ライフサイエンスコーパス: PRR

1 PRR and these pathways regulate the expression/activity

2 PRR-initiated pathways also contribute to bacterial clea

3 PRRs act as transcriptional repressors and associate wit

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

5 PRRs of aortic arch defects increased with maternal obes

6 PRRs of aortic branch defects, ASD, and persistent ductu

7 PRRs of ASD and persistent ductus arteriosus in term inf

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

9 artificial nucleic acid ligands to activate PRRs.

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

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

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

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

14 wn about the mechanics of ligand binding and PRR activation, how cells coordinate RNA sensing with si

15 ed cytokines in intestinal myeloid cells and PRR-enhanced antimicrobial pathways in MDMs.

16 pare bronchial mucosal type I interferon and PRR expression at baseline and after rhinovirus infectio

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

18 6 mice were injected with scramble shRNA and PRR shRNA and followed for a period of eight weeks.

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

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

21 ered signaling through antigen receptors and PRRs.

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

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

24 oligomerization domains 1 and 2 (NOD1/2) are PRRs that recognize and respond to multiple stimuli of m

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

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

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

28 structure shows how ATP6AP1/Ac45 and ATP6AP2/PRR enable assembly of the enzyme's catalytic and membra

29 anchors for cleaved ATP6AP1/Ac45 and ATP6AP2/PRR, the latter of which is the (pro)renin receptor that

30 As for other bacteria, PRR-stimulated type I interferon (IFN-I) induction has b

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

32 lear localization signal is embedded between PRR and WH2 and is subject to similar autoinhibition.

33 garding the antagonistic interaction between PRR and ELABELA/apelin, the mutually stimulatory relatio

34 he mutually stimulatory relationship between PRR and COX-2/PGE(2) or Wnt/beta-catenin signaling in th

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

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 ery, kinase activity, and phosphorylation by PRRs are critical for the function of BSK5 in PTI.

40 ing protein, as a direct target repressed by PRRs in mediating TOR signaling.

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

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

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

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

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

46 eventing delayed activation of the cytosolic PRR NLR pyrin domain 3 (NLRP3) that would otherwise ampl

47 Here, we show that the cytosolic PRR Nod-like Receptor CARD 4 (NLRC4) suppresses, rather

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

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

52 at baseline was not accompanied by deficient PRR expression in asthmatic patients.

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

54 a) isoform, which both contain the described PRR and WH2 domains.

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

56 trast to adjuvants that operate via discrete PRRs.

57 fate of signaling endosomes formed following PRR activation.

58 STAT1 and STAT4 were required for PRR- and live bacterial-induced secretion of multiple cy

59 IRF5 was required for PRR-induced MAPK and NF-kappaB activation, which, in tur

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

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

62 STAT5a, and STAT5b expression determines if PRR-induced proinflammatory cytokines are increased or d

63 required for optimal bacterial clearance in PRR-stimulated, M1-differentiated human macrophages.

64 or-like cytoplasmic kinase subfamily XII, in PRR-initiated immunity.

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

66 monstrated increased Ag uptake and increased PRR-induced costimulatory molecule expression and chemok

67 STAT5a, and STAT5b expression and increased PRR-induced STAT3 and STAT5 phosphorylation relative to

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

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

70 ncreased numbers of subepithelial interferon/PRR-expressing inflammatory cells were related to greate

71 of subepithelial cells expressing interferon/PRRs during infection were also related to greater viral

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

73 The intracellular PRR-signaling pathways that detect DNA viruses have been

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

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

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

77 However, the exact mechanisms involving PRR activity and diabetic kidney dysfunction are unknown

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

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

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

81 wide range of binding properties of the Itch PRR.

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

83 All known PRRs for viral RNA have extranuclear localization.

84 Lastly, we found Dectin-1, a c-type lectin PRR to be reduced at the protein level in both naive neu

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

86 e to fungal chitin is conferred by the major PRRs for chitin recognition, LYK5 and CERK1, the recepto

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

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

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

90 In diabetic mice, PRR knockdown decreased urine albumin to creatinine rati

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

92 autocrine/paracrine cytokines in modulating PRR-initiated signaling.

93 red with offspring of normal weight mothers, PRRs of aortic arch defects and transposition of the gre

94 bserved upon chronic stimulation of multiple PRRs.

95 gent regulators that associate with multiple PRRs in plants(4).

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

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

98 RLCKs from the PRR complex and activation of PRR signalling.

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

100 unostaining revealed increased deposition of PRR, collagen and fibronectin in diabetic kidney.

101 In conclusion, increased expression of PRR localized in renal mitochondria and diabetic kidney

102 iabetic mice showed increased expressions of PRR and NOX4 in both total kidney tissue and renal mitoc

103 reatinine ratio and the renal expressions of PRR, NOX4, UCP2, caspase3, phos-FOXO3a, phos-NF-kappaB,

104 on of the Toll-like receptor (TLR) family of PRR may regulate epithelial barrier integrity by upregul

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

106 ht the latest progress in the involvement of PRR for the vacuolar H(+) -ATPase activity.

