ライフサイエンスコーパス: caspase 11

1 PS binding to inflammatory caspases, such as caspase 11.

2 However, humans do not encode caspase-11.

3 in the cytosol to human caspase-4 and mouse caspase-11.

4 olates was independent of both caspase-1 and caspase-11.

5 spase-4, a potential human homolog of murine caspase-11.

6 cellular inflammasome complex that activates caspase-11.

7 re we demonstrate that this pathway requires caspase-11.

8 eover, LPS-mutant E. coli failed to activate caspase-11.

9 n NLRC4 and ASC, but not NLRP3, caspase-1 or caspase-11.

10 ence of an interferon-inducible activator of caspase-11.

11 s review, we summarize effector functions of caspase-11.

12 gaging TRIF, Gram-negative bacteria activate caspase-11.

13 plying that there is a distinct activator of caspase-11.

14 NLRP3 inflammasome activation that requires caspase-11.

15 re necessary for activation of LPS-bound pro-caspase-11.

16 pithelium when mice lack both NAIP-NLRC4 and Caspase-11.

17 a caspase recruitment domain, caspase-1 and caspase-11.

18 e-1, human caspase-4 and caspase-5, or mouse caspase-11.

19 m mobilization, and potassium efflux but not caspase-11.

20 ) on the C57BL/6 J background that expressed caspase-11.

21 making them deficient in both caspase-1 and caspase-11.

22 site, influences gasdermin D recognition by caspase-11.

23 ype I interferons were insufficient to prime caspase-11.

24 TRIF regulated expression of caspase-11, a caspase-1-related protease that is critica

25 of LPS in macrophages and the activation of caspase-11, a cytosolic LPS receptor that mediates letha

26 We found that caspase-11, a cytosolic LPS receptor, activated the coag

27 Caspase-11, a member of the murine caspase family, has b

28 al inflammasome was described that activates caspase-11, a pro-inflammatory caspase required for lipo

29 lammasome pathway that ultimately results in caspase-11 activation and cell death.

30 Galectin-3 also promotes caspase-11 activation and gasdermin D cleavage in macrop

31 ficient in IRF8 showed substantially reduced caspase-11 activation and gasdermin D cleavage, which ar

32 ed a pro-caspase-11-NLRP3 interaction before caspase-11 activation and inflammasome assembly.

33 polysaccharide (LPS) in the cytosol triggers caspase-11 activation and is central to host defense aga

34 chia coli has recently been shown to trigger caspase-11 activation and pyroptosis, but the cytoplasmi

35 g fraction of immortalized macrophages after caspase-11 activation by lipopolysaccharide.

36 e or absence of RIP3 inhibited caspase-1 and caspase-11 activation by Nlrp3 stimuli but not the Nlrc4

37 During endotoxemia, however, excessive caspase-11 activation causes shock.

38 Here we show that non-canonical caspase-11 activation contributes to macrophage death du

39 Therefore, caspase-11 activation contributes to pathogen control an

40 he cytosolic entry of LPS and, consequently, caspase-11 activation during Gram-negative bacterial inf

41 nt interferon-beta production is crucial for caspase-11 activation in macrophages, but is only partia

42 sion of IcaA in L. pneumophila inhibited the caspase-11 activation in macrophages.

43 saccharide (LPS) is the signal that triggers caspase-11 activation in mice.

44 ng a divergent lipid A structure antagonized caspase-11 activation in response to E. coli LPS or Gram

45 ulated the host components required for this caspase-11 activation pathway.

46 Activation by Legionella differed from caspase-11 activation using previously described agonist

47 iously described agonists in that Legionella caspase-11 activation was rapid and required bacteria wi

48 microbial infection and trigger caspase-1 or caspase-11 activation, culminating in cytokine secretion

49 ssion, and cytosolic LPS directly stimulates caspase-11 activation, promoting the release of proinfla

50 Recognition of LPS mediates caspase-11 activation, which promotes a myriad of downst

51 ophagosomes, which results in a reduction of caspase-11 activation.

