ライフサイエンスコーパス: fibrinogen

1 accelerated clot retraction and spreading on fibrinogen.

2 preading, and migration of cells on iC3b and fibrinogen.

3 aolin as an activator, and blood spiked with fibrinogen.

4 ivity C-reactive protein (hsCRP), and plasma fibrinogen.

5 fibrinogen glycation of 4.0 mol glucose/mol fibrinogen.

6 is not free, but rather circulates bound to fibrinogen.

7 eta-binding site within the alphaC region of fibrinogen.

8 same mechanism through which FnBPB binds to fibrinogen.

9 rin is more reactive with alphaIIbbeta3 than fibrinogen.

10 n-deficient plasma reconstituted with gamma' fibrinogen.

11 reactive with alphaIIbbeta3 than the parent fibrinogen.

12 and multimerin-1 with Efb is independent of fibrinogen.

13 integrin alphaIIbbeta3-mediated spreading on fibrinogen.

14 displayed decreased adhesion to immobilized fibrinogen.

15 preclude thrombin's exosites and binding to fibrinogen.

16 to extracellular matrix components, such as fibrinogen.

17 cells and the extracellular matrix protein, fibrinogen.

18 binds to similar areas on the beta chain of fibrinogen.

19 ides, in the absence of a T cell response to fibrinogen.

20 aIIbbeta3-mediated spreading of CHO cells on fibrinogen.

21 ing order: fibrin polymer > fibrin monomer > fibrinogen.

22 lphaIIbbeta3 binding to monomeric fibrin and fibrinogen.

23 M) adhered to a fibrin matrix (0.1-0.4 mg/mL fibrinogen, 10 nM thrombin) under a variety of venous fl

24 NPs had fast association rate constants with fibrinogen (1x10(6) M(-1) s(-1)) and Al2O3 NPs had a slo

25 otein arginine deiminase 4 (12 sites) and in fibrinogen (25 sites, two previously unknown).

26 in CD11c mediated adhesion of eosinophils to fibrinogen, a significant component of epithelial barrie

27 The first case of hereditary fibrinogen Aalpha-chain amyloidosis was recognized >20 y

28 a French kindred with a novel amyloidogenic fibrinogen Aalpha-chain frameshift variant, Phe521Leufs,

29 Here we show that the coagulation factor fibrinogen activates the bone morphogenetic protein (BMP

30 hypertension-associated biomarkers, namely, fibrinogen, adiponectin, low-density lipoprotein, and 8-

31 mbin failed to release fibrinopeptide-A from fibrinogen(AEK) and failed to induce polymer formation w

32 r formation with Fib(AEK) plasma or purified fibrinogen(AEK) in 37 degrees C mixtures regardless of i

33 elet aggregation in vitro, highlighting that fibrinogen(AEK) retains the functional capacity to suppo

34 ne, we show that UHRA does not interact with fibrinogen, affect fibrin polymerization during clot for

35 Fibrinogen alphaC (233-425) contains a binding site for

36 n of Arf6 in platelets enhances spreading on fibrinogen and accelerates clot retraction (see figure).

37 Significant reductions in adherence to fibrinogen and collagen type I were observed with deleti

38 upon conversion to active plasmin, degraded fibrinogen and complement C3b and contributed to serum r

39 that led to a successful outcome for plasma fibrinogen and discusses implications for future biomark

40 eta3-mediated interactions of platelets with fibrinogen and fibrin.

41 sition of the alpha-granule contents such as fibrinogen and fibronectin were primarily observed in th

42 uantitatively the kinetics and affinities of fibrinogen and human serum albumin (HSA) for TiO2, CeO2,

43 Like alphaIIbbeta3 binding to fibrinogen and monomeric fibrin, we found that alphaIIbb

44 s increase the affinity of alphaIIbbeta3 for fibrinogen and other ligands.

