ライフサイエンスコーパス: PRR

1 PRR and PMd were found to oscillate at similar frequenci

2 PRR complexes are under tight control by protein phospha

3 PRRs act as transcriptional repressors and associate wit

4 PRRs detecting viral RNA, such as toll like receptor (TL

5 PRRs that recognize nucleic acids in cells include sever

6 Our study reveals that EphA2 functions as a PRR for beta-glucans that senses epithelial cell fungal

7 artificial nucleic acid ligands to activate PRRs.

8 In addition, PRR complexes and signaling components are often transcr

9 However, there are additional PRRs that account for the host immune responses to T. cr

10 Finally, NOD2 synergized with additional PRRs to increase Twist1 and Twist2 expression and Twist-

11 er among men with healed MC wounds (adjusted PRR, 0.62; 95% CI, .35-1.08).

12 d prevalence risk ratios (PRRs) and adjusted PRRs (adjPRRs) of HIV shedding were estimated using modi

13 nd that soluble pattern generation might aid PRR-mediated immune activation in cell layers adjacent t

14 When each effector moved alone, PRR inactivation shortened reach but not saccade amplitu

15 Taken together, ICOSL amplifies PRR-initiated outcomes, which might contribute to immune

16 n together, TNFSF15:DR3 interactions amplify PRR-induced signaling and cytokines, and the rs6478108 T

17 Therefore, LACC1 is critical for amplifying PRR-induced outcomes, an effect that is attenuated by th

18 R3 interactions were critical for amplifying PRR-initiated MAPK/NF-kappaB/PI3K signaling and cytokine

19 arin-related protein 3 (MTMR3) in amplifying PRR-induced cytokine secretion in human macrophages and

20 through IL-18RAP was critical in amplifying PRR-induced cytokine secretion in MDMs.

21 emonstrated increased TNFSF15 expression and PRR-induced signaling and cytokines.

22 sk-carriers had reduced ICOSL expression and PRR-initiated signaling and this loss-of-function ICOSLG

23 -like components, such as LCL1-, GmELF4- and PRR-like genes, which had reduced expression in stressed

24 previous studies, we found that both LIP and PRR encode a reward-based decision variable, the target

25 that can be used to identify PAMPs/DAMPs and PRRs.

26 l load, whereas diversification of MAMPs and PRRs emerges as a mechanism that locally sculpts microbi

27 ered signaling through antigen receptors and PRRs.

28 ing recognized by both the invariant TCR and PRRs and inducing immune responses.

29 The Arabidopsis PRR EF-Tu receptor (EFR) recognizes the bacterial PAMP e

30 ong Brassicaceae species are enriched around PRR binding sites, indicating that PRRs associate with f

31 ctable plasma VL compared to men not on ART (PRR = 0.15, 95% CI = 0.05-0.43, p = 0.001).

32 A G-box-like motif was overrepresented at PRR binding regions, and we showed that this motif is ne

33 l: .71/F1-measure: .80) outperforms the best PRR based method (.69/.69/.69) on all four adverse event

34 ere above this threshold; consequently, both PRR-induced pro- and anti-inflammatory cytokines were de

35 r hand, saccade choices were not affected by PRR inactivation.

36 supports the sensing of extracellular DNA by PRRs, leading to calcium-dependent signaling, although n

37 knowledge of early PTI signaling mediated by PRRs and their associated proteins, many downstream sign

38 atterns (DAMPs), which are also perceived by PRRs to modulate PTI responses.

39 eceptor 2 (EphA2) is an oral epithelial cell PRR that binds to exposed beta-glucans on the surface of

40 by peripheral macrophages following chronic PRR stimulation and by human intestinal myeloid cells fo

41 ver, when both effectors moved concurrently, PRR inactivation shortened both reach and saccade amplit

42 omic DNA and exhibit markers of constitutive PRR and checkpoint activation.

43 n, many leucine-rich repeat (LRR)-containing PRRs interact with the LRR-RK BRI1-ASSOCIATED KINASE 1 (

44 or of several leucine-rich repeat-containing PRRs.

