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

22 The serum amyloid A (SAA) family comprises a number of diffe

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 family of acute-phase protein

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

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

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

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

31 iously reported that the acute phase protein serum amyloid A (SAA) is a potent chemoattractant for hu

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 best known for being the main c

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

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

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

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

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

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

44 Serum amyloid A (SAA) promotes neutrophilic inflammation

45 kines to increase the synthesis of precursor serum amyloid A (SAA) protein and the transitory nature

46 The serum amyloid A (SAA) protein has been implicated in the

47 The serum amyloid A (SAA) protein has been implicated in the

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

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

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

51 Serum amyloid A (SAA) proteins were originally identifie

52 Serum amyloid A (SAA) represents an evolutionarily conse

53 Serum amyloid A (SAA) upregulation was subsequently conf

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

79 -6], tumor necrosis factor alpha [TNFalpha], serum amyloid A [SAA], vascular endothelial growth facto

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

81 ter with a zinc finger transcription factor, serum amyloid A activating factor (SAF)-1, was demonstra

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

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

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

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

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

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

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

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

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

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

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

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

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

95 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

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

97 Serum amyloid A increases the ability of acute phase HDL

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

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

100 Serum amyloid A levels were significantly lower in ApoE(

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

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

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

104 Serum amyloid A measurement and a rapid cTnT assay were

105 , tyrosine phosphorylation, and IL-6-induced serum amyloid A mRNA expression.

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

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

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

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

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

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

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

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

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

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

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

117 -1 activity was measured by the induction of serum amyloid A protein in cultured chondrocytes.

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

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

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

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

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

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

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

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

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

127 Serum amyloid A was higher in patients who died compared

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

129 The levels of hs-CRP and serum amyloid A were significant predictors of risk even

130 c lipase, phospholipid transfer protein, and serum amyloid A) could decrease the ability of HDL to pr

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

148 t is characterized by enhanced expression of serum amyloid A, haptoglobin and tissue inhibitor for me

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

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

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

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

153 ke Alzheimer beta-amyloid peptide (Abeta) or serum amyloid A, must undergo significant structural tra

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

155 In mice, it induces serum amyloid A, potentiates the induction by IL-1 of co

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

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

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

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

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

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

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

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

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

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

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

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

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

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

170 s the activating and proinflammatory protein serum amyloid A.

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

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

173 is a receptor for the amyloidogenic form of serum amyloid A.

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

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

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

177 roteins such as C-reactive protein (CRP) and serum amyloid A].

178 d a decrease in serum C-reactive protein and serum amyloid-A and an increase in serum retinol-binding

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

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

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

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

189 ieved by providing cultures with recombinant serum amyloid A2 (rSAA2), a defined, readily produced, a

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

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

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

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

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

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

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

197 distal regulatory element (DRE) in the mouse serum amyloid A3 (SAA3) promoter that functions as a cyt

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

224 s in the levels of two acute-phase proteins (serum amyloid P and C3) at 24, 48, and 72 h after the ex

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

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

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

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

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

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

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

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

233 Serum amyloid P component (SAP), a highly conserved plas

234 uated for changes in plasma concentration of serum amyloid P component (SAP), a protein that is up-re

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

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

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

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

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

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

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

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

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

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

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

246 C-reactive protein and serum amyloid P component are members of the pentraxin f

247 been postulated that C-reactive protein and serum amyloid P component are products of a gene duplica

248 We have isolated serum amyloid P component from the haemolymph of the phy

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 cture of the previously undiscovered Limulus serum amyloid P component, the first invertebrate lectin

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

259 Serum amyloid P concentration was decreased in plasma an

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

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

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

263 Serum amyloid P depletion decreased the inhibitory effec

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

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

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

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

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

269 Serum amyloid P was located in normal and acute respirat

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

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

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 Changes in serum amyloid polypeptide A levels between groups did no

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

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

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

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

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

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

297 Serum amyloid protein has been found to inhibit the gene

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

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

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