45 flammatory functions mediated by cleavage of fibrinogen and PAR1, the trypsin-like protease thrombin

46 er cirrhosis in the intensive care unit, and fibrinogen and platelet count were identified as the bes

47 meters and high DIC scores (primarily due to fibrinogen and platelets) correspond to increased bleedi

48 of Efb (Efb-N) promotes platelet binding of fibrinogen and that Efb-N binding to platelets proceeds

49 elets induced by thrombin in the presence of fibrinogen and the alphaIIbbeta3 blocker eptifibatide.

50 Fibrinogen and the BMP target Id2 are increased in demye

51 The fibrinogen and the percentage of megakaryocytes were sig

52 dent functions such as platelet spreading on fibrinogen and thrombin-mediated fibrin clot retraction.

53 Inflammatory markers (C-reactive protein and fibrinogen) and lifestyle factors were measured repeated

54 o alpha-granules in resting platelets, binds fibrinogen, and acts as a positive regulator of platelet

55 with a significant amelioration of ferritin, fibrinogen, and alanine aminotransferase levels.

56 or blood's hemostatic components (platelets, fibrinogen, and coagulation factors).

57 fectively all FXIII-A2B2 circulates bound to fibrinogen, and excess FXIII-B2 circulates in plasma.

58 ted for high-sensitivity C-reactive protein, fibrinogen, and intercellular adhesion molecule-1, sugge

59 the Xps-mediated degradation of fibronectin, fibrinogen, and the cytokine interleukin-8 (IL-8).

60 was reduced from 8.8 to 5.0 mol glucose/mol fibrinogen, and the healthy individuals had a mean fibri

61 Both fibrinogen- and fibrin-alphaIIbbeta3 interactions were p

62 Two cell wall-associated proteins, the fibrinogen- and fibronectin-binding proteins A and B, we

63 bovine serum albumin antibody (anti-BSA) and fibrinogen antibody (anti-Fg) onto the pCB-coated surfac

64 This led to the FDA qualification of plasma fibrinogen as a prognostic or enrichment biomarker for a

65 e also found to have higher levels of plasma fibrinogen at the time of surgery, with unchanged prothr

66 tural change in the C-terminal region of the fibrinogen beta-chain (beta384-393).

67 monstrate that blood proteins such as bovine fibrinogen (BFG) can absorb onto the graphene surface qu

68 JNK inhibition reduced fibrinogen binding and P-selectin expression of d12 plat

69 n and clarifies the mechanism by which Abeta-fibrinogen binding delays fibrinolysis by plasmin.

70 icles (PLPs), whereas p38 inhibition reduced fibrinogen binding of d12 PLPs.

71 ed by thrombin, which simultaneously induces fibrinogen binding to alphaIIbbeta3 and converts fibrino

72 Fibrinogen binding to the integrin alphaIIbbeta3 mediate

73 In response to fibrinogen binding, SWCNT fluorescence decreases by >80%

74 ceptor 4, activating peptide-induced soluble fibrinogen binding.

75 lphaIIbbeta3 expression and had no effect on fibrinogen binding.

76 Extracellular fibrinogen-binding protein (Efb) from Staphylococcus aur

77 er to prepare an inexpensive electrochemical fibrinogen biosensor.

78 s hPg/hPm to its cell surface indirectly via fibrinogen bound to M-protein, M23.

79 gammaA/gammaA, gamma'/gamma', and Aalpha251 fibrinogens bound FXIII-A2B2 with high affinity (nanomol

80 tion of mechanical ventilation and admission fibrinogen, but not exposure to extracorporeal support,

81 , diabetes, sex, and duration of dialysis or fibrinogen, C-reactive protein, and complement C3) confi

82 cluding ESR, CBC with differential, D-dimer, fibrinogen, C3, C4, IL-6, etc.

83 Fibrinogen-C3 interactions were further studied by pepti

84 <0.001), which significantly correlated with fibrinogen carbonylation level (r(2)=0.33, P<0.0001), re

85 rties relative to fIIa, including diminished fibrinogen cleavage and increased protein C activation.

86 ding variants in CPN1 were associated with a fibrinogen cleavage peptide.

