ライフサイエンスコーパス: ASC

1 ASC specks released by microglia bind rapidly to amyloid

2 ASC were also significantly reduced in the CNS, resultin

3 ASC-conditioned media (CM) collected after 1 week of iAs

4 ASC-JM17 acts on Nrf1, Nrf2 and Hsf1 to increase the exp

5 ASC-mediated cell death leads to the release of IL-1alph

6 ASCs (plasmablasts) have been extensively studied in hum

7 ASCs are highly dependent on exogenous soluble factors s

8 ASCs may therefore provide a promising cell source for v

9 procedures and charges accounted for by (1) ASCs that are strongly connected to their local health s

10 by reducing expression of NLRP3, caspase-1, ASC, AIM2, TNFalpha, IL1beta and proinflammatory genes.

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

12 accharide also is dependent on the caspase-1-ASC axis.

13 ge and dendritic cell death in a caspase-1-, ASC-, and NLRP3-independent manner, whereas the presence

14 sfection impaired transcription of IL-1beta, ASC speck formation, and secretion of mature IL-1beta.

15 r chemical inhibitors dramatically abolished ASC oligomerization, caspase-1 activation, and IL-1beta

16 mRNA expression and inflammasome activation (ASC oligomers and mature IL-1beta).

17 Upon activation, ASC forms large oligomeric filaments, which facilitate p

18 NLRP3 forms an inflammasome with the adapter ASC, resulting in caspase-1 activation, release of proin

19 es the PYRIN domain (PYD)-containing adaptor ASC, and depends on PYD-PYD interactions.

20 sembled by the PYD of the downstream adaptor ASC.

21 trigger assembly of the inflammasome adaptor ASC into specks, large signaling platforms considered ha

22 mplex (DISC) and by the inflammasome adaptor ASC.

23 ost-derived threats, consists of the adaptor ASC (Apoptosis-associated Speck-like protein containing

24 masome, donor MDSCs deficient in the adaptor ASC (apoptosis-associated speck-like protein containing

25 f a complex containing NLRP3 and the adaptor ASC, oligomerization of ASC and activation of caspase-1.

26 ular sensor (NLR), caspase-1 and the adaptor ASC.

27 directly for the most part, via the adaptors ASC and NLRC4.

28 To examine 5-year outcomes after ASC-US cytology with vs without HPV testing.

29 Pdgfa expression is reduced in aged ASCs and is required for ASC proliferation and maintenan

30 re, we characterize a novel curcumin analog, ASC-JM17, as an activator of central pathways controllin

31 with the interaction between NLRPs/ALRs and ASC to prevent nucleation of ASC and therefore prevent a

32 ation in vitro and Fas-induced apoptosis and ASC-mediated caspase-8 recruitment in cells.

33 , we propose molecular models of ASC.ASC and ASC.NLRP3 PYD early supramolecular complexes, providing

34 through double-stranded DNA break (DSB) and ASC-mediated inflammasome assembly in phagocytes.

35 QUC reduced ASC speck formation and ASC oligomerization compared with controls.

36 ase-1 cleavage and interacted with NLRP3 and ASC.

37 mes flippase and floppase, capon, NLRP3, and ASC.

38 x, which, along with ASC oligomerization and ASC speck formation, was abrogated in the absence of NEK

39 RD alone could dampen IL-1beta secretion and ASC speck formation induced by NALP3 mutants associated

40 A to modulate liposarcoma cell survival and ASC differentiation state.

41 ifferentially expressed in human tissues and ASCs from subcutaneous and visceral fat.

42 Moreover, co-application of an anti-ASC antibody blocked the increase in amyloid-beta pathol

43 cytology results per woman were reported as ASC-US.

