1 and in a small secretion of interleukin (IL)-1beta, IL-18, and IFNgamma (Th1).	Fluvastatin	0-11	caspase 1	Homo sapiens	52-61
11164419-7	2000	Not only did mevalonate abolish the effects of the statin but it also prevented the caspase-1 activation induced by the bacteria, suggesting the involvement of isoprenoids in the response to M. tuberculosis.	Terpenes	160-171	caspase 1	Homo sapiens	84-93
11029523-3	2000	To elucidate the caspase-1 activity, which might be a predictor for the effect of chemotherapy, we examined the changes of caspase-1 activity induced after exposure to cisplatin (CDDP) in six gastric cancer cell lines.	Cisplatin	168-177	caspase 1	Homo sapiens	17-26
11029523-3	2000	To elucidate the caspase-1 activity, which might be a predictor for the effect of chemotherapy, we examined the changes of caspase-1 activity induced after exposure to cisplatin (CDDP) in six gastric cancer cell lines.	Cisplatin	168-177	caspase 1	Homo sapiens	123-132
11029523-3	2000	To elucidate the caspase-1 activity, which might be a predictor for the effect of chemotherapy, we examined the changes of caspase-1 activity induced after exposure to cisplatin (CDDP) in six gastric cancer cell lines.	Cisplatin	179-183	caspase 1	Homo sapiens	17-26
11029523-3	2000	To elucidate the caspase-1 activity, which might be a predictor for the effect of chemotherapy, we examined the changes of caspase-1 activity induced after exposure to cisplatin (CDDP) in six gastric cancer cell lines.	Cisplatin	179-183	caspase 1	Homo sapiens	123-132
11029523-4	2000	A high correlation between the 50% inhibitory concentration (IC50) and caspase-1 activity ratio was shown (r=0.83, p=0.041) (caspase-1 activity ratio: the caspase-1 activity of cells at 4 h after CDDP treatment/the caspase-1 activity of untreated cells).	Cisplatin	196-200	caspase 1	Homo sapiens	71-80
11029523-4	2000	A high correlation between the 50% inhibitory concentration (IC50) and caspase-1 activity ratio was shown (r=0.83, p=0.041) (caspase-1 activity ratio: the caspase-1 activity of cells at 4 h after CDDP treatment/the caspase-1 activity of untreated cells).	Cisplatin	196-200	caspase 1	Homo sapiens	125-134
11029523-4	2000	A high correlation between the 50% inhibitory concentration (IC50) and caspase-1 activity ratio was shown (r=0.83, p=0.041) (caspase-1 activity ratio: the caspase-1 activity of cells at 4 h after CDDP treatment/the caspase-1 activity of untreated cells).	Cisplatin	196-200	caspase 1	Homo sapiens	125-134
11029523-4	2000	A high correlation between the 50% inhibitory concentration (IC50) and caspase-1 activity ratio was shown (r=0.83, p=0.041) (caspase-1 activity ratio: the caspase-1 activity of cells at 4 h after CDDP treatment/the caspase-1 activity of untreated cells).	Cisplatin	196-200	caspase 1	Homo sapiens	125-134
11029523-5	2000	Further, we examined the correlation between caspase-1 activity and apoptosis induced by CDDP in two cell lines that have very different CDDP sensitivities; OCUM-2M and OCUM-2M/DDP (IC50; 0.	Cisplatin	89-93	caspase 1	Homo sapiens	45-54
11029523-8	2000	In both cell lines, caspase-1 activity began to increase immediately after exposure to CDDP and peaked at approximately 4 h after cessation of exposure to CDDP, and gradually decreased thereafter.	Cisplatin	87-91	caspase 1	Homo sapiens	20-29
11029523-8	2000	In both cell lines, caspase-1 activity began to increase immediately after exposure to CDDP and peaked at approximately 4 h after cessation of exposure to CDDP, and gradually decreased thereafter.	Cisplatin	155-159	caspase 1	Homo sapiens	20-29
11029523-9	2000	The caspase-1 activity of OCUM-2M was approximately 1.8-times higher than that of OCUM-2M/DDP at 4 h after exposure to CDDP.	Cisplatin	119-123	caspase 1	Homo sapiens	4-13
11029523-10	2000	Taken together, our results indicate that evaluating the changes of caspase-1 activity after exposure to CDDP may be useful to predict apoptosis following CDDP treatment in gastric cancer cells.	Cisplatin	105-109	caspase 1	Homo sapiens	68-77
11029523-10	2000	Taken together, our results indicate that evaluating the changes of caspase-1 activity after exposure to CDDP may be useful to predict apoptosis following CDDP treatment in gastric cancer cells.	Cisplatin	155-159	caspase 1	Homo sapiens	68-77
11129738-5	2000	Both caspase-1 and caspase-3 were activated in Hep G2 cells by HCPT treatment, suggesting that caspase-1 and caspase-3 are involved in the process of apoptosis in Hep G2 cells, and may be the main effectors of the apoptosis.	10-hydroxycamptothecin	63-67	caspase 1	Homo sapiens	5-14
11046058-8	2000	The inhibition of caspase-1 by NCX-4016 was reversible by the addition of DTT, which is consistent with S-nitrosylation as the mechanism of caspase-1 inhibition.	Dithiothreitol	74-77	caspase 1	Homo sapiens	18-27
11046058-12	2000	Caspase-1 inhibition is a new, cycloxygenase-independent antiinflammatory mechanism of NO-aspirin.	Aspirin	90-97	caspase 1	Homo sapiens	0-9
11046058-0	2000	IL-1 beta converting enzyme is a target for nitric oxide-releasing aspirin: new insights in the antiinflammatory mechanism of nitric oxide-releasing nonsteroidal antiinflammatory drugs.	Nitric Oxide	44-56	caspase 1	Homo sapiens	0-27
11046058-0	2000	IL-1 beta converting enzyme is a target for nitric oxide-releasing aspirin: new insights in the antiinflammatory mechanism of nitric oxide-releasing nonsteroidal antiinflammatory drugs.	Aspirin	67-74	caspase 1	Homo sapiens	0-27
11046058-0	2000	IL-1 beta converting enzyme is a target for nitric oxide-releasing aspirin: new insights in the antiinflammatory mechanism of nitric oxide-releasing nonsteroidal antiinflammatory drugs.	Nitric Oxide	126-138	caspase 1	Homo sapiens	0-27
11129738-5	2000	Both caspase-1 and caspase-3 were activated in Hep G2 cells by HCPT treatment, suggesting that caspase-1 and caspase-3 are involved in the process of apoptosis in Hep G2 cells, and may be the main effectors of the apoptosis.	10-hydroxycamptothecin	63-67	caspase 1	Homo sapiens	95-104
10960761-0	2000	Mitomycin C induces apoptosis in a caspases-dependent and Fas/CD95-independent manner in human gastric adenocarcinoma cells.	Mitomycin	0-11	caspase 1	Homo sapiens	35-43
10974198-4	2000	These effects were prevented completely by the pan-caspase inhibitor z-Val-Ala-Asp-(OMe)-fluoromethylketone (z-VAD-fmk), thereby implicating the cysteine aspartase (caspase) cascade in the process.	z-Val-Ala-Asp(Ome)-fluoromethylketone	69-107	caspase 1	Homo sapiens	51-58
10974198-4	2000	These effects were prevented completely by the pan-caspase inhibitor z-Val-Ala-Asp-(OMe)-fluoromethylketone (z-VAD-fmk), thereby implicating the cysteine aspartase (caspase) cascade in the process.	z-Val-Ala-Asp(Ome)-fluoromethylketone	69-107	caspase 1	Homo sapiens	165-172
10974198-4	2000	These effects were prevented completely by the pan-caspase inhibitor z-Val-Ala-Asp-(OMe)-fluoromethylketone (z-VAD-fmk), thereby implicating the cysteine aspartase (caspase) cascade in the process.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	109-118	caspase 1	Homo sapiens	51-58
10974198-4	2000	These effects were prevented completely by the pan-caspase inhibitor z-Val-Ala-Asp-(OMe)-fluoromethylketone (z-VAD-fmk), thereby implicating the cysteine aspartase (caspase) cascade in the process.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	109-118	caspase 1	Homo sapiens	165-172
10974198-5	2000	Dibucaine activated various caspases, such as caspase-3, -6, -8, and -9 (-like) activities, but not caspase-1 (-like) activity, and induced mitochondrial membrane depolarization and the release of cytochrome c (Cyt.c) from mitochondria into the cytosol.	Dibucaine	0-9	caspase 1	Homo sapiens	28-36
10974198-7	2000	Bid, a death agonist member of the Bcl-2 family, was processed by caspases following exposure of cells to dibucaine.	Dibucaine	106-115	caspase 1	Homo sapiens	66-74
10974198-9	2000	Taken together, these data suggest that dibucaine induced apoptosis of HL-60 cells through activation of the caspase cascade in conjunction with Cyt.c release induced by a processed product of Bid and depolarization of the mitochondrial membrane potential.	Dibucaine	40-49	caspase 1	Homo sapiens	109-116
10960761-4	2000	Incubation with z-DEVD-fmk and benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone (z-VAD-fmk) almost completely abrogated MMC-induced DNA fragmentation, indicating that activation of these caspases was crucially involved in MMC-induced apoptosis.	benzoylcarbonyl-aspartyl-glutamyl-valyl-aspartyl-fluoromethyl ketone	16-26	caspase 1	Homo sapiens	187-195
10960761-4	2000	Incubation with z-DEVD-fmk and benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone (z-VAD-fmk) almost completely abrogated MMC-induced DNA fragmentation, indicating that activation of these caspases was crucially involved in MMC-induced apoptosis.	Caspase Inhibitor VI	31-79	caspase 1	Homo sapiens	187-195
10960761-4	2000	Incubation with z-DEVD-fmk and benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone (z-VAD-fmk) almost completely abrogated MMC-induced DNA fragmentation, indicating that activation of these caspases was crucially involved in MMC-induced apoptosis.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	81-90	caspase 1	Homo sapiens	187-195
10960761-4	2000	Incubation with z-DEVD-fmk and benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone (z-VAD-fmk) almost completely abrogated MMC-induced DNA fragmentation, indicating that activation of these caspases was crucially involved in MMC-induced apoptosis.	Mitomycin	120-123	caspase 1	Homo sapiens	187-195
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.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	30-85	caspase 1	Homo sapiens	222-231
11022849-3	2000	The presence of fairly low concentrations of VES inhibited the growth and DNA synthesis of HL-60 cells, and also induced their apoptosis via a mechanism that was inhibited by z-VAD-fluoromethylketone (z-VAD-fmk), an inhibitor of pan-caspases.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	175-199	caspase 1	Homo sapiens	233-241
10854431-12	2000	Tyr-Val-Ala-Asp-chloromethyl ketone, a caspase-1 inhibitor, prevented ATP-induced release of processed interleukin-1beta, but not ATP-dependent SAPK activity.	Tyr-Val-Ala-Asp-chloromethyl ketone	0-35	caspase 1	Homo sapiens	39-48
10854431-12	2000	Tyr-Val-Ala-Asp-chloromethyl ketone, a caspase-1 inhibitor, prevented ATP-induced release of processed interleukin-1beta, but not ATP-dependent SAPK activity.	Adenosine Triphosphate	70-73	caspase 1	Homo sapiens	39-48
10989191-9	2000	Activation of caspase-3/CPP32 and apoptosis upon growth factor withdrawal were inhibited/reduced by the caspase inhibitors, z-VAD-fmk and DEVD-CHO.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	124-133	caspase 1	Homo sapiens	14-21
10989191-9	2000	Activation of caspase-3/CPP32 and apoptosis upon growth factor withdrawal were inhibited/reduced by the caspase inhibitors, z-VAD-fmk and DEVD-CHO.	aspartyl-glutamyl-valyl-aspartal	138-146	caspase 1	Homo sapiens	14-21
10908312-10	2000	Thus, these results indicate that the cytotoxicity of BHA is due to the induction of apoptosis that is mediated by the direct release of cytochrome c and the subsequent activation of caspases.	Butylated Hydroxyanisole	54-57	caspase 1	Homo sapiens	183-191
10947972-5	2000	The S(1) subsite, the major specificity-determining site of the caspases, demonstrates tremendous selectivity, with a 20000-fold preference for cleaving substrates containing aspartic acid over glutamic acid at this position.	Aspartic Acid	175-188	caspase 1	Homo sapiens	64-72
10947972-5	2000	The S(1) subsite, the major specificity-determining site of the caspases, demonstrates tremendous selectivity, with a 20000-fold preference for cleaving substrates containing aspartic acid over glutamic acid at this position.	Glutamic Acid	194-207	caspase 1	Homo sapiens	64-72
10947972-7	2000	We find that the caspases show an unexpected degree of discrimination in the P(1)" position, with a general preference for small amino acid residues such as alanine, glycine and serine, with glycine being the preferred substituent.	Alanine	157-164	caspase 1	Homo sapiens	17-25
10947972-7	2000	We find that the caspases show an unexpected degree of discrimination in the P(1)" position, with a general preference for small amino acid residues such as alanine, glycine and serine, with glycine being the preferred substituent.	Glycine	166-173	caspase 1	Homo sapiens	17-25
10947972-7	2000	We find that the caspases show an unexpected degree of discrimination in the P(1)" position, with a general preference for small amino acid residues such as alanine, glycine and serine, with glycine being the preferred substituent.	Serine	178-184	caspase 1	Homo sapiens	17-25
10947972-7	2000	We find that the caspases show an unexpected degree of discrimination in the P(1)" position, with a general preference for small amino acid residues such as alanine, glycine and serine, with glycine being the preferred substituent.	Glycine	191-198	caspase 1	Homo sapiens	17-25
10938399-0	2000	Induction of apoptosis by ursolic acid through activation of caspases and down-regulation of c-IAPs in human prostate epithelial cells.	ursolic acid	26-38	caspase 1	Homo sapiens	61-69
10938399-5	2000	These apoptotic effects of UA were accompanied by proteolytic cleavage of specific target proteins such as PARP, beta-catenin and Rad51 proteins suggesting the possible involvement of caspases.	ursolic acid	27-29	caspase 1	Homo sapiens	184-192
10938399-6	2000	Western blotting and in vitro assay demonstrated that processing/activation of at least four caspases (caspase-1, -3, -8 and -9) accompanies the generation of UA-mediating apoptotic cell death.	ursolic acid	159-161	caspase 1	Homo sapiens	93-101
10938399-6	2000	Western blotting and in vitro assay demonstrated that processing/activation of at least four caspases (caspase-1, -3, -8 and -9) accompanies the generation of UA-mediating apoptotic cell death.	ursolic acid	159-161	caspase 1	Homo sapiens	103-127
10938399-9	2000	These data suggest that apoptotic signals evoked by UA treatment may converge caspases activation through down-regulation of c-IAPs family and without mitochondrial dysfunction.	ursolic acid	52-54	caspase 1	Homo sapiens	78-86
10937565-9	2000	In addition, doxycycline reduced the steady state level of the cellular ICE protein but did not affect the level of ICE transcripts.	Doxycycline	13-24	caspase 1	Homo sapiens	72-75
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 1	Homo sapiens	222-231
10840014-9	2000	Moreover, we found that the interleukin 1beta-converting enzyme (ICE)/CED-3 family protease (caspase-3) became activated in high glucose-induced apoptosis.	Glucose	129-136	caspase 1	Homo sapiens	28-63
10843724-7	2000	All effects of histamine on cytokine responses were also abolished by the presence of either anti-IL-18 Ab or IL-1beta-converting enzyme/caspase-1 inhibitor, indicating that the histamine action is dependent on mature IL-18 secretion and that IL-18 production is located upstream of the cytokine cascade activated by histamine.	Histamine	15-24	caspase 1	Homo sapiens	110-136
10843724-7	2000	All effects of histamine on cytokine responses were also abolished by the presence of either anti-IL-18 Ab or IL-1beta-converting enzyme/caspase-1 inhibitor, indicating that the histamine action is dependent on mature IL-18 secretion and that IL-18 production is located upstream of the cytokine cascade activated by histamine.	Histamine	15-24	caspase 1	Homo sapiens	137-146
10843724-7	2000	All effects of histamine on cytokine responses were also abolished by the presence of either anti-IL-18 Ab or IL-1beta-converting enzyme/caspase-1 inhibitor, indicating that the histamine action is dependent on mature IL-18 secretion and that IL-18 production is located upstream of the cytokine cascade activated by histamine.	Histamine	178-187	caspase 1	Homo sapiens	110-136
10843724-7	2000	All effects of histamine on cytokine responses were also abolished by the presence of either anti-IL-18 Ab or IL-1beta-converting enzyme/caspase-1 inhibitor, indicating that the histamine action is dependent on mature IL-18 secretion and that IL-18 production is located upstream of the cytokine cascade activated by histamine.	Histamine	178-187	caspase 1	Homo sapiens	137-146
10840014-9	2000	Moreover, we found that the interleukin 1beta-converting enzyme (ICE)/CED-3 family protease (caspase-3) became activated in high glucose-induced apoptosis.	Glucose	129-136	caspase 1	Homo sapiens	65-68
10811013-5	2000	After DMSO treatment, bak, bcl-w, bfl-1, fas, and caspases 1 and 9 were up-regulated, whereas bik, bcl-2, and caspases 2, 3, and 10 were down-regulated at different degrees, achieving mRNA expression levels that correlated with those detected in peripheral blood neutrophils.	Dimethyl Sulfoxide	6-10	caspase 1	Homo sapiens	50-66
10828965-1	2000	We have synthesized (acyloxy)methyl ketone inactivators of papain, cathepsin B, and interleukin-1beta conversion enzyme (ICE) that interact with both the S and S" subsites.	(acyloxy)methyl ketone	20-42	caspase 1	Homo sapiens	121-124
10799503-0	2000	The prodomain of caspase-1 enhances Fas-mediated apoptosis through facilitation of caspase-8 activation.	ammonium ferrous sulfate	36-39	caspase 1	Homo sapiens	17-26
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 1	Homo sapiens	215-224
10799869-1	2000	We report that potassium leakage from cells leads to activation of the Ca2+-independent phospholipase A2 (iPLA2), and the latter plays a pivotal role in regulating the cleavage of pro-IL-1 beta by the IL-converting enzyme caspase-1 in human monocytes.	Potassium	15-24	caspase 1	Homo sapiens	222-231
10752932-8	2000	The activities of interleukin-1beta-converting enzyme (ICE) and CPP32 proteases for cells cultured with 10 microg/ml cholestanol were significantly higher than those observed in control cells.	Cholestanol	117-128	caspase 1	Homo sapiens	18-53
10937621-6	2000	In all cases, the irreversible nonselective caspase inhibitor, Z-VAD-FMK, and the caspase-3-selective inhibitor, Ac-DMQD-CHO, inhibited DEVDase activity and apoptosis, whereas the caspase-1-selective inhibitor, Ac-YVAD-CHO, had no effect.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	63-72	caspase 1	Homo sapiens	180-189
10806046-0	2000	Diacerhein and rhein reduce the ICE-induced IL-1beta and IL-18 activation in human osteoarthritic cartilage.	diacerein	0-10	caspase 1	Homo sapiens	32-35
10752932-8	2000	The activities of interleukin-1beta-converting enzyme (ICE) and CPP32 proteases for cells cultured with 10 microg/ml cholestanol were significantly higher than those observed in control cells.	Cholestanol	117-128	caspase 1	Homo sapiens	55-58
10713065-3	2000	Staurosporine treatment caused time- and concentration-dependent increases in the activities of caspase-3 and caspase-9 but not caspase-1, increased proteolysis of poly(ADP-ribose) polymerase, and induced morphological changes consistent with apoptosis.	Staurosporine	0-13	caspase 1	Homo sapiens	128-137
10745077-2	2000	The breakdown of cellular proteins in apoptosis is mediated by caspases, which comprise a highly conserved family of cysteine proteases with specificity for aspartic acid residues at the P1 positions of their substrates.	Aspartic Acid	157-170	caspase 1	Homo sapiens	63-71
10706869-4	2000	The synthetic caspase inhibitors, N-benzyloxycarbonyl-Val-Ala-Asp-fluoromethyl ketone (Z-VAD-FMK) and N-benzyloxycarbonyl-Asp-glu-Val-Asp-fluoromethyl ketone (Z-DEVD-FMK), effectively blocked apoptosis of Jurkat cells co-incubated with SCCHN cell lines, suggesting the involvement of caspases in tumor-induced apoptosis of lymphocytes.	Z-Asp-Glu-Val-Asp-FMK	102-157	caspase 1	Homo sapiens	284-292
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 1	Homo sapiens	40-49
10897390-7	2000	These effects of Fas-activation on the HSF1/hsp70 stress response were blocked by ICE (caspase 1)-inhibitors, suggesting an ICE-mediated process.	ammonium ferrous sulfate	17-20	caspase 1	Homo sapiens	82-85
10728920-5	2000	Treatment of lovastatin caused a rapid release of mitochondrial cytochrome c into cytosol and subsequent induction of caspase-3, but not caspase-1 activity.	Lovastatin	13-23	caspase 1	Homo sapiens	137-146
10617636-4	2000	The H2B was phosphorylated around the time when nucleosomal DNA fragmentation was initiated and, like this fragmentation, was completely blocked with Z-Asp-CH(2)-DCB, an inhibitor of ICE or ICE-like caspase.	benzyloxycarbonyl-Asp-CH2OC(O)-2,6-dichlorobenzene	150-165	caspase 1	Homo sapiens	183-186
10617636-4	2000	The H2B was phosphorylated around the time when nucleosomal DNA fragmentation was initiated and, like this fragmentation, was completely blocked with Z-Asp-CH(2)-DCB, an inhibitor of ICE or ICE-like caspase.	benzyloxycarbonyl-Asp-CH2OC(O)-2,6-dichlorobenzene	150-165	caspase 1	Homo sapiens	190-193
10897390-7	2000	These effects of Fas-activation on the HSF1/hsp70 stress response were blocked by ICE (caspase 1)-inhibitors, suggesting an ICE-mediated process.	ammonium ferrous sulfate	17-20	caspase 1	Homo sapiens	87-96
10897390-7	2000	These effects of Fas-activation on the HSF1/hsp70 stress response were blocked by ICE (caspase 1)-inhibitors, suggesting an ICE-mediated process.	ammonium ferrous sulfate	17-20	caspase 1	Homo sapiens	124-127
10821442-1	2000	The activities of caspase-1 and caspase-3 were measured by use of fluoropeptides as substrates for the first time in the brain (substantia nigra, caudate nucleus, putamen, cerebellum, and frontal cortex) from control and parkinsonian patients.	fluoropeptides	66-80	caspase 1	Homo sapiens	18-27
10663637-16	2000	These analyses revealed that only CDDP induced apoptosis of HOS cells via activation of caspases.	Cisplatin	34-38	caspase 1	Homo sapiens	88-96
10663637-19	2000	CONCLUSIONS: This study demonstrates that CDDP specifically induces apoptosis via activation of caspases and the other anticancer drugs induce death of HOS cells via different signaling pathways.	Cisplatin	42-46	caspase 1	Homo sapiens	96-104
10652190-7	2000	Pretreatment of ventricular myocytes with the peptide-caspase inhibitor known to block caspases related to caspase 1 (Ac-YVAD-CHO) attenuated cytochrome c release, processing of caspase 3, and apoptosis.	L 709049	118-129	caspase 1	Homo sapiens	87-95
10652190-7	2000	Pretreatment of ventricular myocytes with the peptide-caspase inhibitor known to block caspases related to caspase 1 (Ac-YVAD-CHO) attenuated cytochrome c release, processing of caspase 3, and apoptosis.	L 709049	118-129	caspase 1	Homo sapiens	107-116
10630370-6	1999	These results suggest that Tanshione II-A induced HL60 and K562 cellular apoptosis that may be associated with the selective members of caspase family.	tanshione ii-a	27-41	caspase 1	Homo sapiens	136-143
10652190-8	2000	While the caspase inhibitor (Ac-DEVD-CHO) which blocks caspases related to caspase 3, suppressed the cleavage of PARP and apoptosis, it had no effect on cytochrome c release by mitochondria.	acetyl-aspartyl-glutamyl-valyl-aspartal	29-40	caspase 1	Homo sapiens	55-63
11205147-7	2000	Increased levels of proinflammatory cytokines, cytokine receptors and caspase activities, and reduced levels of neurotrophins in the nigrostriatal region in PD patients, and in MPTP- and 6OHDA-produced parkinsonian animals suggest increased immune reactivity and programmed cell death (apoptosis) of neuronal and/or glial cells.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	177-181	caspase 1	Homo sapiens	70-77
10496353-5	1999	An ICE inhibitor, Acetyl-Tyr-Val-Ala-Asp-CHO (YVAD-CHO) blocked IL-1beta-induced growth inhibition in KU-1 and KU-2.	L 709049	18-44	caspase 1	Homo sapiens	3-6
10567499-9	1999	The magnitude of caspase-1 mRNA increase correlated with the number of new (p=0.01) but not persisting gadolinium enhancing brain MRI lesions.	Gadolinium	103-113	caspase 1	Homo sapiens	17-26
10487526-0	1999	Induction of apoptosis by dexrazoxane (ICRF-187) through caspases in the absence of c-jun expression and c-Jun NH2-terminal kinase 1 (JNK1) activation in VM-26-resistant CEM cells.	Dexrazoxane	26-37	caspase 1	Homo sapiens	57-65
10493505-4	1999	Cell cycle analyses revealed that acetyl-Tyr-Val-Ala-Asp-chloromethylketone-specific and acetyl-Ala-Ala-Val-Ala-Leu-Leu-Pro-Ala-Val-Leu-Leu-Ala-Leu-Leu-Ala-Pro-T yr-Val-Ala-Asp-aldehyde-specific cell-permeable inhibitors of ICE significantly reduced the proliferation of AsPC-1 cells, which suggested a positive influence of ICE on the proliferation in human pancreatic carcinoma cells.	N-acetyl-tyrosyl-valyl-alanyl-aspartyl chloromethyl ketone	34-75	caspase 1	Homo sapiens	224-227
10493505-4	1999	Cell cycle analyses revealed that acetyl-Tyr-Val-Ala-Asp-chloromethylketone-specific and acetyl-Ala-Ala-Val-Ala-Leu-Leu-Pro-Ala-Val-Leu-Leu-Ala-Leu-Leu-Ala-Pro-T yr-Val-Ala-Asp-aldehyde-specific cell-permeable inhibitors of ICE significantly reduced the proliferation of AsPC-1 cells, which suggested a positive influence of ICE on the proliferation in human pancreatic carcinoma cells.	N-acetyl-tyrosyl-valyl-alanyl-aspartyl chloromethyl ketone	34-75	caspase 1	Homo sapiens	325-328
10493505-4	1999	Cell cycle analyses revealed that acetyl-Tyr-Val-Ala-Asp-chloromethylketone-specific and acetyl-Ala-Ala-Val-Ala-Leu-Leu-Pro-Ala-Val-Leu-Leu-Ala-Leu-Leu-Ala-Pro-T yr-Val-Ala-Asp-aldehyde-specific cell-permeable inhibitors of ICE significantly reduced the proliferation of AsPC-1 cells, which suggested a positive influence of ICE on the proliferation in human pancreatic carcinoma cells.	acetyl-ala-ala-val-ala-leu-leu-pro-ala-val-leu-leu-ala-leu-leu-ala-pro-t yr-val-ala-asp-aldehyde	89-185	caspase 1	Homo sapiens	224-227
10601248-0	1999	ATP treatment of human monocytes promotes caspase-1 maturation and externalization.	Adenosine Triphosphate	0-3	caspase 1	Homo sapiens	42-51
10601248-2	1999	In this study, we demonstrate that mature caspase-1 subunits are produced when human monocytes are treated with ATP and, like mature IL-1beta, are released extracellularly.	Adenosine Triphosphate	112-115	caspase 1	Homo sapiens	42-51
10601248-5	1999	Two inhibitors of anion transport, glyburide and ethacrynic acid, blocked maturation of both caspase-1 and pro-IL-1beta and prevented release of the propolypeptides.	Glyburide	35-44	caspase 1	Homo sapiens	93-102
10601248-5	1999	Two inhibitors of anion transport, glyburide and ethacrynic acid, blocked maturation of both caspase-1 and pro-IL-1beta and prevented release of the propolypeptides.	Ethacrynic Acid	49-64	caspase 1	Homo sapiens	93-102
10496353-5	1999	An ICE inhibitor, Acetyl-Tyr-Val-Ala-Asp-CHO (YVAD-CHO) blocked IL-1beta-induced growth inhibition in KU-1 and KU-2.	tyrosyl-valyl-alanyl-aspartal	46-54	caspase 1	Homo sapiens	3-6
10521575-4	1999	The temporal profile of p53, c-Myc, Bcl-2, Bax expression and caspases activation after glutamate treatment suggest that Bcl-2, c-Myc and caspase-3 play important roles in the excitotoxic neuronal cell death.	Glutamic Acid	88-97	caspase 1	Homo sapiens	62-70
10551732-4	1999	The susceptibility of PBMCs to apoptosis was markedly decreased after ritonavir treatment and correlated with lower levels of caspase-1 expression, decreases in annexin V staining, and reduced caspase-3 activity.	Ritonavir	70-79	caspase 1	Homo sapiens	126-135
10438532-5	1999	The apoptotic effect of TNF-alpha in HL-60 and the transfectants was abrogated by fumonisin, an inhibitor of ceramide generation, and by the peptide Ac-YVAD-BoMK, an inhibitor of caspase-1 and -4.	ac-yvad-bomk	149-161	caspase 1	Homo sapiens	179-195
10438532-6	1999	Supplementing HL-525 cells with exogenous ceramides bypassed the PKC-beta deficiency and induced apoptosis, which was also restrained by the caspase-1 and -4 inhibitor.	Ceramides	42-51	caspase 1	Homo sapiens	141-157
10419894-11	1999	In the presence of ritonavir, CD4(+) T cells from HIV-infected patients showed similar changes in ICE intracellular levels without alteration of Fas expression.	Ritonavir	19-28	caspase 1	Homo sapiens	98-101
10430629-6	1999	Programmed cell death induced by etoposide was specifically blocked by peptides inhibitory for the caspase-1 or caspase-3 subfamilies of caspases.	Etoposide	33-42	caspase 1	Homo sapiens	99-108
10430629-6	1999	Programmed cell death induced by etoposide was specifically blocked by peptides inhibitory for the caspase-1 or caspase-3 subfamilies of caspases.	Etoposide	33-42	caspase 1	Homo sapiens	137-145
10634172-6	1999	Caspase-1-like specific activity was detected early and transiently at approximately 15 min, followed by a gradual increase in caspase-3-like-specific activity peaking at 2 h. When the broad-spectrum caspase inhibitor, Z-VAD.FMK, was included in the MDS BM aspirate 4 h culture, apoptosis was attenuated.	z-vad	219-224	caspase 1	Homo sapiens	0-9
10448599-0	1999	Modulatory in vitro effects of interleukin-1 receptor antagonist (IL-1Ra) or antisense oligonucleotide to interleukin-1 beta converting enzyme (ICE) on acute myeloid leukaemia (AML) cell growth.	Oligonucleotides	87-102	caspase 1	Homo sapiens	144-147
10388534-3	1999	In this study, we demonstrate that singlet oxygen induced caspase-3 activation and Z-DEVD-FMK, a caspase-3 inhibitor, blocked apoptosis induction, while caspase-1 activity was not detectable and the caspase-1 inhibitor Z-YVAD-FMK had a very limited effect on apoptosis.	Singlet Oxygen	35-49	caspase 1	Homo sapiens	199-208
10388534-3	1999	In this study, we demonstrate that singlet oxygen induced caspase-3 activation and Z-DEVD-FMK, a caspase-3 inhibitor, blocked apoptosis induction, while caspase-1 activity was not detectable and the caspase-1 inhibitor Z-YVAD-FMK had a very limited effect on apoptosis.	benzyloxycarbonyltyrosyl-valyl-alanyl-aspartic acid fluoromethyl ketone	219-229	caspase 1	Homo sapiens	199-208
10394958-7	1999	Ice and Ced-3 homolog (ICH-1L) expression was significantly lower in PC-9/CDDP and was up-regulated by S-1452 or ONO-NT-126.	Cisplatin	74-78	caspase 1	Homo sapiens	0-3
10394958-7	1999	Ice and Ced-3 homolog (ICH-1L) expression was significantly lower in PC-9/CDDP and was up-regulated by S-1452 or ONO-NT-126.	ono-nt	113-119	caspase 1	Homo sapiens	0-3
10375546-9	1999	In Cos-7 cells, caspase-1 and caspase-3 substrates were cleaved upon induction of apoptosis with staurosporine, a protein-kinase inhibitor, whereas caspase-3 but not caspase-1 substrate was cleaved upon treatment of cells with the DNA-damaging agent mitomycin c.	Staurosporine	97-110	caspase 1	Homo sapiens	16-25
10375546-9	1999	In Cos-7 cells, caspase-1 and caspase-3 substrates were cleaved upon induction of apoptosis with staurosporine, a protein-kinase inhibitor, whereas caspase-3 but not caspase-1 substrate was cleaved upon treatment of cells with the DNA-damaging agent mitomycin c.	Mitomycin	250-261	caspase 1	Homo sapiens	16-25
10892568-7	1999	The interleukin-1 converting enzyme (ICE) inhibitor z-VAD-fmk reduced apoptosis for low-, medium- and high-expressing constructs, whereas the CPP-32 inhibitor z-DEVD-fmk had no effect.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	52-61	caspase 1	Homo sapiens	4-35
10892568-7	1999	The interleukin-1 converting enzyme (ICE) inhibitor z-VAD-fmk reduced apoptosis for low-, medium- and high-expressing constructs, whereas the CPP-32 inhibitor z-DEVD-fmk had no effect.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	52-61	caspase 1	Homo sapiens	37-40
10448599-3	1999	To evaluate the involvement of IL-1 beta converting enzyme (ICE) in the autonomous AML cell growth, the effects of an antisense oligonucleotide on ICE were examined in 19 of these patients.	Oligonucleotides	128-143	caspase 1	Homo sapiens	147-150
10344216-1	1999	BACKGROUND: Caspases are a family of cysteine proteases capable of characteristically cleaving after an aspartic acid residue.	Aspartic Acid	104-117	caspase 1	Homo sapiens	12-20
10381635-8	1999	The cell permeable tripeptide inhibitor of ICE family cysteine proteases, zVAD-fmk, suppressed Mn2+-induced apoptosis.	tripeptide K-26	19-29	caspase 1	Homo sapiens	43-46
10323451-7	1999	Analysis of the involvement of the caspase cascade revealed that the cytotoxic activity of c-myc AS ODN was completely blocked by inhibitors of both caspase 1 (YVAD-FMK) and caspase 3 (DEVD-FMK).	tyrosyl-valyl-alanyl-aspartic acid fluoromethyl ketone	160-168	caspase 1	Homo sapiens	149-158
10381635-8	1999	The cell permeable tripeptide inhibitor of ICE family cysteine proteases, zVAD-fmk, suppressed Mn2+-induced apoptosis.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	74-82	caspase 1	Homo sapiens	43-46
10381635-8	1999	The cell permeable tripeptide inhibitor of ICE family cysteine proteases, zVAD-fmk, suppressed Mn2+-induced apoptosis.	Manganese(2+)	95-99	caspase 1	Homo sapiens	43-46
10381635-9	1999	Furthermore, Mn2+ triggered the activation of interleukin-1beta converting enzyme (ICE/caspase 1), followed by the activation of CPP32/Yama/Apopain/caspase-3.	Manganese(2+)	13-17	caspase 1	Homo sapiens	83-86
10381635-9	1999	Furthermore, Mn2+ triggered the activation of interleukin-1beta converting enzyme (ICE/caspase 1), followed by the activation of CPP32/Yama/Apopain/caspase-3.	Manganese(2+)	13-17	caspase 1	Homo sapiens	87-96
10382944-0	1999	Arsenic trioxide induces apoptosis of myeloid leukemia cells by activation of caspases.	Arsenic Trioxide	0-16	caspase 1	Homo sapiens	78-86
10233770-6	1999	SB203580 pretreatment prevented activation of caspase-3 and caspase-1, and also suppressed the cleavage of poly(ADP) ribose polymerase.	SB 203580	0-8	caspase 1	Homo sapiens	60-69
10103059-9	1999	The time course of SP1 cleavage during anti-IgM-induced apoptosis is paralleled by an increase of caspase activity measured by DEVD-p-nitroanilide (DEVD-pNA) cleavage.	devd-p-nitroanilide	127-146	caspase 1	Homo sapiens	98-105
10103059-9	1999	The time course of SP1 cleavage during anti-IgM-induced apoptosis is paralleled by an increase of caspase activity measured by DEVD-p-nitroanilide (DEVD-pNA) cleavage.	aspartyl-glutamyl-valyl-aspartyl-p-nitroanilide	148-156	caspase 1	Homo sapiens	98-105
10549166-0	1999	Induction of apoptosis in AK-5 cells by rotenone involves participation of caspases.	Rotenone	40-48	caspase 1	Homo sapiens	75-83
10082131-8	1999	However, only Z-Asp, not specific caspase inhibitors (Z-DEVD for caspase 3, Z-YVAD for caspase 1), was effective in the suppression of cell spreading.	benzyloxycarbonyl-asparagine	14-19	caspase 1	Homo sapiens	87-96
10353641-0	1999	A catalytic mechanism for caspase-1 and for bimodal inhibition of caspase-1 by activated aspartic ketones.	aspartic ketones	89-105	caspase 1	Homo sapiens	26-35
10353641-0	1999	A catalytic mechanism for caspase-1 and for bimodal inhibition of caspase-1 by activated aspartic ketones.	aspartic ketones	89-105	caspase 1	Homo sapiens	66-75
10353641-4	1999	We have examined 22 crystallographic structures of caspase-1 complexed as a thiohemiketal with the inhibitors from 8 different ketone classes, and found the Cys285S-C-C(alpha)-leaving group dihedral angle to be near either to 60 degrees or to 180 degrees.	Ketones	127-133	caspase 1	Homo sapiens	51-60
10353641-4	1999	We have examined 22 crystallographic structures of caspase-1 complexed as a thiohemiketal with the inhibitors from 8 different ketone classes, and found the Cys285S-C-C(alpha)-leaving group dihedral angle to be near either to 60 degrees or to 180 degrees.	cys285s	157-164	caspase 1	Homo sapiens	51-60
