ライフサイエンスコーパス: CAPS

1 CAPS (aka CADPS) is one of several factors required for

2 CAPS (aka CADPS) is required for optimal vesicle exocyto

3 CAPS (also known as CADPS) is a 145-kDa cytosolic and pe

4 CAPS (Ca(2+)-dependent activator protein for secretion)

5 CAPS accompanied vesicles to the plasma membrane and was

6 CAPS binding is specific for a subset of exocytic SNARE

7 CAPS binds phosphatidylinositol 4,5-bisphosphate (PI(4,5

8 CAPS bound syntaxin-1, and CAPS truncations that competi

9 CAPS deletion specifically reduced secretion of stationa

10 CAPS dimer formation required its C2 domain based on mut

11 CAPS dimerization may be coupled to oligomeric SNARE com

12 CAPS function in dense core vesicle docking parallels UN

13 CAPS is a result of central sensitization with disinhibi

14 CAPS is found to reside on vesicles but depends on plasm

15 CAPS may function in priming by organizing SNARE complex

16 CAPS outcomes for IPT and prolonged exposure differed by

17 CAPS patients have traditionally been successfully treat

18 CAPS phosphorylation by CK2 was constitutive, but the el

19 CAPS promotes SNARE complex formation on liposomes, but

20 CAPS stimulated trans-SNARE complex formation concomitan

21 CAPS variants containing this exon promote serotonin upt

22 CAPS was cardioprotective: infarct size was 25+/-5 and 4

23 CAPS-1-EYFP expression in DKO neurons restored DCV secre

24 CAPS-DB is a database of clusters of structural patterns

25 CAPS-DB is a relational database that allows the user to

26 -dependent activator protein in secretion 1 (CAPS-1; CADPS/UNC31) and ubMunc13-2 (UNC13B) are PIP2-bi

27 for a C-terminal binding site on syntaxin-1, CAPS stimulates SNARE-dependent liposome fusion with N-t

28 t DCV secretion was reduced by 70% in CAPS-1/CAPS-2 double null mutant (DKO) neurons and remaining fu

29 firmation resulted in the development of 250 CAPS markers distributed evenly over the genome.

30 reviously identified contributions of UNC-31/CAPS to neuropeptide or glutamate transmission.

31 type Ca(2+) channel alpha-subunit and unc-31/CAPS, in addition to unc-13/Munc13 and unc-10/RIM, and e

32 Clinician-Administered PTSD Scale for DSM-5 (CAPS-5), and Structured Clinical Interview for DSM-IV, N

33 A CAPS marker able to distinguish the CBF2A, CBF2B and CBF

34 A CAPS(DeltaC135) protein that does not localize to vesicl

35 Nlrp3 KI mice displayed a CAPS phenotype with many characteristics of autoinflamma

36 not Ser-1281 to Ala substitutions abolished CAPS activity.

37 rticles in the serum of patients with active CAPS but not in that of patients with other inherited au

38 ping study in a 110-kb region at 19q13 among CAPS and JHH study populations revealed that rs887391 wa

39 measurements, a cavity phase shift analyzer (CAPS) for NO2 measurements, and a UV ozone analyzer.

40 Deletion of CAPS-1 and CAPS-2 did not affect DCV biogenesis, loading, transport

41 CAPS bound syntaxin-1, and CAPS truncations that competitively inhibited syntaxin-1

42 Based on SNPs identification and CAPS markers, the resistance gene was identified as ClaP

43 4%, respectively, in the CAPS-pretreated and CAPS-delayed treatment groups versus 56+/-5% in saline c

44 review, we summarize biomarkers in sJIA and CAPS and draw upon the various similarities and differen

45 escribe a strong similarity between sJIA and CAPS at the gene expression level in which several genes

46 The main differences between sJIA and CAPS biomarkers are genetic markers, with CAPS being a f

47 The gene expression data in both sJIA and CAPS show a strong upregulation of innate immunity pathw

48 similarity of clinical response of sJIA and CAPS to anti-interleukin 1 therapies prompted a comparis

49 s signature are upregulated in both sJIA and CAPS.