52 xpresses OspC3, an effector that antagonizes Caspase-11 activity.

53 ion, however, in vitro studies indicate that caspase-11 acts upstream of NLRP3 and caspase-1.

54 on confirmed that galectin-3 associates with caspase-11 after intracellular delivery of LPSs.

55 expression of IL1-beta, TNF-alpha, HSP70 and Caspase 11 all increased over control levels found in un

56 Caspase-11 also detects eukaryotic (i.e., self) lipids.

57 with C57BL/6 Casp11 gene-targeted mice, that caspase-11 (also known as caspase-4) is critical for cas

58 depletion of caspase-4, a human ortholog of caspase-11, also led to increased bacterial colonization

59 daptive immune responses and are elicited by caspase-11, an enzyme that binds oxPAPC and bacterial li

60 binding protein 2, and reducing cleavage of caspase 11 and gasdermin-D.

61 /- and p53+/- mice showed virtual absence of caspase 11 and marked attenuation of caspases 1 and 12,

62 identify gasdermin D as a critical target of caspase-11 and a key mediator of the host response again

63 cytosolic lipopolysaccharide (LPS) receptor caspase-11 and antagonizes IFN-I production mediated by

64 We examined innate immunity, caspase-11 and associated inflammatory pathways in twitc

65 tly, the published Casp1(-/-) mice lack both caspase-11 and caspase-1.

66 eling proteins, interacts and regulates both caspase-11 and caspase-1.

67 In this study, we investigated a role for caspase-11 and caspase-12 in obesity and insulin resista

68 gand binding proteins such as the NAIPs, and caspase-11 and caspase-8 in addition to caspase-1.

69 PS significantly increased the expression of caspase-11 and cleavage of the GSDMD, as evidenced by in

70 ivation indicated by decreased activation of caspase-11 and decreased IL-1beta, compared with other g

71 and proinflammatory cytokine production via caspase-11 and gasdermin D (GSDMD).

72 Caspase-11 and GBPs epistatically protect mice against l

73 Caspase-11 and GSDMD mediate the release of interleukin-

74 interferon (IFN-I)-mediated upregulation of caspase-11 and guanylate-binding proteins (GBP) increase

75 to the molecular basis of LPS recognition by caspase-11 and highlight the fundamental and likely inse

76 the noncanonical pathway, regulated by mouse caspase-11 and human caspase-4/5.

77 nduced sepsis in StB KO mice is dependent on caspase-11 and mitochondrial reactive oxygen species but

78 ributed to the activation of the LPS-sensing caspase-11 and NLRP3 inflammasome by Gram-negative bacte

79 1-activated IL-18 induces IFN-gamma to prime caspase-11 and rapidly clear B. thailandensis infection.

80 ts included, besides Nalp1b, proinflammatory caspase-11 and the caspase-1 substrate alpha-enolase.

81 annexin-1 required the catalytic activity of caspase-11 and was essential for ATP release and P2X7-me

82 ntiation factor 2 complex (TLR4/MD-2), mouse caspase-11, and human caspases 4 and 5.

83 ammasome components, activates caspase-1 and caspase-11, and induces host-cell death and secretion of

84 apping and unique functions of caspase-1 and caspase-11 are difficult to unravel without additional g

85 Therefore, the physiological functions of caspase-11 are much broader than its previously establis

86 Caspase-1 and caspase-11 are proinflammatory caspases that regulate cy

87 The enzymatic activities of caspase-1 and caspase-11 are required for growth inhibition in differe

88 procaspase involved in inflammation (murine caspase-11) are also activated by oligomerization.