10353641-7	1999	We therefore propose a proteolytic mechanism for caspase-1 involving polarization of the scissile carbonyl by the His237 imidazolium group.	imidazolium	121-132	caspase 1	Homo sapiens	49-58
10234300-3	1999	These findings suggest that DNA fragmentation was inhibited through maintenance of delta psi m. Z-Asp-CH2-DCB, interleukin-1 beta-converting enzyme (ICE) specific inhibitor, inhibited ETP-induced DNA fragmentation and delta psi m reduction in U937 cells.	benzyloxycarbonyl-Asp-CH2OC(O)-2,6-dichlorobenzene	96-109	caspase 1	Homo sapiens	111-147
10234300-3	1999	These findings suggest that DNA fragmentation was inhibited through maintenance of delta psi m. Z-Asp-CH2-DCB, interleukin-1 beta-converting enzyme (ICE) specific inhibitor, inhibited ETP-induced DNA fragmentation and delta psi m reduction in U937 cells.	benzyloxycarbonyl-Asp-CH2OC(O)-2,6-dichlorobenzene	96-109	caspase 1	Homo sapiens	149-152
10234300-3	1999	These findings suggest that DNA fragmentation was inhibited through maintenance of delta psi m. Z-Asp-CH2-DCB, interleukin-1 beta-converting enzyme (ICE) specific inhibitor, inhibited ETP-induced DNA fragmentation and delta psi m reduction in U937 cells.	Etoposide	184-187	caspase 1	Homo sapiens	111-147
10234300-3	1999	These findings suggest that DNA fragmentation was inhibited through maintenance of delta psi m. Z-Asp-CH2-DCB, interleukin-1 beta-converting enzyme (ICE) specific inhibitor, inhibited ETP-induced DNA fragmentation and delta psi m reduction in U937 cells.	Etoposide	184-187	caspase 1	Homo sapiens	149-152
10382944-1	1999	The primary objective of this study was to determine whether caspases are involved in arsenic trioxide(ATO)-induced apoptosis of human myeloid leukemia cells.	Arsenic Trioxide	86-102	caspase 1	Homo sapiens	61-69
10382944-1	1999	The primary objective of this study was to determine whether caspases are involved in arsenic trioxide(ATO)-induced apoptosis of human myeloid leukemia cells.	ato	103-106	caspase 1	Homo sapiens	61-69
10382944-9	1999	We conclude that in cultured myeloid leukemia cells ATO-induced apoptosis is executed by caspases from the distal, PARP-cleaving part of the activation cascade and that PKC activation has no effect on apoptosis induced by either ATO or VP-16 in these cells.	ato	52-55	caspase 1	Homo sapiens	89-97
10085120-4	1999	The caspase inhibitors benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone (zVAD-fmk) and benzyloxycarbonyl-Asp-Glu-Val-Asp-fluoromethylketone (zDEVD-fmk) protect cells against apoptosis and inhibit DEVD-specific caspase activity and PARP cleavage without affecting JNK1 and p38 MAPK activations.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	73-81	caspase 1	Homo sapiens	4-11
10085120-4	1999	The caspase inhibitors benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone (zVAD-fmk) and benzyloxycarbonyl-Asp-Glu-Val-Asp-fluoromethylketone (zDEVD-fmk) protect cells against apoptosis and inhibit DEVD-specific caspase activity and PARP cleavage without affecting JNK1 and p38 MAPK activations.	benzyloxycarbonyl-asp-glu-val-asp-fluoromethylketone	87-139	caspase 1	Homo sapiens	4-11
10085120-4	1999	The caspase inhibitors benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone (zVAD-fmk) and benzyloxycarbonyl-Asp-Glu-Val-Asp-fluoromethylketone (zDEVD-fmk) protect cells against apoptosis and inhibit DEVD-specific caspase activity and PARP cleavage without affecting JNK1 and p38 MAPK activations.	Caspase Inhibitor VI	23-71	caspase 1	Homo sapiens	4-11
10085120-4	1999	The caspase inhibitors benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone (zVAD-fmk) and benzyloxycarbonyl-Asp-Glu-Val-Asp-fluoromethylketone (zDEVD-fmk) protect cells against apoptosis and inhibit DEVD-specific caspase activity and PARP cleavage without affecting JNK1 and p38 MAPK activations.	Caspase Inhibitor VI	23-71	caspase 1	Homo sapiens	210-217
10085120-4	1999	The caspase inhibitors benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone (zVAD-fmk) and benzyloxycarbonyl-Asp-Glu-Val-Asp-fluoromethylketone (zDEVD-fmk) protect cells against apoptosis and inhibit DEVD-specific caspase activity and PARP cleavage without affecting JNK1 and p38 MAPK activations.	benzyloxycarbonyl-asp-glu-val-asp-fluoromethylketone	87-139	caspase 1	Homo sapiens	210-217
10085120-4	1999	The caspase inhibitors benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone (zVAD-fmk) and benzyloxycarbonyl-Asp-Glu-Val-Asp-fluoromethylketone (zDEVD-fmk) protect cells against apoptosis and inhibit DEVD-specific caspase activity and PARP cleavage without affecting JNK1 and p38 MAPK activations.	benzoylcarbonyl-aspartyl-glutamyl-valyl-aspartyl-fluoromethyl ketone	141-150	caspase 1	Homo sapiens	4-11
10218585-3	1999	We observed that extracellular ATP induced the activation of multiple caspases including caspase-1, -3 and -8, and subsequent cleavage of the caspase substrates PARP and lamin B.	Adenosine Triphosphate	31-34	caspase 1	Homo sapiens	70-78
10218585-3	1999	We observed that extracellular ATP induced the activation of multiple caspases including caspase-1, -3 and -8, and subsequent cleavage of the caspase substrates PARP and lamin B.	Adenosine Triphosphate	31-34	caspase 1	Homo sapiens	89-109
10218585-3	1999	We observed that extracellular ATP induced the activation of multiple caspases including caspase-1, -3 and -8, and subsequent cleavage of the caspase substrates PARP and lamin B.	Adenosine Triphosphate	31-34	caspase 1	Homo sapiens	70-77
10218585-4	1999	Using caspase inhibitors, it was found that caspases were specifically involved in ATP-induced apoptotic damage such as chromatin condensation and DNA fragmentation.	Adenosine Triphosphate	83-86	caspase 1	Homo sapiens	6-13
10218585-4	1999	Using caspase inhibitors, it was found that caspases were specifically involved in ATP-induced apoptotic damage such as chromatin condensation and DNA fragmentation.	Adenosine Triphosphate	83-86	caspase 1	Homo sapiens	44-52
10218585-6	1999	Our results therefore suggest that the activation of caspases by the P2Z receptor is required for apoptotic but not necrotic alterations of ATP-induced cell death.	Adenosine Triphosphate	140-143	caspase 1	Homo sapiens	53-61
10096572-11	1999	This TGF-beta1-mediated apoptosis induction in TbetaRII transfectant cells was significantly protected by the caspase-1 inhibitor (zVAD-fmk) in a dose-dependent manner.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	131-139	caspase 1	Homo sapiens	110-119
10051653-9	1999	Functional inhibition of caspase-1 activity by acetyl-Tyr-Val-Ala-Asp-chloromethyl ketone blocks macrophage cytotoxicity, and macrophages lacking caspase-1 are not susceptible to Salmonella-induced apoptosis.	N-acetyl-tyrosyl-valyl-alanyl-aspartyl chloromethyl ketone	47-89	caspase 1	Homo sapiens	25-34
10066446-8	1999	As activities of interleukin-1beta-converting enzyme (ICE) and CPP32 protease were increased in cells cultured with cholestanol, all these data taken together suggest that cholestanol induced apoptosis of cerebellar neuronal cells.	Cholestanol	116-127	caspase 1	Homo sapiens	17-52
10066446-8	1999	As activities of interleukin-1beta-converting enzyme (ICE) and CPP32 protease were increased in cells cultured with cholestanol, all these data taken together suggest that cholestanol induced apoptosis of cerebellar neuronal cells.	Cholestanol	116-127	caspase 1	Homo sapiens	54-57
10066446-8	1999	As activities of interleukin-1beta-converting enzyme (ICE) and CPP32 protease were increased in cells cultured with cholestanol, all these data taken together suggest that cholestanol induced apoptosis of cerebellar neuronal cells.	Cholestanol	172-183	caspase 1	Homo sapiens	17-52
10066446-8	1999	As activities of interleukin-1beta-converting enzyme (ICE) and CPP32 protease were increased in cells cultured with cholestanol, all these data taken together suggest that cholestanol induced apoptosis of cerebellar neuronal cells.	Cholestanol	172-183	caspase 1	Homo sapiens	54-57
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.	acetyl-aspartyl-glutamyl-valyl-aspartal	57-68	caspase 1	Homo sapiens	213-222
10092779-8	1999	We could successfully block the activation-induced cell death with z-VAD-fmk, a tripeptide inhibitor of IL-1 beta-converting enzyme homologues, or with anti-Fas mAbs.	tripeptide K-26	80-90	caspase 1	Homo sapiens	104-131
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 1	Homo sapiens	213-222
10200574-7	1999	Furthermore, we have provided evidence that while caspase 3 is activated by both inducers, caspase 1 is essential only for the etoposide-induced apoptosis.	Etoposide	127-136	caspase 1	Homo sapiens	91-100
10051540-4	1999	Treatment of CEM cells with apoptosis-inducing concentrations of merbarone caused activation of c-Jun NH2-terminal kinase/stress-activated protein kinase, c-jun gene induction, activation of caspase-3/CPP32-like protease but not caspase-1, and the proteolytic cleavage of poly(ADP-ribose) polymerase.	merbarone	65-74	caspase 1	Homo sapiens	229-238
10217178-6	1999	We also report a hitherto unrecognized feature of an anti-PARP antiserum, VIC-5, detecting both the 89 kDa and the 24 kDa caspase-generated fragments of PARP.	vic-5	74-79	caspase 1	Homo sapiens	122-129
10224675-7	1999	The formation of 65-72 kDa beta-catenin cleavage fragments was completely prevented by a caspase-1 inhibitor Z-VAD-CH2F and a caspase-3 inhibitor Z-DEVD-CH2F, indicating that the cleavage is associated with caspase-dependent process.	benzyloxycarbonyl-valyl-alanyl-aspartyl-fluoromethane	109-119	caspase 1	Homo sapiens	89-98
10026138-1	1999	Apoptosis was induced in human glioma cell lines by exposure to 100 nM calphostin C, a specific inhibitor of protein kinase C. Calphostin C-induced apoptosis was associated with synchronous down-regulation of Bcl-2 and Bcl-xL as well as activation of caspase-3 but not caspase-1.	calphostin C	71-83	caspase 1	Homo sapiens	269-278
10026138-1	1999	Apoptosis was induced in human glioma cell lines by exposure to 100 nM calphostin C, a specific inhibitor of protein kinase C. Calphostin C-induced apoptosis was associated with synchronous down-regulation of Bcl-2 and Bcl-xL as well as activation of caspase-3 but not caspase-1.	calphostin C	127-139	caspase 1	Homo sapiens	269-278
9931312-7	1999	Additionally, we found that sphingosine-induced apoptosis was accompanied by activation of caspases.	Sphingosine	28-39	caspase 1	Homo sapiens	91-99
10047465-5	1999	In addition, p38 activation is dependent upon the activation of the caspase system since p38 activation is blocked by the pan ICE inhibitor Z-VAD fmk, which also inhibits CD437-mediated apoptosis and PARP cleavage in these cells.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	140-149	caspase 1	Homo sapiens	68-75
10047465-5	1999	In addition, p38 activation is dependent upon the activation of the caspase system since p38 activation is blocked by the pan ICE inhibitor Z-VAD fmk, which also inhibits CD437-mediated apoptosis and PARP cleavage in these cells.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	140-149	caspase 1	Homo sapiens	126-129
10047465-5	1999	In addition, p38 activation is dependent upon the activation of the caspase system since p38 activation is blocked by the pan ICE inhibitor Z-VAD fmk, which also inhibits CD437-mediated apoptosis and PARP cleavage in these cells.	CD 437	171-176	caspase 1	Homo sapiens	68-75
10047465-5	1999	In addition, p38 activation is dependent upon the activation of the caspase system since p38 activation is blocked by the pan ICE inhibitor Z-VAD fmk, which also inhibits CD437-mediated apoptosis and PARP cleavage in these cells.	CD 437	171-176	caspase 1	Homo sapiens	126-129
10047465-6	1999	CD437-mediated activation of JNK/SAPK is not inhibited by Z-VAD fmk, suggesting that it lies upstream of CD437 activation of caspase activity and subsequent apoptosis.	CD 437	0-5	caspase 1	Homo sapiens	125-132
9931312-9	1999	The general caspase inhibitor benzyloxycarbonyl-Val-Ala-Asp fluoromethyl ketone, which exhibits a broad specificity for caspase-family proteases, effectively blocked sphingosine-induced apoptosis.	Caspase Inhibitor VI	30-79	caspase 1	Homo sapiens	12-19
9931312-9	1999	The general caspase inhibitor benzyloxycarbonyl-Val-Ala-Asp fluoromethyl ketone, which exhibits a broad specificity for caspase-family proteases, effectively blocked sphingosine-induced apoptosis.	Sphingosine	166-177	caspase 1	Homo sapiens	12-19
9925765-5	1999	Using various peptide-based caspase inhibitors, our results showed that N-acetyl-Tyr-Val-Ala-Asp chloromethyl ketone and benzyloxycarbonyl-Val-Ala-Asp (OMe) fluoromethyl ketone efficiently blocked Fas-mediated apoptosis in Jurkat T cells, whereas N-acetyl-Tyr-Val-Ala-Asp aldehyde, which is more specific for caspase-1, had little effect.	N-acetyl-tyrosyl-valyl-alanyl-aspartyl chloromethyl ketone	72-116	caspase 1	Homo sapiens	28-35
9986707-4	1999	All the compounds were modeled using the X-ray crystal structure of tetrapeptide aldehyde inhibitor/ICE complex.	Aldehydes	81-89	caspase 1	Homo sapiens	100-103
14634294-5	1999	By using the tetrapeptidic sequence recognized by caspase-3 (DEVD-AMC) or by caspase-1 (YVAD-AMC) linked to fluorogenic substrate, we also demonstrated that only the DEVD sequence was recognized and cleaved after drug treatment, while no significant changes were found for YVAD peptides.	yvad-amc	88-96	caspase 1	Homo sapiens	77-86
9925765-5	1999	Using various peptide-based caspase inhibitors, our results showed that N-acetyl-Tyr-Val-Ala-Asp chloromethyl ketone and benzyloxycarbonyl-Val-Ala-Asp (OMe) fluoromethyl ketone efficiently blocked Fas-mediated apoptosis in Jurkat T cells, whereas N-acetyl-Tyr-Val-Ala-Asp aldehyde, which is more specific for caspase-1, had little effect.	N-acetyl-tyrosyl-valyl-alanyl-aspartyl chloromethyl ketone	72-116	caspase 1	Homo sapiens	309-318
9925765-5	1999	Using various peptide-based caspase inhibitors, our results showed that N-acetyl-Tyr-Val-Ala-Asp chloromethyl ketone and benzyloxycarbonyl-Val-Ala-Asp (OMe) fluoromethyl ketone efficiently blocked Fas-mediated apoptosis in Jurkat T cells, whereas N-acetyl-Tyr-Val-Ala-Asp aldehyde, which is more specific for caspase-1, had little effect.	val-ala-asp (ome) fluoromethyl ketone	139-176	caspase 1	Homo sapiens	28-35
9925765-5	1999	Using various peptide-based caspase inhibitors, our results showed that N-acetyl-Tyr-Val-Ala-Asp chloromethyl ketone and benzyloxycarbonyl-Val-Ala-Asp (OMe) fluoromethyl ketone efficiently blocked Fas-mediated apoptosis in Jurkat T cells, whereas N-acetyl-Tyr-Val-Ala-Asp aldehyde, which is more specific for caspase-1, had little effect.	val-ala-asp (ome) fluoromethyl ketone	139-176	caspase 1	Homo sapiens	309-318
9925765-5	1999	Using various peptide-based caspase inhibitors, our results showed that N-acetyl-Tyr-Val-Ala-Asp chloromethyl ketone and benzyloxycarbonyl-Val-Ala-Asp (OMe) fluoromethyl ketone efficiently blocked Fas-mediated apoptosis in Jurkat T cells, whereas N-acetyl-Tyr-Val-Ala-Asp aldehyde, which is more specific for caspase-1, had little effect.	ammonium ferrous sulfate	197-200	caspase 1	Homo sapiens	28-35
9925765-5	1999	Using various peptide-based caspase inhibitors, our results showed that N-acetyl-Tyr-Val-Ala-Asp chloromethyl ketone and benzyloxycarbonyl-Val-Ala-Asp (OMe) fluoromethyl ketone efficiently blocked Fas-mediated apoptosis in Jurkat T cells, whereas N-acetyl-Tyr-Val-Ala-Asp aldehyde, which is more specific for caspase-1, had little effect.	L 709049	247-280	caspase 1	Homo sapiens	28-35
10022509-3	1999	We found that benzyloxycarbonyl-VAD-fluoromethylketone, a general caspase inhibitor, inhibits didemnin B-induced apoptosis in HL-60 and Daudi cells.	benzyloxycarbonyl-vad-fluoromethylketone	14-54	caspase 1	Homo sapiens	66-73
9990127-12	1999	On the other hand, the ac-YVAD-aldehyde tetrapeptide inhibitor that is dominantly effective on interleukin-1beta converting enzyme failed to block the apoptotic event initiated by LAO.	ac-yvad	23-30	caspase 1	Homo sapiens	95-130
9990127-12	1999	On the other hand, the ac-YVAD-aldehyde tetrapeptide inhibitor that is dominantly effective on interleukin-1beta converting enzyme failed to block the apoptotic event initiated by LAO.	Aldehydes	31-39	caspase 1	Homo sapiens	95-130
10205784-6	1999	The activation of caspases can be inhibited by several molecules, including peptide aldehydes (caspase-1 and or caspase-3 inhibitors) and crmA that target the active-site cysteine of caspase family members, Bcl-2, IAP (inhibitor of apoptosis protein) and NAIP (neuronal apoptosis inhibitory protein).	Aldehydes	84-93	caspase 1	Homo sapiens	18-26
9973403-4	1999	The caspase inhibitor peptides, DEVD-CHO, Z-VAD.fmk, and Boc-Asp.fmk, blocked Fas-induced PS externalization, disruption of Deltapsim, and cell death, suggesting that these events are sequelae of caspase activation.	aspartyl-glutamyl-valyl-aspartal	32-40	caspase 1	Homo sapiens	4-11
9973403-4	1999	The caspase inhibitor peptides, DEVD-CHO, Z-VAD.fmk, and Boc-Asp.fmk, blocked Fas-induced PS externalization, disruption of Deltapsim, and cell death, suggesting that these events are sequelae of caspase activation.	z-vad	42-47	caspase 1	Homo sapiens	4-11
9973403-4	1999	The caspase inhibitor peptides, DEVD-CHO, Z-VAD.fmk, and Boc-Asp.fmk, blocked Fas-induced PS externalization, disruption of Deltapsim, and cell death, suggesting that these events are sequelae of caspase activation.	FMK	48-51	caspase 1	Homo sapiens	4-11
9973403-4	1999	The caspase inhibitor peptides, DEVD-CHO, Z-VAD.fmk, and Boc-Asp.fmk, blocked Fas-induced PS externalization, disruption of Deltapsim, and cell death, suggesting that these events are sequelae of caspase activation.	butyloxycarbonyl-aspartyl-fluoromethyl ketone	57-68	caspase 1	Homo sapiens	4-11
9973403-4	1999	The caspase inhibitor peptides, DEVD-CHO, Z-VAD.fmk, and Boc-Asp.fmk, blocked Fas-induced PS externalization, disruption of Deltapsim, and cell death, suggesting that these events are sequelae of caspase activation.	ammonium ferrous sulfate	78-81	caspase 1	Homo sapiens	4-11
10048577-4	1999	These inhibitors were benzyloxycarbonyl (z-) and fluoromethyl-ketone (FMK) derivatives of peptides that serve as substrates for selected caspases.	benzyloxycarbonyl	22-39	caspase 1	Homo sapiens	137-145
10048577-4	1999	These inhibitors were benzyloxycarbonyl (z-) and fluoromethyl-ketone (FMK) derivatives of peptides that serve as substrates for selected caspases.	fluoromethyl-ketone	49-68	caspase 1	Homo sapiens	137-145
10048577-4	1999	These inhibitors were benzyloxycarbonyl (z-) and fluoromethyl-ketone (FMK) derivatives of peptides that serve as substrates for selected caspases.	FMK	70-73	caspase 1	Homo sapiens	137-145
10205784-6	1999	The activation of caspases can be inhibited by several molecules, including peptide aldehydes (caspase-1 and or caspase-3 inhibitors) and crmA that target the active-site cysteine of caspase family members, Bcl-2, IAP (inhibitor of apoptosis protein) and NAIP (neuronal apoptosis inhibitory protein).	Aldehydes	84-93	caspase 1	Homo sapiens	95-104
10205784-6	1999	The activation of caspases can be inhibited by several molecules, including peptide aldehydes (caspase-1 and or caspase-3 inhibitors) and crmA that target the active-site cysteine of caspase family members, Bcl-2, IAP (inhibitor of apoptosis protein) and NAIP (neuronal apoptosis inhibitory protein).	Aldehydes	84-93	caspase 1	Homo sapiens	18-25
10205784-6	1999	The activation of caspases can be inhibited by several molecules, including peptide aldehydes (caspase-1 and or caspase-3 inhibitors) and crmA that target the active-site cysteine of caspase family members, Bcl-2, IAP (inhibitor of apoptosis protein) and NAIP (neuronal apoptosis inhibitory protein).	crma	138-142	caspase 1	Homo sapiens	18-26
10205784-6	1999	The activation of caspases can be inhibited by several molecules, including peptide aldehydes (caspase-1 and or caspase-3 inhibitors) and crmA that target the active-site cysteine of caspase family members, Bcl-2, IAP (inhibitor of apoptosis protein) and NAIP (neuronal apoptosis inhibitory protein).	crma	138-142	caspase 1	Homo sapiens	18-25
10205784-6	1999	The activation of caspases can be inhibited by several molecules, including peptide aldehydes (caspase-1 and or caspase-3 inhibitors) and crmA that target the active-site cysteine of caspase family members, Bcl-2, IAP (inhibitor of apoptosis protein) and NAIP (neuronal apoptosis inhibitory protein).	Cysteine	171-179	caspase 1	Homo sapiens	18-26
10205784-6	1999	The activation of caspases can be inhibited by several molecules, including peptide aldehydes (caspase-1 and or caspase-3 inhibitors) and crmA that target the active-site cysteine of caspase family members, Bcl-2, IAP (inhibitor of apoptosis protein) and NAIP (neuronal apoptosis inhibitory protein).	Cysteine	171-179	caspase 1	Homo sapiens	95-104
10205784-6	1999	The activation of caspases can be inhibited by several molecules, including peptide aldehydes (caspase-1 and or caspase-3 inhibitors) and crmA that target the active-site cysteine of caspase family members, Bcl-2, IAP (inhibitor of apoptosis protein) and NAIP (neuronal apoptosis inhibitory protein).	Cysteine	171-179	caspase 1	Homo sapiens	18-25
10029205-14	1999	The prevention of the ethanol-induced apoptosis by 4-methylpyrazole and by trolox suggests that production of a prooxidative state as a consequence of ethanol oxidation by CYP2E1 results in eventual activation of caspases such as caspases 1 and 3, which can trigger the apoptotic process.	Ethanol	22-29	caspase 1	Homo sapiens	213-221
11819386-2	1999	Expression of ICE in the tumor cells exposed to 5-FU was examined by the immunocytochemical method.RESULTS:The cells treated with 5-FU displayed disappearance of nucleoli, chromatin gathering under nuclear envelope, karyorrhexis, budding and the formation of apoptotic bodies.The expression of ICE was negative in control cells, and 5-FU could induce the ICE expression in Eca-109 cells undergoing apoptosis.	Fluorouracil	48-52	caspase 1	Homo sapiens	14-17
11819386-2	1999	Expression of ICE in the tumor cells exposed to 5-FU was examined by the immunocytochemical method.RESULTS:The cells treated with 5-FU displayed disappearance of nucleoli, chromatin gathering under nuclear envelope, karyorrhexis, budding and the formation of apoptotic bodies.The expression of ICE was negative in control cells, and 5-FU could induce the ICE expression in Eca-109 cells undergoing apoptosis.	Fluorouracil	130-134	caspase 1	Homo sapiens	14-17
11819386-2	1999	Expression of ICE in the tumor cells exposed to 5-FU was examined by the immunocytochemical method.RESULTS:The cells treated with 5-FU displayed disappearance of nucleoli, chromatin gathering under nuclear envelope, karyorrhexis, budding and the formation of apoptotic bodies.The expression of ICE was negative in control cells, and 5-FU could induce the ICE expression in Eca-109 cells undergoing apoptosis.	Fluorouracil	130-134	caspase 1	Homo sapiens	294-297
11819386-2	1999	Expression of ICE in the tumor cells exposed to 5-FU was examined by the immunocytochemical method.RESULTS:The cells treated with 5-FU displayed disappearance of nucleoli, chromatin gathering under nuclear envelope, karyorrhexis, budding and the formation of apoptotic bodies.The expression of ICE was negative in control cells, and 5-FU could induce the ICE expression in Eca-109 cells undergoing apoptosis.	Fluorouracil	130-134	caspase 1	Homo sapiens	294-297
11819386-2	1999	Expression of ICE in the tumor cells exposed to 5-FU was examined by the immunocytochemical method.RESULTS:The cells treated with 5-FU displayed disappearance of nucleoli, chromatin gathering under nuclear envelope, karyorrhexis, budding and the formation of apoptotic bodies.The expression of ICE was negative in control cells, and 5-FU could induce the ICE expression in Eca-109 cells undergoing apoptosis.	Fluorouracil	130-134	caspase 1	Homo sapiens	14-17
11819386-2	1999	Expression of ICE in the tumor cells exposed to 5-FU was examined by the immunocytochemical method.RESULTS:The cells treated with 5-FU displayed disappearance of nucleoli, chromatin gathering under nuclear envelope, karyorrhexis, budding and the formation of apoptotic bodies.The expression of ICE was negative in control cells, and 5-FU could induce the ICE expression in Eca-109 cells undergoing apoptosis.	Fluorouracil	130-134	caspase 1	Homo sapiens	294-297
11819386-2	1999	Expression of ICE in the tumor cells exposed to 5-FU was examined by the immunocytochemical method.RESULTS:The cells treated with 5-FU displayed disappearance of nucleoli, chromatin gathering under nuclear envelope, karyorrhexis, budding and the formation of apoptotic bodies.The expression of ICE was negative in control cells, and 5-FU could induce the ICE expression in Eca-109 cells undergoing apoptosis.	Fluorouracil	130-134	caspase 1	Homo sapiens	294-297
11819386-3	1999	The number and the staining intensity of positive cells increased with the extension of action time.CONCLUSION: 5-FU may induce apoptosis in human esophageal carcinoma Eca-109 cells; ICE gene may be involved in the regulation of 5-FU induced apoptosis; and ICE protein may mediate apoptosis induced by 5-FU.	Fluorouracil	112-116	caspase 1	Homo sapiens	183-186
11819386-3	1999	The number and the staining intensity of positive cells increased with the extension of action time.CONCLUSION: 5-FU may induce apoptosis in human esophageal carcinoma Eca-109 cells; ICE gene may be involved in the regulation of 5-FU induced apoptosis; and ICE protein may mediate apoptosis induced by 5-FU.	Fluorouracil	112-116	caspase 1	Homo sapiens	257-260
11819386-3	1999	The number and the staining intensity of positive cells increased with the extension of action time.CONCLUSION: 5-FU may induce apoptosis in human esophageal carcinoma Eca-109 cells; ICE gene may be involved in the regulation of 5-FU induced apoptosis; and ICE protein may mediate apoptosis induced by 5-FU.	Fluorouracil	229-233	caspase 1	Homo sapiens	183-186
11819386-3	1999	The number and the staining intensity of positive cells increased with the extension of action time.CONCLUSION: 5-FU may induce apoptosis in human esophageal carcinoma Eca-109 cells; ICE gene may be involved in the regulation of 5-FU induced apoptosis; and ICE protein may mediate apoptosis induced by 5-FU.	Fluorouracil	229-233	caspase 1	Homo sapiens	183-186
10029205-9	1999	Ethanol treatment of the cells expressing CYP2E1 resulted in increased activities of caspases 1 and 3.	Ethanol	0-7	caspase 1	Homo sapiens	85-101
10029205-10	1999	An inhibitor of these caspases prevented the ethanol-induced apoptosis in the stable cell lines and the transiently transfected cell lines.	Ethanol	45-52	caspase 1	Homo sapiens	22-30
10029205-14	1999	The prevention of the ethanol-induced apoptosis by 4-methylpyrazole and by trolox suggests that production of a prooxidative state as a consequence of ethanol oxidation by CYP2E1 results in eventual activation of caspases such as caspases 1 and 3, which can trigger the apoptotic process.	Ethanol	22-29	caspase 1	Homo sapiens	230-246
10029205-14	1999	The prevention of the ethanol-induced apoptosis by 4-methylpyrazole and by trolox suggests that production of a prooxidative state as a consequence of ethanol oxidation by CYP2E1 results in eventual activation of caspases such as caspases 1 and 3, which can trigger the apoptotic process.	6-hydroxy-2,5,7,8-tetramethylchroman-2-carboxylic acid	75-81	caspase 1	Homo sapiens	213-221
10029205-14	1999	The prevention of the ethanol-induced apoptosis by 4-methylpyrazole and by trolox suggests that production of a prooxidative state as a consequence of ethanol oxidation by CYP2E1 results in eventual activation of caspases such as caspases 1 and 3, which can trigger the apoptotic process.	6-hydroxy-2,5,7,8-tetramethylchroman-2-carboxylic acid	75-81	caspase 1	Homo sapiens	230-246
10029205-14	1999	The prevention of the ethanol-induced apoptosis by 4-methylpyrazole and by trolox suggests that production of a prooxidative state as a consequence of ethanol oxidation by CYP2E1 results in eventual activation of caspases such as caspases 1 and 3, which can trigger the apoptotic process.	Ethanol	151-158	caspase 1	Homo sapiens	213-221
10029205-14	1999	The prevention of the ethanol-induced apoptosis by 4-methylpyrazole and by trolox suggests that production of a prooxidative state as a consequence of ethanol oxidation by CYP2E1 results in eventual activation of caspases such as caspases 1 and 3, which can trigger the apoptotic process.	Ethanol	151-158	caspase 1	Homo sapiens	230-246
10193575-3	1999	However, which caspases function as executioners in reactive oxygen species (ROS)-induced apoptosis is not known.	Reactive Oxygen Species	52-75	caspase 1	Homo sapiens	15-23
10380358-0	1999	Peptidyl beta-homo-aspartals (3-amino-4-carboxybutyraldehydes): new specific inhibitors of caspases.	3-amino-4-carboxybutyraldehydes	30-61	caspase 1	Homo sapiens	91-99
10380358-4	1999	The most efficient ICE inhibitors are peptide aldehydes and peptidyl chloro or (acyloxy)methanes.	Aldehydes	46-55	caspase 1	Homo sapiens	19-22
10380358-4	1999	The most efficient ICE inhibitors are peptide aldehydes and peptidyl chloro or (acyloxy)methanes.	peptidyl chloro or	60-78	caspase 1	Homo sapiens	19-22
10380358-4	1999	The most efficient ICE inhibitors are peptide aldehydes and peptidyl chloro or (acyloxy)methanes.	(acyloxy)methanes	79-96	caspase 1	Homo sapiens	19-22
10380358-5	1999	A recent study revealed that both D- and L-Asp are accepted by ICE at the P1 of such inhibitors, and the peptidyl (acyloxy)methane analogues having the beta-homo-aspartyl residue [-NH-CH(CH2COOH)-CH2CO-] are inactive.	d- and l-asp	34-46	caspase 1	Homo sapiens	63-66
10380358-11	1999	Here, we analyzed the inhibition of ICE and apopain in comparison with that of papain, thrombin, and trypsin by peptide L/D-alpha-aldehydes and their L-beta-homo-aldehyde [-NH-CH(R)-CH2-CHO] analogues.	alpha-aldehydes	124-139	caspase 1	Homo sapiens	36-39
10193575-3	1999	However, which caspases function as executioners in reactive oxygen species (ROS)-induced apoptosis is not known.	Reactive Oxygen Species	77-80	caspase 1	Homo sapiens	15-23
10193575-4	1999	The present study was performed to identify the major caspases acting in ROS-induced apoptosis.	Reactive Oxygen Species	73-76	caspase 1	Homo sapiens	54-62
10193575-7	1999	Of these caspase inhibitors, only Ac-DEVD-CHO completely blocked morphological changes, caspase-3 subfamily protease activation and DNA ladder formation in H2O2-treated HL-60 cells.	acetyl-aspartyl-glutamyl-valyl-aspartal	34-45	caspase 1	Homo sapiens	9-16
10193575-7	1999	Of these caspase inhibitors, only Ac-DEVD-CHO completely blocked morphological changes, caspase-3 subfamily protease activation and DNA ladder formation in H2O2-treated HL-60 cells.	Hydrogen Peroxide	156-160	caspase 1	Homo sapiens	9-16
9829999-6	1998	The halomethyl ketone benzyloxycarbonyl-VAD fluoromethyl ketone is a broad specificity irreversible caspase inhibitor, with second-order inactivation rates that range from 2.9 x 10(2) M-1 s-1 for caspase-2 to 2.8 x 10(5) M-1 s-1 for caspase-1.	halomethyl ketone	4-21	caspase 1	Homo sapiens	100-107
9886070-2	1999	We report here that caspases are activated during apoptosis by treatment with NOC18, a nitric oxide (NO) donor.	NOC 18	78-83	caspase 1	Homo sapiens	20-28
9886070-2	1999	We report here that caspases are activated during apoptosis by treatment with NOC18, a nitric oxide (NO) donor.	Nitric Oxide	87-99	caspase 1	Homo sapiens	20-28
9829999-6	1998	The halomethyl ketone benzyloxycarbonyl-VAD fluoromethyl ketone is a broad specificity irreversible caspase inhibitor, with second-order inactivation rates that range from 2.9 x 10(2) M-1 s-1 for caspase-2 to 2.8 x 10(5) M-1 s-1 for caspase-1.	halomethyl ketone	4-21	caspase 1	Homo sapiens	233-242
9829999-6	1998	The halomethyl ketone benzyloxycarbonyl-VAD fluoromethyl ketone is a broad specificity irreversible caspase inhibitor, with second-order inactivation rates that range from 2.9 x 10(2) M-1 s-1 for caspase-2 to 2.8 x 10(5) M-1 s-1 for caspase-1.	-vad fluoromethyl ketone	39-63	caspase 1	Homo sapiens	100-107
9829999-6	1998	The halomethyl ketone benzyloxycarbonyl-VAD fluoromethyl ketone is a broad specificity irreversible caspase inhibitor, with second-order inactivation rates that range from 2.9 x 10(2) M-1 s-1 for caspase-2 to 2.8 x 10(5) M-1 s-1 for caspase-1.	-vad fluoromethyl ketone	39-63	caspase 1	Homo sapiens	233-242
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 1	Homo sapiens	96-117
9834227-4	1998	Proteasome inhibitor-induced DNA fragmentation was associated with activation of caspase/ICE family cysteine protease(s) and was blocked by the caspase antagonist, zVADfmk.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	164-171	caspase 1	Homo sapiens	81-88
9834227-4	1998	Proteasome inhibitor-induced DNA fragmentation was associated with activation of caspase/ICE family cysteine protease(s) and was blocked by the caspase antagonist, zVADfmk.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	164-171	caspase 1	Homo sapiens	89-92
9834227-4	1998	Proteasome inhibitor-induced DNA fragmentation was associated with activation of caspase/ICE family cysteine protease(s) and was blocked by the caspase antagonist, zVADfmk.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	164-171	caspase 1	Homo sapiens	144-151
9828101-0	1998	Brefeldin A-mediated apoptosis requires the activation of caspases and is inhibited by Bcl-2.	Brefeldin A	0-11	caspase 1	Homo sapiens	58-66
9856788-4	1998	Whether the specific tetrapeptide ICE inhibitor Ac-YVAD-CMK affected gamma-irradiation-induced apoptosis in tumor cells was also examined.	ac-yvad	48-55	caspase 1	Homo sapiens	34-37
9856788-8	1998	The apoptotic cell death induced by gamma-irradiation was suppressed by the tetrapeptide ICE inhibitor Ac-YVAD-CMK.	ac-yvad	103-110	caspase 1	Homo sapiens	89-92
9862416-3	1998	Under apoptotic conditions the cleavage of poly(ADP-ribose) polymerase (PARP) into the 85-kDa product is blocked by the caspase inhibitors benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone (z-VAD-fmk) and benzyloxycarbonyl-Asp-Glu-Val-Asp-fluoromethylketone (z-DEVD-fmk).	-val-ala-asp-fluoromethylketone	156-187	caspase 1	Homo sapiens	120-127
9862416-3	1998	Under apoptotic conditions the cleavage of poly(ADP-ribose) polymerase (PARP) into the 85-kDa product is blocked by the caspase inhibitors benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone (z-VAD-fmk) and benzyloxycarbonyl-Asp-Glu-Val-Asp-fluoromethylketone (z-DEVD-fmk).	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	189-198	caspase 1	Homo sapiens	120-127
9862416-3	1998	Under apoptotic conditions the cleavage of poly(ADP-ribose) polymerase (PARP) into the 85-kDa product is blocked by the caspase inhibitors benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone (z-VAD-fmk) and benzyloxycarbonyl-Asp-Glu-Val-Asp-fluoromethylketone (z-DEVD-fmk).	benzyloxycarbonyl-asp-glu-val-asp-fluoromethylketone	204-256	caspase 1	Homo sapiens	120-127