50 or a genetic interaction between tomosyn and CAPS, we generated tom-1;unc-31 double mutants.

51 nd Rab27, rabphilin3a, munc18a, tomosyn, and CAPS.

52 ise the prospect that immunization with anti-CAPS antibodies might provide therapeutic benefit for AD

53 ) were present in 85.7% of catastrophic APS (CAPS), 35.6% of APS (and 68.5% of samples collected with

54 rocedure designed for distributions, such as CAPS in this study, that have an excess of zeroes in add

55 dence of inflammation as part of an atypical CAPS phenotype and was reversed or improved by IL-1beta

56 showed that participants with high baseline CAPS scores receiving oxytocin had significantly lower C

57 llow-up than participants with high baseline CAPS scores receiving placebo.

58 Adjusting for the baseline CAPS score, trauma exposure, and other relevant covariat

59 osis did not depend on the PI(4,5)P2-binding CAPS-proteins, suggesting that PI(4,5)P2 uncaging may by

60 n in DKO neurons restored DCV secretion, but CAPS-1-EYFP and DCVs rarely traveled together.

61 SNARE protein binding by CAPS is novel and mediated by interactions with the SNAR

62 est that SNARE complex formation promoted by CAPS may be mediated by direct interactions of CAPS with

63 uggesting that PI(4,5)P2 uncaging may bypass CAPS-function.

64 aracterization of the location of capsaicin (CAPS) and resiniferatoxin (RTX).

65 ults indicate that dense-core vesicles carry CAPS to sites of exocytosis, where CAPS promotes vesicle

66 The discovery of the mutations that cause CAPS and DIRA led to clinical and basic research that un

67 Genomic and cDNA CAPS analyses of 10 candidate genes revealed that only o

68 istics of sJIA are also seen to characterize CAPS.

69 cal reaction chambers, each with a dedicated CAPS NO2 sensor.

70 nd restored the activity of dephosphorylated CAPS.

71 otton phytochrome genes with newly developed CAPS and dCAPS markers.

72 atable sensorineural hearing loss in DFNA34, CAPS, and possibly in a wide variety of hearing-loss dis

73 particles (< 100 nm in aerodynamic diameter; CAPS) using the Harvard University Concentrated Ambient

74 ompared with controls [group by time effect, CAPS (Clinician-Administered PTSD Scale): F(2, 185) = 5.

75 ulation of lipid-dependent protein effectors CAPS and Munc13.

76 haracterized the sole Caenorhabditis elegans CAPS ortholog UNC-31 (uncoordinated family member) and d

77 Dephosphorylation eliminated CAPS activity in reconstituting Ca(2+)-dependent vesicle

78 Endogenous CAPS-1 co-localized with synaptic markers but was not en

79 ities of the lipid-dependent priming factors CAPS (also known as CADPS) and ubiquitous Munc13-2 in PC

80 rvested at baseline and 10 minutes following CAPS treatment and assayed (by immunoblotting) for 2 pro

81 The binding affinity of cAMP for CAPS-associated mutant NLRP3 is substantially lower than

82 s in sJIA with no such studies described for CAPS.

83 ndicating that dimerization is essential for CAPS function.

84 esults may have therapeutic implications for CAPS patients with partial responses to IL-1-targeted th

85 lation by protein kinase CK2 is required for CAPS activity.

86 open syntaxin can bypass the requirement for CAPS in dense core vesicle docking.

87 The C-terminal site for CAPS binding on syntaxin-1 does not overlap the Munc18-1

88 ge are the most commonly used treatments for CAPS patients.