89 Inflammatory caspases, including caspase-11, are upregulated in CD8(+) T cells after Ag-s

90 or both caspase-1 and -11 but that expressed caspase-11 as a transgene (essentially, caspase-1-defici

91 in 1) inflammasome] consisting of caspase-1, caspase-11, ASC (apoptosis-associated speck-like protein

92 LPS binding to pro-caspase-11 augmented bacterial mRNA-dependent assembly o

93 spase-1 provides priming signals upstream of caspase-11 but not caspase-4 during murine defense again

94 ed, the activation of the cytosolic receptor caspase-11 by LPS is now known to lead to inflammasome a

95 Second, either caspase-1 or caspase-11 can trigger a form of lytic, programmed cell

96 expression of pro-inflammatory non-canonical caspase-11, canonical caspase-1, gasdermin D and cognate

97 l, and cell-based assays, we report that the caspase-11 CARD functions as a bipartite lipid-binding m

98 Caspase-11 (Cas11) is a cysteine protease involved in pr

99 ackgrounds including Il1b/Il18-, caspase-1-, caspase-11- (Casp1/11-), and Tnf-deficient strains.

100 man caspase-4 (CASP4) and its mouse homolog, caspase-11 (CASP11), are up-regulated in SARS-CoV-2 infe

101 ng of bacterial LPS to its cytosolic sensor, caspase-11 (Casp11), promotes Casp11 aggregation within

102 Furthermore, DCs from caspase-11 (casp11)-deficient 129S6 mice failed to secre

103 The caspase-11 (CASP11)-nucleotide-binding oligomerization d

104 d activation of human caspase-4/CASP4 (mouse caspase-11/CASP11), and this process contributes to NLRP

105 aspases (caspase-1, caspase-4, caspase-5 and caspase-11 (caspase-1/-4/-5/-11)) mediate host defense a

106 cognition and activation of pathways such as caspase-11 (caspase-4/5 in humans).

107 Direct activation of caspase-11, caspase-4 and caspase-5 by intracellular LPS

108 , which is activated by cleavage mediated by caspase-11, caspase-4 or caspase-5.

109 th during HS that is dependent on caspase-1, caspase-11, caspase-8, and RIPK3 through the PANoptosis

110 d Burkholderia thailandensis activates mouse caspase-11, causing pyroptotic cell death, interleukin-1

111 3-C3aR pathway in proinflammatory signaling, caspase-11 cell death, and sepsis severity.

112 By reconstituting caspase-1/caspase-11(-/-) cells with a noncleavable or catalytical

113 nsgenic for caspase-4, the human ortholog of caspase-11, cleared B. thailandensis in vivo, they did n

114 Purified active recombinant caspase-11 cleaves and activates procaspase-3 very effic

115 Mechanistically, caspase-11 cleaves gasdermin D, and the resulting amino-

116 further elucidating the mechanisms by which caspase-11 contributes to host defense.

117 Caspase-11 controls a noncanonical inflammasome that res

118 n caspase-4 and caspase-5, homologs of mouse caspase-11, cooperated to restrict L. pneumophila infect

119 Importantly, Caspase-11 deficiency does not decrease the graft-versus

120 Our results show that caspase-11 deficiency was sufficient to recapitulate the

121 We report that caspase-11-deficient (Casp11(-/-)) T cells proliferated

122 To determine the mechanism by which caspase-11-deficient mice developed reduced pathology, t

123 dition to its defect in cytokine maturation, caspase-11-deficient mice have a reduced number of apopt

124 Caspase-11-deficient mice showed reduced dilation in bot

125 colonization in the intestinal epithelium of caspase-11-deficient mice, but not at systemic sites.

126 icantly fewer neutrophils in the oviducts of caspase-11-deficient mice, supporting the observed decre

127 In the caspase-11-deficient mice, we observed increased chlamyd

128 On the other hand, caspase-11 delineates a non-canonical inflammasome that

129 Microbiota depletion led to NLRP6- and caspase 11-dependent loss of CART(+) neurons and impaire

130 Specifically, caspase-11-dependent cell death contributes to pathology

131 These results indicate that caspase-11-dependent cell death is detrimental to the ho

132 ide screen, we identified novel mediators of caspase-11-dependent cell death.

