ライフサイエンスコーパス: type I

1 e narrow angles not as close as those of MPS type I.

2 ergic axonal projections exclusively reached type I acini in the SG of both Ixodes species.

3 In type I acini, the rich network of cholinergic axons term

4 e immune response and a modulatory impact on type I allergy is discussed.

5 of proteins that promote fibrosis (collagen type I alpha 1 chain, tissue inhibitor of metalloprotein

6 R-resident molecular chaperones for collagen type I and bone metabolism and a crucial role of HSP47 i

7 This finding suggests that type I and especially the less adverse effect-prone type

8 cartilage thickness on quantitative MRI and type I and II collagen C-telopeptide biomarkers.

9 targeted cell surface molecule, suggest the Type I and II curves are the primary nanomechanical resp

10 dentified that were associated with impaired type I and II IFN responses.

11 We previously reported that type I and II IFNs control MuPyV infection in non-centra

12 gnatures of nuclear factor-kappaB-dependent, type I and II interferon signaling, and leukocyte activa

13 hways relevant to the human disease, such as type I and II interferon signaling, cell-cell adhesion,

14 ssis infection in adult mice, revealing that type I and III IFN pathways may play an important role i

15 Ultimately, type I and III IFN signaling drove the expression of CXC

16 The ISGs stimulated in common by type I and III IFNs have strong interferon-stimulated re

17 However, pretreatment and posttreatment with type I and III IFNs significantly reduced virus replicat

18 CL9 and CXCL10, in a Dectin-1 and Card9- and type I and III interferon signaling-dependent manner, re

19 uced significantly higher expression of both type I and III interferons in IPEC-DQ cells than the par

20 This response is defined by low levels of type I and III interferons juxtaposed to elevated chemok

21 , and analysis of characteristic biomarkers (type I and III interferons) produced by PBMCs transfecte

22 repertoires were associated with interferon type I and III responses, early CD4(+) and CD8(+) T cell

23 ement of distinct recycling pathways for the type I and type II BMP receptors and highlights the impo

24 eus colonization, we examined the effects of type I and type II IFNs on S. aureus adherence and invas

25 ghly effective photodynamic therapy via both type I and type II mechanisms.

26 that persists in vitro and has properties of Type I and Type II priming.

27 tify two major classes of PVT neurons-termed type I and type II-that differ in terms of gene expressi

28 uction in human and mouse cell lines through type I and type III IFNs.

29 s or vaccines to this ongoing global threat, type I and type III interferons (IFNs) are currently bei

30 Analysis of phase-variable Type I and Type III restriction-modification systems in

31 and supports a developmental model in which Type-I and Type-II hair cells develop in parallel rather

32 ve as a signature to distinguish between the type-I and type-II Weyl semimetals.

33 dentified: one with a deflection transition (Type I) and another with a discontinuous transition (Typ

34 peptide shows that the central NPNA forms a type I beta-turn and is the main recognition motif.

35 Type I blocks all APC activities, whereas type II preser

36 Additionally, BMPR1, a type I BMP receptor normally required for BMP-mediated p

37 ed carboxyl-terminal telopeptide of collagen type I by 4% (95% CI: 1% to 8%; p = 0.02) compared with

38 o-EM structure of the Desulfovibrio vulgaris type I-C Cascade, revealing the molecular mechanisms tha

39 ssive nuclease Cas3, together with a minimal Type I-C Cascade-based system for targeted genome engine

40 Interestingly, the type I-C system employs a minimal Cascade effector compl

41 by true absence of a compound and the later type is caused by a technical detection limit.

42 The former type is caused by true absence of a compound and the lat

43 In normal monkeys, type I causes many adverse effects including animal deat

44 Type I cells (36% of total) displayed localised asynchro

45 Type I cells, and indeed overall density of Type I cells was reduced.

46 , but rates of inferred differentiation into Type I cells, and indeed overall density of Type I cells

47 protectin, osteocalcin, and N-telopeptide of type I collagen (NTx) levels were analyzed by ELISA.