89 cases (n=2,393) and controls (n=1,222) from CAPS and found that rs887391 at 19q13 was highly associa

90 hreshold of activation; blood monocytes from CAPS patients maintain the high levels of secreted IL-1b

91 uncontrolled mature IL-1beta production from CAPS patients' peripheral blood mononuclear cells is att

92 variation (CNV) in additional subjects from CAPS and from Johns Hopkins Hospital (JHH).

93 nightmares, sleep quality, global function, CAPS score, and the CAPS hyperarousal symptom cluster.

94 ucleotide polymorphisms (SNPs) and generates CAPS and/or dCAPS PCR primer sequences.

95 Mouse lines harboring CAPS-associated mutations in Nlrp3 have elevated levels

96 ation and poor growth, similar to some human CAPS patients, and demonstrated early mortality, primari

97 y; however, there are a number of identified CAPS patients who show only a partial response to IL-1 b

98 . barbadense one PHYA1-specific Mbo I/Dpn II CAPS, one PHYB-specific Alu I dCAPS, and one HY5-specifi

99 We imaged CAPS before, during, and after single-vesicle fusion eve

100 In CAPS monocytes, LPS induces the externalization of copio

101 The central role of IL-1beta in CAPS is supported by the response to IL-1-targeted thera

102 sponse, defined as an improvement of >30% in CAPS score, were 63% for IPT, 47% for prolonged exposure

103 ing, but DCV secretion was reduced by 70% in CAPS-1/CAPS-2 double null mutant (DKO) neurons and remai

104 Change in CAPS scores from baseline to 24 weeks in the risperidone

105 , and defibrotide, that can be considered in CAPS patients refractory to traditional treatment.

106 The difference in CAPS between the VRE-DCS (n=13) and VRE-placebo (n=12) g

107 nts also showed no significant difference in CAPS score (risperidone: mean, 64.43; 95% CI, 61.98 to 6

108 ot observe a significant group difference in CAPS total score at 1.5 months posttrauma (primary outco

109 ld, indicating that inflammatory episodes in CAPS may not be entirely a result of IL-1beta but may al

110 cue vesicle docking and evoked exocytosis in CAPS-depleted cells, showing that CAPS residence on vesi

111 pression of an alternatively spliced exon in CAPS leads to enhanced catecholamine content in chromaff

112 imer revealed conserved residues involved in CAPS dimerization.

113 mally inferior (a difference <12.5 points in CAPS score) to prolonged exposure.

114 Reductions in CAPS total, re-experiencing, and hyperarousal scores wer

115 l stress and increased cytokine secretion in CAPS.

116 with the latter exceeding the levels seen in CAPS.

117 tures that are more similar to those seen in CAPS.

118 levation of Ca(2+) in synaptosomes increased CAPS Ser-5 and -6 dephosphorylation, which terminates CA

119 inhibited syntaxin-1 binding also inhibited CAPS-dependent fusion.

120 rning biomass-fueled cookstove intervention (CAPS [Cooking and Pneumonia Study]) in rural Malawi.

121 Secondary outcome measures were the 17-item CAPS, the Hamilton Depression Rating Scale, the Patient

122 ing inflammation in double-cytokine knockout CAPS mice implicated a role for caspase-1-mediated pyrop

123 s receiving oxytocin had significantly lower CAPS scores across follow-up than participants with high

124 to concentrated ambient particulate matter (CAPS) during the first 2 weeks of life, alone or again i

125 Nlrp3 mutant knockin mouse strains to model CAPS to examine the role of other inflammatory mediators

126 pocket and is substantially reduced for most CAPS-associated NLRP3 mutants.

127 d found that vesicle docking requires Munc13/CAPS family priming proteins and all three neuronal SNAR

128 role of inflammasome-driven IL-18 in murine CAPS, we bred Nlrp3 mutations onto an Il18r-null backgro

129 ive of this study was to develop and map new CAPS and dCAPS markers for cotton developmental-regulato

130 flammation driven by wild-type NLRP3 but not CAPS-associated mutants.

131 inversely correlated with avoidance/numbing CAPS symptoms.