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

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

109 study reveals the intertwined regulation of PRR-RLCK complex activation by protein phosphorylation a

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

111 ens, and discuss how classical activation of PRRs and ETI interplay to drive inflammatory responses.

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

113 ve demonstrated that TZF1 acts downstream of PRRs to attenuate TOR signaling.

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

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

116 show that RLP/KSeq enables rapid mapping of PRRs and is especially beneficial for crop plants with l

117 e, our pipeline shows accelerated mapping of PRRs.

118 The null mutants of PRRs display much reduced sensitivities to sugar-activat

119 ion for their ability to activate a panel of PRRs, and analyzed this reactivity in relation to biopsy

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

121 MDA5 that challenge the conventional view of PRRs.

122 hese outcomes were particularly dependent on PRR-initiated autocrine/paracrine IL-12-induced STAT4 ac

123 Ongoing PRR stimulation can confer epigenetic changes in macroph

124 s how sensory neurons utilize TLRs and other PRR pathways to detect danger signals in their environme

125 Sensory neurons also express TLRs and other PRRs that directly sense danger signals after injury or

126 TU RECEPTOR (EFR) and PEP1 RECEPTOR1 (PEPR1) PRRs, and was phosphorylated in vitro by PEPR1 and EFR i

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

128 activated FLS2 and other non-activated plant PRRs are recycled remain not well understood.

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

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

131 sceptible E. coli isolates, whereas positive PRR values, indicating resistance to polymyxins, were ob

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

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

134 We calculated polymyxin resistance ratio (PRR) values from the acquired spectra; PRR values of 0,

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

136 calculated adjusted prevalence rate ratios (PRRs) with 95% confidence intervals.

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

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

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

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

141 pathogens, and pattern recognition receptor (PRR) ligands, and investigating the course of systemic i

142 CMVs), through pattern-recognition receptor (PRR) pathways involving MyD88 or STING constitute a firs

143 intracellular pattern recognition receptor (PRR) responsible for sensing bacterial peptidoglycan fra

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

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

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

147 ht to identify pattern recognition receptor (PRR) signaling pathway(s) that mediates the inflammatory

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

149 nvolvement in pathogen recognition receptor (PRR) signaling.

150 ound that upon pattern-recognition receptor (PRR) stimulation of human monocyte-derived macrophages (

151 in response to pattern-recognition receptor (PRR) stimulation.

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

153 pled and novel pattern recognition receptor (PRR), P2RY10, as a central regulator of these genes.

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

155 variability in pattern recognition receptor (PRR)-induced cytokines in macrophages.

156 variability in pattern-recognition receptor (PRR)-induced cytokines in myeloid cells.

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

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

159 hanisms of the pattern recognition receptor (PRR)-mediated inflammatory response to subvert host cell

160 implicated in pattern recognition receptor (PRR)-triggered immunity (PTI) because its transcript abu

161 ed that increased renal (Pro)renin receptor (PRR) expression in diabetes contributes to development o

162 The (pro)renin receptor (PRR), a key regulator of intrarenal renin-angiotensin sy

163 innate immune pattern recognition receptors (PRR) are expressed at epithelial surfaces and modulate e

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

165 engagement of pattern recognition receptors (PRR) on resident tissue cells and circulating leukocytes

166 onses through pattern-recognition receptors (PRR).

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

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

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

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

171 Pattern recognition receptors (PRRs) are crucial for responses to infections and tissue

172 Pattern recognition receptors (PRRs) expressed in antigen-presenting cells are thought

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

174 by activating pattern-recognition receptors (PRRs) in the host.

175 ns (MAMPs) by pattern recognition receptors (PRRs) induces currents mediated via slow-type (S-type) a

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

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

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

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

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

181 s, important pattern- recognition receptors (PRRs) of the complement system.

182 ucts activate pattern recognition receptors (PRRs) on antigen-presenting cells, including monocytes a

183 Pattern recognition receptors (PRRs) on immune and parenchymal cells can detect danger-

184 activated by pattern recognition receptors (PRRs) on the membrane of innate immune cells play an imp

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

186 ll-associated pattern recognition receptors (PRRs) recognize and respond to microbial ligands.

187 s mediated by pattern recognition receptors (PRRs) remain less utilized.

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

189 Pattern recognition receptors (PRRs) sense microbial patterns and activate innate immun

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

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

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

193 innate immune pattern recognition receptors (PRRs) such as Toll-like receptors (TLRs) stimulates cell

194 AMPs) through pattern recognition receptors (PRRs) such as Toll-like receptors (TLRs), and produce in

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

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

197 TLRs) are the pattern recognition receptors (PRRs) that recognize pathogen-associated molecular patte

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

199 sRNA-sensing pathogen recognition receptors (PRRs) TLR3 and RIG-I specifically respond to poly(I:C) a

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

201 ace-localized pattern recognition receptors (PRRs) to detect pathogen- or damage-associated molecular

202 mal cells use pattern-recognition receptors (PRRs) to detect specific pathogens.