9862416-3	1998	Under apoptotic conditions the cleavage of poly(ADP-ribose) polymerase (PARP) into the 85-kDa product is blocked by the caspase inhibitors benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone (z-VAD-fmk) and benzyloxycarbonyl-Asp-Glu-Val-Asp-fluoromethylketone (z-DEVD-fmk).	benzoylcarbonyl-aspartyl-glutamyl-valyl-aspartyl-fluoromethyl ketone	258-268	caspase 1	Homo sapiens	120-127
9894612-3	1998	Caspases-1, -3, -6 and -7 were shown to cleave fodrin to the 150 kDa fragment in vitro and all were inhibited by 10 microM zVAD-fmk.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	123-131	caspase 1	Homo sapiens	0-25
9828101-7	1998	Both Acetyl-Tyr-Val-Ala-Asp-chloromethylketone and Acetyl-Tyr-Val-Ala-Asp-aldehyde, selective caspase-1 (interleukin-1beta converting enzyme) inhibitors, exerted only partial protection of cells from apoptosis at higher concentrations.	N-acetyl-tyrosyl-valyl-alanyl-aspartyl chloromethyl ketone	5-46	caspase 1	Homo sapiens	94-103
9828101-7	1998	Both Acetyl-Tyr-Val-Ala-Asp-chloromethylketone and Acetyl-Tyr-Val-Ala-Asp-aldehyde, selective caspase-1 (interleukin-1beta converting enzyme) inhibitors, exerted only partial protection of cells from apoptosis at higher concentrations.	L 709049	51-82	caspase 1	Homo sapiens	94-103
9828101-10	1998	Thus, the data indicate that BFA-induced apoptosis requires caspase(s) activation, primarily the activation of caspase-3, and is inhibited by overexpression of Bcl-2.	Brefeldin A	29-32	caspase 1	Homo sapiens	60-67
9928441-2	1998	In the current paradigm for apoptotic cell death, the activity of a family of proteases, caspases, related to interleukin-1 beta-converting enzyme (ICE) orchestrates the multiple downstream events, such as cell shrinkage, membrane blebbing, glutathione (GSH) efflux, and chromatin degradation that constitute apoptosis.	Glutathione	241-252	caspase 1	Homo sapiens	89-97
9815121-6	1998	When applied simultaneously with anti-Fas antibodies, 50 ng/ml of captopril completely abrogated apoptotic indexes based on morphology, DNA fragmentation, and inducible caspase-1 activity and significantly decreased the inducible activity of caspase-3.	Captopril	66-75	caspase 1	Homo sapiens	169-178
9928441-2	1998	In the current paradigm for apoptotic cell death, the activity of a family of proteases, caspases, related to interleukin-1 beta-converting enzyme (ICE) orchestrates the multiple downstream events, such as cell shrinkage, membrane blebbing, glutathione (GSH) efflux, and chromatin degradation that constitute apoptosis.	Glutathione	241-252	caspase 1	Homo sapiens	110-146
9928441-2	1998	In the current paradigm for apoptotic cell death, the activity of a family of proteases, caspases, related to interleukin-1 beta-converting enzyme (ICE) orchestrates the multiple downstream events, such as cell shrinkage, membrane blebbing, glutathione (GSH) efflux, and chromatin degradation that constitute apoptosis.	Glutathione	241-252	caspase 1	Homo sapiens	148-151
9928441-2	1998	In the current paradigm for apoptotic cell death, the activity of a family of proteases, caspases, related to interleukin-1 beta-converting enzyme (ICE) orchestrates the multiple downstream events, such as cell shrinkage, membrane blebbing, glutathione (GSH) efflux, and chromatin degradation that constitute apoptosis.	Glutathione	254-257	caspase 1	Homo sapiens	89-97
9928441-2	1998	In the current paradigm for apoptotic cell death, the activity of a family of proteases, caspases, related to interleukin-1 beta-converting enzyme (ICE) orchestrates the multiple downstream events, such as cell shrinkage, membrane blebbing, glutathione (GSH) efflux, and chromatin degradation that constitute apoptosis.	Glutathione	254-257	caspase 1	Homo sapiens	110-146
9928441-2	1998	In the current paradigm for apoptotic cell death, the activity of a family of proteases, caspases, related to interleukin-1 beta-converting enzyme (ICE) orchestrates the multiple downstream events, such as cell shrinkage, membrane blebbing, glutathione (GSH) efflux, and chromatin degradation that constitute apoptosis.	Glutathione	254-257	caspase 1	Homo sapiens	148-151
9928441-5	1998	The caspases themselves are cysteine-dependent enzymes and, as such, appear to be redox sensitive.	Cysteine	28-36	caspase 1	Homo sapiens	4-12
9928441-9	1998	The possible implications of these dual roles for reactive oxygen species in apoptosis, that is, induction and inhibition of caspases, are discussed in the present review.	Reactive Oxygen Species	50-73	caspase 1	Homo sapiens	125-133
9849900-3	1998	Pretreatment with Z-Asp-CH2-DCB, a caspase inhibitor, suppressed the DNA ladder in response to hypoxia in a concentration-dependent manner.	benzyloxycarbonyl-Asp-CH2OC(O)-2,6-dichlorobenzene	18-31	caspase 1	Homo sapiens	35-42
9801394-9	1998	Arsenic trioxide induced the expression of the proenzymes of caspase 2 and caspase 3 and activation of both caspase 1 and caspase 3.	Arsenic Trioxide	0-16	caspase 1	Homo sapiens	108-117
9766451-10	1998	In both short- and long-term BM cultures, hematopoietic colony-forming cell numbers were increased after ICE blockade with a synthetic ICE inhibitor (Ac-Tyr-Val-Ala-Asp-aldehyde), even in the absence of IFN-gamma, suggesting that ICE regulates the proliferation and cell death of committed and primitive progenitor cells.	L 709049	150-177	caspase 1	Homo sapiens	105-108
9804161-7	1998	Cytochrome c appeared in the cytosol immediately following light activation of the photosensitizer benzoporphyrin derivative monoacid ring A. Activation of caspases 3, 6, 7, and 8 was evident within 1-2 h post PDT.	monoacid	125-133	caspase 1	Homo sapiens	156-164
9780184-7	1998	The NO donor S-nitroso-N-acetyl-DL-penicillamine inhibited caspase-1 activity in cells as well as the activity of purified recombinant caspase-1 and also prevented the cleavage of pro-IL-1beta and pro-IGIF by recombinant caspase-1.	snap	13-48	caspase 1	Homo sapiens	59-68
9780184-7	1998	The NO donor S-nitroso-N-acetyl-DL-penicillamine inhibited caspase-1 activity in cells as well as the activity of purified recombinant caspase-1 and also prevented the cleavage of pro-IL-1beta and pro-IGIF by recombinant caspase-1.	snap	13-48	caspase 1	Homo sapiens	135-144
9780184-7	1998	The NO donor S-nitroso-N-acetyl-DL-penicillamine inhibited caspase-1 activity in cells as well as the activity of purified recombinant caspase-1 and also prevented the cleavage of pro-IL-1beta and pro-IGIF by recombinant caspase-1.	snap	13-48	caspase 1	Homo sapiens	135-144
9873617-1	1998	A systematic study of interleukin-1 beta converting enzyme (ICE, caspase-1) and caspase-3 (CPP32, apopain) inhibitors incorporating a P2-P3 conformationally constrained dipeptide mimetic is reported.	p2-p3	134-139	caspase 1	Homo sapiens	22-58
9873617-1	1998	A systematic study of interleukin-1 beta converting enzyme (ICE, caspase-1) and caspase-3 (CPP32, apopain) inhibitors incorporating a P2-P3 conformationally constrained dipeptide mimetic is reported.	Dipeptides	169-178	caspase 1	Homo sapiens	22-58
9766451-10	1998	In both short- and long-term BM cultures, hematopoietic colony-forming cell numbers were increased after ICE blockade with a synthetic ICE inhibitor (Ac-Tyr-Val-Ala-Asp-aldehyde), even in the absence of IFN-gamma, suggesting that ICE regulates the proliferation and cell death of committed and primitive progenitor cells.	L 709049	150-177	caspase 1	Homo sapiens	135-138
9766451-10	1998	In both short- and long-term BM cultures, hematopoietic colony-forming cell numbers were increased after ICE blockade with a synthetic ICE inhibitor (Ac-Tyr-Val-Ala-Asp-aldehyde), even in the absence of IFN-gamma, suggesting that ICE regulates the proliferation and cell death of committed and primitive progenitor cells.	L 709049	150-177	caspase 1	Homo sapiens	135-138
9917859-4	1998	Although several enzymes associated with inflammatory tissues are capable of processing proIL-1 beta into an active molecule in the extracellular compartment, the IL-1 beta converting enzyme (ICE, also called caspase-1) cuts intracellular proIL-1 beta after the aspartic acid residue in position 116, resulting in a highly active mature IL-1 beta that is secreted into the extracellular space.	Aspartic Acid	262-275	caspase 1	Homo sapiens	163-190
9917859-4	1998	Although several enzymes associated with inflammatory tissues are capable of processing proIL-1 beta into an active molecule in the extracellular compartment, the IL-1 beta converting enzyme (ICE, also called caspase-1) cuts intracellular proIL-1 beta after the aspartic acid residue in position 116, resulting in a highly active mature IL-1 beta that is secreted into the extracellular space.	Aspartic Acid	262-275	caspase 1	Homo sapiens	192-195
9917859-4	1998	Although several enzymes associated with inflammatory tissues are capable of processing proIL-1 beta into an active molecule in the extracellular compartment, the IL-1 beta converting enzyme (ICE, also called caspase-1) cuts intracellular proIL-1 beta after the aspartic acid residue in position 116, resulting in a highly active mature IL-1 beta that is secreted into the extracellular space.	Aspartic Acid	262-275	caspase 1	Homo sapiens	209-218
9917859-6	1998	IL-18 is a member of the IL-1 family, and like IL-1 beta, proIL-18 is cleaved by ICE to yield an active molecule.	proil	58-63	caspase 1	Homo sapiens	81-84
9740225-9	1998	F-II equally hydrolyzed acetyl-Asp-Glu-Val-Asp-methylcoumarinamide, and acetyl-Tyr-Val-Ala-Asp-methylcoumarinamide, caspase-1 (interleukin-1beta converting enzyme)-specific substrate, and was inhibited by acetyl-Tyr-Val-Ala-Asp-aldehyde and acetyl-Tyr-Val-Ala-Asp-aldehyde.	L 709049	205-236	caspase 1	Homo sapiens	116-125
9712143-7	1998	Moreover, blockage of activation of CPP32/caspase-3 by pretreating the cells with two specific tetrapeptidic inhibitors for caspases (Ac-DEVD-cho and Ac-YVAD-cmk) could significantly attenuate the extent of cleavage/activation of PAK2 induced by UV irradiation.	acetyl-aspartyl-glutamyl-valyl-aspartal	134-145	caspase 1	Homo sapiens	124-132
9712143-7	1998	Moreover, blockage of activation of CPP32/caspase-3 by pretreating the cells with two specific tetrapeptidic inhibitors for caspases (Ac-DEVD-cho and Ac-YVAD-cmk) could significantly attenuate the extent of cleavage/activation of PAK2 induced by UV irradiation.	ac-yvad	150-157	caspase 1	Homo sapiens	124-132
9721720-0	1998	Role of caspases in N-methyl-D-aspartate-induced apoptosis in cerebrocortical neurons.	N-Methylaspartate	20-40	caspase 1	Homo sapiens	8-16
9721720-5	1998	To determine whether caspases play a role in NMDA-induced apoptosis, we used two functionally distinct approaches to decrease substrate cleavage by caspases.	N-Methylaspartate	45-49	caspase 1	Homo sapiens	148-156
9770325-0	1998	Activation of interleukin-1beta-converting enzyme by nigericin is independent of apoptosis.	Nigericin	53-62	caspase 1	Homo sapiens	14-49
9770325-2	1998	Since the precursor form of interleukin-1beta (pre-IL-1beta) is one of the well known substrates for ICE, and a potassium/proton ionophore, nigericin, enhances IL-1beta processing, the authors hypothesized that nigericin induces apoptosis through the activation of ICE.	Nigericin	140-149	caspase 1	Homo sapiens	101-104
9770325-2	1998	Since the precursor form of interleukin-1beta (pre-IL-1beta) is one of the well known substrates for ICE, and a potassium/proton ionophore, nigericin, enhances IL-1beta processing, the authors hypothesized that nigericin induces apoptosis through the activation of ICE.	Nigericin	140-149	caspase 1	Homo sapiens	265-268
9770325-4	1998	Under exactly the same conditions, nigericin also induced IL-1beta processing in these cells, which was significantly inhibited by an ICE inhibitor, acetyl-Tyr-Val-Ala-Asp-CHO.	Nigericin	35-44	caspase 1	Homo sapiens	134-137
9770325-4	1998	Under exactly the same conditions, nigericin also induced IL-1beta processing in these cells, which was significantly inhibited by an ICE inhibitor, acetyl-Tyr-Val-Ala-Asp-CHO.	L 709049	149-175	caspase 1	Homo sapiens	134-137
9721720-7	1998	The other is a pseudosubstrate peptide (Z-VAD x fmk) that inhibits caspase activity.	z-vad x fmk	40-51	caspase 1	Homo sapiens	67-74
9721720-8	1998	Pretreatment with either V-ICEinh or Z-VAD-fmk protects cerebrocortical neurons from NMDA-induced apoptosis, suggesting a role for caspases in NMDA-induced apoptosis.	v-iceinh	25-33	caspase 1	Homo sapiens	131-139
9721720-8	1998	Pretreatment with either V-ICEinh or Z-VAD-fmk protects cerebrocortical neurons from NMDA-induced apoptosis, suggesting a role for caspases in NMDA-induced apoptosis.	N-Methylaspartate	143-147	caspase 1	Homo sapiens	131-139
9740225-9	1998	F-II equally hydrolyzed acetyl-Asp-Glu-Val-Asp-methylcoumarinamide, and acetyl-Tyr-Val-Ala-Asp-methylcoumarinamide, caspase-1 (interleukin-1beta converting enzyme)-specific substrate, and was inhibited by acetyl-Tyr-Val-Ala-Asp-aldehyde and acetyl-Tyr-Val-Ala-Asp-aldehyde.	L 709049	241-272	caspase 1	Homo sapiens	116-125
9651388-8	1998	Addition of the irreversible interleukin-1beta-converting enzyme (ICE) inhibitor, Z-Val-Ala-Asp-dichlorobenzoate, or a radicicol analog, inhibited nigericin-induced mature IL-1beta release and activation of p45 ICE precursor.	z-val-ala-asp-dichlorobenzoate	82-112	caspase 1	Homo sapiens	211-214
9657755-5	1998	In addition, in freshly purified human eosinophils, lavendustin A prevented anti-Fas MoAb-induced proteolytic cleavage of lamin B, suggesting that tyrosine kinases may amplify the proteolytic signaling cascade within interleukin-1beta converting enzyme (ICE) family proteases.	lavendustin A	52-65	caspase 1	Homo sapiens	217-252
9657755-5	1998	In addition, in freshly purified human eosinophils, lavendustin A prevented anti-Fas MoAb-induced proteolytic cleavage of lamin B, suggesting that tyrosine kinases may amplify the proteolytic signaling cascade within interleukin-1beta converting enzyme (ICE) family proteases.	lavendustin A	52-65	caspase 1	Homo sapiens	254-257
9785598-10	1998	On the other hand, 6-hydroxydopamine-induced microglial cell death was inhibited by inhibitors of aspartic proteinases and caspases, suggesting the involvement of cathepsins E and D and caspases in microglial cell death.	Oxidopamine	19-36	caspase 1	Homo sapiens	123-131
9785598-10	1998	On the other hand, 6-hydroxydopamine-induced microglial cell death was inhibited by inhibitors of aspartic proteinases and caspases, suggesting the involvement of cathepsins E and D and caspases in microglial cell death.	Oxidopamine	19-36	caspase 1	Homo sapiens	186-194
9651349-6	1998	Apoptotic changes induced by the incubation of nuclei with CaCl2 in the presence of these cytosols were strongly reduced in the presence of an inhibitor of caspase-3 and to a lesser extent by an inhibitor of caspase-1.	Calcium Chloride	59-64	caspase 1	Homo sapiens	208-217
9651388-8	1998	Addition of the irreversible interleukin-1beta-converting enzyme (ICE) inhibitor, Z-Val-Ala-Asp-dichlorobenzoate, or a radicicol analog, inhibited nigericin-induced mature IL-1beta release and activation of p45 ICE precursor.	Nigericin	147-156	caspase 1	Homo sapiens	29-64
9651388-8	1998	Addition of the irreversible interleukin-1beta-converting enzyme (ICE) inhibitor, Z-Val-Ala-Asp-dichlorobenzoate, or a radicicol analog, inhibited nigericin-induced mature IL-1beta release and activation of p45 ICE precursor.	Nigericin	147-156	caspase 1	Homo sapiens	66-69
9651388-8	1998	Addition of the irreversible interleukin-1beta-converting enzyme (ICE) inhibitor, Z-Val-Ala-Asp-dichlorobenzoate, or a radicicol analog, inhibited nigericin-induced mature IL-1beta release and activation of p45 ICE precursor.	Nigericin	147-156	caspase 1	Homo sapiens	211-214
9651388-11	1998	We have therefore shown conclusively, for the first time, that nigericin-induced release of IL-1beta is dependent upon activation of p45 ICE processing.	Nigericin	63-72	caspase 1	Homo sapiens	137-140
9651388-12	1998	So far, the mechanism by which reduced intracellular potassium ion concentration triggers p45 ICE processing is not known, but further investigation in this area could lead to the discovery of novel molecular targets whereby control of IL-1beta production might be effected.	Potassium	53-62	caspase 1	Homo sapiens	94-97
9498817-3	1998	The Nef-induced apoptosis as well as Fas-mediated apoptosis was inhibited by acetyl-Try-Val-Ala-Asp-CHO, an IL-1beta converting enzyme (ICE) inhibitor.	ammonium ferrous sulfate	37-40	caspase 1	Homo sapiens	108-134
9642224-9	1998	In contrast, the CED-3/interleukin-1beta-converting enzyme (ICE) protease inhibitor Z-VADfmk efficiently suppressed Fas-induced apoptosis and only marginally inhibited PKC/Ras-mediated apoptosis.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	84-92	caspase 1	Homo sapiens	23-58
9642224-9	1998	In contrast, the CED-3/interleukin-1beta-converting enzyme (ICE) protease inhibitor Z-VADfmk efficiently suppressed Fas-induced apoptosis and only marginally inhibited PKC/Ras-mediated apoptosis.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	84-92	caspase 1	Homo sapiens	60-63
9642224-9	1998	In contrast, the CED-3/interleukin-1beta-converting enzyme (ICE) protease inhibitor Z-VADfmk efficiently suppressed Fas-induced apoptosis and only marginally inhibited PKC/Ras-mediated apoptosis.	ammonium ferrous sulfate	116-119	caspase 1	Homo sapiens	23-58
9642224-9	1998	In contrast, the CED-3/interleukin-1beta-converting enzyme (ICE) protease inhibitor Z-VADfmk efficiently suppressed Fas-induced apoptosis and only marginally inhibited PKC/Ras-mediated apoptosis.	ammonium ferrous sulfate	116-119	caspase 1	Homo sapiens	60-63
9770120-8	1998	Consistent with this observation, inhibition of ICE proteases by the peptide z-VAD.fmk did not protect against acid-induced cell killing.	z-vad	77-82	caspase 1	Homo sapiens	48-51
9770120-8	1998	Consistent with this observation, inhibition of ICE proteases by the peptide z-VAD.fmk did not protect against acid-induced cell killing.	FMK	83-86	caspase 1	Homo sapiens	48-51
10684020-0	1998	[Effects of mifepristone on ICE expression and Fas expression in early pregnant chorionic villi].	Mifepristone	12-24	caspase 1	Homo sapiens	28-31
10684020-6	1998	In the villi from the pregnant women who received mifepristone for 2 days, expression of Fas increased markely; the ratio of positive nuclear staining cells were significantly raised, but the immunostaining intensity of ICE was slightly increased.	Mifepristone	50-62	caspase 1	Homo sapiens	220-223
9590133-8	1998	Furthermore, the interleukin-1beta-converting enzyme inhibitor, Ac-YVAD-CMK, reversed the augmented cytotoxicity.	N-acetyl-tyrosyl-valyl-alanyl-aspartyl chloromethyl ketone	64-75	caspase 1	Homo sapiens	17-52
9871520-0	1998	Peptidomimetic aminomethylene ketone inhibitors of interleukin-1 beta-converting enzyme (ICE).	aminomethylene ketone	15-36	caspase 1	Homo sapiens	51-87
9871520-0	1998	Peptidomimetic aminomethylene ketone inhibitors of interleukin-1 beta-converting enzyme (ICE).	aminomethylene ketone	15-36	caspase 1	Homo sapiens	89-92
9871520-1	1998	Pyridone-based peptidomimetic inhibitors of recombinant human Interleukin-1 beta-converting enzyme (ICE, caspase-1) with an aminomethylene ketone activating group in the P1" position are described.	Pyridones	0-8	caspase 1	Homo sapiens	62-98
9871520-1	1998	Pyridone-based peptidomimetic inhibitors of recombinant human Interleukin-1 beta-converting enzyme (ICE, caspase-1) with an aminomethylene ketone activating group in the P1" position are described.	Pyridones	0-8	caspase 1	Homo sapiens	100-103
9871520-1	1998	Pyridone-based peptidomimetic inhibitors of recombinant human Interleukin-1 beta-converting enzyme (ICE, caspase-1) with an aminomethylene ketone activating group in the P1" position are described.	Pyridones	0-8	caspase 1	Homo sapiens	105-114
9871520-1	1998	Pyridone-based peptidomimetic inhibitors of recombinant human Interleukin-1 beta-converting enzyme (ICE, caspase-1) with an aminomethylene ketone activating group in the P1" position are described.	aminomethylene ketone	124-145	caspase 1	Homo sapiens	62-98
9871520-1	1998	Pyridone-based peptidomimetic inhibitors of recombinant human Interleukin-1 beta-converting enzyme (ICE, caspase-1) with an aminomethylene ketone activating group in the P1" position are described.	aminomethylene ketone	124-145	caspase 1	Homo sapiens	100-103
9871520-1	1998	Pyridone-based peptidomimetic inhibitors of recombinant human Interleukin-1 beta-converting enzyme (ICE, caspase-1) with an aminomethylene ketone activating group in the P1" position are described.	aminomethylene ketone	124-145	caspase 1	Homo sapiens	105-114
9578463-1	1998	Interleukin-1beta-converting enzyme is a member of a family of human cysteine proteases with specificity for aspartic acid, which have been named caspases.	Aspartic Acid	109-122	caspase 1	Homo sapiens	0-35
9578463-1	1998	Interleukin-1beta-converting enzyme is a member of a family of human cysteine proteases with specificity for aspartic acid, which have been named caspases.	Aspartic Acid	109-122	caspase 1	Homo sapiens	146-154
9578463-4	1998	The three enzymes, ICE, TX and TY, were therefore expressed in baculovirus-infected insect cells, as 30-kDa proteins lacking the propeptide.	propeptide	129-139	caspase 1	Homo sapiens	19-22
9578463-8	1998	T7-tagged ICE, TX and TY were purified by immunoaffinity and tested for their catalytic efficiency on YVAD-containing synthetic substrates and on the ICE natural substrate, pro-interleukin-1beta.	YVAD	102-106	caspase 1	Homo sapiens	10-13
9578463-9	1998	TX cleaved the same synthetic substrates as ICE (Km of 90 microM and k(cat) of 0.4 s(-1) for Suc-YVAD-NH-Mec, where Suc represents succinyl and NH-Mec represents amino-4-methylcoumarin) and could cleave pro-interleukin-1beta into the same peptides as ICE but less efficiently.	succinyl	131-139	caspase 1	Homo sapiens	44-47
9578463-9	1998	TX cleaved the same synthetic substrates as ICE (Km of 90 microM and k(cat) of 0.4 s(-1) for Suc-YVAD-NH-Mec, where Suc represents succinyl and NH-Mec represents amino-4-methylcoumarin) and could cleave pro-interleukin-1beta into the same peptides as ICE but less efficiently.	3-amino-4-methyl-2H-chromen-2-one	162-184	caspase 1	Homo sapiens	44-47
9578463-10	1998	On the other hand, TY showed very little efficacy on the different ICE substrates (Km of 860 microM for Suc-YVAD-NH-Mec).	Thr-Tyr	19-21	caspase 1	Homo sapiens	67-70
9525624-4	1998	Apoptosis was significantly inhibited by an interleukin-1beta (IL-1beta)-converting enzyme (ICE)/CED-3 family protease inhibitor, Ac-DEVD-CHO (CPP32; caspase 3), whereas a similar inhibitor of ICE (caspase 1), Ac-YVAD-CHO, had no effect.	acetyl-aspartyl-glutamyl-valyl-aspartal	130-141	caspase 1	Homo sapiens	92-95
9525624-4	1998	Apoptosis was significantly inhibited by an interleukin-1beta (IL-1beta)-converting enzyme (ICE)/CED-3 family protease inhibitor, Ac-DEVD-CHO (CPP32; caspase 3), whereas a similar inhibitor of ICE (caspase 1), Ac-YVAD-CHO, had no effect.	acetyl-aspartyl-glutamyl-valyl-aspartal	130-141	caspase 1	Homo sapiens	193-196
9525624-4	1998	Apoptosis was significantly inhibited by an interleukin-1beta (IL-1beta)-converting enzyme (ICE)/CED-3 family protease inhibitor, Ac-DEVD-CHO (CPP32; caspase 3), whereas a similar inhibitor of ICE (caspase 1), Ac-YVAD-CHO, had no effect.	acetyl-aspartyl-glutamyl-valyl-aspartal	130-141	caspase 1	Homo sapiens	198-207
9525624-4	1998	Apoptosis was significantly inhibited by an interleukin-1beta (IL-1beta)-converting enzyme (ICE)/CED-3 family protease inhibitor, Ac-DEVD-CHO (CPP32; caspase 3), whereas a similar inhibitor of ICE (caspase 1), Ac-YVAD-CHO, had no effect.	L 709049	210-221	caspase 1	Homo sapiens	92-95
9661894-8	1998	Consistent with this observation, inhibition of interleukin 1beta-converting enzyme proteases by the peptide z-Val-Ala-Asp(OMe)-CH2F did not protect against acid-induced cell killing.	z-val-ala-asp	109-122	caspase 1	Homo sapiens	48-83
9661894-8	1998	Consistent with this observation, inhibition of interleukin 1beta-converting enzyme proteases by the peptide z-Val-Ala-Asp(OMe)-CH2F did not protect against acid-induced cell killing.	Fluoromethyl radical	128-132	caspase 1	Homo sapiens	48-83
9873373-1	1998	Inhibition of interleukin-1 beta converting enzyme (ICE), apopain, papain, thrombin and trypsin with substrate like peptidyl L- and D-alpha-aldehydes and their L-beta-homo-aldehyde analogues was investigated.	peptidyl	116-124	caspase 1	Homo sapiens	14-50
9873373-1	1998	Inhibition of interleukin-1 beta converting enzyme (ICE), apopain, papain, thrombin and trypsin with substrate like peptidyl L- and D-alpha-aldehydes and their L-beta-homo-aldehyde analogues was investigated.	peptidyl	116-124	caspase 1	Homo sapiens	52-55
9873373-1	1998	Inhibition of interleukin-1 beta converting enzyme (ICE), apopain, papain, thrombin and trypsin with substrate like peptidyl L- and D-alpha-aldehydes and their L-beta-homo-aldehyde analogues was investigated.	l- and d-alpha-aldehydes	125-149	caspase 1	Homo sapiens	14-50
9873373-1	1998	Inhibition of interleukin-1 beta converting enzyme (ICE), apopain, papain, thrombin and trypsin with substrate like peptidyl L- and D-alpha-aldehydes and their L-beta-homo-aldehyde analogues was investigated.	l- and d-alpha-aldehydes	125-149	caspase 1	Homo sapiens	52-55
9873373-1	1998	Inhibition of interleukin-1 beta converting enzyme (ICE), apopain, papain, thrombin and trypsin with substrate like peptidyl L- and D-alpha-aldehydes and their L-beta-homo-aldehyde analogues was investigated.	homo-aldehyde	167-180	caspase 1	Homo sapiens	14-50
9622503-0	1998	Bimodal inhibition of caspase-1 by aryloxymethyl and acyloxymethyl ketones.	aryloxymethyl and acyloxymethyl ketones	35-74	caspase 1	Homo sapiens	22-31
10200502-7	1998	Caspase activities were measured using specific fluorogenic peptide derivatives DABCYL-YVADAPV-EDANS and Ac-DEVD-AMC, substrates of the caspase 1-like and caspase 3-like families, respectively.	Ac-aspartyl-glutamyl-valyl-aspartyl-aminomethylcoumarin	105-116	caspase 1	Homo sapiens	136-145
9582351-6	1998	The effects on PP2A could be prevented by the caspase family inhibitors acetyl-Asp-Glu-Val-Asp (DEVD) aldehyde or Ac-DEVD fluoromethyl ketone.	acetyl-asp-glu-val-asp (devd) aldehyde	72-110	caspase 1	Homo sapiens	46-53
9590133-0	1998	Suppression of intracellular resistance factors by adriamycin augments heat-induced apoptosis via interleukin-1beta-converting enzyme activation in pancreatic carcinoma cells.	Doxorubicin	51-61	caspase 1	Homo sapiens	98-133
9581784-6	1998	Z-VAD-FMK inhibited E1A-induced apoptosis in adenovirus-infected Hela cells, suggesting that the ICE family proteases are involved in this apoptosis pathway.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	0-9	caspase 1	Homo sapiens	97-100
9547337-6	1998	Although calcium, prooxidants, and several recombinant caspases (caspases 1, 2, 3, 4, and 6) enhance the permeability of PT pore-containing liposomes, recombinant Bcl-2 or Bcl-XL augment the resistance of the reconstituted PT pore complex to pore opening.	Calcium	9-16	caspase 1	Homo sapiens	65-91
9498817-6	1998	These results suggest that the PK inhibitors specifically act on a cellular protein involved in the upper stream of signal transduction pathway of the Nef-induced apoptosis, which is different from the Fas-mediated pathway but meets it upstream of ICE.	ammonium ferrous sulfate	202-205	caspase 1	Homo sapiens	248-251
9466564-1	1998	During apoptosis, activation of a family of cysteine proteases related to interleukin-1beta-converting enzyme (ICE)-related proteases or "caspases" results in endoproteolytic cleavage of multiple substrates at specific aspartate residues.	Aspartic Acid	219-228	caspase 1	Homo sapiens	111-114
9498817-3	1998	The Nef-induced apoptosis as well as Fas-mediated apoptosis was inhibited by acetyl-Try-Val-Ala-Asp-CHO, an IL-1beta converting enzyme (ICE) inhibitor.	ammonium ferrous sulfate	37-40	caspase 1	Homo sapiens	136-139
9498817-3	1998	The Nef-induced apoptosis as well as Fas-mediated apoptosis was inhibited by acetyl-Try-Val-Ala-Asp-CHO, an IL-1beta converting enzyme (ICE) inhibitor.	acetyl-try-val-ala-asp-cho	77-103	caspase 1	Homo sapiens	108-134
9498817-3	1998	The Nef-induced apoptosis as well as Fas-mediated apoptosis was inhibited by acetyl-Try-Val-Ala-Asp-CHO, an IL-1beta converting enzyme (ICE) inhibitor.	acetyl-try-val-ala-asp-cho	77-103	caspase 1	Homo sapiens	136-139
9425165-6	1998	However, the protease CPP32, a downstream molecule of the CD95 pathway, was activated in UV-exposed HaCaT cells, and UV-induced apoptosis was blocked by the ICE protease inhibitor zVAD, implying that at least similar downstream events are involved in CD95- and UV-induced apoptosis.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	180-184	caspase 1	Homo sapiens	157-160
9536946-7	1998	Ac-Tyr-Val-Ala-Asp-CHO, a specific peptide aldehyde inhibitor of ICE, significantly reduced the amount of mature IL-1 beta released by isolated IBD macrophages (from a median of 1.2 (range 0.78-4.42) ng/ml to 0.43 (0.21-1.6) ng/ml; p &lt; 0.01).	L 709049	0-22	caspase 1	Homo sapiens	65-68
9536946-7	1998	Ac-Tyr-Val-Ala-Asp-CHO, a specific peptide aldehyde inhibitor of ICE, significantly reduced the amount of mature IL-1 beta released by isolated IBD macrophages (from a median of 1.2 (range 0.78-4.42) ng/ml to 0.43 (0.21-1.6) ng/ml; p &lt; 0.01).	Aldehydes	43-51	caspase 1	Homo sapiens	65-68
9427712-3	1998	Caspase-1 belongs to a rapidly growing family of cysteine proteases with substrate specificity for aspartate involved in cellular apoptosis.	Aspartic Acid	99-108	caspase 1	Homo sapiens	0-9
9421482-3	1998	IL-1beta- converting enzyme (ICE) is a key enzyme of the apoptotic machinery involved in Fas-mediated apoptosis of normal lymphocytes.	ammonium ferrous sulfate	89-92	caspase 1	Homo sapiens	0-27
10200444-3	1998	Incubation of follicles in the presence of a putative irreversible and non-competitive inhibitor of caspase-1 (interleukin-1beta-converting enzyme or ICE), sodium aurothiomalate (SAM), completely prevented internucleosomal, but not high MW, DNA cleavage.	Gold Sodium Thiomalate	156-177	caspase 1	Homo sapiens	100-109
9421482-3	1998	IL-1beta- converting enzyme (ICE) is a key enzyme of the apoptotic machinery involved in Fas-mediated apoptosis of normal lymphocytes.	ammonium ferrous sulfate	89-92	caspase 1	Homo sapiens	29-32
9393811-8	1997	IL-1beta maturation was severely retarded by YVAD, indicating that IL-1beta-converting enzyme (ICE; caspase 1) is activated in Shigella-induced apoptosis.	YVAD	45-49	caspase 1	Homo sapiens	95-98
10923408-1	1998	OBJECTIVE: To investigate the effects of Arg-Gly-Asp-Ser (RGDS) tetrapeptide on the expressions of apoptosis-related genes interleukin-1 beta-converting enzyme (ICE) and bcl-2 in human glomerular mesangial cells, so as to provide experimental evidence for regulating proliferation and apoptosis of mesangial cells with RGD-containing polypeptide.	arginyl-glycyl-aspartyl-serine	41-56	caspase 1	Homo sapiens	123-159
10923408-1	1998	OBJECTIVE: To investigate the effects of Arg-Gly-Asp-Ser (RGDS) tetrapeptide on the expressions of apoptosis-related genes interleukin-1 beta-converting enzyme (ICE) and bcl-2 in human glomerular mesangial cells, so as to provide experimental evidence for regulating proliferation and apoptosis of mesangial cells with RGD-containing polypeptide.	arginyl-glycyl-aspartyl-serine	41-56	caspase 1	Homo sapiens	161-164
9550423-4	1997	Baseline levels of ICE mRNA were detected in keratinocyte cultures devoid of Langerhans cells and were up-regulated by nontoxic concentrations of the reactive hapten urushiol and by the irritant chemicals sodium lauryl sulfate and PMA.	Sodium Dodecyl Sulfate	205-226	caspase 1	Homo sapiens	19-22
9550423-4	1997	Baseline levels of ICE mRNA were detected in keratinocyte cultures devoid of Langerhans cells and were up-regulated by nontoxic concentrations of the reactive hapten urushiol and by the irritant chemicals sodium lauryl sulfate and PMA.	Tetradecanoylphorbol Acetate	231-234	caspase 1	Homo sapiens	19-22
9550423-6	1997	Enzymatic conversion from the 31-kDa to the 17.5-kDa form of IL-1beta was blocked by addition of a highly specific aldehyde inhibitor that contained a tetrapeptide recognition sequence specific for ICE, but not by an aldehyde inhibitor of a related ICE-like cysteine protease.	Aldehydes	115-123	caspase 1	Homo sapiens	198-201
9437520-0	1997	Disulfiram is a potent inhibitor of proteases of the caspase family.	Disulfiram	0-10	caspase 1	Homo sapiens	53-60
9420624-4	1997	Addition of the ICE family inhibitor Z-VAD.fmk (50 microM) completely inhibited apoptosis (2.0 +/- 1.5% at 24 h).	z-vad	37-42	caspase 1	Homo sapiens	16-19
9437520-2	1997	Because the processing can be accomplished by caspase activity, we investigated the effect of DC disulfides, such as disulfiram (DSF), on active caspases.	dc disulfides	94-107	caspase 1	Homo sapiens	145-153
9437520-2	1997	Because the processing can be accomplished by caspase activity, we investigated the effect of DC disulfides, such as disulfiram (DSF), on active caspases.	Disulfiram	117-127	caspase 1	Homo sapiens	145-153
9437520-2	1997	Because the processing can be accomplished by caspase activity, we investigated the effect of DC disulfides, such as disulfiram (DSF), on active caspases.	Disulfiram	129-132	caspase 1	Homo sapiens	145-153
9437520-4	1997	Direct interaction of DSF with caspases was confirmed by its inhibition of the purified Ac-DEVD-AMC cleaving protease, caspase-3 (CPP32/apopain).	Ac-aspartyl-glutamyl-valyl-aspartyl-aminomethylcoumarin	88-99	caspase 1	Homo sapiens	31-39
9437520-6	1997	DSF was also observed to inhibit the purified Ac-YVAD-AMC cleaving enzyme, caspase-1 (interleukin-1 beta-converting enzyme, ICE), with a K(app) of 2.2 x 10(3) M(-1)s(-1).	Ac-Tyr-Val-Ala-Asp-AMC	46-57	caspase 1	Homo sapiens	75-84
9437520-6	1997	DSF was also observed to inhibit the purified Ac-YVAD-AMC cleaving enzyme, caspase-1 (interleukin-1 beta-converting enzyme, ICE), with a K(app) of 2.2 x 10(3) M(-1)s(-1).	Ac-Tyr-Val-Ala-Asp-AMC	46-57	caspase 1	Homo sapiens	124-127
9437520-7	1997	In this case protein mixed disulfide formation between DSF and caspase-1 was directly demonstrated using 35S-labeled DSF.	Disulfides	27-36	caspase 1	Homo sapiens	63-72
9437520-7	1997	In this case protein mixed disulfide formation between DSF and caspase-1 was directly demonstrated using 35S-labeled DSF.	Sulfur-35	105-108	caspase 1	Homo sapiens	63-72
9437520-8	1997	The physiological disulfide GSSG was also observed to influence the activity of caspases.	Disulfides	18-27	caspase 1	Homo sapiens	80-88
9437520-8	1997	The physiological disulfide GSSG was also observed to influence the activity of caspases.	Glutathione Disulfide	28-32	caspase 1	Homo sapiens	80-88
9437520-10	1997	In conclusion, our study shows that caspases are quite sensitive to thiol oxidation and that DSF is a very potent oxidant of caspase protein thiol(s), being 700-fold more potent than glutathione disulfide.	Sulfhydryl Compounds	68-73	caspase 1	Homo sapiens	36-44
9437520-10	1997	In conclusion, our study shows that caspases are quite sensitive to thiol oxidation and that DSF is a very potent oxidant of caspase protein thiol(s), being 700-fold more potent than glutathione disulfide.	Sulfhydryl Compounds	68-73	caspase 1	Homo sapiens	36-43
9420624-4	1997	Addition of the ICE family inhibitor Z-VAD.fmk (50 microM) completely inhibited apoptosis (2.0 +/- 1.5% at 24 h).	FMK	43-46	caspase 1	Homo sapiens	16-19
