ライフサイエンスコーパス: serum amyloid

1 ple assayed for C-reactive protein (CRP) and serum amyloid A (30 months after diagnosis) and complete

2 The human acute phase serum amyloid A (A-SAA) genes, SAA1 and SAA2, have a hig

3 The acute-phase protein serum amyloid A (A-SAA) was significantly increased by 2

4 Serum amyloid A (A-SAA/Saa3) was shown before to affect

5 Diary scores improved (P<0.001) and serum amyloid A (from a median of 174 mg to 8 mg per lit

6 with the risk of cardiovascular events were serum amyloid A (relative risk for the highest as compar

7 The fibrillation of Serum Amyloid A (SAA) - a major acute phase protein - is

8 Serum amyloid A (SAA) 1 and 2 are produced predominantly

9 found that the acute-phase response proteins serum amyloid A (SAA) 1 and SAA3 are transcriptional tar

10 -terminal peptide of the acute phase protein serum amyloid A (SAA) 1.

11 Serum amyloid A (SAA) activating factor-1 (SAF-1) is an

12 Inflammatory markers serum amyloid A (SAA) and C-reactive protein (CRP) are p

13 Therefore, serum amyloid A (SAA) and C-reactive protein (CRP) were

14 lpha), circulatory C-reactive protein (CRP), serum amyloid A (SAA) and haptoglobin (Hpt) were analyse

15 Systemic C-reactive protein (CRP) and serum amyloid A (SAA) are measures of low-grade chronic

16 the inflammation-associated genes Fizz1 and serum amyloid A (SAA) are significantly up-regulated in

17 Here, we identify serum amyloid A (SAA) as a candidate mediator of GC refr

18 h reduced expression of TNF-alpha, IL-6, and serum amyloid A (SAA) at all time points compared with l

19 ly interleukin 6, leads to overproduction of serum amyloid A (SAA) by the liver.

20 Since serum amyloid A (SAA) concentrations in HDL increase wit

21 terial lipopolysaccharide (LPS) and purified serum amyloid A (SAA) effectively induced the expression

22 Because AngII increases hepatic serum amyloid A (SAA) expression in an IL-6-dependent ma

23 The fibrillar deposition of serum amyloid A (SAA) has been linked to the disease amy

24 The acute phase protein serum amyloid A (SAA) has been well characterized as an

25 ta demonstrating the multifunctional role of serum amyloid A (SAA) in the pathogenesis of amyloidosis

26 Serum amyloid A (SAA) is a DAMP that is involved in the

27 Serum amyloid A (SAA) is a family of acute-phase protein

28 Serum amyloid A (SAA) is a highly conserved acute phase

29 Induced secretion of acute-phase serum amyloid A (SAA) is a host response to danger signa

30 Serum amyloid A (SAA) is a major acute phase protein inv

31 Serum amyloid A (SAA) is a plasma protein that transport

32 Serum amyloid A (SAA) is a small apolipoprotein that bin

33 Serum amyloid A (SAA) is an acute phase protein whose ex

34 Serum amyloid A (SAA) is an acute-phase plasma protein t

35 Serum amyloid A (SAA) is an acute-phase protein induced

36 Serum amyloid A (SAA) is an apolipoprotein primarily pro

37 Serum amyloid A (SAA) is an evolutionally conserved enig

38 Serum amyloid A (SAA) is best known for being the main c

39 The acute-phase protein serum amyloid A (SAA) is commonly considered a marker fo

40 Serum amyloid A (SAA) is expressed locally in chronic in

41 The acute-phase protein serum amyloid A (SAA) is highly induced during inflammat

42 Serum amyloid A (SAA) is one such marker but its functio

43 Elevated serum amyloid A (SAA) levels are associated with increas

44 ignificantly reduced histological damage and serum amyloid A (SAA) levels in IL-10(-/-) colitis mice,

45 ified in AKU and related to high circulating serum amyloid A (SAA) levels, which are linked with infl

