ライフサイエンスコーパス: inflammasome

1 LR family, pyrin domain-containing 3 (NLRP3) inflammasome.

2 PK3 and caspase-8 to activate the ZBP1-NLRP3 inflammasome.

3 surveillance systems, including cGAS and the inflammasome.

4 fumigatus is a PAMP that activates the NLRP3 inflammasome.

5 of caspase-8 that involves activation of an inflammasome.

6 ainst ischemic stroke by regulating the AIM2 inflammasome.

7 aling and subsequent engagement of the NLRP3 inflammasome.

8 950, a small molecule inhibitor of the NLRP3-inflammasome.

9 ptor that multimerizes with NAIPs to form an inflammasome.

10 c pathways results in the activation of this inflammasome.

11 tion machinery, and thus activated the NLRP3 inflammasome.

12 e also been shown to regulate the ZBP1-NLRP3 inflammasome.

13 r kinase 3 (RIPK3), caspase-8, and the NLRP3 inflammasome.

14 mouse-specific activation of the NAIP-NLRC4 inflammasome.

15 iberating the C-terminal fragment to form an inflammasome.

16 ion can be exploited for sensing by a single inflammasome.

17 the mTOR pathway and regulation of the pyrin inflammasome.

18 is required for the activation of the Nlrp3 inflammasome.

19 tory factor signaling pathways and the NLRP3 inflammasome.

20 engers are also summarized in the context of inflammasomes.

21 sible biological purposes of these enigmatic inflammasomes.

22 nd the targeting of immune mediators such as inflammasomes.

23 eptor signaling and maturational cleavage by inflammasomes.

24 y caspases within signaling platforms called inflammasomes.

25 ice fed with high-fat chow; mechanistically, inflammasome-activating short interspersed nuclear eleme

26 In addition, NLRP3-inflammasome-activating stimuli trigger diverse posttran

27 mal degradation, its role in NLRP3 and pyrin inflammasome activation also provides an inherent mechan

28 ical processes including antiviral immunity, inflammasome activation and antibody class switching; an

29 Inflammasome activation and bacterial numbers were measu

30 ensive and consistent protocol for assessing inflammasome activation and cell death.

31 unctions as a physiologic inhibitor of NLRP3 inflammasome activation and explain why patients with XL

32 s review is to highlight how lipids regulate inflammasome activation and how this leads to the progre

33 2X5 is required for L. monocytogenes-induced inflammasome activation and IL-1beta production and that

34 of this activity, Trx1 is critical for NLRP3 inflammasome activation and IL-1beta production in macro

35 n autoinflammatory diseases, associated with inflammasome activation and IL-1beta secretion, remains

36 ls a novel centrosomal regulatory pathway of inflammasome activation and may provide new therapeutic

37 Noptosis and that ZBP1 plays a vital role in inflammasome activation and PANoptosis in response to fu

38 domain of ZBP1 was required to promote this inflammasome activation and PANoptosis.

39 bes mechanisms by which S. aureus EVs induce inflammasome activation and reveals an unexpected role o

40 ed and shown to be more susceptible to NLRP3 inflammasome activation and to exhibit elevated CASP1 an

41 sinergic signalling, which serves to sustain inflammasome activation and worsen fibrotic reactions.

42 K bound to NLRP3 during the priming phase of inflammasome activation and, in doing so, inhibited LPS-

43 lus fumigatus PAMPs that are responsible for inflammasome activation are not known.

44 tion of immature pro-IL-1beta; subsequently, inflammasome activation by a secondary signal allows cle

45 Noncanoncial inflammasome activation by cytosolic lipopolysaccharide

46 ur results extend our understanding of NLRP3 inflammasome activation by noncellular particulate mater

47 We propose that CaSR-mediated NLRP3 inflammasome activation contributes to inflammatory arth

48 ur findings suggest that IRF8 promotes NLRP3 inflammasome activation during infection with Gram-negat

49 ing and activation events that lead to NLRP3 inflammasome activation during Leishmania spp. infection

50 as dispensable for caspase-11-mediated NLRP3 inflammasome activation during LPS transfection; however

51 r the canonical or non-canonical pathways of inflammasome activation have a limited role on malaria p

52 ids, particularly cholesterol, in regulating inflammasome activation implying key functions for infla

53 r in non-RPE cells promotes CNV, (2) whether inflammasome activation in CNV occurs via NLRP3 or also

54 nd (3) whether complement activation induces inflammasome activation in CNV.

