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1                                              GPIb-IX activates not only the transfected alpha(IIb)bet
2                                              GPIb-IX also induces intracellular signals, stimulating
3                                              GPIb-IX signaling requires SFK (Src family kinase) Lyn.
4                                              GPIb-IX-induced ERK2 phosphorylation is inhibited by PKG
5                                              GPIb-IX-V is a catch bond for it becomes more stable as
6 n and because no dissociation of the ABP-280/GPIb-IX complexes is detected after thrombin activation.
7 ological role of GPIbbeta phosphorylation, a GPIb-IX mutant replacing Ser(166) of GPIbbeta with alani
8 nphosphorylated identical peptide, abolished GPIb-IX binding to 14-3-3zeta.
9 us pulling force of >15 pN to fully activate GPIb-IX.
10    Mechanical unfolding of the MSD activates GPIb-IX signaling into platelets, leading to their activ
11 so showed reduced actin polymerization after GPIb-IX-mediated platelet aggregation, actin polymerizat
12 r botrocetin)-induced vWF binding and allows GPIb-IX-expressing cells to adhere to immobilized vWF un
13  coexpressing integrin alpha(IIb)beta(3) and GPIb-IX adhere and spread on vWF, which is inhibited by
14 rmed for platelet GPla (integrin alpha2) and GPIb-IX-V, but there is support for the 807 T/C polymorp
15 cluding P-selectin, activated GPIIb,IIIa and GPIb-IX), whole-blood platelet aggregation, platelet cou
16 esting that the membrane skeleton-associated GPIb-IX is in a state that prevents access to the A1 dom
17 ires a minimum of two steps, one associating GPIb-IX to the activated cytoskeleton and the second req
18       In this study, the interaction between GPIb-IX and recombinant 14-3-3zeta is reconstituted.
19 than promoted activation of alphaIIbbeta3 by GPIb-IX-V and blocked aggregate formation on collagen at
20 thways in the activation of alphaIIbbeta3 by GPIb-IX-V.
21 rotein Ib-IX-V complex (GPIb-IX), but not by GPIb-IX-independent platelet agonists.
22 atelets show an enhanced reaction to certain GPIb-IX-independent agonists.
23 telet von Willebrand factor receptor complex GPIb-IX-V).
24 d the von Willebrand factor receptor complex GPIb-IX-V, which are essential for thrombus growth and s
25  receptor, the glycoprotein Ib-IX-V complex (GPIb-IX), but not by GPIb-IX-independent platelet agonis
26   The platelet glycoprotein Ib-IX-V complex (GPIb-IX-IV) is the receptor for VWF and is responsible f
27  Akt1 and Akt2 play important roles in early GPIb-IX signaling independent of Syk, adenosine diphosph
28                             Cells expressing GPIb-IX adhere to vWF in the presence of botrocetin but
29 ts of Chinese hamster ovary cells expressing GPIb-IX complexes containing wild-type or mutant GPIbalp
30 h is critical for not only the extracellular GPIb-IX ligand-induced intracellular signaling but also
31 ld type 14-3-3zeta has a higher affinity for GPIb-IX complex than recombinant GPIbalpha cytoplasmic d
32  dimerization and decreases its affinity for GPIb-IX.
33  therefore necessary, but not sufficient for GPIb-IX centralization.
34 omain before the dissociation of VWF-A1 from GPIb-IX.
35 nst cell-specific glycoproteins (GPIIb-IIIa, GPIb-IX and others) accelerate platelet destruction.
36 /y) platelets exhibited a marked decrease in GPIb-IX-V function and agonist-mediated integrin alphaII
37 me, a bleeding disorder caused by defects in GPIb-IX-V.
38 tification of the mechanosensitive domain in GPIb-IX has significant implications for the pathogenesi
39  unfolding of the mechanosensitive domain in GPIb-IX, which may possibly contribute to platelet mecha
40  mutant complexes confirmed its existence in GPIb-IX and enabled localization of this quasi-stable me
41 s, 14-3-3 binding to GPIb-IX is important in GPIb-IX signaling.
42  model, and show that 14-3-3 is important in GPIb-IX signaling.
43 rotein kinase (MAPK) pathway is important in GPIb-IX-dependent activation of platelet integrin alpha(
44 indicate that Lyn is critically important in GPIb-IX-mediated activation of the cGMP pathway.
45 sphoinositol 3-kinase (PI3K) is important in GPIb-IX-mediated signaling.
46        The defect of LIMK1(-/-) platelets in GPIb-IX-mediated platelet activation is attributed to a
47  vitro leads to the concomitant reduction in GPIb-IX complex expression due to ER-associated degradat
48 n outside-in signaling distinct from that in GPIb-IX-mediated inside-out signaling.
49 These results indicate that thrombin-induced GPIb-IX centralization requires a minimum of two steps,
50 (SFKs) play an important role in VWF-induced GPIb-IX signaling.