46 Serum amyloid A (SAA) promotes neutrophilic inflammation

47 Serum amyloid A (SAA) protein has recently been linked t

48 Abundantly expressed serum amyloid A (SAA) protein under chronic inflammatory

49 Serum amyloid A (SAA) proteins are acute-phase reactant

50 Serum amyloid A (SAA) proteins are strongly induced in t

51 Serum amyloid A (SAA) proteins are strongly induced in t

52 activated vitamin A-dependent expression of serum amyloid A (SAA) proteins by binding directly to Sa

53 Serum amyloid A (SAA) proteins were originally identifie

54 Serum amyloid A (SAA) represents an evolutionarily conse

55 Serum amyloid A (SAA) upregulation was subsequently conf

56 C-reactive protein (CRP) and serum amyloid A (SAA) were measured by latex-enhanced ne

57 about the association between fibrinogen and serum amyloid A (SAA), a highly fibrillogenic protein th

58 We evaluated the ability of serum amyloid A (SAA), alone and in combination with a r

59 ctant protein B (SP-B), apolipoprotein C-II, serum amyloid A (SAA), and alpha-1-microglobulin/bikunin

60 We measured C-reactive protein (CRP), serum amyloid A (SAA), and interleukin 6 (IL-6) in 2402

61 C-reactive protein (CRP), serum amyloid A (SAA), and lipoprotein levels were compa

62 markers including C-reactive protein (CRP), serum amyloid A (SAA), and S100 calcium-binding protein

63 acute-phase proteins, C-reactive protein and serum amyloid A (SAA), are biomarkers of infection and i

64 rs associated with neonatal sepsis including Serum Amyloid A (SAA), C - reactive protein (CRP), Proca

65 pocyte-derived factors, e.g., hyaluronan and serum amyloid A (SAA), can facilitate monocyte adhesion

66 ior day stressors, C-reactive protein (CRP), serum amyloid A (SAA), intercellular adhesion molecule-1

67 igh-sensitivity C-reactive protein (hs-CRP), serum amyloid A (SAA), interleukin-6 (IL-6), leukocyte,

68 Concentrations of HDL-bound serum amyloid A (SAA), lipopolysaccharide binding protei

69 ucose-stimulated production by adipocytes of serum amyloid A (SAA), monocyte chemoattractant protein

70 f high-sensitivity C-reactive protein (CRP), serum amyloid A (SAA), plasminogen activator inhibitor-1

71 SFB cause an increase in serum amyloid A (SAA), suggesting that SAA might mediate

72 e expression of C-reactive protein (CRP) and serum amyloid A (SAA), the prototype acute-phase respons

73 The transcription factor serum amyloid A (SAA)-activating factor (SAF), a family

74 temic deposition of the acute-phase reactant serum amyloid A (SAA).

75 increased levels of the acute-phase protein, serum amyloid A (SAA).

76 in the blood of acute-phase proteins such as serum amyloid A (SAA).

77 histological injury score (HIS), and plasma serum amyloid A (SAA).

78 served significantly increased expression of serum amyloid A (Saa3) and serine protease inhibitor 3n

79 We now show that systemic serum amyloid A 1 (SAA-1) controls the plasticity of neu

80 lated the IL-1beta-induced expression of the serum amyloid A 1 (SAA1) and SAA2 genes.

81 daily activities, and C-reactive protein and serum amyloid A [SAA] levels).

82 high-sensitivity C-reactive protein [hsCRP], serum amyloid A [SAA], and IL-6) were determined at 3, 6

83 -6], tumor necrosis factor alpha [TNFalpha], serum amyloid A [SAA], vascular endothelial growth facto

84 e to the generation of lipid-poor apoA-I and serum amyloid A acceptors for cholesterol efflux.

85 l that overexpresses a transcription factor, serum amyloid A activating factor-1 (SAF-1), leading to

86 f amyloidosis was systemic AL (N = 14, 47%), serum amyloid A amyloidosis (AA) (N = 11, 37%), localize

87 motactic peptide fMet-Leu-Phe, lipoxin A(4), serum amyloid A and beta-amyloid peptides.

