ライフサイエンスコーパス: ASC

1 ASC downregulate their surface BCR upon differentiation,

2 ASC were also significantly reduced in the CNS, resultin

3 ASC-1 depletion in C2C12 and in patient-derived fibrobla

4 ASCs are highly dependent on exogenous soluble factors s

5 ASCs were isolated from clinical lipoaspirates and cultu

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

7 , LRR, and PYD domain-containing protein 3), ASC (apoptosis-associated speck-like protein containing

8 Using C57BL/6 ASC-mCitrine transgenic inflammasome reporter mice, we s

9 In Abdsc ASCs, low concentrations of dexamethasone suppressed TGF

10 compared with abdominal subcutaneous (Abdsc) ASCs was associated with greater secretion of TGFbeta li

11 bitor 1 (PAI-1), which was the most abundant ASC adipokine, led to reversal of cellular distribution

12 Accordingly, ASCs cultured in scaffolds with thicker fibers were more

13 tralis, suggesting that rickettsiae activate ASC inflammasome via a Toll-like receptor 4 (TLR4)-depen

14 y showed that Rickettsia australis activates ASC inflammasome in macrophages.

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

16 ally inhibits NLRP3 inflammasome activation, ASC speck formation and pyroptosis.

17 t caspase-1, but not its upstream activator, ASC, contributes to oviduct pathology during mouse genit

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

19 Caspase-1 and its adaptor ASC contributed to the perinatal lethal phenotype becaus

20 ased IL-18, IL-1beta, caspase-1 activity and ASC speck release (Scambler et al. eLife 2019).

21 s of IL-18, IL-1beta, caspase-1 activity and ASC-speck release in monocytes, epithelia and serum with

22 coronavirus to track virus-specific Bmem and ASC, this report demonstrates that both subsets only eme

23 he molecular trajectories of B cell fate and ASC formation.

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

25 lls highlighting its importance in iBMSC and ASC adipogenesis and circadian biology.

26 embles an inflammasome complex with NEK7 and ASC to activate caspase-1 and drive the maturation of pr

27 , we show that IRGM interacts with NLRP3 and ASC and hinders inflammasome assembly by blocking their

28 asdermin D, and the recruitment of NLRP3 and ASC into a novel RIPK1 kinase activity-independent cell

29 elective autophagic degradation of NLRP3 and ASC.

30 semble into a linear molecular platform, and ASC is recruited to form higher molecular structures, in

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

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

33 -derived macrophages (BMMs) of TLR4(-/-) and ASC(-/-) mice were significantly greater than those in B

34 ared with the tumour parenchyma, B cells and ASCs were preferentially localized in the tumour stroma,

35 tivated B cells, germinal centre B cells and ASCs within the tumour microenvironment.

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

37 ssemble into cytosolic compartments known as ASC specks to facilitate the activation of caspase-1.

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

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

40 ms with or without cardiomyopathy, associate ASC-1 depletion with isolated primary muscle involvement

41 that the administration of the bioengineered ASCs in combination with irinotecan prodrug in the desig

42 experimental ectopic cRel expression blocked ASC differentiation by inhibiting the transcription fact

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

44 The assembly is mediated by ASC self-association and protein interactions via its tw

45 r data suggest that persistent repression by ASC adipokines leads to promoter hypermethylation of GJA

46 ciated speck-like protein containing a CARD (ASC) oligomerization and speck formation.

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

48 ciated speck-like protein containing a CARD (ASC) speck; cleavage of caspase-1 and gasdermin D; relea

49 ciated speck-like protein containing a CARD (ASC)-speck formation and caspase-1 activation by NLRC4-H

50 e protein surfaces involved in the ASC(CARD)-ASC(CARD) interaction.

51 All mutations caused ASC-1 protein depletion.

52 mma) and long-lived antibody-secreting cell (ASC) responses, the roles for IFN-gamma and IFN-gamma-in

53 iming) will delay adipose-derived stem cell (ASC) transition to a pro-fibrotic phenotype, expanding t

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

55 ections, with antibody (Ab)-secreting cells (ASC) contributing to local protection.

56 Ab-secreting cells (ASC) or plasma cells are essential components of the hum

57 and differentiation into Ab-secreting cells (ASC)-a finding that coincided with increased AgR signali

58 fferentiating into antibody-secreting cells (ASC).