9362518-5	1997	Then, to dissect various cellular responses induced by Fas, we used several peptide inhibitors for ICE family proteases in Fas-treated Jurkat cells and KB cells.	ammonium ferrous sulfate	55-58	caspase 1	Homo sapiens	99-102
9334240-7	1997	These activities were blocked separately by the caspase inhibitors Ac-YVAD-CHO and Ac-DEVD-CHO.	acetyl-aspartyl-glutamyl-valyl-aspartal	83-94	caspase 1	Homo sapiens	48-55
9334376-6	1997	We show that z-VAD-fmk, a tripeptide inhibitor of ICE homologues, can inhibit Fas-induced apoptosis of peripheral blood CD4(+) and CD8+ T cells from asymptomatic HIV+ individuals.	tripeptide K-26	26-36	caspase 1	Homo sapiens	50-53
9334376-6	1997	We show that z-VAD-fmk, a tripeptide inhibitor of ICE homologues, can inhibit Fas-induced apoptosis of peripheral blood CD4(+) and CD8+ T cells from asymptomatic HIV+ individuals.	ammonium ferrous sulfate	78-81	caspase 1	Homo sapiens	50-53
9334376-11	1997	The above findings show that Fas-induced T cell apoptosis is ICE dependent in HIV infection.	ammonium ferrous sulfate	29-32	caspase 1	Homo sapiens	61-64
9409756-4	1997	The caspase-1 inhibitor (YVAD-CHO) effectively blocked apoptosis, whereas the caspase-3 inhibitor (DEVD-CHO) did not.	tyrosyl-valyl-alanyl-aspartal	25-33	caspase 1	Homo sapiens	4-13
9334376-6	1997	We show that z-VAD-fmk, a tripeptide inhibitor of ICE homologues, can inhibit Fas-induced apoptosis of peripheral blood CD4(+) and CD8+ T cells from asymptomatic HIV+ individuals.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	13-22	caspase 1	Homo sapiens	50-53
9376593-3	1997	Apoptosis induced in tumor cells by cytarabine, doxorubicin, and methotrexate required the activation of ICE/Ced-3 proteases (caspases), similarly to the CD95 system.	Cytarabine	36-46	caspase 1	Homo sapiens	126-134
9406913-3	1997	In the present study we demonstrate by in situ hybridization analysis that expression of CPP-32, an ICE-related protease, is significantly upregulated in CA1 hippocampal neurons following global ischemia induced by cardiac arrest and in hippocampal neurons of the CA3/CA4 region after kainate-mediated epilepsy, respectively.	Kainic Acid	285-292	caspase 1	Homo sapiens	100-103
9326666-3	1997	Glutamate-induced apoptosis of CGNs is, however, associated with a concentration- and time-dependent activation of the interleukin 1beta-converting enzyme (ICE)/CED-3-related protease, CPP32/Yama/apopain (now designated caspase 3).	Glutamic Acid	0-9	caspase 1	Homo sapiens	119-154
9326666-3	1997	Glutamate-induced apoptosis of CGNs is, however, associated with a concentration- and time-dependent activation of the interleukin 1beta-converting enzyme (ICE)/CED-3-related protease, CPP32/Yama/apopain (now designated caspase 3).	Glutamic Acid	0-9	caspase 1	Homo sapiens	156-159
9326666-7	1997	Our data demonstrate that glutamate-induced apoptosis of CGNs is mediated by a posttranslational activation of the ICE/CED-3-related cysteine protease caspase 3.	Glutamic Acid	26-35	caspase 1	Homo sapiens	115-118
9325297-5	1997	Caspase activity is not affected by concentrations of Ca2+ below 100 mM, but is abolished by Zn2+ in the submicromolar range, a common characteristic of cysteine proteases.	Zinc	93-97	caspase 1	Homo sapiens	0-7
9376593-3	1997	Apoptosis induced in tumor cells by cytarabine, doxorubicin, and methotrexate required the activation of ICE/Ced-3 proteases (caspases), similarly to the CD95 system.	Doxorubicin	48-59	caspase 1	Homo sapiens	126-134
9376593-3	1997	Apoptosis induced in tumor cells by cytarabine, doxorubicin, and methotrexate required the activation of ICE/Ced-3 proteases (caspases), similarly to the CD95 system.	Methotrexate	65-77	caspase 1	Homo sapiens	126-134
9377572-4	1997	The immunohistochemical studies and Western analyses as well as the terminal dUTP-biotin nick end labeling (TUNEL) method revealed that both ICE and CPP32 were translocated from the cytoplasm into the nuclei in regressing, apoptotic tumor cells.	dutp-biotin	77-88	caspase 1	Homo sapiens	141-144
14555975-6	1997	Z-Asp, an inhibitor of interleukin-1beta converting enzyme (ICE) family proteases, inhibited the appearance of the 50 kDa protein and the emergence of the cell-free apoptosis activity in the etoposide-treated U937 cytosol.	benzyloxycarbonyl-asparagine	0-5	caspase 1	Homo sapiens	23-58
9357850-8	1997	Additionally, an increased formation of the active p20 fragments of ICE and Ich-1L as well as degradation of the inactive zymogen form of cpp32beta protein were observed in silica-treated human alveolar macrophages, indicating activation of these proteases.	Silicon Dioxide	173-179	caspase 1	Homo sapiens	68-71
9357850-10	1997	These results suggest that silica-induced apoptosis involves activation of the ICE family of proteases and is the first step in elucidating the intracellular mechanism of particulate-induced apoptosis in human alveolar macrophages.	Silicon Dioxide	27-33	caspase 1	Homo sapiens	79-82
9357850-0	1997	Involvement of the ICE family of proteases in silica-induced apoptosis in human alveolar macrophages.	Silicon Dioxide	46-52	caspase 1	Homo sapiens	19-22
9357850-7	1997	Pretreatment of cells with 10 microM of the ICE inhibitor z-Val-Ala-Asp-fluoromethyl ketone and the cpp32beta inhibitor Asp-Glu-Val-Asp-fluoromethyl ketone completely blocked silica-induced apoptosis.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	58-91	caspase 1	Homo sapiens	44-47
14555975-6	1997	Z-Asp, an inhibitor of interleukin-1beta converting enzyme (ICE) family proteases, inhibited the appearance of the 50 kDa protein and the emergence of the cell-free apoptosis activity in the etoposide-treated U937 cytosol.	benzyloxycarbonyl-asparagine	0-5	caspase 1	Homo sapiens	60-63
14555975-6	1997	Z-Asp, an inhibitor of interleukin-1beta converting enzyme (ICE) family proteases, inhibited the appearance of the 50 kDa protein and the emergence of the cell-free apoptosis activity in the etoposide-treated U937 cytosol.	Etoposide	191-200	caspase 1	Homo sapiens	23-58
14555975-6	1997	Z-Asp, an inhibitor of interleukin-1beta converting enzyme (ICE) family proteases, inhibited the appearance of the 50 kDa protein and the emergence of the cell-free apoptosis activity in the etoposide-treated U937 cytosol.	Etoposide	191-200	caspase 1	Homo sapiens	60-63
14555976-2	1997	In this study, we show for the first time that photodynamic therapy (PDT), using benzoporphyrin derivative monoacid ring A (BPD-MA, verteporfin) as the photosensitizer, induces the complete cleavage and subsequent activation of caspase-3 (CPP32/Yama/Apopain) but not caspase-1 (ICE) in human promyelocytic leukemia HL-60 cells.	Benzoporphyrin	81-95	caspase 1	Homo sapiens	267-282
14555976-2	1997	In this study, we show for the first time that photodynamic therapy (PDT), using benzoporphyrin derivative monoacid ring A (BPD-MA, verteporfin) as the photosensitizer, induces the complete cleavage and subsequent activation of caspase-3 (CPP32/Yama/Apopain) but not caspase-1 (ICE) in human promyelocytic leukemia HL-60 cells.	monoacid	107-115	caspase 1	Homo sapiens	267-282
14555976-2	1997	In this study, we show for the first time that photodynamic therapy (PDT), using benzoporphyrin derivative monoacid ring A (BPD-MA, verteporfin) as the photosensitizer, induces the complete cleavage and subsequent activation of caspase-3 (CPP32/Yama/Apopain) but not caspase-1 (ICE) in human promyelocytic leukemia HL-60 cells.	Verteporfin	132-143	caspase 1	Homo sapiens	267-282
9317114-0	1997	B cell receptor cross-linking prevents Fas-induced cell death by inactivating the IL-1 beta-converting enzyme protease and regulating Bcl-2/Bcl-x expression.	ammonium ferrous sulfate	39-42	caspase 1	Homo sapiens	82-109
14555976-4	1997	The general caspase inhibitor Z-Asp-2,6 dichlorobenzoyloxymethylketone (Z-Asp-DCB) blocked PARP cleavage while the serine protease inhibitors 3,4-dichloroisocoumarin (DCI) and N-tosyl-lysyl chloromethyl ketone (TLCK) blocked the cleavage of caspase-3 suggesting that they act upstream of caspase-3 activation.	Z-Asp-2,6-dichlorobenzoyl-oxymethylketone	30-70	caspase 1	Homo sapiens	12-19
9317114-5	1997	Since the PKC inhibitor bisindolylmaleimide I completely abolishes the protective effect of the sIgG signal, a member of the PKC family is probably responsible for the prevention of ICE cascade activation.	bisindolylmaleimide I	24-45	caspase 1	Homo sapiens	182-185
14555976-4	1997	The general caspase inhibitor Z-Asp-2,6 dichlorobenzoyloxymethylketone (Z-Asp-DCB) blocked PARP cleavage while the serine protease inhibitors 3,4-dichloroisocoumarin (DCI) and N-tosyl-lysyl chloromethyl ketone (TLCK) blocked the cleavage of caspase-3 suggesting that they act upstream of caspase-3 activation.	Z-Asp-2,6-dichlorobenzoyl-oxymethylketone	72-81	caspase 1	Homo sapiens	12-19
9271410-10	1997	Moreover, both EGF-induced apoptosis and IFN-gamma-induced apoptosis were effectively blocked by Z-Val-Ala-Asp-fluoromethylketone (ZVAD) in all the cells tested, and studies from ICE-deficient cells indicated that ICE gene expression was necessary for IFN-gamma-induced apoptosis.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	97-129	caspase 1	Homo sapiens	214-217
9305545-2	1997	Z-Asp-CH2-DCB (100 microM), an inhibitor of interleukin-1 beta-converting enzyme (caspase-1) and caspase-1-like proteases, markedly inhibited UVB-induced cell death and DNA fragmentation.	benzyloxycarbonyl-Asp-CH2OC(O)-2,6-dichlorobenzene	0-13	caspase 1	Homo sapiens	44-80
9305545-2	1997	Z-Asp-CH2-DCB (100 microM), an inhibitor of interleukin-1 beta-converting enzyme (caspase-1) and caspase-1-like proteases, markedly inhibited UVB-induced cell death and DNA fragmentation.	benzyloxycarbonyl-Asp-CH2OC(O)-2,6-dichlorobenzene	0-13	caspase 1	Homo sapiens	82-91
9305545-2	1997	Z-Asp-CH2-DCB (100 microM), an inhibitor of interleukin-1 beta-converting enzyme (caspase-1) and caspase-1-like proteases, markedly inhibited UVB-induced cell death and DNA fragmentation.	benzyloxycarbonyl-Asp-CH2OC(O)-2,6-dichlorobenzene	0-13	caspase 1	Homo sapiens	97-106
9288794-6	1997	Drug-induced apoptosis involved activation of caspases (interleukin 1beta-converting enzyme/Ced-3-like proteases) and processing of the prototype caspase substrate PARP and was completely blocked by benzyloxycarbonyl-Val-Ala-Asp-fluoromethyl ketone, a peptide inhibitor of caspases.	Caspase Inhibitor VI	199-248	caspase 1	Homo sapiens	46-54
9288794-6	1997	Drug-induced apoptosis involved activation of caspases (interleukin 1beta-converting enzyme/Ced-3-like proteases) and processing of the prototype caspase substrate PARP and was completely blocked by benzyloxycarbonyl-Val-Ala-Asp-fluoromethyl ketone, a peptide inhibitor of caspases.	Caspase Inhibitor VI	199-248	caspase 1	Homo sapiens	56-91
9288794-6	1997	Drug-induced apoptosis involved activation of caspases (interleukin 1beta-converting enzyme/Ced-3-like proteases) and processing of the prototype caspase substrate PARP and was completely blocked by benzyloxycarbonyl-Val-Ala-Asp-fluoromethyl ketone, a peptide inhibitor of caspases.	Caspase Inhibitor VI	199-248	caspase 1	Homo sapiens	46-53
9288794-6	1997	Drug-induced apoptosis involved activation of caspases (interleukin 1beta-converting enzyme/Ced-3-like proteases) and processing of the prototype caspase substrate PARP and was completely blocked by benzyloxycarbonyl-Val-Ala-Asp-fluoromethyl ketone, a peptide inhibitor of caspases.	Caspase Inhibitor VI	199-248	caspase 1	Homo sapiens	273-281
9271410-10	1997	Moreover, both EGF-induced apoptosis and IFN-gamma-induced apoptosis were effectively blocked by Z-Val-Ala-Asp-fluoromethylketone (ZVAD) in all the cells tested, and studies from ICE-deficient cells indicated that ICE gene expression was necessary for IFN-gamma-induced apoptosis.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	131-135	caspase 1	Homo sapiens	214-217
9223451-3	1997	The ICE inhibitor (Z-Val-Ala-Asp-CH2F) and CPP32 inhibitor (Z-Asp-Glu-Val-Asp-CH2F) blocked the apoptotic cell death caused by UVB irradiation.	benzyloxycarbonyl-valyl-alanyl-aspartyl-fluoromethane	19-37	caspase 1	Homo sapiens	4-7
9261102-6	1997	Our results suggest that the first cleavage of caspase-2 is accomplished by a caspase-3-like activity, and other ICE-like proteases less sensitive to DEVD-CHO may be responsible for activation of caspase-3 and loss of mitochondrial function.	aspartyl-glutamyl-valyl-aspartal	150-158	caspase 1	Homo sapiens	113-116
9236222-4	1997	Cell death after serum/K+ deprivation was significantly attenuated by the CPP32-like inhibitor z-DEVD-fmk; however, the ICE-like inhibitor z-YVAD-fmk had only slightly protective effects at the highest concentration used.	benzyloxycarbonyltyrosyl-valyl-alanyl-aspartic acid fluoromethyl ketone	139-149	caspase 1	Homo sapiens	120-123
9276475-6	1997	Differential Bcl-2 and ICE mRNA expression was also found when granulocytic differentiation was stimulated by DMSO.	Dimethyl Sulfoxide	110-114	caspase 1	Homo sapiens	23-26
9276475-8	1997	De novo caspase expression was responsible for the development of spontaneous apoptosis, since specific inhibitors of ICE (YVAD-CMK) and CPP32 (DEVD-CHO), inhibited retinoic acid induced spontaneous apoptosis.	YVAD	123-127	caspase 1	Homo sapiens	118-121
9276475-8	1997	De novo caspase expression was responsible for the development of spontaneous apoptosis, since specific inhibitors of ICE (YVAD-CMK) and CPP32 (DEVD-CHO), inhibited retinoic acid induced spontaneous apoptosis.	Tretinoin	165-178	caspase 1	Homo sapiens	118-121
9240442-2	1997	NO generated from (+/-)-(E)-methyl-2-[(E)-hydroxyimino]-5-nitro-6-methoxy-S-hexen eamide (NOR1) inhibited CPP32-like protease, which constitute a family of interleukin-1beta-converting enzyme (ICE)-like proteases in a dose-dependent manner.	(+/-)-(e)-methyl-2-[(e)-hydroxyimino	18-54	caspase 1	Homo sapiens	156-191
9240442-2	1997	NO generated from (+/-)-(E)-methyl-2-[(E)-hydroxyimino]-5-nitro-6-methoxy-S-hexen eamide (NOR1) inhibited CPP32-like protease, which constitute a family of interleukin-1beta-converting enzyme (ICE)-like proteases in a dose-dependent manner.	(+/-)-(e)-methyl-2-[(e)-hydroxyimino	18-54	caspase 1	Homo sapiens	193-196
9240442-2	1997	NO generated from (+/-)-(E)-methyl-2-[(E)-hydroxyimino]-5-nitro-6-methoxy-S-hexen eamide (NOR1) inhibited CPP32-like protease, which constitute a family of interleukin-1beta-converting enzyme (ICE)-like proteases in a dose-dependent manner.	-5-nitro-6-methoxy-s-hexen eamide	55-88	caspase 1	Homo sapiens	156-191
9240442-2	1997	NO generated from (+/-)-(E)-methyl-2-[(E)-hydroxyimino]-5-nitro-6-methoxy-S-hexen eamide (NOR1) inhibited CPP32-like protease, which constitute a family of interleukin-1beta-converting enzyme (ICE)-like proteases in a dose-dependent manner.	-5-nitro-6-methoxy-s-hexen eamide	55-88	caspase 1	Homo sapiens	193-196
9206994-5	1997	Transfection with the cowpox protease inhibitor crmA or culture in the presence of the synthetic ICE-specific inhibitor Ac-YVAD.cmk both prevent the DeltaPsim collapse and subsequent apoptosis.	ac-yvad	120-127	caspase 1	Homo sapiens	97-100
9233790-7	1997	Our experiments show that selective inhibition of some caspases protects human T cells (Jurkat and CEM-C7) from Fas-induced apoptosis, dramatically increasing their survival (up to 320-fold) in a colony-forming assay.	ammonium ferrous sulfate	112-115	caspase 1	Homo sapiens	55-63
9096388-8	1997	Inhibition of Fas killing by an interleukin 1beta-converting enzyme (ICE)-like protease inhibitor peptide did not modify Fas-induced JNK activation upon Fas ligation.	ammonium ferrous sulfate	14-17	caspase 1	Homo sapiens	32-67
9128256-9	1997	The ICE-like protease inhibitor, benzyloxycarbonyl-Val-Ala-Asp (OMe) fluoromethyl ketone (Z-VAD.FMK), inhibited apoptosis and cleavage of Ich-1, CPP32, Mch3alpha, Mch2alpha, PARP, U1-70K, and lamins.	benzyloxycarbonyl-val-ala-asp (ome) fluoromethyl ketone	33-88	caspase 1	Homo sapiens	4-7
9128256-9	1997	The ICE-like protease inhibitor, benzyloxycarbonyl-Val-Ala-Asp (OMe) fluoromethyl ketone (Z-VAD.FMK), inhibited apoptosis and cleavage of Ich-1, CPP32, Mch3alpha, Mch2alpha, PARP, U1-70K, and lamins.	z-vad	90-95	caspase 1	Homo sapiens	4-7
9128256-9	1997	The ICE-like protease inhibitor, benzyloxycarbonyl-Val-Ala-Asp (OMe) fluoromethyl ketone (Z-VAD.FMK), inhibited apoptosis and cleavage of Ich-1, CPP32, Mch3alpha, Mch2alpha, PARP, U1-70K, and lamins.	mch3alpha	152-161	caspase 1	Homo sapiens	4-7
9128256-9	1997	The ICE-like protease inhibitor, benzyloxycarbonyl-Val-Ala-Asp (OMe) fluoromethyl ketone (Z-VAD.FMK), inhibited apoptosis and cleavage of Ich-1, CPP32, Mch3alpha, Mch2alpha, PARP, U1-70K, and lamins.	mch2alpha	163-172	caspase 1	Homo sapiens	4-7
9173887-5	1997	Whereas actin cleavage and nuclear/cell surface markers of apoptosis were co-ordinately diminished by zVAD-fmk, an inhibitor of the ICE-like family of proteases, only acetyl-leucyl-leucylnormethional, an inhibitor of calpains, was capable of completely inhibiting actin cleavage.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	102-110	caspase 1	Homo sapiens	132-135
9084431-2	1997	Here we report the ability of peptide inhibitors of ICE-like proteases to inhibit apoptosis of cultured cerebellar granule neurones caused by reduction of extracellular K+ levels and by the broad-spectrum protein kinase inhibitor staurosporine.	Staurosporine	230-243	caspase 1	Homo sapiens	52-55
9084431-4	1997	The ICE-like protease inhibitor benzyloxycarbonyl-Val-Ala-Asp (O-methyl)fluoromethyl ketone (zVAD-fmk) was found to be extremely effective at preventing staurosporine-induced death of cerebellar granule neurones and yet was completely ineffective in preventing K+ deprivation-induced death.	benzyloxycarbonyl-val-ala-asp (o-methyl)fluoromethyl ketone	32-91	caspase 1	Homo sapiens	4-7
9084431-4	1997	The ICE-like protease inhibitor benzyloxycarbonyl-Val-Ala-Asp (O-methyl)fluoromethyl ketone (zVAD-fmk) was found to be extremely effective at preventing staurosporine-induced death of cerebellar granule neurones and yet was completely ineffective in preventing K+ deprivation-induced death.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	93-101	caspase 1	Homo sapiens	4-7
9084431-4	1997	The ICE-like protease inhibitor benzyloxycarbonyl-Val-Ala-Asp (O-methyl)fluoromethyl ketone (zVAD-fmk) was found to be extremely effective at preventing staurosporine-induced death of cerebellar granule neurones and yet was completely ineffective in preventing K+ deprivation-induced death.	Staurosporine	153-166	caspase 1	Homo sapiens	4-7
9084431-5	1997	Staurosporine induced cleavage of the 116-kDa poly (ADP-ribose) polymerase enzyme, a substrate of ICE-like proteases, to the 85-kDa product, and this cleavage was also blocked by zVAD.	Staurosporine	0-13	caspase 1	Homo sapiens	98-101
9084431-5	1997	Staurosporine induced cleavage of the 116-kDa poly (ADP-ribose) polymerase enzyme, a substrate of ICE-like proteases, to the 85-kDa product, and this cleavage was also blocked by zVAD.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	179-183	caspase 1	Homo sapiens	98-101
9166725-1	1997	We characterized the activation of interleukin-1beta-converting enzyme (ICE)-like proteases (caspases) in human neuroblastoma cells (SH-SY5Y) following challenge with staurosporine, an established agent known to induce apoptosis.	Staurosporine	167-180	caspase 1	Homo sapiens	72-75
9166725-1	1997	We characterized the activation of interleukin-1beta-converting enzyme (ICE)-like proteases (caspases) in human neuroblastoma cells (SH-SY5Y) following challenge with staurosporine, an established agent known to induce apoptosis.	Staurosporine	167-180	caspase 1	Homo sapiens	93-101
9166725-9	1997	It is important that a pan ICE inhibitor [carbobenzoxy-Asp-CH2OC(O)-2,6-dichlorobenzene] was able to attenuate lactate dehydrogenase release and PARP and CPP32 cleavage and altered immunohistochemical staining patterns for PARP and CPP32 following staurosporine challenge.	carbobenzoxy-asp-ch2oc(o)-2,6-dichlorobenzene	42-87	caspase 1	Homo sapiens	27-30
9166725-9	1997	It is important that a pan ICE inhibitor [carbobenzoxy-Asp-CH2OC(O)-2,6-dichlorobenzene] was able to attenuate lactate dehydrogenase release and PARP and CPP32 cleavage and altered immunohistochemical staining patterns for PARP and CPP32 following staurosporine challenge.	Staurosporine	248-261	caspase 1	Homo sapiens	27-30
9175767-2	1997	The present study describes the effects of GGO on the activity of cysteine-dependent aspartate-directed proteases (caspases) in human leukemia U937 cells.	geranylgeraniol	43-46	caspase 1	Homo sapiens	115-123
9175767-2	1997	The present study describes the effects of GGO on the activity of cysteine-dependent aspartate-directed proteases (caspases) in human leukemia U937 cells.	Cysteine	66-74	caspase 1	Homo sapiens	115-123
9130145-2	1997	Using primary culture methods, we report that neurons and astrocytes require the activity of the ICE/CED-3 family of proteases to undergo apoptosis induced by staurosporine, ceramide, and serum-free media.	Staurosporine	159-172	caspase 1	Homo sapiens	97-100
9130145-2	1997	Using primary culture methods, we report that neurons and astrocytes require the activity of the ICE/CED-3 family of proteases to undergo apoptosis induced by staurosporine, ceramide, and serum-free media.	Ceramides	174-182	caspase 1	Homo sapiens	97-100
9130145-5	1997	To determine which member of the ICE/CED-3 family was activated in neurons and astrocytes during apoptosis, we developed a novel affinity-labeling technique that labeled the active site cysteine and identified a 17-kDa subunit of the activated protease.	Cysteine	186-194	caspase 1	Homo sapiens	33-36
9142649-0	1997	4-Hydroxynonenal inhibits interleukin-1 beta converting enzyme.	4-hydroxy-2-nonenal	0-16	caspase 1	Homo sapiens	26-62
9142649-8	1997	HNE inhibited ICE activity in lysed cells in a similar dose-dependent manner, measured by hydrolysis of the fluorogenic substrate YVAD-AMC and recombinant proIL-1 beta.	yvad-amc	130-138	caspase 1	Homo sapiens	14-17
9142649-11	1997	Thus, low levels of HNE can suppress mononuclear cell release of IL-1 beta, probably by interacting with the active site cysteine of ICE.	Cysteine	121-129	caspase 1	Homo sapiens	133-136
9096388-8	1997	Inhibition of Fas killing by an interleukin 1beta-converting enzyme (ICE)-like protease inhibitor peptide did not modify Fas-induced JNK activation upon Fas ligation.	ammonium ferrous sulfate	14-17	caspase 1	Homo sapiens	69-72
9058728-3	1997	To study the mechanism of PS externalization during development of apoptosis, we examined the correlation between the activation of interleukin-1 beta-converting enzyme (ICE) family protease and PS externalization in human monocytic leukemia U937 cells and in their apoptosis-resistant variants, UK711 and UK110, after treatment with etoposide and anti-Fas antibody.	Etoposide	334-343	caspase 1	Homo sapiens	170-173
9058728-5	1997	Furthermore, inhibitors of ICE family proteases, Z-Asp and Z-VAD, prevented apoptosis and PS externalization in etoposide-treated U937 cells.	benzyloxycarbonyl-asparagine	49-54	caspase 1	Homo sapiens	27-30
9058728-5	1997	Furthermore, inhibitors of ICE family proteases, Z-Asp and Z-VAD, prevented apoptosis and PS externalization in etoposide-treated U937 cells.	z-vad	59-64	caspase 1	Homo sapiens	27-30
9058728-5	1997	Furthermore, inhibitors of ICE family proteases, Z-Asp and Z-VAD, prevented apoptosis and PS externalization in etoposide-treated U937 cells.	Etoposide	112-121	caspase 1	Homo sapiens	27-30
9054391-9	1997	Pretreatment of the cells with benzyloxycarbonyl-Val-Ala-Asp-(OMe)-fluoromethylketone (zVAD.fmk), a tetrapeptide inhibitor of caspases, prevented the induction of apoptosis for 24 h. Even after 72 h of treatment, some cells were still alive and progressing through the cell cycle, suggesting that blockage of caspase activity is able to protect cells.	benzyloxycarbonyl-val-ala-asp-(ome)-fluoromethylketone	31-85	caspase 1	Homo sapiens	126-134
9054443-0	1997	Activation of multiple interleukin-1beta converting enzyme homologues in cytosol and nuclei of HL-60 cells during etoposide-induced apoptosis.	Etoposide	114-123	caspase 1	Homo sapiens	23-58
9054443-2	1997	In the present study, three complementary techniques were utilized to follow caspase activation during the course of etoposide-induced apoptosis in HL-60 human leukemia cells.	Etoposide	117-126	caspase 1	Homo sapiens	77-84
9054443-9	1997	These results not only indicate that etoposide-induced apoptosis in HL-60 cells is accompanied by the selective activation of multiple caspases in cytosol and nuclei, but also suggest that other caspase precursors such as procaspase-2 are present but not activated during apoptosis.	Etoposide	37-46	caspase 1	Homo sapiens	135-143
9054443-9	1997	These results not only indicate that etoposide-induced apoptosis in HL-60 cells is accompanied by the selective activation of multiple caspases in cytosol and nuclei, but also suggest that other caspase precursors such as procaspase-2 are present but not activated during apoptosis.	Etoposide	37-46	caspase 1	Homo sapiens	135-142
9054391-9	1997	Pretreatment of the cells with benzyloxycarbonyl-Val-Ala-Asp-(OMe)-fluoromethylketone (zVAD.fmk), a tetrapeptide inhibitor of caspases, prevented the induction of apoptosis for 24 h. Even after 72 h of treatment, some cells were still alive and progressing through the cell cycle, suggesting that blockage of caspase activity is able to protect cells.	benzyloxycarbonyl-val-ala-asp-(ome)-fluoromethylketone	31-85	caspase 1	Homo sapiens	126-133
9054391-9	1997	Pretreatment of the cells with benzyloxycarbonyl-Val-Ala-Asp-(OMe)-fluoromethylketone (zVAD.fmk), a tetrapeptide inhibitor of caspases, prevented the induction of apoptosis for 24 h. Even after 72 h of treatment, some cells were still alive and progressing through the cell cycle, suggesting that blockage of caspase activity is able to protect cells.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	87-95	caspase 1	Homo sapiens	126-134
9054391-9	1997	Pretreatment of the cells with benzyloxycarbonyl-Val-Ala-Asp-(OMe)-fluoromethylketone (zVAD.fmk), a tetrapeptide inhibitor of caspases, prevented the induction of apoptosis for 24 h. Even after 72 h of treatment, some cells were still alive and progressing through the cell cycle, suggesting that blockage of caspase activity is able to protect cells.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	87-95	caspase 1	Homo sapiens	126-133
9045680-6	1997	In addition, the P1 carbonyl of the ketone inhibitor is pointing into the oxyanion hole and forms a hydrogen bond with the peptidic nitrogen of Gly-122, resulting in a different state compared with the tetrahedral intermediate observed in the structure of ICE and CPP32 in complex with an aldehyde inhibitor.	Ketones	36-42	caspase 1	Homo sapiens	256-259
9045680-6	1997	In addition, the P1 carbonyl of the ketone inhibitor is pointing into the oxyanion hole and forms a hydrogen bond with the peptidic nitrogen of Gly-122, resulting in a different state compared with the tetrahedral intermediate observed in the structure of ICE and CPP32 in complex with an aldehyde inhibitor.	Hydrogen	100-108	caspase 1	Homo sapiens	256-259
9045680-6	1997	In addition, the P1 carbonyl of the ketone inhibitor is pointing into the oxyanion hole and forms a hydrogen bond with the peptidic nitrogen of Gly-122, resulting in a different state compared with the tetrahedral intermediate observed in the structure of ICE and CPP32 in complex with an aldehyde inhibitor.	Nitrogen	132-140	caspase 1	Homo sapiens	256-259
9045680-6	1997	In addition, the P1 carbonyl of the ketone inhibitor is pointing into the oxyanion hole and forms a hydrogen bond with the peptidic nitrogen of Gly-122, resulting in a different state compared with the tetrahedral intermediate observed in the structure of ICE and CPP32 in complex with an aldehyde inhibitor.	Glycine	144-147	caspase 1	Homo sapiens	256-259
9045680-6	1997	In addition, the P1 carbonyl of the ketone inhibitor is pointing into the oxyanion hole and forms a hydrogen bond with the peptidic nitrogen of Gly-122, resulting in a different state compared with the tetrahedral intermediate observed in the structure of ICE and CPP32 in complex with an aldehyde inhibitor.	Aldehydes	289-297	caspase 1	Homo sapiens	256-259
9070907-7	1997	The protective effect of ICE inhibitor III was not dependent upon pH, but was associated with decreased release of arachidonic acid from cells.	Arachidonic Acid	115-131	caspase 1	Homo sapiens	25-28
9070648-3	1997	We previously showed that actin is cleaved in vitro by an ICE family protease, distinct from ICE itself, which is activated during VP-16-induced apoptosis.	Etoposide	131-136	caspase 1	Homo sapiens	58-61
9070648-3	1997	We previously showed that actin is cleaved in vitro by an ICE family protease, distinct from ICE itself, which is activated during VP-16-induced apoptosis.	Etoposide	131-136	caspase 1	Homo sapiens	93-96
9034139-0	1997	Suppression of apoptosis by nitric oxide via inhibition of interleukin-1beta-converting enzyme (ICE)-like and cysteine protease protein (CPP)-32-like proteases.	Nitric Oxide	28-40	caspase 1	Homo sapiens	59-94
9034139-0	1997	Suppression of apoptosis by nitric oxide via inhibition of interleukin-1beta-converting enzyme (ICE)-like and cysteine protease protein (CPP)-32-like proteases.	Nitric Oxide	28-40	caspase 1	Homo sapiens	96-99
9034139-8	1997	Inhibition of CPP-32 enzyme activity was due to specific S-nitrosylation of Cys 163, a functionally essential amino acid conserved among ICE/CPP-32-like proteases.	Cysteine	76-79	caspase 1	Homo sapiens	137-140
9034139-8	1997	Inhibition of CPP-32 enzyme activity was due to specific S-nitrosylation of Cys 163, a functionally essential amino acid conserved among ICE/CPP-32-like proteases.	Amino Acids, Essential	100-120	caspase 1	Homo sapiens	137-140
9190289-6	1997	The results indicate that the optimal tetrapeptide recognition sequence for ICE is WEHD, not YVAD, as previously believed, and this led to the synthesis of an unusually potent aldehyde inhibitor, Ac-WEHD-CHO (Ki = 56 pM).	Aldehydes	176-184	caspase 1	Homo sapiens	76-79
9020192-2	1997	In this study, we found that either etoposide (VP-16) or camptothecin (CPT) activated c-Jun N-terminal kinase 1/stress-activated protein kinase (JNK1/SAPK), transient c-jun expression, and ICE (interleukin-1beta converting enzyme)/CED-3-like proteases in U937 cells.	Etoposide	36-45	caspase 1	Homo sapiens	189-192
9020192-2	1997	In this study, we found that either etoposide (VP-16) or camptothecin (CPT) activated c-Jun N-terminal kinase 1/stress-activated protein kinase (JNK1/SAPK), transient c-jun expression, and ICE (interleukin-1beta converting enzyme)/CED-3-like proteases in U937 cells.	Etoposide	36-45	caspase 1	Homo sapiens	194-229
9020192-2	1997	In this study, we found that either etoposide (VP-16) or camptothecin (CPT) activated c-Jun N-terminal kinase 1/stress-activated protein kinase (JNK1/SAPK), transient c-jun expression, and ICE (interleukin-1beta converting enzyme)/CED-3-like proteases in U937 cells.	Camptothecin	57-69	caspase 1	Homo sapiens	189-192
9020192-2	1997	In this study, we found that either etoposide (VP-16) or camptothecin (CPT) activated c-Jun N-terminal kinase 1/stress-activated protein kinase (JNK1/SAPK), transient c-jun expression, and ICE (interleukin-1beta converting enzyme)/CED-3-like proteases in U937 cells.	Camptothecin	57-69	caspase 1	Homo sapiens	194-229
9020192-2	1997	In this study, we found that either etoposide (VP-16) or camptothecin (CPT) activated c-Jun N-terminal kinase 1/stress-activated protein kinase (JNK1/SAPK), transient c-jun expression, and ICE (interleukin-1beta converting enzyme)/CED-3-like proteases in U937 cells.	Camptothecin	71-74	caspase 1	Homo sapiens	189-192
9020192-2	1997	In this study, we found that either etoposide (VP-16) or camptothecin (CPT) activated c-Jun N-terminal kinase 1/stress-activated protein kinase (JNK1/SAPK), transient c-jun expression, and ICE (interleukin-1beta converting enzyme)/CED-3-like proteases in U937 cells.	Camptothecin	71-74	caspase 1	Homo sapiens	194-229
9020192-5	1997	As reported previously, benzyloxycarbonyl-Asp-CH2OC(O)-2,6-dichlorobenzene (Z-Asp), a preferential inhibitor of ICE/CED-3-like proteases, blocked the apoptosis of U937 cells.	benzyloxycarbonyl-Asp-CH2OC(O)-2,6-dichlorobenzene	24-74	caspase 1	Homo sapiens	112-115
9020192-5	1997	As reported previously, benzyloxycarbonyl-Asp-CH2OC(O)-2,6-dichlorobenzene (Z-Asp), a preferential inhibitor of ICE/CED-3-like proteases, blocked the apoptosis of U937 cells.	benzyloxycarbonyl-asparagine	76-81	caspase 1	Homo sapiens	112-115
9020192-9	1997	These results indicate that JNK1 triggers the DNA damaging drug-induced apoptosis of U937 cells by activating Z-Asp-sensitive ICE/CED-3-like proteases.	benzyloxycarbonyl-asparagine	110-115	caspase 1	Homo sapiens	126-129
9106306-1	1997	Members of the ICE/Ced3 family are cysteine endoproteases that have been found to induce many of the proteolytic events observed during apoptosis.	Cysteine	35-43	caspase 1	Homo sapiens	15-18
9030233-3	1997	We found that a selective inhibitor of ICE/ced 3 family proteases, benzyloxycarbonyl Asp CH2OC(O) 2 6,-dichlorobenzene (Z-Asp-CH2-DCB).	asp ch2oc(o) 2 6,-dichlorobenzene	85-118	caspase 1	Homo sapiens	39-42
9038883-5	1997	The interleukin-1 beta-converting enzyme (ICE) family protease inhibitor, Z-Val-Ala-Asp chloromethylketone, inhibited apoptosis in a concentration-dependent manner.	CHEMBL2370692	74-106	caspase 1	Homo sapiens	4-40
9038883-5	1997	The interleukin-1 beta-converting enzyme (ICE) family protease inhibitor, Z-Val-Ala-Asp chloromethylketone, inhibited apoptosis in a concentration-dependent manner.	CHEMBL2370692	74-106	caspase 1	Homo sapiens	42-45
9374378-0	1997	Reduced expression of the ICE-related protease CPP32 is associated with radiation-induced cisplatin resistance in HeLa cells.	Cisplatin	90-99	caspase 1	Homo sapiens	26-29
9374378-5	1997	Cisplatin resistance correlated with reduced expression of ICE-related proteases (interleukin-1beta-converting enzyme).	Cisplatin	0-9	caspase 1	Homo sapiens	59-62
16465209-4	1997	Since cytosolic proteases related to interleukin-1beta-converting enzyme (ICE) are implicated as key activators of apoptosis in many different systems, we investigated the possible involvement of such proteases in TPEN-induced apoptosis.	N,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamine	214-218	caspase 1	Homo sapiens	74-77
16465209-6	1997	This could be inhibited by Z-Val-Ala-Asp-chloromethylketone (VADcmk), an inhibitor of ICE-like proteases, but not by an inhibitor of Ca2+-regulated serine protease.	CHEMBL2370692	27-59	caspase 1	Homo sapiens	86-89
16465209-6	1997	This could be inhibited by Z-Val-Ala-Asp-chloromethylketone (VADcmk), an inhibitor of ICE-like proteases, but not by an inhibitor of Ca2+-regulated serine protease.	vadcmk	61-67	caspase 1	Homo sapiens	86-89
16465209-9	1997	The apoptosis-inducing activity in cytosolic fraction from TPEN-treated Jurkat cells was blocked by incubating cells in the presence of VADcmk or another inhibitor of ICE-like proteases, Ac - Asp - Glu - Val - Asp-aldehyde (DEVD-CHO), which has been found to competitively inhibit CPP32/apopain.	N,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamine	59-63	caspase 1	Homo sapiens	167-170