88 ation and acute phase proteins, particularly serum amyloid A and group IIa secretory phospholipase A2

89 LVS-infected IL-6 KO mice produced much less serum amyloid A and haptoglobin (two acute-phase protein

90 culating levels of the acute phase proteins, serum amyloid A and IL-6, and the neutrophil-selective C

91 therosclerosis, serum levels of CD40 ligand, serum amyloid A and monocyte chemoattractant protein-1,

92 inflammation markers C-reactive protein and serum amyloid A and quality-of-life scores were signific

93 model for the acute phase response in which serum amyloid A and sPLA2-IIa, present at sites of infla

94 r, C-reactive protein (CRP), fibrinogen, and serum amyloid A are associated independently with functi

95 SIGNIFICANCE STATEMENT In the present study, serum amyloid A can induce that activation of the inflam

96 Amyloid A deposits regress upon reduction of serum amyloid A concentration, indicating that the amylo

97 reased apoA-I content and markedly increased serum amyloid A content in HDL during the acute phase re

98 These effects were associated with reduced serum amyloid A expression in ileum and synovial tissue.

99 e inflammation, including three genes of the serum amyloid A family, three major histocompatibility c

100 o 2.5 +/- 0.5 mg/L (P < 0.01), decreased HDL serum amyloid A from 10.3 +/- 1.8 to 5.7 +/- 1.3 mg/L (P

101 Serum amyloid A functions efficiently in a lipid-free or

102 Serum amyloid A increases the ability of acute phase HDL

103 Serum amyloid A is an acute phase protein that is carrie

104 ad increased IL-1beta, IL-6, IL-23, C3a, and serum amyloid A levels in BAL fluid, and these correlate

105 Serum amyloid A levels were significantly lower in ApoE(

106 ammation as assessed by circulating IL-6 and serum amyloid A levels.

107 and matrix metalloproteinase-9, and systemic serum amyloid A levels.

108 The displacement of paraoxonase by serum amyloid A may explain in part the proinflammatory

109 Serum amyloid A measurement and a rapid cTnT assay were

110 By comparison, serum amyloid A non-genomic responses were reliant on ex

111 Peak interleukin-6 and serum amyloid A plasma levels were observed at 2 and 7 d

112 n in mice, while not affecting IL-22-induced serum amyloid A production or EPO-induced reticulocytosi

113 journal to induce an acute phase response of serum amyloid A protein (SAA) and of CRP itself, and to

114 that develops when proteolytic fragments of serum amyloid A protein (SAA) are deposited in tissues a

115 inflammatory protein 1beta (MIP-1beta), and serum amyloid A protein (SAA) during acute SIVmac251 inf

116 Serum amyloid A protein (SAA) is an acute-phase reactant

117 ed from the circulating acute-phase reactant serum amyloid A protein (SAA), but the relation between

118 is of levels of C-reactive protein (CRP) and serum amyloid A protein (SAA).

119 From these peaks, two peptides (serum amyloid A protein and transthyretin) were identifi

120 ry assessments, including measurement of the serum amyloid A protein concentration.

121 -1 activity was measured by the induction of serum amyloid A protein in cultured chondrocytes.

122 ation, including immunoglobulin light chain, serum amyloid A protein, and transthyretin.

123 cute-phase reactants, C-reactive protein and serum amyloid A protein, were measured by immunonephelom

124 egates derived from the acute-phase reactant serum amyloid A protein.

125 Acute phase serum amyloid A proteins (A-SAAs) are multifunctional ap

126 g, their cytokine production is regulated by serum amyloid A proteins (SAA1 and SAA2) secreted by adj

127 rect contact with the epithelium and induces serum amyloid A proteins 1 and 2 (SAA1/2), which promote

128 During inflammation, serum amyloid A proteins transport retinol to infected t

129 colleagues shows that hepatic and intestinal serum amyloid A proteins, which are induced in response

130 ncluding induction of fibrinogen, CXCL1, and serum amyloid A that likely contribute to the reported c

131 ced IFN-gamma production and IL-22-dependent serum amyloid A to similar extents, indicating that, in

132 Serum amyloid A was higher in patients who died compared

133 r levels of D-dimer, C-reactive protein, and serum amyloid A were associated with higher all-cause mo

134 ha1-antichymotrypsin, C-reactive protein, or serum amyloid A) from 15 studies of apparently healthy i

135 inflammation markers (C-reactive protein and serum amyloid A), and quality-of-life assessments (Derma

136 acute-phase proteins (C-reactive protein and serum amyloid A), however, has been found to be associat

137 C-reactive protein, alpha-1-antitrypsin, and serum amyloid A), immune response (high IgA), leakage of

138 ein, 25% for C-reactive protein, and 32% for serum amyloid A).