132 d by sequential PIP2-dependent activation of CAPS and PIP2-dependent recruitment of Munc13.

133 Moreover, administration of CAPS was associated with increased expression of both pr

134 The contents of CAPS-DB might be of interest to a wide range of scientis

135 Deletion of CAPS does not alter acidification of vesicles.

136 Deletion of CAPS-1 and CAPS-2 did not affect DCV biogenesis, loading

137 The unique tandem C2-PH domain of CAPS may serve as a PI(4,5)P2-triggered switch for dimer

138 g; however, the localization and dynamics of CAPS at sites of exocytosis in live neuroendocrine cells

139 hronized schedule, eliminating the effect of CAPS baseline offsets on the calculated peroxy radical c

140 plice-variant-dependent modulatory effect of CAPS on catecholamine content in LDCVs.SIGNIFICANCE STAT

141 To investigate whether the efficacy of CAPS was maintained with "delayed" treatment, additional

142 However, the active form of CAPS bound to PC12 cell membranes or to liposomes contai

143 Although an influence of CAPS on monoamine transporter function and on vesicle ac

144 PS may be mediated by direct interactions of CAPS with each of the three SNARE proteins required for

145 Here we show that the intestines of CAPS model mice carrying an Nlrp3 (R258W) mutation maint

146 The knockdown of CAPS by shRNA eliminated the VAMP-2-dependent docking an

147 Synaptic localization of CAPS-1-EYFP in DKO neurons was calcium dependent and DCV

148 mutations or deletions resulted in a loss of CAPS function in regulated vesicle exocytosis, indicatin

149 out any other target-organ manifestations of CAPS.

150 to accurately determine the binding mode of CAPS and RTX and experimentally validate the computation

151 scued neonatal lethality in a mouse model of CAPS and was active in ex vivo samples from individuals

152 p a novel Nlrp3 knock-in (KI) mouse model of CAPS to study amyloidosis, a severe CAPS complication, a

153 nflammatory pathology in two mouse models of CAPS.

154 omplement components) in the pathogenesis of CAPS and the therapeutic benefit of complement inactivat

155 tical roles in the molecular pathogenesis of CAPS.

156 te the immunologic and clinical phenotype of CAPS.

157 , correlating inversely with the presence of CAPS protein on purified vesicles.

158 posomes, but the SNARE binding properties of CAPS are unknown.

159 nt vesicle exocytosis, but the regulation of CAPS activity has not been characterized.

160 A modulatory role of CAPS in catecholamine loading of vesicles has been sugge

161 e acidification has been reported, a role of CAPS in vesicle loading is disputed.

162 To genetically assess the functional role of CAPS, we characterized the sole Caenorhabditis elegans C

163 vement in the clinical signs and symptoms of CAPS, and normalized the levels of SAA from those associ

164 of drugs targeting IL -1 in the treatment of CAPS and DIRA have encouraged their wider use in other a

165 3 inflammasome pathway, for the treatment of CAPS and other diseases.

166 f complement activation, in the treatment of CAPS demonstrates both the importance of complement (spe

167 Treatment of CAPS focuses on anticoagulation therapy and on removal o

168 Epigenetic tuning of CAPS variants may allow modulation of endocrine adrenali

169 alence (95% CI) of 4.5% (1.7%-7.3%) based on CAPS-5 criteria for a current PTSD diagnosis; 10.8% (6.5

170 PTSD diagnosis; 10.8% (6.5%-15.1%) based on CAPS-5 full plus subthreshold PTSD; and 11.2% (8.3%-14.2

171 Protein kinase CK2 phosphorylated CAPS in vitro at these sites and restored the activity o

172 core raised predicted 3-month postdeployment CAPS scores by factors of 1.02 (P < .001; 95% CI, 1.02-1

173 nificant overall predictor of postdeployment CAPS scores (P = .002): each 10-fold increment in CRP co

174 e plasma CRP concentration on postdeployment CAPS using zero-inflated negative binomial regression (Z

175 Postnatal CAPS exposure produces an enhanced bias towards immediat

176 FR response rates, mice exposed to postnatal CAPS displayed increased FR resets that reinstated short

177 Predeployment CAPS score and combat intensity score raised predicted 3

178 Deployment-related mild TBI raised predicted CAPS scores by a factor of 1.23 (P < .001; 95% CI, 1.11-

179 mutants lacking unc-31 (encoding the protein CAPS) or unc-13 (encoding Munc13).

