ライフサイエンスコーパス: PAMP

1 PAMP binding activates RIG-I to induce innate immune sig

2 PAMP perception leads to BIR2 release from the BAK1 comp

3 PAMP perception results in rapid and transient activatio

4 PAMP recognition of T/F HCV variants by RIG-I may theref

5 PAMP responses include changes in intracellular protein

6 A PAMP selectivity test was carried out in line with our i

7 In addition, lipoteichoic acid, a PAMP produced by Gram-positive bacteria that activates T

8 CV-infected liver and has features of both a PAMP and a genomic reservoir.

9 plies that the immune response elicited by a PAMP is more complex than predicted by the examination o

10 P. syringae strains were able to overcome a PAMP pretreatment in tobacco or Arabidopsis (Arabidopsis

11 ciently present Ags linked to the activating PAMP and prime naive T cells.

12 s represents the first description of active PAMP masking by a Candida species, a process that reduce

13 ) MPK6 and MPK3, are rapidly activated after PAMP treatment, and are thought to positively regulate a

14 ogen-associated molecular patterns (DAMP and PAMP, respectively) through pattern recognition receptor

15 EG3 acted as PAMPs to trigger cell death and PAMP-triggered immunity (PTI) independent of their enzym

16 s a component of ethylene (ET) signaling and PAMP-triggered immunity (PTI) to fungal pathogens.

17 Mitochondrial DAMPs and PAMPs share the same pattern recognition receptors.

18 gen-associated molecular patterns (DAMPs and PAMPs).

19 ceptors (TLRs) that recognize such DAMPs and PAMPs, or the downstream effector molecules they engende

20 pathway in discriminating between DAMPs and PAMPs.

21 hamiana and cotton, VdEG1 and VdEG3 acted as PAMPs and virulence factors, respectively indicative of

22 lium dahliae Vd991, VdEG1 and VdEG3 acted as PAMPs to trigger cell death and PAMP-triggered immunity

23 hat recognize the long stretches of dsRNA as PAMPs to activate interferon-mediated antiviral pathways

24 ort the identification of a novel Ascomycete PAMP, RcCDI1, recognized by Solanaceae but not by monoco

25 n of a special class of viability-associated PAMPs (vita-PAMPs).

26 c analyses demonstrate that CPK28 attenuates PAMP-triggered immune responses and antibacterial immuni

27 F-Tu receptor (EFR) recognizes the bacterial PAMP elongation factor Tu (EF-Tu) and its derived peptid

28 and PG-LPS prior to stimulation by bacterial PAMPs.

29 are still required to identify new bacterial PAMPs.

30 only the continuous expression of bacterial PAMPs on transgenic T. cruzi sustains these responses, r

31 ionarily conserved similarities to bacterial PAMPs into the circulation.

32 ng T3Es, provides a mechanistic link between PAMP-triggered immunity (PTI) and effector-triggered imm

33 calcium-dependent protein kinases, and both PAMP-induced BIK1 activation and BIK1-mediated phosphory

34 vivo phosphorylation of RBOHD occurs on both PAMP- and ROS stimulation.

35 Both PAMPs and DAMPs can be liberated by early insults to the

36 tis cinerea and Alternaria brassisicola Both PAMPs and osmotic stress activate some of the same MPKs

37 st, EBOV VP35 can inhibit activation by both PAMPs.

38 Confirming our idea that both PAMPs and DAMPs are likely to cooccur at infection sites

39 In vitro, hepcidin induction by PAMPs in primary human hepatocytes was abolished by the

40 The vast majority of PRRs controlling PAMP-triggered immunity (PTI) and the mechanisms used by

41 e lumen of MHC II compartments and cytosolic PAMPs to endosomal TLRs, (ii) it is crucial in T cell re

42 lant upon treatment with a bacterial-derived PAMP, flg22.

43 TLR activation requires bacterially derived PAMPs and that endogenously produced alarmins are not su

44 n is down-regulated in response to different PAMPs.

