ライフサイエンスコーパス: caspase 1

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

2 its ability to form ASC specks and activate caspase-1.

3 nd freeing the NLRP1B C terminus to activate caspase-1.

4 s ASC specks to facilitate the activation of caspase-1.

5 S-rich CF lung by the NLRP3 inflammasome via caspase-1.

6 active IL-1beta by proteolytic cleavage via caspase-1.

7 landensis in vitro upon processing by active caspase-1.

8 is further reduced by the presence of active caspase-1.

9 te immunity by recruitment and activation of caspase-1.

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

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

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

13 proteolytic activity of a cysteine protease caspase-1.

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

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

16 prevented by co-ablation of either Ripk1 or Caspase-1.

17 ese alterations are independent of NLRP3 and caspase-1.

18 to the recruitment of ASC and activation of caspase-1.

19 phages deficient for diverse combinations of caspases-1, -11, -12, and -8 and receptor interacting se

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

21 g analysis; however, Aldara treatment led to caspase 1/11-, caspase 8-, and RIPK3-independent keratin

22 dermin-D dependent, and that gasdermin-D and caspase-1/11 deficient mice show deficits in brain infla

23 by low relative humidity was ameliorated in caspase-1/11-deficient Mx1 mice, independent of viral bu

24 e, antihelminth responses were unaffected in caspase-1/11-deficient or WT mice treated with the NLRP3

25 ntary, but independent role of caspase-8 and caspases-1/11/GSDM-D in the pathogenesis of malaria.

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

27 avage of gasdermin D (GSDMD) by inflammatory caspases-1, 4, 5, and 11 are essential steps in initiati

28 nocytes from malaria patients express active caspases-1, -4 and -8 suggesting that these inflammatory

29 pase-1, caspase-4, caspase-5 and caspase-11 (caspase-1/-4/-5/-11)) mediate host defense against micro

30 SERPINB1 prompted spontaneous activation of caspase-1/-4/-5/-11, release of the cytokine IL-1beta an

31 nding motif restrained the activation of pro-caspase-1/-4/-5/-11.

32 Pharmacologic inhibition with Ac-YVAD-cmk of caspase 1, a critical component of the NLRP3 inflammasom

33 The mutation D20A prevents cleavage of caspase-1, a step required for IL-37 nuclear translocati

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

35 cell death that is induced upon formation of caspase-1-activating inflammasomes.

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

37 Blocking caspase-1 activation abrogated the therapeutic effects o

38 on of HOIP or Sharpin resulted in heightened caspase-1 activation and cell death in response to infla

39 Increased caspase-1 activation and cell death were observed in mou

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

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

42 le to monitor the spatiotemporal dynamics of caspase-1 activation and onset of inflammation in indivi

43 omes are multiprotein complexes facilitating caspase-1 activation and subsequent gasdermin D-mediated

44 We found that NLRP3 inflammasome-mediated caspase-1 activation and subsequent IL-1beta production

45 as further confirmed by functional assays of caspase-1 activation and subsequent secretion of cytokin

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

47 omplexes with NLRC4 and negatively regulates caspase-1 activation by NLRC4-H443P in human cells.

48 containing a CARD (ASC)-speck formation and caspase-1 activation by NLRC4-H443P.

49 ts identify HSC70 as a negative regulator of caspase-1 activation by the temperature-sensitive NLRC4-

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

51 rkable attenuation of IL-1beta secretion and caspase-1 activation in patients with an NLRP3-associate

52 mutation sensitizes cells to necroptosis and caspase-1 activation in response to TLRs signaling.

53 Caspase-1 activation mediated release of mature IL-1beta

54 aureus EVs were critical for NLRP3-dependent caspase-1 activation of human macrophages, but not for T

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

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

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

58 tosis of monosodium urate (MSU) crystals and caspase-1 activation were determined by flow cytometer.