16465209-12	1997	Our results suggest that activation of cytosolic ICE-like proteases is an essential step in TPEN-induced apoptosis, and that CPP32/apopain is critically involved in this process.	N,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamine	92-96	caspase 1	Homo sapiens	49-52
9030233-3	1997	We found that a selective inhibitor of ICE/ced 3 family proteases, benzyloxycarbonyl Asp CH2OC(O) 2 6,-dichlorobenzene (Z-Asp-CH2-DCB).	benzyloxycarbonyl-Asp-CH2OC(O)-2,6-dichlorobenzene	120-133	caspase 1	Homo sapiens	39-42
8972182-0	1997	Fas activation of the p38 mitogen-activated protein kinase signalling pathway requires ICE/CED-3 family proteases.	ammonium ferrous sulfate	0-3	caspase 1	Homo sapiens	87-90
8972182-4	1997	Fas has been shown to require ICE (interleukin-1 beta-converting enzyme) family proteases to induce apoptosis from studies utilizing the cowpox ICE inhibitor protein CrmA, the synthetic tetrapeptide ICE inhibitor YVAD-CMK, and the tripeptide pan-ICE inhibitor Z-VAD-FMK.	tripeptide K-26	231-241	caspase 1	Homo sapiens	30-33
8940132-4	1996	Studies in cells treated with these apoptotic stimuli reveal that both fodrin and poly(ADP-ribose) polymerase proteolysis are inhibited by acetyl-Tyr-Val-Ala-Asp chloromethyl ketone and CrmA, specific inhibitors of ICE/Ced-3 proteases.	N-acetyl-tyrosyl-valyl-alanyl-aspartyl chloromethyl ketone	139-181	caspase 1	Homo sapiens	215-218
8972182-4	1997	Fas has been shown to require ICE (interleukin-1 beta-converting enzyme) family proteases to induce apoptosis from studies utilizing the cowpox ICE inhibitor protein CrmA, the synthetic tetrapeptide ICE inhibitor YVAD-CMK, and the tripeptide pan-ICE inhibitor Z-VAD-FMK.	tripeptide K-26	231-241	caspase 1	Homo sapiens	35-71
8972182-4	1997	Fas has been shown to require ICE (interleukin-1 beta-converting enzyme) family proteases to induce apoptosis from studies utilizing the cowpox ICE inhibitor protein CrmA, the synthetic tetrapeptide ICE inhibitor YVAD-CMK, and the tripeptide pan-ICE inhibitor Z-VAD-FMK.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	260-269	caspase 1	Homo sapiens	30-33
8972182-4	1997	Fas has been shown to require ICE (interleukin-1 beta-converting enzyme) family proteases to induce apoptosis from studies utilizing the cowpox ICE inhibitor protein CrmA, the synthetic tetrapeptide ICE inhibitor YVAD-CMK, and the tripeptide pan-ICE inhibitor Z-VAD-FMK.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	260-269	caspase 1	Homo sapiens	35-71
8940103-3	1996	VAD-chloromethylketone (VAD-cmk), an inhibitor of ICE-like proteases, effectively inhibited ICE-like activity in both cell types studied, whereas the calpain inhibitor calpeptin was ineffective.	vad-chloromethylketone	0-22	caspase 1	Homo sapiens	50-53
8962091-2	1996	This included the activation of interleukin 1 beta-converting enzyme (ICE)-like proteases with cleavage of the endogenous substrates poly(ADP ribose) polymerase and D4-GDI (GDP dissociation inhibitor for the rho family), as well as the fluorogenic peptide acetyl-Asp-Glu-Val-Asp-aminotrifluoromethylcoumarin (DEVD-AFC).	acetyl-asp-glu-val-asp-aminotrifluoromethylcoumarin	256-307	caspase 1	Homo sapiens	32-68
8940103-3	1996	VAD-chloromethylketone (VAD-cmk), an inhibitor of ICE-like proteases, effectively inhibited ICE-like activity in both cell types studied, whereas the calpain inhibitor calpeptin was ineffective.	vad-chloromethylketone	0-22	caspase 1	Homo sapiens	92-95
8940103-3	1996	VAD-chloromethylketone (VAD-cmk), an inhibitor of ICE-like proteases, effectively inhibited ICE-like activity in both cell types studied, whereas the calpain inhibitor calpeptin was ineffective.	VAD I protocol	0-3	caspase 1	Homo sapiens	50-53
8940103-3	1996	VAD-chloromethylketone (VAD-cmk), an inhibitor of ICE-like proteases, effectively inhibited ICE-like activity in both cell types studied, whereas the calpain inhibitor calpeptin was ineffective.	VAD I protocol	0-3	caspase 1	Homo sapiens	92-95
8940103-4	1996	VAD-cmk also effectively inhibited all three extranuclear events, as well as nuclear fragmentation, in Jurkat cells stimulated by anti-Fas monoclonal antibody, indicating that ICE-like proteases play an important role in the regulation of this apoptotic system.	VAD I protocol	0-3	caspase 1	Homo sapiens	176-179
8962091-2	1996	This included the activation of interleukin 1 beta-converting enzyme (ICE)-like proteases with cleavage of the endogenous substrates poly(ADP ribose) polymerase and D4-GDI (GDP dissociation inhibitor for the rho family), as well as the fluorogenic peptide acetyl-Asp-Glu-Val-Asp-aminotrifluoromethylcoumarin (DEVD-AFC).	acetyl-asp-glu-val-asp-aminotrifluoromethylcoumarin	256-307	caspase 1	Homo sapiens	70-73
8980142-5	1996	Furthermore, the etoposide-induced RB cleavage was inhibited by a specific tetrapeptide ICE-like inhibitor.	Etoposide	17-26	caspase 1	Homo sapiens	88-91
8962091-2	1996	This included the activation of interleukin 1 beta-converting enzyme (ICE)-like proteases with cleavage of the endogenous substrates poly(ADP ribose) polymerase and D4-GDI (GDP dissociation inhibitor for the rho family), as well as the fluorogenic peptide acetyl-Asp-Glu-Val-Asp-aminotrifluoromethylcoumarin (DEVD-AFC).	aspartyl-glutamyl-valyl-aspartyl-7-amino-4-trifluoromethylcoumarin	309-317	caspase 1	Homo sapiens	32-68
8962091-2	1996	This included the activation of interleukin 1 beta-converting enzyme (ICE)-like proteases with cleavage of the endogenous substrates poly(ADP ribose) polymerase and D4-GDI (GDP dissociation inhibitor for the rho family), as well as the fluorogenic peptide acetyl-Asp-Glu-Val-Asp-aminotrifluoromethylcoumarin (DEVD-AFC).	aspartyl-glutamyl-valyl-aspartyl-7-amino-4-trifluoromethylcoumarin	309-317	caspase 1	Homo sapiens	70-73
8912861-5	1996	ICE/ced-3 family protease inhibitors such as Z-VAD-CH2DCB and Z-EVD-CH2DCB at 100 microg/ml prevented both the emergence of ACA and the morphological change, characteristics of apoptosis, in cisplatin-treated OVCAR-3 cells.	z-vad-ch2dcb	45-57	caspase 1	Homo sapiens	0-3
20650253-3	1996	Ac-Tyr-Val-Ala-Asp-aldehyde (YVAD) and Ac-Asp-Glu-Val-Asp-aldehyde (DEVD), synthesized tetrapeptide inhibitors of interleukin(1beta)-converting enzyme (ICE)- and CPP32/Yama-like proteases, were used to examine the CPT-11-induced death signal transduction.	L 709049	0-27	caspase 1	Homo sapiens	114-157
20650253-3	1996	Ac-Tyr-Val-Ala-Asp-aldehyde (YVAD) and Ac-Asp-Glu-Val-Asp-aldehyde (DEVD), synthesized tetrapeptide inhibitors of interleukin(1beta)-converting enzyme (ICE)- and CPP32/Yama-like proteases, were used to examine the CPT-11-induced death signal transduction.	acetyl-aspartyl-glutamyl-valyl-aspartal	39-66	caspase 1	Homo sapiens	114-157
8942655-3	1996	N-His (D381E) ICE was expressed in Escherichia coli and purified by nickel-chelating Sepharose and size-exclusion chromatography (SEC).	n-his	0-5	caspase 1	Homo sapiens	14-17
8942655-3	1996	N-His (D381E) ICE was expressed in Escherichia coli and purified by nickel-chelating Sepharose and size-exclusion chromatography (SEC).	Nickel	68-74	caspase 1	Homo sapiens	14-17
8942655-3	1996	N-His (D381E) ICE was expressed in Escherichia coli and purified by nickel-chelating Sepharose and size-exclusion chromatography (SEC).	Sepharose	85-94	caspase 1	Homo sapiens	14-17
8942655-6	1996	An oxidized adduct of ICE with glutathione, formed by disulfide rearrangement with oxidized glutathione to inhibit and stabilize the enzyme during purification, was rapidly reduced upon exposure to 5 mM DTT.	Glutathione	31-42	caspase 1	Homo sapiens	22-25
8942655-6	1996	An oxidized adduct of ICE with glutathione, formed by disulfide rearrangement with oxidized glutathione to inhibit and stabilize the enzyme during purification, was rapidly reduced upon exposure to 5 mM DTT.	Disulfides	54-63	caspase 1	Homo sapiens	22-25
8942655-6	1996	An oxidized adduct of ICE with glutathione, formed by disulfide rearrangement with oxidized glutathione to inhibit and stabilize the enzyme during purification, was rapidly reduced upon exposure to 5 mM DTT.	Glutathione	92-103	caspase 1	Homo sapiens	22-25
8942655-6	1996	An oxidized adduct of ICE with glutathione, formed by disulfide rearrangement with oxidized glutathione to inhibit and stabilize the enzyme during purification, was rapidly reduced upon exposure to 5 mM DTT.	Dithiothreitol	203-206	caspase 1	Homo sapiens	22-25
8942655-8	1996	Of the nine cysteines in ICE, eight were present in their reduced form in the glutathione adduct.	Cysteine	12-21	caspase 1	Homo sapiens	25-28
8942655-8	1996	Of the nine cysteines in ICE, eight were present in their reduced form in the glutathione adduct.	Glutathione	78-89	caspase 1	Homo sapiens	25-28
8942655-9	1996	N-His (D381E) ICE cleaved Ac-YVAD-Amc with the Michaelis-Menten parameters K(M) = 14 microM and Kcat = 0.7 s-1, values essentially identical to those reported for enzyme from natural sources.	n-his	0-5	caspase 1	Homo sapiens	14-17
8942655-9	1996	N-His (D381E) ICE cleaved Ac-YVAD-Amc with the Michaelis-Menten parameters K(M) = 14 microM and Kcat = 0.7 s-1, values essentially identical to those reported for enzyme from natural sources.	Ac-Tyr-Val-Ala-Asp-AMC	26-37	caspase 1	Homo sapiens	14-17
8912861-5	1996	ICE/ced-3 family protease inhibitors such as Z-VAD-CH2DCB and Z-EVD-CH2DCB at 100 microg/ml prevented both the emergence of ACA and the morphological change, characteristics of apoptosis, in cisplatin-treated OVCAR-3 cells.	benzyloxycarbonyl-Glu-Val-Asp-CH2OC(O)-2,6-dichlorobenzene	62-74	caspase 1	Homo sapiens	0-3
8912861-5	1996	ICE/ced-3 family protease inhibitors such as Z-VAD-CH2DCB and Z-EVD-CH2DCB at 100 microg/ml prevented both the emergence of ACA and the morphological change, characteristics of apoptosis, in cisplatin-treated OVCAR-3 cells.	Cisplatin	191-200	caspase 1	Homo sapiens	0-3
8910464-1	1996	Dipeptides containing fluorescein or biotin have been incorporated into proteolytic substrate cleavage products of bovine serum albumin generated by human cathepsin S or neutrophil elastase and into a fragment of the 31-kDa interleukin 1beta precursor by human interleukin 1beta-converting enzyme.	Dipeptides	0-10	caspase 1	Homo sapiens	261-296
8910464-1	1996	Dipeptides containing fluorescein or biotin have been incorporated into proteolytic substrate cleavage products of bovine serum albumin generated by human cathepsin S or neutrophil elastase and into a fragment of the 31-kDa interleukin 1beta precursor by human interleukin 1beta-converting enzyme.	Fluorescein	22-33	caspase 1	Homo sapiens	261-296
8915583-5	1996	Oligonucleotides to interleukin-1 beta convertase (ICE), which detected the expected 2-kb transcript and two lesser 1.5- and 3-kb hybridizing species, demonstrated slight mRNA induction in the CA1 region at 72 h following ischemia.	Oligonucleotides	0-16	caspase 1	Homo sapiens	20-49
8912630-1	1996	In this study, we investigated the IL-1 beta converting enzyme (ICE) family cysteine proteases responsible for the Fas-mediated apoptosis of rheumatoid arthritis (RA) synoviocytes and their involvement in proinflammatory cytokine production.	ammonium ferrous sulfate	115-118	caspase 1	Homo sapiens	35-62
8912630-1	1996	In this study, we investigated the IL-1 beta converting enzyme (ICE) family cysteine proteases responsible for the Fas-mediated apoptosis of rheumatoid arthritis (RA) synoviocytes and their involvement in proinflammatory cytokine production.	ammonium ferrous sulfate	115-118	caspase 1	Homo sapiens	64-67
8920967-4	1996	The formation of the 120 kDa SBDP was insensitive to calpain inhibitors but was completely blocked by an interleukin 1 beta-converting-enzyme (ICE)-like protease inhibitor, Z-Asp-CH2OC(O)-2,6-dichlorobenzene.	sbdp	29-33	caspase 1	Homo sapiens	105-141
8920967-4	1996	The formation of the 120 kDa SBDP was insensitive to calpain inhibitors but was completely blocked by an interleukin 1 beta-converting-enzyme (ICE)-like protease inhibitor, Z-Asp-CH2OC(O)-2,6-dichlorobenzene.	sbdp	29-33	caspase 1	Homo sapiens	143-146
8920967-4	1996	The formation of the 120 kDa SBDP was insensitive to calpain inhibitors but was completely blocked by an interleukin 1 beta-converting-enzyme (ICE)-like protease inhibitor, Z-Asp-CH2OC(O)-2,6-dichlorobenzene.	z-asp-ch2oc(o)-2,6-dichlorobenzene	173-207	caspase 1	Homo sapiens	105-141
8920967-4	1996	The formation of the 120 kDa SBDP was insensitive to calpain inhibitors but was completely blocked by an interleukin 1 beta-converting-enzyme (ICE)-like protease inhibitor, Z-Asp-CH2OC(O)-2,6-dichlorobenzene.	z-asp-ch2oc(o)-2,6-dichlorobenzene	173-207	caspase 1	Homo sapiens	143-146
8915583-5	1996	Oligonucleotides to interleukin-1 beta convertase (ICE), which detected the expected 2-kb transcript and two lesser 1.5- and 3-kb hybridizing species, demonstrated slight mRNA induction in the CA1 region at 72 h following ischemia.	Oligonucleotides	0-16	caspase 1	Homo sapiens	51-54
8892627-2	1996	To determine the relationship between ICE and its substrate IL-1beta, we examined six human cell lines for susceptibility to Fas-mediated apoptosis and Fas induction of ICE-like activity.	ammonium ferrous sulfate	152-155	caspase 1	Homo sapiens	169-172
8892627-9	1996	These results suggest that Fas-mediated apoptosis is mediated by ICE cleavage of proteolytic substrates other than IL-1beta and that IL-1beta is an endogenous inhibitor of Fas-mediated apoptosis.	ammonium ferrous sulfate	27-30	caspase 1	Homo sapiens	65-68
8892627-4	1996	ICE mRNA was highly expressed in SKW6.4, H-9, and HL-60 cells, and ICE-like activity increased during Fas-mediated apoptosis in SKW6.4 cells.	ammonium ferrous sulfate	102-105	caspase 1	Homo sapiens	0-3
8892627-4	1996	ICE mRNA was highly expressed in SKW6.4, H-9, and HL-60 cells, and ICE-like activity increased during Fas-mediated apoptosis in SKW6.4 cells.	ammonium ferrous sulfate	102-105	caspase 1	Homo sapiens	67-70
8892627-6	1996	Acetyl-Tyr-Val-Ala-Asp-chloromethylketone, a tetrapeptidyl inhibitor of ICE, prevented Fas-mediated apoptosis strongly in SKW6.4 and H-9 cells but weakly or marginally in other cells.	N-acetyl-tyrosyl-valyl-alanyl-aspartyl chloromethyl ketone	0-41	caspase 1	Homo sapiens	72-75
8892627-6	1996	Acetyl-Tyr-Val-Ala-Asp-chloromethylketone, a tetrapeptidyl inhibitor of ICE, prevented Fas-mediated apoptosis strongly in SKW6.4 and H-9 cells but weakly or marginally in other cells.	ammonium ferrous sulfate	87-90	caspase 1	Homo sapiens	72-75
8898109-2	1996	We report here that cell-permeable ceramide induced cleavage and activation of CPP32, a Ced-3/ICE-like protease, but not ICE.	Ceramides	35-43	caspase 1	Homo sapiens	94-97
8917679-11	1996	Further, we examined the involvement of interleukin-converting enzyme (ICE) in silica-mediated apoptosis using an ICE inhibitor, Z-Val-Ala-Asp-fluoromethyl ketone.	Silicon Dioxide	79-85	caspase 1	Homo sapiens	40-69
8917679-11	1996	Further, we examined the involvement of interleukin-converting enzyme (ICE) in silica-mediated apoptosis using an ICE inhibitor, Z-Val-Ala-Asp-fluoromethyl ketone.	Silicon Dioxide	79-85	caspase 1	Homo sapiens	71-74
8917679-14	1996	Additionally, silica-induced apoptosis of alveolar macrophages may be due to the interaction of silica particulates with the SR, initiating one or a number of signaling pathways involving ICE, ultimately leading to apoptosis.	Silicon Dioxide	14-20	caspase 1	Homo sapiens	188-191
8917679-14	1996	Additionally, silica-induced apoptosis of alveolar macrophages may be due to the interaction of silica particulates with the SR, initiating one or a number of signaling pathways involving ICE, ultimately leading to apoptosis.	Silicon Dioxide	96-102	caspase 1	Homo sapiens	188-191
8841000-10	1996	Fas sensitivity was reconstituted in the IFN-gamma-resistant cell line by transfection of ICE into that cell line.	ammonium ferrous sulfate	0-3	caspase 1	Homo sapiens	90-93
8840958-5	1996	Specific tetrapeptide inhibitors of ICE (Acetyl-Tyr-Val-Ala-Asp-chloromethylketone) or CPP32beta (Acetyl-Asp-Glu-Val-Asp-aldehyde) prevented the anti-Fas antibody-mediated activation of p34cdc2 and inhibited apoptosis.	N-acetyl-tyrosyl-valyl-alanyl-aspartyl chloromethyl ketone	41-82	caspase 1	Homo sapiens	36-39
8896444-3	1996	This effect was inhibited by the tetrapeptide Ac-DEVD-CHO, a competitive inhibitor of the interleukin-1 beta-converting enzyme (ICE)-related protease CPP32, but was not influenced by Ac-YVAD-CHO and Ac-YVAD-CMK, two specific inhibitors of ICE.	acetyl-aspartyl-glutamyl-valyl-aspartal	46-57	caspase 1	Homo sapiens	128-131
8896444-3	1996	This effect was inhibited by the tetrapeptide Ac-DEVD-CHO, a competitive inhibitor of the interleukin-1 beta-converting enzyme (ICE)-related protease CPP32, but was not influenced by Ac-YVAD-CHO and Ac-YVAD-CMK, two specific inhibitors of ICE.	acetyl-aspartyl-glutamyl-valyl-aspartal	46-57	caspase 1	Homo sapiens	239-242
8839858-7	1996	On the other hand, a specific tetrapetide-aldehyde inhibitor of ICE significantly retarded the apoptotic death of BMAM cells at 1 mumol/L in 5/6 MDS cases studied (AI% = 2.99 +/- 0.30 in controls v 1.58 +/- 0.40 with ICE-inhibitor, P = .05) and also reduced the levels of active IL-1 beta synthesized (5.59 +/- 2.63 v 2.24 +/- 0.93 pg/10(6) cells, respectively).	tetrapetide	30-41	caspase 1	Homo sapiens	64-67
8837753-9	1996	Benzyloxycarbonyl-Val-Ala-Asp fluoromethyl ketone and iodoacetamide, inactivators of interleukin 1beta-converting enzyme (ICE)-like proteases, did not produce apoptosis and inhibited the induction of apoptosis by cycloheximide, calpain inhibitors, or serine protease inhibitors.	Caspase Inhibitor VI	0-49	caspase 1	Homo sapiens	85-120
8837753-9	1996	Benzyloxycarbonyl-Val-Ala-Asp fluoromethyl ketone and iodoacetamide, inactivators of interleukin 1beta-converting enzyme (ICE)-like proteases, did not produce apoptosis and inhibited the induction of apoptosis by cycloheximide, calpain inhibitors, or serine protease inhibitors.	Iodoacetamide	54-67	caspase 1	Homo sapiens	85-120
8839858-7	1996	On the other hand, a specific tetrapetide-aldehyde inhibitor of ICE significantly retarded the apoptotic death of BMAM cells at 1 mumol/L in 5/6 MDS cases studied (AI% = 2.99 +/- 0.30 in controls v 1.58 +/- 0.40 with ICE-inhibitor, P = .05) and also reduced the levels of active IL-1 beta synthesized (5.59 +/- 2.63 v 2.24 +/- 0.93 pg/10(6) cells, respectively).	tetrapetide	30-41	caspase 1	Homo sapiens	217-220
8839858-7	1996	On the other hand, a specific tetrapetide-aldehyde inhibitor of ICE significantly retarded the apoptotic death of BMAM cells at 1 mumol/L in 5/6 MDS cases studied (AI% = 2.99 +/- 0.30 in controls v 1.58 +/- 0.40 with ICE-inhibitor, P = .05) and also reduced the levels of active IL-1 beta synthesized (5.59 +/- 2.63 v 2.24 +/- 0.93 pg/10(6) cells, respectively).	Aldehydes	42-50	caspase 1	Homo sapiens	64-67
8855298-6	1996	Using the peptide inhibitor Ac-DEVD-CHO, apoptosis as well as p45 ICE hydrolysis are suppressed in HeLa cells, suggesting that a CPP32-like protease is upstream of ICE.	acetyl-aspartyl-glutamyl-valyl-aspartal	28-39	caspase 1	Homo sapiens	62-65
8879205-5	1996	This apoptosis-inducing factor (AIF) is blocked by N-benzyloxycarbonyl-Val-Ala-Asp.fluoromethylketone (Z-VAD.fmk), an antagonist of interleukin-1 beta-converting enzyme (ICE)-like proteases that is also an efficient inhibitor of apoptosis in cells.	n-benzyloxycarbonyl-val-ala-asp.fluoromethylketone	51-101	caspase 1	Homo sapiens	132-168
8879205-5	1996	This apoptosis-inducing factor (AIF) is blocked by N-benzyloxycarbonyl-Val-Ala-Asp.fluoromethylketone (Z-VAD.fmk), an antagonist of interleukin-1 beta-converting enzyme (ICE)-like proteases that is also an efficient inhibitor of apoptosis in cells.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	103-112	caspase 1	Homo sapiens	132-168
8855298-6	1996	Using the peptide inhibitor Ac-DEVD-CHO, apoptosis as well as p45 ICE hydrolysis are suppressed in HeLa cells, suggesting that a CPP32-like protease is upstream of ICE.	acetyl-aspartyl-glutamyl-valyl-aspartal	28-39	caspase 1	Homo sapiens	66-69
8855298-6	1996	Using the peptide inhibitor Ac-DEVD-CHO, apoptosis as well as p45 ICE hydrolysis are suppressed in HeLa cells, suggesting that a CPP32-like protease is upstream of ICE.	acetyl-aspartyl-glutamyl-valyl-aspartal	28-39	caspase 1	Homo sapiens	164-167
8670889-4	1996	Nanomolar concentrations of several proteasome inhibitors, including the highly selective inhibitor lactacystin, not only prolonged survival of NGF-deprived neurons but also prevented processing of poly(ADP-ribose) polymerase which is known to be cleaved by an ICE/Ced-3 family member during PCD.	lactacystin	100-111	caspase 1	Homo sapiens	261-264
8702962-0	1996	An interleukin-1beta converting enzyme-like protease is a key component of Fas-mediated apoptosis.	ammonium ferrous sulfate	75-78	caspase 1	Homo sapiens	3-38
8702962-4	1996	Here we use activity assays and peptide inhibitors of ICE/Ced-3 proteases to study their role in Fas-mediated killing.	ammonium ferrous sulfate	97-100	caspase 1	Homo sapiens	54-57
8702962-8	1996	Although ICE activity (as measured by a fluorogenic substrate) is present in cell lysates from anti-Fas-treated cells, we found no pro-IL-1beta-cleaving activity in these lysates.	ammonium ferrous sulfate	100-103	caspase 1	Homo sapiens	9-12
8670889-6	1996	This order of events was confirmed in macrophages where lactacystin inhibited the proteolytic activation of precursor ICE and the subsequent generation of active interleukin-1beta.	lactacystin	56-67	caspase 1	Homo sapiens	118-121
8757963-7	1996	On the other hand, the IL-1beta-converting enzyme (ICE)-like protease tetrapeptide inhibitor Ac-YVAD-cmk partially inhibited Fas-based cytotoxicity, while the specific inhibitor of CPP32/Yama Ac-DEVD-CHO was a much more effective inhibitor of Fas-induced apoptosis.	N-acetyl-tyrosyl-valyl-alanyl-aspartyl chloromethyl ketone	93-104	caspase 1	Homo sapiens	23-49
8663439-0	1996	Fas-induced activation of the cell death-related protease CPP32 Is inhibited by Bcl-2 and by ICE family protease inhibitors.	ammonium ferrous sulfate	0-3	caspase 1	Homo sapiens	93-96
8663439-6	1996	CPP32 activation is blocked by cell-permeable inhibitors of aspartate-directed, cysteine proteases, suggesting that pro-CPP32 is cleaved by active CPP32 or by other ICE family members.	Aspartic Acid	60-69	caspase 1	Homo sapiens	165-168
8764657-0	1996	Potassium deprivation-induced apoptosis of cerebellar granule neurons: a sequential requirement for new mRNA and protein synthesis, ICE-like protease activity, and reactive oxygen species.	Potassium	0-9	caspase 1	Homo sapiens	132-135
8764657-2	1996	Using a fluorogenic substrate for interleukin-1beta converting enzyme (ICE), we show that K+ deprivation of cerebellar granule neurons induces cycloheximide-sensitive ICE-like protease activity.	Cycloheximide	143-156	caspase 1	Homo sapiens	34-69
8764657-2	1996	Using a fluorogenic substrate for interleukin-1beta converting enzyme (ICE), we show that K+ deprivation of cerebellar granule neurons induces cycloheximide-sensitive ICE-like protease activity.	Cycloheximide	143-156	caspase 1	Homo sapiens	71-74
8764657-2	1996	Using a fluorogenic substrate for interleukin-1beta converting enzyme (ICE), we show that K+ deprivation of cerebellar granule neurons induces cycloheximide-sensitive ICE-like protease activity.	Cycloheximide	143-156	caspase 1	Homo sapiens	167-170
8764657-3	1996	A peptide inhibitor of ICE-like protease activity, Ac-YVAD-chloromethylketone (Ac-YVAD-CMK), prevents K+ deprivation-induced apoptosis.	ac-yvad-chloromethylketone	51-77	caspase 1	Homo sapiens	23-26
8764657-3	1996	A peptide inhibitor of ICE-like protease activity, Ac-YVAD-chloromethylketone (Ac-YVAD-CMK), prevents K+ deprivation-induced apoptosis.	ac-yvad	51-58	caspase 1	Homo sapiens	23-26
8764657-5	1996	Using fluorescent assays, we show that ROS production after K+ deprivation is blocked by actinomycin D, cycloheximide, and Ac-YVAD-CMK, suggesting that ROS act downstream of gene transcription, mRNA translation, and ICE activation.	Reactive Oxygen Species	39-42	caspase 1	Homo sapiens	216-219
8764657-5	1996	Using fluorescent assays, we show that ROS production after K+ deprivation is blocked by actinomycin D, cycloheximide, and Ac-YVAD-CMK, suggesting that ROS act downstream of gene transcription, mRNA translation, and ICE activation.	Dactinomycin	89-102	caspase 1	Homo sapiens	216-219
8764657-5	1996	Using fluorescent assays, we show that ROS production after K+ deprivation is blocked by actinomycin D, cycloheximide, and Ac-YVAD-CMK, suggesting that ROS act downstream of gene transcription, mRNA translation, and ICE activation.	Cycloheximide	104-117	caspase 1	Homo sapiens	216-219
8764657-5	1996	Using fluorescent assays, we show that ROS production after K+ deprivation is blocked by actinomycin D, cycloheximide, and Ac-YVAD-CMK, suggesting that ROS act downstream of gene transcription, mRNA translation, and ICE activation.	ac-yvad	123-130	caspase 1	Homo sapiens	216-219
8764657-5	1996	Using fluorescent assays, we show that ROS production after K+ deprivation is blocked by actinomycin D, cycloheximide, and Ac-YVAD-CMK, suggesting that ROS act downstream of gene transcription, mRNA translation, and ICE activation.	Reactive Oxygen Species	152-155	caspase 1	Homo sapiens	216-219
8752894-0	1996	Defective Rho GTPase regulation by IL-1 beta-converting enzyme-mediated cleavage of D4 GDP dissociation inhibitor.	Guanosine Diphosphate	87-90	caspase 1	Homo sapiens	35-62
8663307-7	1996	We also examined the requirement for protease activation for cytoplasmic acidification to occur and found that inhibition of interleukin-1beta converting enzyme/CED-3 family proteases (using carbobenzoxy-Val-Ala-Asp-fluoromethylketone, an inhibitor of these proteases) prevents acidification and apoptosis mediated by Fas ligation.	carbobenzoxy-val-ala-asp-fluoromethylketone	191-234	caspase 1	Homo sapiens	125-160
8757963-7	1996	On the other hand, the IL-1beta-converting enzyme (ICE)-like protease tetrapeptide inhibitor Ac-YVAD-cmk partially inhibited Fas-based cytotoxicity, while the specific inhibitor of CPP32/Yama Ac-DEVD-CHO was a much more effective inhibitor of Fas-induced apoptosis.	N-acetyl-tyrosyl-valyl-alanyl-aspartyl chloromethyl ketone	93-104	caspase 1	Homo sapiens	51-54
8757963-7	1996	On the other hand, the IL-1beta-converting enzyme (ICE)-like protease tetrapeptide inhibitor Ac-YVAD-cmk partially inhibited Fas-based cytotoxicity, while the specific inhibitor of CPP32/Yama Ac-DEVD-CHO was a much more effective inhibitor of Fas-induced apoptosis.	ammonium ferrous sulfate	125-128	caspase 1	Homo sapiens	23-49
8757963-7	1996	On the other hand, the IL-1beta-converting enzyme (ICE)-like protease tetrapeptide inhibitor Ac-YVAD-cmk partially inhibited Fas-based cytotoxicity, while the specific inhibitor of CPP32/Yama Ac-DEVD-CHO was a much more effective inhibitor of Fas-induced apoptosis.	ammonium ferrous sulfate	125-128	caspase 1	Homo sapiens	51-54
8757963-7	1996	On the other hand, the IL-1beta-converting enzyme (ICE)-like protease tetrapeptide inhibitor Ac-YVAD-cmk partially inhibited Fas-based cytotoxicity, while the specific inhibitor of CPP32/Yama Ac-DEVD-CHO was a much more effective inhibitor of Fas-induced apoptosis.	acetyl-aspartyl-glutamyl-valyl-aspartal	192-203	caspase 1	Homo sapiens	23-49
8757963-7	1996	On the other hand, the IL-1beta-converting enzyme (ICE)-like protease tetrapeptide inhibitor Ac-YVAD-cmk partially inhibited Fas-based cytotoxicity, while the specific inhibitor of CPP32/Yama Ac-DEVD-CHO was a much more effective inhibitor of Fas-induced apoptosis.	acetyl-aspartyl-glutamyl-valyl-aspartal	192-203	caspase 1	Homo sapiens	51-54
8757963-7	1996	On the other hand, the IL-1beta-converting enzyme (ICE)-like protease tetrapeptide inhibitor Ac-YVAD-cmk partially inhibited Fas-based cytotoxicity, while the specific inhibitor of CPP32/Yama Ac-DEVD-CHO was a much more effective inhibitor of Fas-induced apoptosis.	ammonium ferrous sulfate	243-246	caspase 1	Homo sapiens	23-49
8757963-7	1996	On the other hand, the IL-1beta-converting enzyme (ICE)-like protease tetrapeptide inhibitor Ac-YVAD-cmk partially inhibited Fas-based cytotoxicity, while the specific inhibitor of CPP32/Yama Ac-DEVD-CHO was a much more effective inhibitor of Fas-induced apoptosis.	ammonium ferrous sulfate	243-246	caspase 1	Homo sapiens	51-54
8757963-8	1996	It was concluded that Fas-induced cytotoxicity was clearly dependent on ICE-like protease activation, and especially on that of CPP32 in Fas-sensitive cells, including mitochondrial DNA-depleted ones.	ammonium ferrous sulfate	22-25	caspase 1	Homo sapiens	72-75
8655577-0	1996	Role of Ced-3/ICE-family proteases in staurosporine-induced programmed cell death.	Staurosporine	38-51	caspase 1	Homo sapiens	14-17
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 1	Homo sapiens	2-5
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 1	Homo sapiens	2-5
8662843-4	1996	The addition of L-742,395, a biotinylated irreversible ICE inhibitor, to these extracts labels only p45 and simultaneously inhibits p45 processing, demonstrating that the p45 has catalytic activity.	l-742	16-21	caspase 1	Homo sapiens	55-58
8662843-4	1996	The addition of L-742,395, a biotinylated irreversible ICE inhibitor, to these extracts labels only p45 and simultaneously inhibits p45 processing, demonstrating that the p45 has catalytic activity.	l-742	16-21	caspase 1	Homo sapiens	100-103
8662843-4	1996	The addition of L-742,395, a biotinylated irreversible ICE inhibitor, to these extracts labels only p45 and simultaneously inhibits p45 processing, demonstrating that the p45 has catalytic activity.	l-742	16-21	caspase 1	Homo sapiens	132-135
8662843-4	1996	The addition of L-742,395, a biotinylated irreversible ICE inhibitor, to these extracts labels only p45 and simultaneously inhibits p45 processing, demonstrating that the p45 has catalytic activity.	l-742	16-21	caspase 1	Homo sapiens	132-135
8662843-5	1996	Following a cleavage of p45 at a site that becomes the COOH terminus of p20, a more active intermediate is formed which migrates on SDS-polyacrylamide gel electrophoresis with an molecular mass of 35 kDa (ED50 of approximately 0.1 microM L-742,395 labeling versus 5 microM for p45).	Sodium Dodecyl Sulfate	132-135	caspase 1	Homo sapiens	24-27
8662843-5	1996	Following a cleavage of p45 at a site that becomes the COOH terminus of p20, a more active intermediate is formed which migrates on SDS-polyacrylamide gel electrophoresis with an molecular mass of 35 kDa (ED50 of approximately 0.1 microM L-742,395 labeling versus 5 microM for p45).	polyacrylamide	136-150	caspase 1	Homo sapiens	24-27
8662843-9	1996	Less than 50% of the p45 is cleaved down to active p20 or p22 ICE as determined by band shift on SDS-polyacrylamide gel electrophoresis of the biotinylated fragments, indicating that the in vitro activation is highly inefficient.	Sodium Dodecyl Sulfate	97-100	caspase 1	Homo sapiens	62-65
8662843-9	1996	Less than 50% of the p45 is cleaved down to active p20 or p22 ICE as determined by band shift on SDS-polyacrylamide gel electrophoresis of the biotinylated fragments, indicating that the in vitro activation is highly inefficient.	polyacrylamide	101-115	caspase 1	Homo sapiens	62-65
8662843-11	1996	Cleavage of p45 by exogenous p20/p10 ICE differs from that of the endogenous p45 cleavage activity in that the p20/p10 activity is more salt sensitive, and it produces a different pattern of cleavage fragments, principally 35- and 12-kDa fragments.	Salts	136-140	caspase 1	Homo sapiens	12-15
8662843-11	1996	Cleavage of p45 by exogenous p20/p10 ICE differs from that of the endogenous p45 cleavage activity in that the p20/p10 activity is more salt sensitive, and it produces a different pattern of cleavage fragments, principally 35- and 12-kDa fragments.	Salts	136-140	caspase 1	Homo sapiens	37-40
8662843-11	1996	Cleavage of p45 by exogenous p20/p10 ICE differs from that of the endogenous p45 cleavage activity in that the p20/p10 activity is more salt sensitive, and it produces a different pattern of cleavage fragments, principally 35- and 12-kDa fragments.	Salts	136-140	caspase 1	Homo sapiens	77-80
8656677-0	1996	Role of serine and ICE-like proteases in induction of apoptosis by etoposide in human leukemia HL-60 cells.	Etoposide	67-76	caspase 1	Homo sapiens	19-22
8647264-7	1996	A tripeptide inhibitor of ICE family cysteine proteases, Z-Val-Ala-Asp-fluoromethylketone (zVAD-fmk) inhibits ionomycin- and AgR-triggered CPP32 activation, PARP cleavage and apoptosis, but not growth arrest, in Ramos-BL B cells.	tripeptide K-26	2-12	caspase 1	Homo sapiens	26-29
8647264-7	1996	A tripeptide inhibitor of ICE family cysteine proteases, Z-Val-Ala-Asp-fluoromethylketone (zVAD-fmk) inhibits ionomycin- and AgR-triggered CPP32 activation, PARP cleavage and apoptosis, but not growth arrest, in Ramos-BL B cells.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	57-89	caspase 1	Homo sapiens	26-29
8647264-7	1996	A tripeptide inhibitor of ICE family cysteine proteases, Z-Val-Ala-Asp-fluoromethylketone (zVAD-fmk) inhibits ionomycin- and AgR-triggered CPP32 activation, PARP cleavage and apoptosis, but not growth arrest, in Ramos-BL B cells.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	91-99	caspase 1	Homo sapiens	26-29
8647264-7	1996	A tripeptide inhibitor of ICE family cysteine proteases, Z-Val-Ala-Asp-fluoromethylketone (zVAD-fmk) inhibits ionomycin- and AgR-triggered CPP32 activation, PARP cleavage and apoptosis, but not growth arrest, in Ramos-BL B cells.	Ionomycin	110-119	caspase 1	Homo sapiens	26-29
8665848-2	1996	One of these proteases, granzyme B, has an unusual substrate site preference for Asp residues, a property that it shares with members of the emerging interleukin-1beta-converting enzyme (ICE)/CED-3 family of proteases.	Aspartic Acid	81-84	caspase 1	Homo sapiens	150-185
8665848-2	1996	One of these proteases, granzyme B, has an unusual substrate site preference for Asp residues, a property that it shares with members of the emerging interleukin-1beta-converting enzyme (ICE)/CED-3 family of proteases.	Aspartic Acid	81-84	caspase 1	Homo sapiens	187-190
8656677-6	1996	An inhibitor of interleukin 1-beta-converting enzyme (ICE), Z-Val-Ala-Asp-fluoromethyl ketone (VAD-FMK), had no effect on this DNA fragmenting activity in vitro.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	60-93	caspase 1	Homo sapiens	16-52
8656677-6	1996	An inhibitor of interleukin 1-beta-converting enzyme (ICE), Z-Val-Ala-Asp-fluoromethyl ketone (VAD-FMK), had no effect on this DNA fragmenting activity in vitro.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	60-93	caspase 1	Homo sapiens	54-57
8656677-8	1996	Our data indicate that serine and ICE-like proteases may be involved in etoposide-induced apoptosis at the different stages, and especially a serine protease may be closely associated with the final step for induction of internucleosomal DNA fragmentation during apoptosis in HL-60 cells.	Etoposide	72-81	caspase 1	Homo sapiens	34-37
8967341-3	1996	JNK1 (p45) and JNK2 (p54) isoforms phosphorylated His-c-jun in mesangial cells.	Histidine	50-53	caspase 1	Homo sapiens	6-9
