ライフサイエンスコーパス: caspase 1

1 dently of NLRP3, its adaptor protein ASC, or caspase 1.

2 ted with an NLRP3 inhibitor or inhibitors of caspase 1.

3 NLRP3(R258W) activating mutation to activate caspase-1.

4 a in the extracellular space by the protease caspase-1.

5 ich leads to the activation of the protease, caspase-1.

6 of the NLRP3 inflammasome and activation of caspase-1.

7 ndent of the inflammasome components ASC and caspase-1.

8 dent on the presence of IL-1beta, IL-18, and caspase-1.

9 reby preventing processing and activation of caspase-1.

10 wn origin harbor mutations in CASP1 encoding caspase-1.

11 e p.C284A caspase-1 variant compared with WT caspase-1.

12 nd with increased intensity compared with WT caspase-1.

13 SC, oligomerization of ASC and activation of caspase-1.

14 mmasomes, multi-protein complexes activating caspase-1.

15 d lipolysis by decreasing levels of MAOA and caspase-1.

16 ed IL-8 and MCP-1 synthesis through TLR4 and caspase-1.

17 cleaved caspase-3 levels and the absence of caspase-1.

18 s on immune/cell death regulators, including caspase-1.

19 We monitored survival, Il1beta/18, and caspase 1/11 levels in plasma and organs and deciphered

20 The release of IL-1alpha occurred by a caspase 1/11- and P2XR7-independent mechanism but was de

21 asopharynx, which required activation of the caspase-1/11 inflammasome, mucosal T cells, and macropha

22 signaling but dependent on bacterial burden, caspase-1/11, and neutrophil-dependent tissue damage.

23 Interestingly, injection of caspase-1/11-deficient mice with anti-COL7 IgG led to th

24 Caspases 1, 3, and 8 decreased significantly in cells co

25 Inflammatory caspases (caspases 1, 4, 5 and 11) are activated in response to mi

26 nse because its cleavage by the inflammatory caspases 1, 4, 5, and 11 yields an N-terminal p30 fragme

27 tination and degradation of the inflammatory caspases 1, 4, and 11.

28 athogenesis was not enhanced in mice lacking caspase-1, a critical inflammasome component.

29 Caspase-1-activated IL-18 induces IFN-gamma to prime cas

30 ducible protein (IFI)16, bind dsDNA and form caspase-1-activating inflammasomes that are important in

31 ated by IL-1beta The NLRP3 inflammasome is a caspase-1-activating multiprotein complex that links sen

32 Increased caspase 1 activation causing maturation of IL1beta/18 re

33 ulates inflammation, with unknown effects on caspase 1 activation.

34 Blocking caspase-1 activation abrogated the therapeutic effects o

35 gen-associated molecular patterns leading to caspase-1 activation and cytokine release, which mediate

36 t of ASC to upstream sensors, which prevents caspase-1 activation and cytokine release.

37 In the absence of NEK7, caspase-1 activation and IL-1beta release were abrogated

38 a pyrin domain 3 are partially required for caspase-1 activation and IL-1beta secretion, suggesting

39 This led to caspase-1 activation and IL-1beta secretion.

40 ficient mice showed substantial reduction in caspase-1 activation and in interleukin (IL)-1beta and I

41 pite their low CD14 expression, LPS-sensing, caspase-1 activation and P2X7R activity were comparable

42 Their activation induces caspase-1 activation and release of interleukin-1beta, a

43 assembly inhibitors prevented Pyrin-mediated caspase-1 activation and secretion of IL-1beta and IL-18

44 aining a CARD (caspase recruitment domain)), caspase-1 activation by another danger-signaling sensor

45 es demonstrate a role of Nedd8 in regulating caspase-1 activation following inflammasome activation,

46 MP1 association correlated with the level of caspase-1 activation in individual cells.

47 her effectors cooperate with YopM to inhibit caspase-1 activation in LPS-activated macrophages has no

48 ficantly increased Stat3 phosphorylation and caspase-1 activation in the kidneys of nephritic Mer-KO

49 ating caspase-1, but different mechanisms of caspase-1 activation occur, depending on the bacterial g

50 The NLRP3 inflammasome, a caspase-1 activation platform, plays a key role in the m

51 Whereas NLRP3 regulation of caspase-1 activation requires the adaptor protein ASC (a

52 terminal CARD domain that facilitates direct caspase-1 activation via CARD-CARD interaction.

