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1 nd thrombosis, in part, by supporting stable platelet adhesion.
2 ing events are crucial for the initiation of platelet adhesion.
3 e the ability to significantly reduce static platelet adhesion.
4 elet aggregation and beta1 integrin-mediated platelet adhesion.
5 a receptor other than GPIbalpha can mediate platelet adhesion.
6 lted in the loss of alpha(IIb)beta3-mediated platelet adhesion.
7 hat could serve as a driving force for tight platelet adhesion.
8 nt ligand resulted in a greater stability in platelet adhesion.
9 role of circulating VWF in the initiation of platelet adhesion.
10 VWF multimers that, as a result, can mediate platelet adhesion.
11 < .05 vs wild-type), but not in the initial platelet adhesion.
12 the manifestation of functional activity in platelet adhesion.
13 bind to von Willebrand factor, resulting in platelet adhesion.
14 -coated substrates to examine flow-dependent platelet adhesion.
15 lusters, even in the absence of any platelet-platelet adhesion.
16 von Willebrand factor multimers could reduce platelet adhesion.
17 s show normal bleeding times despite reduced platelet adhesion.
18 ne cytoskeleton and for the stabilization of platelet adhesion.
19 f LIMK1(-/-) platelets in VWF-induced stable platelet adhesion.
20 as observed using fluorescence imaging, and platelet adhesion (81.7 +/- 2.5%) in vitro over a 2 h pe
21 uced protein absorption (64.7% decrease) and platelet adhesion (85.6% decrease) compared to bare PCL
22 ng cleavage by ADAMTS13, may promote initial platelet adhesion above glomerular endothelial cells.
23 transmitted cellular forces are critical for platelet adhesion, activation, aggregation and contracti
28 involved in several key steps of thrombosis: platelet adhesion/activation, thrombus growth, and stabi
33 nteracts with CLEC-2 on platelets, mediating platelet adhesion, aggregation, and secretion to guide t
34 cidating the molecular mechanisms leading to platelet adhesion, aggregation, shape change, and secret
35 lation in a dose-dependent manner as well as platelet adhesion, although total plaque area was reduce
36 nin-211 (alpha2beta1gamma1), allow efficient platelet adhesion and activation across a wide range of
38 nti-GP VI antibody completely inhibited both platelet adhesion and activation of the GP IIb-IIIa comp
40 eatment with MMP inhibitors partly prevented platelet adhesion and activation, as well as vWF express
41 coating prevents fibrin attachment, reduces platelet adhesion and activation, suppresses biofilm for
47 roles of alpha2beta1 and GPVI in supporting platelet adhesion and aggregate formation on collagen at
48 m the basis of a unifying two-state model of platelet adhesion and aggregate formation on collagen th
49 ation of nitric oxide synthase (NOS), limits platelet adhesion and aggregation after a prothrombotic
50 is a plasma metalloproteinase that regulates platelet adhesion and aggregation by cleaving ultra-larg
52 lular matrices (ECMs) that are essential for platelet adhesion and aggregation during hemo stasis and
61 ves von Willebrand factor multimers, reduces platelet adhesion and aggregation, and downregulates thr
62 BSA coating of thrombogenic surfaces reduces platelet adhesion and aggregation, possibly by increasin
74 (Fn1(syn/syn)) suffer from surprisingly mild platelet adhesion and bleeding defects due to delayed th
75 binding site for alpha(IIb)beta3 involved in platelet adhesion and clot retraction and define the new
76 eptides duplicating these segments inhibited platelet adhesion and clot retraction but not platelet a
78 we show that the physical interplay between platelet adhesion and hemodynamics in a microchannel man
79 nd factor (VWF) to GP Ib-IX mediates initial platelet adhesion and increases the subsequent adhesive
80 ptor, glycoprotein Ib-IX (GPIb-IX), mediates platelet adhesion and induces signaling leading to integ