87 beta-band intensity (r(2)=0.07, P<0.01), and fibrinogen clotting ability (r(2)=0.073, P<0.01) CONCLUS

88 Binding of plasminogen and fibrinogen co-localized with PAC-1 in the center of spre

89 Fibrinogen, coagulation factor VII (FVII), and factor VI

90 Resting platelets adhering to fibrinogen-coated electrodes were activated by different

91 diates platelet aggregation and spreading on fibrinogen-coated surfaces.

92 Intravenous, single-dose administration of fibrinogen concentrate (n = 60) or placebo (n = 60), tar

93 To determine whether fibrinogen concentrate infusion dosed to achieve a plasm

94 Fibrinogen concentrate might partly restore coagulation

95 5 minutes) were randomized to receive either fibrinogen concentrate or placebo.

96 high-risk cardiac surgery, administration of fibrinogen concentrate, compared with placebo, resulted

97 cation in neurosurgical patients, and plasma fibrinogen concentration has been identified as a potent

98 The established platform can monitor the fibrinogen concentration ranging from 1-6g/L (yielding R

99 41 loci explain 3% of the variance in plasma fibrinogen concentration.

100 23 genetic loci associated with circulating fibrinogen concentration.

101 gels shows that fiber density increases with fibrinogen concentration.

102 gels act as thermal networks independent of fibrinogen concentration.

103 t loads >500 nM and sensitive to the initial fibrinogen concentration.

104 emonstrated detection of clinically relevant fibrinogen concentrations (938-44,542mug/dL) from human

105 erum environment, at the clinically relevant fibrinogen concentrations in the human blood.

106 However,in vivoalphaIIbbeta3 activation and fibrinogen conversion to fibrin occur simultaneously, al

107 isseminated intravascular coagulation (DIC) (fibrinogen, D-dimer, alpha-2-antiplasmin, antitrombin, p

108 DIC score was calculated based on platelets, fibrinogen, d-dimer, and prothrombin index.

109 Six biomarkers (white blood cell count, fibrinogen, D-dimer, troponin T, N-terminal pro-brain na

110 SEP inequalities in fibrinogen decreased with age.

111 Therapeutic depletion of fibrinogen decreases BMP signaling and enhances remyelin

112 Tumors harvested from fibrinogen-deficient mice displayed a relative reduction

113 ction dose-dependent survival advantage over fibrinogen-deficient mice following peritonitis challeng

114 Although fibrinogen-deficient mice or mice with combined deficien

115 one fracture repair, as healing fractures in fibrinogen-deficient mice were indistinguishable from th

116 re, tumor growth was dramatically impeded in fibrinogen-deficient mice, offering the first direct evi

117 Unlike fibrinogen-deficient mice, platelet-rich plasma from Fib

118 llowing intraperitoneal infection similar to fibrinogen-deficient mice, yet Fib(AEK) mice displayed a

119 Assays on reconstituted PRP and PRP from fibrinogen-deficient patients revealed a fibrinogen-depe

120 plasma for high thrombin concentrations and fibrinogen-deficient plasma reconstituted with gamma' fi

121 trations at 6, and 8 hours, and blood fibrin/fibrinogen degradation products at 4 hours after NK admi

122 ination with low-dose r-tPA, did not lead to fibrinogen degradation, did not cause bleeding (versus c

123 rom fibrinogen-deficient patients revealed a fibrinogen-dependent enhancement of thrombin generation,

124 ule (ICAM)-1 identified a marked decrease in fibrinogen-dependent platelet-monocyte interactions, esp

125 Fibrinogen deposition at sites of blood-brain barrier br

126 deletion in adult mice resulted in increased fibrinogen deposition in lungs and kidneys, indicating e

127 sma thrombin-antithrombin complex levels and fibrinogen deposition on islet grafts, which correlated

128 age in plasma and reduced neuroinflammation, fibrinogen deposition, and neurodegeneration in the brai

129 Fibrinogen effects are rescued by BMP type I receptor in

130 , sigmaPre2 could generate fibrin clots from fibrinogen, either in solution or in blood plasma, and c

131 sylation factor 6 (Arf6) plays a key role in fibrinogen engulfment.