53 IL-1beta secretion and caspase-1 activation were also dependent on IRAK-4 signa

54 mutant NLRC4 S533A had only a mild defect in caspase-1 activation when compared with NLRC4-deficient

55 NG is required to induce IL-1beta secretion, caspase-1 activation, and GBP2 and GBP3 expression.

56 dramatically abolished ASC oligomerization, caspase-1 activation, and IL-1beta secretion in response

57 r IFI16, resulting in inflammasome assembly, caspase-1 activation, and pyroptosis.

58 lrp3 inflammasome in MLVECs accompanied with caspase-1 activation, IL-1beta release and induction of

59 osome maturation arrest, while NOD2 promoted caspase-1 activation, IL-1beta secretion and autophagy m

60 ause Naip5 deletion in macrophages abolished caspase-1 activation, interleukin (IL)-1beta secretion,

61 The inflammasome, which leads to caspase-1 activation, is implicated in neuroinflammation

62 lammasome with the adapter ASC, resulting in caspase-1 activation, release of proinflammatory cytokin

63 distinct inflammasome complexes that promote caspase-1 activation, secretion of the proinflammatory c

64 ugh all the mutations result in constitutive caspase-1 activation, their phenotypic presentations are

65 ar patterns by cytosolic sensory proteins to caspase-1 activation.

66 nflammatory cytokines through pyroptosis and caspase-1 activation.

67 HIV-induced podocyte injury was mediated by caspase-1 activation.

68 limiting upstream inflammasome assembly and caspase-1 activation.

69 ct in NLRC4 inflammasome oligomerization and caspase-1 activation.

70 duced pyroptotic cell death characterized by caspase-1 activation.

71 s showed reduction in IL-1beta secretion and caspase-1 activation.

72 f mitochondrial ROS, ASC speck formation and caspase-1 activation.

73 We analyzed caspase 1 activity and cytokine secretion.

74 AM5 is a novel regulator of inflammasome and caspase 1 activity that functions independently of RIPK3

75 accord with our in vitro findings, lesional caspase 1 activity was abolished in P2X7(-/-) mice.

76 -like protein containing a CARD) expression, caspase 1 activity, or IL-1beta (interleukin-1beta) prot

77 In addition, inhibition or deficiency of caspase-1 activity blocked NMII-induced B1a cell death.

78 sponsible for increased NLRP3 expression and caspase-1 activity in adipose tissues and liver.

79 nd caspase-1 cleavage, whereas YopM inhibits caspase-1 activity via an incompletely understood mechan

80 Mechanistic studies showed that caspase-1 activity, IL-1beta production, IL-1beta secret

81 have been reported to influence inflammasome caspase-1 activity; YopJ promotes caspase-8-dependent ce

82 eficient macrophages showed no activation of caspase 1 after sequential stimulation while still expre

83 Results show enhanced activation of caspase-1 after infection with the yopJ yopM mutant rela

84 Caspase-1, also known as interleukin-1beta (IL-1beta)-co

85 eracting protein kinase-1 (RIPK1), RIPK3, or caspase-1] also serve other functions.

86 SHARPIN bound caspase 1 and disrupted p20/p10 dimer formation, the las

87 timulation with ATP, led to an activation of caspase 1 and interleukin-1beta in P2X7-competent macrop

88 3 inflammasome, leading to the activation of caspase 1 and production of interleukin 1beta (IL-1beta)

89 Thus, a coordinated IEC-intrinsic, Caspase-1 and -8 inflammasome response plays a key role

90 ASC inflammasome led to the up-regulation of caspase-1 and a proinflammatory cytokine, interleukin-1b

91 fected astrocytes and microglia deficient in caspase-1 and apoptosis-associated speck-like protein co

92 Caspase-1 and apoptosis-associated speck-like protein co

93 The overlapping and unique functions of caspase-1 and caspase-11 are difficult to unravel withou

94 The enzymatic activities of caspase-1 and caspase-11 are required for growth inhibit

95 We further demonstrated that caspase-1 and caspase-11 differentially contributed to t

96 Activation of caspase-1 and caspase-11 initiates pyroptotic host cell

97 ery of Gasdermin D (GSDMD) as a substrate of caspase-1 and caspase-11 upon detection of cytosolic lip

98 s, essentially making them deficient in both caspase-1 and caspase-11.

