ライフサイエンスコーパス: DAMP

1 DAMP recognition by dendritic cells (DCs) has also been

2 DAMPs are recognized by the innate immune system via pat

3 DAMPs encompass a group of heterogenous molecules, inclu

4 DAMPs represent a heterogeneous group of molecules that

5 DAMPs trigger innate immunity by activating Toll-like re

6 DAMPs within the tumor microenvironment stimulate tumor-

7 observed that circulating levels of these 2 DAMPs are increased in hypertension, and activation of T

8 4-DAMP inhibited neurogenic secretion by 80 and 95%, respe

9 and blocked by atropine methylbromide and 4-DAMP mustard, an M(3) muscarinic receptor selective anta

10 5.0 nM for telenzepine, methoctramine and 4-DAMP, respectively.

11 elective muscarinic M3 receptor antagonist 4-DAMP (100 nmol/L) but was blocked by the M2 receptor ant

12 The M3 mAChR antagonist 4-DAMP abolished the stimulatory effect of oxotremorine-M

13 The M3 muscarinic receptor antagonist 4-DAMP effectively reversed muscarine-induced inhibition o

14 s inhibited by the m3 receptor antagonist, 4-DAMP, and binding to Galphai3 antibody was inhibited by

15 In contrast, the M3-selective antagonist, 4-DAMP-mustard, blocked muscarinic excitations in a majori

16 activity was also completely inhibited by 4-DAMP in both species.

17 potentials (EJP) were partially blocked by 4-DAMP in half of the cells tested.

18 y gallamine (10(-5) M), and 72% +/- 11% by 4-DAMP mustard (10(-5) M).

19 dispersed muscle cells was accentuated by 4-DAMP or Gbeta antibody (55 +/- 8 to 63 +/- 6%).

20 6%); the increase in cAMP was abolished by 4-DAMP or Gbeta antibody.

21 yperpolarization was reversibly blocked by 4-DAMP, charybdotoxin or BAPTA-AM, but not by N(omega)-nit

22 an increase in cAMP that was abolished by 4-DAMP.

23 ts, identifying both rapidly dissociating (4-DAMP, himbacine) and slowly dissociating (tiotropium, gl

24 (3) receptor pathway was blocked by either 4-DAMP or by intracellular dialysis with anti-Galphaq anti

25 -(2-chloroethyl)-piperidine hydrochloride (4-DAMP mustard; M3) were incubated with carbachol to deter

26 -(2-chloroethyl)-piperidine hydrochloride (4-DAMP; 10(-5) M) for 10 minutes.

27 nylacetoxy-N-methyl-piperidine methiodide (4-DAMP) was 57-244-fold smaller than that of pirenzepine,

28 enylacetoxy-N-methylpiperidine methiodide (4-DAMP; M1 and M3).

29 ylacetoxy-N-methylpiperidine methobromide (4-DAMP) for the M3 receptor.

30 act cells, and the m3-mAChR selectivity of 4-DAMP and pFHHSiD was 2.4- and 3.9-fold less in membranes

31 The m3-mAChR selectivity of 4-DAMP in intact cells was unaffected by cytoskeletal depo

32 onses were blocked by atropine (10 mum) or 4-DAMP (100 nm), an M(3) receptor antagonist.

33 order of potency (atropine > pirenzepine = 4-DAMP >> gallamine) consistent with regulation by M1, rat

34 response curve to methoctramine but not to 4-DAMP, pirenzepine, or tropicamide.

35 y doubled the stimulated response, whereas 4-DAMP abolished the stimulated secretory response.

36 Here we report that actin is also a DAMP in invertebrates that lack DCs and adaptive immunit

37 coding double-stranded RNA (dsRNAs) act as a DAMP in the skin and how the human cathelicidin AMP LL-3

38 ypothesis that OGs released in vivo act as a DAMP signal to trigger plant immunity and suggest that c

39 ased from necrotic liver cells and acts as a DAMP to mediate acetaminophen-induced liver injury.