59 idence indicates that adipose stromal cells (ASC) are recruited to enhance cancer development.

60 studies indicate that adipose stromal cells (ASC), the progenitors of adipocytes, are recruited by tu

61 of Mp-specific IgM antibody-secreting cells (ASCs) by enzyme-linked immunospot (ELISpot) assay allowe

62 c immunoglobulin M antibody-secreting cells (ASCs) by enzyme-linked immunospot assay allowed for diff

63 munoglobulin (Ig)M antibody-secreting cells (ASCs) improved diagnosis of Mp infection.

64 Antibody-secreting cells (ASCs) or plasma cells secrete antibodies and form a corn

65 HBsAg-specific antibody-secreting cells (ASCs) response was not different between these groups, y

66 HPV-specific antibody secreting cells (ASCs) were present in the tumour microenvironment, with

67 fferentiation into antibody-secreting cells (ASCs).

68 ponses in the biology of Ab-secreting cells (ASCs).

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

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

71 the lineages of adipose-derived stem cells (ASCs) and bone marrow-derived MSCs (BMSCs).

72 Adipose-derived stem cells (ASCs) are a potential adult mesenchymal stem cell source

73 Adipose-derived stromal/stem cells (ASCs) are multipotent in nature that can be differentiat

74 Adipose-derived stem cells (ASCs) can be chemically differentiated towards a SC-like

75 confirming that adipose-derived stem cells (ASCs) exhibit enriched colocalization with endothelial c

76 th factor conditions, such adult stem cells (ASCs) grow as 3D organoids that recapitulate essential f

77 Human adipose-derived stem cells (ASCs) have potential to improve wound healing; however,

78 t and differentiation of adipose stem cells (ASCs) is associated with adipose tissue inflammation and

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

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

81 Adipose-derived stem cells (ASCs) were genetically engineered to express recombinant

82 are expressed in adipose-derived stem cells (ASCs).

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

84 st differentiation of adipose stromal cells (ASCs) independent of bulk stiffness.

85 y associated with adventitial stromal cells (ASCs), a mesenchymal fibroblast-like subset that express

86 ction of aromatase in adipose stromal cells (ASCs).

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

88 e, the goal of our study was to characterize ASCs isolated from the subcutaneous fat of domestic pigs

89 edictors of colectomy, acute severe colitis (ASC), chronically active pediatric UC, cancer and mortal

90 Acid-soluble collagen (ASC) derived from a mixed by-product of different fish s

91 iatric disorders: autism spectrum condition (ASC), bipolar disorder (BD), major depressive disorder (

92 ostic feature of autism spectrum conditions (ASC).

93 The widely conserved ASC-1 complex (ASCC) containing the ASCC3 helicase disas

94 ESBL-E through active surveillance cultures (ASC) and the implementation of contact precautions (CP)

95 Our goal was to define ASC-1 neuromuscular function and the phenotypical spectr

96 then applied to show that locally delivered ASCs have enriched colocalization with murine retinal mi

97 g and TLR7/8 ligand and that IL-21 dependent ASC formation is significantly enhanced by IFNgamma or I

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

99 transducing events that ultimately determine ASC differentiation.

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

101 l role of the secretome from differentiating ASCs in the vascular development and its integration wit

102 with elevated myofibroblast differentiation, ASCs in scaffolds with thicker fibers exhibited a more p

103 Deep learning-based direct ASC at whole-body PET is feasible and potentially can be

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

105 ed version of ASC with only the CARD domain (ASC(CARD)) forms different filaments (~3-4-nm width), pr

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

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

108 ein containing a caspase recruitment domain (ASC).

109 ll fate programming and heterogeneity during ASC differentiation using T cell-independent models.

110 cells cRel was dynamically repressed during ASC differentiation by Blimp1 binding the Rel locus.

111 38 (syndecan-1), which is upregulated during ASC maturation, is required in a cell-intrinsic manner t

112 a shared ASC signature was identified, each ASC isotype-specific population expressed distinct trans

113 compared BCR clonotypes and found that each ASC isotype contained a unique, clonally related CDR3 re

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

115 caspase-8, enabling its prodomain to engage ASC.

