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 appears to act upstream of fusion in the biogenesis

7 CAPS binding is specific for a subset of exocytic SNARE

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

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

10 CAPS deletion specifically reduced secretion of stationa

11 CAPS dimer formation required its C2 domain based on mut

12 CAPS dimerization may be coupled to oligomeric SNARE com

13 CAPS function in dense core vesicle docking parallels UN

14 CAPS is a result of central sensitization with disinhibi

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

16 CAPS may function in priming by organizing SNARE complex

17 CAPS outcomes for IPT and prolonged exposure differed by

18 CAPS patients have traditionally been successfully treat

19 CAPS phosphorylation by CK2 was constitutive, but the el

20 CAPS promotes SNARE complex formation on liposomes, but

21 CAPS stimulated trans-SNARE complex formation concomitan

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

23 CAPS-1 activity and binding to the plasma membrane depen

24 CAPS-1 activity depended upon prior ATP-dependent primin

25 CAPS-1 increased the initial rate of Ca2+-triggered vesi

26 CAPS-1 is required for Ca2+-triggered fusion of dense-co

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

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

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

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

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

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

33 a Clinician Administered PTSD Scale Part 2 (CAPS-2) minimum total severity score of at least 50 at b

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

35 e dense-core vesicle priming protein UNC-31 (CAPS) share highly similar phenotypes with mutants lacki

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

37 ic and novel genetic interaction with UNC-31/CAPS, a protein that has been shown in other systems to

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

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

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

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

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

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

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

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

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

47 Regulation of PIP2 levels and CAPS-1 activity would control the secretion of neuropept

48 4%, respectively, in the CAPS-pretreated and CAPS-delayed treatment groups versus 56+/-5% in saline c

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

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

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

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

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

54 s signature are upregulated in both sJIA and CAPS.

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

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

57 In contrast, anti-CAPS antibodies in AD plasma were found to be significan

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

73 istics of sJIA are also seen to characterize CAPS.

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

75 nd restored the activity of dephosphorylated CAPS.

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

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

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

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

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

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

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

83 th distinct binding specificities may enable CAPS to bind both target membranes to facilitate DCV-pla

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

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

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

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

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

89 ding properties that were each essential for CAPS activity in regulated exocytosis.

90 erties but not the latter were essential for CAPS function.

91 ndicating that dimerization is essential for CAPS function.

92 rect mapping of 124 SSRs and exploration for CAPS and SNPs illustrate the "portability" of these STS

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

109 In CAPS monocytes, LPS induces the externalization of copio

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

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

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

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

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

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

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

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

118 We identified two domains in CAPS with distinct membrane-binding properties that were

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

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

121 imer revealed conserved residues involved in CAPS dimerization.

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

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

124 l stress and increased cytokine secretion in CAPS.

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

126 with the latter exceeding the levels seen in CAPS.

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

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

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

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

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

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

133 prising distal C-terminal sequences mediated CAPS targeting to and association with neuroendocrine DC

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

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

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

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

138 triggering vesicle fusion in the absence of CAPS-1 but instead promoted desensitization to CAPS-1 re

139 and the subsequent PIP2-dependent action of CAPS-1.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

154 out any other target-organ manifestations of CAPS.

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

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

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

158 tical roles in the molecular pathogenesis of CAPS.

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

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

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

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

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

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

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

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

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

168 tagged sites, primarily detected as dCAPS or CAPS (n = 131) and VNTRs (n = 31), in addition to AFLPs

169 by varying the pH maintained by Tris-HCl or CAPS buffer (pH 8.0 and 10.3) and keeping the ionic stre

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

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

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

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

174 Postnatal CAPS exposure produces an enhanced bias towards immediat

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

176 Predeployment CAPS score and combat intensity score raised predicted 3

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

193 ed of the Clinician-Administered PTSD Scale (CAPS-2) total severity score, the patient-rated Impact o

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

195 +-dependent activator protein for secretion (CAPS) is a cytosolic protein essential for the Ca2+-depe

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

197 +-dependent activator protein for secretion (CAPS) is an evolutionarily conserved secretory protein t

198 Calcium-activated protein for secretion (CAPS) is proposed to play an essential role in Ca2+-regu

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

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

201 31 [calcium-activated protein for secretion (CAPS)] acts through an inhibitory pathway not explained

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

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

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

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

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

207 contain autoantibodies specific for soluble CAPS.

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

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

210 c cross-linked beta-amyloid protein species (CAPS).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

233 med cryopyrin-associated periodic syndromes (CAPS).

234 ith cryopyrin-associated periodic syndromes (CAPS).

235 as cryopyrin-associated periodic syndromes (CAPS).

236 of cryopyrin-associated periodic syndromes (CAPS).

237 the cryopyrin-associated periodic syndromes (CAPS).

238 rum cryopyrin-associated periodic syndromes (CAPS).

239 the cryopyrin-associated periodic syndromes (CAPS).

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

241 5 and -6 dephosphorylation, which terminates CAPS activity.

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

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

244 We conclude that CAPS-1 functions following ATP-dependent priming as a PI

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

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

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

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

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

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

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

252 et al. (this issue of Neuron) now show that CAPS function may have been misunderstood.

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

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

255 Recent studies also suggest that CAPS may be the primary neurotoxic agent in AD.

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

257 The CAPS C-terminal domain was also essential for optimal ac

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

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

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

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

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

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

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

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

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

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

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

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

270 t genetic insight into possible roles of the CAPS protein in mediating dense core vesicle fusion and

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

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

273 n the PSS, Cohen d = 1.00; P<.001 and on the CAPS, Cohen d = 1.53; P<.001).

274 for sertraline compared with placebo on the CAPS-2 (t = 2.96, P =.003), the IES (t = 2.26, P =.02),

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

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

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

280 PS-1 but instead promoted desensitization to CAPS-1 resulting from decreased plasma membrane PIP2.

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

282 plasma were analyzed for immunoreactivity to CAPS and Abetamon.

283 ly (p=0.041) with plasma immunoreactivity to CAPS.

284 Targeted transgenic CAPS expression in identified motoneurons fails to rescu

285 kstrin homology domain may mediate transient CAPS interactions with the plasma membrane during Ca2+-t

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

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

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

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

290 The mechanism by which CAPS functions in exocytosis and the means by which it a

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

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

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

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

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

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

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

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.