81 ycoprotein Ibalpha (GPIbalpha) promotes both platelet adhesion and inflammatory actions of platelets
84 c binding site for alphaIIbbeta3 involved in platelet adhesion and platelet-mediated fibrin clot retr
86 decipher mechanisms of A1-GPIbalpha-mediated platelet adhesion and resolve dynamic secondary structur
88 nd shear microfluidic assays, Slit2 impaired platelet adhesion and spreading on diverse extracellular
93 n (nominal values) tensions generated during platelet adhesion and tensions above 54 piconewton gener
94 d by their ability to support flow-dependent platelet adhesion and their ability to inhibit ristoceti
95 endothelial collagen acts as a substrate for platelet adhesion and thrombus formation after vascular
97 that vWF plays a critical role in mediating platelet adhesion and thrombus formation following mesen
98 ne deficiency significantly accelerates both platelet adhesion and thrombus formation in mice followi
100 wed that nanofibrous scaffolds alone induced platelet adhesion and thrombus formation, which was supp
103 ), glycoprotein (GP) Ib-IX, mediates initial platelet adhesion and transmits signals leading to plate
105 kindlin-3 was introduced into HEL cells and platelets; adhesion and spreading of both cell types wer
106 ltimers adhere to endothelial cells, support platelet adhesion, and may induce microvascular thrombos
107 Free Hb (>/=50 mg/dL) effectively augmented platelet adhesion, and microthrombi formation on fibrin(
109 vities, including factor XIIIa crosslinking, platelet adhesion, and platelet-mediated clot retraction
110 PS was enriched dramatically and decreased platelet adhesion as well as secretion from delta-, alph
111 ks VWFpp binding to VWF-D'D3, also abrogated platelet adhesion, as shown by shear-induced platelet ag
112 recombinant VWFpp in both flow-chamber-based platelet adhesion assays and viscometer-based shear-indu
114 e in hemostasis and thrombosis by initiating platelet adhesion at sites of arterial injury through in
116 (VWF) is a multimeric protein that mediates platelet adhesion at sites of vascular injury, and ADAMT
120 coprotein Ib-IX-V complex, not only mediates platelet adhesion but also transmits signals leading to
121 nce of endothelial cells in stenoses reduces platelet adhesion but increases sickle cell disease (SCD
122 -111 (alpha1beta1gamma1) is known to support platelet adhesion but is absent from most blood vessels,
123 tirofiban (anti-GPIIb/IIIa) did not prevent platelet adhesion but nearly eliminated the deposition o
124 deficiency of pFN did not affect the initial platelet adhesion, but a delay of several minutes in thr
125 is a multidomain metalloprotease that limits platelet adhesion by a feedback mechanism in which fluid
126 gands may promote the feedback inhibition of platelet adhesion by stimulating the cleavage of domain
127 tween the thrombin and collagen receptors in platelet adhesion by utilizing a collagen-related peptid
129 tigate the effect of a drug known to inhibit platelet adhesion (clopidogrel) and, in the presence of
130 cant reductions in I/R-induced leukocyte and platelet adhesion compared with wild-type mice exposed t
131 M: 146.2 +/- 20.4 min, p < 0.05) and reduced platelet adhesion, complement activation, coagulation ac
132 brinogen binding to alpha(IIb)beta(3) during platelet adhesion decreased integrin-associated PP2A act
133 balpha) and genetically engineered mice with platelet adhesion defects, we investigated the role of p
134 daptor absent in patients with leukocyte and platelet adhesion deficiency syndrome and is critical fo
135 y of von Willebrand factor (VWF) to initiate platelet adhesion depends on the number of monomers in i
136 F in plasma of patients with ALI/ALF support platelet adhesion, despite a relative loss of function o
137 ogrel) and, in the presence of the drug, the platelet adhesion due to activation by 5.00 microM ADP d
138 in long string-like structures that initiate platelet adhesion during hemostasis and thrombosis.