51 ermeant calcium chelator Quin-2 AM inhibited GPIb-IX centralization by 70%, but did not prevent its a
52 e 14-3-3-binding site in GPIbalpha inhibited GPIb-IX-mediated fibrinogen binding to alpha(IIb)beta(3)
53                         Anti-pS609 inhibited GPIb-IX binding to the intracellular signaling molecule,
54 n to the activated cytoskeleton and inhibits GPIb-IX centralization by 50%, without affecting actin a
55 or vWF interaction with different integrins, GPIb-IX-mediated activation of alpha(IIb)beta(3) require
56 to the platelet membrane glycoprotein Ib-IX (GPIb-IX) results in platelet activation.
57 s receptor, the platelet glycoprotein Ib-IX (GPIb-IX), and p38 inhibitors diminish platelet aggregati
58 Willebrand factor (vWF), glycoprotein Ib-IX (GPIb-IX), mediates initial platelet adhesion and activat
59 d factor (vWF) receptor, glycoprotein Ib-IX (GPIb-IX), mediates platelet adhesion and induces signali
60 o its platelet receptor, glycoprotein Ib-IX (GPIb-IX), via the protein kinase G (PKG) signaling pathw
61 hear sensing and provide a mechanism linking GPIb-IX to platelet clearance.
62 zed and tested for its interference with Lyn-GPIb-IX co-immunoprecipitation, platelet adhesion, risto
63                  Thus, Akt1 and Akt2 mediate GPIb-IX signaling via the cGMP-dependent signaling pathw
64                                 Lyn-mediated GPIb-IX signaling is critical for platelet adhesion and
65 However, it remains unclear how Lyn mediates GPIb-IX signaling, whether Lyn directly binds to GPIb-IX
66  plays a novel role in selectively mediating GPIb-IX-dependent TXA2 synthesis and thrombosis and repr
67 mples are treated with inhibitors of myosin, GPIb-IX-V, integrin alpha(IIb)beta(3,) P2Y(12), or throm
68              The cytoskeletal association of GPIb-IX involves ABP-280, as it correlates with the inco
69 fecting actin assembly or the association of GPIb-IX to the cytoskeleton.
70 ledge, mechanism in which the catch bonds of GPIb-IX-V/VWF can be supported by internal forces produc
71                Because the centralization of GPIb-IX is inhibited by cytochalasin, it is believed to
72                         Dephosphorylation of GPIb-IX with potato acid phosphatase inhibited anti-pS60
73 ent with romiplostim decreased expression of GPIb-IX-V complex and GPVI, but not of GPIIbIIIa, and bl
74 mbrane skeleton-associated and free forms of GPIb-IX.
75 e, activation of the VWF binding function of GPIb-IX induced by GPIbbeta dephosphorylation is diminis
76   We show here that the receptor function of GPIb-IX is regulated intracellularly via its link to the
77 sm that controls the VWF binding function of GPIb-IX, and also suggest a new type of antiplatelet age
78                However, the incorporation of GPIb-IX into the cytoskeleton is complete within 1 minut
79 trate that signals induced by interaction of GPIb-IX with von Willebrand factor lead to alpha(IIb)bet
80  have further characterized the mechanism of GPIb-IX centralization in platelets in suspension.
81                              The movement of GPIb-IX to the cytoskeleton of activated platelets is th
82 ype and filamin binding-deficient mutants of GPIb-IX is comparable, suggesting that the membrane skel
83 sensitive domain in the GPIbalpha subunit of GPIb-IX was identified.
84 domain (MSD) within the GPIbalpha subunit of GPIb-IX.
85           Because MSD refolding may turn off GPIb-IX's mechanosensory signals, our results provide a
86  pulling of the A1 domain of VWF (VWF-A1) on GPIb-IX captured by its cytoplasmic domain induced unfol
87 P elevation, and their inhibitory effects on GPIb-IX-dependent platelet adhesion were reversed by exo
88 bodies against glycoprotein (GP) IIb-IIIa or GPIb-IX and occasionally against GPIa-IIa or GPV.
89 , the ligand-binding subunit of the platelet GPIb-IX complex and a marker for platelet senescence and
90 unctionally dominant subunit of the platelet GPIb-IX-V receptor complex, with the von Willebrand fact
91 mannin, high enough to inhibit MLCK, prevent GPIb-IX centralization.
92  connects the Von Willebrand factor receptor GPIb-IX-V to the underlying cytoskeleton in platelets.