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

60 o significantly blocked IL-1beta production, caspase-1 activation, and pyroptosis caused by several i

61 ates had contrasting effects on IL-1beta and caspase-1 activation, but all clinical isolates induced

62 ing, BCAP inhibited NLRP3- and NLRC4-induced caspase-1 activation, cell death, and IL-1beta release f

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

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

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

66 ibitor, NSA, blocks inflammasome priming and caspase-1 activation, thereby preventing pyroptosis inde

67 Inflammasome assembly often results in caspase-1 activation, which is an inflammatory caspase t

68 straining the NLRP3 inflammasome and, hence, caspase-1 activation.

69 control and oviduct disease independently of caspase-1 activation.

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

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

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

73 tion, cation flux-induced cell swelling, and caspase-1 activation.

74 carboxyl-terminal fragment that is a potent caspase-1 activator.

75 t of the GSDMD N- and C-domain linker by the caspase-1 active site, an anti-parallel beta sheet at th

76 We analyzed caspase 1 activity and cytokine secretion.

77 in soluble NET components, and increases in caspase 1 activity and IL-1beta (all P values <0.001).

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

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

80 me signature with increased IL-18, IL-1beta, caspase-1 activity and ASC speck release (Scambler et al

81 nced by increased levels of IL-18, IL-1beta, caspase-1 activity and ASC-speck release in monocytes, e

82 IL-1beta precursor pro-IL-1beta, as well as caspase-1 activity and processing of pro-IL-1beta to IL-

83 version of procaspase-1 to active caspase-1, caspase-1 activity and resultant generation of mature IL

84 d in BD patients, followed by an increase in caspase-1 activity as well as IL-1beta and IL-18 levels.

85 asome-associated structures (ASC specks) and caspase-1 activity by microscopy is time consuming and l

86 VU0155069 indirectly inhibited caspase-1 activity caused by LPS + nigericin in BMDMs in

87 and cellular distribution of ASC specks and caspase-1 activity in mouse and human cells.

88 taneously detect and quantify ASC specks and caspase-1 activity, both at the population and single-ce

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

90 tion (TOFIE), cannot visualize ASC specks or caspase-1 activity, making colocalization studies of inf

91 ates IL-1beta generation by interfering with caspase-1 activity.

92 lting in alterations in IL-1beta, IL-18, and caspase-1 activity.

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

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

95 Caspase 1 analysis in sorafenib-treated MPhi revealed an

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

97 Further, mice that were deficient for both caspase-1 and -11 but that expressed caspase-11 as a tra

98 we studied the independent contributions of caspase-1 and -11 during genital Chlamydia infection.

99 We have previously shown that caspase-1 and -11 promoted the dermatitis pathology of c

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

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

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

103 e the effect of the combined absence of both caspase-1 and caspase-11 on oviduct pathology.

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

105 ukin-1beta (IL-1beta) release occurs through caspase-1 and caspase-11-mediated gasdermin D pore forma

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

107 SYK centrally mediates signaling upstream of caspase-1 and caspase-8 activation and principally up-re

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

109 eading to increased cleavage and activity of caspase-1 and downstream interleukin-1beta release(2).

110 masome complex with NEK7 and ASC to activate caspase-1 and drive the maturation of proinflammatory cy

111 n containing a CARD (ASC) speck; cleavage of caspase-1 and gasdermin D; release of IL-1beta, IL-18, c

112 Inflammasomes and their downstream mediators caspase-1 and IL-1beta are expressed by gestational tiss

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

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

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

116 cytosolic sensor of bacteria that activates caspase-1 and initiates potent immune responses.