55 ne, improves insulin sensitivity and reduces inflammasome activation in diabetic and insulin resistan

56 link between oncogenic Kras(G12D) and NLRP3 inflammasome activation in murine and human cells.

57 his study, we found that IRF8 promotes NLRP3 inflammasome activation in murine bone marrow-derived ma

58 in a neovascular AMD mouse model that NLRP3 inflammasome activation in non-RPE cells but not in RPE

59 hanism by which PPARalpha attenuates hepatic inflammasome activation in response to metabolic stress

60 found that the NLRP1 variant M1184V reduces inflammasome activation in the context of dipeptidyl pep

61 acting protein kinase (RIPK) 3 impacts pyrin inflammasome activation independent of its role in necro

62 Inflammasome activation is a constituent of the inflamma

63 Inflammasome activation is a ubiquitous but poorly under

64 Here, we show that NLRP3 inflammasome activation is suppressed by a centrosomal p

65 sion.Measurements and Main Results: Platelet-inflammasome activation led to generation of IL-1beta an

66 Key open questions are (1) whether NLRP3 inflammasome activation mainly in retinal pigment epithe

67 t both NLRP3-dependent and NLRP3-independent inflammasome activation mechanisms induce CNV.

68 lammation reveal a protective role for NLRP1 inflammasome activation reducing eosinophilia in this se

69 ole in Gram-negative bacteria-mediated NLRP3 inflammasome activation remains unknown.

70 agellin to act as a "safety net" to maintain inflammasome activation under conditions of suboptimal N

71 Our workflow assesses inflammasome activation via the formation of the apoptos

72 sults in increased lysosomal activity, NLRP3 inflammasome activation, and IL-1beta release.

73 NLR family pyrin domain containing 3 (NLRP3) inflammasome activation, caspase-1 (CASP1) cleavage, and

74 In response to caspase-8 inflammasome activation, GSDMD, chaperoned by Cdc37/Hsp9

75 ficient to promote Mefv expression and pyrin inflammasome activation, highlighting the cross-talk bet

76 ming of TAK1-deficient macrophages triggered inflammasome activation, including the activation of cas

77 nt understanding of innate immune responses, inflammasome activation, inflammatory cell death pathway

78 Further, downstream of inflammasome activation, polymorphisms that cause loss o

79 l agents that target a critical component of inflammasome activation, signaling leading to cellular p

80 or family, pyrin domain containing 3 (NLRP3) inflammasome activation, since the genetic ablation and

81 ve been shown to intersect with and modulate inflammasome activation, thereby affecting host defense.

82 e-1 activation and cell death in response to inflammasome activation, unlike what is observed in macr

83 production by tumor cells through TLR4-NLRP3 inflammasome activation.

84 erovar Typhimurium (S. Typhimurium) leads to inflammasome activation.

85 HIV-1 and hepatitis B infections, also block inflammasome activation.

86 onicity-induced, but not DAMP-induced, NLRP3 inflammasome activation.

87 fluenza A virus-induced PANoptosis and NLRP3 inflammasome activation.

88 action with NLRP3 and causes increased NLRP3 inflammasome activation.

89 inflammasome during the activation phase of inflammasome activation.

90 bolism has numerous but complex functions in inflammasome activation.

91 ionally, loss of GSDMD promoted robust NLRP3 inflammasome activation.

92 m stress, cholesterol crystal formation, and inflammasome activation.

93 min D cleavage, which are required for NLRP3 inflammasome activation.

94 fect pyrin dephosphorylation associated with inflammasome activation.

95 RP3 interaction, which is required for NLRP3 inflammasome activation.

96 ll as NF-kappaB (nuclear factor kappa B) and inflammasome activation.

97 rting direct effects on sodium transport and inflammasome activation.

98 Deep-targeted sequencing and NLRP3-inflammasome-activation assays were used to identify the

99 xygen species (ROS) production causing NLRP3 inflammasome-activation.

100 Identification of endogenous inflammasome activators is essential for the development

101 NLRP3 inflammasome activity must be tightly controlled, as its

102 ing IL-1Rsignaling pathways with Anakinra or inflammasome activity with parthenolide provides a promi

103 globulinemia (XLA) exhibited increased NLRP3 inflammasome activity; this was also the case for BMDMs

104 K, JNK)-mediated priming signal of the NLRP3 inflammasome and by regulating the autophagy/NLRP3 infla

105 cally establish the activation status of the inflammasome and cell death pathways.