116 tochemistry results show that the engineered ASCs actively targeted and localized at both tumor strom

117 of NLRP3 inflammasome signaling and exosomal ASC release.

118 lation in the CNS, late GC reactions favored ASC accumulation, although Bmem outnumbered ASC in drain

119 Finally, ASC can be further subseted based on their differential

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

121 SC70, and an increase in its ability to form ASC specks and activate caspase-1.

122 al reprogramming in order to ultimately form ASC.

123 thin the Akt1 pathway in CD4(+) T cells from ASC and SCZ patients, in addition to increased correlati

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

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

126 -induced osteogenic differentiation of human ASC (hASCs) in vitro.

127 Thus, in human ASCs growth factor-like gene regulation is transiently i

128 s study, we dissect such a response in human ASCs using an in vitro model.

129 They also identify ASC-1 as a novel cell cycle regulator with a key role in

130 iposarcoma but also promotes adipogenesis in ASC.

131 gamma-induced transcription factors (TFs) in ASC development are unclear.

132 ired host control of R. australis in vivo in ASC(-/-) mice was associated with dramatically reduced l

133 In ASCs, treatment with PGE(2), which is increased in obese

134 medium induced downregulation of miR-145 in ASCs and promoted endothelial differentiation.

135 rmore, in vivo, downregulation of miR-145 in ASCs enhanced angiogenesis in subcutaneously implanted p

136 Downregulation of miR-145 in ASCs induce vascular network formation in ischemic muscl

137 Upregulation of miR-145 in ASCs, by mimic miR-145, suppressed ETS1 expression and c

138 Modulation of miR-145 in ASCs, using a miR-145 inhibitor, regulated their differe

139 ulted in significantly higher fold change in ASCs among patients with HBsAg <100 IU/ml compared to pa

140 h a significant shift in response to SDF1 in ASCs with amplified ERK1/2 activation, growth factor-lik

141 cking bFGF-receptor or PI3K/AKT signaling in ASCs increased miR-145 levels.

142 estrain cell-autonomous TGFbeta signaling in ASCs to facilitate adipogenesis and healthy remodeling i

143 on by AIM2, which induced GSDMD-independent, ASC-, and caspase-8-dependent apoptosis.

144 transcriptome profile of osteogenic induced ASCs to understand the associated genotype changes.

145 bFGF released by ECs induces ASCs differentiation toward ECs through miR-145-regulate

146 During helminth infection, ASC depletion impaired lung ILC2 and Th2 cell accumulati

147 h patients are at risk of ESBL-E infections, ASC results appear of limited value to rationalize the e

148 computational analysis to investigate intact ASC structures.

149 stimulated to divide and differentiate into ASC upon Ag re-encounter when Ag-specific IgG levels dec

150 ded, class switched, and differentiated into ASC in response to Ag in vivo, but this was inhibited in

151 activated inflammatory effector B cells into ASCs in the setting of IFN-gamma-, but not IL-4-, induce

152 cell-induced differentiation of B cells into ASCs.

153 ation on the filaments formed by full-length ASC is needed to construct a meaningful model of inflamm

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

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

156 ther these changes were functionally linked, ASCs were utilized.

157 bet was required for formation of long-lived ASCs and secondary ASCs following viral, but not nematod

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

159 tissue TGFbeta signaling activity and lower ASC differentiation.

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

161 icance of charge complementarity in the M013-ASC-1 interaction was further confirmed by functional as

162 S recruitment of tdTomato(+) B cells, mainly ASC, primed late during GC reactions.

163 We find that maximal ASC induction requires at least eight cell divisions in

164 umes had plasma exosomes that contained more ASC than did those from a matched control group.

165 Moreover, ASC-J9, an AR degradation enhancer, suppressed FAK/CAT-i

166 Here, we aimed to describe Mp ASC kinetics and duration in comparison to conventional

167 The Mp ASC response correlated with clinical disease, but it di

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

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

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

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

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

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

174 This is dependent on NLRP3, ASC, caspase-1, and NEK7, but not on NLRC4, NLRP1, NLRP6

175 levels of the NLRP3-related proteins NLRP3, ASC, and pro-casp1 were upregulated in BD patients, foll

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

177 ctivation-by both direct inhibition of NLRP3/ASC oligomerization and selective autophagic destruction

178 nd selective autophagic destruction of NLRP3/ASC.