99 Furthermore, caspase-1 and caspase-8 can interact with ASC to mediate

100 mmunofluorescence studies exhibited distinct caspase-1 and caspase-8 puncta in diseasedPtpn6(spin)neu

101 e provides similar protection as observed in caspase-1 and caspase-8-deficientPstpip2(cmo)mice, demon

102 s associated with an epidermal activation of caspase-1 and cutaneous overexpression of IL-1beta.

103 r not only attenuated podocyte expression of caspase-1 and IL-1beta but also provided protection agai

104 LPS, which is also accompanied by increased Caspase-1 and IL-1beta cleavage upon NLRP3, but not AIM2

105 e also time-dependently increased the mature caspase-1 and IL-1beta levels and enhanced the IL-1beta

106 s induced, with the downstream activation of caspase-1 and IL-1beta.

107 of the NLRP3 inflammasome and processing of caspase-1 and IL-1beta.

108 ants result in reduced enzymatic activity of caspase-1 and impaired IL-1beta secretion.

109 how inflammasomes are regulated to activate caspase-1 and implicated in human diseases.

110 and sensors that regulate the activation of caspase-1 and induce inflammation in response to infecti

111 IKV-infected patients showed elevated NLRP3, caspase-1 and interleukin-18 messenger RNA expression an

112 tro, that increased concentrations of active caspase-1 and interleukin-1beta are related to an increa

113 absence of AIM2 or its downstream effectors, caspase-1 and interleukin-1beta, erases the ability of E

114 ehenate), and TLR7/8 (R848) greatly enhanced caspase-1 and NF-kappaB activation, Th1 polarizing cytok

115 erized by targeted gene expression analysis, caspase-1 and NF-kappaB studies, cytokine multiplex and

116 phages exhibit reduced expression of cleaved caspase-1 and NLRP3.

117 LR12 decreased expression of the NLRP3, pro-caspase-1 and pro-IL-1beta, and inhibited priming of the

118 n demonstrated that it was unable to recruit caspase-1 and process IL-1beta.

119 flammasome activation leads to maturation of caspase-1 and processing of IL1beta, contributing to man

120 er that these particles induce activation of caspase-1 and secretion of IL-1beta by macrophages.

121 gocytosed and could induce the activation of caspase-1 and subsequent activation of caspase-7; this r

122 ome comprises an intracellular sensor (NLR), caspase-1 and the adaptor ASC.

123 2 prevents the autoproteolytic activation of caspase-1 and the maturation of IL-1beta through inducti

124 te immune defenses through the activation of caspase-1 and the maturation of proinflammatory cytokine

125 d caspase-1 that result in the activation of caspase-1 and the release of IL-1beta and IL-18.

126 masome activation leads to the activation of caspase-1 and the release of pro-inflammatory cytokines

127 NLRP3 inflammasome by binding both NLRP3 and caspase-1 and thereby preventing processing and activati

128 te that these fusion proteins are cleaved by caspases-1 and -11 at Asp-276.

129 d enrichment in mature Il1beta/18 and active caspase 1, and shortened survival.

130 ecruitment domain (ASC), cysteine aspartase (caspase)-1, and interleukin (IL)-1beta from individuals

131 e to L. braziliensis was dependent on NLRP3, caspase-1, and caspase-recruiting domain (ASC).

132 distinctive, increased expression of NLRP3, caspase-1, and IL-1beta in individuals with clinically e

133 d expression of NLRP3, ASC (a CARD protein), caspase-1, and IL-1beta proteins, confirming NLRP3 infla

134 tential for targeting of NLRP3 inflammasome, caspase-1, and IL-1beta responses in experimental severe

135 n NLRP3 knockout mice, up-regulation of ASC, caspase-1, and IL-1beta were all reduced, and, important

136 ons of inflammasome markers (NLRP3, ASC, and caspase-1, and IL-1beta).