139 tokine-mediated transcriptional induction of serum amyloid A, an acute-phase plasma protein that is a

140 itive C-reactive protein, interleukin 6, HDL serum amyloid A, and adiponectin concentrations were mea

141 oid-beta(1-40), alpha-synuclein, ABri, ADan, serum amyloid A, and amylin undergo supramolecular confo

142 is-suppressing signals from myeloperoxidase, serum amyloid A, and bacterial DNA, shifting the balance

143 ave high circulating concentrations of IL-6, serum amyloid A, and C-reactive protein, each of which d

144 ol was required for elevation of circulating serum amyloid A, and cholate was required for accumulati

145 e-1-phosphate, apolipoproteins A-I and A-IV, serum amyloid A, and complement 3 protein (in apolipopro

146 s apolipoprotein J, fibrinogen, haptoglobin, serum amyloid A, and complement factors (B, C3, and C9).

147 ions of high-sensitivity C-reactive protein, serum amyloid A, and fibrinogen from baseline to end of

148 ric oxide, oxidized low-density lipoprotein, serum amyloid A, and lipid peroxidation, were significan

149 igh levels of apolipoproteins A-II and B and serum amyloid A, and low levels of haptoglobin dimers an

150 estingly, some of the serum proteins such as Serum amyloid A, Apolipoprotein A1, C-reactive protein,

151 ficant elevation of transcripts for the APPs serum amyloid A, complement C3, pentraxin 3, and alpha2-

152 n shown to regulate several genes, including serum amyloid A, gamma-fibrinogen, and matrix metallopro

153 les were enriched with acute-phase proteins (serum amyloid A, haptoglobin, and hemopexin) and deplete

154 Blood C-reactive protein, serum amyloid A, IL-6, IL-1ra, G-CSF, but not TNF-alpha

155 igh-sensitivity C-reactive protein (hs-CRP), serum amyloid A, interleukin-6, and soluble intercellula

156 ding amyloid-beta, tau, alpha-synuclein, and serum amyloid A, misfold into distinct conformers linked

157 sedimentation rates, and C-reactive protein, serum amyloid A, myeloid-related protein 8/14, and S100A

158 etin, p53, superoxide dismutase 1, lysozyme, serum amyloid A, prions, vasopressin receptor 2, and alp

159 all OxLDL biomarkers and C-reactive protein, serum amyloid A, tissue plasminogen activator, interleuk

160 y was found in the case of those formed from serum amyloid A, transthyretin, and islet amyloid polype

161 amyloidogenic precursor proteins, including serum amyloid A, transthyretin, islet amyloid polypeptid

162 inflammation, including C-reactive protein, serum amyloid A, tumor necrosis factor-alpha, and IL-6.

163 RNA inhibited cytokine induction of the APP serum amyloid A-1, demonstrating that both transcription

164 t promoter constructs of MMP-9, we show that serum amyloid A-activating factor (SAF)-1, a novel trans

165 The role of serum amyloid A-activating factor 1 (SAF-1) in MMP-1 exp

166 nflammation-responsive transcription factor, serum amyloid A-activating factor 1 (SAF-1), has been sh

167 The transcription factor serum amyloid A-activating factor-1 (SAF-1) has been ide

168 Serum amyloid A-activating factor-1 (SAF-1) is a zinc fi

169 report, IL-6 failed to induce activation of serum amyloid A-activating factor-1/c-Myc-associated zin

170 Serum amyloid A-activating transcription factor-1 (SAF-1

171 t congophilic fibrillar material composed of serum amyloid A-related protein that acted as a potent A

172 s the activating and proinflammatory protein serum amyloid A.