40 As a DAMP, S100A4 is sensitive to oxidation whereas uric acid

41 the host response to DAMP is controlled by a DAMP-CD24-Siglec axis.

42 Actin is a DAMP detected in mammals by the receptor, DNGR-1, expres

43 In summary, CypA is a DAMP that mediates acetaminophen poisoning.

44 uggest that under disease relevant acidosis, DAMPs and lactic acid induce the secretion of IL-1beta i

45 Although DAMPs such as endogenous DNA and nuclear high-mobility g

46 nose (PCAM), 1-deoxy-1-aminomannopyranoside (DAMP), glucosamine and low molecular weight chitosan bon

47 Microglia morphology and DAMP signaling in enriched rat hippocampal microglia wer

48 are whether and how the response to PAMP and DAMP are regulated differentially.

49 In addition, a role for PAMP and DAMP perception in bolstering effector-triggered immunit

50 Confirming our idea that both PAMPs and DAMPs are likely to cooccur at infection sites, cotreatm

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

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

53 age-associated molecular patterns (PAMPs and DAMPs) orchestrate inflammatory responses to infection a

54 This work focuses on the Arabidopsis DAMPs plant elicitor peptides (Peps) and their receptors

55 tanding that oxidation-specific epitopes are DAMPs, and thus the target of multiple arcs of innate im

56 ctors, as well as unsolved questions such as DAMP release from non-tumor cells as well as the existen

57 demonstrated that both S100A4 and UA act as DAMPs and, as such, may play a critical role in promotin

58 report that endogenous histones function as DAMPs after ischemic injury through the pattern recognit

59 esis that bone matrix components function as DAMPs for the NLRP3 inflammasome and regulate osteoclast

60 additional signals such as aging-associated DAMPs.

61 irect toward strategies aimed at attenuating DAMP-mediated inflammation while preserving antimicrobia

62 the increasingly complex connection between DAMPs and kidney diseases.

63 D24-Siglec pathway in discriminating between DAMPs and PAMPs.

64 eristics, and signaling pathways elicited by DAMPs will be critically evaluated.

65 ve immune responses are triggered in vivo by DAMPs induced by tumor progression are not well characte

66 we will review the contribution of candidate DAMPs and their receptors, and discuss the evidence for

67 A12; a potent mucosa- and neutrophil-derived DAMP.

68 ytotoxic anticancer treatment, tumor-derived DAMPs (damage-associated molecular patterns) can be sens

69 ATP acts as an effective DAMP when released into extracellular space from damaged

70 MRP8/MRP14 is an endogenous DAMP involved in various inflammatory diseases, though i

71 that the production of HMGB1, an established DAMP released by dying cells, was critical for tumor pro

72 Further evidence for DAMP signaling in behavioral responses is provided by ev

73 heir receptors, and discuss the evidence for DAMPs as tumor-promoting and anti-tumor effectors, as we

74 luble RAGE, an inhibitory decoy receptor for DAMPs.

75 These results identify a novel role for DAMPs and AMPs in the stimulation of repair and highligh

76 culture conditions, and it is not known how DAMPs signal under disease relevant conditions such as a

77 fecting activation, some recently identified DAMP receptors control specialised DC functions such as

78 TLR9 and P2X(7) are important DAMP receptors upstream of inflammasome activation, and

79 initiated by the lipid-soluble azo initiator DAMP, dimethyl 2,2'-azobis (2-methylpropionate), while Q

80 Cryopyrin activation and microbial ligand-, DAMP-, and crystal-induced IL-1beta secretion.

81 Recent evidence has indicated that the major DAMP driving host antitumor immune responses is tumor-de

82 Many DAMPs represent intracellular contents that are released

83 Mitochondrial DAMPs and PAMPs share the same pattern recognition recep

84 e we show that injury releases mitochondrial DAMPs (MTDs) into the circulation with functionally impo

85 disruption by trauma releases mitochondrial DAMPs with evolutionarily conserved similarities to bact

86 the hypothesis that acidic conditions modify DAMP-induced IL-1beta release from cultured primary mous

87 mage-associated molecular pattern molecules (DAMPs) are cell-derived and initiate and perpetuate immu

88 mage-associated molecular pattern molecules (DAMPs) including AGEs, HMGB1, S100s, and DNA.

