ライフサイエンスコーパス: GPIb

1 GPIb alpha is present, as detected by immunohistochemist

2 GPIb alpha plays a critical role in the co-localization

3 GPIb alpha, a glycoprotein component of the GPIb-IX-V co

4 GPIb beta and GPIX chimeras corresponding to predicted b

5 GPIb-IX activates not only the transfected alpha(IIb)bet

6 GPIb-IX-induced ERK2 phosphorylation is inhibited by PKG

7 GPIb-IX-V is a catch bond for it becomes more stable as

8 flavocetin-A, which has long been known as a GPIb inhibitor, efficiently targets alpha2beta1 integrin

9 itherto, flavocetin-A has been reported as a GPIb inhibitor.

10 ta cytoskeletal translocation may serve as a GPIb post-receptor occupancy signaling event.

11 ological role of GPIbbeta phosphorylation, a GPIb-IX mutant replacing Ser(166) of GPIbbeta with alani

12 , no difference in activity was seen using a GPIb complex-binding assay that is independent of ristoc

13 o-inflammatory diseases such as stroke via a GPIb-dependent mechanism.

14 nphosphorylated identical peptide, abolished GPIb-IX binding to 14-3-3zeta.

15 us pulling force of >15 pN to fully activate GPIb-IX.

16 regulatory mechanism by which flow activates GPIb alpha via inducing a loop-to-beta-hairpin conformat

17 Mechanical unfolding of the MSD activates GPIb-IX signaling into platelets, leading to their activ

18 agen-induced platelet aggregation even after GPIb was blocked with other inhibitors.

19 so showed reduced actin polymerization after GPIb-IX-mediated platelet aggregation, actin polymerizat

20 ited by LJ1b1, a monoclonal antibody against GPIb.

21 r botrocetin)-induced vWF binding and allows GPIb-IX-expressing cells to adhere to immobilized vWF un

22 Interaction of glycoprotein Ib alpha (GPIb alpha) with von Willebrand factor (VWF) initiates p

23 the platelet glycoprotein receptor Ib alpha (GPIb(alpha)) and the A1 domain of von Willebrand factor

24 reacted with GPV independent of GPIb alpha, GPIb beta, or GPIX.

25 coexpressing integrin alpha(IIb)beta(3) and GPIb-IX adhere and spread on vWF, which is inhibited by

26 other thrombin receptors, PAR-3, PAR-4, and GPIb; and (2) greater sensitivity of PAR-1 transfected B

27 rmed for platelet GPla (integrin alpha2) and GPIb-IX-V, but there is support for the 807 T/C polymorp

28 pulated the expression levels of filamin and GPIb in cultured embryonic stem cells (ESCs) that were s

29 itment was dependent upon both GPIIbIIIa and GPIb (CD42B).

30 factors such as shear rate, hematocrit, and GPIb and GPIIbIIIa receptor densities have also been ide

31 ed agglutination-induced TxA2 production and GPIb-dependent stable arterial thrombus formation in viv

32 Aberrant interactions between pvWF and GPIb play a significant role in DIC associated with pulm

33 ion of activated GPIIb/IIIa, P-selectin, and GPIb was measured with and without low and high adenosin

34 ets are continuous, identical structures and GPIb is homogeneously distributed on external and intern

35 of GPIb beta and GPIX, we developed an anti-GPIb beta monoclonal antibody MBC 257.4, whose epitope w

36 ated monoclonal antibodies (mAb) CD42b (anti-GPIb), CD41a (anti-GPIIb/IIIa), and CD62 (anti-P-selecti

37 by function-blocking murine monoclonal anti-GPIb alpha antibodies.

38 Platelet absorption of anti-GPIb autoantibodies in ITP plasmas resulted in double th

39 a with no detectable anti-GPIIb/IIIa or anti-GPIb autoantibodies.

40 In vivo, the anti-GPIb antibody prevented platelet deposition and prevente

41 atelet count after immunodepletion with anti-GPIb or anti-CD41 antibody.

42 080 human fibrosarcoma cells, which lack any GPIb, on collagen.