8620480-2	1996	Interleukin-1beta-converting enzyme (ICE), which shows substantial homology to the product of the cell death gene, ced-3, of Caenorhabditis elegans, is reported to be involved in Fas-mediated apoptosis.	ammonium ferrous sulfate	179-182	caspase 1	Homo sapiens	37-40
8620480-4	1996	Fas-mediated apoptosis is inhibited by the CPP32/Yama inhibitor DEVD-CHO, but not by the ICE inhibitor YVAD-CHO, suggesting a dominant role for the CPP32/Yama(-like) proteases and not ICE itself in Fas-mediated apoptosis of the human carcinoma cell lines.	ammonium ferrous sulfate	0-3	caspase 1	Homo sapiens	184-187
8617266-8	1996	In addition, as already observed for ICE and TX, TY is able to induce apoptosis when overexpressed in COS cells.	Thr-Tyr	49-51	caspase 1	Homo sapiens	37-40
8670109-2	1996	We now demonstrate that benzyloxycarbonyl-Val-Ala-Asp (OMe) fluoromethylketone (Z-VAD.FMK), an ICE-like protease inhibitor, inhibits apoptosis by preventing the processing of CPP32 to its active form.	benzyloxycarbonyl-val-ala-asp (ome) fluoromethylketone	24-78	caspase 1	Homo sapiens	95-98
8670109-2	1996	We now demonstrate that benzyloxycarbonyl-Val-Ala-Asp (OMe) fluoromethylketone (Z-VAD.FMK), an ICE-like protease inhibitor, inhibits apoptosis by preventing the processing of CPP32 to its active form.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	80-89	caspase 1	Homo sapiens	95-98
8617266-9	1996	TY therefore represents a new member of the growing family of apoptosis-inducing ICE-related cysteine proteases.	Thr-Tyr	0-2	caspase 1	Homo sapiens	81-84
8567626-0	1996	CPP32/apopain is a key interleukin 1 beta converting enzyme-like protease involved in Fas-mediated apoptosis.	ammonium ferrous sulfate	86-89	caspase 1	Homo sapiens	23-59
8812723-0	1996	Stimulation of interleukin-1beta-converting enzyme activity during growth inhibition by CPT-11 in the human myeloid leukemia cell line K562.	Irinotecan	88-94	caspase 1	Homo sapiens	15-50
8812723-6	1996	To determine how CPT-11 brings about cell death by apoptosis, we investigated the effects of CPT-11 on the expression of ICE activity in K562 cells, which represent human myeloid leukemia cells.	Irinotecan	93-99	caspase 1	Homo sapiens	121-124
8812723-8	1996	We also found that the levels of mRNA for ICE in the cells were increased in the presence of CPT-11.	Irinotecan	93-99	caspase 1	Homo sapiens	42-45
8812723-10	1996	These features suggested that CPT-11 enhances the apoptotic cell death in K562 cells and that a part of induction of apoptosis by CPT-11 may be correlated with the stimulation of the ICE activity.	Irinotecan	30-36	caspase 1	Homo sapiens	183-186
8812723-10	1996	These features suggested that CPT-11 enhances the apoptotic cell death in K562 cells and that a part of induction of apoptosis by CPT-11 may be correlated with the stimulation of the ICE activity.	Irinotecan	130-136	caspase 1	Homo sapiens	183-186
8631956-8	1996	Aurintricarboxylic acid, an inhibitor of apoptosis in mammalian cells, blocked Ced-3 autocatalytic activity, suggesting that an aurintricarboxylic acid-sensitive Ced-3/ICE-related protease might be involved in the apoptosis pathway(s) in mammalian cells.	Aurintricarboxylic Acid	0-23	caspase 1	Homo sapiens	168-171
8567626-1	1996	Cysteine proteases of the interleukin 1 beta Converting Enzyme (ICE)/CED-3 family have been implicated in the effector process of apoptosis in several systems, including Fas-mediated apoptosis.	ammonium ferrous sulfate	170-173	caspase 1	Homo sapiens	26-62
8567626-1	1996	Cysteine proteases of the interleukin 1 beta Converting Enzyme (ICE)/CED-3 family have been implicated in the effector process of apoptosis in several systems, including Fas-mediated apoptosis.	ammonium ferrous sulfate	170-173	caspase 1	Homo sapiens	64-67
8856983-6	1996	On the other hand, tumor sensitization may result from activation of "killing" proteins such as interleukin-1 beta converting enzyme (ICE) or other ICE-like proteases, possibly through TNF/LT-induced oxygen free radicals.	Oxygen	200-206	caspase 1	Homo sapiens	96-132
8856983-6	1996	On the other hand, tumor sensitization may result from activation of "killing" proteins such as interleukin-1 beta converting enzyme (ICE) or other ICE-like proteases, possibly through TNF/LT-induced oxygen free radicals.	Oxygen	200-206	caspase 1	Homo sapiens	134-137
8856983-6	1996	On the other hand, tumor sensitization may result from activation of "killing" proteins such as interleukin-1 beta converting enzyme (ICE) or other ICE-like proteases, possibly through TNF/LT-induced oxygen free radicals.	Oxygen	200-206	caspase 1	Homo sapiens	148-151
8856983-6	1996	On the other hand, tumor sensitization may result from activation of "killing" proteins such as interleukin-1 beta converting enzyme (ICE) or other ICE-like proteases, possibly through TNF/LT-induced oxygen free radicals.	Free Radicals	207-220	caspase 1	Homo sapiens	96-132
8856983-6	1996	On the other hand, tumor sensitization may result from activation of "killing" proteins such as interleukin-1 beta converting enzyme (ICE) or other ICE-like proteases, possibly through TNF/LT-induced oxygen free radicals.	Free Radicals	207-220	caspase 1	Homo sapiens	134-137
8856983-6	1996	On the other hand, tumor sensitization may result from activation of "killing" proteins such as interleukin-1 beta converting enzyme (ICE) or other ICE-like proteases, possibly through TNF/LT-induced oxygen free radicals.	Free Radicals	207-220	caspase 1	Homo sapiens	148-151
8541550-4	1995	To do this, we used bocaspartyl (benzyl) chloromethylketone (BACMK) an inhibitor designed to penetrate cells and bind covalently to the active site of ICE.	N-tert-butyloxycarbonyl-aspartyl (benzyl)chloromethylketone	20-59	caspase 1	Homo sapiens	151-154
8521409-4	1995	We show here that cis-diamminedichloroplatinum (cisplatin) induces the expression of interleukin-1 beta-converting enzyme (ICE), a mammalian homologue of the Caenorhabditis elegans cell death gene ced-3, in murine and human malignant glioma cells during apoptosis regardless of their p53 status.	Cisplatin	18-46	caspase 1	Homo sapiens	85-121
8521409-4	1995	We show here that cis-diamminedichloroplatinum (cisplatin) induces the expression of interleukin-1 beta-converting enzyme (ICE), a mammalian homologue of the Caenorhabditis elegans cell death gene ced-3, in murine and human malignant glioma cells during apoptosis regardless of their p53 status.	Cisplatin	18-46	caspase 1	Homo sapiens	123-126
8521409-4	1995	We show here that cis-diamminedichloroplatinum (cisplatin) induces the expression of interleukin-1 beta-converting enzyme (ICE), a mammalian homologue of the Caenorhabditis elegans cell death gene ced-3, in murine and human malignant glioma cells during apoptosis regardless of their p53 status.	Cisplatin	48-57	caspase 1	Homo sapiens	85-121
8521409-4	1995	We show here that cis-diamminedichloroplatinum (cisplatin) induces the expression of interleukin-1 beta-converting enzyme (ICE), a mammalian homologue of the Caenorhabditis elegans cell death gene ced-3, in murine and human malignant glioma cells during apoptosis regardless of their p53 status.	Cisplatin	48-57	caspase 1	Homo sapiens	123-126
8557034-8	1995	The specific tetrapeptide ICE inhibitor (YVAD) blocked both proteolytic activation of PKC delta and internucleosomal DNA fragmentation in IR-treated cells.	YVAD	41-45	caspase 1	Homo sapiens	26-29
8541550-4	1995	To do this, we used bocaspartyl (benzyl) chloromethylketone (BACMK) an inhibitor designed to penetrate cells and bind covalently to the active site of ICE.	BACMK ketone	61-66	caspase 1	Homo sapiens	151-154
7595215-12	1995	Likewise, labeling of fixed ultrathin cryosections of monocytes with a biotinylated irreversible ICE inhibitor [Ac-Tyr-Val-Lys(biotin)-Asp-(acyloxy)-methyl-ketone] showed that the compound localized on the outer cell surface as well, and to a lesser extent, within the cytoplasmic ground substance.	ac-tyr-val-lys(biotin)-asp-(acyloxy)-methyl-ketone	112-162	caspase 1	Homo sapiens	97-100
8554575-3	1995	This ACA was inhibited by inhibitors of interleukin-1 beta-converting enzyme (ICE)/ced-3 family proteases, such as Z-Asp-CH2-DCB, YVAD-CHO, TPCK, TLCK, and iodoacetamide.	benzyloxycarbonyl-Asp-CH2OC(O)-2,6-dichlorobenzene	115-128	caspase 1	Homo sapiens	40-76
8554575-3	1995	This ACA was inhibited by inhibitors of interleukin-1 beta-converting enzyme (ICE)/ced-3 family proteases, such as Z-Asp-CH2-DCB, YVAD-CHO, TPCK, TLCK, and iodoacetamide.	benzyloxycarbonyl-Asp-CH2OC(O)-2,6-dichlorobenzene	115-128	caspase 1	Homo sapiens	78-81
8554575-3	1995	This ACA was inhibited by inhibitors of interleukin-1 beta-converting enzyme (ICE)/ced-3 family proteases, such as Z-Asp-CH2-DCB, YVAD-CHO, TPCK, TLCK, and iodoacetamide.	tyrosyl-valyl-alanyl-aspartal	130-138	caspase 1	Homo sapiens	40-76
8554575-3	1995	This ACA was inhibited by inhibitors of interleukin-1 beta-converting enzyme (ICE)/ced-3 family proteases, such as Z-Asp-CH2-DCB, YVAD-CHO, TPCK, TLCK, and iodoacetamide.	Iodoacetamide	156-169	caspase 1	Homo sapiens	40-76
8554575-3	1995	This ACA was inhibited by inhibitors of interleukin-1 beta-converting enzyme (ICE)/ced-3 family proteases, such as Z-Asp-CH2-DCB, YVAD-CHO, TPCK, TLCK, and iodoacetamide.	Iodoacetamide	156-169	caspase 1	Homo sapiens	78-81
8964658-0	1995	Effect of peptide aldehydes with IL-1 beta converting enzyme inhibitory properties on IL-1 alpha and IL-1 beta production in vitro.	Aldehydes	18-27	caspase 1	Homo sapiens	33-60
8964658-1	1995	Tripeptide and pentapeptide aldehydes as substrate-base inhibitors of cysteine proteases were designed in our laboratory for the inhibition of interleukin-1 beta converting enzyme (ICE), a recently described cysteine protease responsible for the processing of IL-1 beta.	tripeptide K-26	0-10	caspase 1	Homo sapiens	143-179
8964658-1	1995	Tripeptide and pentapeptide aldehydes as substrate-base inhibitors of cysteine proteases were designed in our laboratory for the inhibition of interleukin-1 beta converting enzyme (ICE), a recently described cysteine protease responsible for the processing of IL-1 beta.	tripeptide K-26	0-10	caspase 1	Homo sapiens	181-184
8964658-1	1995	Tripeptide and pentapeptide aldehydes as substrate-base inhibitors of cysteine proteases were designed in our laboratory for the inhibition of interleukin-1 beta converting enzyme (ICE), a recently described cysteine protease responsible for the processing of IL-1 beta.	pentapeptide aldehydes	15-37	caspase 1	Homo sapiens	143-179
8964658-1	1995	Tripeptide and pentapeptide aldehydes as substrate-base inhibitors of cysteine proteases were designed in our laboratory for the inhibition of interleukin-1 beta converting enzyme (ICE), a recently described cysteine protease responsible for the processing of IL-1 beta.	pentapeptide aldehydes	15-37	caspase 1	Homo sapiens	181-184
8964658-11	1995	These findings indicate that these peptide aldehydes might be used as IL-beta inhibitory agents in experimental models in which IL-1 beta is a key mediator or ICE is implicated.	Aldehydes	43-52	caspase 1	Homo sapiens	159-162
7499971-4	1995	Activated cells treated with YVAD-emk and ATP or CTL showed no mature IL-1 beta in either the cell lysates or the culture supernatants, indicating effective inhibition of ICE activity; however, the YVAD-treated macrophages showed no detectable change in 51Cr release or nuclear fragmentation, indicating failure to inhibit apoptotic cell death.	YVAD	29-33	caspase 1	Homo sapiens	171-174
7499971-4	1995	Activated cells treated with YVAD-emk and ATP or CTL showed no mature IL-1 beta in either the cell lysates or the culture supernatants, indicating effective inhibition of ICE activity; however, the YVAD-treated macrophages showed no detectable change in 51Cr release or nuclear fragmentation, indicating failure to inhibit apoptotic cell death.	Adenosine Triphosphate	42-45	caspase 1	Homo sapiens	171-174
7499971-4	1995	Activated cells treated with YVAD-emk and ATP or CTL showed no mature IL-1 beta in either the cell lysates or the culture supernatants, indicating effective inhibition of ICE activity; however, the YVAD-treated macrophages showed no detectable change in 51Cr release or nuclear fragmentation, indicating failure to inhibit apoptotic cell death.	YVAD	198-202	caspase 1	Homo sapiens	171-174
7797592-3	1995	Both were highly homologous to human ICE (52% identical) and CED-3 (25% identical) and both contained the absolutely conserved pentapeptide sequence Gln-Ala-Cys-Arg-Asp containing the catalytic cysteine residue.	Glutamine	149-152	caspase 1	Homo sapiens	37-40
7629113-4	1995	The cleavage enzyme, designated SREBP cleavage activity (SCA), belongs to a new class of cysteine proteases of the interleukin-1 beta-converting enzyme (ICE) family, all of which cleave at aspartic acid residues.	Aspartic Acid	189-202	caspase 1	Homo sapiens	153-156
7797592-3	1995	Both were highly homologous to human ICE (52% identical) and CED-3 (25% identical) and both contained the absolutely conserved pentapeptide sequence Gln-Ala-Cys-Arg-Asp containing the catalytic cysteine residue.	Alanine	153-156	caspase 1	Homo sapiens	37-40
7797592-3	1995	Both were highly homologous to human ICE (52% identical) and CED-3 (25% identical) and both contained the absolutely conserved pentapeptide sequence Gln-Ala-Cys-Arg-Asp containing the catalytic cysteine residue.	Cysteine	157-160	caspase 1	Homo sapiens	37-40
7797592-3	1995	Both were highly homologous to human ICE (52% identical) and CED-3 (25% identical) and both contained the absolutely conserved pentapeptide sequence Gln-Ala-Cys-Arg-Asp containing the catalytic cysteine residue.	Arginine	161-164	caspase 1	Homo sapiens	37-40
7797592-3	1995	Both were highly homologous to human ICE (52% identical) and CED-3 (25% identical) and both contained the absolutely conserved pentapeptide sequence Gln-Ala-Cys-Arg-Asp containing the catalytic cysteine residue.	Aspartic Acid	165-168	caspase 1	Homo sapiens	37-40
7797592-3	1995	Both were highly homologous to human ICE (52% identical) and CED-3 (25% identical) and both contained the absolutely conserved pentapeptide sequence Gln-Ala-Cys-Arg-Asp containing the catalytic cysteine residue.	Cysteine	194-202	caspase 1	Homo sapiens	37-40
7822802-2	1995	WIN 67694, Z-Val-Ala-Asp-CH2O(CO)[2,6-(CI2)]Ph, is a potent, selective inhibitor of human ICE.	WIN 67694	0-9	caspase 1	Homo sapiens	90-93
7876192-4	1995	In ICE gamma, most of the propeptide (amino acids 20-112) is deleted, which suggests that it may function as a catalyst for ICE autoprocessing in vivo.	propeptide	26-36	caspase 1	Homo sapiens	3-6
7876192-4	1995	In ICE gamma, most of the propeptide (amino acids 20-112) is deleted, which suggests that it may function as a catalyst for ICE autoprocessing in vivo.	propeptide	26-36	caspase 1	Homo sapiens	124-127
7876192-6	1995	Intriguingly, in ICE epsilon amino acids 20-335, which encompass most of the propeptide and the p20 subunit, are deleted resulting in the formation of a molecule that is homologous to the p10 subunit.	propeptide	77-87	caspase 1	Homo sapiens	17-20
7629564-2	1995	To examine the role of pro-IL-1 processing, antisense technology was employed with 16-mer phosphorothioate oligodeoxynucleotide directed against human IL-1 beta converting enzyme (ICR) in 7 randomly selected AML cases.	16-mer phosphorothioate oligodeoxynucleotide	83-127	caspase 1	Homo sapiens	151-178
7629564-2	1995	To examine the role of pro-IL-1 processing, antisense technology was employed with 16-mer phosphorothioate oligodeoxynucleotide directed against human IL-1 beta converting enzyme (ICR) in 7 randomly selected AML cases.	16-mer phosphorothioate oligodeoxynucleotide	83-127	caspase 1	Homo sapiens	180-183
7629564-4	1995	Similarly, spontaneous as well as induced CFU-AML colony formation was inhibited by human ICE antisense oligonucleotide with sample-to-sample variability.	Oligonucleotides	104-119	caspase 1	Homo sapiens	90-93
7538907-4	1995	Overexpression of FADD in MCF7 and BJAB cells induces apoptosis, which, like Fas-induced apoptosis, is blocked by CrmA, a specific inhibitor of the interleukin-1 beta-converting enzyme.	ammonium ferrous sulfate	77-80	caspase 1	Homo sapiens	148-184
7538907-4	1995	Overexpression of FADD in MCF7 and BJAB cells induces apoptosis, which, like Fas-induced apoptosis, is blocked by CrmA, a specific inhibitor of the interleukin-1 beta-converting enzyme.	crma	114-118	caspase 1	Homo sapiens	148-184
7737968-3	1995	Previously we have shown CrmA to be an inhibitor of the cysteine proteinase interleukin-1 beta-converting enzyme (ICE).	crma	25-29	caspase 1	Homo sapiens	114-117
7722467-4	1995	ICE and granzyme B share the rare substrate site of aspartic acid, after which amino acid cleavage of precursor IL-1 beta (pIL-1 beta) occurs.	Aspartic Acid	52-65	caspase 1	Homo sapiens	0-3
7733983-0	1995	Aspartate-based inhibitor of interleukin-1 beta-converting enzyme prevents antitumor agent-induced apoptosis in human myeloid leukemia U937 cells.	Aspartic Acid	0-9	caspase 1	Homo sapiens	29-65
7733983-3	1995	These results indicate that ICE or ICE-like proteases inhibited by Z-Asp-CH2-DCB are involved in a common pathway of apoptotic cell death in U937 cells.	-dcb	76-80	caspase 1	Homo sapiens	28-31
7733983-3	1995	These results indicate that ICE or ICE-like proteases inhibited by Z-Asp-CH2-DCB are involved in a common pathway of apoptotic cell death in U937 cells.	-dcb	76-80	caspase 1	Homo sapiens	35-38
7822802-2	1995	WIN 67694, Z-Val-Ala-Asp-CH2O(CO)[2,6-(CI2)]Ph, is a potent, selective inhibitor of human ICE.	z-val-ala-asp-ch2o	11-29	caspase 1	Homo sapiens	90-93
7822802-2	1995	WIN 67694, Z-Val-Ala-Asp-CH2O(CO)[2,6-(CI2)]Ph, is a potent, selective inhibitor of human ICE.	co)	30-33	caspase 1	Homo sapiens	90-93
7822802-2	1995	WIN 67694, Z-Val-Ala-Asp-CH2O(CO)[2,6-(CI2)]Ph, is a potent, selective inhibitor of human ICE.	2,6-(ci2)	34-43	caspase 1	Homo sapiens	90-93
8077669-5	1994	Immunoprecipitation of [35S]Met-labeled LPS-stimulated monocyte extracts revealed only p45 with no other co-precipitating protein.	Sulfur-35	24-27	caspase 1	Homo sapiens	87-90
7966144-0	1994	Aspartyl alpha-((1-phenyl-3-(trifluoromethyl)-pyrazol-5-yl)oxy)methyl ketones as interleukin-1 beta converting enzyme inhibitors.	aspartyl alpha-((1-phenyl-3-(trifluoromethyl)-pyrazol-5-yl)oxy)methyl ketones	0-77	caspase 1	Homo sapiens	81-117
7830263-0	1995	Aspartyl alpha-((diphenylphosphinyl)oxy)methyl ketones as novel inhibitors of interleukin-1 beta converting enzyme.	aspartyl alpha-((diphenylphosphinyl)oxy)methyl ketones	0-54	caspase 1	Homo sapiens	78-114
8034697-5	1994	It is conformationally unstable, unfolding around 3 M urea, and stable to denaturation in 8 M urea upon complex formation with ICE.	Urea	54-58	caspase 1	Homo sapiens	127-130
7982761-1	1994	Aspartyl aldehyde, Ac-Tyr-Val-Ala-Asp-H 1 (L-709,049), has been reported to be a potent, reversible inhibitor of interleukin-1 beta converting enzyme (ICE) [Thornberry, N.A.	aspartyl aldehyde	0-17	caspase 1	Homo sapiens	113-149
7982761-1	1994	Aspartyl aldehyde, Ac-Tyr-Val-Ala-Asp-H 1 (L-709,049), has been reported to be a potent, reversible inhibitor of interleukin-1 beta converting enzyme (ICE) [Thornberry, N.A.	aspartyl aldehyde	0-17	caspase 1	Homo sapiens	151-154
7982761-1	1994	Aspartyl aldehyde, Ac-Tyr-Val-Ala-Asp-H 1 (L-709,049), has been reported to be a potent, reversible inhibitor of interleukin-1 beta converting enzyme (ICE) [Thornberry, N.A.	L 709049	19-39	caspase 1	Homo sapiens	113-149
7982761-1	1994	Aspartyl aldehyde, Ac-Tyr-Val-Ala-Asp-H 1 (L-709,049), has been reported to be a potent, reversible inhibitor of interleukin-1 beta converting enzyme (ICE) [Thornberry, N.A.	L 709049	19-39	caspase 1	Homo sapiens	151-154
7982761-7	1994	Biological evaluation of these aspartyl aldehydes and derivatives suggests that the tripeptide scaffold, Z-Val-Ala-Asp, is a peptide scaffold that retains good potency and selectivity for ICE.	aspartyl aldehydes	31-49	caspase 1	Homo sapiens	188-191
7982761-7	1994	Biological evaluation of these aspartyl aldehydes and derivatives suggests that the tripeptide scaffold, Z-Val-Ala-Asp, is a peptide scaffold that retains good potency and selectivity for ICE.	tripeptide K-26	84-94	caspase 1	Homo sapiens	188-191
7982761-7	1994	Biological evaluation of these aspartyl aldehydes and derivatives suggests that the tripeptide scaffold, Z-Val-Ala-Asp, is a peptide scaffold that retains good potency and selectivity for ICE.	z-val-ala-asp	105-118	caspase 1	Homo sapiens	188-191
8046336-1	1994	Human interleukin 1 beta (IL-1 beta) is synthesized as an inactive precursor that is cleaved by IL-1 converting enzyme (ICE) between Asp116 and Ala117 to form COOH-terminal mature IL-1 beta and NH2-terminal IL-1 beta propeptide.	Carbonic Acid	159-163	caspase 1	Homo sapiens	96-118
8046336-1	1994	Human interleukin 1 beta (IL-1 beta) is synthesized as an inactive precursor that is cleaved by IL-1 converting enzyme (ICE) between Asp116 and Ala117 to form COOH-terminal mature IL-1 beta and NH2-terminal IL-1 beta propeptide.	Carbonic Acid	159-163	caspase 1	Homo sapiens	120-123
8046336-1	1994	Human interleukin 1 beta (IL-1 beta) is synthesized as an inactive precursor that is cleaved by IL-1 converting enzyme (ICE) between Asp116 and Ala117 to form COOH-terminal mature IL-1 beta and NH2-terminal IL-1 beta propeptide.	propeptide	217-227	caspase 1	Homo sapiens	96-118
8046336-1	1994	Human interleukin 1 beta (IL-1 beta) is synthesized as an inactive precursor that is cleaved by IL-1 converting enzyme (ICE) between Asp116 and Ala117 to form COOH-terminal mature IL-1 beta and NH2-terminal IL-1 beta propeptide.	propeptide	217-227	caspase 1	Homo sapiens	120-123
8034697-5	1994	It is conformationally unstable, unfolding around 3 M urea, and stable to denaturation in 8 M urea upon complex formation with ICE.	Urea	94-98	caspase 1	Homo sapiens	127-130
7931364-0	1994	L-741,494, a fungal metabolite that is an inhibitor of interleukin-1 beta converting enzyme.	l-741	0-5	caspase 1	Homo sapiens	55-91
8044845-2	1994	The crystal structure at 2.5 A resolution of a recombinant human ICE-tetrapeptide chloromethylketone complex reveals that the holoenzyme is a homodimer of catalytic domains, each of which contains a p20 and a p10 subunit.	chloromethylketone	82-100	caspase 1	Homo sapiens	65-68
7931364-2	1994	This substance is a water-soluble, competitive, irreversible inhibitor of Interleukin-1 beta Converting Enzyme that is inactive against papain and trypsin.	Water	20-25	caspase 1	Homo sapiens	74-110
8126694-0	1994	P1 aspartate-based peptide alpha-((2,6-dichlorobenzoyl)oxy)methyl ketones as potent time-dependent inhibitors of interleukin-1 beta-converting enzyme.	alpha-((2,6-dichlorobenzoyl)oxy)methyl ketones	27-73	caspase 1	Homo sapiens	113-149
8142397-0	1994	Inactivation of interleukin-1 beta converting enzyme by peptide (acyloxy)methyl ketones.	peptide (acyloxy)methyl ketones	56-87	caspase 1	Homo sapiens	16-52
8142397-6	1994	Affinity labeling of THP.1 monocytic cell cytosol with a biotinylated tetrapeptide (acyloxy)methyl ketone for 28 half-lives resulted in labeling of only ICE, demonstrating the selectivity of these inhibitors.	(acyloxy)methyl ketone	83-105	caspase 1	Homo sapiens	153-156
8012123-1	1994	Interleukin 1 beta converting enzyme (ICE) is responsible for processing an inactive 31-kDa precursor to the active, mature 17-kDa Il-1 beta with cleavage occurring between the Asp116-Ala117 amide bond.	Amides	191-196	caspase 1	Homo sapiens	0-36
8012123-1	1994	Interleukin 1 beta converting enzyme (ICE) is responsible for processing an inactive 31-kDa precursor to the active, mature 17-kDa Il-1 beta with cleavage occurring between the Asp116-Ala117 amide bond.	Amides	191-196	caspase 1	Homo sapiens	38-41
8012123-3	1994	Upon cleavage of DABCYL-Tyr-Val-Ala-Asp-Ala-Pro-Val-EDANS (DABCYL-ICE-EDANS), an increase in fluorescence is observed at the EDANS emission wavelength of 490 nm, permitting a continuous assay of ICE that is useful in the screening of inhibitory compounds.	4-(4'-dimethylaminophenylazo)benzoyl-tyrosyl-valyl-alanyl-aspartyl-alanyl-prolyl-valyl-5((2-aminoethyl)amino)naphthalene-1-sulfonic acid	17-57	caspase 1	Homo sapiens	66-69
8012123-3	1994	Upon cleavage of DABCYL-Tyr-Val-Ala-Asp-Ala-Pro-Val-EDANS (DABCYL-ICE-EDANS), an increase in fluorescence is observed at the EDANS emission wavelength of 490 nm, permitting a continuous assay of ICE that is useful in the screening of inhibitory compounds.	4-(4'-dimethylaminophenylazo)benzoyl-tyrosyl-valyl-alanyl-aspartyl-alanyl-prolyl-valyl-5((2-aminoethyl)amino)naphthalene-1-sulfonic acid	17-57	caspase 1	Homo sapiens	195-198
8012123-4	1994	The Km and kcat results for hydrolysis of DABCYL-ICE-EDANS by ICE were 11.4 +/- 1.6 microM and 0.79 +/- 0.4 s-1.	5-((2-aminoethyl)amino)naphthalene-1-sulfonic acid	53-58	caspase 1	Homo sapiens	49-52
8012123-4	1994	The Km and kcat results for hydrolysis of DABCYL-ICE-EDANS by ICE were 11.4 +/- 1.6 microM and 0.79 +/- 0.4 s-1.	5-((2-aminoethyl)amino)naphthalene-1-sulfonic acid	53-58	caspase 1	Homo sapiens	62-65
25728492-6	2015	Mechanistically, Cyr61 induced proIL-1beta production in FLS via the AKT-dependent NF-kappaB signaling pathway, and ATP caused Cyr61-induced proIL-1beta to generate IL-1beta in a caspase-1-dependent manner.	Adenosine Triphosphate	116-119	caspase 1	Homo sapiens	179-188
8349684-1	1993	Interleukin-1 beta-converting enzyme (ICE) was purified from dialyzed cytoplasmic extracts of THP.1 human monocytic cells by a combination of DEAE-5PW and SP-5PW ion exchange and C4 reverse phase high performance liquid chromatography.	deae-5pw	142-150	caspase 1	Homo sapiens	0-36
8349684-1	1993	Interleukin-1 beta-converting enzyme (ICE) was purified from dialyzed cytoplasmic extracts of THP.1 human monocytic cells by a combination of DEAE-5PW and SP-5PW ion exchange and C4 reverse phase high performance liquid chromatography.	deae-5pw	142-150	caspase 1	Homo sapiens	38-41
8349684-1	1993	Interleukin-1 beta-converting enzyme (ICE) was purified from dialyzed cytoplasmic extracts of THP.1 human monocytic cells by a combination of DEAE-5PW and SP-5PW ion exchange and C4 reverse phase high performance liquid chromatography.	sp-5pw	155-161	caspase 1	Homo sapiens	0-36
8349684-1	1993	Interleukin-1 beta-converting enzyme (ICE) was purified from dialyzed cytoplasmic extracts of THP.1 human monocytic cells by a combination of DEAE-5PW and SP-5PW ion exchange and C4 reverse phase high performance liquid chromatography.	sp-5pw	155-161	caspase 1	Homo sapiens	38-41
8349684-2	1993	Sequence information from tryptic and Asp.N peptides on the isolated 20-kDa (p20) and a 10-kDa (p10) proteins enabled the subsequent cloning of ICE (Thornberry, N. A., Bull, H. G., Calaycay, J. R., Chapman, K. T., Howard, A. D., Kostura, M. J., Miller, D. K., Molineaux, S. M., Weidner, J. R., Aunins, J., Elliston, K. O., Ayala, J. M., Casano, F. J., Chin, J., Ding, G. J.-F., Egger, L. A., Gaffney, E. P., Limjuco, G., Palyha, O. C., Raju, S. M., Rolando, A. M., Salley, J. P., Yamin, T.-T., Lee, T. D., Shively, J. E., MacCross, M., Mumford, R. A., Schmidt, J.	Aspartic Acid	38-41	caspase 1	Homo sapiens	144-147
1919001-6	1991	Analysis of human IL-1 beta precursor mutants containing amino acid substitutions or deletions within each processing site demonstrated that omission or replacement of Asp at site 1 or site 2 prevented cleavage by ICE.	Aspartic Acid	168-171	caspase 1	Homo sapiens	214-217
1919001-12	1991	These results show that ICE is a highly specific IL-1 beta convertase with absolute requirements for Asp in P1 and a small hydrophobic amino acid in P1".	Aspartic Acid	101-104	caspase 1	Homo sapiens	24-27
33760701-0	2021	Inhibition of Caspase-1 with Tetracycline Ameliorates Acute Lung Injury.	Tetracycline	29-41	caspase 1	Homo sapiens	14-23
33760701-4	2021	Recent studies indicate that tetracycline can be used to treat inflammatory diseases mediated by IL-1beta and IL-18 while the molecular mechanism by which tetracycline inhibits inflammasome-caspase-1 signaling remains unknown.	Tetracycline	155-167	caspase 1	Homo sapiens	190-199
33760701-5	2021	OBJECTIVES: To identify patients with ARDS characterized by IL-1beta and IL-18 expression and investigate the ability of tetracycline to inhibit inflammasome-caspase-1 signaling in ARDS.	Tetracycline	121-133	caspase 1	Homo sapiens	158-167
8138355-0	1994	Peptidic p-nitroanilide substrates of interleukin-1 beta-converting enzyme.	p-nitroanilide	9-23	caspase 1	Homo sapiens	38-74
8138355-2	1994	With the aim of developing a convenient, quantitative assay for inhibitors of interleukin-1 beta-converting enzyme (ICE), we have explored three approaches to the synthesis of peptidic p-nitroanilides relevant to this enzyme.	p-nitroanilides	185-200	caspase 1	Homo sapiens	78-114
8138355-2	1994	With the aim of developing a convenient, quantitative assay for inhibitors of interleukin-1 beta-converting enzyme (ICE), we have explored three approaches to the synthesis of peptidic p-nitroanilides relevant to this enzyme.	p-nitroanilides	185-200	caspase 1	Homo sapiens	116-119
8138355-5	1994	While each approach had it merits and limitations, all three produced p-nitroanilides that were substrates for ICE.	p-nitroanilides	70-85	caspase 1	Homo sapiens	111-114
8446594-6	1993	The active site Cys284 lies within a completely conserved stretch of 18 residues; however, Ser289 in hICE, which aligns with the catalytic region of serine and viral cysteinyl proteases, is absent from mICE.	Serine	149-155	caspase 1	Homo sapiens	101-105
33760701-10	2021	In experimental ALI, tetracycline significantly diminished lung injury and pulmonary inflammation by selectively inhibiting caspase-1-dependent IL-1beta and IL-18 production leading to improved survival.	Tetracycline	21-33	caspase 1	Homo sapiens	124-133
33760701-12	2021	CONCLUSIONS: Tetracycline may be effective in the treatment of direct ARDS in patients with elevated caspase-1 activity.	Tetracycline	13-25	caspase 1	Homo sapiens	101-110
33801204-6	2021	Among the apoptosis-related reagents, caspase-family inhibitor almost completely inhibited HOEA-induced DNA fragmentation.	hoea	91-95	caspase 1	Homo sapiens	38-45
33801204-7	2021	In the analyses using specific caspase-substrates, extremely high cleavage activity toward caspase-3/7/8 substrate was observed in HOEA-treated U937 cells, and weak activities of caspase-1 and -3 were detected.	hoea	131-135	caspase 1	Homo sapiens	31-38
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 1	Homo sapiens	20-28
34766707-3	2022	We isolated primary AEC from three healthy adults and treated them with silica particles at different concentrations for 48 h. We found evidence for silica-induced inflammasome activation by the co-localization of Caspase-1 and NLRP3, as well as increased levels of IL-1beta and IL-18.	Silicon Dioxide	72-78	caspase 1	Homo sapiens	214-223
34766707-3	2022	We isolated primary AEC from three healthy adults and treated them with silica particles at different concentrations for 48 h. We found evidence for silica-induced inflammasome activation by the co-localization of Caspase-1 and NLRP3, as well as increased levels of IL-1beta and IL-18.	Silicon Dioxide	149-155	caspase 1	Homo sapiens	214-223
34904823-5	2022	PA treatment suppresses the nuclear translocation of NF-kappaB, enhances PARKIN translocation into the mitochondria, and maintains cellular redox homeostasis in both mouse and human microglial cells that limit NLRP3 inflammasome activation along with processing of active caspase-1, IL-1beta, and IL-18.	perillyl alcohol	0-2	caspase 1	Homo sapiens	272-281
34823899-0	2022	Design, synthesis and biological evaluation of 1,5-disubstituted alpha-amino tetrazole derivatives as non-covalent inflammasome-caspase-1 complex inhibitors with potential application against immune and inflammatory disorders.	1,5-disubstituted	47-64	caspase 1	Homo sapiens	128-137
34823899-0	2022	Design, synthesis and biological evaluation of 1,5-disubstituted alpha-amino tetrazole derivatives as non-covalent inflammasome-caspase-1 complex inhibitors with potential application against immune and inflammatory disorders.	alpha-amino tetrazole	65-86	caspase 1	Homo sapiens	128-137
34415562-10	2022	RESULTS: We found that carbachol increased the expression of NLRP3 inflammasome (NLRP3, ASC, cleaved caspase-1, IL-1beta, and IL-18).	Carbachol	23-32	caspase 1	Homo sapiens	101-110
34696918-6	2022	Placental explants from NT cultured with H2O2 showed increased gene and protein expression of NLRP1, NLRP3, caspase-1, IL-1beta, TNF-alpha and HMGB1, while H2O2 was also able to increase TNF-alpha and caspase-1 gene expression in PE.	Hydrogen Peroxide	41-45	caspase 1	Homo sapiens	108-117
34976136-13	2022	Notably, NaHS and L-cysteine significantly suppressed the expression levels of NLRP3 and cleaved caspase-1, and the production of IL-1 and IL-18 in human placental cells.	sodium bisulfide	9-13	caspase 1	Homo sapiens	97-106
34976136-13	2022	Notably, NaHS and L-cysteine significantly suppressed the expression levels of NLRP3 and cleaved caspase-1, and the production of IL-1 and IL-18 in human placental cells.	Cysteine	18-28	caspase 1	Homo sapiens	97-106
34696918-6	2022	Placental explants from NT cultured with H2O2 showed increased gene and protein expression of NLRP1, NLRP3, caspase-1, IL-1beta, TNF-alpha and HMGB1, while H2O2 was also able to increase TNF-alpha and caspase-1 gene expression in PE.	Hydrogen Peroxide	156-160	caspase 1	Homo sapiens	201-210
34696918-7	2022	Treatment with H2O2 + VD decreased gene/protein expression of NLRP1, NLRP3, caspase-1, HMGB1, IL-1beta, TNF-alpha and IL-18 in PE and NT explants with H2O2.	Hydrogen Peroxide	15-19	caspase 1	Homo sapiens	76-85
34696918-7	2022	Treatment with H2O2 + VD decreased gene/protein expression of NLRP1, NLRP3, caspase-1, HMGB1, IL-1beta, TNF-alpha and IL-18 in PE and NT explants with H2O2.	Hydrogen Peroxide	151-155	caspase 1	Homo sapiens	76-85
34843717-8	2022	Investigation of the mechanism disclosed that luxeptinib does not inhibit the assembly of the NLRP3 inflammasome but disables its ability to cleave and activate caspase-1 that is required for IL-1beta release.	Luxeptinib	46-56	caspase 1	Homo sapiens	161-170
34822855-0	2022	Suppression of the caspase-1/GSDMD-mediated pyroptotic signaling pathway through dexamethasone alleviates corneal alkali injuries.	Dexamethasone	81-94	caspase 1	Homo sapiens	19-28
34822855-4	2022	Here, we presented evidence that the effect of Dex on the pyroptosis-related caspase-1/GSDMD pathway in corneal alkali burns (CABs).	Dexamethasone	47-50	caspase 1	Homo sapiens	77-86
34696918-6	2022	Placental explants from NT cultured with H2O2 showed increased gene and protein expression of NLRP1, NLRP3, caspase-1, IL-1beta, TNF-alpha and HMGB1, while H2O2 was also able to increase TNF-alpha and caspase-1 gene expression in PE.	Hydrogen Peroxide	41-45	caspase 1	Homo sapiens	201-210
34963193-8	2022	Based on gene set enrichment analysis, hyper-methylation of CASP1, CFH, and TTLL7 were found enriched in tumor-related KEGG terms, such as "RNA degradation", "apyruvate metabolism", and "nitrogen metabolism".	apyruvate	159-168	caspase 1	Homo sapiens	60-65
34494385-0	2022	VX-765 ameliorates renal injury and fibrosis in diabetes by regulating caspase-1-mediated pyroptosis and inflammation.	belnacasan	0-6	caspase 1	Homo sapiens	71-80
34494385-2	2022	VX-765 is a safe and effective inhibitor of caspase-1, that was well tolerated in a phase II clinical trial in patients with epilepsy, but its application in DN is still undefined.	belnacasan	0-6	caspase 1	Homo sapiens	44-53