137 Notably, genes (IFI16, caspase-1, and interleukin 1beta [IL-1beta]) in the cano

138 ne increased the expression of NLRP3, active caspase-1, and mature interleukin-1beta in human periphe

139 tivation and Recruitment Domain (CARD)), pro-caspase-1, and NLRP3 (NOD-Like Receptor family Pyrin dom

140 activates caspase-4 (caspase-11 in mice) and caspase-1, and requires cyclic GMP-AMP synthase (cGAS)-d

141 RP3) inflammasome controls the activation of caspase-1, and the release of proinflammatory cytokines

142 his study, we show that RIPK3 is crucial for caspase 1- and caspase 8-mediated pro-IL-1beta and pro-I

143 a form of mitochondrial (mt) damage that is caspase-1- and NLRP3-independent and causes release of d

144 peck-like protein containing a CARD) and pro-caspase-1, as well as its downstream targets IL-1beta an

145 activation by reducing expression of NLRP3, caspase-1, ASC, AIM2, TNFalpha, IL1beta and proinflammat

146 urthermore, the disorder is dependent on the caspase-1-ASC axis, whereas caspase-8 is dispensable.

147 lipopolysaccharide also is dependent on the caspase-1-ASC axis.

148 ced macrophage and dendritic cell death in a caspase-1-, ASC-, and NLRP3-independent manner, whereas

149 ouse MC protease 4 [mMCPT4]), BECs underwent caspase-1-associated cytolysis and exfoliation.

150 y, not only does inhibition of the NF-kappaB/caspase-1 axis disrupt the inflammatory phase of the wou

151 masome complex by competing with ASC for pro-caspase-1 binding.

152 genous NLRC3 interacts with both ASC and pro-caspase-1 but not with NALP3, disrupts ASC speck formati

153 spond to translocation of Yops by activating caspase-1, but different mechanisms of caspase-1 activat

154 Inhibition of the inflammasome enzyme caspase-1 by chemical inhibition or genetic knockdown wi

155 NLRC4 S533A activated caspase-1 by recruiting NLRP3 and its adaptor protein AS

156 toxic to neuronal culture, and inhibition of caspase-1 by shRNA or a specific chemical inhibitor impr

157 asome-induced activation of an intracellular caspase-1/calpain cysteine protease cascade degraded fil

158 ilarly, interaction of endogenous Nedd8 with caspase-1 CARD was detected in inflammasome-activated ma

159 roportions of monocytes expressing activated caspase-1 (casp1) pre-cART, compared with HIV patients w

160 various KO backgrounds including Il1b/Il18-, caspase-1-, caspase-11- (Casp1/11-), and Tnf-deficient s

161 totic speck containing protein with a CARD), caspase-1, cathepsin-mediated degradation, calcium mobil

162 with three biologically important proteins: caspase-1, CheY, and h-Ras, correctly predicting key all

163 nflammasome activation indicated by enhanced caspase 1 cleavage and increased IL-1beta maturation and

164 a prerequisite for sustained NLRP3 mediated caspase-1 cleavage and inflammasome activation.

165 containing a CARD (ASC) speck formation and caspase-1 cleavage and interacted with NLRP3 and ASC.

166 masome, resulting in attenuated IL-1beta and caspase-1 cleavage and secretion, as well as diminished

167 the absence of YopM, YopJ minimally affects caspase-1 cleavage but suppresses IL-1beta, IL-18, and o

168 We found increased caspase-1 cleavage within patient monocytes indicative o

169 duced IL-1beta maturation and secretion, pro-caspase-1 cleavage, and speck formation by apoptosis-ass

170 , unlike the N-terminal fragment produced by caspase-1 cleavage, this fragment fails to trigger cell

171 promotes caspase-8-dependent cell death and caspase-1 cleavage, whereas YopM inhibits caspase-1 acti

172 and inhibited the assembly of the NRLP3/ASC/caspase-1 complex.