48 deposition was accelerated with upregulated type I collagen and interleukin-1beta, and downregulated

49 the cell line faithfully reports changes in type I collagen expression with at least threefold enhan

50 r cells exposed to a physiological matrix of type I collagen fibers form elongated collagenolytic inv

51 Type I collagen is a key protein of most connective tiss

52 st levels of carboxy-terminal telopeptide of type I collagen were observed in ZOL (P < 0.05), and sho

53 The fibrotic areas mainly consisted of type I collagen with only a minor cellular component (es

54 However, type I collagen, RUNX2, type X collagen (CoL10A1), Oster

55 Deletion of IFT80 in type I collagen-positive cells led to a disorganized out

56 N-terminal peptide], CITP [C-telopeptide for type I collagen], IGFBP7 [insulin-like growth factor-bin

57 differential plasticity between the two cell types is coordinated.

58 mperate phages (which can become lysogenic), type I CRISPR-Cas immune systems cannot eliminate the ph

59 Type I CRISPR-Cas systems typically target foreign DNA f

60 protospacer adjacent motif (PAM) in several type I CRISPR-Cas systems, but how the prespacers are pr

61 Rather, elimination of type I cytokine interferon-gamma activity enhanced insul

62 Here we show that the Sulfolobus islandicus type I-D Cas10d large subunit exhibits an unusual domain

63 y preserved and morphologically complex cyst type is described from a 48 million year old early Eocen

64 ng multiple sclerosis, rheumatoid arthritis, type-I diabetes, and cancer.

65 -day mortality were: P: age, gender and ACLF type; I: drug, infection, surgery, and variceal bleeding

66 ocessed in systems lacking Cas4, such as the type I-E and I-F systems, is not understood.

67 In Escherichia coli, which has a type I-E system, Cas1-Cas2 preferentially selects prespa

68 ntify active regulons within a specific cell type, i.e., cell-type-specific regulons (CTSR), provides

69 A second novel sub-type, i.e., Type II cells (64% of total) generated rhyth

70 sociation between these conditions and gamer types (i.e., non-problematic, engaged, problematic and a

71 strikingly different responses of community types, i.e., the almost imperceptible response of mollus

72 utational inefficient or not able to control type I error and provide decent power for whole exome or

73 n simulations, PMR-Egger provides calibrated type I error control for causal effect testing in the pr

74 retation) and performs causal inference with type I error control.

75 eal WES data identified two major sources of type I error inflation in this case-only test: linkage d

76 In contrast, Census suffers from severe type I error inflation, whereas DEXSeq is more conservat

77 With an 80% statistical power and a type I error probability of 0.1, 48 patients were to be

78 We find that when the type I error rates are controlled to be the same for all

79 er than the Firth correction and can control type I error rates at the genome-wide significance level

80 analyze large-sample data (N > 400,000) with type I error rates well controlled.

81 at the new method is more powerful with less Type I error than the other two methods.

82 our trial, which may increase the risk of a type I error; and potential low statistical power to dem

83 esis testing, providing effective control of type I errors and yielding high statistical power.

84 We uncover 11 type I-F and/or I-E anti-CRISPR genes encoded on chromos

85 activation domain to Pseudomonas aeruginosa type I-F Cas proteins, we activate gene transcription in

86 SPR protein IF9 (AcrIF9) in complex with the type I-F CRISPR RNA-guided surveillance complex (Csy).

87 expression and activity of the P. aeruginosa Type I-F CRISPR-Cas system.

88 Furthermore, type I-F system activates target genes specifically with

89 ter the HFHC diet, IMTG content increased in type I fibres only (+101%; P < 0.001), whereas there was

90 distributed PLIN2 to lipid droplet stores in type I fibres.

91 mbrane potentials; the potassium efflux from type I hair cells results from the interdependent gating

92 ses confirmed the formation of an inhibitory type I heme-clobetasol complex in CYP3A5 but not in CYP3

93 erent classes of kinase inhibitors including types I, I(1)/(2), and II as well as allosteric inhibito

94 phils displayed significant up-regulation of type I IFN (IFN)-stimulated genes (ISGs).

95 Type I IFN (IFN-I) is thought to be rapidly internalized

96 macrophage death is dependent on the host's type I IFN (IFN-I) response.