93 IIbbeta3, the von Willebrand factor receptor GPIb-IX-V, the tyrosine kinase Syk, and the signaling pa
94 orylation at Ser(609) of GPIbalpha regulates GPIb-IX interaction with 14-3-3 and may play important r
95              Following thrombin stimulation, GPIb-IX shifts from the membrane skeleton of the resting
96    The involvement of myosin II implies that GPIb-IX/ABP-280 complexes, linked to actin filaments, ar
97 binding to alpha(IIb)beta(3) indicating that GPIb-IX mediates a cellular signal leading to alpha(IIb)
98                                 We show that GPIb-IX-induced platelet aggregation and stable adhesion
99                            Here we show that GPIb-IX-mediated activation of integrin alpha(IIb)beta(3
100                                  Because the GPIb-IX-V complex plays a part in regulating hemostasis
101                   It remains unclear how the GPIb-IX-V complex is assembled and whether there is a ro
102  Akt1 and Akt2 are both required only in the GPIb-IX-mediated integrin activation (inside-out signali
103 ellular calcium; and (iv) independent of the GPIb-IX and GPIIb-IIIa complexes.
104                           Mutagenesis of the GPIb-IX complex, which contains GPIbalpha, GPIbbeta, and
105  a decrease in the surface expression of the GPIb-IX complex, which is redistributed from the platele
106 we identify the platelet GPIX subunit of the GPIb-IX-V complex as an obligate and novel client of gp9
107 nt study, we report that the assembly of the GPIb-IX-V complex depends critically on a molecular chap
108 alpha is an integral membrane protein of the GPIb-IX-V complex found on the platelet surface that int
109           Here, we evaluated the role of the GPIb-IX-V complex in the transmission of cytoskeletal fo
110                                  Loss of the GPIb-IX-V complex is pathogenic for Bernard-soulier Synd
111  GPIb alpha, a glycoprotein component of the GPIb-IX-V complex, serves as a platelet membrane recepto
112 ith increased platelet surface levels of the GPIb-IX-V receptor complex.
113                    In resting platelets, the GPIb-IX complex, the receptor for the von Willebrand fac
114 brand factor) and its platelet receptor, the GPIb-IX (glycoprotein Ib-IX) complex.
115                                    Thus, the GPIb-IX-V/VWF bond is able to transmit force, and uses t
116 SZ-2) that disrupts factor XI binding to the GPIb-IX-V complex also disrupted factor XI-raft associat
117 mes activated and captures platelets via the GPIb-IX complex.
118 letal forces were transmitted to VWF through GPIb-IX-V, an unexpected finding given the widely held n
119                                        Thus, GPIb-IX-dependent platelet adhesion is doubly controlled
120 ctivation pathway in which ligand binding to GPIb-IX activates PKG that stimulates MAPK pathway, lead
121                               vWF binding to GPIb-IX also activates soluble fibrinogen binding to alp
122 Ser(166) negatively regulates VWF binding to GPIb-IX and is one of the mechanisms by which PKA mediat
123 a (residues 202-231) required for binding to GPIb-IX complex and to the cytoplasmic domain of GPIbalp
124                  Furthermore, vWF binding to GPIb-IX induces phosphorylation of Thr-202/Tyr-204 of ex
125                      Thus, 14-3-3 binding to GPIb-IX is important in GPIb-IX signaling.
126                         Thus, vWF binding to GPIb-IX is negatively regulated by the filamin-associate
127 phorylation and also enhanced VWF binding to GPIb-IX.
128 ffects of prostaglandin E1 on vWF binding to GPIb-IX.
129 alpha is important for 14-3-3zeta binding to GPIb-IX.
130 -IX signaling, whether Lyn directly binds to GPIb-IX, and if it is possible to target this signaling
131 a interaction has the potential for treating GPIb-IX-dependent thrombosis.
132 he 14-3-3zeta binds to recombinant wild type GPIb-IX but not to the GPIb-alpha mutants lacking C-term
133  Treatment of CHO cells expressing wild type GPIb-IX with a PKA inhibitor, PKI, reduced Ser(166) phos
134 VWF-binding function compared with wild type GPIb-IX.
135 actin also enhances vWF binding to wild type GPIb-IX.
136                        Glycoprotein Ib-IX-V (GPIb-IX-V) mediates platelet tethering to von Willebrand
137 lso transmits outbound signals enhancing VWF-GPIb-IX interaction.
138 demonstrate an important role for Lyn in VWF/GPIb-IX-induced integrin activation mediated via the cGM
139  attributed to a selective inhibition in VWF/GPIb-IX-induced phosphorylation of cytosolic phospholipa
140 ct binding of Lyn to GPIbbeta mediates 2-way GPIb-IX signaling to activate platelets and modulate VWF
141 keleton is complete within 1 minute, whereas GPIb-IX centralization requires 5 to 10 minutes for comp
142 suggest that the signaling pathways by which GPIb-IX induces alpha(IIb)beta(3) activation are differe
143 a patient with Bernard-Soulier syndrome with GPIb-IX-V deficiency, and platelets from mice deficient
144 tion occurred even in cells transfected with GPIb-IX lacking the domain on GPIbalpha that binds 14-3-

 
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