45 Insights on differential PAMP recognition and inhibition of IFN induction by a si

46 5 are essential PRRs that recognize distinct PAMPs that accumulate during WNV replication.

47 1 (MKP1) as a negative regulator of diverse PAMP responses, including activation of MPK6 and MPK3, t

48 phorylation in the regulation of MKP1 during PAMP signaling and resistance to bacteria.

49 We found that MKP1 was phosphorylated during PAMP elicitation and that phosphorylation stabilized the

50 planta expressed HopM1 suppresses two early PAMP-triggered responses, the oxidative burst and stomat

51 t increase in resistance to Pto and enhanced PAMP-induced growth inhibition observed in mkp1 seedling

52 e mkp1 mutant lacking MKP1 displays enhanced PAMP responses and resistance against the virulent bacte

53 In agreement with the enhanced PAMP response phenotypes observed in the mkp1 mutant, we

54 Thus, GCK is an essential PAMP effector coupling JNK and p38, but not ERK or NF-ka

55 rthe oryzae and Neurospora crassa, exhibited PAMP activity, inducing cell death in Solanaceae but not

56 Thus endogenous danger signals and exogenous PAMPs elicit similar responses through seemingly similar

57 ng of and transgenic expression of exogenous PAMPs all result in enhanced early adaptive immune respo

58 o phosphorylated by MPK4 and, upon flagellin PAMP treatment, PAT1 accumulates and localizes to cytopl

59 he nucleus, whose levels increased following PAMP treatment or infection with an avirulent pathogen.

60 cell surface TLR2, requiring degradation for PAMP recognition.

61 identify LRR-type RKs and RLPs required for PAMP perception/responsiveness, even when the active pur

62 function of 14-3-3 proteins is required for PAMP-triggered oxidative burst and stomatal immunity, an

63 In addition, a role for PAMP and DAMP perception in bolstering effector-triggere

64 A direct role for PAMPs in TLR activation was not supported in a transacti

65 Arabidopsis has at least four PAMP/pathogen-responsive MAPKs: MPK3, MPK6, MPK4 and MPK

66 We characterized a novel fungal PAMP, Cell Death Inducing 1 (RcCDI1), identified in the

67 This activation in response to the fungal PAMP chitin requires a chitin receptor and one or more M

68 e BAK1-independent recognition of the fungal PAMP chitin.

69 The HCV PAMP RNA stimulated RIG-I-dependent signalling to induce

70 analysis for the first time identifies RIG-I PAMPs under natural infection conditions and implies tha

71 fferent methods that can be used to identify PAMPs/DAMPs and PRRs.

72 t disruption of gck in mice strongly impairs PAMP-stimulated macrophage cytokine and chemokine releas

73 ovel specific requirement for AO activity in PAMP-triggered RBOHD-dependent ROS burst and stomatal im

74 roles of long-known signalling components in PAMP-triggered immunity (PTI).

75 or some, but not all, of MKP1's functions in PAMP responses and defense against bacteria.

76 mammalian Sterile 20 (STE20) orthologue, in PAMP signaling, and systemic inflammation.

77 ansgenically expressing HopK1 are reduced in PAMP-triggered immune responses compared with wild-type

78 Consistent with its role in PAMP-triggered immunity, CRT1 interacted with the PAMP r

79 ociated molecular patterns (PAMPs) to induce PAMP-triggered immunity (PTI) also restricts T3SS effect

80 sociated molecular patterns (PAMPs) inducing PAMP-triggered immunity (PTI) or by recognizing pathogen

81 function experiments show that HBI1 inhibits PAMP-induced growth arrest, defense gene expression, rea

82 However, in contrast to other known PAMPs/DAMPs, cellobiose stimulates neither detectable re

83 Here, we comprehensively review known PAMPs/DAMPs recognized by plants as well as the plant PR

84 Furthermore, because many PAMPs on microbes share molecular identity and/or mimicr

85 KP1 as a negative regulator of MPK6-mediated PAMP responses.

86 enic Escherichia coli (CFT073) and microbial PAMPs including flagellin, LPS and peptidoglycan.