97 Although TLRs are known to activate type I IFN (T1IFN) signaling, the role of T1IFN and IFN-

98 demonstrated the ability of ICP0 to inhibit type I IFN activity downstream of pathogen recognition r

99 Poly(I:C) or type I IFN administration was sufficient to cause breakt

100 Moreover, type I IFN alone was sufficient to induce cytokine and c

101 ssion of IFN-stimulated genes in response to type I IFN and leads to 1) promotion of cell-to-cell spr

102 this study, we identified and characterized type I IFN antagonism of MERS-CoV open reading frame (OR

103 on activation, and MERS-CoV ORF8b suppresses type I IFN expression by competing with IKKepsilon for i

104 cterial T6SS5-dependent cell fusion triggers type I IFN gene expression in the host and leads to acti

105 We also observed type I IFN gene expression, micronuclei formation, and d

106 of sfRNA to new susceptible cells to inhibit type I IFN induction before gRNA replication and without

107 e IECs, and the response of IEC organoids to type I IFN is strikingly increased in magnitude and scop

108 l inhibition of IFN-beta, a key component of type I IFN mechanisms to address its role in TBI pathoph

109 lymphopenic patients and decreased following type I IFN neutralisation with anifrolumab in the SLE ph

110 of indoles on goblet cells do not depend on type I IFN or on IL-22 signaling, pathways responsible f

111 1 tyrosine phosphorylation induced either by type I IFN or overexpressed Jak1, paralleling MARV VP40.

112 we determined the effects of hypoxia on the type I IFN pathway in breast cancer and the mechanisms i

113 models, mRNA and protein expressions of the type I IFN pathway were downregulated under hypoxic cond

114 out the relationship between hypoxia and the type I IFN pathway, which comprises the sensing of doubl

115 heterogenous activation of six genes in the type I IFN pathway.

116 ure and death, we reveal that IFN-lambda and type I IFN production were both diminished and delayed,

117 tem promotes phagosomal permeabilization and type I IFN production, key features of tuberculosis path

118 nd places this channel as a key modulator of type I IFN production, the hallmark function of pDCs, co

119 lator of IFN genes (STING) pathway to induce type I IFN production.

120 r viral clearance and a higher IFN-lambda to type I IFN ratio correlated with improved outcome for cr

121 Degradation of type I IFN receptor (IFNAR) is one known method of subve

122 uch strategy is to induce the degradation of type I IFN receptor 1 (IFNAR1) by utilizing viral hemagg

123 Notably, both type I IFN receptor blockade and CD8 T cell depletion pr

124 C organoids have increased expression of the type I IFN receptor relative to neonate IECs, and the re

125 which was associated with regulation of the type I IFN receptor signaling pathway.

126 ulating virus levels after ZIKV challenge in type I IFN receptor-deficient mice and wildtype mice adm

127 e mice administered neutralizing Abs against type I IFN receptor.

128 rolling viral HA-induced degradation of host type I IFN receptor.

129 mmunization even in the absence of recipient type I IFN receptors.

130 ain, is a critical negative regulator of the type I IFN response in Mus musculus macrophages.

131 Further, we provide evidence that the type I IFN response is central to the development of sev

132 onsistent with a defect in resolution of the type I IFN response, Trim14 knockout macrophages have mo

133 nocytogenes spread through modulation of the type I IFN response, which is known to be exploited by L

134 ation) is not required for regulation of the type I IFN response.

135 n unappreciated role for TRIM14 in resolving type I IFN responses and controlling M. tuberculosis inf

136 tion and pathogenicity in vivo by modulating type I IFN responses.

137 ' whole blood revealed strong correlation of type I IFN score and IL18 expression, whereas JAK/STAT i

138 regulation of endosomal pH to ensure strong type I IFN secretion exclusively during infection, avoid

139 ly correlating with mitochondrial abundance, type I IFN signaling and effector immunity.

140 Type I IFN signaling caused tight junction dysregulation

141 ined through adulthood, and requires ongoing type I IFN signaling to maintain it.

142 absence of LGP2, MDA5-mediated activation of type I IFN signaling was abrogated.

143 (SLE), a condition characterized by aberrant type I IFN signaling, has not been determined.

144 and promote epithelial repair via IL-22 and type I IFN signaling.

145 educed the ability of the protein to repress type I IFN signaling.

146 creases in BAFF expression were dependent on type I IFN signaling.