44 IM2 inflammasomes but not NLRC4, we assessed ASC speck formation.

45 ow that endogenous NLRC3 interacts with both ASC and pro-caspase-1 but not with NALP3, disrupts ASC s

46 Pyk2 directly phosphorylates ASC and brings ASC into an oligomerization-competent state by allowing

47 opped significantly; thus, NLRP3 mediated by ASC appears to be the pattern recognition receptor drivi

48 ost common malignant pediatric brain cancer; ASC is also expressed in human medulloblastomas.

49 ciated speck-like protein containing a CARD (ASC) and NLRP3 play key roles in the regulation of apopt

50 ciated speck-like protein containing a CARD (ASC) formed cytosolic macromolecular complexes (so-calle

51 ciated speck-like protein containing a CARD (ASC) protein in response to NALP3 activators.

52 ciated speck-like protein containing a CARD (ASC) speck formation and caspase-1 cleavage and interact

53 ciated speck-like protein containing a CARD (ASC) speck formation, without affecting potassium efflux

54 ciated speck-like protein containing a CARD (ASC)- or caspase-4-dependent inflammasome.

55 Antibody-secreting cell (ASC) and memory B-cell (MBC) responses were enumerated i

56 IgG2a switch and impaired Ab-secreting cell (ASC) differentiation.

57 Human Ab-secreting cell (ASC) populations in circulation are not well studied.

58 f the FMDV-specific antibody-secreting cell (ASC) response following homologous and heterologous inac

59 y (Bmem) cells and antibody-secreting cells (ASC) accumulate in various models of central nervous sys

60 genesis in human adipose-derived stem cells (ASC).

61 f virus-specific antibody-secreting B cells (ASCs) and its relationship with serological response, cl

62 transplanted adipose stem/progenitor cells (ASCs) and recruited endogenous cells.

63 lls bifurcate into antibody-secreting cells (ASCs) and memory B cells (MBCs) after infection or vacci

64 Antibody secreting cells (ASCs) are critical effector cells and long-lived sentine

65 of class-switched antibody-secreting cells (ASCs) in germinal centers.

66 or numbers of IgE antibody secreting cells (ASCs) in the BM.

67 ion factor for IgM antibody-secreting cells (ASCs).

68 y ELISPOT that these are Ab-secreting cells (ASCs).

69 ansplantation of adipose-derived stem cells (ASCs) accelerates the process of acid burn wound-healing

70 genetic mutations in human adult stem cells (ASCs) during life is associated with various age-related

71 perties of human adipose-derived stem cells (ASCs) from visceral depots are compromised compared with

72 (DP) cells with adipose-derived stem cells (ASCs) in promoting hair formation.

73 lated with human adipose-derived stem cells (ASCs) is studied as a potential treatment strategy for A

74 ed STEMPRO human adipose-derived stem cells (ASCs) on both PCL+FA and PCL scaffolds to investigate th

75 and differentiation of adipocyte stem cells (ASCs) to form postmitotic, lipid-filled mature adipocyte

76 fferentiation of adipose-derived stem cells (ASCs) was significantly enhanced as indicated by increas

77 Culturing adipose-derived stem cells (ASCs), we explore the dynamic relationship between the a

78 ellularized with adipose-derived stem cells (ASCs).

79 neration due to its unique adult stem cells (ASCs).

80 eeded with human adipose-derived stem cells (ASCs).

81 Adipose stromal cells (ASCs) can become mobilized from WAT, recruited by tumour

82 ation of adipose-derived stem/stromal cells (ASCs) for engineering the pulmonary vasculature in a dec

83 pose-derived mesenchymal stem/stromal cells (ASCs).

84 are performed in Ambulatory Surgery Center (ASC) and Hospital Outpatient Department (HOPD) locations

85 and nonfacility/ambulatory surgical center (ASC)-based setting.

86 sis of their function, we have characterized ASC and NLRP3 PYD self-association and their intermolecu

87 that chemokines CXCL1 and CXCL8 chemoattract ASC by signalling through their receptors, CXCR1 and CXC

88 ly, pro-IL-1beta and inflammasome components ASC and caspase-1 were released by ATP-activated macroph

89 s independent of the inflammasome components ASC and caspase-1.

