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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

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