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

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

119 Caspase-1 and its adaptor ASC contributed to the perinat

120 Here, we describe a reciprocal regulation of caspase-1 and LUBAC activities in keratinocytes.

121 d bleomycin- or silica-induced activation of caspase-1 and maturation of pro-IL-1beta to secrete clea

122 ein 3 (NLRP3) inflammasome, cathepsin B, and caspase-1 and may play a role in the pathogenesis of neu

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

124 pproved IL-1R antagonist; or parthenolide, a caspase-1 and nuclear factor kappa-light-chain-enhancer

125 We demonstrate that caspase-1 and Prdx4 form a redox-sensitive regulatory co

126 ro-IL-1beta and NLRP3 as well as cleavage of caspase-1 and pro-IL-1beta, indicating inflammasome prim

127 with ATP stimulation led to cleavage of pro-caspase-1 and pro-IL-1beta, resulting in TLR4-dependent

128 crystal structure of a complex between human caspase-1 and the full-length murine GSDMD.

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

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

131 d receptors, which mediate the activation of Caspase-1 and the subsequent release of mature interleuk

132 AT1-dependent activation of the inflammatory caspases 1 and 11.

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

134 of pyroptosis and apoptosis, where initiator caspases-1 and -8 also functioned as executioners when a

135 inflammasome pathways, canonical (involving caspase-1) and noncanonical (involving caspase-4 and -5

136 sponsiveness to MAC by increasing NLRP3, pro-caspase 1, and gasdermin D expression.

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

138 ly target the inflammasome components NLRP3, caspase-1, and caspase-8.

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

140 e inflammasome response by increasing NLRP3, caspase-1, and IL-1beta protein levels in the liver.

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

142 and gasdermin D; release of IL-1beta, IL-18, caspase-1, and lactate dehydrogenase from the cell; and

143 This is dependent on NLRP3, ASC, caspase-1, and NEK7, but not on NLRC4, NLRP1, NLRP6, AIM

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

145 pathways: the canonical pathway, signaled by caspase-1, and the noncanonical pathway, regulated by mo

146 We identified caspase-1 as a unique gene up-regulated only in pathogen

147 pharmacological inhibition of ATM, YAP1, or caspase-1 as well as antibiotic treatment, dramatically

148 atory molecules, namely TNF, IL-1beta, iNOS, caspase-1 as well as the activation and morphologic chan

149 Reciprocally, caspase-1, as well as caspase-8, regulated LUBAC activit

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

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

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

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

154 ransgenic mice constitutively expressing the caspase-1 biosensor.

155 orectal carcinoma cell line expresses little caspase-1 but instead utilizes caspase-4 to respond to S

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

157 It has been shown that caspase-1, but not its upstream activator, ASC, contribu

158 t low-temperature-induced hyperactivation of caspase-1 by NLRC4-H443P is due to loss of inhibition by

159 the mechanism involved in hyperactivation of caspase-1 by NLRC4-H443P upon exposure of cells to lower

160 lammasome-dependent shedding of IL-1beta and caspase-1-carrying platelet EVs promote lung vasoocclusi

161 activation led to generation of IL-1beta and caspase-1-carrying platelet extracellular vesicles (EVs)

162 ontaining 3 (NLRP3) inflammasome activation, caspase-1 (CASP1) cleavage, and proinflammatory interleu

163 kin (IL)1-beta, tumor necrosis factor alpha, caspase-1 (CASP1), intercellular adhesion molecule 1, IL

164 ced the conversion of procaspase-1 to active caspase-1, caspase-1 activity and resultant generation o

165 Gasdermin-D (GSDMD) is cleaved by caspase-1, caspase-4, and caspase-11 in response to cano

166 Inflammatory caspases (caspase-1, caspase-4, caspase-5 and caspase-11 (caspase-

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

168 ogen sensing mechanisms, we show MYD88/TRIF, Caspase-1/Caspase-11 inflammasome, and NOD1/NOD2 nodosom

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

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

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

172 2+) substantially augmented NLRP3 abundance, caspase-1 cleavage, and maturation of the inflammatory c

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

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

175 Caspase-1 cleaves and activates the pro-inflammatory cyt

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

177 man GBP2, and GBP5 support the activation of caspase-1-containing inflammasome complexes or caspase-4

178 orm a redox-sensitive regulatory complex via caspase-1 cysteine 397 that leads to caspase-1 sequestra

179 ssed caspase-11 as a transgene (essentially, caspase-1-deficient mice) had no significant difference

180 ent absence of caspase-11 in previously used caspase-1-deficient mice.