173 amyloid fibrils from the acute phase protein serum amyloid A.

174 rleukin-1beta, interleukin-6, fibrinogen, or serum amyloid A.

175 f IgM, IgE, IgG2b, IgG3, anti-dsDNA Abs, and serum amyloid A.

176 um-derived factor, surfactant protein B, and serum amyloid A.

177 ivity was monitored by serial measurement of serum amyloid A.

178 Serum amyloid A: an ozone-induced circulating factor wit

179 oles of high-sensitivity C-reactive protein, serum amyloid-A, lipoprotein(a), and homocysteine were a

180 Fiber formation from murine serum amyloid A1 (SAA) was compared to the linear aggreg

181 roduction of acute phase proteins, typically serum amyloid A1 (SAA1) and serum amyloid A2 (SAA2), ana

182 ocols for measuring Flt3 ligand (Flt3lg) and serum amyloid A1 (Saa1) in small amounts of blood collec

183 tissue-specific repressor element in the rat serum amyloid A1 (SAA1) promoter.

184 n male mice and determined the expression of serum amyloid A1 (SAA1), an apolipoprotein, induced at t

185 volutionarily conserved acute-phase protein, serum amyloid A1 (SAA1), that promotes pulmonary type 2

186 TAT3) signalling and increased production of serum amyloid A1 and A2 (referred to collectively as SAA

187 Upregulated transcripts included serum amyloid A1 and A2, metallothionein, and apolipopro

188 epatic induction of the acute-phase reactant serum amyloid A1 resulted in its incorporation into HDL

189 ha, defensin-beta4A, chemokine ligand 5, and serum amyloid A1.

190 ron, macrophage-induced protein 1 alpha, and serum amyloid A1.

191 We found that rIL-22 also induced serum amyloid A2 (SAA2) and that SAA2 had anti-K. pneumo

192 teins, typically serum amyloid A1 (SAA1) and serum amyloid A2 (SAA2), analysis of the differential ex

193 ted early in murine cutaneous GVHD including serum amyloid A2 (SAA2), SAA3, serpins a3g and a3n, secr

194 e plasminogen activator receptor (uPAR), and serum amyloid A2 (SAA2), which elicit paracrine effects

195 ee STAT-3 responsive genes, Socs3, Cd14, and serum amyloid A2 were also blocked.

196 ter-alpha-trypsin inhibitor chain H4], SAA2 [serum amyloid A2], APOA4 [apolipoprotein A-IV], CLU [clu

197 , analysis of the differential expression of serum amyloid A3 (SAA3) by mammary epithelial cells is l

198 Serum amyloid A3 (Saa3) derives mainly from extrahepatic

199 In this study, we identified the serum amyloid A3 (Saa3) gene as a key adipocyte-derived

200 te phase reactants at high levels, including serum amyloid A3 (SAA3), alphal-acid glycoprotein, the l

201 y protein (MIP) 1alpha and 1beta, eotaxin-2, serum amyloid A3 (Saa3), and insulin-like growth factor

202 In the lung, serum amyloid A3 mRNA expression decreased in the airway

203 on, and 2) decreased lung cytokine and liver serum amyloid A3 mRNA expression.

204 rix metalloproteinase 3, ECM-1, haptoglobin, serum amyloid A3, and clusterin.

205 cluding many known NF-kappaB targets such as serum amyloid A3, C3, interleukin (IL)-6, IL-11, IL-1 re

206 Lipocalin 2, haptoglobin, serum amyloid A3, stearoyl-CoA desaturase, and 11beta-hy

207 ophage genes, mannose receptor type-1, Cd68, serum amyloid-A3, chemokine ligands (Ccl2, Ccl7, Ccl9),

208 ine oxidase 1, paraoxonase 1, transthyretin, serum amyloid A4, and fibrinogen alpha chain.

209 Serum amyloid-alpha (SAA) is a sensitive marker of an ac

210 , ferritin (OR = 4.20, CI = 1.40-12.65), and serum amyloid P (OR = 3.05, CI = 1.16-8.01) were associa

211 obulin, haptoglobin, C-reactive protein, and serum amyloid P (P < 0.001).