43 esting that the membrane skeleton-associated GPIb-IX is in a state that prevents access to the A1 dom

44 disrupted by phenylalanine substitutions at GPIb alpha tyrosine-276, tyrosine-278, and tyrosine-279,

45 A major contact between GPIb alpha and VWF involves the beta-switch region, whic

46 e the recently described interaction between GPIb and platelet 14-3-3zeta, and provide evidence for t

47 e was 51% to 59% reduced interaction between GPIb and three 14-3-3zeta deletion mutants compared with

48 VWF domain A1 that were involved in binding GPIb or botrocetin.

49 Both GPIb alpha and alpha(2)beta(1) contributed to primary ad

50 mAbs specific for CD9 (mAb7), IAP (BRIC126), GPIb (SZ1), GPIX (GR-P), beta3 (AP3) and alphaIIb (C3).

51 nd signaling network or pathway activated by GPIb-mediated agglutination to cause TxA2 production hav

52 transduction network or pathway activated by GPIb-mediated agglutination to cause TxA2 production.

53 than promoted activation of alphaIIbbeta3 by GPIb-IX-V and blocked aggregate formation on collagen at

54 thways in the activation of alphaIIbbeta3 by GPIb-IX-V.

55 inhibition of fibrinogen turnover caused by GPIb alpha binding to these mutants, and the K(d) values

56 e demonstrate that the signaling elicited by GPIb-mediated agglutination that results in TxA2 product

57 rotein Ib-IX-V complex (GPIb-IX), but not by GPIb-IX-independent platelet agonists.

58 atelets show an enhanced reaction to certain GPIb-IX-independent agonists.

59 telet von Willebrand factor receptor complex GPIb-IX-V).

60 d the von Willebrand factor receptor complex GPIb-IX-V, which are essential for thrombus growth and s

61 specific for the glycoprotein Ib/IX complex (GPIb/IX).

62 d the platelet glycoprotein Ib-IX-V complex (GPIb).

63 receptor, the glycoprotein Ib-IX-V complex (GPIb-IX), but not by GPIb-IX-independent platelet agonis

64 The platelet glycoprotein Ib-IX-V complex (GPIb-IX-IV) is the receptor for VWF and is responsible f

65 Lastly, CVX fails to bind to denatured GPIb alpha in detergent extracts of platelets.

66 Akt1 and Akt2 play important roles in early GPIb-IX signaling independent of Syk, adenosine diphosph

67 yndrome demonstrate that mutations in either GPIb beta or GPIX result in an absence of platelet GPIb

68 Functional deficiency of either GPIb or Cdc42 impairs transendothelial proplatelet forma

69 equired the coinhibition of GPVI with either GPIb alpha or alpha(2)beta(1).

70 Cells expressing GPIb-IX adhere to vWF in the presence of botrocetin but

71 ts of Chinese hamster ovary cells expressing GPIb-IX complexes containing wild-type or mutant GPIbalp

72 ntracellular signaling immediately following GPIb receptor occupancy connecting the adhesive event to

73 ld type 14-3-3zeta has a higher affinity for GPIb-IX complex than recombinant GPIbalpha cytoplasmic d

74 dimerization and decreases its affinity for GPIb-IX.

75 0B12, together with specific antagonists for GPIb alpha (12G1 Fab(2)) and alpha(2)beta(1) (6F1 mAb or

76 Modeling revealed that the kinetics for GPIb/VWF binding rate are significantly lower for type O

77 sults show that (1) GPV is not necessary for GPIb expression and function in platelets and that GPV d

78 The differential distribution proposed for GPIb differs from that reported for the fibrinogen recep

79 so activates the nearby VWF-binding site for GPIb that involves Lys(599) on helix 3.

80 omain before the dissociation of VWF-A1 from GPIb-IX.

81 ht similarly regulate signals emanating from GPIb/FcR gamma, we compared activation and aggregation r

82 (GPIb) interactions using a gain-of-function GPIb construct (tGPIbalpha(235Y;239V)) as a receptor to

83 ur data confirm the presence of a functional GPIb complex expressed on HUVECs in low density.

84 yed cytoplasmic maturation (ie, glycoprotein GPIb and platelet factor 4 expression) and reduced the a

85 a, a process involving platelet glycoprotein GPIb and bacterial opsonization with activated complemen

86 is the shedding of the surface glycoproteins GPIb-alpha and GPV.

