ライフサイエンスコーパス: human platelet

1 ), we developed a computational model of the human platelet.

2 n, and proteolytic processing of proteins in human platelets.

3 augmented TRAP-induced TGF-beta1 release in human platelets.

4 of BCL-2-dependent tumors in vivo and spares human platelets.

5 diverse functional proteins associated with human platelets.

6 phorylation was also potentiated with GFX in human platelets.

7 ovel pathway of Syk regulation by PKCbeta in human platelets.

8 fine the effects of PGN on the activation of human platelets.

9 m responsible for Syk negative regulation in human platelets.

10 the investigation of signal transduction in human platelets.

11 ubjects, we studied the function of PEAR1 in human platelets.

12 ced the collagen-induced STAT3 activation in human platelets.

13 e humanized mice had extremely low levels of human platelets.

14 lly regulated platelet aggregation in washed human platelets.

15 ffects of anthrax lethal and edema toxins on human platelets.

16 s required for effective receptor traffic in human platelets.

17 tion of the protease-activated receptor 1 on human platelets.

18 associates with SHP-2, as well as SHP-1, in human platelets.

19 n and functional relevance of MS channels in human platelets.

20 ect binding and entry of anthrax toxins into human platelets.

21 and vesicle-associated membrane protein-8 in human platelets.

22 e polymers of the size secreted by activated human platelets.

23 ined in VWF(R1326H) mutant mice infused with human platelets.

24 inhibition assays with fluorescently labeled human platelets.

25 nomotors cloaked with the plasma membrane of human platelets.

26 Kv1.3 (KCNA3) is substantially expressed in human platelets.

27 ADP, resembling those in clopidogrel-treated human platelets.

28 resembling those in PAR1 antagonist-treated human platelets.

29 characterizing the ADP signaling pathways in human platelets.

30 integrin in Chinese hamster ovary cells and human platelets.

31 for talin regulation of integrin activity in human platelets.

32 ructural properties and ability to stimulate human platelets.

33 icoid receptor have all been found active in human platelets.

34 at murine VWF-A1 supports limited binding of human platelets.

35 enotype that can be corrected by infusion of human platelets.

36 ptor protease activated receptor-1 (PAR1) in human platelets.

37 of antithrombotics that specifically target human platelets.

38 s mitis strain SF100 that mediate binding to human platelets.

39 r the direct activation of G(i/o) by PAR1 in human platelets.

40 ability to affect alphaIIbbeta3 activity in human platelets.

41 mTOR by rapamycin blocks clot retraction by human platelets.

42 is known to be the most potent activator of human platelets.

43 use of a FLIPR to study the calcium flux in human platelets.

44 myocytes and the open canalicular system of human platelets.

45 for their xenogeneic hepatic consumption of human platelets.

46 PACSIN2 associated with FlnA in human platelets.

47 sed on the plasma membrane of both mouse and human platelets.

48 RE syntaxin 8 (STX8) (Qc SNARE) in mouse and human platelets.

49 n a PI3K-dependent manner upon activation of human platelets.

50 plays a role in binding and phagocytosis of human platelets.

51 ns of apolipoproteins in HDL and proteins in human platelets.

52 with a putative role in granule ontogeny in human platelets.

53 eticulocyte 15-lipoxygenase-1 (15-hLO-1) and human platelet 12-lipoxygenase (12-hLO) have been implic

54 Human platelet 12-lipoxygenase (hp-12LOX, 662 residues+i

55 Here we show that circRNAs are enriched in human platelets 17- to 188-fold relative to nucleated ti

56 To investigate DUSP3 function in human platelets, a novel small-molecule inhibitor of DUS

57 G), an extracellular matrix preparation from human platelets able to support the proliferation of end

58 osphate (of the size secreted from activated human platelets) accelerates factor V activation, comple

59 ontact with an allosteric inhibitor impaired human platelet accrual in damaged arterioles.

60 Here we demonstrate that human platelets activated with thrombin preferentially r

61 nium salt (2MeSAMP) and ARC69931MX), inhibit human platelet activation.