173 Pro-caspase-1 consists of three domains, CARD, p20, and p10.

174 Here, we generated caspase-1-deficient mouse (Casp1(Null)) on the C57BL/6 J

175 Tumor progression was diminished when WT or caspase-1-deficient, but not NLRC4-deficient, macrophage

176 nflammasome through an AIM2, NLRP3, ASC, and caspase-1 dependent process.

177 ion of mitochondrial LigIIIalpha activated a caspase 1-dependent apoptotic pathway, which is known to

178 Inflammasome activation and caspase-1-dependent (CASP1-dependent) processing and sec

179 the STING pathway, in part through promoting caspase-1-dependent cell death.

180 The nature of the caspase-1-dependent change in plasma membrane (PM) perme

181 uric acid or ATP, via NLRP3, which leads to caspase-1-dependent cleavage of pro-IL-1beta to active I

182 se against bacterial pathogens by activating caspase-1-dependent cytokine secretion and cell death.

183 AIM2 mediates the caspase-1-dependent death of intestinal epithelial cells

184 We observed QS-21 to elicit caspase-1-dependent IL-1beta and IL-18 release in antige

185 ch in turn leads to AM pyroptosis, a type of caspase-1-dependent inflammatory cell death.

186 ns did not induce pyroptosis, as measured by caspase-1-dependent interleukin-1beta release, though th

187 embles in human CD4(+) T cells and initiates caspase-1-dependent interleukin-1beta secretion, thereby

188 mmasome is a protein complex responsible for caspase-1-dependent maturation of the proinflammatory cy

189 n of the inflammasome is critical to promote caspase-1-dependent maturation of the proinflammatory cy

190 M1 served as a second signal for caspase-1-dependent NLRP3 inflammasome activation, induc

191 This results in caspase-1-dependent pro-inflammatory cytokine maturation

192 These results suggest that NMII induces a caspase-1-dependent pyroptosis in murine peritoneal B1a

193 These data suggest that NMII-induced caspase-1-dependent pyroptosis may require its T4SS and

194 ivation of the NLRP3 inflammasome results in caspase-1-dependent secretion of the proinflammatory cyt

195 Macrophages with variant p.C284A caspase-1 did not secrete IL-1beta and exhibited reduced

196 In vitro characterization confirmed that caspase-1 directly cleaves aSyn, generating a highly agg

197 on, but the mechanism by which they activate caspase-1 diverges at the level of the pannexin-1/ATP/P2

198 Hence, caspase-1-driven pore-induced cell death triggers a mult

199 Thus, caspase-1-driven pyroptosis requires induction of initia

200 LXR through negative regulation of both pro-caspase 1 expression and activation.

201 spase activation and recruitment domain), or caspase-1 failed to process and secrete IL-1beta.

202 Canonical inflammasome activation induces a caspase-1/gasdermin D (Gsdmd)-dependent lytic cell death

203 ed NLRP3 complexes that direct activation of caspase-1, generation of interleukin-1beta (IL-1beta) an

204 The inflammatory protease caspase-1 has been implicated in metabolic dysfunction;

205 inal truncation by the inflammatory protease caspase-1 has recently been implicated in the mechanisms

206 l death pathway activated by human and mouse caspase-1, human caspase-4 and caspase-5, or mouse caspa

207 oteins of inflammasome pathways, NLRP3, ASC, caspase 1, IL-1 and IL-18.

208 a and Haemophilus infections increase NLRP3, caspase-1, IL-1beta responses that drive steroid-resista

209 HARPIN correlated with enhancement of active caspase 1 in circulating mononuclear cells.

210 de or ATP stimulation alone did not activate caspase 1 in isolated macrophages.

211 Blocking IL-1beta or caspase 1 in vivo had little effect on NanoSiO2 adjuvant

212 red an important role for YopJ in inhibiting caspase-1 in activated macrophages and in promoting Yers

213 Inflammasomes activate caspase-1 in response to cytosolic contamination or pert

214 Although the concentration of caspase-1 in saliva samples makes its determination usel

215 The pharmacological inhibition of caspase-1, in vivo knockdown of NLRP3, or HIF-1alpha oth

216 cell damage; cytosolic sensors activate pro-caspase-1, indirectly for the most part, via the adaptor

217 impaired the quality of lung grafts through caspase-1-induced pyroptotic cell death during EVLP.