133 or caspase-11 gene expression and subsequent caspase-11-dependent cell death.

134 found that cytosolic LPS stimulation induced caspase-11-dependent cleavage of the pannexin-1 channel

135 hat delivers LPS into the cytosol triggering caspase-11-dependent effector responses in vitro and in

136 Here, we show that heparin prevented caspase-11-dependent immune responses and lethality in s

137 Intracellular LPS can then trigger caspase-11-dependent inflammasome activation in the cyto

138 Both lipids induce caspase-11-dependent interleukin-1 release, but only LPS

139 of the colonic mucus in an NLRP6-, ASC-, and caspase-11-dependent manner, consistent with the activat

140 b transcription, which in turn triggered the caspase-11-dependent NLRP3 inflammasome activation in th

141 Here, we briefly review the burgeoning caspase-11-dependent non-canonical inflammasome field, f

142 induce GBP-dependent pyroptosis through both caspase-11-dependent noncanonical and caspase-1-dependen

143 re we show that gasdermin D is essential for caspase-11-dependent pyroptosis and interleukin-1beta ma

144 We found that the induction of caspase-11-dependent pyroptosis by cytoplasmic L. pneumo

145 I IFN receptor, there was a severe defect in caspase-11-dependent pyroptosis in these cells.

146 Caspase-11-dependent pyroptosis is triggered in IFN-acti

147 racellular lipopolysaccharide (LPS) leads to caspase-11-dependent pyroptosis, which is critical for i

148 Induction of caspase-11-dependent responses occurred in macrophages d

149 ate binding protein (Gbp) proteins stimulate caspase-11-dependent, cell-autonomous immunity in respon

150 Caspase-11 detection of intracellular lipopolysaccharide

151 We further demonstrated that caspase-1 and caspase-11 differentially contributed to the host defens

152 , LPS of L. interrogans efficiently prevents caspase 11 dimerization and subsequent massive gasdermin

153 as independent of inflammatory caspase-1 and caspase-11, dominated cytosolic secretion of IL-33 by fo

154 Caspase-11 enhanced the activation of tissue factor (TF)

155 How caspase-11 executes these downstream signalling events i

156 In vivo, we observed increased caspase-11 expression and a significant decrease in the

157 n, and was mediated through the induction of caspase-11 expression and activation of caspase-3.

158 We observed elevated caspase-11 expression and caspase-1 processing in BCG-tr

159 , these data suggest that IFN-gamma-mediated caspase-11 expression has a key role maintaining intesti

160 We find the Cpb1-C3-C3aR pathway induces caspase-11 expression through amplification of MAPK acti

161 polycytidylic acid [poly(I:C)] to induce pro-caspase-11 expression were as susceptible as wild-type m

162 rough TLR4 and interferon receptors, induces caspase-11 expression, and cytosolic LPS directly stimul

163 ages, but is only partially required for pro-caspase-11 expression, consistent with the existence of

164 -11(-/-) ) or sufficient (129 x C57BL/6) for caspase-11 expression, we found that caspase-11 was disp

165 mutation in the Casp11 locus that attenuated caspase-11 expression.

166 imally affected by the absence of caspase-1, caspase-11, Fas ligand, and TNF.

167 l role for pannexin-1 and P2X7 downstream of caspase-11 for pyroptosis and susceptibility to sepsis i

168 -)Casp11(129mt/129mt) macrophages expressing caspase-11 from a C57BL/6 bacterial artificial chromosom

169 ere, we review the emerging understanding of caspase-11 functions and the mechanisms of activation an

170 We further showed that increased caspase-11 gene expression and better pro-inflammatory c

171 rboxypeptidase B1 (Cpb1), to be required for caspase-11 gene expression and subsequent caspase-11-dep

172 nic mice were not altered by the ablation of caspase-11 gene.