180 delayed" treatment, additional pigs received CAPS (20 mg/kg) at 30 minutes after occlusion.

181 In the current work, we reconstituted CAPS function in a SNARE-dependent liposome fusion assay

182 ur patient was a young man who had recurrent CAPS characterized by multiple arterial thromboses in la

183 Such conditions reduce CAPS activity and enhance Munc13 activity, establishing

184 terminal phosphorylation site that regulates CAPS activity in priming vesicle exocytosis.

185 several encoding proteins with known roles (CAPS [calcium-dependent activator protein for secretion

186 The Clinician-Administered PTSD Scale (CAPS) (range, 0-136).

187 re on the Clinician-Administered PTSD Scale (CAPS) 3 months after deployment.

188 ressed on Clinician-Administered PTSD Scale (CAPS) symptoms.

189 The Clinician-Administered PTSD Scale (CAPS) was administered at baseline (within 10 days postt

190 (TEI) and Clinician-Administered PTSD Scale (CAPS) were used to measure lifetime trauma burden and PT

191 em of the Clinician-Administered PTSD Scale (CAPS), the Pittsburgh Sleep Quality Index, and the chang

192 50 on the Clinician-Administered PTSD Scale (CAPS).

193 ed by the Clinician-Administered PTSD Scale (CAPS).

194 e was the Clinician Administered PTSD Scale (CAPS).

195 e was the Clinician-Administered PTSD Scale (CAPS).

196 -dependent activator proteins for secretion (CAPS) are priming factors for synaptic and large dense-c

197 m-dependent activator protein for secretion (CAPS) homolog UNC-31.

198 )-dependent activator protein for secretion (CAPS) is an essential factor for regulated vesicle exocy

199 The calcium activator protein for secretion (CAPS) promotes and stabilizes the entry of catecholamine

200 the calcium-activated protein for secretion (CAPS) protein is required for dense core vesicle docking

201 of calcium-activator protein for secretion (CAPS) proteins in neuronal DCV secretion at single vesic

202 the calcium-activated protein for secretion (CAPS) UNC-31, suggesting it has a neuropeptidergic mecha

203 31 [calcium-activated protein for secretion (CAPS)] acts through an inhibitory pathway not explained

204 sed calcium activator for protein secretion (CAPS) homolog unc-31.

205 cDNA cleaved amplified polymorphic sequence (CAPS) analyses, we found differences in the evolution an

206 ed a cleaved amplified polymorphic sequence (CAPS) marker tightly linked to the Prs locus and demonst

207 d by cleaved amplified polymorphic sequence (CAPS), a simple and robust PCR-based assay that reliably

208 model of CAPS to study amyloidosis, a severe CAPS complication, and test novel therapeutic approaches

209 quantified by cavity attenuated phase shift (CAPS) spectroscopy, a highly sensitive spectroscopic det

210 We characterized purified soluble CAPS as mainly monomer in equilibrium with small amounts

211 ime in a counselor-assisted problem-solving (CAPS) intervention.

212 In the later phase after LPS stimulation, CAPS monocytes undergo oxidative stress, which impairs p

213 he Combined Analysis of Psychiatric Studies (CAPS) project conducted extensive review and regularizat

214 dy, pigs received chloramphenicol succinate (CAPS) (an agent that purportedly upregulates autophagy;

215 in Sweden [CAncer of the Prostate in Sweden (CAPS)] using Affymetrix SNP arrays.