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

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

183 Assembly of the NLRP3 inflammasome leads to caspase 1-dependent release of the pro-inflammatory cyto

184 s priming allowed for effective induction of caspase-1-dependent cell death upon treatment with muram

185 Accordingly, caspase-1-dependent clearance of a Yersinia pseudotuberc

186 on of ASC (also known as PYCARD) specks, and caspase-1-dependent cleavage of GSDMD and caspases 3 and

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

188 from inflammasome activation and subsequent caspase-1-dependent cleavage of the trafficking adaptor

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

190 occus granulosus LL (pLL) trigger NLRP3- and caspase-1-dependent IL-1beta in lipopolysaccharide (LPS)

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

192 rogrammed cell death pathway pyroptosis in a caspase-1-dependent manner.

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

194 is released from parasite-infected cells via caspase-1-dependent mechanisms.

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

196 om factors other than abortive infection and caspase-1-dependent pyroptosis in bystander CD4 T cells.

197 sensing, inflammasome assembly, and death by caspase-1-dependent pyroptosis.

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

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

200 acterized by cold-induced hyperactivation of caspase-1, enhanced interleukin-1beta maturation, and in

201 T cells lacking caspase-1 failed to induce colitis or confer protection

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

203 homologues in humans (caspase-4/5) belong to caspase-1 family of cysteine proteases, and play a role

204 mmation and bone resorption in vivo and that Caspase-1 has a pro-resorptive role in experimental peri

205 Increased expression of IL-1beta and caspase-1 has been observed in IPF patients, indicating

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 LA-4 antibodies through mechanisms involving caspase-1/IL-1beta activation.

210 owering of prenylation isoprenoids activates caspase-1/IL-1beta inflammasome responses that impair en

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

212 of NLRP3 inflammasome and its main effector Caspase-1 in inflammation and alveolar bone resorption a

213 th the dual function of IL-37 and a role for caspase-1 in limiting inflammation.

214 tudies determined the influence of Nlrp3 and Caspase-1 in Rankl-induced osteoclast differentiation an

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

216 covered a critical role for T cell-intrinsic caspase-1, independent of inflammasome, in optimal primi

217 and interleukin-1 (IL-1) receptor-dependent, caspase-1-independent inflammatory disease.

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

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

220 ased NLRP3 inflammasome signaling (NLRP3 and caspase 1 induction and IL-1beta processing) in isolated

221 ired for protein prenylation triggered NLRP3/caspase-1 inflammasome activation and interleukin-1beta

222 increases inflammatory cytokines, activates caspase-1 inflammasome and increases Gasdermin D, an eff

223 by pyrin, which, once activated, assembles a caspase-1 inflammasome, which generates cytokines such a

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

225 In addition, caspase-1 inhibition rapidly upregulated GATA1 protein i

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

227 1a, Il1b, and Nlrp3, and pretreatment with a caspase 1 inhibitor decreased IL-1beta secretion in resp

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

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

230 Cell death was also blocked by a caspase-1 inhibitor, a key enzyme promoting pyroptosis,

231 Caspase-1 inhibitors blocked all of these responses.

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

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

234 ss whether mice lacking the pro-inflammatory caspase 1, interferon gamma-receptor, and nitric oxide s

235 ed speck-like protein (ASC) containing CARD, caspase-1, interleukin-1beta (IL-1beta), interleukin-18

236 llograft biopsies showing chronic rejection, caspase-1 is activated in C4d(+) ECs of interstitial mic

237 Typhimurium infection in vitro We show that caspase-1 is important for restricting intracellular S T

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

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

240 ive site, an anti-parallel beta sheet at the caspase-1 L2 and L2' loops bound a hydrophobic pocket wi

241 e alpha-hemolysin (HlyA) induced cleavage of caspase-1 leading to the maturation of IL-1beta, while i