87 P)VI, C-type lectin-like receptor-2 (CLEC-2)>GPIb>alpha6beta1, alphaIIbbeta3>alpha2beta1>CD36, alpha5

88 -type, GPVI(-/-), FcR gamma (-/-), and human GPIb transgenic mice.

89 ntal baboons (n=3) received mouse anti-human GPIb monoclonal antibody before undergoing orthotopic pu

90 both GPVI and native but not denatured human GPIb alpha.

91 First, CVX binds to human GPIb alpha expressed on the surface of CHO cells.

92 Third, the binding of CVX to human GPIb alpha is inhibited by soluble, recombinant human GP

93 We characterized HUVEC GPIb using viper venom proteins: alboaggregins A and B,

94 been shown to bind to human glycoprotein Ib (GPIb) and cause activation of human (or primate) platele

95 sma containing antiplatelet glycoprotein Ib (GPIb) autoantibodies (P <.001) as compared with both the

96 The glycoprotein Ib (GPIb) complex is composed of GPIb alpha covalently attac

97 xpression and function of a glycoprotein Ib (GPIb) complex on human umbilical vein endothelial cells

98 studies have suggested that Glycoprotein Ib (GPIb) has a different distribution on external (surface)

99 (ELISA)-based assay of VWF-glycoprotein Ib (GPIb) interactions using a gain-of-function GPIb constru

100 rant platelet immunorelated glycoprotein Ib (GPIb) receptor expressed by human tumor cells appears to

101 Glycoprotein Ib (GPIb) shedding, exposure of P-selectin, and activated in

102 interaction of the platelet glycoprotein Ib (GPIb) surface receptor and its arterial subendothelial v

103 Platelets use receptor glycoprotein Ib (GPIb), specifically its alpha subunit (GPIbalpha), to si

104 eceptors that bind VWF: the glycoprotein Ib (GPIb)-IX-V complex and the integrin alphaIIbbeta3, but t

105 through binding to platelet glycoprotein Ib (GPIb).

106 e platelet receptor complex glycoprotein Ib (GPIb).

107 e antihuman CD42b [platelet glycoprotein Ib (GPIb)] mAb, had sizes and cargo protein contents similar

108 Rapid chilling causes glycoprotein-Ib (GPIb) receptors to cluster on blood platelets.

109 n, the soluble form of glycoprotein Ibalpha (GPIb alpha).

110 nst cell-specific glycoproteins (GPIIb-IIIa, GPIb-IX and others) accelerate platelet destruction.

111 doxically, flow enhances rather than impedes GPIb alpha-VWF binding.

112 /y) platelets exhibited a marked decrease in GPIb-IX-V function and agonist-mediated integrin alphaII

113 me, a bleeding disorder caused by defects in GPIb-IX-V.

114 tification of the mechanosensitive domain in GPIb-IX has significant implications for the pathogenesi

115 unfolding of the mechanosensitive domain in GPIb-IX, which may possibly contribute to platelet mecha

116 mutant complexes confirmed its existence in GPIb-IX and enabled localization of this quasi-stable me

117 rement for Btk and TxA2 receptor function in GPIb-dependent arterial thrombosis was confirmed in vivo

118 s, 14-3-3 binding to GPIb-IX is important in GPIb-IX signaling.

119 model, and show that 14-3-3 is important in GPIb-IX signaling.

120 rotein kinase (MAPK) pathway is important in GPIb-IX-dependent activation of platelet integrin alpha(

121 indicate that Lyn is critically important in GPIb-IX-mediated activation of the cGMP pathway.

122 sphoinositol 3-kinase (PI3K) is important in GPIb-IX-mediated signaling.

123 gation, suggesting that the role of LIMK1 in GPIb-mediated platelet activation is independent of acti

124 The defect of LIMK1(-/-) platelets in GPIb-IX-mediated platelet activation is attributed to a

125 vitro leads to the concomitant reduction in GPIb-IX complex expression due to ER-associated degradat

126 Deletion of the filamin binding site in GPIb(alpha) markedly enhances ristocetin- (or botrocetin

127 n outside-in signaling distinct from that in GPIb-IX-mediated inside-out signaling.