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

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

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

206 Pathogen pattern recognition receptors (PRRs) trigger innate immune responses to invading pathog

207 ns (MAMPs) by pattern recognition receptors (PRRs) triggers the first line of inducible defence again

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

209 ownstream of pathogen recognition receptors (PRRs) which are known to be involved in host antiviral d

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

211 Pattern recognition receptors (PRRs), including the Toll-like receptor (TLR) family are

212 ction through pattern recognition receptors (PRRs), leading to type I interferon production.

213 RNase L bind pattern recognition receptors (PRRs), like retinoic acid-inducible I (Rig-I) and melano

214 f RNA-sensing pattern recognition receptors (PRRs), or their co-receptors, in the LFRT contributes to

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

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

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

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

219 hat stimulate pattern-recognition receptors (PRRs).

220 n by specific pattern recognition receptors (PRRs).

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

222 ctivate other pattern recognition receptors (PRRs).

223 the family of pattern recognition receptors (PRRs).

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

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

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

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

228 rminal domain (NTD) and proline-rich region (PRR) in regulating interactions of Tau with soluble tubu

229 domain and an upstream proline-rich region (PRR) that by themselves are sufficient for actin interac

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

231 CK interact with TSAD's proline-rich region (PRR) through their Src homology 3 (SH3) domains.

232 negative charge in the proline-rich region (PRR), and a decrease in positive charge in the microtubu

233 ains (TAD1 and TAD2), a proline-rich region (PRR), and multiple phosphorylation sites.

234 that the STAT1/STAT4 variant might regulate PRR-initiated responses in a complementary and cooperati

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

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

237 have found that Pseudo Response Regulators (PRRs), essential components of circadian core oscillator

238 s of these two prominent and closely related PRR families.

239 glycan sensing, NOD1 and the closely related PRR NOD2 have been linked to inflammation by responding

240 pplied to evaluate the activation of related PRRs and engagement of adaptors.

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

242 asis of these results, we propose that Tau's PRR can serve as a core tubulin-binding domain, whereas

243 We found that Tau's PRR is an independent tubulin-binding domain that has tu

244 Our findings support a role for RNA-sensing PRRs in the dampened innate immunity against ZIKV in the

245 Alternatively, activation of specific PRR pathways can aid pathogen survival.

246 atio (PRR) values from the acquired spectra; PRR values of 0, indicating polymyxin susceptibility, we

247 Both epithelial and subepithelial PRR expression were induced during rhinovirus infection.

248 atory function, increasing evidence suggests PRR can also act in a variety of intracellular signaling

249 precise identification of plants with target PRRs, and subsequent RLP/K enrichment sequencing (RLP/KS

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

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

252 We hypothesized that PRR is localized in renal mitochondria and contributes t

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

254 Our findings support a notion that PRR-TZF1-TOR molecular axis modulates root meristem cell

255 rather than from self, it is now clear that PRRs can also be activated by endogenous ligands, bacter

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

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

258 Here, we show that TAD2 and the PRR inhibit DNA binding by directly interacting with the

259 NMR spectroscopy revealed that TAD2 and the PRR interact with the DBD at or near the DNA binding sur

260 we demonstrate that interactions between the PRR and MTBR are reduced by the NTD through a conserved

261 in heterogeneous Tau: tubulin complexes, the PRR bound tubulin tightly and stoichiometrically.

262 to the release of BIK1 family RLCKs from the PRR complex and activation of PRR signalling.

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

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

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

266 dynamics that are distinct from those of the PRR FLS2.

267 tudy draw attention to a central role of the PRR in Tau function and provide mechanistic insight into

268 We found that short-term stimulation of the PRR NOD2 in primary human monocyte-derived macrophages r

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 terns flg22 and flgII-28, which activate the PRRs Fls2 and Fls3, respectively.

274 t expression of IFN-alpha, IFN-beta, and the PRRs: Toll-like receptor 3, melanoma differentiation-ass

275 CIRCADIAN CLOCK ASSOCIATED 1 and PRR9 by the PRRs.

276 The repressive action of the PRRs on both growth and DTG expression requires the PIFs

277 Protein interaction assays indicate that the PRRs exert their repressive activity by binding directly

278 ese findings support the conclusion that the PRRs function as direct outputs from the core circadian

279 We show that the PRRs function to suppress PIF-stimulated growth in the l

280 Whether the PRRs of the C-type lectin receptor (CLR) family includin

281 ning of portal blood for reactivity to these PRRs might prove useful for prediction and/or therapeuti

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

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

284 nd overlapping binding sites within the TSAD PRR amino acids (aa) 239-274.

285 and IL-12-associated outcomes, and in turn, PRR-induced outcomes, highlighting that these genes coop

286 K1 is thus expected to interact with unknown PRRs.

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

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

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

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

291 mulated by representative bacterial or viral PRR ligands.

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

293 .74-2.38) and 14.8% (23 of 155) at 2 weeks (PRR, 1.50; 95% CI, .86-2.62) after MC.

294 at the C terminus and downstream of the WH2-PRR domain produces a long (SHTN1L or shootin1b) and a s

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