ライフサイエンスコーパス: serum amyloid A

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

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

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

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

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

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

7 s the activating and proinflammatory protein serum amyloid A.

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

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

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

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

12 Levels of serum amyloid A-1, a vitamin A transport protein with pr

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

29 nd organs derived from the precursor protein serum amyloid A, an acute phase reactant synthesized exc

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

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

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

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

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

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

36 at stress decreased plasma concentrations of serum amyloid A and lipopolysaccharide-binding protein,

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

52 cortisol, serum haptoglobin, liver enzymes, serum amyloid A, and prostaglandin E(2) concentrations.

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

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

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

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

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

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

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

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

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

62 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

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

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

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

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

67 at stress increased plasma concentrations of serum amyloid A, haptoglobin and lipocalin-2, and admini

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

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

70 eductions were also observed for fibrinogen, serum amyloid A, haptoglobin, secretory phospholipase A2

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

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

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

74 onal to that of either C-reactive protein or serum amyloid A in both HD and PD patients.

75 Serum amyloid A increases the ability of acute phase HDL

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

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

78 as no significant difference in steady-state serum amyloid A level in the serum of aged non-Tg and Fa

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

80 promoter activity and sustained elevation of serum amyloid A levels that segregated in an autosomal d

81 Serum amyloid A levels were significantly lower in ApoE(

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

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

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

85 lteration in the induction of APP, including serum amyloid A, LPS-binding protein, fibrinogen, or cer

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

87 Serum amyloid A measurement and a rapid cTnT assay were

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

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

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

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

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

93 lted in significantly higher serum levels of serum amyloid A on day 2 and IL-6 on days 1 and 2 and a

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

95 significantly higher C-reactive protein and serum amyloid A plasma levels.

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

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

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

99 alamus-pituitary-adrenal axis, hypoglycemia, serum amyloid A production, and anorexia.

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

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

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

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

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

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

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

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

108 r necrosis factor-alpha inhibitors to reduce serum amyloid A protein formation.

109 -1 activity was measured by the induction of serum amyloid A protein in cultured chondrocytes.

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

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

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

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

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

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

116 ed to increased production and deposition of serum amyloid A proteins secondary to inflammatory condi

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

118 mic deposition of amyloid A originating from serum amyloid A proteins with the kidneys being the most

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

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

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

122 PON-1) activity (P < 0.0001) were lower, and serum amyloid A (SAA) (P < 0.0001) was higher in partici

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

140 Serum amyloid A (SAA) has been linked to atherosclerosis

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

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

143 on of procathepsin-L (pCTS-L) was induced by serum amyloid A (SAA) in innate immune cells, contributi

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

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

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

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

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

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

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

151 Serum amyloid A (SAA) is a plasma protein that is associ

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

153 Serum amyloid A (SAA) is a plasma protein which has been

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

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

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

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

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

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

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

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

162 Serum amyloid A (SAA) is bound to high-density lipoprote

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

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

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

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

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

168 that blood levels of lipocalin-2 (LCN2) and serum amyloid A (SAA) levels are positively correlated w

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

170 used to compare C-reactive protein (CRP) and serum amyloid A (SAA) levels in prerandomization blood s

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

172 Serum amyloid A (SAA) promotes neutrophilic inflammation

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

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

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

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

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

178 ion via interleukin-6/STAT3 and secretion of serum amyloid A (SAA) proteins 1 and 2 as important regu

179 Serum amyloid A (SAA) proteins are a family of inflammat

180 The serum amyloid A (SAA) proteins are a polymorphic family

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

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

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

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

185 Here, we show that serum amyloid A (SAA) proteins retinol-binding proteins

186 Serum amyloid A (SAA) proteins were originally identifie

187 Serum amyloid A (SAA) represents an evolutionarily conse

188 Serum amyloid A (SAA) upregulation was subsequently conf

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

190 ones, cytokines, and the acute phase protein serum amyloid a (SAA) were then measured in serum and br

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

192 Neither the normal role of serum amyloid A (SAA), a major acute phase response prot

193 Serum amyloid A (SAA), a plasma protein inducible in res

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

195 ius, the enigmatic VanZ proteins, the animal Serum Amyloid A (SAA), and a further host of uncharacter

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

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

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

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

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

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

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

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

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

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

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

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

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

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

210 The amino-terminal region of serum amyloid A (SAA), the subunit precursor protein in

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

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

213 on its ligands, which include lipoxin A4 or serum amyloid A (SAA).

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

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

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

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

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

219 -6], tumor necrosis factor alpha [TNFalpha], serum amyloid A [SAA], vascular endothelial growth facto

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

221 inflammatory molecules (C-reactive protein, serum amyloid A, soluble intercellular adhesion molecule

222 ation, and levels of complement component 3, serum amyloid A, sphingosine-1-phosphate, triglycerides,

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

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

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

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

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

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

229 Serum amyloid A was higher in patients who died compared

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

231 No differences for haptoglobin or serum amyloid A were observed.

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

233 ines studied induced the acute-phase protein serum amyloid A when administered alone.