132 ar CD3-positive T-lymphocyte clustering, and fibrinogen extravasation were demonstrated in the core o

133 a (HFg) results in vascular remodelling, and fibrinogen (Fg) and amyloid beta (Abeta) complex formati

134 eats are required for interaction of M1 with fibrinogen (Fg) and consequent proinflammatory activatio

135 Endocytosis is key to fibrinogen (Fg) uptake, trafficking of integrins (alphaI

136 resulting in the release of the host protein fibrinogen (Fg), which coated the bladder and implant.

137 e accompanied by an increased blood level of fibrinogen (Fg).

138 -fibrinogen interaction or thrombin-mediated fibrinogen-fibrin polymerization is a critical step in v

139 using the calcium-dependent IF-1 mAb against fibrinogen for additional investigation using mass spect

140 (390-396A) FXIII-B2 also coprecipitated with fibrinogen from FXIII-A-deficient mouse and human plasma

141 We also purified fibrinogen from healthy controls and patients on hemodia

142 Whereas purified fibrinogen from healthy controls displayed no post-trans

143 In vitro guanidinylation of fibrinogen from healthy subjects increased the formation

144 Clots made of purified fibrinogen from patients on hemodialysis exhibited signi

145 splayed no post-translational modifications, fibrinogen from patients on hemodialysis was glycosylate

146 ex-matched healthy controls; in all patients fibrinogen function and structure, fibrin susceptibility

147 s, altered fibrinogen structure and impaired fibrinogen function are associated with neutrophil activ

148 n = 2) and rare (n = 10) variants across the fibrinogen, FVII, FVIII, and vWF traits that were indepe

149 indings provide insight into assembly of the fibrinogen/FXIII-A2B2 complex in both physiologic and th

150 95% CI, 1.03-1.23]; p = 0.011) and admission fibrinogen (g/L) (odds ratio, 0.73 [0.57-0.91]; p = 0.00

151 measured by epitope exposure, AGDV, like the fibrinogen gamma C-terminal peptide and RGD, caused inte

152 formation, with significant upregulation of fibrinogen gamma polypeptide, apolipoproteins A-Ib and A

153 , in fully hydrated conditions, thrombin and fibrinogen gamma' have dramatic effects on protofibril c

154 was to investigate the role of thrombin and fibrinogen gamma' in modulating fibrin structure under f

155 an important mechanism by which thrombin and fibrinogen gamma' modulate fibrin clot structure and str

156 s studies have shown effects of thrombin and fibrinogen gamma' on clot structure.

157 Fibers produced with fibrinogen gamma' showed reduced protofibril packing ove

158 Fibrin made from a fibrinogen gamma'/gamma' variant lacking the gammaC alph

159 alphaIIbbeta3 binds to a KQAGDV motif at the fibrinogen gamma-chain C terminus and to RGD motifs pres

160 d significant impairment in the formation of fibrinogen-gamma dimers (FGG-dimer) in the plasma of new

161 Using a fibrinogen gel bead angiogenesis assay experiment, FCSC

162 le is the strong upregulation of albumin and fibrinogen genes, which suggest significant liver pathol

163 Our goal was to determine whether fibrinogen glycation and fibrin fiber diameter have an e

164 We found that fibrinogen glycation had no significant systematic effec

165 ogen, and the healthy individuals had a mean fibrinogen glycation of 4.0 mol glucose/mol fibrinogen.

166 The fibrinogen glycation of the diabetic patients was reduce

167 he primary outcome, median blood loss in the fibrinogen group was 50 mL (interquartile range [IQR], 2

168 cases with reoperative thoracotomy (4 in the fibrinogen group).

169 n group); 4 myocardial infarctions (3 in the fibrinogen group); 2 deaths (both in the fibrinogen grou

170 troke or transient ischemic attack (4 in the fibrinogen group); 4 myocardial infarctions (3 in the fi

171 the fibrinogen group); 2 deaths (both in the fibrinogen group); 5 cases with renal insufficiency or f

172 ith renal insufficiency or failure (3 in the fibrinogen group); and 9 cases with reoperative thoracot

173 ith combined deficiencies of plasminogen and fibrinogen had decreased EAE severity, they did not exhi

174 se including acute-phase reactants proteins (fibrinogen, haptoglobin and CRP), cell adhesion molecule

175 An antibody, specific to fibrinogen, has been covalently attached to graphene and

176 that mediate interaction of FXIII-A2B2 with fibrinogen have been elusive.