173 strate that during sepsis, activation of the caspase-11/GSDMD pathway controls NET release by neutrop

174 and FOXF2, BMP-2, p75 neurotrophin receptor, caspase-11, guanylate-binding proteins 1 and 2, ApoJ/clu

175 ion, and insulin resistance, whereas loss of caspase-11 had no effect.

176 ding capability is conserved across numerous caspase-11 homologs and orthologs.

177 Most Gram-negative bacteria that activate caspase-11, however, are not cytosolic, and the mechanis

178 rate specificities of the human orthologs of caspase-11, i.e. caspase-4 and caspase-5, are ruled by t

179 Recent studies indicate that caspase-8, caspase-11, IL-1R-associated kinases (IRAK), and recepto

180 We discuss the importance of caspase-1 and caspase-11 in host defense, and we examine the downstrea

181 ll recruitment, suggesting a contribution of caspase-11 in infection control.

182 flammatory caspases and revealed the role of caspase-11 in mediating septic shock in response to leth

183 Caspase-11 in mice and its homologues in humans (caspase

184 flammasome pathway that activates caspase-4 (caspase-11 in mice) and caspase-1, and requires cyclic G

185 al (involving caspase-4 and -5 in humans and caspase-11 in mice).

186 4, and caspase-5 in human, and caspase-1 and caspase-11 in mouse.

187 chotomy is due to the inadvertent absence of caspase-11 in previously used caspase-1-deficient mice.

188 ) and Case et al. (2013) identify a role for caspase-11 in rapid responses to bacterial pathogens tha

189 DMD) is cleaved by caspase-1, caspase-4, and caspase-11 in response to canonical and noncanonical inf

190 A related set of caspases, caspase-11 in rodents and caspase-4 and caspase-5 in hum

191 light on the lesser-studied proinflammatory caspase-11 in the combat between host and pathogens.

192 hich LPS from these bacteria gains access to caspase-11 in the cytosol remains elusive.

193 assessed the participation of caspase-1 and caspase-11 in the functions of the NLRC4 inflammasome an

194 highlight a unique pro-inflammatory role for caspase-11 in the innate immune response to clinically s

195 pregulation of the lipopolysaccharide sensor caspase-11 in the intestines of both Casp8(C362A/C362A)M

196 aled colocalization of LPSs, galectin-3, and caspase-11 independent of host N-glycans.

197 haride (LPS), or S. typhimurium LPS activate caspase-11 independently of the LPS receptor Toll-like r

198 Legionella activation of caspase-11 induced pyroptosis by a mechanism independent

199 IV secretion system and interferes with the caspase-11-induced, non-canonical activation of the infl

200 y, a noncanonical inflammasome controlled by caspase-11 induces cell death and IL-1 release.

201 Caspase-11 induces pyroptosis, a form of programmed cell

202 nt that is both necessary and sufficient for caspase-11 induction and autoactivation.

203 plasmic sensor for LPS and components of the caspase-11 inflammasome are not yet defined.

204 d for the full activity of the non-canonical caspase-11 inflammasome during infections with vacuolar

205 ng mechanisms, we show MYD88/TRIF, Caspase-1/Caspase-11 inflammasome, and NOD1/NOD2 nodosome signalin

206 We find that the Caspase-11 inflammasome, which senses Shigella LPS, rest

207 interleukin-1beta) through the non-canonical caspase-11 inflammasome.

208 nflammasome and did not affect non-canonical caspase-11, inflammasome activation.

209 Gasdermin D (GSDMD) cleavage by caspase-1 or caspase-11 inflammasomes triggers pyroptosis, a lytic fo

210 osis, and combined caspase-1, caspase-8, and caspase-11 inhibition increased TNF, suggesting a mechan

211 Activation of caspase-1 and caspase-11 initiates pyroptotic host cell death that rel

212 Allo-HSCT markedly increases the LPS-caspase-11 interaction, leading to the cleavage of gasde

213 on of Caspase-11 or Gsdmd, inhibition of LPS-caspase-11 interaction, or neutralizing IL-1alpha unifor

214 Our data suggest that caspase-11 is a component of ICE complex and is required

215 Our results suggest that caspase-11 is a critical initiator caspase responsible f

216 Caspase-11 is a key regulator of caspase-1 and caspase-3

217 Caspase-11 is an innate immune pattern recognition recep

218 Thus, caspase-11 is critical for surviving exposure to ubiquit

219 to ATP and monosodium urate, indicating that caspase-11 is engaged by a non-canonical inflammasome.