87 systemic inflammation triggered by molecular PAMPs, inflammasome component NLRP3 mutation, and ASC da

88 se to a panel of pathogen-derived molecules (PAMPs) in mice and human primary hepatocytes.

89 ogen-associated molecular pattern molecules (PAMPs) are derived from microorganisms and recognized by

90 ogen-associated molecular pattern molecules (PAMPs) elicited a normal response; however, NF-kappaB-me

91 ogen-associated molecular pattern molecules (PAMPs) including bacterial endotoxin, respiratory viruse

92 ogen-associated molecular pattern molecules (PAMPs) such as LPS activate the endothelium and can lead

93 ogen-associated molecular pattern molecules (PAMPs), which are recognized by pattern recognition rece

94 Most PAMPs and DAMPs serve as so-called 'Signal 0s' that bind

95 ), is intrinsically adjuvanted with multiple PAMPs and induces a vigorous anti-WNV humoral response.

96 set of bioassays to study the activation of PAMP-triggered immunity (PTI) in wheat.

97 of Exo70B2 contributes to the attenuation of PAMP-induced signaling.

98 knowledge about the spatial distribution of PAMP-induced Ca(2+) signals is limited.

99 munity was sceptical about the importance of PAMP perception in plants.

100 ciated molecular patterns (PAMPs) as part of PAMP-triggered immunity (PTI).

101 In contrast, negative regulation of PAMP responses by downstream phosphatases remains poorly

102 with BIR2 acting as a negative regulator of PAMP-triggered immunity by limiting BAK1-receptor comple

103 h PUB23 and PUB24 as a negative regulator of PAMP-triggered responses.

104 ignaling, the regulation and significance of PAMP-induced ion fluxes in immunity remain unknown.

105 oxygen species, accumulation of a subset of PAMP-regulated transcripts, and inhibition of seedling g

106 basal resistance, i.e., poor suppression of PAMP-triggered defense by effectors.

107 tin proteasome system for the suppression of PAMP-triggered immunity in plants.

108 ation of airborne fungi, surface exposure of PAMPs and melanin removal, are necessary for LAP activat

109 Surface exposure of PAMPs during germination can leave the pathogen vulnerab

110 requirement for the continuous expression of PAMPs for optimal anti-pathogen immunity.

111 se deposition independent of the presence of PAMPs.

112 by signal two, which involves recognition of PAMPs or damage-associated molecular patterns (DAMPs), s

113 ition receptor that recognizes many types of PAMPs that originate from gram-positive bacteria.

114 distinct from that triggered by the oomycete PAMP INF1.

115 s a pathogen-associated molecular pattern or PAMP) to trigger intracellular signaling events that ind

116 tion, which we find can be primed with other PAMPs, including hepatitis C virus RNA.

117 ing to pathogen associated molecular patter (PAMP) motifs within RNA ligands that accumulate during v

118 es as pathogen-associated molecular pattern (PAMP) and is a potent immune stimulator for innate immun

119 nized pathogen-associated molecular pattern (PAMP) capable of activating a type I IFN response via th

120 erial pathogen-associated molecular pattern (PAMP) counterpart, has been achieved using hybridized to

121 erial pathogen-associated molecular pattern (PAMP) driving host type I IFN responses and autophagy.

122 f the pathogen-associated molecular pattern (PAMP) encountered by endogenous DC.

123 a key pathogen-associated molecular pattern (PAMP) located at the cell surface of C. albicans and oth

124 and a pathogen-associated molecular pattern (PAMP) motif located within the 3' untranslated region co

125 nizes pathogen-associated molecular pattern (PAMP) motifs to differentiate between viral and cellular

126 have pathogen-associated molecular pattern (PAMP) receptors for dsRNA because of the presence of hos

127 cific pathogen-associated molecular pattern (PAMP) recognition pathways, we determined that the dampe

128 ommon pathogen-associated molecular pattern (PAMP) recognized by TLR7.

129 , and pathogen-associated molecular pattern (PAMP) signals repress HBI1 transcription.