177 beta3 inhibitors, suggesting that fibrin and fibrinogen have distinct binding requirements.

178 ity, and many of these strains express human fibrinogen (hFg) binding Pattern A-C M-proteins, e.g. M1

179 interacting with antiphagocytotic human-host fibrinogen (hFg).

180 and transendothelial migration via an ICAM1-fibrinogen-ICAM1 bridge.

181 PGI2 over activated and spread platelets on fibrinogen, identified a significant reduction in platel

182 usion revealed that the highest intensity of fibrinogen immunoreactivity was at 14 days.

183 Arf6-dependent endocytosis is restricted to fibrinogen, implying that Arf6 also modulates traffickin

184 biosensor responds in a selective manner to fibrinogen in aqueous media even in the presence of plas

185 correlated with white blood cell counts and fibrinogen in free-ranging dolphins.

186 t evidence of a critical functional role for fibrinogen in malignant tumor growth.

187 role for thrombin and its targets PAR-1 and fibrinogen in the pathogenesis of colonic adenocarcinoma

188 e, the biosensor was shown to reliably sense fibrinogen in the presence of high background serum albu

189 essed by the presence of increased levels of fibrinogen in the surrounding parenchyma and enhanced le

190 band beta3, and enhanced platelet binding to fibrinogen in vivo and in vitro.

191 gamma390-396A mice carrying a mutant form of fibrinogen incapable of binding leukocyte alphaMbeta2-in

192 Plasma C-reactive protein and fibrinogen increased with MK-7123 treatment.

193 ependent mechanisms: fibrinogen-mediated and fibrinogen-independent.

194 vealed that Abeta42 binding to fragment D of fibrinogen induced a structural change in the C-terminal

195 Fibrinogen induces phosphorylation of Smad 1/5/8 and inh

196 (2017) show that the blood clotting protein fibrinogen inhibits nerve repair by preventing oligodend

197 mon resonance (SPR) measurements showed that fibrinogen interacted with TiO2 and CeO2 NPs with high a

198 Overall, our study elucidates the Abeta-fibrinogen interaction and clarifies the mechanism by wh

199 Platelet activation following bacterial-fibrinogen interaction or thrombin-mediated fibrinogen-f

200 of effective therapeutics against the Abeta-fibrinogen interaction to treat cerebrovascular abnormal

201 of fibrin clot lysis by interfering with C3-fibrinogen interaction within the beta chain.

202 chemical and structural details of the Abeta-fibrinogen interaction.

203 Fibrinogen interacts with beta-amyloid (Abeta), forming

204 s snake venom metalloproteinases that cleave fibrinogen into fibrin split products without inducing c

205 pendent on coagulase-catalyzed conversion of fibrinogen into fibrin.

206 yzed conversion of a soluble plasma protein, fibrinogen, into a polymeric fibrin clot, is conserved i

207 em repeats of a 27-residue peptide that bind fibrinogen, is conserved at the C terminus of all Coa mo

208 on admission, platelet count <30 < 10(9) /L, fibrinogen level <60 mg/dL, and activated partial thromb

209 ncentrate infusion dosed to achieve a plasma fibrinogen level of 2.5 g/L in high-risk cardiac surgery

210 ), targeted to achieve a postinfusion plasma fibrinogen level of 2.5 g/L.

211 thrombus resistance, and for a supplemented fibrinogen level of 48%, the thrombus resistance increas

212 indings indicate that Cv-PC increases plasma fibrinogen levels and may provide a promising therapy fo

213 tion in vitro, along with plasma d-dimer and fibrinogen levels were also measured.

214 easurement of serum hsCRP levels, and plasma fibrinogen levels were determined using an automated ana

215 ontrast, P-SEL expression and PAC-1 binding, fibrinogen levels, and d-dimers were not associated with

216 gy was observed as platelet counts, d-dimer, fibrinogen levels, and serum chemistries remained normal

217 rinogen spilt products, thereby upregulating fibrinogen levels, ultimately improving perioperative he

218 rinogen production, thereby elevating plasma fibrinogen levels.