45 In contrast, PRR encoded target desirability only for reaches and not

46 acid-inducible gene I (RIG-I) is a cytosolic PRR that senses viral nucleic acids and induces innate i

47 xtracellular and endosomal but not cytosolic PRRs.

48 burnetii NMII by TLRs, rather than cytosolic PRRs, in enabling C57BL/6 macrophages to restrict bacter

49 sk carrier macrophages demonstrate decreased PRR-induced mtROS, signalling, cytokine secretion and ba

50 MTMR3 decreased PRR-induced phosphatidylinositol 3-phosphate (PtdIns3P)

51 ges, lower INAVA expression led to decreased PRR-induced activation of MAPK and NF-kappaB pathways, c

52 sed MTMR3 expression and, in turn, decreased PRR-induced PtdIns3P and autophagy and increased PRR-ind

53 Here, we have specifically deleted PRR from T cells.

54 NSITIVE1-ASSOCIATED KINASE1 (BAK1)-dependent PRRs FLS2 and EFR, as well as with the BAK1-independent

55 ic trafficking is conserved across different PRR protein families as well as across different plant s

56 gly, these risk-carrier MDMs show diminished PRR-, IL-18-, and IL-1-induced MAPK and NF-kappaB signal

57 ignaling promotes defenses and downregulates PRRs, whereas later (within 24 to 48 h) SA signaling upr

58 EF-PRR bypasses DNA incongruities that impede replication b

59 whether genetic variation in genes encoding PRRs influences the susceptibility to cSSSIs.

60 ced outcomes, ultimately leading to enhanced PRR-induced cytokines.

61 fate of signaling endosomes formed following PRR activation.

62 vaginal epithelial cells were evaluated for PRR expression and C. albicans-induced S100A8 and S100A9

63 Our study thus identifies a new role for PRR in T-cell development.

64 ts implicate multiple modes of signaling for PRRs in response to PAMPs and SA.

65 Signal relay from PRR complexes to the nuclear transcriptional machinery v

66 Our results further our understanding of how PRRs target specific promoters and provide an extensive

67 Human PRR over-expression alone increased ROS levels, NADPH ox

68 In PRR analyses, whereas Toll-like receptor 4 (TLR4)- and S

69 litionally control single-neuron activity in PRR by preferentially exploring and exploiting their nat

70 movements causes the spatial information in PRR to influence the otherwise independent eye control p

71 activity in the brain, action potentials in PRR anti-synchronize with PMd oscillations.

72 us single-nucleotide polymorphisms (SNPs) in PRR genes coding for Toll-like receptors (TLRs) 1, 2, 4,

73 induced PtdIns3P and autophagy and increased PRR-induced caspase-1 activation, signaling, and cytokin

74 es the prorenin receptor (PRR) and increases PRR/V-ATPase-driven ATP release, thereby enhancing the p

75 3P) and autophagy levels, thereby increasing PRR-induced caspase-1 activation, autocrine IL-1beta sec

76 nd EFR, as well as with the BAK1-independent PRR CERK1.

77 Finally, SA induces PRR- and ACD6-dependent signaling to induce callose depo

78 , successful pathogens must evade or inhibit PRR-triggered immunity to cause disease.

79 evaluation of the PMN response in inoculated PRR-deficient mice.

80 t their temporal coupling requires an intact PRR.

81 earance of endosomes containing internalized PRRs, failure of which resulted in enhanced signaling an

82 gh nucleic acid recognition by intracellular PRRs such as endosomal TLRs (TLR3, TLR7, TLR8, and TLR9)

83 discuss recent advances in how intracellular PRRs respond to microbial nucleic acids and emerging vie

84 new information on the role of intracellular PRRs in the pathogenesis of oral diseases including peri

85 vaginal PMN response to C. albicans involves PRRs in addition to SIGNR1 and TLR4, or other induction

86 These structures depict the position of Itch PRR engaged in a 1:2 protein complex with beta-PIX and a

87 spectrometry analysis, we show that the Itch PRR preferentially forms complexes with endophilins, amp

88 s reveal the binding preferences of the Itch PRR toward its most common SH3 domain-containing partner

89 wide range of binding properties of the Itch PRR.