130 e and pathogen-associated molecular pattern (PAMP) stimulation had a strong cooperative effect on mac

131 se to pathogen-associated molecular pattern (PAMP) stimulation.

132 ommon pathogen-associated molecular pattern (PAMP) that induces potent innate immune responses.

133 y the pathogen-associated molecular pattern (PAMP) that initiated this cell-autonomous response.

134 NA, a pathogen-associated molecular pattern (PAMP), comprised 52% (standard deviation, 28%) of the HC

135 duced pathogen-associated molecular pattern (PAMP)-induced gene expression and callose deposition in

136 (DC) pathogen-associated molecular pattern (PAMP)-induced pro-inflammatory cytokine production, inhi

137 tween pathogen-associated molecular pattern (PAMP)-triggered immunity (PTI) and brassinosteroid (BR)-

138 both pathogen-associated molecular pattern (PAMP)-triggered immunity (PTI) and effector-triggered im

139 FR in pathogen-associated molecular pattern (PAMP)-triggered immunity (PTI) and the LRR-RLK BRI1 in b

140 nt is pathogen-associated molecular pattern (PAMP)-triggered immunity (PTI).

141 d for pathogen-associated molecular pattern (PAMP)-triggered immunity (PTI).

142 uring pathogen-associated molecular pattern (PAMP)-triggered immunity in plants.

143 press pathogen-associated molecular pattern (PAMP)-triggered immunity in rice.

144 d for pathogen-associated molecular pattern (PAMP)-triggered immunity, basal resistance, non-host res

145 nize pathogen-associated molecular patterns (PAMP) and mediate innate immune responses, and TLR agoni

146 e to pathogen associated molecular patterns (PAMP), and (iii) it is an effector of Th1-Th2 polarizati

147 s to pathogen-associated molecular patterns (PAMP), enhanced cell death, and resistance to bacterial

148 n- and damage-associated molecular patterns (PAMPs and DAMPs) orchestrate inflammatory responses to i

149 en- or danger-associated molecular patterns (PAMPs or DAMPs).

150 n- or microbe-associated molecular patterns (PAMPs or MAMPs, respectively), such as flagellin, initia

151 bial pathogen-associated molecular patterns (PAMPs) activate innate immunocytes through pattern recog

152 rved pathogen-associated molecular patterns (PAMPs) and activate MAP kinase cascades, which regulate

153 nize pathogen-associated molecular patterns (PAMPs) and activate signaling pathways that lead to immu

154 s to pathogen-associated molecular patterns (PAMPs) and bacterial type III effector proteins (T3Es).

155 nous pathogen-associated molecular patterns (PAMPs) and danger-associated molecular patterns (DAMPs)

156 rous pathogen-associated molecular patterns (PAMPs) and have been shown to combat various viral, para

157 s as pathogen-associated molecular patterns (PAMPs) and initiate an antiviral immune response.

158 n of pathogen-associated molecular patterns (PAMPs) and other environmental stresses trigger transien

159 n of pathogen-associated molecular patterns (PAMPs) and recognition by the host Pto kinase of pathoge

160 e of pathogen-associated molecular patterns (PAMPs) and their binding to pattern recognition receptor

161 d by pathogen-associated molecular patterns (PAMPs) and undergo maturation.

162 Pathogen-associated molecular patterns (PAMPs) are detected by plant pattern recognition recepto

163 Pathogen-associated molecular patterns (PAMPs) are known to be fundamental in instigating immune

164 s to pathogen-associated molecular patterns (PAMPs) are mediated by cell surface pattern recognition

165 and pathogen-associated molecular patterns (PAMPs) as part of PAMP-triggered immunity (PTI).

166 zing pathogen-associated molecular patterns (PAMPs) but have also been implicated in the recognition

167 rved pathogen-associated molecular patterns (PAMPs) by host pattern recognition receptors (PRRs) resu

168 cing pathogen-associated molecular patterns (PAMPs) by influenza A viruses using inhibitors of these

169 n of pathogen-associated molecular patterns (PAMPs) by pattern recognition receptors (PRRs).