220 Caspase-11 is found in reactive microglia/macrophages as

221 Whether either ortholog functions similar to caspase-11 is poorly defined.

222 Here, we report that caspase-11 is required for innate immunity to cytosolic,

223 However, the signaling pathway downstream of caspase-11 is unknown.

224 We show here that the expression of caspase-11 is upregulated in the spinal cord of superoxi

225 sensor caspase-4, unlike its mouse homologue caspase-11, is constitutively expressed and activates pr

226 iated inactivating passenger mutation on the caspase-11 locus, essentially making them deficient in b

227 erial RNA by NLRP3 and binding of LPS by pro-caspase-11 mediated a pro-caspase-11-NLRP3 interaction b

228 -1beta) release occurs through caspase-1 and caspase-11-mediated gasdermin D pore formation.

229 utants of C. burnetii failed to suppress the caspase-11-mediated inflammasome activation induced by L

230 egulatory factor (IRF) 8 was dispensable for caspase-11-mediated NLRP3 inflammasome activation during

231 of macrophages with C. burnetii inhibits the caspase-11-mediated non-canonical activation of the NLRP

232 Caspase-11-mediated pyroptosis in response to cytosolic

233 Caspase-11 mediates caspase-1 activation in response to

234 A second inflammatory caspase, mouse caspase-11, mediates pyroptotic death through an unknown

235 We find that caspase-11(-/-) mice display enhanced susceptibility to

236 These data indicate that caspase-11 negatively regulates TCR signaling, possibly

237 ding of LPS by pro-caspase-11 mediated a pro-caspase-11-NLRP3 interaction before caspase-11 activatio

238 Thus, the pro-caspase-11-NLRP3 interaction nucleated a scaffold for th

239 pore formation and not through activation of caspase 11/noncanonical inflammasome.

240 pase-1 - as well as caspase-4, caspase-5 and caspase-11 of the noncanonical inflammasome, and the inf

241 f the combined absence of both caspase-1 and caspase-11 on oviduct pathology.

242 Deletion of Caspase-11 or Gsdmd, inhibition of LPS-caspase-11 intera

243 in mice deficient in IL-1B, ASC, caspase-1, caspase-11, or gasdermin D.

244 NEK7, but not on NLRC4, NLRP1, NLRP6, AIM2, caspase-11, or GSDMD.

245 gered macrophage cell death, indicating that caspase-11 orchestrates both caspase-1-dependent and -in

246 e show C3aR is required for up-regulation of caspase-11 orthologues, caspase-4 and -5, in primary hum

247 Thus, although caspase-11 participates in flagellin-independent noncano

248 Priming the caspase-11 pathway in vivo resulted in extreme sensitivi

249 Priming the caspase-11 pathway in vivo with LPS or Toll-like recepto

250 Furthermore, we found that pro-caspase-11 physically interacts with pro-ICE in cells, a

251 ays with recombinant proteins confirmed that caspase-11 prefers cleaving gasdermin D over the pro-ILs

252 anonical stimuli required NLRP3 and ASC, but caspase-11 processing and cell death did not, implying t

253 nt signaling pathway is required for in vivo caspase-11 production in intestinal epithelial cells dur

254 Caspase-11 promoted the fusion of the L. pneumophila vac

255 es activation of HSCs through decreasing MPT-Caspase-11 pyroptosis in hepatocytes.

256 ochondrial permeability transition (MPT) and Caspase-11 pyroptosis in mice.