90 intained the deacetylation status of the key PRR signaling molecule TBK1 and enhanced its kinase acti

91 drug-AE correlation tests (i.e., class-level PRR, Chi-squared, and minimal case reports) were also mo

92 However, the signaling cascades linking PRR activation by MAMPs to cytoskeleton remodeling are n

93 ption of elicitors by cell surface-localized PRRs, leading to subsequent downstream immune signaling.

94 While many PRRs that recognize mycobacteria have been identified, n

95 ) and remained suppressed at 12 wk after MC (PRR = 0.19, 95% CI = 0.06-0.64, p = 0.008).

96 HIV shedding was decreased by 6 wk after MC (PRR = 0.27, 95% CI = 0.09-0.83, p = 0.023) and remained

97 D-associated polymorphisms in INAVA modulate PRR-initiated signaling, cytokines, and intracellular ba

98 increases MTMR3 expression, which modulates PRR-induced outcomes, ultimately leading to enhanced PRR

99 than G carriers upon stimulation of multiple PRRs, including nucleotide-binding oligomerization domai

100 As novel PRRs are identified, their transfer between plant famili

101 Although Mtuberculosis activates numerous PRRs, for reasons that are poorly understood LAP does no

102 The concerted actions of PRR signaling, specific viral-restriction factors, innat

103 se type 2A (PP2A) controls the activation of PRR complexes by modulating the phosphostatus of the co-

104 e with the known reach-selective activity of PRR.

105 tes of these proteins using a combination of PRR sub-sequences and mutants.

106 host and pathogen compete to take control of PRR tyrosine phosphorylation used to initiate antibacter

107 er poxvirus genomes, is a novel inhibitor of PRR- and cytokine-stimulated NF-kappaB activation.

108 Wevers et al. (2014) uncover a mechanism of PRR antagonism where fungal-induced Mincle signaling sup

109 ular, biochemical, and genetic mechanisms of PRR activation, and dissecting the complex signaling net

110 est these hypotheses, we inactivated part of PRR in the macaque, located in the medial bank of the in

111 slational modifications in the regulation of PRR signaling and activation of antiviral innate immune

112 ucing oxidative stress; however, the role of PRR-mediated Ang II-independent signaling pathways in ox

113 The use of PRR agonists and the underlying molecular mechanisms hav

114 (RIG-I, encoded by DDX58) forms one class of PRRs that mediates apoptosis and the elimination of infe

115 To evaluate the collective contribution of PRRs and IL-1R signalling to RSV immunity, we generated

116 ute an immune signaling module downstream of PRRs, linking protein phosphorylation cascades to metabo

117 We evaluated the expression of PRRs on APCs in mice infected with the helminth parasite

118 o members of the NOD-like receptor family of PRRs, are important mediators of ER-stress-induced infla

119 mic effect on the regulation and function of PRRs.

120 accumulation also causes increased levels of PRRs and potentiates the responsiveness of plants to PAM

121 in MDMs upon stimulation of a broad range of PRRs.

122 effect of SA causes a transient reduction of PRRs and ACD6-dependent reduced responsiveness to PAMPs.

123 MDMs and in mice, continuous stimulation of PRRs induces expression of metallothioneins.

124 e emerging biotechnological potential use of PRRs to improve broad-spectrum, and potentially durable,

125 MDA5 that challenge the conventional view of PRRs.

126 Accordingly, previous studies on PRRs, such as RIG-I and MDA5, have primarily focused on

127 presses IL-12 transcription induced by other PRRs and thereby abates antifungal immunity.

128 at, rather than driving PMd during planning, PRR neurons fire in such a way that they are less likely

129 Plant PRRs are either surface-localized receptor kinases (RKs)

130 Plant PRRs are surface-localized receptor-like kinases, which

131 Plant PRRs contribute to both basal and non-host resistances,

132 lecular patterns (DAMPs) recognized by plant PRRs induces both local and systemic immunity.