147 STAT1, and STAT3 phosphorylation and impairs type I IFN signaling; BGLF2 also counteracts the ability

148 ases, interferon regulatory factor-dependent type I IFN synthesis followed by JAK/STAT-dependent inte

149 Surprisingly, cGAS-STING activation leads to type I IFN transcription but not its production.

150 nitially capable of producing high levels of type I IFN, but rapidly lost this capacity, even before

151 ow that viral infection with LCMV results in type I IFN-dependent Treg cell loss that is rapidly comp

152 g Hv1 as an attractive target for modulating type I IFN-driven autoimmunity.

153 new therapeutic avenue for the treatment of type I IFN-linked autoimmune disorders.

154 cause a syndrome overlapping clinically with type I IFN-mediated disease due to gain-of-function in S

155 Type I IFN-mediated JAK-STAT signaling is severely impai

156 promoter motifs, whereas the expanded set of type I IFN-specific ISGs, including proapoptotic genes,

157 The expanded type I IFN-specific response includes proapoptotic genes

158 activation in a plasmacytoid dendritic cell-type I IFN-T/B lymphocyte network.

159 jor role for STING activation was to produce type I IFN.

160 els, CX-6258 induced a potent cGAS-dependent type-I IFN response in tumor cells, increased IFNgamma-p

161 However, TS cells expressed high levels of type I IFNR subunits (Ifnar1 and Ifnar2) and responded t

162 toid dendritic cells (pDCs) produce abundant type I IFNs (IFN-I) in response to viral nucleic acids.

163 Interestingly, induction of type I IFNs after A. fumigatus challenge was only partia

164 epithelial barrier permeability and reveals type I IFNs and CD8 T cells as causative factors of inte

165 Many of the antiviral genes induced by type I IFNs are repressed in the presence of butyrate, r

166 Type I IFNs play a complex role in determining the fate

167 Type I IFNs stimulate JAK/STAT signaling in DRG neurons

168 nterferon alpha (IFN-alpha) and IFN-beta are type I IFNs that are induced by virus infection and are

169 Endogenous release of type I IFNs with the double-stranded RNA mimetic poly(I:

170 ew also had auto-Abs against the other three type I IFNs.

171 he IFI16/STING pathway and the production of type I IFNs.

172 to type III, VI and X collagens, but not to type I, II or V collagens.

173 Type I, II, and III interferons (IFNs), which all signal

174 To this end, mice deficient in type I, II, or III IFN receptors or STAT1 were infected

175 We found that STAT1, but not type I, II, or III IFNs, mediated viral control during a

176 ority of which encode the fibrillar collagen types I, III and V, modifying or processing enzymes for

177 nal and three different C-terminal products (type I-III).

178 f taste cells: three mature, elongate types, Types I-III; and basally situated, immature postmitotic

179 In B. pertussis-infected mice, lung type I/III IFN responses correlated with increased proin

180 Signaling through the type I IL-1R has recently been shown to control disease

181 is dependent on intact signaling through the type I IL-1R receptor.

182 essing the frequency of stressor interaction types is imperative for a better understanding of how st

183 47 and FKBP65 along with reduced procollagen type I in culture media.

184 networks and functional output across cancer types is instrumental to realize the full potential of i

185 depletion, mediated by CD8 T cell-intrinsic type I interferon (IFN) and signal transducer and activa

186 Type I interferon (IFN) antiviral responses and SARS-CoV

187 pneumonia, and we have shown previously that type I interferon (IFN) contributes to the pathogenesis

188 Type I interferon (IFN) drives pathology in systemic lup

189 Type I interferon (IFN) is a major output of STING signa

190 Unlike TLR7-mediated disease, which requires type I interferon (IFN) receptor signaling, TLR9-driven

191 Type I interferon (IFN) response is commonly recognized

192 utation also increased early infectivity and type I interferon (IFN) responses in mouse bone marrow-d

193 onuclear cells from the patients, downstream type I interferon (IFN) signaling was transcriptionally

194 l encephalitis in the Western world, and the type I interferon (IFN) system is important for antivira

195 eficient cells secreted increased amounts of type I interferon (IFN), which could be limited by CGAS

196 SG15, stabilize USP18, a potent inhibitor of type I interferon (IFN)-I.

197 -2, Vaccinia virus, and Zika virus through a type I interferon (IFN)-independent mechanism.

198 omputational modeling to investigate how the type I interferon (IFN)-responsive regulatory network op

199 roptosis by mammalian reovirus requires both type I interferon (IFN)-signaling and viral replication

200 lls (pDCs) and blunts systemic production of type I interferon (IFN).