170 n of pathogen-associated molecular patterns (PAMPs) by pattern-recognition receptors (PRRs) located o

171 n of pathogen-associated molecular patterns (PAMPs) by plasma membrane-localized pathogen recognition

172 n of pathogen-associated molecular patterns (PAMPs) by surface-localized pattern recognition receptor

173 n of pathogen-associated molecular patterns (PAMPs) by surface-localized pattern recognition receptor

174 n of pathogen-associated molecular patterns (PAMPs) by surface-localized pattern-recognition receptor

175 s) or pattern-associated molecular patterns (PAMPs) by the innate immune system.

176 inct pathogen-associated molecular patterns (PAMPs) containing 5' triphosphate and double-stranded RN

177 d by pathogen associated molecular patterns (PAMPs) during infection, including RNA and proteins from

178 and pathogen-associated molecular patterns (PAMPs) in oomycetes.

179 and pathogen-associated molecular patterns (PAMPs) induced IL-1beta release have been demonstrated i

180 n as pathogen-associated molecular patterns (PAMPs) inducing PAMP-triggered immunity (PTI) or by reco

181 ling pathogen-associated molecular patterns (PAMPs) is a principal strategy used by fungi to avoid im

182 ) by pathogen-associated molecular patterns (PAMPs) is in essence sufficient to stop pathogen invasio

183 tive pathogen-associated molecular patterns (PAMPs) leads to production of proinflamatory cytokines,

184 eive pathogen-associated molecular patterns (PAMPs) or damage-associated molecular patterns (DAMPs).

185 ough pathogen associated molecular patterns (PAMPs) or through danger associated molecular patterns (

186 wall pathogen-associated molecular patterns (PAMPs) orientate the host response toward either fungal

187 ough pathogen-associated molecular patterns (PAMPs) produced by Gram-positive bacteria are likely to

188 the pathogen-associated molecular patterns (PAMPs) responsible for T. denticola activation of the in

189 n of pathogen-associated molecular patterns (PAMPs) such as bacterial flagellin-derived flg22 trigger

190 s to pathogen-associated molecular patterns (PAMPs) that are conserved across broad classes of infect

191 rved pathogen-associated molecular patterns (PAMPs) that are recognized by pattern recognition recept

192 n of pathogen-associated molecular patterns (PAMPs) that are targeted to specific immune cells.

193 ense pathogen-associated molecular patterns (PAMPs) that are typical of whole classes of microbes.

194 p of pathogen-associated molecular patterns (PAMPs) that efficiently trigger innate immune activation

195 Pathogen-associated molecular patterns (PAMPs) that signal through Toll-like receptors (TLRs) ca

196 n of pathogen-associated molecular patterns (PAMPs) through pattern-recognition receptors (PRRs) on d

197 n- or microbe-associated molecular patterns (PAMPs) to elicit defenses and provide protection against

198 with pathogen-associated molecular patterns (PAMPs) to induce PAMP-triggered immunity (PTI) also rest

199 n of pathogen-associated molecular patterns (PAMPs) triggers a phosphorylation relay leading to PAMP-

200 iral Pathogen-Associated Molecular Patterns (PAMPs), and by the potential for 'arms race' coevolution

201 OS), pathogen-associated molecular patterns (PAMPs), and damage-associated molecular patterns (DAMPs)

202 bial pathogen-associated molecular patterns (PAMPs), are repressed by the interaction [corrected] of

203 Ps), pathogen-associated molecular patterns (PAMPs), danger-associated molecular patterns (DAMPs), an

204 iple pathogen-associated molecular patterns (PAMPs), including beta-glucan.

205 n of pathogen-associated molecular patterns (PAMPs), such as bacterial flagellin (or the peptide flg2

206 iral pathogen-associated molecular patterns (PAMPs), such as double-strandedness and dsRNA blunt ends

207 n of pathogen-associated molecular patterns (PAMPs), such as LPS or other colonizing/invading microbe

208 rial pathogen associated molecular patterns (PAMPs), such as LPS, is well established to induce toler

209 Pathogen-associated molecular patterns (PAMPs), which are detected by the immune system, are pre

210 tent pathogen-associated molecular patterns (PAMPs).