90 uals affected by autism spectrum conditions (ASC) are considerably heterogeneous.

91 ostic feature of autism spectrum conditions (ASC).

92 Although weakly and strongly connected ASCs are similar from an organizational perspective, unc

93 Imaging of MLKL-dependent ASC speck formation demonstrated that necroptotic stimul

94 t only antigen-primed, peripheral GC-derived ASC infiltrate the CNS, thereby limiting potentially har

95 Ptn stimulated human adipose tissue derived ASCs to differentiate into lipid-laden adipocytes by upr

96 asia and is functionally required for dermal ASC proliferation.

97 equiaxial strain favorable to differentiate ASCs towards AF lineage and that ASCs-embedded biphasic

98 , we find replicable evidence for 5 discrete ASC subgroups that are highly differentiated in item-lev

99 d pro-caspase-1 but not with NALP3, disrupts ASC speck formation through its CARD, and impairs the AS

100 d at steady-state consists of three distinct ASC populations.

101 3, caspase-1, and caspase-recruiting domain (ASC).

102 a caspase activation and recruitment domain (ASC) and trigger caspase-1 processing of the proinflamma

103 ike protein with caspase recruitment domain (ASC) measured in the serum of Schnitzler syndrome patien

104 ein containing a caspase recruitment domain (ASC) micrometer-sized perinuclear structures (specks).

105 ein containing a caspase recruitment domain (ASC), cysteine aspartase (caspase)-1, and interleukin (I

106 ining C-terminal caspase recruitment domain (ASC), or pro-IL-1beta prevented the hyperglycemia-induce

107 a caspase activation and recruitment domain (ASC)-dependent inflammasome in response to infection.

108 a caspase activation and recruitment domain (ASC).

109 sh, describing the molecular domains driving ASC speck assembly and identifying a key role for macrop

110 are hypersensitive to Wnt activation during ASC differentiation.

111 many autophagy-related genes changes during ASC differentiation.

112 38 (syndecan-1), which is upregulated during ASC maturation, is required in a cell-intrinsic manner t

113 cial network analysis, we then measured each ASC's strength of connection to nearby hospitals on the

114 ive but HPV 16/18-negative women with either ASC-US or LSIL.

115 or CIN3+ was about 70% for women with either ASC-US or LSIL.

116 tools has prevented the study of endogenous ASC dynamics, we generated a live ASC reporter through C

117 ures allowed the visualization of endogenous ASC(PYD) filaments for the first time.

118 opy to track fluorescently tagged endogenous ASC in the zebrafish, describing the molecular domains d

119 mesenchyme-targeting growth factor, enhanced ASC differentiation into pericytes but overstimulated th

120 entified signal with AR degradation enhancer ASC-J9 may help us to better suppress the melanoma metas

121 ntly, 83% of the $4.3 billion in charges for ASC-based care originate from facilities that have subst

122 ensive survey of the materials developed for ASC electrodes, as well as covering the progress made in

123 is reduced in aged ASCs and is required for ASC proliferation and maintenance in the dermis, but not

124 Because most are freestanding, ASCs may have little connection to local health systems,

125 state cancer cell viability, whereas CM from ASCs that received no iAs exposure decreased cell viabil

126 ted B cells' (ABCs), that were distinct from ASCs and were committed to the MBC lineage.

127 Conditional medium from ASCs, but not differentiated adipocytes, promoted DP mar

128 -principle for the view that newly generated ASCs can acquire a mature PC phenotype that is accompani

129 ells of undetermined significance (hereafter ASC-US cytology).

130 ll intestine, probably reflecting their high ASC division rate.

131 In IL-6 and APRIL-deficient hosts, ASCs underwent extensive apoptosis independently of CD13

132 ch specifically recognizes the CARD of human ASC via its type II interface.

133 Ptn-primed human ASCs seeded in 3D-bioprinted biomaterial scaffolds yield

134 of differentiating into peanut-specific IgE ASCs.