133 tiple molecular strategies employed by plant PRRs to activate innate immune signaling to survive.

134 Many plant PRRs are kinases.

135 Notably, plant PRRs appear as central components of multiprotein comple

136 , I summarize our current knowledge of plant PRRs and their ligands, illustrating the multiple molecu

137 erception and subsequent activation of plant PRRs.

138 Ps recognized by plants as well as the plant PRRs described to date.

139 exes PhB(MesIm)3Fe-N horizontal linePRR'R'' (PRR'R'' = PMePh2, PMe2Ph, PMe3, and P(n)Pr3) undergo a t

140 The fast parasite reduction ratio (PRR) and gametocytocidal effect of ACT-451840 were recen

141 ed in the in vitro parasite reduction ratio (PRR) assay coupled with the extended survival highlights

142 Proportional reporting ratio (PRR) was used to detect statistically significant associ

143 lity analysis (proportional reporting ratio, PRR) and quantify the improvement in signal detection wi

144 Unadjusted prevalence risk ratios (PRRs) and adjusted PRRs (adjPRRs) of HIV shedding were e

145 Prevalence risk ratios (PRRs) of GUD were estimated using log binomial regressio

146 Prevalence risk ratios (PRRs) were estimated using Poisson regression.

147 OB lineage stabilizes the prorenin receptor (PRR) and increases PRR/V-ATPase-driven ATP release, ther

148 of prorenin (P = 0.049), prorenin receptor (PRR; P = 0.0004), and angiotensin type 1 receptor (AT1R,

149 The use of pathogen recognition receptor (PRR) agonists and the molecular mechanisms involved have

150 te of multiple pattern recognition receptor (PRR) complexes.

151 a predominant pathogen recognition receptor (PRR) for DNA-directed type I interferon (IFN) innate imm

152 , we show that pattern recognition receptor (PRR) ligands, including lipid A, LPS, poly(I:C), poly(dA

153 cytokines upon pattern recognition receptor (PRR) restimulation; cytokine attenuation to PRR stimulat

154 virus-induced pattern recognition receptor (PRR) signaling and cellular activation by virus-induced

155 regulation of pattern recognition receptor (PRR) signaling is critical for intestinal immune homeost

156 n receptor and pattern recognition receptor (PRR) signaling.

157 nvolvement in pathogen recognition receptor (PRR) signaling.

158 onse following pattern recognition receptor (PRR) stimulation of whole blood from 2-year-old infants

159 tection by the pattern-recognition receptor (PRR) Toll-like receptor 8 (TLR8).

160 affects viral pattern recognition receptor (PRR)-driven cytokine production.

161 studies linked pattern-recognition receptor (PRR)-expressing HSCs, EMH, and immune responses to micro

162 we found that pattern-recognition receptor (PRR)-induced cytokine secretion was diminished in human

163 ing determined pattern-recognition receptor (PRR)-induced outcomes; whereas anti-inflammatory cytokin

164 and amplifies pattern recognition receptor (PRR)-induced SDH activity, an important contributor to m

165 or decrease in pattern-recognition receptor (PRR)-induced signaling and cytokine secretion can lead t

166 ed T3SEs or in pattern recognition receptor (PRR)-triggered immunity.

167 Regulation of pattern-recognition-receptor (PRR)-induced signaling and cytokines is crucial for immu

168 enin or prorenin to the (pro)renin receptor (PRR) promotes angiotensin (Ang) II formation and mediate

169 The (pro)renin receptor (PRR) was originally thought to be important for regulati

170 itiated when pathogen recognition receptors (PRR) engage viral pathogen-associated molecular patterns

171 Pattern recognition receptors (PRR) promote pathogen eradication and shape adaptive imm

172 Pattern recognition receptors (PRR) sense certain molecular patterns uniquely expressed

173 teria via the pattern recognition receptors (PRR) Toll-like receptor (TLR)-4 and nucleotide-binding o

174 eceptor) and pathogen recognition receptors (PRRs) (i.e., TLR3; TLR4), revealing a stimulus-selective

175 ace-localized pattern-recognition receptors (PRRs) activates plant innate immunity, mainly through ac

176 ace-localized pattern recognition receptors (PRRs) activates the NADPH oxidase RBOHD by hitherto unkn

177 ace-localized pattern recognition receptors (PRRs) also plays a role in basal resistance to insects,

178 nself by host pattern recognition receptors (PRRs) and activate pattern-triggered immunity (PTI).