106 r particles triggers activation of the NLRP3 inflammasome and consequent secretion of interleukin 1be

107 vivo (in mice) strategies for activating the inflammasome and explain how to subsequently assess mult

108 linical isolates differentially activate the inflammasome and how inflammasome inhibition can lead to

109 y, pyrin domain-containing protein 3 (NLRP3) inflammasome and inflammasome-associated cytokines IL-1b

110 se hepatitis virus (MHV) activated the NLRP3 inflammasome and inflammatory cell death in the form of

111 id metabolism (P < .001) and in TAC2 for the inflammasome and interferon signalling pathways (P < .00

112 This study investigates the role of NLRP3 inflammasome and its main effector Caspase-1 in inflamma

113 nally, P2X4 agonist ivermectin induced NLRP3 inflammasome and pro-inflammatory cytokines in cultured

114 Bacillus cereus is an activator of the NLRP3 inflammasome and pyroptosis.

115 by activation of a fibroblast-specific NLRP3 inflammasome and subsequent IL-1beta production.

116 underlying the activation of the ZBP1-NLRP3 inflammasome and the formation of the PANoptosome.

117 e is overwhelming evidence linking the NLRP3 inflammasome and the IL-1 cytokines with the pathogenesi

118 ew insights into the regulation of the NLRP3 inflammasome and the pathophysiological role of triglyce

119 controls, highlighting the important role of inflammasome and these molecules in controlling ricketts

120 suggest that combination therapies targeting inflammasomes and complement may offer synergistic benef

121 nt research findings indicate a key role for inflammasomes and derailed proteostasis as root causes o

122 The interactions of R. parkeri with inflammasomes and interferons are similar to those of vi

123 Moreover, potential interactions between the inflammasomes and proteostasis pathways are discussed an

124 ing methylation of NLRC5, a regulator of the inflammasome, and associated pQTMs implicating key prote

125 ms, we show MYD88/TRIF, Caspase-1/Caspase-11 inflammasome, and NOD1/NOD2 nodosome signaling to be ind

126 ecture and structural basis of potential pre-inflammasome, and suggests a novel molecular assembly pa

127 pyroptotic cell death via the non-canonical inflammasome, and that lipopolysaccharide transfection i

128 did not elicit protective activation of the inflammasome, and this strain exhibited enhanced virulen

129 priming and activation signals of the NLRP3 inflammasome; and 3) suppress the phosphorylation of JNK

130 progress in understanding how the different inflammasomes are activated, how infection is sensed by

131 Although inflammasomes are generally thought to promote Shigella

132 Inflammasomes are highly sophisticated and effective orc

133 Inflammasomes are important for host defence against pat

134 Inflammasomes are important sentinels of innate immune d

135 Inflammasomes are intracellular signaling complexes that

136 Inflammasomes are multimeric heterogeneous mega-Dalton p

137 Inflammasomes are multiprotein complexes facilitating ca

138 Inflammasomes are multiprotein complexes of the innate i

139 Inflammasomes are multiprotein complexes of the innate i

140 Inflammasomes are supramolecular complexes that play key

141 Our findings identify the inflammasome as a crucial player in establishing a prope

142 This scientific commentary refers to 'NLRP3 inflammasome as prognostic factor and therapeutic target

143 Prior studies identified the canonical inflammasome as the major pathway leading to interleukin

144 Inflammasome assembly drives the maturation and secretio

145 the expression of pro-IL-1beta and enhances inflammasome assembly in vivo and in vitro.

146 Inflammasome assembly often results in caspase-1 activat

147 aining protein 3 (NLRP3)- and pyrin-mediated inflammasome assembly, caspase activation, and IL-1beta

148 ve been found to be important for ZBP1-NLRP3 inflammasome assembly, including molecules involved in t

149 ive regulation mechanisms to avoid premature inflammasome assembly.

150 ontaining protein 3 (NLRP3) inflammasome and inflammasome-associated cytokines IL-1beta and IL-18 in

151 on cell death, and decreased NOX2- and NLRP3 inflammasome-associated neuroinflammation.

152 n implicated in maintenance of the autophagy-inflammasome axis in innate murine immune cells.

153 masome and by regulating the autophagy/NLRP3 inflammasome axis.

154 microtubule transport and assembly of these inflammasomes both in vitro and in mice.