219 eir correlations with serum hsCRP and plasma fibrinogen levels.

220 The fibrinogen-like (FBG) domain of FREP1 is highly conserve

221 matrilin-3, tissue factor pathway inhibitor, fibrinogen-like 1, and plasminogen activator inhibitor-1

222 -coil domain (CCD) connected to a C-terminal fibrinogen-like domain (FLD) via a cleavable linker, and

223 lecule-1, intercellular adhesion molecule-1, fibrinogen-like protein 2, and PAI-1, the secretion of T

224 of cell surface markers (adhesion molecules, fibrinogen-like protein 2, plasminogen activator inhibit

225 obulin G, complement, fibrin, tissue factor, fibrinogen-like protein 2, tissue plasminogen activator

226 s C and S, antithrombin, factors VIII/IX/XI, fibrinogen, lipoprotein(a), homocysteine, lupus anticoag

227 We identified 41 genome-wide significant fibrinogen loci; of which, 18 were newly identified.

228 The peak areas of the fibrinogen marker peptides were increased by a factor of

229 Targeting fibrinogen may be an upstream therapeutic strategy to pr

230 the following proteins compared to Group II: fibrinogen (median (interquartile range) Group I: 0.09 (

231 ets proceeds via two independent mechanisms: fibrinogen-mediated and fibrinogen-independent.

232 eins such as Albumin, Alpha Fetoprotein, and Fibrinogen, metabolized ammonia, and displayed cytochrom

233 ned whether neutrophil activation can affect fibrinogen modifications and consequently elicit thrombo

234 Sequential binding of the three fibrinogen nodules is suggested by selective fluorescenc

235 ntly thinner fibers compared with clots from fibrinogen of control individuals (mean+/-SD =63+/-2 and

236 degradation of iC3b by hPm that is bound to fibrinogen on the cells.

237 he bloodstream, and yet avidly bind immobile fibrinogen on the surface of other platelets at the prim

238 Activated platelets display immobilized fibrinogen on their surface, thus mediating further recr

239 and immunological side effects, while use of fibrinogen or coagulation factors provides only partial

240 ty, because unlike r-tPA, it did not degrade fibrinogen or enhance experimental bleeding.

241 Targeting fibrinogen or its downstream BMP signaling pathway may h

242 A microscopic bead coated with fibrinogen or monomeric fibrin produced by treating the

243 (high-sensitive C-reactive protein, lipids, fibrinogen, oxidative stress, and endothelial function a

244 (P<0.001) and with a marked carbonylation of fibrinogen (P<0.001), whose secondary structure appeared

245 s to PAD and IgG antibodies to citrullinated fibrinogen peptides, in the absence of a T cell response

246 ailed to develop antibodies to citrullinated fibrinogen peptides.

247 by CCA (ie, international normalized ratio, fibrinogen, platelet count).

248 Moreover, fibrinogen, platelets, and activated partial thromboplas

249 Separately, fibrinogen split products induce fibrinogen production, thereby elevating plasma fibrinog

250 ntly, dysregulation of circulating levels of fibrinogen, protein C activity, and antifibrinolytic pro

251 Platelets, fibrinogen, prothrombin index, activated partial thrombo

252 Inhibition of the fibrinogen receptor CD11b/CD18 protects from all immune

253 Fibrinogen receptor subunits Itga2b (alphaIIb) and Itgb3

254 ocyte chemoattractant protein-1, P-selectin, fibrinogen, receptor activator of nuclear factor-kappaB

255 pon active plasmin, yet independent of known fibrinogen receptors.