218 n activation within an inflammasome complex, caspase-1 induces pyroptosis and converts pro-IL-1beta a

219 RhoA deamidation induces caspase-1 inflammasome activation, which is mediated by

220 When the NLRP3-ASC-caspase-1 inflammasome-induced pathway was inhibited by

221 OD-like receptors leads to the activation of caspase-1 inflammasomes, and the production of the pro-i

222 d deciphered mechanisms of SHARPIN-dependent caspase 1 inhibition.

223 a processing and secretion were sensitive to Caspase-1 inhibition, NLRP3 knockdown, and K(+) efflux i

224 indings identify SHARPIN as a potent in vivo caspase 1 inhibitor and propose the caspase 1-SHARPIN in

225 1a, Il1b, and Nlrp3, and pretreatment with a caspase 1 inhibitor decreased IL-1beta secretion in resp

226 aride-induced endotoxemia, and injected with caspase 1 inhibitor.

227 tals were shown to be IL-1-dependent using a caspase-1 inhibitor (inhibits IL-1 maturation) and IL-1R

228 ective NLRP3 inhibitor, MCC950; the specific caspase-1 inhibitor Ac-YVAD-cho; and neutralizing anti-I

229 Caspase-1 inhibitor not only attenuated podocyte express

230 vivo proof of concept of the ability of the caspase-1 inhibitor prodrug VX-765 to mitigate alpha-syn

231 inflammatory response if a LF was used or a caspase-1 inhibitor was administered during EVLP.

232 Caspase-1 inhibitors blocked all of these responses.

233 Furthermore, the administration of caspase-1 inhibitors or the infusion of bone marrow-deri

234 Furthermore, enzymatically inactive caspase-1 interacted with ASC longer and with increased

235 hrough its CARD, and impairs the ASC and pro-caspase-1 interaction.

236 ia augmenting autoprocessing/cleavage of pro-caspase-1 into its corresponding catalytically active su

237 Caspase-1 is a key player during the initiation of pro-i

238 or to Yersinia pseudotuberculosis infection, caspase-1 is activated by a rapid inflammasome-dependent

239 Here we report that caspase-1 is activated in macrophages under hypertonic c

240 wild-type (WT), NLRP3 knockout (NLRP3(-/-)), caspase-1 knockout (Casp-1(-/-)), and interleukin-1 rece

241 roblastic transition and its amelioration in caspase-1 knockout mice.

242 hermore, disruption of IL-1beta signaling by caspase-1(KO) specifically within bone marrow-derived ce

243 ein complex that regulates the activation of caspase-1 leading to the maturation of the proinflammato

244 t the common adaptor protein ASC to activate caspase-1, leading to the secretion of mature IL-1beta a

245 no significant differences were observed for caspase-1 levels between clinical groups, and only NLRP3

246 Despite the observation that merely raising caspase-1 levels is sufficient to induce inflammation, t

247 hat Arabidopsis BAG6 is cleaved in vivo in a caspase-1-like-dependent manner and via a combination of

248 Nlrc4 phosphorylation, but failed to elicit caspase-1 maturation, IL-1beta secretion, and pyroptosis

249 nd AIM2 mediated inflammasomes that leads to caspase 1 mediated apoptosis.

250 Caspase-1-mediated cell death with accompanying cytokine

251 In contrast to the rapid caspase-1-mediated death of wild type (WT) BMDC via NLRP

252 ome activation in HCV-infected cells enables caspase-1-mediated degradation of insulin-induced gene p

253 r studies have uncovered a specific role for caspase-1-mediated IL-1beta release in the manifestation

254 r stress-associated stimuli, activating both caspase-1-mediated inflammatory cytokine secretion and p

255 l morphogenesis, sufficient for induction of caspase-1-mediated macrophage lysis.

256 Activation of the inflammasome promotes caspase-1-mediated secretion of proinflammatory cytokine

257 the NLRP3 and AIM2 inflammasomes, leading to caspase-1-mediated tumour regression that is dependent o

258 saccharide induction of IL-1beta, NLRP3, and caspase-1 mRNAs.