179 activation of pro-caspase-1 within the NLRP3/ASC preinflammasome through its association with Flightl

180 ow that deubiquitination inhibited the NLRP6-ASC inflammasome complex and regulated the maturation of

181 Meanwhile, the non-ASC branch expresses an inflammatory signature, and main

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

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

184 suggesting that PAI-1 may mediate actions of ASC on transcriptional regulation in EEC.

185 ese observations indicate that activation of ASC inflammasome, most likely driven by interaction of T

186 CLCs into the lungs promoted the assembly of ASC complexes in infiltrating immune cells (neutrophils

187 ecent studies have challenged the benefit of ASC and CP in controlling the spread of ESBL-E in ICUs w

188 Binding of ASC to pyrin by a PYD-PYD interaction triggers inflammas

189 requency, area, and cellular distribution of ASC specks and caspase-1 activity in mouse and human cel

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

191 mutant CASP8(C362A) induces the formation of ASC (also known as PYCARD) specks, and caspase-1-depende

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 ssion serving as a potential early marker of ASC fate commitment.

196 and compare the gene expression programs of ASC subsets that were responding to the same Ags followi

197 ion of Bmem dominated over the proportion of ASC throughout infection.

198 ly comprised mainly Bmem, the proportions of ASC and Bmem became similar as tdTomato(+) B cells incre

199 h K(+) efflux, leading to the recruitment of ASC and activation of caspase-1.

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

201 Here, we investigated the role of ASC in cancer chemoresistance and invasiveness, the attr

202 to pre-existing filaments match the size of ASC dimer structures generated by NMR-based protein dock

203 at the presence of NLRP3 reduces the size of ASC specks, which is further reduced by the presence of

204 In the present study, host susceptibility of ASC inflammasome-deficient mice to R. australis was sign

205 A truncated version of ASC with only the CARD domain (ASC(CARD)) forms differen

206 Truncated versions of ASC have been shown to form filaments, but information o

207 e effect of ET1 on enhancing adipogenesis of ASCs and osteogenesis of BMSCs was attenuated by blockin

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

209 Examining the effects of ASCs on the transcriptome of endometrial epithelial cell

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 growth factor) released by ECs as inducer of ASCs differentiation through receptor-induced AKT (prote

213 murine hindlimb ischemia model injection of ASCs with downregulated miR-145 induced collateral flow

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

215 ngiogenic markers during the osteogenesis of ASCs.

216 We analyzed subpopulations of ASCs and BMSCs with or without ETAR and/or ETBR, and we

217 TBR(-) and ETAR(-)/ETBR(+) subpopulations of ASCs and those of BMSCs pretreated with ET1 were prone t

218 Inhibition of TGFbeta signaling rescued Om ASC differentiation.

219 Om ASCs were resistant to these dexamethasone effects; reco

220 and function, which are in part dependent on ASC-derived IL-33.

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

222 ASC accumulation, although Bmem outnumbered ASC in draining lymph nodes throughout infection.

223 attenuation- and scatter-corrected PET (PET(ASC)).

224 ated quantitatively high similarity with PET(ASC).

225 Physiological ASCs survive in niche microenvironments, but how niche s

226 ygen levels has not been demonstrated in pig ASCs.

227 Mycoplasma pneumoniae ASCs measured by enzyme-linked immunospot assay were ass

228 Mycoplasma pneumoniae ASCs of the isotype IgM were found in 29 (46%), IgG were

229 Mycoplasma pneumoniae ASCs were detected from 2 days to a maximum of 6 weeks a

230 Mycoplasma pneumoniae ASCs were undetectable in HCs, in contrast to detection

231 (neg) (DN2) pre-antibody secreting cell (pre-ASC) subset.

232 strate that naive B cells form T-bet(hi) pre-ASCs following stimulation with either Th1 cells or with

233 elial cell-conditioned medium-preconditioned ASCs; whereas, overexpression of ETS1 reversed the abrog

234 Predifferentiated ASCs and BMSCs were treated with ET1 for 2 cell passages

235 s showed that adipogenesis of ET1-pretreated ASCs and osteogenesis of ET1-pretreated BMSCs were incre

236 of the ASC differentiation circuit prevented ASC generation in simulations.

237 e program that, if not restrained, prevented ASC formation.