211 ying pathogen-associated molecular patterns (PAMPs).

212 rved pathogen-associated molecular patterns (PAMPs).

213 d to pathogen-associated molecular patterns (PAMPs).

214 g to pathogen-associated molecular patterns (PAMPs).

215 rved pathogen-associated molecular patterns (PAMPs).

216 rial pathogen-associated molecular patterns (PAMPs).

217 n as pathogen-associated molecular patterns (PAMPs).

218 n of pathogen associated molecular patterns (PAMPs).

219 s by pathogen-associated molecular patterns (PAMPs).

220 d by pathogen associated molecular patterns (PAMPs).

221 iral pathogen-associated molecular patterns (PAMPs).

222 with pathogen-associated molecular patterns (PAMPs)/danger-associated molecular patterns, including d

223 iral pathogen-associated molecular patterns (PAMPs)/live virus, alone and in combination.

224 via pathogen-associated molecular patterns (PAMPs, such as lipopolysaccharides), which leads to prem

225 hogen/microbe-associated molecular patterns (PAMPs/MAMPs) and pathogen effectors.

226 n- or microbe-associated molecular patterns (PAMPs/MAMPs) are detected as nonself by host pattern rec

227 (or microbe)-associated molecular patterns (PAMPs/MAMPs) by pattern recognition receptors (PRRs) is

228 ogen-/microbe-associated molecular patterns (PAMPs/MAMPs) or damage-associated molecular patterns (DA

229 ngage pathogen-associated molecule patterns (PAMPs) present in viral products.

230 al "pathogen-associated molecular patterns" (PAMPs), we postulate that host-derived, oxidation-specif

231 ens (pathogen-associated molecular patterns, PAMPs), whereas others bind endogenous plant compounds (

232 r with proadrenomedullin N-terminal peptide (PAMP), by the Adm gene (adrenomedullin gene).

233 hich selectively abrogated AM, but preserved PAMP, expression (Adm(AM+/Delta) animals).

234 tokine/chemokine production, thus preserving PAMP-mediated TLR4-MD-2 responses.

235 equesters chitin oligosaccharides to prevent PAMP-triggered immunity in rice, thereby facilitating ra

236 Such PRR-PAMP interactions lead to PRR-dependent nonself-recognit

237 The few PRR/PAMP pairs that are characterised provide useful models

238 esponsiveness, even when the active purified PAMP has not been defined.

239 receptor; PRR, pattern recognition receptor; PAMP, pathogen-associated molecular pattern; LPS, lipopo

240 lular and endosomal receptors that recognize PAMPs from a wide range of microbial pathogens.

241 eptic shock where Toll receptor 4 recognizes PAMPs.

242 HBI1 overexpression leads to reduced PAMP-triggered responses.

243 Disruption of gck substantially reduces PAMP activation of macrophage Jun-N-terminal kinase (JNK

244 A5) activation by double strandedness of RNA PAMPs (coating backbone) but is unable to inhibit activa

245 vely gauges the infectious risk by searching PAMPs for signatures of microbial life and thus infectiv

246 hibits immune responses triggered by several PAMPs and anti-bacterial immunity.

247 studies have focused on LPS, a TLR4-specific PAMP produced by Gram-negative bacteria.

248 panosoma cruzi, which is deficient in strong PAMPs, we demonstrate a requirement for the continuous e

249 Upon binding to such PAMP motifs, RIG-I initiates a signalling cascade that i

250 micry with oxidation-specific epitopes, such PAMPs provide a strong secondary selecting pressure for

251 HKPG and PG-LPS differentially suppress PAMP-induced TNFalpha, IL-6 and IL-10 but fail to suppre

252 host tissue, indicating that XopN suppresses PAMP-triggered immune responses during Xcv infection.