135 We show that BM natural IgM ASC arise from a fetal-lineage progenitor that is neithe

136 at is neither B1a nor B1b, and that this IgM ASC compartment contains a substantial fraction of long-

137 VHHASC not only impairs ASC(CARD) interactions in vitro, but also inhibits infla

138 iposarcoma but also promotes adipogenesis in ASC.

139 some evaluation, which detects the change in ASC distribution within the cell.

140 HMOX1 and a decrease in THBS1 expression in ASC following iAs exposure.

141 nd identifying a key role for macrophages in ASC speck removal in vivo.

142 g and spreading of amyloid-beta pathology in ASC-deficient APPSwePSEN1dE9 mice.

143 d that autophagy played an important role in ASC differentiation on the PCL+FA scaffold.

144 imeric complex formation previously shown in ASC PYD fibril assemblies.

145 m a decrease in stromal TGFbeta signaling in ASC following iAs exposure.

146 s a direct PDGFA target that is activated in ASCs during WAT hyperplasia and is functionally required

147 We demonstrate that alphaSMA expression in ASCs is induced by chemokine signalling and mediates the

148 e determine genome-wide mutation patterns in ASCs of the small intestine, colon and liver of human do

149 ly invasive cataract procedures performed in ASCs and HOPDs.

150 sting that intrinsic mutational processes in ASCs can initiate tumorigenesis.

151 l niches as dominated by PPARalpha signal in ASCs to induce the greater hair induction than MA-DPS or

152 rmore, we showed that Wnt signaling inhibits ASC differentiation possibly through repression of Blimp

153 uding memory B cells that differentiate into ASC soon after contact with the infective virus.

154 IL-1beta produced by a T(H)17 cell-intrinsic ASC-NLRP3-caspase-8 inflammasome during inflammation of

155 ath induction in vivo requires a full-length ASC.

156 enge, we measured increased antibody levels, ASCs and HAI titers with reduced viral load and inflamma

157 endogenous ASC dynamics, we generated a live ASC reporter through CRISPR/Cas9 tagging of the endogeno

158 t IgE levels may be maintained by long-lived ASCs.

159 We have found indication of short-lived ASCs in the local lymphoid tissue, further evidence of a

160 ASCs, indicating the presence of short-lived ASCs, a hallmark of a T-independent 2 (TI-2) antigenic r

161 Liver ASCs, however, have different mutation spectra compared

162 d early in the CNS do not give rise to local ASC differentiation and that only antigen-primed, periph

163 xpression and activity as evidenced by lower ASC (apoptosis-associated speck-like protein containing

164 High-molecular mass ASC complexes were also detected, consistent with oligom

165 el in which CD138 expression on fully mature ASCs provides a selective survival advantage over less m

166 val advantage over less mature, newly minted ASCs, by enhancing pro-survival cytokine signaling.

167 ination, CD19(pos), CD19(low), and CD19(neg) ASCs secrete vaccine-specific Abs and show linked IGHV r

168 Next, ASCs isolated from rats were co-cultured with DP spheres

169 tes the inflammasome through an AIM2, NLRP3, ASC, and caspase-1 dependent process.

170 sitive significant correlations among NLRP3, ASC, and IL-1beta salivary concentrations and clinical p

171 deficient for inflammasome components NLRP3, ASC (apoptosis speck-like protein containing a caspase a

172 expressions of inflammasome markers (NLRP3, ASC, and caspase-1, and IL-1beta).

173 26) displayed increased expression of NLRP3, ASC (a CARD protein), caspase-1, and IL-1beta proteins,

174 macological inhibition or deletion of NLRP3, ASC (apoptosis-associated speck-like protein containing

175 d/or its severity, salivary levels of NLRP3, ASC, and IL-1beta may act as strong/independent indicato

176 d a strong/independent association of NLRP3, ASC, and IL-1beta salivary levels with CP and AgP.