128 ound 48/80 resulted in transiently increased GPIb alpha expression by dermal dendrocytes.

129 (SFKs) play an important role in VWF-induced GPIb-IX signaling.

130 e 14-3-3-binding site in GPIbalpha inhibited GPIb-IX-mediated fibrinogen binding to alpha(IIb)beta(3)

131 Anti-pS609 inhibited GPIb-IX binding to the intracellular signaling molecule,

132 or vWF interaction with different integrins, GPIb-IX-mediated activation of alpha(IIb)beta(3) require

133 to the platelet membrane glycoprotein Ib-IX (GPIb-IX) results in platelet activation.

134 s receptor, the platelet glycoprotein Ib-IX (GPIb-IX), and p38 inhibitors diminish platelet aggregati

135 Willebrand factor (vWF), glycoprotein Ib-IX (GPIb-IX), mediates initial platelet adhesion and activat

136 d factor (vWF) receptor, glycoprotein Ib-IX (GPIb-IX), mediates platelet adhesion and induces signali

137 o its platelet receptor, glycoprotein Ib-IX (GPIb-IX), via the protein kinase G (PKG) signaling pathw

138 hear sensing and provide a mechanism linking GPIb-IX to platelet clearance.

139 ownstream of the MK-specific mechanoreceptor GPIb to coordinate polarized transendothelial platelet b

140 Thus, Akt1 and Akt2 mediate GPIb-IX signaling via the cGMP-dependent signaling pathw

141 ng an important role for Lyn in VWF-mediated GPIb signaling but not in integrin outside-in signaling.

142 plays a novel role in selectively mediating GPIb-IX-dependent TXA2 synthesis and thrombosis and repr

143 or more components of the platelet membrane GPIb-V-IX complex.

144 immunofluorescence and confocal microscopy, GPIb alpha-positive cells within the dermal interstitium

145 mples are treated with inhibitors of myosin, GPIb-IX-V, integrin alpha(IIb)beta(3,) P2Y(12), or throm

146 VX exhibits dual specificity for both native GPIb alpha and GPVI.

147 with GPIX involve residues 15 through 32 of GPIb beta

148 t activation rather than enhanced binding of GPIb-V-IX to vWF.

149 ledge, mechanism in which the catch bonds of GPIb-IX-V/VWF can be supported by internal forces produc

150 ppears to be mediated by reduced cleavage of GPIb by tumor necrosis factor-alpha-converting enzyme an

151 lycoprotein Ib (GPIb) complex is composed of GPIb alpha covalently attached to GPIb beta and noncoval

152 terminus is critical for the conformation of GPIb beta that interacts with GPIX and further suggests

153 Therefore, a contribution of GPIb alpha to CVX-induced platelet responses needs to be

154 Deficiency of GPIb or GPIX results in Bernard-Soulier syndrome (BSS),

155 e to the endothelium, and that deficiency of GPIb-alpha greatly abrogated the recruitment of platelet

156 Dephosphorylation of GPIb-IX with potato acid phosphatase inhibited anti-pS60

157 describe the expression and distribution of GPIb alpha in normal adult and neonatal human skin.

158 e present study explored the distribution of GPIb on external and internal membranes of resting plate

159 ta associates with the cytoplasmic domain of GPIb subunits Ibalpha and Ibbeta in transformed yeast ce

160 ntre of a molecular checkpoint downstream of GPIb that controls transendothelial platelet biogenesis.

161 directed against the vWf binding epitope of GPIb alpha and against the GPIb binding epitope of plasm

162 ent with romiplostim decreased expression of GPIb-IX-V complex and GPVI, but not of GPIIbIIIa, and bl

163 mbrane skeleton-associated and free forms of GPIb-IX.

164 cocalicin and the amino-terminal fragment of GPIb alpha reduced the release of fibrinopeptide A from

165 Compound 1 did not affect the function of GPIb, alpha2beta1, or the other beta3 family receptor al

166 e, activation of the VWF binding function of GPIb-IX induced by GPIbbeta dephosphorylation is diminis

167 We show here that the receptor function of GPIb-IX is regulated intracellularly via its link to the

168 sm that controls the VWF binding function of GPIb-IX, and also suggest a new type of antiplatelet age

169 e antibodies reacted with GPV independent of GPIb alpha, GPIb beta, or GPIX.