257 Lastly, loss of caspase-11 rather than caspase-1 protected mice from a l

258 Caspase-11 rather than caspase-1, however, was required

259 However, we found that caspase-11 recognizes protein substrates through a mecha

260 In addition, mouse caspase-11 (represented in humans by its orthologs, casp

261 For example, caspase-11 responds to LPS introduced into the cytosol a

262 Specifically, caspase-11 responds to penta- and hexa-acylated lipid A,

263 f the noncanonical inflammasome, mediated by caspase-11, serves as an additional pathway for the prod

264 CT, as pharmacological interference with the caspase-11 signaling might reduce GVHD while preserving

265 e-11-/-;SOD1 G93A mice compared with that of caspase-11+/-; SOD1 G93A mice.

266 ly reduced in the spinal cord of symptomatic caspase-11-/-;SOD1 G93A mice compared with that of caspa

267 We conclude that caspase-11 specificity is mediated by the P1'-P4' region

268 Legionella activation of caspase-11 stimulated activation of caspase-1 through NL

269 Caspase-11 subsequently synergizes with the assembled NL

270 Thus, TLR4- and TRIF-induced caspase-11 synthesis is critical for noncanonical Nlrp3

271 t mediate a capsase-11 response and that the caspase-11 system provides an alternative pathway for ra

272 Here we show that caspase-11, the cytosolic receptor for bacterial endotox

273 estored fully by inhibition of Caspase-1 and Caspase-11, the murine homolog of Caspase-4.

274 These effects were mediated by caspase-11, TLR4, and complement, each of which trigger

275 t caspase-1 activity is required upstream of caspase-11 to control infection.

276 ASC in turn recruits caspase-1 and/or caspase-11 to form the AIM2 inflammasome.

277 ' region into pro-IL18 enhanced catalysis by caspase-11 to levels comparable with that of gasdermin D

278 Flightless-I targets caspase-11 to the Triton X-100-insoluble cytoskeleton fr

279 he individual contributions of caspase-1 and caspase-11 to this phenotype are not known.

280 ysaccharide triggers human caspase-4 (murine caspase-11) to cleave gasdermin-D and induce pyroptotic

281 The identification of TRIF as a regulator of caspase-11 underscores the importance of TLRs as master

282 in D (GSDMD) as a substrate of caspase-1 and caspase-11 upon detection of cytosolic lipopolysaccharid

283 oxPAPC and LPS bind caspase-11 via distinct domains and elicit different inf

284 TRIF activates caspase-11 via type I IFN signaling, an event that is bo

285 , we found that the optimal cleavage site of caspase-11 was (I/L/V/P)EHD, similar to that of upstream

286 Here, we demonstrated that caspase-11 was dispensable for caspase-1 activation in r

287 However, caspase-11 was dispensable for the fusion of lysosomes w

288 /6) for caspase-11 expression, we found that caspase-11 was dispensable for the restriction of Legion

289 Although caspase-11 was produced in macrophages deficient in the

290 e-11, we demonstrated that caspase-1 but not caspase-11 was required for pore formation, pyroptosis,

291 We also determined that active mouse caspase-11 was required for restriction of L. pneumophil

292 sing mice double deficient for caspase-1 and caspase-11, we assessed the participation of caspase-1 a

293 a and mice singly deficient for caspase-1 or caspase-11, we demonstrated that caspase-1 but not caspa

294 to identify new intracellular regulators of caspase-11, we found that Flightless-I, a member of the

295 as well as heat shock protein 70 (HSP70) and Caspase 11 were found to be increased up to 24 fold high

296 which includes murine Caspase 4 (also called Caspase 11), which we show is a direct p53 target gene.

297 These mutants triggered caspase-11, which enhanced clearance of S. typhimurium s

298 naturally invade the cytosol also triggered caspase-11, which protected mice from lethal challenge w

299 The observed increase in Caspase 11 with over-expression of miR-34a indicates tha

300 IP/NLRC4, NLRP6, and noncanonical caspase-4 (caspase-11) - within epithelial cells of the gut in muco