177 Significantly higher levels of NLRP3, ASC, and IL-1beta were detected in periodontitis groups

178 he proteins of inflammasome pathways, NLRP3, ASC, caspase 1, IL-1 and IL-18.

179 Activation of NLRP3-ASC inflammasome led to the up-regulation of caspase-1 a

180 ntuates the priming of Nlrp3, promotes Nlrp3-ASC inflammasome assembly, and results in the activation

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

182 hology in the facility/hospital (nonfacility/ASC)-based setting was $65 to $190 ($25-$71) depending o

183 he rates and patterns of mutations in normal ASCs remain unknown.

184 eus, and inhibited the assembly of the NRLP3/ASC/caspase-1 complex.

185 Three subgroups comprising 45-62% of ASC adults show evidence for large impairments (Cohen's

186 ments via ASC(CARD) mediates the assembly of ASC foci.

187 osphate, P5P) modulates the self-assembly of ASC, we rationally designed an N-terminal capped nonapep

188 VHHASC leaves the Pyrin domain of ASC functional and stabilizes a filamentous intermediate

189 ear-atomic structures of the PYRIN domain of ASC in the protein filament of inflammasomes and the obs

190 ut not Hsf1, blocks the protective effect of ASC-JM17 on mutant AR-induced eye degeneration in flies.

191 ring the progress made in the fabrication of ASC devices over the last few decades.

192 involves inflammasome-dependent formation of ASC specks in microglia.

193 e we show that intrahippocampal injection of ASC specks resulted in spreading of amyloid-beta patholo

194 se pathogenesis; although elevated levels of ASC, IL-6, and IL-18 in patients' serum, and the respons

195 These data revealed that cross-linking of ASC(PYD) filaments via ASC(CARD) mediates the assembly o

196 uctural data, we propose molecular models of ASC.ASC and ASC.NLRP3 PYD early supramolecular complexes

197 NLRPs/ALRs and ASC to prevent nucleation of ASC and therefore prevent an oligomeric platform for cas

198 proposed to depend on the lifetime number of ASC divisions, owing to unavoidable random mutations tha

199 LRP3 and the adaptor ASC, oligomerization of ASC and activation of caspase-1.

200 ium orthovanadate-induced phosphorylation of ASC Y144, necessary and sufficient for Nlrp3 inflammasom

201 ASC and interfering with the recruitment of ASC to upstream sensors, which prevents caspase-1 activa

202 In NLRP3 knockout mice, up-regulation of ASC, caspase-1, and IL-1beta were all reduced, and, impo

203 nt signaling as a physiological regulator of ASC differentiation and establish a role for the Wnt pat

204 owth to uncover an unrecognized regulator of ASC self-renewal and proliferation, PDGFA, which activat

205 ssed in living cells, highlighting a role of ASC in all three types of inflammasomes.

206 ctivity impedes the adipogenic capability of ASCs at early but not late stages of adipogenesis, which

207 Pre-conditioning of ASCs using ascorbic acid (AA) or hypoxic conditions prov

208 d induced region-specific differentiation of ASCs within the inner and outer regions of the biphasic

209 ling and mediates the stimulatory effects of ASCs on endothelial cells.

210 llenges and a future outlook of the field of ASCs are also discussed.

211 Recent progress made in the field of ASCs is critically reviewed, with the main focus on an e

212 e found that the canonical surface marker of ASCs, CD138 (syndecan-1), which is upregulated during AS

213 ogenic differentiation and mineralization of ASCs in the 3-dimensional model.

214 ermine their interactions; a mixed sphere of ASCs with DP cells (MA-DPS), or a core-shell structure,

215 epots are compromised compared with those of ASCs from subcutaneous depots, but little is known about

216 of CD138 increased heparan sulfate levels on ASCs, which are known to bind pro-survival cytokines, le

217 s (MA-DPS), or a core-shell structure, outer ASCs shell and an inner DP core (CSA-DPS).