62 maging and electron microscopy, we show that human platelets adherent to collagen are transformed int

63 al forms of human properdin bind directly to human platelets after activation by strong agonists in t

64 ed time-resolved phosphorylation patterns in human platelets after treatment with iloprost, a stable

65 Maternal alloantibodies against the human platelet Ag (HPA)-1a allotype of the platelet beta

66 Human platelet Ag (HPA)-1a, located on integrin beta3, i

67 roscopy we visualised membrane ballooning in human platelet aggregates adherent to collagen-coated su

68 9%), was associated with higher PAR4-induced human platelet aggregation and Ca2+ flux, and generated

69 shown to specifically block collagen-induced human platelet aggregation and granule secretion.

70 Thrombin initiates human platelet aggregation by coordinately activating pr

71 10k inhibited serotonin-amplified human platelet aggregation with an IC(50) = 8.7 nM and h

72 n- and C-type lectin-like receptor 2-induced human platelet aggregation, thereby phenocopying the eff

73 and functional activities as an inhibitor of human platelet aggregation.

74 5-HT release and SERT activity in efficient human platelet aggregation.

75 g site moderately decreased thrombin-induced human platelet aggregation.

76 In human platelets, aldose reductase synergistically modula

77 Human platelet alloantigens (HPAs) reside on functionall

78 We show that Cbl-b is expressed in human platelets along with c-Cbl, but in contrast to c-C

79 Similar to recombinant CXCL4, releasate from human platelets also reduced CD163 expression.

80 s and for the receptor expressed normally in human platelets an agonist-selective engagement of G(q)

81 sitol 3,4,5-trisphosphate-binding protein in human platelets and a key regulator of integrin alphaIIb

82 Using isolated human platelets and a mouse model of myocardial infarcti

83 We show that PAR1 couples to G(i/o) in human platelets and activates phosphoinositide-3 kinase

84 elet-membrane-cloaked nanomotors disguise as human platelets and display efficient propulsion in bloo

85 PAR4 associate as a heterodimeric complex in human platelets and fibroblasts.

86 also evaluated E. faecalis interactions with human platelets and found that growth of E. faecalis in

87 ated a superadditive Ca(2+) increase in both human platelets and human embryonic kidney 293 (HEK293)

88 Here, we used human platelets and human erythroleukemia (HEL) cells, w

89 he effect of shear stress on Ca(2+) entry in human platelets and Meg-01 megakaryocytic cells loaded w

90 hibition of alpha2beta1-mediated adhesion of human platelets and other cells to collagen.

91 ed human blood were used to study binding of human platelets and platelet-white blood cell aggregatio

92 uced aggregation and calcium mobilization in human platelets and reduce 12-HETE in beta-cells.

93 t ATX is stored in alpha-granules of resting human platelets and released upon tumor cell-induced pla

94 stinct sialylated carbohydrate structures on human platelets and salivary proteins.

95 e for PKC downstream of 12-LOX activation in human platelets and suggest 12-LOX as a possible target

96 stem cells to introduce FVIII expression in human platelets and that human platelet-derived FVIII ca

97 rin alphaIIbbeta3, enhances SERT activity in human platelets and that integrin alphaIIbbeta3 interact

98 us serum significantly enhanced adherence to human platelets and that sortase deletion mutants (the D

99 Our results show that LXR-beta is present in human platelets and the LXR ligands, GW3965 and T0901317

100 , we validate extracellular flux analysis in human platelets and use this technique to screen for mit

101 ppraisal of protein networks and pathways in human platelets, and indicate the feasibility of differe

102 ptor 1, the primary receptor for thrombin on human platelets, and reduces recurrent thrombotic events

103 elet transfusions without evidence of HLA or human platelet antigen (HPA) antibodies.

104 aused by maternal alloantibodies against the human platelet antigen (HPA)-1a, which opsonizes fetal p

105 al antigenic difference; Leu33 generates the human platelet antigen 1a (HPA-1a), whereas Pro33 genera

106 Incompatibility of the human platelet antigen-1 (HPA-1) system is the most comm

107 ernal generation of antibodies against fetal human platelet antigen-1a (HPA-1a), can result in intrac

108 sera with respect to alloantibodies against human platelet antigens (HPA).