139 intracellular binding partners, anchors the platelet adhesion glycoprotein (GP) Ib-IX-V receptor to
140 t glycoprotein Ibalpha that supports initial platelet adhesion in absence of von Willebrand factor (V
142 iolar vasodilation and venular leukocyte and platelet adhesion in mice after injection with either mo
144 -induced thrombosis model, we report similar platelet adhesion in Tsp1(-/-)/Vwf(-/-) mice compared wi
145 A NPs have also proven capable of inhibiting platelet adhesion in vitro with a reduced IC50 of 1.83 +
147 in a ristocetin cofactor ELISA and increased platelet adhesion in whole blood to collagen under arter
148 ha(IIb)beta(3) by immobilized ligands during platelet adhesion induces a transmembrane conformation c
151 cal importance of rapid bond dissociation in platelet adhesion is demonstrated by kinetic characteriz
153 cally in a number of settings such as during platelet adhesion, leukocyte trans-migration, and angiog
154 of von Willebrand disease, whereas too much platelet adhesion may cause thrombotic thrombocytopenic
155 Ibalpha, thrombin could potentially act as a platelet adhesion molecule or receptor dimerisation trig
157 f platelets with blocking antibodies against platelet adhesion molecules did not alter their effect o
158 focused solely on recapitulating aspects of platelet adhesion; more complex platelet behaviours such
159 pite the presence of arterial shear, delayed platelet adhesion occurred and stable thrombi formed.
162 on by NO of alphaIIb/beta3 integrin-mediated platelet adhesion on immobilized fibrinogen, mediated in
166 or glycoprotein VI and strongly affects firm platelet adhesion on von Willebrand factor (VWF) under a
168 ew NO-release coating exhibit no significant platelet adhesion or thrombus formation, but control sen
171 shared with those elicited by the inhibitory platelet adhesion receptor PECAM-1 (platelet endothelial
172 an polymorphism in the Kozak sequence of the platelet adhesion receptor, glycoprotein (GP) Ibalpha, a
174 ty due to molecular abnormalities in a major platelet adhesion receptor, integrin alphaIIbbeta3.
176 dhesion defects, we investigated the role of platelet adhesion receptors in stabilizing tumor vessels
178 in genetically engineered mice lacking major platelet adhesion receptors or their activators (alphaII
179 into thrombi is mediated by interactions of platelet adhesion receptors with ligands on the injured
180 ntibody M3/38) or collagen receptor-mediated platelet adhesion (revacept, a dimeric platelet collagen
182 sduce those cues into differential levels of platelet adhesion, spreading, and activation provides bi
183 tivity mediate substrate stiffness-dependent platelet adhesion, spreading, and activation to differen
185 shear stress conditions effectively blocked platelet adhesion, suggesting that the initial interacti
188 to lowering lipids, statins favorably affect platelet adhesion, thrombosis, endothelial function, inf
189 injury, von Willebrand factor (VWF) mediates platelet adhesion through binding to platelet glycoprote
191 ing high-affinity GPIbalpha binding and firm platelet adhesion to a partially disordered A1 domain.
192 mechanism for the regulation of rheological platelet adhesion to A1 based on cooperative flexibility
195 al microscopy revealed a >3-fold increase in platelet adhesion to angiogenic vessels of Matrigel comp
196 alpha may alter the mechanical regulation of platelet adhesion to cause hemostatic defects as found i
197 activation of the GP IIb-IIIa complex after platelet adhesion to collagen and generation of thrombox
198 m-Fab-F inhibits both GPVI-dependent static platelet adhesion to collagen and thrombus formation on
199 tivation were confirmed in vitro by studying platelet adhesion to collagen in flow conditions, integr
200 ficient beta1 integrin show strongly reduced platelet adhesion to collagen in vitro and in a carotis
202 egrin alpha2beta1 play significant roles for platelet adhesion to collagen under flow and that the lo
203 nder static conditions and completely blocks platelet adhesion to collagen under flow conditions at h
204 genetic approaches to study human and mouse platelet adhesion to collagen under flow conditions.