34494385-4	2022	In vitro, selective caspase-1 inhibitors VX-765 and Z-YVAD-FMK were administered.	belnacasan	41-47	caspase 1	Homo sapiens	20-29
34494385-4	2022	In vitro, selective caspase-1 inhibitors VX-765 and Z-YVAD-FMK were administered.	benzyloxycarbonyltyrosyl-valyl-alanyl-aspartic acid fluoromethyl ketone	52-62	caspase 1	Homo sapiens	20-29
34963193-8	2022	Based on gene set enrichment analysis, hyper-methylation of CASP1, CFH, and TTLL7 were found enriched in tumor-related KEGG terms, such as "RNA degradation", "apyruvate metabolism", and "nitrogen metabolism".	Nitrogen	187-195	caspase 1	Homo sapiens	60-65
34930938-8	2021	Functionally, using CCK-8, TUNEL, and Transwell migration assays, these results showed that activation of NLRP3/caspase-1 inflammasome by LPS + ATP could enhance the ability of proliferation and migration; and decrease the apoptosis of LNCaP and PC3 cell lines.	Adenosine Triphosphate	144-147	caspase 1	Homo sapiens	112-121
34965405-9	2022	NLRP3, caspase-1 and IL1-beta expression significantly increased in human lens cells exposed to H2O2 or irradiated with white LED light.	Hydrogen Peroxide	96-100	caspase 1	Homo sapiens	7-16
34935985-4	2022	In both differentiated and non-differentiated human monocytic THP-1 cells, clozapine, but not its structural analogues fluperlapine and olanzapine, caused inflammasome-dependent caspase-1 activation and IL-1beta release that was inhibited using the caspase-1 inhibitor yVAD-cmk.	Clozapine	75-84	caspase 1	Homo sapiens	178-187
34935985-4	2022	In both differentiated and non-differentiated human monocytic THP-1 cells, clozapine, but not its structural analogues fluperlapine and olanzapine, caused inflammasome-dependent caspase-1 activation and IL-1beta release that was inhibited using the caspase-1 inhibitor yVAD-cmk.	Clozapine	75-84	caspase 1	Homo sapiens	249-258
34935985-4	2022	In both differentiated and non-differentiated human monocytic THP-1 cells, clozapine, but not its structural analogues fluperlapine and olanzapine, caused inflammasome-dependent caspase-1 activation and IL-1beta release that was inhibited using the caspase-1 inhibitor yVAD-cmk.	YVAD	269-273	caspase 1	Homo sapiens	178-187
34935985-4	2022	In both differentiated and non-differentiated human monocytic THP-1 cells, clozapine, but not its structural analogues fluperlapine and olanzapine, caused inflammasome-dependent caspase-1 activation and IL-1beta release that was inhibited using the caspase-1 inhibitor yVAD-cmk.	YVAD	269-273	caspase 1	Homo sapiens	249-258
34930938-9	2021	Western blotting assay showed that the activation of caspase-1 would increase after the stimulation of NLRP3 inflammasome by LPS + ATP.	Adenosine Triphosphate	131-134	caspase 1	Homo sapiens	53-62
34956386-7	2021	What is more, upregulated protein expression of p-IKKalpha/beta, p-NF-kappaB p65, NLRP3, cleaved caspase 1, and mature IL-1beta occurred in HepG2 cells in response to PA stress while rescued with the PCB2 intervention.	Protactinium	167-169	caspase 1	Homo sapiens	97-106
34956386-8	2021	In conclusion, our study demonstrated that PA induces ERS in HepG2 cells and subsequently activates downstream NLRP3 inflammasome-mediated cellular injury, while PCB2 inhibits NLRP3/caspase 1/IL-1beta pathway, inflammation, and apoptosis with the presence of ERS, thereby promoting cell survival, which may provide pharmacological evidence for clinical approaches on NAFLD.	Protactinium	43-45	caspase 1	Homo sapiens	182-191
34858005-8	2021	When PA was added to cultured human sebocytes, caspase-1 activation and IL-1beta secretion were significantly enhanced.	Palmitic Acid	5-7	caspase 1	Homo sapiens	47-56
34975454-7	2021	Among the tested flavones, 7,8-DHF, quercetin, and apigenin reduced Tau aggregation, oxidative stress, and caspase-1 activity as well as improved neurite outgrowth in SH-SY5Y cells expressing DeltaK280 TauRD-DsRed folding reporter.	Flavones	17-25	caspase 1	Homo sapiens	107-116
34975454-7	2021	Among the tested flavones, 7,8-DHF, quercetin, and apigenin reduced Tau aggregation, oxidative stress, and caspase-1 activity as well as improved neurite outgrowth in SH-SY5Y cells expressing DeltaK280 TauRD-DsRed folding reporter.	6,7-dihydroxyflavone	27-34	caspase 1	Homo sapiens	107-116
34975454-7	2021	Among the tested flavones, 7,8-DHF, quercetin, and apigenin reduced Tau aggregation, oxidative stress, and caspase-1 activity as well as improved neurite outgrowth in SH-SY5Y cells expressing DeltaK280 TauRD-DsRed folding reporter.	Quercetin	36-45	caspase 1	Homo sapiens	107-116
34975454-7	2021	Among the tested flavones, 7,8-DHF, quercetin, and apigenin reduced Tau aggregation, oxidative stress, and caspase-1 activity as well as improved neurite outgrowth in SH-SY5Y cells expressing DeltaK280 TauRD-DsRed folding reporter.	Apigenin	51-59	caspase 1	Homo sapiens	107-116
34226664-8	2021	Moreover, darapladib substantially reduced the Ang II infusion-induced expression of nucleotide-binding oligomerization domain-like receptor with pyrin domain 3 (NLRP3) and interleukin (IL)-1beta and markedly attenuated caspase-1 activation in cardiac tissues.	darapladib	10-20	caspase 1	Homo sapiens	220-229
34922061-9	2021	After anthocyanin administration, both mRNA expression of NLRP3 inflammasome components (caspase-1, IL-1beta, and IL-18) in PBMCs and plasma levels of IL-1beta and IL-18 decreased dramatically in NAFLD patients compared with controls.	Anthocyanins	6-17	caspase 1	Homo sapiens	89-98
34848447-10	2021	CONCLUSION: Increased levels of intracellular ROS promoted activity of caspase-1 and induced cell death in MCF-7 cells.	Reactive Oxygen Species	46-49	caspase 1	Homo sapiens	71-80
34643000-0	2021	Cannabidiol inhibits SARS-Cov-2 spike (S) protein-induced cytotoxicity and inflammation through a PPARgamma-dependent TLR4/NLRP3/Caspase-1 signaling suppression in Caco-2 cell line.	Cannabidiol	0-11	caspase 1	Homo sapiens	129-138
34710506-5	2021	IFN-gamma (100 ng/mL) plus poly (dA:dT) (2 mg/mL) induced the increased AURKA, secretion of IL-1beta, IL-18 and the active form of caspase-1 (p20).	poly(dA)	27-36	caspase 1	Homo sapiens	131-140
34710506-5	2021	IFN-gamma (100 ng/mL) plus poly (dA:dT) (2 mg/mL) induced the increased AURKA, secretion of IL-1beta, IL-18 and the active form of caspase-1 (p20).	Thymidine	36-39	caspase 1	Homo sapiens	131-140
34643253-8	2021	Similar in HPDE6C7 cells, CAE treatment caused supernatant IL-1beta level, NLRP3 and caspase-1 mRNA expression levels to significantly increase.	Ceruletide	26-29	caspase 1	Homo sapiens	85-94
34663173-10	2021	Expressions of p16, p21, TXNIP, NLRP3, cleaved caspase-3 and cleaved caspase-1 in H2O2-treated HUVECs were inhibited by Gen, while the inhibition as such was partially reversed by overexpressed TXNIP.	Hydrogen Peroxide	82-86	caspase 1	Homo sapiens	69-78
34663173-10	2021	Expressions of p16, p21, TXNIP, NLRP3, cleaved caspase-3 and cleaved caspase-1 in H2O2-treated HUVECs were inhibited by Gen, while the inhibition as such was partially reversed by overexpressed TXNIP.	Genistein	120-123	caspase 1	Homo sapiens	69-78
34496682-5	2021	RESULTS: High cobalt chloride exposure mediated significant increase in caspase-1 activity, cytokine levels, and IL1B and NLRP3 expression with a corresponding regulatory decrease for CASP1 and PYCARD expression.	cobaltous chloride	14-29	caspase 1	Homo sapiens	72-81
34496682-5	2021	RESULTS: High cobalt chloride exposure mediated significant increase in caspase-1 activity, cytokine levels, and IL1B and NLRP3 expression with a corresponding regulatory decrease for CASP1 and PYCARD expression.	cobaltous chloride	14-29	caspase 1	Homo sapiens	184-189
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 1	Homo sapiens	324-333
34872043-5	2021	1,25(OH)2VD3 suppressed nigericin-induced interleukin-1beta (IL-1beta) secretion and caspase-1 activation in human primary keratinocytes.	Nigericin	24-33	caspase 1	Homo sapiens	85-94
34606909-4	2021	LPS induced-tissue damage promotes an elevation of extracellular ATP, triggering the NRLP3-inflammasome assembly and activation that, sequentially, induces caspase-1 cleavage and IL-1beta processing and secretion.	Adenosine Triphosphate	65-68	caspase 1	Homo sapiens	156-165
34785631-2	2021	In this article, they found that astrocytes that were pretreated with paeonol significantly rescued MPP+-induced cell viability reduction, and inhibited up-regulation of cell apoptosis, caspase-1 activity, COX2, iNOS, and Bax/Bcl-2 ratio, as well as p-JNK and p-ERK.	paeonol	70-77	caspase 1	Homo sapiens	186-195
34830395-5	2021	Using our method to measure ASC, stimulation of PBMC with lipopolysaccharide and nigericin or adenosine triphosphate resulted in microscopic identification of intracellular ASC specks, as well as interleukin 1 (IL-1) beta and caspase-1 p10 in the periphery.	Nigericin	81-90	caspase 1	Homo sapiens	226-235
34830395-5	2021	Using our method to measure ASC, stimulation of PBMC with lipopolysaccharide and nigericin or adenosine triphosphate resulted in microscopic identification of intracellular ASC specks, as well as interleukin 1 (IL-1) beta and caspase-1 p10 in the periphery.	Adenosine	94-103	caspase 1	Homo sapiens	226-235
34624334-8	2021	Caspase-1 and GSDMD expression levels in all hLEC groups changed with blue light exposure times (8, 16, 24, and 32 h) and were higher in the AC-YVAD-CMK and SWBL exposure groups than in the NC group.	ac-yvad	141-148	caspase 1	Homo sapiens	0-9
34767572-6	2021	RESULTS: PKD activation/auto-phosphorylation always preceded cleavage of caspase-1 and gasdermin D, and treatment with the PKD inhibitor CRT0066101 could block NLRP3 inflammasome assembly and interleukin-1beta production.	CRT 0066101	137-147	caspase 1	Homo sapiens	73-82
34582774-4	2021	The inhibition of ICl, vol and RVD by the chloride channel blockers, tamoxifen or DCPIB, led to the emergence of pyroptosis-like phenotypes such as activated-caspase-1, pyroptotic-body-like bubbles, and a fried-egg-like appearance.	Chlorides	42-50	caspase 1	Homo sapiens	158-167
34582774-4	2021	The inhibition of ICl, vol and RVD by the chloride channel blockers, tamoxifen or DCPIB, led to the emergence of pyroptosis-like phenotypes such as activated-caspase-1, pyroptotic-body-like bubbles, and a fried-egg-like appearance.	Tamoxifen	69-78	caspase 1	Homo sapiens	158-167
34582774-4	2021	The inhibition of ICl, vol and RVD by the chloride channel blockers, tamoxifen or DCPIB, led to the emergence of pyroptosis-like phenotypes such as activated-caspase-1, pyroptotic-body-like bubbles, and a fried-egg-like appearance.	4-(2-butyl-6,7-dichlor-2-cyclopentyl-indan-1-one-5-yl)oxybutyric acid	82-87	caspase 1	Homo sapiens	158-167
34831318-4	2021	In SH-SY5Y cells expressing the GFP-tagged Abeta-folding reporter, both ZN compounds reduced Abeta aggregation, oxidative stress, activities of caspase-1 and AChE, as well as increased neurite outgrowth.	Zinc	72-74	caspase 1	Homo sapiens	144-153
34681898-13	2021	In conclusion, the data suggested that ardisianone induced the apoptosis and pyroptosis of leukemic cells through downregulation of IAPs and activation of caspase pathways that caused gasdermin D cleavage and DNA double-stranded breaks and ultimately led to programmed cell death.	Ardisianone	39-50	caspase 1	Homo sapiens	155-162
34686215-5	2021	Further results showed that famotidine triggered cell pyroptosis in gastric cancer cells by activation of NLPR3 inflammasomes including ASC, Caspase-1 and NLRP, leading to enhanced IL-18, not IL-1beta, mature and secretion.	Famotidine	28-38	caspase 1	Homo sapiens	141-150
34769294-0	2021	The Fibrotic Effects of TMAO on Human Renal Fibroblasts Is Mediated by NLRP3, Caspase-1 and the PERK/Akt/mTOR Pathway.	trimethyloxamine	24-28	caspase 1	Homo sapiens	78-87
34769294-5	2021	We found that TMAO promoted renal fibroblast activation and fibroblast proliferation via the PERK/Akt/mTOR pathway, NLRP3, and caspase-1 signaling.	trimethyloxamine	14-18	caspase 1	Homo sapiens	127-136
34769294-8	2021	We have unraveled that the PERK/Akt/mTOR pathway, NLRP3, and caspase-1 mediates TMAO"s fibrotic effect on human renal fibroblasts.	trimethyloxamine	80-84	caspase 1	Homo sapiens	61-70
34628106-7	2021	In human trophoblast cells, BHB reduced ASC and activated-caspase-1 expression, resulting in the inhibition of IL-1beta secretion.	3-Hydroxybutyric Acid	28-31	caspase 1	Homo sapiens	58-67
34598017-3	2021	2) Nuclear pro-caspase-1 exports back to the cytosol, which is facilitated by a leptomycin B-inhibited mechanism.	leptomycin B	80-92	caspase 1	Homo sapiens	15-24
34598017-4	2021	3) Increased nuclear localization of pro-caspase-1 by a new NES peptide inhibitor upregulates inflammatory genes in oxidative stress and Th17 pathways; and SUMO activator N106 enhances nuclear localization of pro-caspase-1 and caspase-1 activation (p20) in the nucleus.	N-(4-methoxybenzo[d]thiazol-2-yl)-5-(4-methoxyphenyl)-1,3,4-oxadiazol-2-amine	171-175	caspase 1	Homo sapiens	227-236
34600334-5	2021	Whole-genome deep sequencing analysis revealed that Nrf2, NLRP3 and caspase-1 in SNc may be associated with the neuroprotective actions of celastrol in PD.	celastrol	139-148	caspase 1	Homo sapiens	68-77
34599154-7	2021	Consistently, miR-138-5p inhibition reversed the effects of lncRNA NLRP3 silencing on the expression of NLRP3-related molecules and inhibition of the NLRP3/caspase-1/IL-1beta signalling pathway.	mir-138-5p	14-24	caspase 1	Homo sapiens	156-165
34182399-6	2021	Additionally, the caspase-1/IL-1beta axis is involved in inflammatory responses but not cell pyroptosis in EA.hy926 cells following the exposure to PM SRM1648a.	srm1648a	151-159	caspase 1	Homo sapiens	18-27
34182399-10	2021	In a conclusion, mitochondrial fission enables EA.hy926 cells to facilitate caspase-1 activation in response to PM SRM1648a, which is a crucial step for inflammatory reaction in vascular endothelial cells.	srm1648a	115-123	caspase 1	Homo sapiens	76-85
34681768-7	2021	BAY-117082 at higher concentrations significantly reduced NLRP3, ASC, caspase-1, IL-1beta, and IL-18 expression.	3-(4-methylphenylsulfonyl)-2-propenenitrile	0-10	caspase 1	Homo sapiens	70-79
34619679-5	2022	We found that beta-TCP activates NLRP3 inflammasomes, and increases interleukin (IL)-1beta production in primary cultured mouse dendritic cells (DCs) and macrophages, and human THP-1 cells in caspase-1 dependent manner.	beta-tricalcium phosphate	14-22	caspase 1	Homo sapiens	192-201
34675809-7	2021	Notably, the increased expression levels of TLR4, NLRP3, interleukin 1beta, and interleukin 18 proteins and the elevated activities of caspase-1 and lactic dehydrogenase in in vivo and in vitro disease models were markedly reversed by the treatment with BHGZD.	bhgzd	254-259	caspase 1	Homo sapiens	135-144
34332276-6	2021	RESULTS: The SP-induced hyperlipidemic cell model demonstrated increased expression of NLRP3 and caspase-1 proteins (P < 0.05) and elevated ROS levels (P < 0.01), and decreased phosphorylated-Akt and phosphorylated-eNOS expression (P < 0.05).	Palmitic Acid	13-15	caspase 1	Homo sapiens	97-106
34098069-5	2021	Elevated ROS and NLRP3, caspase-1, IL-1beta and IL-18 were detected, which was attenuated by N-acetylcysteine.	Acetylcysteine	93-109	caspase 1	Homo sapiens	24-33
34229177-9	2021	Confocal microscopy results showed that licochalcone E dramatically reduced the generation of ROS and the expressions of NLRP3 and its downstream caspase-1 in PA-treated HepG2 model.	licochalcone E	40-54	caspase 1	Homo sapiens	146-155
34547129-7	2021	Only cysteine and antioxidants (catechin hydrate) could inhibit caspase-1 activation and IL-1beta secretion in itaconate-stimulated macrophages.	Cysteine	5-13	caspase 1	Homo sapiens	64-73
34547129-7	2021	Only cysteine and antioxidants (catechin hydrate) could inhibit caspase-1 activation and IL-1beta secretion in itaconate-stimulated macrophages.	(+)-Catechin Hydrate	32-48	caspase 1	Homo sapiens	64-73
34229177-9	2021	Confocal microscopy results showed that licochalcone E dramatically reduced the generation of ROS and the expressions of NLRP3 and its downstream caspase-1 in PA-treated HepG2 model.	Palmitic Acid	159-161	caspase 1	Homo sapiens	146-155
34229177-10	2021	Western blot results further indicated that licochalcone E significantly reduced the expression of NLRP3, caspase-1 and IL-1beta in the model.	licochalcone E	44-58	caspase 1	Homo sapiens	106-115
34680443-4	2021	Exposure of human conditionally immortalized proximal tubule epithelial cells to indoxyl sulfate (IS) and a mixture of anionic PBUTs (UT mix) increased expression levels of NLRP3, caspase-1 and IL-1beta, accompanied by a significant increase in IL-1beta secretion and caspase-1 activity.	Indican	81-96	caspase 1	Homo sapiens	180-189
34368883-10	2021	Concurrently, oxymatrine inhibited ox-LDL-induced NLRP3 inflammasome-mediated pyroptosis in HUVECs, as evidenced by the significant decreases in the expression of NLRP3, apoptosis-associated speck-like protein containing a C-terminal caspase recruitment domain (ASC), cleaved caspase-1, interleukin (IL)-1beta and IL-18 in HUVECs.	oxymatrine	14-24	caspase 1	Homo sapiens	276-285
34445863-4	2021	The Cas-NP was prepared by the assembly of three different fluorophores-labeled peptides, specific response to caspases-1/3/4 on Au nanoparticles via the Au-Se bond to in situ monitor caspase-1/3/4 with high selectivity and sensitivity.	Peptides	80-88	caspase 1	Homo sapiens	111-125
34551296-4	2021	Treating microglia with pTau-containing neuronal media, exosomes, or PHFs causes IL-1beta activation, which is NLRP3, ASC, and caspase-1 dependent.	ptau	24-28	caspase 1	Homo sapiens	127-136
34537816-5	2021	Dexamethasone also induced pyroptosis, indicated by upregulated pyroptosis-related protein NLR family pyrin domain containing 3 (NLRP3), Caspase-1, and gasdermin-D (GSDMD).	Dexamethasone	0-13	caspase 1	Homo sapiens	137-146
34537816-8	2021	Activation of NLRP3 using LPS and ATP not only increased the cleavage and activation of Caspase-1 and GSDMD, but also increased the expression levels of atrophy markers MuRF1 and Atrogin-1 in trimetazidine-treated C2C12 myotubes.	Adenosine Triphosphate	34-37	caspase 1	Homo sapiens	88-97
34537816-8	2021	Activation of NLRP3 using LPS and ATP not only increased the cleavage and activation of Caspase-1 and GSDMD, but also increased the expression levels of atrophy markers MuRF1 and Atrogin-1 in trimetazidine-treated C2C12 myotubes.	Trimetazidine	192-205	caspase 1	Homo sapiens	88-97
34680443-4	2021	Exposure of human conditionally immortalized proximal tubule epithelial cells to indoxyl sulfate (IS) and a mixture of anionic PBUTs (UT mix) increased expression levels of NLRP3, caspase-1 and IL-1beta, accompanied by a significant increase in IL-1beta secretion and caspase-1 activity.	Indican	81-96	caspase 1	Homo sapiens	268-277
34680443-4	2021	Exposure of human conditionally immortalized proximal tubule epithelial cells to indoxyl sulfate (IS) and a mixture of anionic PBUTs (UT mix) increased expression levels of NLRP3, caspase-1 and IL-1beta, accompanied by a significant increase in IL-1beta secretion and caspase-1 activity.	Indican	98-100	caspase 1	Homo sapiens	180-189
34680443-4	2021	Exposure of human conditionally immortalized proximal tubule epithelial cells to indoxyl sulfate (IS) and a mixture of anionic PBUTs (UT mix) increased expression levels of NLRP3, caspase-1 and IL-1beta, accompanied by a significant increase in IL-1beta secretion and caspase-1 activity.	Indican	98-100	caspase 1	Homo sapiens	268-277
34680443-5	2021	Furthermore, IS and UT mix induced the production of intracellular reactive oxygen species, and caspase-1 activity and IL-1beta secretion were reduced in the presence of antioxidant N-acetylcysteine.	Acetylcysteine	182-198	caspase 1	Homo sapiens	96-105
34445863-4	2021	The Cas-NP was prepared by the assembly of three different fluorophores-labeled peptides, specific response to caspases-1/3/4 on Au nanoparticles via the Au-Se bond to in situ monitor caspase-1/3/4 with high selectivity and sensitivity.	Peptides	80-88	caspase 1	Homo sapiens	184-197
34445863-4	2021	The Cas-NP was prepared by the assembly of three different fluorophores-labeled peptides, specific response to caspases-1/3/4 on Au nanoparticles via the Au-Se bond to in situ monitor caspase-1/3/4 with high selectivity and sensitivity.	Gold	129-131	caspase 1	Homo sapiens	111-125
34445863-4	2021	The Cas-NP was prepared by the assembly of three different fluorophores-labeled peptides, specific response to caspases-1/3/4 on Au nanoparticles via the Au-Se bond to in situ monitor caspase-1/3/4 with high selectivity and sensitivity.	Gold	129-131	caspase 1	Homo sapiens	184-197
34445863-4	2021	The Cas-NP was prepared by the assembly of three different fluorophores-labeled peptides, specific response to caspases-1/3/4 on Au nanoparticles via the Au-Se bond to in situ monitor caspase-1/3/4 with high selectivity and sensitivity.	Gold	154-156	caspase 1	Homo sapiens	111-125
34445863-4	2021	The Cas-NP was prepared by the assembly of three different fluorophores-labeled peptides, specific response to caspases-1/3/4 on Au nanoparticles via the Au-Se bond to in situ monitor caspase-1/3/4 with high selectivity and sensitivity.	Gold	154-156	caspase 1	Homo sapiens	184-197
34445863-6	2021	During the pyroptosis of cancer cells induced by adenosine triphosphate (ATP), only the fluorescence of caspase-1 significantly increases.	Adenosine	49-58	caspase 1	Homo sapiens	104-113
34445863-6	2021	During the pyroptosis of cancer cells induced by adenosine triphosphate (ATP), only the fluorescence of caspase-1 significantly increases.	Adenosine Triphosphate	73-76	caspase 1	Homo sapiens	104-113
34106394-9	2021	NaB notably ameliorated apoptotic regulatory proteins p-53, Caspase-3 and caspase-1 level, and reversed phosphorylation of extracellular signal-regulated kinases and p-38 proteins.	nab	0-3	caspase 1	Homo sapiens	74-83
34288031-8	2021	Importantly, a small-molecular caspase-1 inhibitor CZL80 attenuated seizures in pharmacoresistant TLE models, and decreased the neural excitability in the brain slices obtained from pharmacoresistant TLE patients.	czl80	51-56	caspase 1	Homo sapiens	31-40
34146852-0	2021	Chloroquine attenuates thymic stromal lymphopoietin production via suppressing caspase-1 signaling in mast cells.	Chloroquine	0-11	caspase 1	Homo sapiens	79-88
34146852-5	2021	CQ down-regulated caspase-1 (CASP1), MAPKs, and NF-kappaB levels enhanced by stimulation with PMA + A23187.	Chloroquine	0-2	caspase 1	Homo sapiens	18-27
34146852-5	2021	CQ down-regulated caspase-1 (CASP1), MAPKs, and NF-kappaB levels enhanced by stimulation with PMA + A23187.	Chloroquine	0-2	caspase 1	Homo sapiens	29-34
34146852-5	2021	CQ down-regulated caspase-1 (CASP1), MAPKs, and NF-kappaB levels enhanced by stimulation with PMA + A23187.	Tetradecanoylphorbol Acetate	94-97	caspase 1	Homo sapiens	18-27
34146852-5	2021	CQ down-regulated caspase-1 (CASP1), MAPKs, and NF-kappaB levels enhanced by stimulation with PMA + A23187.	Tetradecanoylphorbol Acetate	94-97	caspase 1	Homo sapiens	29-34
34146852-5	2021	CQ down-regulated caspase-1 (CASP1), MAPKs, and NF-kappaB levels enhanced by stimulation with PMA + A23187.	Calcimycin	100-106	caspase 1	Homo sapiens	18-27
34146852-5	2021	CQ down-regulated caspase-1 (CASP1), MAPKs, and NF-kappaB levels enhanced by stimulation with PMA + A23187.	Calcimycin	100-106	caspase 1	Homo sapiens	29-34
34146852-7	2021	CQ decreased CASP1 and NF-kappaB levels in the ear tissue.	Chloroquine	0-2	caspase 1	Homo sapiens	13-18
34217687-7	2021	Ox-LDL induced NF-kappaB/NLRP3 pathway activation by inducing C-reactive protein expression, NLRP3 activation, caspase-1 activation, and IL-1beta secretion, which were inhibited by pretreatment with the combination of PAVA and RSV.	pelargonic acid vanillylamide	218-222	caspase 1	Homo sapiens	111-120
34217687-7	2021	Ox-LDL induced NF-kappaB/NLRP3 pathway activation by inducing C-reactive protein expression, NLRP3 activation, caspase-1 activation, and IL-1beta secretion, which were inhibited by pretreatment with the combination of PAVA and RSV.	Rosuvastatin Calcium	227-230	caspase 1	Homo sapiens	111-120
34142814-6	2021	The supernatant from the incubation of amiodarone with FLC-4 cells for 7 days increased caspase-1 activity and production of IL-1ss by THP-1 cells.	Amiodarone	39-49	caspase 1	Homo sapiens	88-97
34445530-4	2021	The aim of this study was to evaluate the effect of vitamin D on the expression of IL-33, IL-37, macrophages, and caspase-1 in the neointimal tissue of coronary artery in Yucatan microswine with vitamin D deficient, sufficient, and supplemented status.	Vitamin D	52-61	caspase 1	Homo sapiens	114-123
34492927-5	2021	Besides, both 3-MA and CQ addition increased NLRP3, Caspase-1, NEK7, ASC, GSDMA, GSDME, IL-1beta, IL-18 mRNA levels, NLRP3, Caspase-1 p20, ASC, GSDMD protein and ROS levels, and NO, LDH, IL-1beta, IL-18 releases.	Chloroquine	23-25	caspase 1	Homo sapiens	52-61
34119493-0	2021	Necrosulfonamide reverses pyroptosis-induced inhibition of proliferation and differentiation of osteoblasts through the NLRP3/caspase-1/GSDMD pathway.	N-(4-(N-(3-methoxypyrazin-2-yl)sulfamoyl)phenyl)-3-(5-nitrothiophene-2-yl)acrylamide	0-16	caspase 1	Homo sapiens	126-135
34492927-5	2021	Besides, both 3-MA and CQ addition increased NLRP3, Caspase-1, NEK7, ASC, GSDMA, GSDME, IL-1beta, IL-18 mRNA levels, NLRP3, Caspase-1 p20, ASC, GSDMD protein and ROS levels, and NO, LDH, IL-1beta, IL-18 releases.	Chloroquine	23-25	caspase 1	Homo sapiens	124-133
34492927-5	2021	Besides, both 3-MA and CQ addition increased NLRP3, Caspase-1, NEK7, ASC, GSDMA, GSDME, IL-1beta, IL-18 mRNA levels, NLRP3, Caspase-1 p20, ASC, GSDMD protein and ROS levels, and NO, LDH, IL-1beta, IL-18 releases.	3-methyladenine	14-18	caspase 1	Homo sapiens	52-61
34492927-5	2021	Besides, both 3-MA and CQ addition increased NLRP3, Caspase-1, NEK7, ASC, GSDMA, GSDME, IL-1beta, IL-18 mRNA levels, NLRP3, Caspase-1 p20, ASC, GSDMD protein and ROS levels, and NO, LDH, IL-1beta, IL-18 releases.	3-methyladenine	14-18	caspase 1	Homo sapiens	124-133
34439523-0	2021	Isoorientin Attenuated the Pyroptotic Hepatocyte Damage Induced by Benzo(a)pyrene via ROS/NF-kappaB/NLRP3/Caspase-1 Signaling Pathway.	homoorientin	0-11	caspase 1	Homo sapiens	106-115
34439523-0	2021	Isoorientin Attenuated the Pyroptotic Hepatocyte Damage Induced by Benzo(a)pyrene via ROS/NF-kappaB/NLRP3/Caspase-1 Signaling Pathway.	Benzo(a)pyrene	67-81	caspase 1	Homo sapiens	106-115
34515145-7	2022	Furthermore, we show that pneumococcal H2O2 causes cell death via the activation of both apoptotic as well as pyroptotic pathways which are mediated by the activation of caspase-3/7 and caspase-1, respectively.	Hydrogen Peroxide	39-43	caspase 1	Homo sapiens	186-195
34216617-4	2021	We found that antimycin A-induced mitochondrial dysfunction caused caspase-1-dependent inflammasome activation and subsequent production of mature IL-1beta and IL-18 in human RPE cells.	Antimycin A	14-25	caspase 1	Homo sapiens	67-76
34341353-7	2021	Notably, N-induced lung injury and cytokine production are blocked by MCC950 (a specific inhibitor of NLRP3) and Ac-YVAD-cmk (an inhibitor of caspase-1).	Nitrogen	9-10	caspase 1	Homo sapiens	142-151
34355546-8	2022	The findings revealed that genes of CASP1 and ASC were dysregulated by melatonin regulating the inflammasome complex.	Melatonin	71-80	caspase 1	Homo sapiens	36-41
34356509-4	2021	The pan-caspase inhibitor, z-VAD-fmk, and the caspase-1 inhibitor, z-YVAD-fmk, but not the JNK inhibitor, SP600125, significantly reversed apoptosis and caspase activation in TNF-alpha/MCPIP1-treated cells.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	27-36	caspase 1	Homo sapiens	8-15
34452150-3	2021	5-FU activity leads to caspase-1 activation, secretion and maturation of interleukins (IL)-1, IL-18 and reactive oxygen species (ROS) generation.	Fluorouracil	0-4	caspase 1	Homo sapiens	23-32
34452150-5	2021	Exposure of tumor cells to P.CNF/5-FU resulted in a strong cytotoxic effect, an increased level of caspase-1 released in the culture media and ROS production-the latter directly proportional to the concentration of anti-tumor agent embedded in the scaffolds.	Fluorouracil	33-37	caspase 1	Homo sapiens	99-108
34452150-6	2021	Simultaneously, 5-FU determined the increase of p53 and caspase-1 expressions, both at gene and protein levels.	Fluorouracil	16-20	caspase 1	Homo sapiens	56-65
34266494-8	2021	Further analysis showed that ASC, NLRP3 and Caspase-1, was significantly repressed in response to Rabeprazole stimulation, resulting in decreasing cleaved-caspase-1 expression.	Rabeprazole	98-109	caspase 1	Homo sapiens	44-53
34335569-6	2021	Through the modulation of the GAL1 promoter by using different galactose:glucose ratios in the culture medium, we have established a scenario in which caspase-1 is sufficiently expressed to become activated while yeast growth is not impaired.	Galactose	63-72	caspase 1	Homo sapiens	151-160
34335569-6	2021	Through the modulation of the GAL1 promoter by using different galactose:glucose ratios in the culture medium, we have established a scenario in which caspase-1 is sufficiently expressed to become activated while yeast growth is not impaired.	Glucose	73-80	caspase 1	Homo sapiens	151-160
34356509-4	2021	The pan-caspase inhibitor, z-VAD-fmk, and the caspase-1 inhibitor, z-YVAD-fmk, but not the JNK inhibitor, SP600125, significantly reversed apoptosis and caspase activation in TNF-alpha/MCPIP1-treated cells.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	27-36	caspase 1	Homo sapiens	153-160
34356509-4	2021	The pan-caspase inhibitor, z-VAD-fmk, and the caspase-1 inhibitor, z-YVAD-fmk, but not the JNK inhibitor, SP600125, significantly reversed apoptosis and caspase activation in TNF-alpha/MCPIP1-treated cells.	benzyloxycarbonyltyrosyl-valyl-alanyl-aspartic acid fluoromethyl ketone	67-77	caspase 1	Homo sapiens	46-55
34356509-4	2021	The pan-caspase inhibitor, z-VAD-fmk, and the caspase-1 inhibitor, z-YVAD-fmk, but not the JNK inhibitor, SP600125, significantly reversed apoptosis and caspase activation in TNF-alpha/MCPIP1-treated cells.	benzyloxycarbonyltyrosyl-valyl-alanyl-aspartic acid fluoromethyl ketone	67-77	caspase 1	Homo sapiens	153-160
34326697-0	2021	Cisplatin Induces Pyroptosis via Activation of MEG3/NLRP3/caspase-1/GSDMD Pathway in Triple-Negative Breast Cancer.	Cisplatin	0-9	caspase 1	Homo sapiens	58-67
34262321-0	2021	Calcitriol Alleviates Hyperosmotic Stress-Induced Corneal Epithelial Cell Damage via Inhibiting the NLRP3-ASC-Caspase-1-GSDMD Pyroptosis Pathway in Dry Eye Disease.	Calcitriol	0-10	caspase 1	Homo sapiens	110-119
34262321-11	2021	More importantly, we demonstrated that, in line with the effect of disulfiram, calcitriol could also alleviate HS-induced pyroptosis, through inhibiting the NLRP3-ASC-caspase-1-GSDMD pyroptosis pathway.	Disulfiram	67-77	caspase 1	Homo sapiens	167-176
34262321-11	2021	More importantly, we demonstrated that, in line with the effect of disulfiram, calcitriol could also alleviate HS-induced pyroptosis, through inhibiting the NLRP3-ASC-caspase-1-GSDMD pyroptosis pathway.	Calcitriol	79-89	caspase 1	Homo sapiens	167-176
34262321-13	2021	We demonstrated that calcitriol was able to effectively alleviate HS-induced corneal epithelial cell damage through inhibiting the NLRP3-ASC-caspase-1-GSDMD pyroptosis pathway.	Calcitriol	21-31	caspase 1	Homo sapiens	141-150
34326697-6	2021	Furthermore, knockdown of MEG3 not only partly abolished the activation effect of DDP on NLRP3/caspase-1/GSDMD pathway-mediated pyroptosis, but also reversed the suppression of DDP on tumor growth and metastasis ability in vitro and in vivo, further confirming that MEG3 may partially mediate the pyroptotic signaling upon DDP treatment.	Cisplatin	323-326	caspase 1	Homo sapiens	95-104
34326697-4	2021	In the present study, NLRP3/caspase-1/GSDMD pyroptosis pathway was involved in the DDP-induced anti-tumor effect of TNBC in vitro and in vivo, providing evidence that DDP might induce pyroptosis in TNBC.	Cisplatin	83-86	caspase 1	Homo sapiens	28-37
34326697-4	2021	In the present study, NLRP3/caspase-1/GSDMD pyroptosis pathway was involved in the DDP-induced anti-tumor effect of TNBC in vitro and in vivo, providing evidence that DDP might induce pyroptosis in TNBC.	Cisplatin	167-170	caspase 1	Homo sapiens	28-37
34066647-5	2021	Our results indicated that ethyl pyruvate significantly suppressed LPS and ATP-induced NLRP3 inflammasome activation, decreased active caspase-1 level, secretion of IL-1beta and IL-18 cytokines, and reduced the level of pyroptotic cell death resulting from inflammasome activation.	ethyl pyruvate	27-41	caspase 1	Homo sapiens	135-144
34350239-12	2021	We also found decreased DA secretion and TH expression, as well as increased NLRP3, caspase-1, ASC, IL-1alpha, and IL-18 expression in the MPP+ induced PD model.	mangion-purified polysaccharide (Candida albicans)	139-143	caspase 1	Homo sapiens	84-93
34069836-0	2021	Antioxidant Ascorbic Acid Modulates NLRP3 Inflammasome in LPS-G Treated Oral Stem Cells through NFkappaB/Caspase-1/IL-1beta Pathway.	Ascorbic Acid	12-25	caspase 1	Homo sapiens	105-114
34066647-5	2021	Our results indicated that ethyl pyruvate significantly suppressed LPS and ATP-induced NLRP3 inflammasome activation, decreased active caspase-1 level, secretion of IL-1beta and IL-18 cytokines, and reduced the level of pyroptotic cell death resulting from inflammasome activation.	Adenosine Triphosphate	75-78	caspase 1	Homo sapiens	135-144
35439536-0	2022	Involvement of NLRP3/Caspase-1/GSDMD-Dependent Pyroptosis in BPA-Induced Apoptosis of Human Neuroblastoma Cells.	bisphenol A	61-64	caspase 1	Homo sapiens	21-30
34062977-10	2021	Our findings show that TAS-116 could prevent the activation of caspase-1, subsequently reducing the release of mature IL-1beta.	TAS-116	23-30	caspase 1	Homo sapiens	63-72
34100379-8	2021	The Starbase database predicted that CASP1 is a potential target of miR-16-5p, which was verified through a luciferase reporter assay.	mir-16-5p	68-77	caspase 1	Homo sapiens	37-42
34100379-9	2021	Moreover, CASP1 expression was determined after miR-16-5p silencing in HG-stimulated HRECs with puerarin exposure.	puerarin	96-104	caspase 1	Homo sapiens	10-15
34100379-13	2021	CASP1 was confirmed as a direct target gene of miR-16-5p.	mir-16-5p	47-56	caspase 1	Homo sapiens	0-5
34100379-14	2021	Taken together, puerarin alleviates oxidative stress and pyroptosis in HG-stimulated HRECs through regulating the miR- 16-5p/CASP1 axis.	puerarin	16-24	caspase 1	Homo sapiens	125-130
35346830-8	2022	The overexpression of miR-1656 can induce increased expression of pyroptosis-related genes including NLRP3, Caspase-1, IL-18, and IL-1beta by inhibiting the release of GPX4.	mir-1656	22-30	caspase 1	Homo sapiens	108-117
35633614-7	2022	Then, flow cytometry, LDH assay and western blotting demonstrated that tCQA could inhibit LPS- and nigericin-induced Caspase-1 activation and gasdermin D cleavage, thereby suppressing inflammatory cell death.	tcqa	71-75	caspase 1	Homo sapiens	117-126
35633614-7	2022	Then, flow cytometry, LDH assay and western blotting demonstrated that tCQA could inhibit LPS- and nigericin-induced Caspase-1 activation and gasdermin D cleavage, thereby suppressing inflammatory cell death.	Nigericin	99-108	caspase 1	Homo sapiens	117-126