212 Two closely related human serum proteins, serum amyloid P (SAP) and C-reactive protein (CRP), stro

213 Patients with amyloidosis also underwent serum amyloid P (SAP) component scintigraphy so that spe

214 ecently published crystal structure of human serum amyloid P (SAP) in complex with FcgammaRIIA furthe

215 The plasma protein Serum Amyloid P (SAP) inhibits fibrocyte differentiation

216 reviously found that a plasma protein called serum amyloid P (SAP) inhibits fibrocyte differentiation

217 A sialylated glycoprotein called serum amyloid P (SAP) inhibits fibrocyte differentiation

218 The systemic pentraxin serum amyloid P (SAP) inhibits inflammation.

219 h concentrations of interleukin-6 (IL-6) and serum amyloid P (SAP) is uncertain.

220 Administration of serum amyloid P (SAP) prevented the presence of this cel

221 The plasma protein serum amyloid P (SAP) reduces neutrophil adhesion, inhib

222 collapse was most noticeable for pentameric serum amyloid P (SAP) which contains a large central cav

223 the serum level of C-reactive protein (CRP), serum amyloid P (SAP), and alpha-2-macroglobulin (A2M).

224 is strongly inhibited by the plasma protein serum amyloid P (SAP), and healthy tissues contain very

225 ssays, several of these molecules, including serum amyloid P (SAP), PG D synthase, superoxide dismuta

226 phenotype we have shown to be influenced by serum amyloid P (SAP).

227 pearance of fibrocytes, and identified it as serum amyloid P (SAP).

228 xenograft mice with the fibrocyte inhibitor serum amyloid P (SAP; pentraxin-2) significantly prolong

229 d P originated, in part, from the release of serum amyloid P associated with lung connective tissue d

230 The pentraxins, serum amyloid P component (SAP) and C-reactive protein (

231 The classical pentraxins include serum amyloid P component (SAP) and C-reactive protein,

232 R), avidin, concanavalin A (conA), and human serum amyloid P component (SAP) at elevated temperatures

233 The normal plasma protein serum amyloid P component (SAP) binds to fibrils in all

234 wo monoclinic (P2(1)) crystal forms of human serum amyloid P component (SAP) in complex with the 4,6-

235 Serum amyloid P component (SAP) is a member of the pentr

236 Serum amyloid P component (SAP) is a non-fibrillar glyco

237 f the constitutive plasma pentraxin protein, serum amyloid P component (SAP), in serum samples obtain

238 C-reactive protein (CRP) and serum amyloid P component (SAP), two major classical pen

239 nd basic fibroblast growth factor (bFGF) and serum amyloid P component (SAP), we investigated a novel

240 The serum amyloid P component (SAP)-like pentraxin Limulus p

241 Activating FcgammaRs are also involved in serum amyloid P component (SAP)-mediated clearance of ap

242 amyloidophilic dyes and for the presence of serum amyloid P component (SAP).

243 e normal, non-fibrillar plasma glycoprotein, serum amyloid P component (SAP).

244 ve endogenous acute phase reactants, SAA and serum amyloid P component (SAP).

245 um proteins C-reactive P component (CRP) and serum amyloid P component (SAP).

246 rils, hyper-sulphated glycosaminoglycans and serum amyloid P component (SAP).

247 tain the nonfibrillar normal plasma protein, serum amyloid P component (SAP).

248 macrophages secrete cathepsin B (CATB), and serum amyloid p component (SAPC), inducing neuronal apop

249 ase, and mice with targeted deletions of the serum amyloid P component gene (Sap) develop a lupus-lik

250 ted lipopolysaccharide-induced mouse CRP and serum amyloid P component gene expression in the liver,

251 Although sequence homology with human serum amyloid P component is relatively low, structural

252 based on amino-acid residues 27-38 of human serum amyloid P component represent a novel type of hepa

253 and his amyloid deposits were monitored with serum amyloid P component scintigraphy.

254 l amyloid deposits were assessed annually by serum amyloid P component scintigraphy.