170 To characterize the interaction of GPIb beta and GPIX, we developed an anti-GPIb beta monoc

171 The precise sites of interaction of GPIb beta with GPIX are not known.

172 ther suggests that a critical interaction of GPIb beta with GPIX involve residues 15 through 32 of GP

173 e used to define the sites of interaction of GPIb beta with GPIX.

174 trate that signals induced by interaction of GPIb-IX with von Willebrand factor lead to alpha(IIb)bet

175 Replacing the N-terminal disulfide loops of GPIb beta (amino acids 1-14) with the corresponding disu

176 embly of actin, and, reportedly, movement of GPIb.

177 ype and filamin binding-deficient mutants of GPIb-IX is comparable, suggesting that the membrane skel

178 lts suggest that the cysteine knot region of GPIb beta in the N terminus is critical for the conforma

179 hose epitope was in the N-terminal region of GPIb beta.

180 our findings suggest that the separation of GPIb- and alpha2beta1 integrin-blocking members within t

181 sensitive domain in the GPIbalpha subunit of GPIb-IX was identified.

182 domain (MSD) within the GPIbalpha subunit of GPIb-IX.

183 However, when the N terminus of GPIb beta was replaced to residue 32 with the N terminus

184 To verify the topology of GPIb-FLNa interaction we also purified the native comple

185 N-terminal truncations of GPIb beta were expressed in mammalian cells.

186 N-terminal truncations of GPIb beta, missing the first 14, 26, or 31 amino acids,

187 Because MSD refolding may turn off GPIb-IX's mechanosensory signals, our results provide a

188 pulling of the A1 domain of VWF (VWF-A1) on GPIb-IX captured by its cytoplasmic domain induced unfol

189 P elevation, and their inhibitory effects on GPIb-IX-dependent platelet adhesion were reversed by exo

190 Furthermore, the binding site on GPIb alpha for CVX may be close to that for von Willebra

191 Thrombin bound to one GPIb alpha molecule, via ABE-II on its posterior surface

192 -3-3zeta element may be required for optimal GPIb interaction.

193 educed in half by antibodies against CD36 or GPIb, but not by antibodies against GPIIb/IIIa, von Will

194 bodies against glycoprotein (GP) IIb-IIIa or GPIb-IX and occasionally against GPIa-IIa or GPV.

195 active antibodies specific for GPIIb/IIIa or GPIb/IX were identified in each case.

196 Platelet GPIb and activated GPIIb/IIIa expression without added a

197 ding to immobilized GPIbalpha-N and platelet GPIb nearly as much as aptamer HD22 and heparin, both ex

198 that autoantibodies against either platelet GPIb or platelet GPIIb/IIIa in ITP plasma not only are i

199 Ib alpha but more strongly to human platelet GPIb alpha, as evidenced by comparative binding to wild-

200 Second, CVX binds weakly to murine platelet GPIb alpha but more strongly to human platelet GPIb alph

201 eta or GPIX result in an absence of platelet GPIb alpha.

202 ukocytes but was independent of the platelet GPIb and P-selectin receptors.

203 ough transcript also containing the platelet GPIb beta coding region.

204 lboaggregins act as agonists of the platelet GPIb complex.

205 , the ligand-binding subunit of the platelet GPIb-IX complex and a marker for platelet senescence and

206 unctionally dominant subunit of the platelet GPIb-IX-V receptor complex, with the von Willebrand fact

207 The platelet GPIb-V-IX complex is the receptor for the initial bindin

208 Blocking the pvWF-GPIb interaction with a monoclonal antibody to GPIb prev

209 connects the Von Willebrand factor receptor GPIb-IX-V to the underlying cytoskeleton in platelets.

210 IIbbeta3, the von Willebrand factor receptor GPIb-IX-V, the tyrosine kinase Syk, and the signaling pa

211 beta1 and the von Willebrand factor receptor GPIb.