209 2 beta 1 integrin is a critical mediator of platelet adhesion to collagen within the vessel wall aft
214 ha) to von Willebrand factor (VWF) initiates platelet adhesion to disrupted vascular surface under ar
216 , we found that ADAMTS13 down-regulates both platelet adhesion to exposed subendothelium and thrombus
217 The von Willebrand factor (vWF) mediates platelet adhesion to exposed subendothelium at sites of
220 we studied the effect of hemoglobin (Hb) on platelet adhesion to fibrin(ogen) under conditions of di
222 demonstrate this technique by measurement of platelet adhesion to fibrinogen as a means to quantify t
227 trated that alphaIIb beta3 integrin mediates platelet adhesion to fibrinogen, whereas both alphav bet
230 , Y731 and Y774 undergo phosphorylation upon platelet adhesion to immobilized fibrinogen, which was i
231 e-rich repeat (LRR) protein family, mediates platelet adhesion to immobilized von Willebrand factor (
233 ) with von Willebrand factor (VWF) initiates platelet adhesion to injured vascular wall to stop bleed
234 Ibalpha and von Willebrand factor initiates platelet adhesion to injured vessel walls, and the adhes
235 e blood von Willebrand factor (VWF) mediates platelet adhesion to injured vessels by sequestering pla
237 the avidity of thrombin- and ADP-stimulated platelet adhesion to intact or thrombin-cleaved human os
239 intravascular inflammatory events, including platelet adhesion to neutrophils, an important event in
240 mediated adhesion, L-selectin expression, or platelet adhesion to neutrophils, suggesting that cytosk
242 and elicited anti-pig antibodies, recipient platelet adhesion to pig hematopietic progenitor cells,
243 Src family and Syk tyrosine kinases promotes platelet adhesion to primary mouse lymphatic endothelial
244 e glycoprotein (GP) Ib-IX-V complex mediates platelet adhesion to reactive substrates under high shea
249 nt of the GP Ib-IX-V complex, which mediates platelet adhesion to subendothelium at sites of injury.
250 e show that in ferric chloride-injured veins platelet adhesion to subendothelium is decreased and thr
251 1 EMI domain (GST-EMI) competitively reduced platelet adhesion to surface-coated PEAR1, diminished pl
253 gs support the hypothesis that inhibition of platelet adhesion to the brain microvasculature protects
254 oprotein ligand 1 axis, followed by (2) firm platelet adhesion to the endothelium via interaction of
255 e (NO) production, a recognized inhibitor of platelet adhesion to the endothelium, increased the numb
257 optimization studies, and studies involving platelet adhesion to the immobilized endothelium, were p
259 Cs to participate in thrombosis by mediating platelet adhesion to the intact endothelial surface.
260 were implicated in recognition of P3, since platelet adhesion to the peptide was blocked by function
262 s interaction may play a significant role in platelet adhesion to the site of endothelial injury.
263 monstrating the role of P2Y(12) in mediating platelet adhesion to thrombogenic surfaces (collagen, vo
266 complex plays a critical role in initiating platelet adhesion to von Willebrand factor (vWF) at the
267 ural integrity to the plasma membrane during platelet adhesion to von Willebrand factor (VWF) under h
268 bocytopenia, shedding of GPIbalpha, impaired platelet adhesion to von Willebrand factor, and inabilit
269 mutation, Gly233Val, promotes and stabilizes platelet adhesion to VWF at shear rates that do not supp
273 kout platelets were also defective in stable platelet adhesion to VWF under shear stress that is inde
278 ucidate the mechanism of thrombus growth and platelet adhesion under conditions of arterial shear rat
282 latelet activation as well as CXCL16-induced platelet adhesion under high arterial shear stress in vi
286 In both cases, we find that the rate of platelet adhesion varies greatly with the RBC hematocrit
288 or PI3KC2alpha in regulating shear-dependent platelet adhesion via regulation of membrane structure,
290 cificity of Cyr61- and Fisp12/mCTGF-mediated platelet adhesion was demonstrated by specific inhibitio
291 nhibition and 5.00 microM ADP, the affect on platelet adhesion was further increased to 127 +/- 5.2.
293 I [CalDAG-GEFI]), thus indicating that firm platelet adhesion was not necessary for their supporting
297 sclerosis reduces endothelial activation and platelet adhesion, which are likely responsible for the
298 o the surface of biomaterial correlates with platelet adhesion, which is mediated by von Willebrand f
299 e of Weibel-Palade bodies, induced immediate platelet adhesion (within 15 seconds) and translocation
300 endorepellin supported alpha2beta1-dependent platelet adhesion, without appreciably activating or agg
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