255 Human serum amyloid P component, a pentraxin protein that is v

256 Serum amyloid P component, apolipoprotein E, immunoglobu

257 epharose exclusion and failure to bind human serum amyloid P component, which acts as a lectin for te

258 Serum amyloid P concentration was decreased in plasma an

259 Plasma and broncho-alveolar lavage fluid serum amyloid P contents were determined by western blot

260 ivated transthyretin tetramer and nativelike serum amyloid P decamer, were separated in ion mobility

261 igate glutamate dehydrogenase dodecamers and serum amyloid P decamers as a function of protein concen

262 Serum amyloid P depletion decreased the inhibitory effec

263 monstrated that PTX3 and the short pentraxin serum amyloid P express sialic acids that are recognized

264 nti-CD4 therapy also caused normalization of serum amyloid P levels.

265 Alveolar serum amyloid P originated, in part, from the release of

266 roncho-alveolar lavage fluid by 60%, whereas serum amyloid P replenishment of serum amyloid P-deplete

267 The amyloid load was measured by serum amyloid P scintigraphy.

268 Serum amyloid P was located in normal and acute respirat

269 monstrated by reduced plasma levels of IL-6, serum amyloid P, and soluble vascular cell adhesion mole

270 he serum fibrocyte differentiation inhibitor serum amyloid P, but dominates over the fibroblast-secre

271 ace of monocytes (which, in conjunction with serum amyloid P, is responsible for clearing residual hy

272 roteins (alpha-2 macroglobulin, haptoglobin, serum amyloid P, procalcitonin, and tissue plasminogen a

273 nents, including vitronectin, clusterin, and serum amyloid P, thus suggesting that specific protein-p

274 lammatory mediators, the acute phase protein serum amyloid P, vascular endothelial growth factor and

275 e of chaperones such as apolipoprotein E and serum amyloid P-component (arrows) as well as the identi

276 activate transcription of the genes encoding serum amyloid P-component (SAP) and C-reactive protein (

277 Serum amyloid P-component (SAP), an acute-phase response

278 nduction of the acute-phase proteins CRP and serum amyloid P-component (SAP).

279 ntaining serum glycoproteins, ceruloplasmin, serum amyloid P-component, and amyloid precursor protein

280 rombospondin-1 and 5, alpha-1B-glycoprotein, serum amyloid P-component, and tenascin-X, were selected

281 Additionally, serum amyloid P-component, the murine homologue of C-rea

282 0%, whereas serum amyloid P replenishment of serum amyloid P-depleted acute respiratory distress synd

283 rosion and in normalization of the levels of serum amyloid P.

284 he alveolar environment, mainly dependent on serum amyloid P.

285 ors involved in this modulation, focusing on serum amyloid P.

286 ains to the antiviral activities of PTX3 and serum amyloid P.

287 collagen, and with the innate immune protein serum amyloid P.

288 asting plasma levels of glucose, insulin and serum amyloid-P (SAP) and body weight in 234 female F2 m

289 The serum-amyloid-P-component-like pentraxin from Limulus po

290 C-reactive protein, serum amyloid polypeptide A, inteleukin-6, and lipoprote

291 port that glycoproteins such as haptoglobin, serum amyloid protein (SAP), and carboxylesterase that b

292 , C-reactive protein [CRP], haptoglobin, and serum amyloid protein A [SAA]), inflammatory markers (ma

293 and the proinflammatory signals elicited by serum amyloid protein A and cathelicidins, among others.

294 th the largest median fold changes were SAA (serum amyloid protein A), NPS-PLA2 (secreted phospholipa

295 the receptors; significantly, AnxA1, but not serum amyloid protein A, could activate ALX homodimers.

296 Serum amyloid protein has been found to inhibit the gene

297 n, bovine serum albumin, concanavalin, human serum amyloid protein, and Immunoglobulin G) from those

298 en observed that the sera have low levels of serum amyloid protein.

299 T cells were analyzed by flow cytometry, and serum amyloid proteins (SAA) were analyzed by quantitati

300 ich then activates acute-phase genes such as serum amyloid proteins and orosomucoids.