218 lowing Tyr146 phosphorylation to participate ASC speck formation and subsequent NLRP3 inflammation.

219 2, but not FAK, could directly phosphorylate ASC at Tyr146, and only the phosphorylated ASC could par

220 activation, and secretion of phosphorylated ASC were inhibited by ethanol.

221 e ASC at Tyr146, and only the phosphorylated ASC could participate in speck formation and trigger IL-

222 ctivation, only Pyk2 directly phosphorylates ASC and brings ASC into an oligomerization-competent sta

223 Early polyclonal ASC expansion, GC formation, and virus-specific ASC were

224 he NLRP3 and AIM2 inflammasome by preventing ASC oligomerization and may be a potential therapeutic c

225 Mechanistically, PGAM5 promotes ASC polymerization, maintenance of mitochondrial integri

226 study demonstrates that antiviral protective ASC in the CNS are dependent on CD19 activation and peri

227 s JHMV infection, infiltration of protective ASC occurs after T cell-mediated viral control and is pr

228 se-1 activation requires the adaptor protein ASC (apoptosis-associated speck-like protein containing

229 lammasome complexes with the adaptor protein ASC and caspase-1 that result in the activation of caspa

230 ibed that recruit the common adaptor protein ASC to activate caspase-1, leading to the secretion of m

231 was dependent on NLRP3, its adaptor protein ASC, or caspase 1, the cleavage of intracellular pro-IL-

232 independently of NLRP3, its adaptor protein ASC, or caspase 1.

233 by recruiting NLRP3 and its adaptor protein ASC.

234 The inflammasome adaptor protein, ASC, contributes to both innate immune responses and inf

235 The inflammasome complex proteins ASC (apoptosis-associated speck-like protein containing

236 QUC reduced ASC speck formation and ASC oligomerization compared wit

237 efore reveal active mechanisms that regulate ASC self-renewal in the skin and show that distinct regu

238 uncover the molecular mechanisms regulating ASC specification in vivo.

239 nger-signaling sensor NLRP1 does not require ASC because NLRP1 contains a C-terminal CARD domain that

240 LPC-activated inflammasome also requires ASC (apoptotic speck containing protein with a CARD), ca

241 followed by production of mitochondrial ROS, ASC speck formation and caspase-1 activation.

242 We found that pre-seeded ASCs differentiated into pericytes and stabilized the en

243 nt, proliferation and survival of the seeded ASCs, and up-regulates the expression of their neurotrop

244 Furthermore, several ASC progeny markers were downregulated, and regeneration

245 squamous cells of undetermined significance (ASC-US) or low-grade squamous intraepithelial lesions (L

246 squamous cells of undetermined significance (ASC-US) or low-grade squamous intraepithelial lesions (L

247 squamous cells of undetermined significance (ASC-US), a cervical scrape specimen was taken, placed in

248 show high similarity to the tissue-specific ASC mutation spectra, suggesting that intrinsic mutation

249 The presence of a virus-specific ASC response serves an early cellular marker of an EV71-

250 expansion, GC formation, and virus-specific ASC were all significantly impaired in CLN of CD19(-/-)

251 By simultaneously analyzing antigen-specific ASCs and ABCs in human blood after vaccination against i

252 lymphoid tissue had detectable FMDV-specific ASCs in the absence of circulating FMDV-specific ASCs, i

253 in the absence of circulating FMDV-specific ASCs, indicating the presence of short-lived ASCs, a hal

254 We see strong ASC expression in the skin and other epithelia that act

255 Asymmetric supercapacitors (ASCs) assembled using two dissimilar electrode materials

256 both PCL+FA and PCL scaffolds could sustain ASC growth but only the PCL+FA scaffold could sustain ce

257 mulation of virus-specific, isotype-switched ASC requires CD19-dependent GC formation in CLN.