155 Viruses activate inflammasomes but then subvert resulting inflammatory re

156 oded pattern recognition receptors that form inflammasomes, but their activation mechanisms and biolo

157 been shown to activate a novel, noncanonical inflammasome by directly binding in the cytosol to human

158 t mechanism for the down-regulation of these inflammasomes by autophagy.

159 w Leishmania amazonensis inhibits macrophage inflammasomes by modifying histone H3 activation marks o

160 By inducing pyroptosis, inflammasomes can also drive the release of the alarmin

161 anisms related to a PKG/VASP/NF-kappaB/NLRP3 inflammasome circuit.

162 ably assess the successful activation of the inflammasome complex and cell death.

163 hat deubiquitination inhibited the NLRP6-ASC inflammasome complex and regulated the maturation of IL-

164 Assembly of the inflammasome complex following infection or injury begin

165 The innate immune sensor NLRP3 assembles an inflammasome complex with NEK7 and ASC to activate caspa

166 n via activation of the multimolecular NLRP3-inflammasome complex.

167 nate immune sensor that can form cytoplasmic inflammasome complexes.

168 ated uric acid; and increased NLRP3, a major inflammasome component.

169 in enhancing the expression and assembly of inflammasome components and suggest that while blocking

170 Deleting NLRP3 inflammasome components or the downstream cell death exe

171 Loss of inflammasome components, including il1b, reduced CD41(+)

172 , monoamines, monosaturated fatty acids, and inflammasome components.

173 Fitzgerald discuss the basic concepts about inflammasome composition, assembly and activation, effec

174 Furthermore, we show that the AIM2 inflammasome contributes to central nervous system (CNS)

175 Here we show that the AIM2 inflammasome contributes to normal brain development and

176 matory diseases, autoimmunity, and cancer in inflammasome-dependent and inflammasome-independent mann

177 s LTB(4) can be used as an adjuvant to boost inflammasome-dependent host defense.

178 rapeutic potential of targeting the platelet-inflammasome-dependent innate immune pathway to prevent

179 itis induced by dextran sulfate sodium in an inflammasome-dependent manner.

180 ults are the first to identify that platelet-inflammasome-dependent shedding of IL-1beta and caspase-

181 tive study, these results suggest that Nlrp3 inflammasome does not play a significant role in inflamm

182 NLRP3-inflammasome-driven inflammation is involved in the path

183 protective vs pathogenic roles of the NLRP3 inflammasome during Leishmania spp. infection.

184 and nigericin-induced assembly of the NLRP3 inflammasome during the activation phase of inflammasome

185 d critical roles for cytoplasmic sensors and inflammasomes during Leishmania spp. infection and patho

186 Inhibition of the inflammasome effector caspase-1 or IL-1beta pathway atte

187 NF-kappaB-dependent transcription, assemble inflammasomes, enabling processing, and facilitate secre

188 Activation of noncanonical inflammasome exerts two major effects: it activates the

189 We now show that RBP4 primes the NLRP3 inflammasome for interleukin-1beta (IL1beta) release, in

190 or family, pyrin domain containing 3 (NLRP3) inflammasome for mediating the long-term consequences of

191 ings uncover an unexpected role of non-NLRP3 inflammasomes for CNV and suggest that combination thera

192 ins with the oligomerization of the upstream inflammasome-forming sensor and proceeds through a multi

193 oronavirus infection and that impaired NLRP3 inflammasome function or pyroptosis can lead to negative

194 e a requirement for phosphorylation in NLRC4 inflammasome function.

195 and tuberculosis (TB), but the relevance of inflammasome gene polymorphisms in TB-associated pulmona

196 We identified polymorphisms in inflammasome genes interferon gamma inducible protein 16

197 cholesterol metabolism in the activation of inflammasomes have been comprehensively discussed.

198 Inflammasomes have been implicated in the detection and

199 , and that genetic inactivation of the NLRP3 inflammasome improves behavioral tests and synaptic plas

200 were applied to investigate the role of this inflammasome in asthma at the molecular level.

201 nslocate to the gut, where they activate the inflammasome in colonic mononuclear phagocytes, triggeri

202 ere we explore attempts to inhibit the NLRP3 inflammasome in light of clinical and preclinical data a

203 rough mechanisms involving activation of the inflammasome in macrophages.

204 owed that Rickettsia australis activates ASC inflammasome in macrophages.