201 mulating plasmacytoid dendritic cells-(pDCs)-Type I interferon (IFN-I) and acts as autoantigen for pa

202 Plasmacytoid dendritic cells (pDCs) produce type I interferon (IFN-I) and are traditionally defined

203 tory stimuli by inhibiting the NF-kappaB and type I interferon (IFN-I) pathways.

204 osphorylation of IRF3 (not TBK1) and enhance type I interferon (IFN-I) production in macrophages.

205 Type I interferon (IFN-I) provides effective antiviral i

206 In this report, we evaluate type I interferon (IFN-I) sensitivity of SARS-CoV-2 rela

207 ression depends on Mtb-induced production of type I interferon (IFN-I).

208 initiating capacity through activation of a type I interferon (IFN-I)/STAT1 pathway when caspases ar

209 on downregulation of the IFNAR1 chain of the type I interferon (IFN1) receptor.

210 ging phenotype accompanying inborn errors of type I interferon immunity.

211 Basal levels of type I interferon in the long-term infected bat cells we

212 leading to activation of inflammatory genes, type I interferon production, autophagy, and cell death.

213 nducible gene I (RIG-I), thereby stimulating type I interferon production.

214 tion or defective negative regulation of the type I interferon response can lead to autoinflammation.

215 g and nonexpressing mice, but enrichment for type I interferon response gene changes was specifically

216 might protect virus-infected cells from the type I interferon response in cells undergoing lytic vir

217 xed with nucleic acids triggers an antiviral type I interferon response in neuroglia, resulting in co

218 racy, rather than uniquely to antagonize the type I interferon response.

219 poptotic cells within tumors and triggered a type I interferon response.

220 ssembly, including molecules involved in the type I interferon signaling pathway and caspase-6.

221 2 tegument protein binds to a protein in the type I interferon signaling pathway Tyk2 and inhibits th

222 ition, an enrichment in the IL-12 family and type I interferon signaling pathways was observed among

223 nd is punctuated by a late prenatal spike in type I interferon signaling that promotes perinatal HPC

224 smacytoid DCs (pDCs), the major producers of type I interferon, are principally recognized as key med

225 Interferon-alpha (IFNalpha), a type I interferon, is expressed in the islets of type 1

226 rference includes suppression of hundreds of type I interferon-regulated genes due to lower interfero

227 plicative capacity (p = 0.0005) and are more type I interferon-resistant (p = 0.007) than those trans

228 ngeal swabs demonstrated that in addition to type-I interferon and interleukin-6-dependent inflammato

229 and administrated using different routes in type-I interferon receptor deficient A129 mice.

230 various cytokines and chemokines, including type I interferons (IFN-I).

231 respond to intracellular dsRNA by expressing type I interferons (IFNs) and inducing apoptosis, but th

232 tionally repressing STAT1/2 and secretion of Type I Interferons (IFNs).

233 ion factor with many target genes, including type I interferons (IFNs).

234 G is phosphorylated, leading to induction of type I interferons (IFNs).

235 focused response that predominantly involves type I interferons and interferon-related genes, whereas

236 , mediating the transcriptional induction of type I interferons and other genes that collectively est

237 lpha to suppress EBV reactivation.IMPORTANCE Type I interferons are important for controlling virus i

238 Moreover, we show that type I interferons do not control SARS-CoV-2 replication

239 Type I interferons have a crucial role in the progressio

240 lic GMP-AMP, which mediates the induction of type I interferons through the STING-TBK1-IRF3 signallin

241 Type I interferons, particularly interferon-alpha (IFN-a

242 nflammatory cytokines, but the production of type I interferons, which are key antiviral mediators, i

243 CE Viral infection triggers the secretion of type I interferons, which in turn induce the expression

244 otice" the infection and respond by inducing type I interferons, which limits virus replication.

245 inhibits the expression of genes induced by type I interferons.

246 lation of antiviral effectors in response to type I interferons.IMPORTANCE Viral infection triggers t

247 esponses, characterized by the production of type-I interferons (IFN) including IFNbeta.