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

239 Primary ASCs isolated from rat and human subcutaneous fat exhibi

240 Soft primed ASCs injected into our rat model of post-traumatic elbow

241 IFNgamma promotes ASC development by synergizing with IL-2 and TLR7/8 liga

242 However, the mechanism that promotes ASCs differentiation toward endothelial cells (ECs) is n

243 The adapter protein ASC assembles inflammasome components by acting as a mol

244 transfer of the inflammasome adaptor protein ASC in exosomes.

245 ing apoptosis-associated speck-like protein (ASC) containing CARD, caspase-1, interleukin-1beta (IL-1

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

247 pro-survival stress granules and pyroptotic ASC specks.

248 proach to simultaneously detect and quantify ASC specks and caspase-1 activity, both at the populatio

249 ILC2s and IL-13 drove reciprocal ASC expansion and IL-33 expression.

250 that the NLRP6 PYD filament uses to recruit ASC PYD.

251 QUC reduced ASC speck formation and ASC oligomerization compared wit

252 r formation of long-lived ASCs and secondary ASCs following viral, but not nematode, infection.

253 Intriguingly, whereas a shared ASC signature was identified, each ASC isotype-specific

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

255 Similarly, ASCs responding to survival conditions initially induce

256 e transcriptional programming of Ag-specific ASC populations.

257 suggesting a localized and antigen-specific ASC response.

258 HPV-specific ASC responses correlated with titres of plasma IgG and w

259 xpression allowed tracking of virus-specific ASC and Bmem in priming and effector sites throughout in

260 Mycoplasma pneumoniae-specific ASCs are short-lived and associated with clinical diseas

261 ed for release of large inflammatory stimuli-ASC specks, mitochondria, nuclei, and bacteria.

262 aluating inflammasome-associated structures (ASC specks) and caspase-1 activity by microscopy is time

263 e caused by nigericin or ATP, and subsequent ASC oligomerization caused by several inflammasome-activ

264 er, a solid-state asymmetric supercapacitor (ASC) was built utilising the NiCo(2)O(4) nanosheets, car

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

266 TGF-beta3 supports ASC survival while having a limited effect on gene expre

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

268 with some transport taking place via system ASC.

269 ide D-CAN, previously developed for targeted ASC ablation, suppressed the obesity-associated EMT and

270 lymph nodes, tdTomato-positive (tdTomato(+)) ASC were most prevalent prior to germinal center (GC) fo

271 cell co-culture models, we demonstrate that ASC induce epithelial-mesenchymal transition (EMT) in pr

272 results for the first time demonstrate that ASC interaction renders cancer cells more migratory and

273 Our data demonstrate that ASC promote tumor aggressiveness and identify them as a

274 We show that ASC forms ~6-7-nm-wide filaments that stack laterally to

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

276 The ASC displayed great electrochemical properties with a 42

277 The ASC-destined branch requires induction of IRF4, MYC-targ

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

279 e distinct functions, it is not known if the ASC that secrete each isotype are also distinct.

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

281 ntified the protein surfaces involved in the ASC(CARD)-ASC(CARD) interaction.

282 nteractions into a mathematical model of the ASC differentiation circuit prevented ASC generation in

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

284 scular atrophy (SMA), and 3 mutations of the ASC-1 gene TRIP4 have been associated with SMA or congen

285 Recently, the ASC-1 complex has been identified as a mechanistic link

286 e conformational changes and can recruit the ASC adaptor using PYD-PYD interactions.

287 R-based protein docking, suggesting that the ASC dimer could be a basic building block for filament f

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

289 on via antigen presentation or conversion to ASC.

290 ry B-1b cell division and differentiation to ASC upon Ag restimulation.

291 rols the switch from B cell proliferation to ASC generation phases and hence the respective cell popu

292 from MDD on one end, through BD and SCZ, to ASC on the other end.

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

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

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

296 mmasome evaluation (TOFIE), cannot visualize ASC specks or caspase-1 activity, making colocalization

297 In vitro, ASCs produced TSLP that supported ILC2 accumulation and

298 adventitial niches are conserved sites where ASCs regulate type 2 lymphocyte expansion and function.

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

300 idues reveal their role in interactions with ASC-1.

301 administered to synaesthetes and people with ASC.

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