205 Ca(2+)](ex)) trigger activation of the NLRP3 inflammasome in monocytes through calcium-sensing recept

206 ke receptor family pyrin domain-containing 3 inflammasome in naive neutrophils and promote interleuki

207 ase of HDAC3 and absent in melanoma 2 (AIM2) inflammasome in primary cultured microglia.

208 e, we report an unexpected role of the NLRC4 inflammasome in promoting expression of its microbial li

209 During infection, activation of the AIM2 inflammasome in response to double-stranded DNA damage t

210 ers of the nod-like receptor family assemble inflammasome in response to specific ligands.

211 masome activation implying key functions for inflammasomes in diseases with defective lipid metabolis

212 ty, and cancer in inflammasome-dependent and inflammasome-independent manners.

213 Here, we describe an inflammasome-independent pathway of IL-1beta production

214 erentially activate the inflammasome and how inflammasome inhibition can lead to enhanced bacterial c

215 ot currently approved, as well as oral NLRP3 inflammasome inhibitors currently in clinical developmen

216 k the IL-1 isoforms, and possibly oral NLRP3 inflammasome inhibitors, across a wide spectrum of cardi

217 dy sheds light on the mystery of LPS-induced inflammasome initiation, reveals the architecture and st

218 ke receptor family pyrin domain-containing 3 inflammasome, interleukin-1beta) in neutrophils suppress

219 or family, pyrin domain containing 3 (NLRP3) inflammasome into a mature and active form.

220 T, LRR, and PYD domains-containing protein 3 inflammasome is a critical component of the innate immun

221 The NAIP/NLRC4 inflammasome is a cytosolic sensor of bacteria that acti

222 The NLRP3 inflammasome is a multi-molecular protein complex that c

223 se pathogenesis and that the NLRP3-dependent inflammasome is a potential therapeutic target for the c

224 The NAIP/NLRC4 inflammasome is activated by multiple bacterial protein

225 Innate immune signaling through the NLRP3 inflammasome is activated by multiple diabetes-related s

226 Modulating the inflammasome is an attractive adjunct to current anti-my

227 related stressors, but whether targeting the inflammasome is beneficial for diabetes is still unclear

228 The NLRP3 inflammasome is frequently associated with the damaging

229 The inflammasome is integral to innate immune responses but

230 At the same time, the NLRP3 inflammasome is part of a larger pro-inflammatory pathwa

231 ults suggest that targeting ENT1/2 and NLRP3 inflammasome may be novel strategies for prevention and

232 A common SNP in the NLRC4 inflammasome may modify TB-associated inflammation in cl

233 Inflammasomes mediate inflammation in adults living with

234 a promising therapeutic strategy to prevent inflammasome-mediated diseases, exogenous LTB(4) can be

235 keri is sensitive to IFN-I and benefits from inflammasome-mediated host cell death that antagonizes I

236 e zebrafish model, we demonstrate that NLRP3 inflammasome-mediated interleukin-1-beta (IL1beta) signa

237 ens, flagellin is a major activator of NLRC4 inflammasome-mediated macrophage pyroptosis and pathogen

238 These results indicate that inflammasome-mediated RILP cleavage, and sequence-specif

239 Inhibiting the NLRP3 inflammasome mediates inflammation in an extensive numbe

240 The inflammasome modulates the release of key proinflammator

241 the expression of proteins that regulate the inflammasome, namely pyrin domain-only proteins (POPs),

242 leukin) IL1B (interleukin 1B), IL6, IL8, the inflammasome NLRP3, and the macrophage inflammatory prot

243 The inflammasome NLRP6 plays a crucial role in regulating in

244 , LRR, and PYD domains-containing protein 3) inflammasome on AF pathogenesis and cardiomyocyte remode

245 Ten functional SNPs in 5 inflammasome pathway genes were related to circulating i

246 avirus 2, we highlight the importance of the inflammasome pathway.

247 beta (IL-1beta) independent of the canonical inflammasome pathway.

248 tamidine, AmB induced gene expression of the inflammasome pathway.

249 Our results showed that TLR4 and inflammasome pathways are enhanced in low-quality kidney

250 The IL-1 and NLRP3 inflammasome pathways are markedly less responsive to SA

251 regulate the specificity and sensitivity of inflammasome pathways provides a fine-tuning balance bet

252 There are two primary inflammasome pathways, canonical (involving caspase-1) a

253 The NLRP3 inflammasome plays a major role in inflammation, particu

254 Finally, inhibition of inflammasome prevented P. aeruginosa-induced acute lung

255 ge of caspase-1 and pro-IL-1beta, indicating inflammasome priming and activation.