248 The poliovirus type I IRES is able to recruit ribosomal machinery only

249 Altered microarchitecture of collagen type I is a hallmark of wound healing and cancer that is

250 All hiatal hernia types (I-IV) were collected.

251 tein (myelin) and scored for cortical lesion types I-IV (mixed grey matter/white matter, intracortica

252 Synthesis of type I LacNAc (Galbeta1 -> 3GlcNAc) oligosaccharides usu

253 tcome of glycosylations for the synthesis of type I LacNAc hexasaccharides.

254 acceptors had to be more than 6311 to obtain type I LacNAc tetrasaccharides in 72-86% yields, with mi

255 othalamus (POA-AH) of nest-holding, courting type I males during spawning compared to cuckolding type

256 We also established the first database of type I modular PKSs, featuring a comprehensive annotatio

257 the biosynthetic pathways of the products of type I modular polyketide synthase (PKS) with the focus

258 A 52-bp deletion (type I mutation) and a 5-bp insertion (type II mutation)

259 Neither type I nor type II IFNs are required to generate CD122+M

260 The androgen receptor (AR) is a type I nuclear hormone receptor and the primary drug tar

261 of subjects available for rare cancer (sub-)types is often limited.

262 n for patients with focal cortical dysplasia type I or mild malformation of cortical development (50.

263 r eQTL detection, which results in increased Type I or Type II errors.

264 MPS type I patients are prone to have glaucoma with narrow o

265 e first machine learning based algorithm for type I PKS DD affinity and pathway prediction.

266 ate the approach by isolating and sequencing type I polyketide synthase gene clusters from an Antarct

267 for at least one of the polyketide synthase type I, polyketide synthase type II or non-ribosomal pep

268 d its variation across and within vegetation types is poorly understood, which hinders our capacity t

269 This way, type I porphyrins could be obtained as the only type iso

270 A targeted synthesis of dodecasubstituted type I porphyrins that utilizes the reaction of unsymmet

271 Here, we evaluate the effect of type I PRMT inhibition on arginine methylation in normal

272 (hnRNP-A1) as a pharmacodynamic biomarker of type I PRMT inhibition.

273 ilize a broad proteomic approach to identify type I PRMT substrates.

274 GSK3368715 is a small molecule inhibitor of type I PRMTs currently in clinical development.

275 ptation and virulence beyond the role of the Type I R-M systems against phage infection.

276 suggests that, similar to its action against type I R-M systems, Ocr associates with as yet unidentif

277 ubstrates to form radicals and radical ions (Type I reaction); whereas in photodynamic therapy, the t

278 flammatory role by identifying interleukin 1 type I receptor kinase-1 (IRAK-1) as a Nck1-selective bi

279 Together with previous findings that the type I receptor SMA-6 is recycled via the retromer compl

280 e specific interactions between BMPs and BMP type I receptors.

281 Ryanodine receptor type I-related myopathies (RYR1-RMs) are a common group

282 rdinated growth among these major brain cell types is required for neural development.

283 e-variable system of Bacteroides fragilis, a Type I restriction modification system (R-M).

284 A phase variable type I restriction-modification (R-M) system (SpnIII) ha

285 Type I restriction-modification (R-M) systems consist of

286 tects the phage from the defensive action of type I restriction-modification systems, is also active

287 Unlike type I rosetting that involves direct interaction of ros

288 uter membrane via a variant of the classical type I secretion system.

289 nding on the alternative splicing of exon 1, type I splice variants (MOCS1A) either localize to the m

290 e-nuclease Cas3(4,5), but nuclease-deficient type I systems lacking Cas3 have been repurposed for RNA

291 f these structures are produced in nature by type I terpene cyclase enzymes from one single substrate

292 Lastly, we demonstrate type I TGFbeta receptor kinase inhibition abrogates VehM

293 One such interneuron type is the low-threshold, somatostatin (SST)-expressing

294 In contrast, the B type is the most common type in East Asia, and its ances

295 ere, these questions were investigated for a type I toxin-antitoxin system (AapA1-IsoA1) expressed fr

296 The seventh member, PC7, is a type-I transmembrane (TM) protein with a 97-residue-long

297 rosis formation was enhanced by 19%, and the type I/type III collagen ratio was shifted toward higher

298 ghtly controlled: a given eukaryotic protein type is typically associated with a narrow, specific gly

299 rms associated with heparin differ by cancer type is unclear.

300 tal cells, the survival rate of various cell types is very high.