109 ulin G (IgG) formed during pregnancy against human platelet antigens (HPAs) of the fetus mediates fet

110 patibility Complex of different species; IPD-human platelet antigens, alloantigens expressed only on

111 ng patients who have developed antibodies to human platelet antigens.

112 bed functional disparities between mouse and human platelets are reflected in differences at the tran

113 operties of 5G6 Fab fragment to GPIbalpha on human platelets as those to KL10 suggests that such an i

114 hysically proximal to talin and kindlin-3 in human platelets, as assessed biochemically, and by immun

115 Human platelets at a physiologic ratio of 1 platelet to

116 blocking antibodies resulted in reduction of human platelet binding and phagocytosis.

117 GTA1, CMAH LSECs exhibited reduced levels of human platelet binding in vitro when compared with GGTA1

118 18 expression by siRNA resulted in decreased human platelet binding.

119 mbopoiesis, we have developed a microfluidic human platelet bioreactor that recapitulates bone marrow

120 ted this dephosphorylation on Tyr-525/526 in human platelets but not in wild type murine platelets.

121 e not involved in the activation of purified human platelets by pneumococci.

122 l also reduces the xenogeneic consumption of human platelets by the porcine liver.

123 ere inhibited in TLR2-deficient mice and, in human platelets, by pretreatment with TLR2-blocking anti

124 sence of dual phosphorylated G6B-b in washed human platelets can reduce the EC(50) for both CRP and c

125 eived 2bF8LV-transduced hCB cells as long as human platelet chimerism persisted.

126 haIIbbeta3 and P2Y(1)(2) inhibitors to limit human platelet clot formation at doses recommended by th

127 Human platelets cocultured with HT29 cells rapidly adher

128 fibrinogen was augmented by niacin in washed human platelets, coincident with increased thromboxane (

129 Human platelets contain microRNAs (miRNAs) and miRNA pro

130 We also showed that human platelets contain the enzyme hyaluronidase-2 (HYAL

131 New activities of human platelets continue to emerge.

132 The direct binding of bacteria to human platelets contributes to the pathogenesis of infec

133 Mechanistically, human platelets correct the phenotype by forming occlusi

134 rug target retaining potential for enhancing human platelet counts.

135 he defective hemostatic function of mouse or human platelets deficient in cPLA(2)alpha.

136 We have recently reported that human platelets degrade HA from the surfaces of activate

137 In this study, we show that human platelets degrade the proinflammatory matrix HA th

138 FVIII expression in human platelets and that human platelet-derived FVIII can improve hemostasis in h

139 membrane (CM) with xenograft and recombinant human platelet-derived growth factor (rhPDGF) in guided

140 Recombinant human platelet-derived growth factor (rhPDGF) is safe an

141 al matrix (ADM) with and without recombinant human platelet-derived growth factor (rhPDGF).

142 d defect with the application of recombinant human platelet-derived growth factor (rhPDGF-BB) combine

143 The proximal 5'-flanking region of the human platelet-derived growth factor A (PDGF-A) promoter

144 Human platelet-derived growth factor B (hPDGFB) has been

145 tein human alpha-thrombin and an oncoprotein human platelet-derived growth factor B-chain (PDGF-BB) u

146 neralized bone allograft (FDBA), recombinant human platelet-derived growth factor mixture with a tita

147 lution structure of PDGFRbeta [a full-length human platelet-derived growth factor receptor], in compl

148 is systematic review, the use of recombinant human platelet-derived growth factor-BB (rhPDGF-BB) led

149 phosphate (beta-TCP) + 0.3 mg/ml recombinant human platelet-derived growth factor-BB (rhPDGF-BB) with

150 evaluating two concentrations of recombinant human platelet-derived growth factor-BB (rhPDGF-BB) with

151 amel matrix derivative (EMD) and recombinant human platelet-derived growth factor-BB (rhPDGF-BB) with

152 uine origin (eHAC), infused with recombinant human platelet-derived growth factor-BB (rhPDGF-BB), to

153 tissue graft (CTG) (control) or recombinant human platelet-derived growth factor-BB + beta-tricalciu

154 cs (enamel matrix derivative and recombinant human platelet-derived growth factor-BB plus beta-trical

155 Initial studies revealed that human platelets did not efficiently transmigrate across

156 rast to the murine study, galactosylation of human platelets did not prevent the accelerated platelet

157 Human platelets display a unique dual receptor system fo

158 tion or in blood plasma, and could aggregate human platelets, either isolated or in whole blood.