89 mage-associated molecular pattern molecules (DAMPs) such as S100 proteins and high-mobility group box

90 mage-Associated Molecular Pattern molecules (DAMPs) suggested that, at best, early application at a s

91 Moreover, DAMPs may incite distinct downstream cellular responses

92 s who developed MODS also had elevated mtDNA DAMP levels compared with those who did not (32.57 +/- 0

93 er threshold cycles indicate increased mtDNA DAMP content.

94 with SIRS had significantly increased mtDNA DAMP levels in all 4 sequences examined (32.14 +/- 0.90

95 Patients with above-median mtDNA DAMP levels had a significantly elevated relative risk f

96 determine relationships between plasma mtDNA DAMP levels and the occurrence of systemic inflammatory

97 MtDNA DAMPs were quantified as PCR threshold cycle number.

98 tion; however, the link between plasma mtDNA DAMPs and outcome in severely injured human subjects has

99 rst observational evidence that plasma mtDNA DAMPs is associated with the evolution of SIRS, MODS, an

100 ions in animal models demonstrate that mtDNA DAMPs contribute to organ dysfunction; however, the link

101 cute myeloid leukemia (AML) exposed multiple DAMPs, including calreticulin (CRT), heat-shock protein

102 ted extracellular release of the necroptotic DAMP, IL-33, and reduced Myd88-dependent inflammation.

103 ecroptosis, and increased release of nuclear DAMPs compared with controls.

104 eveal that histones represent a new class of DAMP molecules and serve as a crucial link between initi

105 ical data have established the importance of DAMPs, which signal through innate pattern recognition r

106 On the other hand, cell death and release of DAMPs may also trigger chronic inflammation and, thereby

107 IRGM regulates necroptosis and release of DAMPs to induce gastrointestinal inflammation, linking I

108 Here we focus on the role of DAMPs and their putative receptors in the pathogenesis o

109 A growing understanding of the role of DAMPs in directing the immune response to transplantatio

110 nce of suitable models, the relative role of DAMPs released because of necrosis or leukocyte activati

111 nate pattern recognition receptors (PRRs) or DAMP-specific receptors, in regulating the alloresponse

112 nger-associated molecular patterns (PAMPs or DAMPs).

113 t methods that can be used to identify PAMPs/DAMPs and PRRs.

114 Here, we comprehensively review known PAMPs/DAMPs recognized by plants as well as the plant PRRs des

115 However, in contrast to other known PAMPs/DAMPs, cellobiose stimulates neither detectable reactive

116 he mito-damage-associated molecular pattern (DAMP) cardiolipin can be detected in the lungs.

117 totypic damage-associated molecular pattern (DAMP) molecule and has been implicated in several inflam

118 P) is a damage-associated molecular pattern (DAMP) molecule which stimulates proinflammatory cytokine

119 art via danger-associated molecular pattern (DAMP) molecules, such as high mobility group box 1 prote

120 ellular damage-associated molecular pattern (DAMP) molecules.

121 ease of damage-associated molecular pattern (DAMP) molecules.

122 nstream damage-associated molecular pattern (DAMP) pathway activation in vivo and in vitro and in pat

123 tion of damage-associated molecular pattern (DAMP) receptors and a cytosolic complex termed the infla

124 mediate damage-associated molecular pattern (DAMP) response including elevations in heat-shock protei

125 ts as a danger-associated molecular pattern (DAMP) that initiates helminth-induced type 2 immune resp

126 ts as a danger-associated molecular pattern (DAMP) that is potently proinflammatory.