258 We found that ASC self-associates and binds NLRP3 PYD through equivale

259 Here, we show that ASC is highly expressed in a model of medulloblastoma, t

260 We show that ASC-JM17 ameliorates toxicity of the mutant androgen rec

261 Our data suggest that ASC recruitment to tumours, driven by CXCL1 and CXCL8, p

262 fferentiate ASCs towards AF lineage and that ASCs-embedded biphasic scaffold can potentially be utili

263 Thus, we provide strong evidence that ASCs ameliorate inflammation-induced systemic bone loss

264 Literature suggests that ASCs exhibit cancer-promoting properties, influence/are

265 The ASC-mediated stabilization of the ECs clearly reduced va

266 nt progress on the filament formation by the ASC (apoptosis-associated speck-like protein containing

267 formation through its CARD, and impairs the ASC and pro-caspase-1 interaction.

268 extent of somatic hypermutation (SHM) in the ASC (effector) and ABC (memory) lineages.

269 Assembly of the ASC speck is critical for signaling by the inflammasome.

270 This study reveals that the ASC speck can present different oligomerization assembli

271 Furthermore, our data suggest that the ASC-NLRP3 inflammasome is responsible for QS-21-induced

272 ted by the kinase Syk and relocalizes to the ASC specks upon NLRP3 inflammasome activation.

273 neate robust natural subdivisions within the ASC population that may allow for more individualized in

274 ight chain 3 (LC3)-II protein changes of the ASCs grown on the 2- or 3-dimensional environments at 6

275 inhibits inflammasome assembly by binding to ASC and interfering with the recruitment of ASC to upstr

276 ture by NMR and characterized its binding to ASC PYD.

277 xial strains and frequencies were applied to ASCs-encapsulated scaffolds to identify the optimal load

278 MRI as a reliable method with which to track ASCs after transplantation to skin wounds.

279 nes were immobilized to the PCL to transduce ASCs upon seeding, and constructs were cultured in chond

280 hat, despite being short-lived, transplanted ASCs can accelerate wound-healing and reduce hair loss i

281 Bioluminescent imaging (BLI) of transplanted ASCs revealed a gradual loss of transplanted cells, with

282 is required for the obesity-dependent tumour ASC recruitment, vascularization and tumour growth promo

283 e, there is a trend toward fewer unconnected ASCs over time (P = 0.080).

284 Mechanisms underlying ASC trafficking are unclear.

285 triggered T cell production of IL-1beta via ASC-NLRP3-dependent caspase-8 activation.

286 that cross-linking of ASC(PYD) filaments via ASC(CARD) mediates the assembly of ASC foci.

287 endogenous level of RA is higher in visceral ASCs; this is associated with upregulation of the RA syn

288 r-mass NLRP3-NEK7 complex, which, along with ASC oligomerization and ASC speck formation, was abrogat

289 e-8 assembles with FADD at the DISC and with ASC at the inflammasome through its tandem death effecto

290 Concomitantly, we observe that cells with ASC phenotype are mobilized and infiltrate tumours in ob

291 NALP3 inflammasome complex by competing with ASC for pro-caspase-1 binding.

292 e, caspase-1 and caspase-8 can interact with ASC to mediate secretion of IL-1 cytokines.

293 matically inactive caspase-1 interacted with ASC longer and with increased intensity compared with WT

294 administered to synaesthetes and people with ASC.

295 od-quality studies involving 8587 women with ASC-US and 5284 with LSIL were found.

296 od-quality studies involving 8587 women with ASC-US and 5284 with LSIL were found.

297 was 83% (95% CI, 80% to 86%) for women with ASC-US and 76% (CI, 74% to 79%) for those with LSIL.

298 17% and 19% in HPV 16/18-positive women with ASC-US and LSIL, respectively, and was 5% in hrHPV-posit

299 ssembling of a core-shell sphere for DP with ASCs could reconstruct the HF cellular arrangement for h

300 ognitive datasets of adults with and without ASC (n = 694; n = 249), we find replicable evidence for