159 However, we observe that anucleate human platelets, either maintained in suspension culture

160 We found that this prodrug binds tightly to human platelets even after gel filtration, has a prolong

161 onment allowing us to manufacture functional human platelets ex vivo.

162 Human platelets express 2 thrombin receptors: protease-a

163 We found that human platelets express 284 miRNAs.

164 Human platelets express dual thrombin receptors, proteas

165 se data provide the first demonstration that human platelets express functional TLR2 capable of recog

166 Human platelets express RXRalpha and RXRbeta.

167 In the present study, we demonstrate that human platelets express TLR2, TLR1, and TLR6.

168 Human platelets express two thrombin receptors, protease

169 FcgammaRIIa phosphorylation did not occur in human platelets expressing a truncated beta3 cytoplasmic

170 t thrombin, collagen, or ionophore-activated human platelets externalize two phosphatidylserines (PSs

171 to affinity purify potential regulators from human platelet extracts.

172 ated by antibodies against complexes between human platelet factor 4 (hPF4) and heparin.

173 screened a panel of HDPs and determined that human platelet factor 4 (hPF4) kills malaria parasites i

174 In human platelets, Fc receptor gamma-chain IIa (FcgammaRII

175 PAR4, plays a central role in regulation of human platelet function in that it is known to be the mo

176 Human platelet FVIII expression was introduced by 2bF8LV

177 the feasibility for lentivirus (LV)-mediated human platelet gene therapy of hemophilia A.

178 by using lipidomics that thrombin-activated human platelets generate a new type of eicosanoid that b

179 Recent studies show that human platelets have high levels of miR-30c and synthesi

180 In human platelet, higher sensitivity of PDE5 for sildenafi

181 c analysis of dematin-associated proteins in human platelets identified inositol 1,4,5-trisphosphate

182 In mice expressing both hPF4+ and human platelet IgG Fc receptor IIA (FcgammaRIIA), infusi

183 inhibited collagen-stimulated activation of human platelets in a dose-dependent manner but displayed

184 collagen-adhered, thrombin-activated, washed human platelets in a flow chamber.

185 Rapid increase in human platelets in blood to levels comparable with those

186 AS to predict calcium signaling responses of human platelets in EDTA-treated plasma to six different

187 ristocetin-induced platelet agglutination of human platelets in plasma with no influence on platelet

188 of histones on the procoagulant potential of human platelets in platelet-rich plasma (PRP) and in pur

189 ibitory effect of ADP-induced aggregation of human platelets in platelet-rich plasma.

190 ifications have on xenogeneic consumption of human platelets in the absence of immune-mediated graft

191 s also have shown the ability to phagocytose human platelets in the absence of immune-mediated injury

192 In human platelets in vitro, both BSDL and a peptide corres

193 ry glioblastoma cells induced aggregation of human platelets in vitro, which could be abrogated by an

194 serine protease not previously identified in human platelets, increases with aging ( approximately 9-

195 Patient sera incubated with washed human platelets induced more C3 and C9 deposition on the

196 DRA/DRB3*0101, in complex with an N-terminal human platelet integrin alphaII(B)betaIII glycoprotein p

197 The binding of bacteria to human platelets is a likely central mechanism in the pat

198 Bacterial binding to human platelets is an important step in the pathogenesis

199 Even though GPCR signaling in human platelets is directly involved in hemostasis and t

200 Complement activation on human platelets is known to cause platelet degranulation

201 y expressed oxylipin-producing enzyme in the human platelet, is an essential component of FcgammaRIIa

202 GrmA is present and bioactive in human platelets, is higher in older adults, and controls

203 ures of the mammalian PFK1 tetramer, for the human platelet isoform (PFKP), in complex with ATP-Mg(2+

204 anules and releases functional FV(+)CD42b(+) human platelet-like particles in vitro and when infused

205 Proteomic analysis of human platelet LRRFIP1-interacting proteins indicated th

206 We describe the generation of human platelet lysate gel (hPLG), an extracellular matri

207 In human platelets, margatoxin reduced the P2X(1)- and thro

208 r 1 kg of body weight) significantly reduced human platelet-mediated thrombus formation in laser-inju

209 gue infection that had significant levels of human platelets, monocytes/macrophages, and hepatocytes.