127 ng as a danger-associated molecular pattern (DAMP) that stimulates cytokine production in neighboring

128 ectious damage-associated molecular pattern (DAMP), heparan sulfate (HS),(1) aggravates graft-versus-

129 id is a damage-associated molecular pattern (DAMP), released from ischemic tissues and dying cells wh

130 and pathogen-associated molecular patterns (DAMP and PAMP, respectively) through pattern recognition

131 ted by damage-associated molecular patterns (DAMP).

132 and pathogen-associated molecular patterns (DAMPs and PAMPs).

133 al DNA damage-associated molecular patterns (DAMPs) accumulate in the circulation after severe injury

134 ), and damage-associated molecular patterns (DAMPs) activate families of pattern recognition receptor

135 danger/damage associated molecular patterns (DAMPs) and a reduction in immunoinhibitory miRNA, which

136 ion of damage-associated molecular patterns (DAMPs) and a response that includes secretion of cytokin

137 ure of damage-associated molecular patterns (DAMPs) and cytokines/chemokines.

138 abolic damage-associated molecular patterns (DAMPs) and discuss potential targets for therapeutic int

139 act as damage-associated molecular patterns (DAMPs) and interact with pattern recognition receptors t

140 Damage-associated molecular patterns (DAMPs) are considered key inducers of sterile inflammati

141 Damage-associated molecular patterns (DAMPs) are critical mediators of information concerning

142 Damage-associated molecular patterns (DAMPs) are molecules released by dead cells that trigger

143 Damage-associated molecular patterns (DAMPs) are released in response to cell death and stress

144 hrough danger associated molecular patterns (DAMPs) as a response to an insult (systemic inflammatory

145 ion by danger associated molecular patterns (DAMPs) can be deleterious to the host.

146 ing as damage-associated molecular patterns (DAMPs) for pattern recognition receptors (PRRs) may repr

147 L) are danger-associated molecular patterns (DAMPs) generated in response to infection that can preve

148 ase of damage-associated molecular patterns (DAMPs) is a characteristic feature of most advanced tumo

149 ted by damage-associated molecular patterns (DAMPs) like HMGB1.

150 zed as damage-associated molecular patterns (DAMPs) or pattern-associated molecular patterns (PAMPs)

151 Ps) or damage-associated molecular patterns (DAMPs) recognized by plant PRRs induces both local and s

152 ing to damage-associated molecular patterns (DAMPs) released by injured host cells unleashes an infla

153 uch as damage-associated molecular patterns (DAMPs) released from injured cells to stimulate innate i

154 ogenic damage-associated molecular patterns (DAMPs) released into the circulation from football-induc

155 iverse damage-associated molecular patterns (DAMPs) such as extracellular ATP, excess glucose, cerami

156 nous 'damage'-associated molecular patterns (DAMPs) that activate innate immunity.

157 s) and danger-associated molecular patterns (DAMPs) to influence the activation and trafficking of DC

158 ensing damage associated molecular patterns (DAMPs) to sensing all particulate matter irrespective of

159 ept of damage-associated molecular patterns (DAMPs) was proposed to describe plant elicitors like oli

160 gands, danger-associated molecular patterns (DAMPs), and crystals.

161 ase of damage-associated molecular patterns (DAMPs), and progressing through innate and adaptive immu

162 AMPs), danger-associated molecular patterns (DAMPs), and the more recent discovery of the role of the

163 ls, or damage-associated molecular patterns (DAMPs), are generated in response to cell stress and act

164 o host danger-associated molecular patterns (DAMPs), but not to microbial pathogen-associated molecul

165 rosis, damage-associated molecular patterns (DAMPs), cause inflammation.

166 termed damage-associated molecular patterns (DAMPs), have been proposed to activate dendritic cells (

167 to as danger associated molecular patterns (DAMPs), including those triggered by crystalline particu

168 MPs or damage-associated molecular patterns (DAMPs), such as uric acid or ATP, via NLRP3, which leads

169 er- or damage-associated molecular patterns (DAMPs), which are also perceived by PRRs to modulate PTI

170 Ps) or damage-associated molecular patterns (DAMPs).

171 ion of damage-associated molecular patterns (DAMPs).

172 to as damage-associated molecular patterns (DAMPs).