216 in Sweden [Cancer of the Prostate in Sweden (CAPS)].

217 fusion probability correlated with synaptic CAPS-1-EYFP expression.

218 Catastrophic antiphospholipid syndrome (CAPS) is a potentially lethal disease that presents with

219 Catastrophic antiphospholipid syndrome (CAPS) is characterized by histopathologic evidence of sm

220 Centrally Mediated Abdominal Pain Syndrome (CAPS), formerly known as Functional Abdominal Pain Syndr

221 h as cryopyrin-associated periodic syndrome (CAPS) and complex diseases such as multiple sclerosis, t

222 The cryopyrin-associated periodic syndrome (CAPS) is a rare inherited inflammatory disease associate

223 Cryopyrin-associated periodic syndrome (CAPS) patients with NLRP3 mutations have autoinflammatio

224 s in cryopyrin-associated periodic syndrome (CAPS).

225 n as cryopyrin-associated periodic syndrome (CAPS).

226 yopyrin-associated periodic fever syndromes (CAPS) caused by inherited NLRP3 mutations.

227 ith cryopyrin-associated periodic syndromes (CAPS) and familial Mediterranean fever, 2 archetypical m

228 the cryopyrin-associated periodic syndromes (CAPS) and trigger spontaneous inflammasome activation an

229 Cryopyrin-associated periodic syndromes (CAPS) are a group of autoinflammatory diseases linked to

230 Cryopyrin-associated periodic syndromes (CAPS) are caused by aberrant interleukin-1beta (IL-1beta

231 the cryopyrin-associated periodic syndromes (CAPS) disease spectrum.

232 in Cryopyrin-Associated Periodic Syndromes (CAPS) macrophages, where NLRP3 inflammasome is constitut

233 ted cryopyrin-associated periodic syndromes (CAPS) release greater amounts of IL-1beta than monocytes

234 ith cryopyrin-associated periodic syndromes (CAPS) stimulated further activation of caspase-1 extrace

235 ith cryopyrin-associated periodic syndromes (CAPS), a rare monogenetic disease driven by uncontrolled

236 se, cryopyrin-associated periodic syndromes (CAPS).

237 ith cryopyrin-associated periodic syndromes (CAPS).

238 as cryopyrin-associated periodic syndromes (CAPS).

239 of cryopyrin-associated periodic syndromes (CAPS).

240 rum cryopyrin-associated periodic syndromes (CAPS).

241 the cryopyrin-associated periodic syndromes (CAPS).

242 med cryopyrin-associated periodic syndromes (CAPS).

243 the cryopyrin-associated periodic syndromes (CAPS).

244 and early-onset autoinflammatory syndromes, CAPS (cryopyrin associated periodic syndromes) and DIRA

245 5 and -6 dephosphorylation, which terminates CAPS activity.

246 ered) DCVs in presynaptic terminals and that CAPS-1 localization to DCVs is probably not essential fo

247 We conclude that CAPS functions as a C2 domain-mediated dimer in regulate

248 ase-1-mediated pyroptosis and confirmed that CAPS is inflammasome dependent.

249 However, the precise events that CAPS regulates to promote vesicle fusion are unclear.

250 These data indicate that CAPS-1 promotes fusion competence of immobile (tethered)

251 These findings indicate that CAPS/UNC-31 function is not restricted to catecholaminer

252 Previous studies indicated that CAPS (calcium-dependent activator protein for secretion)

253 It also indicated that CAPS is entirely mediated by IL-1beta and that canakinum

254 The current work revealed that CAPS exhibits high affinity binding to syntaxin-1 and SN

255 lecular target of MCC950/CRID3 and show that CAPS-related NLRP3 mutants escape efficient MCC950/CRID3

256 cytosis in CAPS-depleted cells, showing that CAPS residence on vesicles is essential.