179 the different pattern-recognition receptors (PRRs) and cell wall pathogen-associated molecular patter

180 cognition via pattern recognition receptors (PRRs) and cell:cell communication conducted by soluble m

181 Pattern recognition receptors (PRRs) and cytokine receptors are key players in the init

182 muli through pathogen-recognition receptors (PRRs) and decode, integrate, and present information der

183 cell surface pattern recognition receptors (PRRs) and include the accumulation of reactive oxygen sp

184 al infection, pattern recognition receptors (PRRs) and their associated adaptors recruit TANK-binding

185 ived by plant pattern recognition receptors (PRRs) and whether host hydrolytic activities facilitate

186 e detected by pattern recognition receptors (PRRs) are (i) flagellin, detected by TLR5 and NLRC4 (Ipa

187 Host pattern recognition receptors (PRRs) are critical in regulating these interactions.

188 Pattern recognition receptors (PRRs) are essential sentinels for pathogens or tissue da

189 how endosomal pattern recognition receptors (PRRs) detect HRV replication products that are generated

190 They employ pattern-recognition receptors (PRRs) for sensitive and rapid detection of the potential

191 The pattern recognition receptors (PRRs) in epithelial cells that mediate this differential

192 face-resident pattern recognition receptors (PRRs) induces rapid, robust, and selective transcription

193 MPs/MAMPs) by pattern recognition receptors (PRRs) is a key component of plant innate immunity.

194 microbes with pattern recognition receptors (PRRs) is essential for protective immunity.

195 ns (PAMPs) by pattern-recognition receptors (PRRs) located on the host cell's surface.

196 s (DAMPs) for pattern recognition receptors (PRRs) may represent one such signal, these RNAs must rem

197 ecognized by pathogen-recognition receptors (PRRs) of infected cells, which triggers a signaling casc

198 recognized by pattern-recognition receptors (PRRs) of the innate immune system.

199 are sensed by pattern recognition receptors (PRRs) on cells of plants and animals.

200 AMPs) through pattern-recognition receptors (PRRs) on dendritic cells (DCs).

201 eptors called pattern recognition receptors (PRRs) on dendritic cells, which translate these inflamma

202 hrough innate pattern recognition receptors (PRRs) or DAMP-specific receptors, in regulating the allo

203 sponses, and pathogen recognition receptors (PRRs) play a key role in maintaining this balance.

204 he roles that pattern recognition receptors (PRRs) play in regulating APC phenotypes are just now bei

205 Rs) and other pattern-recognition receptors (PRRs) sense microbial ligands and initiate signaling to

206 s to mammals, pattern recognition receptors (PRRs) specifically recognize DNA, as a potential marker

207 ane-localized pattern recognition receptors (PRRs) such as FLAGELLIN SENSING2 (FLS2), EF-TU RECEPTOR

208 ly target the pattern recognition receptors (PRRs) such as the Toll-like receptors (TLRs) that recogn

209 of proteins: pattern recognition receptors (PRRs) that detect viral infection and induce the interfe

210 es as well as pattern-recognition receptors (PRRs) that initiate cellular-based signals as a first li

211 ns (MAMPs) by pattern recognition receptors (PRRs) that initiate quantitative immune responses to con

212 d to evaluate pattern recognition receptors (PRRs) that initiate the response.

213 hat activate pathogen-recognition receptors (PRRs) through a lysosomal-trafficking pathway called "LC

214 recognized by pattern recognition receptors (PRRs) to activate pattern-triggered immunity (PTI).