259 Notably, knockdown of NLRP3 or caspase-1, neutralization of S100A9, and pharmacologic i

260 ium integrity but did not absolutely require Caspase-1 or Gasdermin D.

261 R12 also reduced the expression of NLRP3 and caspase-1 p10 protein, and secretion of the IL-1beta, in

262 This latter step is reliant on active caspase-1, pannexin-1, and P2X7 receptor activation.

263 optosis and pyroptosis; 26% were pyroptotic (Caspase-1-positive).

264 Therefore, targeting the caspase-1/PPARgamma/MCAD pathway might be a promising th

265 tic or pharmacological targeting of NLRP3 or caspase-1 prevented MLKL-induced IL-1beta secretion, the

266 ed p20/p10 dimer formation, the last step of caspase 1 processing, thereby inhibiting enzyme activati

267 ion and recruitment domain (ASC) and trigger caspase-1 processing of the proinflammatory cytokine IL-

268 tein with a CARD domain oligomerization, and caspase-1 processing, key events during inflammasome act

269 , apoptosis-associated specklike protein, or caspase-1 produced markedly higher IFN-beta in response

270 Caspase-1 promotes pyroptotic cell death and the maturat

271 Here, the author show that caspase-1 promotes TAMs differentiation by attenuating m

272 Here, we report that caspase-1 promotes tumor-associated macrophage different

273 tment and activation of the pro-inflammatory CASPASE-1 protease.

274 -like protein containing a CARD complex), or caspase-1 protected against PDA and was associated with

275 induction of a cellular state inhibitory to caspase-1 proteolytic function.

276 ysiological aberration, drives activation of caspase-1, pyroptosis, and the release of the pro-inflam

277 Inhibition of caspase 1 reduced levels of Il1beta/18 and splenic cell

278 component of this effect, and inhibition of caspase-1 reduced cell death, augmenting phosphorylation

279 in vivo caspase 1 inhibitor and propose the caspase 1-SHARPIN interaction as a target in sepsis.

280 eta) secreted by BECs after inflammasome and caspase-1 signaling.

281 ining enzymatically inactive variant p.C284A caspase-1 spread during cell division.

282 In conclusion, variant p.C284A caspase-1 stabilizes pyroptosome formation, potentially

283 Gasdermin D (GSDMD), the pore-forming caspase-1 substrate required for efficient NLRP3-trigger

284 e complexes with the adaptor protein ASC and caspase-1 that result in the activation of caspase-1 and

285 endent on NLRP3, its adaptor protein ASC, or caspase 1, the cleavage of intracellular pro-IL-1beta to

286 block all caspases including proinflammatory caspase-1, the effect of specific caspase-3 inhibition d

287 rol the innate immune response by activating caspase-1, thus promoting the secretion of cytokines in

288 They process pro-caspase-1 to active caspase-1, which cleaves pro-inflamm

289 complexes with the adaptor proteins Asc and caspase-1 to promote the maturation of interleukin (Il)-

290 umber and size in cells carrying the p.C284A caspase-1 variant compared with WT caspase-1.

291 A correlation between LUBAC and active caspase 1 was found in blood mononuclear cells from sept

292 aspase-3 or PARP-1 cleavage, but cleavage of caspase-1 was detected in NMII-infected B1a cells.

293 Activation of caspase-1 was measured by cleavage of the enzyme, releas

294 ed speck-like protein containing a CARD, and caspase-1), we further show that the activation of the N

295 -1R or the inflammasome components NLRP3 and caspase-1 were protected from aldosterone-induced vascul

296 IL-1beta and inflammasome components ASC and caspase-1 were released by ATP-activated macrophages thr

297 y is the activation of the cysteine protease caspase-1, which activates the pro-inflammatory cytokine

298 They process pro-caspase-1 to active caspase-1, which cleaves pro-inflammatory IL-1beta o mat

299 tion of IL-1beta requires a unique protease, caspase-1, which is activated by various protein platfor

300 Association of pro-caspase-1 with the inflammasome results in initiation of