173 called danger associated molecular patterns (DAMPs).

174 ted by damage-associated molecular patterns (DAMPs).

175 resent danger-associated molecular patterns (DAMPs).

176 termed damage-associated molecular patterns (DAMPs).

177 own as damage-associated molecular patterns (DAMPs).

178 erived damage-associated molecular patterns (DAMPs).

179 ase of damage-associated molecular patterns (DAMPs).

180 nse to damage-associated molecular patterns (DAMPs).

181 ing as damage-associated molecular patterns (DAMPs).

182 ase of danger-associated molecular patterns (DAMPs).

183 re the damage-associated molecular patterns (DAMPs).

184 (or damage)-associated molecular patterns" (DAMPs).

185 s of 'danger associated molecular patterns' (DAMPs), against which a concerted innate immune response

186 ounds (damage-associated molecular patterns, DAMPs) such as peptides released from cells upon attack.

187 lled "damage-associated molecular patterns," DAMPs), as they die in the context of failing adaptive r

188 cells (damage-associated molecular patterns; DAMPs) activate cellular receptors leading to downstream

189 density-associated mutation-rate plasticity (DAMP) at multiple loci in both eukaryotes and bacteria,

190 physema development and progression via RAGE-DAMP signaling.

191 ross-talk with various non-immune receptors, DAMPs determine the downstream signaling outcome of sept

192 ating into injured tissues tonically release DAMPs, including the high mobility group box 1 protein (

193 ent with the notion that osteolysis releases DAMPs from bone matrix, pharmacologic inhibition of bone

194 ity and, potentially, tolerance that renders DAMPs nonredundant players in responses to both sterile

195 es stromal activation with deployment of RNA DAMPs that promote aggressive features of cancer.

196 Since some DAMPs confer tissue-specific activation of the inflammas

197 of defense against atherosclerosis-specific DAMPs, and engage adaptive immune responses, provided by

198 Kidney-specific DAMPs include crystals and uromodulin released by renal

199 h, but the relative contribution of specific DAMPs, including high-mobility group box 1 (HMGB1), is i

200 protein recognize common oxidation-specific DAMPs, such as oxidized phospholipids and oxidized chole

201 s as well as the existence of tumor-specific DAMPs.

202 ll-like receptors (TLRs) that recognize such DAMPs and PAMPs, or the downstream effector molecules th

203 As such, DAMPs may exert protective functions by alerting the imm

204 ablishes HMGB1 as a bona fide and targetable DAMP that selectively triggers a neutrophil-mediated inj

205 Nonetheless, in each domain tested, DAMP requires proteins scavenging the mutagenic oxidised

206 However, recent evidence revealed that DAMPs also trigger re-epithelialization upon kidney inju

207 Thus, these discoveries suggest that DAMPs drive not only immune injury but also kidney regen

208 Recent evidence suggests that DAMPs may also have a key role in the development of can

209 eficient in the IL-1 family receptor for the DAMP, IL-33 (called ST2), displayed reduced intestinal T

210 oy were associated with up-regulation of the DAMP-related signaling pathway via Nrf2.

211 ur opinion that these function to remove the DAMP (ATP) released by host cells in response to schisto

212 These DAMPs are sensed by a pattern recognition receptor calle

213 growth factor production in response to this DAMP.

214 onstrated recently that the host response to DAMP is controlled by a DAMP-CD24-Siglec axis.

215 se initiated by the accumulation of OSE type DAMPs and perpetuated by maladaptive response of the inn

216 tein (HMGB1), but the receptor(s) underlying DAMP signaling have not been identified.

217 ricted receptor specific for an unidentified DAMP that is exposed by necrotic cells and is necessary

218 In this study, we examined whether DAMP-receptors and the inflammasome provide the link bet

219 Widespread DAMP, which we manipulate genetically in disparate organ

220 Concurrent with DAMP presentation, significant elevations in proinflamma

221 LPS-primed glial cells were stimulated with DAMPs under acidic conditions (pH 6.2), the predominant