215 stem utilizes pattern-recognition receptors (PRRs) to detect the invasion of pathogens and initiate h

216 nses that use pattern-recognition receptors (PRRs) to detect viral pathogens, and that subsequently i

217 nt cytosolic pathogen recognition receptors (PRRs) to induce antiviral genes.

218 ins (RLPs) as pattern recognition receptors (PRRs) to monitor their apoplastic environment and detect

219 ins (RLPs) as pattern recognition receptors (PRRs) to sense pathogen-associated molecular patterns (P

220 cognition of pathogen recognition receptors (PRRs) via their cognate ligands are critical for enhanci

221 triggered by pattern-recognition receptors (PRRs), but not that of the proinflammatory cytokines TNF

222 timulation of pattern recognition receptors (PRRs), including nucleotide-binding oligomerization doma

223 ace-localized pattern recognition receptors (PRRs), leading to an innate immune response that prevent

224 ding how host pattern recognition receptors (PRRs), specifically toll-like receptors (TLRs), sense an

225 riggered when pattern recognition receptors (PRRs), such as Toll-like receptors or nucleotide-binding

226 o families of pattern recognition receptors (PRRs), Toll-like receptors (TLRs) and NOD-like receptors

227 cted by plant pattern recognition receptors (PRRs), which gives rise to PAMP-triggered immunity (PTI)

228 hways are the pattern recognition receptors (PRRs), which must be present at the plasma membrane to s

229 n by specific pattern recognition receptors (PRRs).

230 line-encoded pattern recognition receptors (PRRs).

231 ns (PAMPs) by pattern recognition receptors (PRRs).

232 s (TLRs), key pattern recognition receptors (PRRs).

233 the nearby histidines (249,250) have reduced PRR-induced outcomes.

234 resence of a C-terminal pseudorepeat region (PRR) greatly increased MT binding by a greater-than-sixf

235 (Macaca mulatta): the parietal reach region (PRR) and the dorsal premotor cortex (PMd).

236 s in area LIP and the parietal reach region (PRR) of the parietal cortex.

237 sibly inactivated the parietal reach region (PRR), the area of the PPC that is specialized for reachi

238 e explore whether the parietal reach region (PRR), the region of the PPC that is specialized for reac

239 or pathway, e.g., the parietal reach region (PRR), would not affect the other effector.

240 intraparietal sulcus [parietal reach region (PRR)] specifically biased choices made using arm movemen

241 mains, Itch possesses a proline-rich region (PRR) that has been shown to interact with several Src ho

242 l repressors Twist1 and Twist2 in regulating PRR-induced cytokine outcomes is poorly understood and h

243 le of INAVA and INAVA genotype in regulating PRR-initiated outcomes in primary human cells.

244 Pseudo response regulators (PRRs) comprise a five-member family that is essential to

245 PSEUDO-RESPONSE REGULATORs (PRRs) play overlapping and distinct roles in maintaining

246 gh homology-mediated postreplication repair (PRR) events.

247 ronic activation of post-replication repair (PRR) and genome instability.

248 hagy or restoring NFkappaB signaling rescued PRR-induced cytokines.

249 aced the RSC chromatin remodeler in the same PRR pathway, and Rsc2 recruitment was coincident with H4

250 cognition and signal transduction by several PRR families at distinct subcellular compartments.

251 ositively regulates the abundance of several PRRs and affects the responsiveness of plants to two PAM

252 bacterial matrices and generation of soluble PRR ligands.