253 and later responses triggered by all tested PAMPs, suggestive of a role in signaling.

254 Previous evidences suggest that PAMP-triggered immunity (PTI) is under constant negative

255 er in length and complexity, suggesting that PAMP diversity in T/F genomes could regulate innate immu

256 These findings demonstrate that PAMPs function to potentiate adaptive immune responses w

257 These results support the hypothesis that PAMPs produced by low levels of bacterial colonization m

258 lation of these residues is critical for the PAMP-induced ROS burst and antibacterial immunity.

259 se results unveil the impact of HopM1 on the PAMP-triggered oxidative burst and stomatal immunity in

260 triggered immunity, CRT1 interacted with the PAMP recognition receptor FLS2.

261 In the absence of PDIM, these PAMPs signal a Toll-like receptor (TLR)-dependent recrui

262 This PAMP-independent effect of SA causes a transient reducti

263 re investigated, understanding the known TLR-PAMP interactions, through the exploitation of this elec

264 particles (SVLPs) carrying hydrophobic TLR2 PAMPs within di- and triacylated lipopeptide cores (P2Cy

265 ecognized intracellular exposure of the TLR2 PAMPs carried by di- and triacylated SVLP cores, which i

266 triggers a phosphorylation relay leading to PAMP-triggered immunity (PTI).

267 the insensitivity of g6pd6 mutant plants to PAMP-induced growth inhibition was complemented by a pho

268 ss clear are whether and how the response to PAMP and DAMP are regulated differentially.

269 nition receptors (PRRs), which gives rise to PAMP-triggered immunity (PTI).

270 potentiates the responsiveness of plants to PAMPs.

271 They can also respond to PAMPs, but the previous encounter of inflammatory signal

272 e modes of signaling for PRRs in response to PAMPs and SA.

273 had greatly diminished hepcidin response to PAMPs.

274 phosphorylated and activated in response to PAMPs.

275 , and plants are rendered more responsive to PAMPs.

276 and ACD6-dependent reduced responsiveness to PAMPs.

277 affects the responsiveness of plants to two PAMPs.

278 length of the U-core motif of the poly-U/UC PAMP and are recognized by RIG-I to induce innate immune

279 al cell wall peptidoglycan (CW), a universal PAMP for TLR2, traverses the murine placenta into the de

280 The perception of several unrelated PAMPs rapidly induced ASKalpha kinase activity.

281 gered by the perception of several unrelated PAMPs.

282 In contrast to its expression pattern upon PAMP treatment, HBI1 expression is enhanced by BR treatm

283 interacts with and phosphorylates RBOHD upon PAMP perception.

284 turnover of PUB22, which is stabilized upon PAMP perception.

285 Targeting antigen to immune cells via PAMP-modified biomaterials is a new strategy to control

286 IFN responses induced by CS plus virus/viral PAMP in combination.

287 These studies demonstrate that CS and viral PAMPs/live virus interact in a synergistic manner to sti

288 While the exact nature of the viral PAMPs remains to be determined, our data suggest that in

289 ling responses induced by CS and virus/viral PAMPs in lungs from RNase L null and wild-type mice.

290 erimental system the major influenza A virus PAMPs are distinct from those of incoming genomes or pro

291 identify prokaryotic messenger RNA as a vita-PAMP present only in viable bacteria, the recognition of

292 ate in live Gram-positive bacteria is a vita-PAMP, engaging the innate sensor stimulator of interfero

293 y STING-dependent sensing of a specific vita-PAMP and elucidate how innate receptors engage multilaye

294 This vita-PAMP-induced ER-phagy additionally orchestrates an inter

295 Vita-PAMPs denote microbial viability, signaling the danger o

296 Vaccine formulations that incorporate vita-PAMPs could thus combine the superior protection of live

297 Detection of vita-PAMPs triggers a state of alert not warranted for dead b

298 al class of viability-associated PAMPs (vita-PAMPs).

299 and innate immune activation correlate with PAMP sequence characteristics.

300 cated into the host cell and interferes with PAMP-triggered immunity (PTI).