210 Desialylation of human platelet monolayers reduced adherence of SF100, wh

211 g of substrates (TAILS), to characterize the human platelet N-terminome, proteome, and posttranslatio

212 iously undescribed biosynthetic route during human platelet-neutrophil interactions for the proresolv

213 Human platelet numbers decreased from 102 +/- 33 at begi

214 d approximately 80% of thrombus formation of human platelets on a collagen matrix.

215 y either pharmacologic inhibition of NOX2 in human platelets or genetic ablation of NOX2 in murine pl

216 Inhibition of Cx40 in human platelets or its deletion in mice reduces platelet

217 Pharmacological inhibition of PP2Ac in human platelets or PP2Acalpha knockdown in primary murin

218 erization, we have begun to characterize the human platelet palmitoylome.

219 PAR4, a low-affinity thrombin receptor in human platelets, participates in sustained platelet acti

220 In human platelets, PKC-theta-selective antagonistic (RACK;

221 Contact phase activation of human platelet-poor plasma by kaolin led to cleavage of

222 s, Bacillus cereus, initiated coagulation of human platelet-poor plasma only when confined.

223 E protein syntaxin-4 was strongly reduced in human platelets pretreated with PKC-theta RACK peptide,

224 ctional integrin alphaIIbbeta3 complexes and human platelets pretreated with the fibrinogen receptor

225 and Tymp(-/-) platelets, and in wild type or human platelets pretreated with TYMP inhibitor KIN59.

226 em for the study of pathologic mechanisms of human platelet production.

227 The acid-induced unfolding of human platelet profilin (HPP) can be minimally modeled a

228 ium unfolding studies have been performed on human platelet profilin1 (HPP) and monitored by far-UV c

229 study demonstrates an extensive spectrum of human platelet protein phosphorylation in response to AD

230 ted the first comprehensive and quantitative human platelet proteome, comprising almost 4000 unique p

231 In human platelets, recombinant PDI(ss-oo) inhibited aggreg

232 use macrophages are responsible for the poor human platelet reconstitution in humanized mice.

233 ss spectrometry analyses and immunoassays of human platelet releasates coupled with angiogenesis assa

234 In contrast, human platelets released by intrapulmonary-entrapped meg

235 se a cautionary note for the clinical use of human platelets released under standard ex vivo conditio

236 for the several-fold range in GPVI levels of human platelets remains to be determined.

237 Here we introduce a comprehensive human platelet repository (PlateletWeb) for systems biol

238 CE-mediated receptor shedding from mouse and human platelets requires p38 MAP kinase signaling.

239 Pharmacologic inhibition of 12-LOX in human platelets resulted in significant attenuation of F

240 sed traction forces in mouse fibroblasts and human platelets, revealing alignment between the organiz

241 ion of platelet aggregation as measured in a human platelet rich plasma (PRP) assay.

242 n generation time (TGT) coagulation assay in human platelet rich plasma (PRP).

243 ar inhibition of platelet aggregation in the human platelet rich plasma assay with IC(5)(0) values be

244 In human platelet-rich plasma (PRP), RvE1 selectively block

245 d its antiplatelet activity both in vitro in human platelet-rich plasma and in vivo in mice.

246 Microarray analyses of human platelet RNA demonstrated the presence of SVIL iso

247 Compared with human platelets, rodent platelets are less responsive to

248 sue of Blood, Kapur et al show that maternal human platelet-specific antigen 1a (HPA 1a)-specific ant

249 ells, nor do I observe affinity increases in human platelets stimulated with thrombin.

250 their rapid clearance, in agreement with the human platelet study.

251 e serotonin release from thrombin-stimulated human platelet suspensions was successfully measured, an

252 GGTA1 CMAH livers also consumed fewer human platelets than ASGR1 livers in a single-pass model

253 sion model, GGTA1 CMAH livers consumed fewer human platelets than GGTA1 and WT livers.