212 nor platelet glycoprotein Ib-alpha receptor (GPIb-alpha) is required for RBCs to adhere to the endoth

213 is a subunit of the von Willebrand receptor, GPIb-V-IX, which mediates adhesion of platelets to the s

214 he concerted interplay of several receptors: GPIb in synergy with alpha(2)beta(1) mediating primary a

215 Transient expression of recombinant GPIb alpha deltaAT in 293T cells also generated a solubl

216 orylation at Ser(609) of GPIbalpha regulates GPIb-IX interaction with 14-3-3 and may play important r

217 Similarly, GPIb alpha caused in thrombin an allosteric reduction in

218 These data demonstrate that GPIb alpha binds to thrombin exosite II and in so doing

219 Recent data have demonstrated that GPIb alpha is not restricted to platelets, but is also e

220 Recent studies indicate that GPIb/V/IX may be functionally coupled with the Fc recept

221 binding to alpha(IIb)beta(3) indicating that GPIb-IX mediates a cellular signal leading to alpha(IIb)

222 We show that GPIb-IX-induced platelet aggregation and stable adhesion

223 Here we show that GPIb-IX-mediated activation of integrin alpha(IIb)beta(3

224 ative complex from platelets and showed that GPIb interacts with the C-terminus of FLNa, which is in

225 The GPIb-binding site within vWF has been localized to the v

226 inding epitope of GPIb alpha and against the GPIb binding epitope of plasma vWf, respectively.

227 of this enzyme, and we confirmed this as the GPIb alpha-binding site on thrombin by using thrombin mu

228 Because the GPIb-IX-V complex plays a part in regulating hemostasis

229 n and increases its binding affinity for the GPIb complex.

230 It remains unclear how the GPIb-IX-V complex is assembled and whether there is a ro

231 Akt1 and Akt2 are both required only in the GPIb-IX-mediated integrin activation (inside-out signali

232 e used several approaches to investigate the GPIb alpha-thrombin interaction in more detail and to st

233 The cytoplasmic domains of the GPIb alpha and beta subunits contain binding sites for t

234 ta support the notion that engagement of the GPIb complex, in addition to sending activation signals,

235 residues that might form all or part of the GPIb interaction site.

236 suggest that these residues form part of the GPIb interaction site.

237 operties are the predominant features of the GPIb(alpha)-vWF-A1 tether bond that in part may explain

238 ellular calcium; and (iv) independent of the GPIb-IX and GPIIb-IIIa complexes.

239 Mutagenesis of the GPIb-IX complex, which contains GPIbalpha, GPIbbeta, and

240 we identify the platelet GPIX subunit of the GPIb-IX-V complex as an obligate and novel client of gp9

241 nt study, we report that the assembly of the GPIb-IX-V complex depends critically on a molecular chap

242 alpha is an integral membrane protein of the GPIb-IX-V complex found on the platelet surface that int

243 Here, we evaluated the role of the GPIb-IX-V complex in the transmission of cytoskeletal fo

244 Loss of the GPIb-IX-V complex is pathogenic for Bernard-soulier Synd

245 GPIb alpha, a glycoprotein component of the GPIb-IX-V complex, serves as a platelet membrane recepto

246 ith increased platelet surface levels of the GPIb-IX-V receptor complex.

247 Glycoprotein (GP) V is a component of the GPIb-V-IX complex, the platelet receptor for vWF.

248 The inhibition of the GPIb-VWF axis in guinea pigs prevents cerebral artery th

249 bbeta3, but this ABO effect is likely on the GPIb-VWF interaction, which is regulated by fluid shear

250 bodies against platelet GPIIbIIIa and/or the GPIb complex.

251 We now report that the GPIb(alpha)-vWF-A1 tether bond displays similar kinetic

252 Thus, the GPIb-IX-V/VWF bond is able to transmit force, and uses t

253 SZ-2) that disrupts factor XI binding to the GPIb-IX-V complex also disrupted factor XI-raft associat

254 To identify the mechanism by which the GPIb:filamin ratio regulates platelet size, we manipulat

255 Therefore, GPIb modification might permit cold platelet storage.

256 letal forces were transmitted to VWF through GPIb-IX-V, an unexpected finding given the widely held n

257 Thus, GPIb-IX-dependent platelet adhesion is doubly controlled

258 An antibody to GPIb (SZ-2) that disrupts factor XI binding to the GPIb-

259 Ib interaction with a monoclonal antibody to GPIb prevented the agglutination of human and baboon pla

260 omposed of GPIb alpha covalently attached to GPIb beta and noncovalently complexed with GPIX and GPV.