257 These data suggest that CAPS are true inflammasome-mediated diseases and provide

258 Our results suggest that CAPS/UNC-31 and UNC-13 serve parallel and dedicated role

259 The CAPS stimulation of fusion required PI(4,5)P(2) in accep

260 In older (>14 to 17 years) adolescents, the CAPS intervention was associated with lower GEC ratings

261 the Five City Project questionnaire, and the CAPS Four Week Activity Recall overestimated (P < 0.05)

262 uality, global function, CAPS score, and the CAPS hyperarousal symptom cluster.

263 in molecular breeding of crop plants are the CAPS and dCAPS markers derived from the genes of interes

264 Both the CAPS and UNC-13 docking pathways converge on syntaxin, a

265 was required for macrophages containing the CAPS-associated NLRP3(R258W) activating mutation to acti

266 was 25+/-5 and 41+/-4%, respectively, in the CAPS-pretreated and CAPS-delayed treatment groups versus

267 Secondary efficacy measures included the CAPS subscales, the Davidson Trauma Scale, the Positive

268 Comparison of the CAPS C2 domain to a structurally defined Munc13-1 C2A do

269 Use of the CAPS intervention clinically should be considered; howev

270 Delivery of the CAPS intervention early after TBI in older adolescents i

271 There was no effect of the CAPS intervention on any of the secondary trial outcomes

272 Munc13-4 is a widely expressed member of the CAPS/Munc13 protein family proposed to function in primi

273 A change of 15 points on the CAPS scale and 1 dependence criterion on the CIDI were c

274 etric abnormalities and no evidence that the CAPS intervention had effects on the secondary trial out

275 ased absorption spectrometer showed that the CAPS-based instrument was able to reliably and quantitat

276 62%, 16%, and 11%, respectively, whereas the CAPS Typical Week Activity Recall underestimated (P < 0.

277 N475K mutation, which is associated with the CAPS phenotype, into the mouse Nlrp3 gene.

278 skin inflammation in neonatal mice with the CAPS-associated Nlrp3 mutation.

279 Thus, CAPS likely promotes the open state of syntaxin, which t

280 sistent asthma in children (LRRC23, TMEM231, CAPS, PTPRC, and FYB); and (3) master regulator genes of

281 These data suggest that autoantibodies to CAPS are depleted in AD patients and raise the prospect

282 UNC-13, which exhibits sequence homology to CAPS/UNC-31, was found to be essential for synaptic vesi

283 inhibitor of complement activation to treat CAPS that was refractory to conventional therapy.

284 resident on cytoplasmic dense-core vesicles, CAPS was present in clusters of approximately nine molec

285 CK2 is the likely in vivo CAPS protein kinase based on inhibition of phosphorylati

286 les carry CAPS to sites of exocytosis, where CAPS promotes vesicle docking and fusion competence, pro

287 ctivation, as well as the mechanism by which CAPS-associated mutations activate NLRP3, remain to be e

288 enuation of ischemia-reperfusion injury with CAPS and are consistent with the concept that induction

289 nd CAPS biomarkers are genetic markers, with CAPS being a family of monogenic diseases with mutations

290 ants to the anti-IL-1 drugs in patients with CAPS and other IL-1-driven diseases.

291 ave important implications for patients with CAPS and residual disease, emphasizing the need to explo

292 Finally, patients with CAPS have high rates of rare germline variants in comple

293 to thrombosis in APS, whereas patients with CAPS have underlying mutations in complement regulatory

294 Interestingly, patients with CAPS treated with anti-IL-1 drugs display methylation le

295 ions, monocytes from untreated patients with CAPS undergo more efficient DNA demethylation than those

296 Forty-seven adult patients with CAPS, as defined by mutations in the causative NLRP3 (CI

297 ta secretion by monocytes from patients with CAPS.

298 mmasome activity in cells from patients with CAPS.

299 drawal study of canakinumab in patients with CAPS.

300 remission of symptoms in most patients with CAPS.