254 y longer time to the onset of aggregation of human platelets than that of the parent strain.

255 Further, we demonstrated in human platelets that ABCC4 inhibition, when coupled with

256 ptor-1, the primary receptor for thrombin on human platelets that is also present on vascular endothe

257 e "canaliculi" structures for secretion from human platelets, the secretory machinery in single-cell

258 e of circular RNAs (circRNAs) in circulating human platelets, thereby revealing yet another facet of

259 cade, drives fibrin deposition and activates human platelets through protease-activated receptor-1 (P

260 xenoantibodies and therefore allows infused human platelets to circulate, can be used to study drug-

261 Integrin alpha2beta1-mediated adhesion of human platelets to monomeric type I collagen or to the G

262 Ex vivo, there was less adhesion of human platelets to von Willebrand factor under high shea

263 Human platelet transformation into balloons is part of t

264 ed in PP1calpha(-/-) murine platelets and in human platelets treated with a small-molecule inhibitor

265 ent in PI3K effectors, Akt1 and Akt2, and in human platelets treated with an Akt inhibitor, SH-6.

266 cPLA(2)alpha-deficient mouse platelets or in human platelets treated with pyrrophenone, a cPLA(2)alph

267 Perfusion models were used to measure human platelet uptake in livers from WT, ASGR1, GGTA1, a

268 Our studies demonstrate that human platelets use Clk1-dependent splicing pathways to

269 To investigate this model, we interrogate human platelets using approaches that include the suppor

270 escent gold nanoparticles are delivered into human platelets via a rapid, pH-controlled mechanism usi

271 e, lysin mediates the binding of S. mitis to human platelets via its interaction with fibrinogen on t

272 between GP Ib from transfected CHO cells and human platelets was attributed to a combination of seque

273 s12041331 and expression of PEAR1 protein in human platelets was confirmed by Western blotting and EL

274 Consistent with reports utilizing human platelets, we found significantly reduced bleeding

275 In human platelets, we show that maximally activated P2X1 r

276 (RNA-Seq) and ribosome profiling of primary human platelets, we show the platelet transcriptome enco

277 Because LPA(5) transcripts are abundant in human platelets, we tested its antagonists on platelet a

278 uced hCB cells, whereas 5 of 7 survived when human platelets were 0.3% to 2%.

279 rescein diacetate succinimidyl ester-labeled human platelets were exposed to PAEC/PFAEC/PLSEC and ana

280 Human platelets were incubated with Aspergillus conidia

281 Millions of human platelets were produced and showed to be functiona

282 In support of this possibility, human platelets were rapidly rejected after infusion int

283 When washed human platelets were stimulated with thrombin, cAMP-depe

284 P2Y12 overexpressed in HEK293, CHO cells and human platelets were used and responsiveness to differen

285 PMPs, generated from purified human platelets, were isolated by ultracentrifugation an

286 particles enclosed in the plasma membrane of human platelets, which are a unique population of cellul

287 robes per nanoparticle to be internalized in human platelets, which are not susceptible to transfecti

288 V-1-infected patients (n = 23) and in washed human platelets, which are the main source of circulatin

289 The treatment of human platelets with a selective PAR4 agonist (AYPGKF-NH

290 density lipoprotein (HDL) and interaction of human platelets with a specific oxPL, and demonstrated i

291 Activation of human platelets with adenosine diphosphate (ADP) stimula

292 Treatment of human platelets with cyclosporin A gave a similar phenot

293 Treatment of human platelets with GSK3 inhibitors renders them more s

294 est that primary pig KC bind and phagocytose human platelets with involvement of CD18.

295 as established to measure the association of human platelets with liver sinusoidal endothelial cells

296 rker for its activation, upon stimulation of human platelets with PAR agonists SFLLRN and AYPGKF or G

297 iate platelet clearance, we incubated normal human platelets with patient serum containing an alphaII

298 Moreover, treating activated human platelets with phospholipase D enhanced the rates

299 Stimulation of washed human platelets with protease-activated receptor agonist

300 ets, ex vivo treatment of wild-type mouse or human platelets with the Vps34-specific inhibitors, SAR4