261 Fourth, CVX binding to GPIb alpha is disrupted by phenylalanine substitutions a

262 Fifth, CVX binding to GPIb alpha on Chinese hamster ovary cell transfectants i

263 lebrand factor and alpha-thrombin binding to GPIb alpha.

264 I of thrombin) inhibited thrombin binding to GPIb alpha.

265 in-induced and botrocetin-induced binding to GPIb both were decreased by mutations at Lys(599), Arg(6

266 (642), whereas botrocetin-induced binding to GPIb was decreased selectively by mutations at Arg(636)

267 Ristocetin-induced binding to GPIb was reduced selectively by substitutions at positio

268 LISA may be useful in testing VWF binding to GPIb, discrimination of type 2 variants, and in the diag

269 rand factor (VWF) that blocks VWF binding to GPIb, of the thrombolytic agent recombinant tissue plasm

270 ctivation pathway in which ligand binding to GPIb-IX activates PKG that stimulates MAPK pathway, lead

271 vWF binding to GPIb-IX also activates soluble fibrinogen binding to alp

272 Ser(166) negatively regulates VWF binding to GPIb-IX and is one of the mechanisms by which PKA mediat

273 a (residues 202-231) required for binding to GPIb-IX complex and to the cytoplasmic domain of GPIbalp

274 Furthermore, vWF binding to GPIb-IX induces phosphorylation of Thr-202/Tyr-204 of ex

275 Thus, 14-3-3 binding to GPIb-IX is important in GPIb-IX signaling.

276 Thus, vWF binding to GPIb-IX is negatively regulated by the filamin-associate

277 phorylation and also enhanced VWF binding to GPIb-IX.

278 ffects of prostaglandin E1 on vWF binding to GPIb-IX.

279 alpha is important for 14-3-3zeta binding to GPIb-IX.

280 We conclude that factor XI is localized to GPIb in membrane rafts and that this association is impo

281 2 activity and MK hyperpolarization triggers GPIb-dependent transmigration of entire MKs into BM sinu

282 Treatment of CHO cells expressing wild type GPIb-IX with a PKA inhibitor, PKI, reduced Ser(166) phos

283 VWF-binding function compared with wild type GPIb-IX.

284 actin also enhances vWF binding to wild type GPIb-IX.

285 ch region, which is a loop in the unliganded GPIb alpha but switches to a beta-hairpin in the complex

286 Glycoprotein Ib-IX-V (GPIb-IX-V) mediates platelet tethering to von Willebrand

287 o alterations in von Willebrand factor (VWF)-GPIb adhesive function or platelet activation, but inste

288 Hence, inhibiting VWF-GPIb interactions is an effective way to prevent and tre

289 demonstrate an important role for Lyn in VWF/GPIb-IX-induced integrin activation mediated via the cGM

290 attributed to a selective inhibition in VWF/GPIb-IX-induced phosphorylation of cytosolic phospholipa

291 suggest that the signaling pathways by which GPIb-IX induces alpha(IIb)beta(3) activation are differe

292 of a novel variant BSS in a patient in which GPIb alpha was absent from the platelet surface but pres

293 unoprecipitated primarily alphaIIbbeta3 with GPIb and IAP.

294 esting that Lys(599) interacts directly with GPIb.

295 occurs through the interaction of GPIX with GPIb beta.

296 in had little effect on its interaction with GPIb alpha.

297 the K(d) values for their interactions with GPIb alpha were similar to those of wild-type thrombin.

298 interactions of these thrombin mutants with GPIb alpha by 10- and 25-fold, respectively.

299 pendent antibody reacted preferentially with GPIb/IX/V.

300 tion occurred even in cells transfected with GPIb-IX lacking the domain on GPIbalpha that binds 14-3-