256 roinflammatory effects of RBP4 require NLRP3-inflammasome priming.

257 Finally, we find that complement and inflammasomes promote CNV through independent mechanisms

258 Induction of the inflammasome protein cryopyrin (NLRP3) in visceral adipo

259 ied novel associations in genes encoding the inflammasome protein NLRP1 and the ER protein Sarcalumen

260 hosphorylation, it was proposed that another inflammasome protein, NLRP3, can induce NLRC4 activation

261 role that DPP9's protein structure plays in inflammasome regulation, and the emerging link between N

262 pathways related to sterile inflammation and inflammasome regulation.

263 ntal disease may result in downregulation of inflammasome regulators that may increase the activity o

264 Whether LTB(4) directly activates the inflammasome remains to be determined.

265 Inflammasomes respond to pathogen or tissue "danger" sig

266 Antagonism of PAFR amplified the inflammasome response by increasing NLRP3, caspase-1, an

267 r knockdown cells were compromised for Nlrp3 inflammasome responses.

268 s (MEKs/MKKs) and some variants of the NLRP1 inflammasome sensor, targeting of these pathways does no

269 experiments reveal that EBV exploits several inflammasome sensors to actually activate its replicativ

270 Mechanistically, induction of kidney NLRP3 inflammasome signaling after renal IR was significantly

271 in domain-containing protein 3 (PD-L1/NLRP3) inflammasome signaling cascade that ultimately led to th

272 the innate immune response-particularly the inflammasome signaling pathway.

273 Recent studies have determined that inflammasome signaling plays an important role in drivin

274 transformed our mechanistic understanding of inflammasome signaling, cell death decisions, and cytoki

275 exacerbates ischemic AKI and promotes NLRP3 inflammasome signaling.

276 Here, we provide an updated view of inflammasome signaling; mechanisms underpinning IL-1alph

277 mised CNS cells, we find that defective AIM2 inflammasome signalling results in decreased neural cell

278 m patients with CF exhibit an enhanced NLRP3-inflammasome signature with increased IL-18, IL-1beta, c

279 ctivation of P2X7 receptors leading to NLRP3 inflammasome stimulation as a key mediator of neuroinvas

280 induction of active IL1beta or pharmacologic inflammasome stimulation increased HSPC number as assess

281 iPSC-derived hemogenic precursors, transient inflammasome stimulation increased multilineage hematopo

282 ave demonstrated that activation of the AIM2 inflammasome substantially contributes to the pathophysi

283 , LRR, and PYD domains-containing protein-3)-inflammasome system in atrial whole-tissue homogenates a

284 ellin, but not PrgI, now activated the NLRP3 inflammasome through a reactive oxygen species- and/or c

285 r to those of viruses, which can exploit the inflammasome to avoid IFN-I(12), are restricted by IFN-I

286 tor family pyrin domain containing 3 (NLRP3) inflammasome to trigger the maturation and release of th

287 rr virus (EBV), an oncoherpesvirus, exploits inflammasomes to activate its replicative or lytic phase

288 abetes, which frequently activates the NLRP3 inflammasome, to deregulation of a tumor virus, and 4) d

289 t of pharmacological inhibition of the NLRP3 inflammasome using dapansutrile (OLT1177), an oral NLRP3

290 receptor pyrin domain-containing protein 3) inflammasome via a Rab5-ZFYVE21-NIK axis and upregulates

291 is, suggesting that rickettsiae activate ASC inflammasome via a Toll-like receptor 4 (TLR4)-dependent

292 The ability of RGFP966 to inhibit the AIM2 inflammasome was confirmed in an experimental mouse mode

293 In addition, in C6(-/-) mice, the NLRP3 inflammasome was defective both in PMNs and in macrophag

294 Activation of Nlrc4 or Aim2 inflammasomes were intact in cells lacking Mm47.

295 h and the mTOR pathway to regulate the pyrin inflammasome, which can be harnessed for therapeutic int

296 ssembles a macromolecular complex called the inflammasome, which unleashes the proteolytic activity o

297 elial cells assembles large complexes called inflammasomes, which activate inflammatory caspases to p

298 Inflammasomes, which are canonically formed upstream of

299 Improved understanding of the ZBP1-NLRP3 inflammasome will direct the development of therapeutic

300 sing clodronate liposomes and inhibiting the inflammasome with a specific inhibitor of NOD-, LRR-, an