35633614-9	2022	Western blotting and autophagosome staining results suggested tCQA could significantly enhance LPS-induced autophagic flux in macrophages and ATG5/ATG7 knockdown reverses the inhibitory effect of tCQA on NLRP3 expression and Caspase-1 activation, indicating that tCQA induces NLRP3 degradation via autophagy.	tcqa	62-66	caspase 1	Homo sapiens	225-234
35633614-9	2022	Western blotting and autophagosome staining results suggested tCQA could significantly enhance LPS-induced autophagic flux in macrophages and ATG5/ATG7 knockdown reverses the inhibitory effect of tCQA on NLRP3 expression and Caspase-1 activation, indicating that tCQA induces NLRP3 degradation via autophagy.	tcqa	196-200	caspase 1	Homo sapiens	225-234
35439536-3	2022	The results showed that BPA increased the mRNA levels of IL-18, ASC, GSDMD and protein levels of NLRP3, caspase-1 and GSDMD in both cell lines in a nonlinear manner.	bisphenol A	24-27	caspase 1	Homo sapiens	104-113
35439536-8	2022	In summary, BPA may induce pyroptosis in neuroblastoma cells through NLRP3/caspase-1/GSDMD pathway, as mediated by ER; caspase-1-dependent pyroptosis may also contribute to BPA-induced apoptosis, an effect alleviated by EGCG.	bisphenol A	12-15	caspase 1	Homo sapiens	75-84
35439536-8	2022	In summary, BPA may induce pyroptosis in neuroblastoma cells through NLRP3/caspase-1/GSDMD pathway, as mediated by ER; caspase-1-dependent pyroptosis may also contribute to BPA-induced apoptosis, an effect alleviated by EGCG.	bisphenol A	12-15	caspase 1	Homo sapiens	119-128
35439536-8	2022	In summary, BPA may induce pyroptosis in neuroblastoma cells through NLRP3/caspase-1/GSDMD pathway, as mediated by ER; caspase-1-dependent pyroptosis may also contribute to BPA-induced apoptosis, an effect alleviated by EGCG.	bisphenol A	173-176	caspase 1	Homo sapiens	119-128
35565057-11	2022	CMap-CTD database analyses indicated the expression levels of Tlr2, Ccl2, Cxcl10, Fas, Irf8, Socs3, Stat3, Gbp6, Casp1 and Syk could be reversed by folic acid.	Folic Acid	148-158	caspase 1	Homo sapiens	113-118
35439536-8	2022	In summary, BPA may induce pyroptosis in neuroblastoma cells through NLRP3/caspase-1/GSDMD pathway, as mediated by ER; caspase-1-dependent pyroptosis may also contribute to BPA-induced apoptosis, an effect alleviated by EGCG.	epigallocatechin gallate	220-224	caspase 1	Homo sapiens	75-84
35439536-8	2022	In summary, BPA may induce pyroptosis in neuroblastoma cells through NLRP3/caspase-1/GSDMD pathway, as mediated by ER; caspase-1-dependent pyroptosis may also contribute to BPA-induced apoptosis, an effect alleviated by EGCG.	epigallocatechin gallate	220-224	caspase 1	Homo sapiens	119-128
34997266-14	2022	PQQ inhibits ROS generation and NF-kappaB activation, which stimulates activation of the NLRP3 inflammasome and regulates the expression of caspase-1, IL-1beta, and IL-18.	PQQ Cofactor	0-3	caspase 1	Homo sapiens	140-149
35331853-7	2022	Puerarin ameliorated LPS-induced cytotoxicity and apoptosis, while repressing LPS-stimulated NLRP3 inflammasome-mediated pyroptosis in GES-1 cells, as evidenced by significantly decreased expression of NLRP3, ASC, cleaved caspase-1, IL-1beta and IL-18.	puerarin	0-8	caspase 1	Homo sapiens	222-231
35584771-10	2022	GW9508 can attenuate inflammation by reducing the expression of NLRP3, ASC, caspase-1, IL-1beta, and IL-18 under HG.	GW9508	0-6	caspase 1	Homo sapiens	76-85
35634294-6	2022	Consistently, SHED could inhibit the elevated expression of NLRP3, GSDMD and Caspase-1 induced by CCl4 treatment in vitro co-culture system, which was mediated by decreasing reactive oxygen species (ROS) generation.	Reactive Oxygen Species	174-197	caspase 1	Homo sapiens	77-86
35634294-6	2022	Consistently, SHED could inhibit the elevated expression of NLRP3, GSDMD and Caspase-1 induced by CCl4 treatment in vitro co-culture system, which was mediated by decreasing reactive oxygen species (ROS) generation.	Reactive Oxygen Species	199-202	caspase 1	Homo sapiens	77-86
35615587-5	2022	Twenty-four hour treatment with olanzapine, quetiapine, risperidone, or haloperidol dose-dependently increased the protein expression of astrocytic NLRP3, NLRP6, caspase-1, caspase-4, and GSDMD.	Olanzapine	32-42	caspase 1	Homo sapiens	162-171
35615587-5	2022	Twenty-four hour treatment with olanzapine, quetiapine, risperidone, or haloperidol dose-dependently increased the protein expression of astrocytic NLRP3, NLRP6, caspase-1, caspase-4, and GSDMD.	Quetiapine Fumarate	44-54	caspase 1	Homo sapiens	162-171
35615587-5	2022	Twenty-four hour treatment with olanzapine, quetiapine, risperidone, or haloperidol dose-dependently increased the protein expression of astrocytic NLRP3, NLRP6, caspase-1, caspase-4, and GSDMD.	Risperidone	56-67	caspase 1	Homo sapiens	162-171
35615587-5	2022	Twenty-four hour treatment with olanzapine, quetiapine, risperidone, or haloperidol dose-dependently increased the protein expression of astrocytic NLRP3, NLRP6, caspase-1, caspase-4, and GSDMD.	Haloperidol	72-83	caspase 1	Homo sapiens	162-171
35615587-6	2022	Co-treatment with a histamine H1 receptor agonist, 2-(3-trifluoromethylphenyl) histamine (FMPH), dose-dependently reduced the increased expression of NLRP3, caspase-1 and GSDMD induced by olanzapine, quetiapine, risperidone, or haloperidol.	2-(3-trifluoromethylphenyl)histamine	51-88	caspase 1	Homo sapiens	157-166
35615587-6	2022	Co-treatment with a histamine H1 receptor agonist, 2-(3-trifluoromethylphenyl) histamine (FMPH), dose-dependently reduced the increased expression of NLRP3, caspase-1 and GSDMD induced by olanzapine, quetiapine, risperidone, or haloperidol.	fmph	90-94	caspase 1	Homo sapiens	157-166
35521772-12	2022	Furthermore, oleic acid treatment induced ROS production and inflammasome activation, which is manifested by enhanced caspase-1 activity and mature IL-18 protein level.	Oleic Acid	13-23	caspase 1	Homo sapiens	118-127
35521772-12	2022	Furthermore, oleic acid treatment induced ROS production and inflammasome activation, which is manifested by enhanced caspase-1 activity and mature IL-18 protein level.	ros	42-45	caspase 1	Homo sapiens	118-127
35385822-8	2022	Moreover, the expression of Caspase-1, NLRP3, GSDMA, IL-18, and IL-1beta and caused membrane perforation, suggesting the development of pyroptosis by chTERT in LMH cells.	chtert	150-156	caspase 1	Homo sapiens	28-37
35092164-7	2022	While blocking the fusion of autophagosomes with lysosomes by bafilomycin A1(BafA1), the reduced NLRP3 inflammasome activity induced by RAPA was significantly restored, with increased protein levels of NLRP3 and cleaved Casp-1(p10), as well as IL-1beta secretion.	bafilomycin A1	62-76	caspase 1	Homo sapiens	220-226
35092164-7	2022	While blocking the fusion of autophagosomes with lysosomes by bafilomycin A1(BafA1), the reduced NLRP3 inflammasome activity induced by RAPA was significantly restored, with increased protein levels of NLRP3 and cleaved Casp-1(p10), as well as IL-1beta secretion.	Sirolimus	136-140	caspase 1	Homo sapiens	220-226
35529876-3	2022	In this study, a stable model of cisplatin-induced MC damage was established in vitro, and the results of PCR and Western blotting showed increased expressions of NLRP3, Caspase-1, IL-1beta, and GSDMD in MCs.	Cisplatin	33-42	caspase 1	Homo sapiens	170-179
35490837-1	2022	We previously showed that increases in reactive oxygen species (ROS) generation upregulate NLRP3 inflammasome and inflammation through increases in both caspase-1 activity and rises in IL-1beta expression levels in animal models of dry eye (DE).	Reactive Oxygen Species	39-62	caspase 1	Homo sapiens	153-162
35490837-1	2022	We previously showed that increases in reactive oxygen species (ROS) generation upregulate NLRP3 inflammasome and inflammation through increases in both caspase-1 activity and rises in IL-1beta expression levels in animal models of dry eye (DE).	Reactive Oxygen Species	64-67	caspase 1	Homo sapiens	153-162
35472101-0	2022	Secoisolariciresinol diglucoside induces pyroptosis by activating caspase-1 to cleave GSDMD in colorectal cancer cells.	secoisolariciresinol	0-20	caspase 1	Homo sapiens	66-75
35472101-0	2022	Secoisolariciresinol diglucoside induces pyroptosis by activating caspase-1 to cleave GSDMD in colorectal cancer cells.	diglucoside	21-32	caspase 1	Homo sapiens	66-75
35472101-6	2022	Furthermore, SDG induced cell pyroptosis by enhancing cleavage of the N-terminal fragment of gasdermin D (GSDMD) in CRC cells, accompanied by increased caspase-1 cleavage.	secoisolariciresinol diglucoside	13-16	caspase 1	Homo sapiens	152-161
35472101-7	2022	Consistent with this, SDG-induced GSDMD-N-terminal fragment cleavage and pyroptosis were reduced by siRNA-mediated silencing of caspase-1 or treatment with the specific caspase-1 inhibitor VX-765 treatment, suggesting that active caspase-1 further induces pyroptosis.	secoisolariciresinol diglucoside	22-25	caspase 1	Homo sapiens	128-137
35472101-7	2022	Consistent with this, SDG-induced GSDMD-N-terminal fragment cleavage and pyroptosis were reduced by siRNA-mediated silencing of caspase-1 or treatment with the specific caspase-1 inhibitor VX-765 treatment, suggesting that active caspase-1 further induces pyroptosis.	secoisolariciresinol diglucoside	22-25	caspase 1	Homo sapiens	169-178
35472101-7	2022	Consistent with this, SDG-induced GSDMD-N-terminal fragment cleavage and pyroptosis were reduced by siRNA-mediated silencing of caspase-1 or treatment with the specific caspase-1 inhibitor VX-765 treatment, suggesting that active caspase-1 further induces pyroptosis.	secoisolariciresinol diglucoside	22-25	caspase 1	Homo sapiens	230-239
35472101-7	2022	Consistent with this, SDG-induced GSDMD-N-terminal fragment cleavage and pyroptosis were reduced by siRNA-mediated silencing of caspase-1 or treatment with the specific caspase-1 inhibitor VX-765 treatment, suggesting that active caspase-1 further induces pyroptosis.	belnacasan	189-195	caspase 1	Homo sapiens	169-178
35472101-7	2022	Consistent with this, SDG-induced GSDMD-N-terminal fragment cleavage and pyroptosis were reduced by siRNA-mediated silencing of caspase-1 or treatment with the specific caspase-1 inhibitor VX-765 treatment, suggesting that active caspase-1 further induces pyroptosis.	belnacasan	189-195	caspase 1	Homo sapiens	230-239
35448938-6	2022	In our results, the three SCFAs could inhibit ROS expressions, NLRP3, Caspase-1, IL-1beta, IL-6, IL-18, Beclin-1 and LC3-II, when induced by 5-FU.	Fluorouracil	141-145	caspase 1	Homo sapiens	70-79
35394753-10	2022	The presence of mitochondrial reactive oxygen species (mitoROS) led to oxidative damage of mitochondrial DNA (mitoDNA), which further activates NLRP3/Caspase-1/gasdermin D (GSDMD)-dependent pyroptosis and could promote dendritic cell (DC) maturation by pyroptosis.	Reactive Oxygen Species	30-53	caspase 1	Homo sapiens	150-159
35212946-0	2022	A20 alleviated caspase-1-mediated pyroptosis and inflammation stimulated by Porphyromonas gingivalis lipopolysaccharide and nicotine through autophagy enhancement.	Nicotine	124-132	caspase 1	Homo sapiens	15-24
35144218-0	2022	Combination of ruthenium (II) polypyridyl complex Delta-Ru1 and Taxol enhances the anti-cancer effect on Taxol-resistant cancer cells through Caspase-1/GSDMD-mediated pyroptosis.	ruthenium (ii) polypyridyl complex delta-ru1	15-59	caspase 1	Homo sapiens	142-151
35144218-0	2022	Combination of ruthenium (II) polypyridyl complex Delta-Ru1 and Taxol enhances the anti-cancer effect on Taxol-resistant cancer cells through Caspase-1/GSDMD-mediated pyroptosis.	Paclitaxel	64-69	caspase 1	Homo sapiens	142-151
35144218-0	2022	Combination of ruthenium (II) polypyridyl complex Delta-Ru1 and Taxol enhances the anti-cancer effect on Taxol-resistant cancer cells through Caspase-1/GSDMD-mediated pyroptosis.	Paclitaxel	105-110	caspase 1	Homo sapiens	142-151
35144218-9	2022	Taken together, the Delta-Ru1 & Taxol combination can induce cell death through Caspase-1/GSDMD-mediated pyroptosis to enhance the therapeutic effect on HeLa/Taxol cells.	delta-ru1	20-29	caspase 1	Homo sapiens	80-89
35144218-9	2022	Taken together, the Delta-Ru1 & Taxol combination can induce cell death through Caspase-1/GSDMD-mediated pyroptosis to enhance the therapeutic effect on HeLa/Taxol cells.	Paclitaxel	32-37	caspase 1	Homo sapiens	80-89
35138513-6	2022	Elevated expression of NEK7 and active caspase-1 was also shown in TGF-beta-induced LX-2 cells, and this level was reduced by (5Z)-oxozeaenol, a TAK inhibitor.	(5z)-oxozeaenol	126-141	caspase 1	Homo sapiens	39-48
35406727-3	2022	METHODS: Caspase activity was measured in ischemic and perfused human myoblasts in response to the NLRP3 and AIM2 inflammasome agonists (nigericin and poly(dA:dT), respectively) with and without specific caspase-1 or pan-caspase inhibition.	Nigericin	137-146	caspase 1	Homo sapiens	9-16
35514993-10	2022	Whether oleamide functioned as a second signal that activated the NLRP3 inflammasome and mediated IL-1beta production was further investigated using LPS-primed MDMs followed by oleamide treatment that induced activation of inflammasome-related proteins including NLRP3, ASC, cleaved casp-1, and cleaved IL-1beta.	oleylamide	8-16	caspase 1	Homo sapiens	283-289
35433045-6	2022	Specifically, caspase-1 activation and secretion of its downstream product interleukin (IL)-1beta were unchanged following 14 days of C8 MCT oil supplementation when measured in unstimulated and LPS-stimulated whole blood cultures (all P > 0.05).	Oils	141-144	caspase 1	Homo sapiens	14-23
35571391-9	2022	The protein expression levels of Caspase-1, NLRP3, TLR4, MyD88, and NF-kappaB in the LPS + EB1089 group were evidently lower than those in the LPS group; however, the VDR protein expression evidently increased in the LPS + EB1089 group.	seocalcitol	91-97	caspase 1	Homo sapiens	33-42
35178861-15	2022	In both CVB3 FB and HL-1 cells, colchicine down-regulated the NLRP3 inflammasome-related components ASC, caspase-1, and IL-1beta.	Colchicine	32-42	caspase 1	Homo sapiens	105-114
35350102-8	2022	In addition, spermine significantly reduced NLR family pyrin domain containing 3, cleaved caspase-1, N-gasdermin D and IL-1beta expression, as well as IL-1beta levels in the supernatant.	Spermine	13-21	caspase 1	Homo sapiens	90-99
35137954-5	2022	DMI, 4OI, DMF and monomethyl fumarate (MMF), another fumarate derivative, also directly inhibited biochemical markers of NLRP3 activation in LPS-primed macrophages, mixed glia, OHSCs and human macrophages in response to nigericin and imiquimod, including ASC speck formation, caspase-1 activation, gasdermin D cleavage and IL-1beta release.	dimethyl itaconate	0-3	caspase 1	Homo sapiens	276-285
35137954-5	2022	DMI, 4OI, DMF and monomethyl fumarate (MMF), another fumarate derivative, also directly inhibited biochemical markers of NLRP3 activation in LPS-primed macrophages, mixed glia, OHSCs and human macrophages in response to nigericin and imiquimod, including ASC speck formation, caspase-1 activation, gasdermin D cleavage and IL-1beta release.	citraconic acid	39-42	caspase 1	Homo sapiens	276-285
35435672-7	2022	The cell swelling, ROS storm, and GSH exhaustion of NaCl@ssss-VHMS effectively eradicated tumor cells by caspase-1-dependent pyroptosis, caspase-3-dependent apoptosis, and GPX4-dependent ferroptosis, respectively, thus synergistically inhibiting tumor growth.	Sodium Chloride	52-56	caspase 1	Homo sapiens	105-114
35437791-7	2022	Furthermore, we found that nitrosamines co-exposure also promoted cell pyroptosis through the NLRP3/caspase-1/GSDMD pathway, which was demonstrated by adding the caspase-1 inhibitor Z-YVAD-FMK and constructing NLRP3 downregulated Het-1A cell line.	Nitrosamines	27-39	caspase 1	Homo sapiens	100-109
35437791-7	2022	Furthermore, we found that nitrosamines co-exposure also promoted cell pyroptosis through the NLRP3/caspase-1/GSDMD pathway, which was demonstrated by adding the caspase-1 inhibitor Z-YVAD-FMK and constructing NLRP3 downregulated Het-1A cell line.	Nitrosamines	27-39	caspase 1	Homo sapiens	162-171
35437791-7	2022	Furthermore, we found that nitrosamines co-exposure also promoted cell pyroptosis through the NLRP3/caspase-1/GSDMD pathway, which was demonstrated by adding the caspase-1 inhibitor Z-YVAD-FMK and constructing NLRP3 downregulated Het-1A cell line.	benzyloxycarbonyltyrosyl-valyl-alanyl-aspartic acid fluoromethyl ketone	182-192	caspase 1	Homo sapiens	100-109
35437791-7	2022	Furthermore, we found that nitrosamines co-exposure also promoted cell pyroptosis through the NLRP3/caspase-1/GSDMD pathway, which was demonstrated by adding the caspase-1 inhibitor Z-YVAD-FMK and constructing NLRP3 downregulated Het-1A cell line.	benzyloxycarbonyltyrosyl-valyl-alanyl-aspartic acid fluoromethyl ketone	182-192	caspase 1	Homo sapiens	162-171
35445025-9	2022	The administration of miR-513c-5p mimics through tail vein injection or caspase-1 inhibitor (vx-765) by intraperitoneal injection remarkably decreased the volume of blood clots in vivo, whereas miR-513c-5p inhibitor aggravated thrombosis formation and this effect was dramatically weakened when treated in combination with vx-765.	belnacasan	93-99	caspase 1	Homo sapiens	72-81
35445025-9	2022	The administration of miR-513c-5p mimics through tail vein injection or caspase-1 inhibitor (vx-765) by intraperitoneal injection remarkably decreased the volume of blood clots in vivo, whereas miR-513c-5p inhibitor aggravated thrombosis formation and this effect was dramatically weakened when treated in combination with vx-765.	mir-513c-5p	194-205	caspase 1	Homo sapiens	72-81
35445025-9	2022	The administration of miR-513c-5p mimics through tail vein injection or caspase-1 inhibitor (vx-765) by intraperitoneal injection remarkably decreased the volume of blood clots in vivo, whereas miR-513c-5p inhibitor aggravated thrombosis formation and this effect was dramatically weakened when treated in combination with vx-765.	belnacasan	323-329	caspase 1	Homo sapiens	72-81
35406727-3	2022	METHODS: Caspase activity was measured in ischemic and perfused human myoblasts in response to the NLRP3 and AIM2 inflammasome agonists (nigericin and poly(dA:dT), respectively) with and without specific caspase-1 or pan-caspase inhibition.	Nigericin	137-146	caspase 1	Homo sapiens	204-213
35406727-3	2022	METHODS: Caspase activity was measured in ischemic and perfused human myoblasts in response to the NLRP3 and AIM2 inflammasome agonists (nigericin and poly(dA:dT), respectively) with and without specific caspase-1 or pan-caspase inhibition.	Nigericin	137-146	caspase 1	Homo sapiens	221-228
35406727-3	2022	METHODS: Caspase activity was measured in ischemic and perfused human myoblasts in response to the NLRP3 and AIM2 inflammasome agonists (nigericin and poly(dA:dT), respectively) with and without specific caspase-1 or pan-caspase inhibition.	poly(dA)	151-158	caspase 1	Homo sapiens	9-16
35431927-3	2022	Consistent data indicate the existence of estrogen receptor-independent targets of tamoxifen in macrophages that include lipid mediators and signaling pathways, such as NRF2 and caspase-1, which allow these cells to undergo phenotypic adaptation and potentiate the inflammatory response, without the induction of cell death.	Tamoxifen	83-92	caspase 1	Homo sapiens	178-187
35406727-3	2022	METHODS: Caspase activity was measured in ischemic and perfused human myoblasts in response to the NLRP3 and AIM2 inflammasome agonists (nigericin and poly(dA:dT), respectively) with and without specific caspase-1 or pan-caspase inhibition.	Thymidine	159-161	caspase 1	Homo sapiens	9-16
35406727-3	2022	METHODS: Caspase activity was measured in ischemic and perfused human myoblasts in response to the NLRP3 and AIM2 inflammasome agonists (nigericin and poly(dA:dT), respectively) with and without specific caspase-1 or pan-caspase inhibition.	Thymidine	159-161	caspase 1	Homo sapiens	204-213
35406727-3	2022	METHODS: Caspase activity was measured in ischemic and perfused human myoblasts in response to the NLRP3 and AIM2 inflammasome agonists (nigericin and poly(dA:dT), respectively) with and without specific caspase-1 or pan-caspase inhibition.	Thymidine	159-161	caspase 1	Homo sapiens	221-228
35406727-6	2022	Ischemic myoblasts also had significantly higher enzymatic caspase activity with poly(dA:dT) (p < 0.001), but not nigericin stimulation.	poly(dA)	81-88	caspase 1	Homo sapiens	59-66
35406727-6	2022	Ischemic myoblasts also had significantly higher enzymatic caspase activity with poly(dA:dT) (p < 0.001), but not nigericin stimulation.	Thymidine	89-92	caspase 1	Homo sapiens	59-66
35406727-7	2022	Inhibition of caspase activity including caspase-4/-5, but not caspase-1, blocked activation effects of poly(dA:dT).	poly	104-108	caspase 1	Homo sapiens	14-21
35406727-7	2022	Inhibition of caspase activity including caspase-4/-5, but not caspase-1, blocked activation effects of poly(dA:dT).	amsonic acid	109-111	caspase 1	Homo sapiens	14-21
35406727-7	2022	Inhibition of caspase activity including caspase-4/-5, but not caspase-1, blocked activation effects of poly(dA:dT).	Thymidine	112-114	caspase 1	Homo sapiens	14-21
35360199-10	2022	In addition, IP-Se-06 displayed significant inhibition of p38 MAPK and p-p38, leading to inhibition of inflammasome complex proteins (NLRP3 and caspase-1) in glioblastoma cells.	ip-se-06	13-21	caspase 1	Homo sapiens	144-153
35227133-6	2022	Experiments in vitro showed that cholesterol crystals promote MUC5AC secretion; they also increase expression of NLRP3, NLR family CARD domain-containing 4 (NLRC4), apoptosis-associated speck-like protein containing caspase recruitment domain (ASC), and cleaved caspase-1 in biliary epithelial cells.	Cholesterol	33-44	caspase 1	Homo sapiens	262-271
35342027-0	2022	Simvastatin Inhibits Tumor Growth and Migration by Mediating Caspase-1-dependent Pyroptosis in Glioblastoma Multiforme.	Simvastatin	0-11	caspase 1	Homo sapiens	61-70
35342027-10	2022	Simvastatin inhibits GBM progression by suppressing caspase-1 dependent pyroptosis, regulated by miR-214.	Simvastatin	0-11	caspase 1	Homo sapiens	52-61
35183871-7	2022	Further studies showed that J114 displayed remarkable inhibitory activity against NLRP3- and AIM2-but not NLRC4-dependent activation of caspase-1 and the release of IL-1beta in human THP-1 macrophages.	Cancell	28-32	caspase 1	Homo sapiens	136-145
35310096-4	2022	Modafinil treatment attenuated inflammasome activity and reduced neuronal pyroptosis involving the NLRP3/NLRP1/NLRC4-caspase-1-IL-1beta pathway.	Modafinil	0-9	caspase 1	Homo sapiens	117-126
35238869-6	2022	Proteasome (bortezomib, MG132) and caspase-1 (VX-765, Z-VAD-FMK) inhibitors block NLRP1 activation and downstream pyroptosis, respectively.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	54-63	caspase 1	Homo sapiens	35-44
35246004-11	2022	Emodin treatment decreased the levels of TNF-alpha, IL-1beta, IL-6, NLRP3, SDC-1, GSDMD-N, and Caspase-1, while increasing the levels of IL-10 in LPS-treated 1321N1 cells.	Emodin	0-6	caspase 1	Homo sapiens	95-104
35298317-6	2022	Under FBC treatment, the reductions of NLRP3 and Caspase-1 mRNA levels were 53.5% (p < 0.001) and 34.2% (p < 0.	4-(3,5-difluorophenyl)benzoic acid	6-9	caspase 1	Homo sapiens	49-58
35227133-8	2022	Also, the IL-1 receptor antagonist, IL1RA, and caspase-1 inhibitor, Ac-YVAD, both inhibited MUC5AC secretion induced by cholesterol crystals.	ac-yvad	68-75	caspase 1	Homo sapiens	47-56
35227133-8	2022	Also, the IL-1 receptor antagonist, IL1RA, and caspase-1 inhibitor, Ac-YVAD, both inhibited MUC5AC secretion induced by cholesterol crystals.	Cholesterol	120-131	caspase 1	Homo sapiens	47-56
35219847-0	2022	Silica nanoparticles induce pyroptosis and cardiac hypertrophy via ROS/NLRP3/Caspase-1 pathway.	Silicon Dioxide	0-6	caspase 1	Homo sapiens	77-86
35219847-0	2022	Silica nanoparticles induce pyroptosis and cardiac hypertrophy via ROS/NLRP3/Caspase-1 pathway.	ros	67-70	caspase 1	Homo sapiens	77-86
35219847-7	2022	For in vitro study, SiNPs increased the intracellular ROS generation and activated the NLRP3/Caspase-1/GSDMD signaling pathway in cardiomyocytes.	sinps	20-25	caspase 1	Homo sapiens	93-102
35219847-9	2022	Moreover, transfected with si-NLRP3 or adopted with Caspase-1 inhibitor VX-765 in cardiomyocytes showed an inhibitory effect on SiNPs-induced pyroptosis and cardiac hypertrophy.	belnacasan	72-78	caspase 1	Homo sapiens	52-61
35219847-9	2022	Moreover, transfected with si-NLRP3 or adopted with Caspase-1 inhibitor VX-765 in cardiomyocytes showed an inhibitory effect on SiNPs-induced pyroptosis and cardiac hypertrophy.	sinps	128-133	caspase 1	Homo sapiens	52-61
35188323-8	2022	MtROS reduction inhibited IL-1beta and IL-8 secretions by NLRP3/caspase-1/IL-1beta/IL-8 pathway.	mtros	0-5	caspase 1	Homo sapiens	64-73
35059736-12	2022	Furthermore, nicotine exposure increased the expression levels of caspase-1, IL-1beta, IL-18, NLRP3, apoptosis-associated speck-like protein and gasdermin D in 16HBE cells.	Nicotine	13-21	caspase 1	Homo sapiens	66-75
35023144-9	2022	After HSP70 stimulation, the expression of ROS, NLRP3, Caspase-1, and interleukin-18 (IL-18) increased significantly and could be reduced by ROS inhibitor NAC.	ros	141-144	caspase 1	Homo sapiens	55-64
35023144-9	2022	After HSP70 stimulation, the expression of ROS, NLRP3, Caspase-1, and interleukin-18 (IL-18) increased significantly and could be reduced by ROS inhibitor NAC.	Acetylcysteine	155-158	caspase 1	Homo sapiens	55-64
35023144-11	2022	In beagle models that received TmLRP, HSP70, NLRP3, Caspase-1, IL-1beta, and IL-18 were highly expressed in the wound tissue or urine, and could also be reduced by NAC pretreatment.	Acetylcysteine	164-167	caspase 1	Homo sapiens	52-61
35193116-7	2022	And the Caspase-1 inhibitor, Belnacasan, has been proved to modify the active site of Caspase-1 and lead to the blocking of Caspase-1, thus correlating with tissue protection of inflammatory diseases in animal models.	belnacasan	29-39	caspase 1	Homo sapiens	8-17
35193116-7	2022	And the Caspase-1 inhibitor, Belnacasan, has been proved to modify the active site of Caspase-1 and lead to the blocking of Caspase-1, thus correlating with tissue protection of inflammatory diseases in animal models.	belnacasan	29-39	caspase 1	Homo sapiens	86-95
35193116-7	2022	And the Caspase-1 inhibitor, Belnacasan, has been proved to modify the active site of Caspase-1 and lead to the blocking of Caspase-1, thus correlating with tissue protection of inflammatory diseases in animal models.	belnacasan	29-39	caspase 1	Homo sapiens	124-133
35221708-2	2022	Methods: A Dox-controlled system was utilized to induce the expression of the ASC transgene in HEK293 cells while simultaneously overexpressing NLRP3 and CASP1.	Doxorubicin	11-14	caspase 1	Homo sapiens	154-159
35221708-5	2022	The applicability and effectiveness of the CASPorter cell line were tested by co-treatment with Dox and four known CASP1/NLRP3 inhibitors (MCC950, Glyburide, VX-765 and VRT-043198).	Glyburide	147-156	caspase 1	Homo sapiens	115-120
35221708-7	2022	Results: Dox treatment significantly induced ASC expression and increased levels of cleaved and catalytically active CASP1, co-IPs further demonstrated that CASP1 was pulled-down with NLRP3 in HEK293-iASC-NLRP3/CASP1 cells after induction of ASC by Dox treatment.	Doxorubicin	9-12	caspase 1	Homo sapiens	117-122
35221708-7	2022	Results: Dox treatment significantly induced ASC expression and increased levels of cleaved and catalytically active CASP1, co-IPs further demonstrated that CASP1 was pulled-down with NLRP3 in HEK293-iASC-NLRP3/CASP1 cells after induction of ASC by Dox treatment.	Doxorubicin	9-12	caspase 1	Homo sapiens	157-162
35221708-7	2022	Results: Dox treatment significantly induced ASC expression and increased levels of cleaved and catalytically active CASP1, co-IPs further demonstrated that CASP1 was pulled-down with NLRP3 in HEK293-iASC-NLRP3/CASP1 cells after induction of ASC by Dox treatment.	Doxorubicin	9-12	caspase 1	Homo sapiens	211-216
35221708-7	2022	Results: Dox treatment significantly induced ASC expression and increased levels of cleaved and catalytically active CASP1, co-IPs further demonstrated that CASP1 was pulled-down with NLRP3 in HEK293-iASC-NLRP3/CASP1 cells after induction of ASC by Dox treatment.	Doxorubicin	249-252	caspase 1	Homo sapiens	117-122
35221708-7	2022	Results: Dox treatment significantly induced ASC expression and increased levels of cleaved and catalytically active CASP1, co-IPs further demonstrated that CASP1 was pulled-down with NLRP3 in HEK293-iASC-NLRP3/CASP1 cells after induction of ASC by Dox treatment.	Doxorubicin	249-252	caspase 1	Homo sapiens	157-162
35221708-7	2022	Results: Dox treatment significantly induced ASC expression and increased levels of cleaved and catalytically active CASP1, co-IPs further demonstrated that CASP1 was pulled-down with NLRP3 in HEK293-iASC-NLRP3/CASP1 cells after induction of ASC by Dox treatment.	Doxorubicin	249-252	caspase 1	Homo sapiens	211-216
35221708-8	2022	In HEK293-iASC-NLRP3/CASP1-CASPorter cell system, cleavage of the CASP1 consensus site (YVAD) in the CASPorter protein after Dox treatment causing excitation/emission of green fluorescence and the 71% GFP+ cell population increase quantified by FC (78.1% vs 6.90%).	Doxorubicin	125-128	caspase 1	Homo sapiens	21-26
35221708-8	2022	In HEK293-iASC-NLRP3/CASP1-CASPorter cell system, cleavage of the CASP1 consensus site (YVAD) in the CASPorter protein after Dox treatment causing excitation/emission of green fluorescence and the 71% GFP+ cell population increase quantified by FC (78.1% vs 6.90%).	Doxorubicin	125-128	caspase 1	Homo sapiens	66-71
35221708-9	2022	Dox-induced activation of the NLRP3 inflammasome was dose-dependently inhibited by Dox co-treatment with four known CASP1/NLRP3 inhibitors.	Doxorubicin	0-3	caspase 1	Homo sapiens	116-121
35221708-9	2022	Dox-induced activation of the NLRP3 inflammasome was dose-dependently inhibited by Dox co-treatment with four known CASP1/NLRP3 inhibitors.	Doxorubicin	83-86	caspase 1	Homo sapiens	116-121
35172755-6	2022	RESULTS: We found that Caspase-1 variant was significantly associated with FDG PET levels and CSF t-tau levels at baseline in total non-demented elderly group, and especially in mild cognitive impairment (MCI) subgroup.	Fluorodeoxyglucose F18	75-78	caspase 1	Homo sapiens	23-32
35163769-3	2022	The anti-inflammatory drug colchicine (which is reported in the literature to be a caspase-1 inhibitor) and the corticosteroid drugs, dexamethasone and methylprednisolone, are among the most effective active compounds for COVID-19 treatment.	Colchicine	27-37	caspase 1	Homo sapiens	83-92
35211530-8	2022	In vitro studies demonstrated that exogenous C18-ceramide promoted macrophage inflammation and matrix metalloprotein (MMP) expression through the NLRP3-caspase 1 pathway.	C18-CERAMIDE	45-57	caspase 1	Homo sapiens	152-161
35163148-8	2022	We found that sENG increased the gene expression of VEGF-A, pro-inflammatory cytokines/inflammasome mediators (TNF-alpha, IL-6, NLRP3, ASC, Caspase-1, and IL-1beta), and proteolytic enzyme (MMP-9) in BV2 microglia.	seng	14-18	caspase 1	Homo sapiens	140-149
35184413-13	2022	The caspase-1-gasdermin D (GSDMD) axis-mediated pyroptosis was the key to extra antitumour effect of the combination of apatinib and melittin.	apatinib	120-128	caspase 1	Homo sapiens	4-13
35184413-16	2022	CONCLUSIONS: Through pyroptosis mediated by caspase-1-GSDMD and caspase-3-GSDME axes synchronically, low-dosage apatinib and melittin could synergistically achieve a comparable therapeutic potential with reduced AEs.	apatinib	112-120	caspase 1	Homo sapiens	44-53
35280692-8	2022	Collectively, these findings suggest that PyrBDs are mainly released by macrophages in a caspase-1-dependent manner and serve as mediators of LPS-induced ALI.	pyrbds	42-48	caspase 1	Homo sapiens	89-98
35087283-0	2022	Pyrroloquinoline Quinone Disodium (PQQ2Na) Has an NLRP Inflammasome-Induced Caspase-1 Release Influence in UVB-Irradiated but Not ATP-Treated Human Keratinocytes but Has No Influence in Increasing Skin Cell Mitochondrial Biogenesis in Either Human Keratinocytes or Fibroblasts.	Methoxatin disodium salt	0-33	caspase 1	Homo sapiens	76-85
35087283-0	2022	Pyrroloquinoline Quinone Disodium (PQQ2Na) Has an NLRP Inflammasome-Induced Caspase-1 Release Influence in UVB-Irradiated but Not ATP-Treated Human Keratinocytes but Has No Influence in Increasing Skin Cell Mitochondrial Biogenesis in Either Human Keratinocytes or Fibroblasts.	pqq2na	35-41	caspase 1	Homo sapiens	76-85
35087283-6	2022	Methods: The inflammation studies followed previously published methods that demonstrated both UVB and ATP were able to upregulate the NLRP-activated release of caspase-1 in NHEKs.	Adenosine Triphosphate	103-106	caspase 1	Homo sapiens	161-170
35087283-10	2022	In NHEKs irradiated with 60mJ/cm2 of UVB radiation as previously described and treated with 0.05 microg/mL to 50 microg/mL of PQQ2Na, the molecule showed a dose-dependent benefit at reducing the expression of active caspase-1 in the irradiated cells.	pqq2na	126-132	caspase 1	Homo sapiens	216-225
35111001-4	2021	In addition, elamipretide has been shown to attenuate neural oxidative stress (hydrogen peroxide, lipid peroxidation, and ROS), neuroinflammation (TNF, IL-6, COX-2, iNOS, NLRP3, cleaved caspase-1, IL-1beta, and IL-18), and toxic protein accumulation (Abeta).	arginyl-2,'6'-dimethyltyrosyl-lysyl-phenylalaninamide	13-25	caspase 1	Homo sapiens	186-195
35095880-4	2021	Those cells also showed aberrant levels of mitochondrial superoxide and lipid peroxidation, both hallmarks of the oxidative stress response, which strongly correlated with caspase-1 activity.	Superoxides	57-67	caspase 1	Homo sapiens	172-181
35615856-9	2022	When HEK293T cells were transfected with inflammasome components NLRP3 or Pyrin, along with ASC, pro-caspase-1, pro-IL-1beta, and B2M, ThT fluorescence intensity increased.	thioflavin T	135-138	caspase 1	Homo sapiens	101-110
35237974-5	2022	Importantly, activation of the nucleotide oligomerization domain leucine-rich repeat and pyrin domain containing protein 3 (NLRP3) inflammasome activates the caspase-1 protease and results in the generation and release of potent pro-inflammatory cytokines, IL-1beta and IL-18.	Leucine	65-72	caspase 1	Homo sapiens	158-167
35042538-12	2022	The expression of Caspase1 in glioblastoma cells treated with 4, 5-dimethoxycanthin-6-one increased, and the number of apoptotic cells increased.	4,5-dimethoxycanthin-6-one	62-89	caspase 1	Homo sapiens	18-26
35022395-10	2022	Such an effect was abrogated when THP-1 cells were incubated with YVAD (caspase-1 inhibitor) or when Caco-2 were incubated with anakinra, while butyrate incubation did not prevent such decrease.	YVAD	66-70	caspase 1	Homo sapiens	72-81
34874326-0	2022	PEG-PEI/siROCK2 inhibits Abeta42-induced microglial inflammation via NLRP3/caspase 1 pathway.	poly(ethylene glycol)-co-poly(ethyleneimine)	0-7	caspase 1	Homo sapiens	75-84
34874326-0	2022	PEG-PEI/siROCK2 inhibits Abeta42-induced microglial inflammation via NLRP3/caspase 1 pathway.	sirock2	8-15	caspase 1	Homo sapiens	75-84
34874326-12	2022	In addition, we found that PPSR suppressed the Abeta-induced NLRP3/caspase 1 pathway in primary microglial cells.	UNII-042A8N37WH	47-52	caspase 1	Homo sapiens	67-76