253 T-cell-specific PRR-knockout mice had a significant decrease in thymic c

254 Although evidence suggests PRRs can antagonize each other, few detailed mechanisms

255 However, it is now emerging that PRR has instead a generic role in cellular development.

256 We found that PRR binding sites are located within genomic regions of

257 We found that PRR inactivation led to a strong reduction of contralesi

258 ysis on sorted DN3 thymocytes indicated that PRR-deficient thymocytes have perturbations in key cellu

259 T-cell progenitors leads us to propose that PRR deletion affects thymocyte survival and development

260 We further show that PRR pathway preference in 0.001% MMS depends on timing a

261 ed around PRR binding sites, indicating that PRRs associate with functionally relevant cis-regulatory

262 It is now recognized that PRRs are paramount in instructing an appropriate adaptiv

263 This work shows that PRRs associate with and are part of the ACD6/SA feedback

264 ancer cells, unshielded RN7SL1 activates the PRR RIG-I to enhance tumor growth, metastasis, and thera

265 Disease-associated tau mutations in the PRR (K369I, G389R) did not influence apparent MT binding

266 We inactivated the PRR while two monkeys performed reach and saccade choice

267 re crucially affected by the presence of the PRR and tau hyperphosphorylation.

268 ase BIK1, which is a direct substrate of the PRR complex, directly interacts with and phosphorylates

269 Bioinformatic analysis revealed that the PRR contained a highly conserved motif of 18 amino acids

270 containing partners and demonstrate that the PRR region is sufficient for binding.

271 nd affinities for their interaction with the PRR of Itch.

272 The PRRs shared a significant number of binding regions, and

273 receptor kinases EFR and FLS2, which are the PRRs for bacterial EF-Tu and flagellin, respectively.

274 CIRCADIAN CLOCK ASSOCIATED 1 and PRR9 by the PRRs.

275 tanding of the structure and function of the PRRs will improve future prospects of therapeutic target

276 of CD8(+) T cells, but signaling through the PRRs TLR7 and RIG-I was not.

277 NOD2 synergized with the PRRs Toll-like receptors 5 and 9 increase the effects of

278 in vitro, inoculated mice deficient in these PRRs showed PMN migration similar to that in wild-type c

279 ved cells are stimulated continually through PRRs; metallothionein expression was up-regulated in hum

280 Thus, PRR is a part of a network for making reach decisions.

281 (PRR) restimulation; cytokine attenuation to PRR stimulation is similarly observed in intestinal macr

282 nisms mediating TNFSF15:DR3 contributions to PRR outcomes included TACE-induced TNFSF15 cleavage to s

283 SF15:death receptor 3 (DR3) contributions to PRR responses have not been described.

284 differences in innate cytokine responses to PRR stimulation exist among different populations of inf

285 glance, the stronger oscillator of the two, PRR, would seem to drive the weaker, PMd.

286 K1 is thus expected to interact with unknown PRRs.

287 Upon PRR stimulation, INAVA was required for optimal MAPK and

288 (within 24 to 48 h) SA signaling upregulates PRRs, and plants are rendered more responsive to PAMPs.

289 In addition to sensing pathogens via PRRs, emerging evidence suggests that DCs can also sense

290 anti-inflammatory responses evoked by viral PRR ligands or infectious RSV.

291 electively reducing the sensitivity of viral PRR responses to modulation.

292 mulated by representative bacterial or viral PRR ligands.

293 , compared with 12.9% (22 of 170) at 1 week (PRR, 1.33; 95% confidence interval [CI], .74-2.38) and 1

294 .74-2.38) and 14.8% (23 of 155) at 2 weeks (PRR, 1.50; 95% CI, .86-2.62) after MC.

295 e JAK signaling threshold determines whether PRR-induced pro- and anti-inflammatory cytokines are rec

296 However, it is not clear which PRRs have a major role in inducing inflammation during E

297 as significantly increased after MC at 1 wk (PRR = 1.87, 95% CI = 1.12-3.14, p = 0.012), 2 wk (PRR =

298 1.87, 95% CI = 1.12-3.14, p = 0.012), 2 wk (PRR = 3.16, 95% CI = 1.94-5.13, p < 0.001), and 3 wk (PR

299 6, 95% CI = 1.94-5.13, p < 0.001), and 3 wk (PRR = 1.98, 95% CI = 1.19-3.28, p = 0.008) after MC.

300 wer in PE at altitude than at sea level, yet PRR, angiotensinogen (AGT) and AT1R proteins were all in