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

243 PRL also reduced active cleaved-caspase-1 levels independent of pannexin-1 activity.

244 Caspase-1-mediated cell death with accompanying cytokine

245 Their activation prompts the caspase-1-mediated cleavage of the proinflammatory cytok

246 mbly of the NLRP3 inflammasome, resulting in caspase-1-mediated depletion of the heterochromatin-indu

247 pression by BALF macrophages, as well as the caspase-1-mediated generation of mature IL-1beta secrete

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

249 gens or internal distress signals, initiates caspase-1-mediated interleukin-1beta maturation and an i

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

251 ts two major effects: it activates the NLRP3-caspase-1-mediated processing and secretion of IL-1beta

252 yrin is an inflammasome sensor that promotes caspase-1-mediated pyroptotic cell death and maturation

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

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

255 rleukin-1 receptor knockout (IL-1R(-/-)) and caspase-1(-/-) mice had 350 and 30 copies/mug RNA, respe

256 pyroptosis effector protein gasdermin D, but caspase-1 mostly activates the inflammatory cytokine pre

257 Here, we show how M. tuberculosis causes caspase-1/NLRP3/gasdermin D-mediated pyroptosis of human

258 Gasdermin D (GSDMD) cleavage by caspase-1 or caspase-11 inflammasomes triggers pyroptosi

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

260 Inhibition of the inflammasome effector caspase-1 or IL-1beta pathway attenuated platelet EV gen

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

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

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

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

265 ing geranylgeranyl isoprenoids or inhibiting caspase-1 prevented statin-induced defects in insulin si

266 in mice was initiated by macrophage-derived, caspase 1-processed cytokines and required activation of

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 to enhance their assembly and subsequent pro-caspase-1 processing.

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

274 ion of PAFR restored the levels of NLPR3 and caspase-1 proteins.

275 d that BCAP specifically associated with the caspase-1 pseudosubstrate inhibitor Flightless-1 and its

276 eta, pro-IL-18, and gasdermin-D by activated caspase-1 resulted in the cellular release of the mature

277 MCC950 significantly reduced IL-1beta and/or caspase-1 secretion and attenuated leukocyte-smooth musc

278 t regulate the cleavage of cysteine protease caspase-1, secretion of inflammatory cytokines, and indu

279 lex via caspase-1 cysteine 397 that leads to caspase-1 sequestration and inactivation.

280 ld against model peptide substrates, such as caspase-1 substrate and Bradykinin-analog.

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

282 To this end, we inserted a known caspase-1 target sequence into a circularly permuted luc

283 lammasomes assemble and recruit and activate caspase-1, the cysteine protease that cleaves numerous d

284 Inflammasome assembly leads to activation of caspase 1, thereby promoting the secretion of bioactive

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

286 ammasome-activated macrophages is cleaved by caspase-1 to generate N-GSDMD fragments.

287 Neat1 also stabilizes the mature caspase-1 to promote interleukin-1beta production and py

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

289 permeability and vascular inflammation (p65, caspase 1, VCAM [vascular cell adhesion molecule-1], ICA

290 llance pathways are coupled to activation of caspase-1 via canonical inflammasome complexes.

291 We show that LUBAC interacted with caspase-1 via HOIP and modified its CARD domain with lin

292 In (LPS/ATP-stimulated) PBMCs, IL-18/TNF/caspase-1 were all significantly decreased and IL-10 was

293 me stimulates cytosolic receptors activating caspase-1 which cleaves pro-IL-18 into mature IL-18, lea

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

295 pase-recruitment domain), and active cleaved-caspase-1, which are components of the NLRP3 inflammasom

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

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

298 eveals dual-interface engagement of GSDMD by caspase-1, which may be applicable to other physiologica

299 family pyrin domain-containing 3 (NLRP3) and caspase-1 with caspase-8 in instigating cmo However, the

300 elayed the recruitment and activation of pro-caspase-1 within the NLRP3/ASC preinflammasome through i