256 The fibrinogen recognition also occurs in serum environment,

257 6 is important because they are located in a fibrinogen region susceptible to physiological truncatio

258 A genetic variation within mosquito fibrinogen related-protein 30 (FBN30) was previously ide

259 we showed that genetic polymorphisms in the fibrinogen-related protein 1 (FREP1) gene are significan

260 sting will have an important role in guiding fibrinogen replacement for hemostatic therapy in clinica

261 maA and Fibgamma(390-396A) clots, suggesting fibrinogen residues gamma390-396 accelerate FXIII-A2B2 a

262 did not bind FXIII-A2B2 These data indicate fibrinogen residues gamma390-396 comprise the major bind

263 y, these data indicate that FXIII-A2B2 binds fibrinogen residues gamma390-396 via the B subunits, and

264 two peptide motifs within the beta chain of fibrinogen (residues 424-433, 435-445) that bound to C3.

265 in G, glutaredoxin-1, thioredoxin, GP1b, and fibrinogen, showed a bias for oxidation, whereas annexin

266 of TG (five markers), and bovine and porcine fibrinogen (six markers each).

267 onditioning with C. atrox venom will produce fibrinogen spilt products, thereby upregulating fibrinog

268 Separately, fibrinogen split products induce fibrinogen production,

269 Fibrinogen stimulates a unique transcriptional signature

270 P<0.01) CONCLUSIONS: In BD patients, altered fibrinogen structure and impaired fibrinogen function ar

271 model with a mutation in the Aalpha chain of fibrinogen such that no fibrin polymer is formed in vivo

272 Fibrinogen supplementation in normal blood resulted in a

273 is process, platelets are bridged by soluble fibrinogen that binds surface integrin receptors.

274 cted reduced binding of FXIII-A2B2 to murine fibrinogen that has gamma-chain residues 390-396 mutated

275 n reduced RBC retention in clots formed with fibrinogen that lacks gamma-chain crosslinking sites, bu

276 In the presence of LPS together with iC3b or fibrinogen, the expression levels of IL-6 and TNF-alpha

277 Accumulating evidence suggests that fibrinogen, the main protein component of blood clots, p

278 ains to how resting platelets ignore soluble fibrinogen, the third most abundant protein in the blood

279 Fibrinogen therapy is an important component of a multim

280 ptomyces mobaraensis, and bovine and porcine fibrinogen/thrombin in restructured meat was developed u

281 y revealed direct binding of plasminogen and fibrinogen to different platelet subpopulations.

282 interaction of alphaIIbbeta3 with fibrin and fibrinogen to explore their differential effects.

283 suggest a role of CPN1 in the conversion of fibrinogen to fibrin.

284 inogen binding to alphaIIbbeta3 and converts fibrinogen to fibrin.

285 d plasma powder and PPFG using the ratios of fibrinogen to serotransferrin peptide peak areas seems t

286 enables bloodstream infections by directing fibrinogen to the staphylococcal surface, generating a p

287 II, IX, and X while simultaneously restoring fibrinogen (to 88% of its normal level) in diluted blood

288 s covalent interaction with the host protein fibrinogen using an unusual internal thioester bond as a

289 D-dimers (6.00-27.0 mg/L) increased, whereas fibrinogen values dropped from 5.8 to 4.1 g/L.

290 sing human components, including recombinant fibrinogen variants, FXIII-A2B2, and isolated FXIII-A2 a

291 -assessed using C-reactive protein (CRP) and fibrinogen- varied across the adult age span.

292 irst time the differentiation of the role of fibrinogen vs fibrin oligomer or polymer in antimicrobia

293 However, the precise contribution of soluble fibrinogen vs insoluble fibrin matrices to vascular inte

294 and platelet count, endotoxin, Protein C and fibrinogen were independent predictors of a hypocoagulab

295 ks of serum levels of C-reactive protein and fibrinogen were noticed in the first postoperative week.

296 a'/gamma'), and alphaC-truncated (Aalpha251) fibrinogens, whereas coprecipitation with human Fibgamma

297 nt Rasa3 (H794L) show increased spreading on fibrinogen, which in contrast to wild-type platelets is

298 ling a specific corona phase that recognizes fibrinogen with high selectivity.

299 ly reduces plasma levels of IL-6, hsCRP, and fibrinogen with little change in atherogenic lipids.

300 fibrin produced by treating the immobilized fibrinogen with thrombin was captured by a laser beam an