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1 ting that TFPI is not stored within platelet alpha granules.
2 ng FV is found in plasma and within platelet alpha granules.
3 nhibited secretion of dense granules but not alpha granules.
4 , a basic protein found normally in platelet alpha granules.
5 (TS1), the most abundant protein of platelet alpha granules.
6 cytoplasmic membranes and reduced numbers of alpha granules.
7 the trans-Golgi network, late endosomes and alpha-granules.
8 s characterized by large platelets that lack alpha-granules.
9 ion requires release of stored proteins from alpha-granules.
10 odies packed with respiring mitochondria and alpha-granules.
11 n platelets and megakaryocytes and stored in alpha-granules.
12 re demonstrated, as was its association with alpha-granules.
13 delivered both in the plasma and in platelet alpha-granules.
14 rs and inhibitors into separate and distinct alpha-granules.
15 along with CD62P, into both MK and platelet alpha-granules.
16 VIII can be expressed and stored in platelet alpha-granules.
17 is accompanied by uptake of fibrinogen into alpha-granules.
18 secretion of plasma fibrinogen from platelet alpha-granules.
19 inogen) and then package these proteins into alpha-granules.
20 bitor, a trace protein contained in platelet alpha-granules.
21 been immunized with purified human platelet alpha-granules.
22 in a rapidly releasable form within platelet alpha-granules.
23 leads to degradation of most proteins of the alpha-granules.
24 diathesis and a marked reduction in platelet alpha-granules.
25 cytoplasm and Dock7 on the membrane of or in alpha-granules.
26 acrothrombocytopenia, with platelets lacking alpha-granules.
27 in that traffics FVIII more effectively into alpha-granules.
28 PS), a rare recessive platelet disorder with alpha-granule abnormalities and mutations in NBEAL2.
29 t a marked defect in exocytosis of delta and alpha granules, alphaIIbbeta3 activation, actin assembly
30 dense granule secretion; and (3) diminished alpha granule and lysosome secretion might contribute to
31 n microscopy, we confirmed that CD154 was an alpha granule and not a cell surface protein, and therea
32 P-1 helps to sequester TGF-beta1 in platelet alpha granules and activates TGF-beta1 once both protein
33 hibited platelet secretion of both dense and alpha granules and the secretion-dependent platelet aggr
34 caused increased platelet CD62P expression, alpha-granule and dense granule release, and the classic
35 tion, integrin alphaIIbbeta3 activation, and alpha-granule and dense granule secretion in response to
36 oprotein IIb or in embryos in which platelet alpha-granule and dense granule secretion is abolished.
38 hat mimic NSF sequence motifs inhibited both alpha-granule and dense-granule secretion in permeabiliz
39 ine signal to potentiate platelet release of alpha-granule and lysosome cargo and protein disulfide i
41 von Willebrand factor (VWF) is stored within alpha-granules and accounts for approximately 20% of tot
43 es can enable the storage of FIX in platelet alpha-granules and corrects the murine hemophilia B phen
44 a patient with gray platelet syndrome lacked alpha-granules and demonstrated only minimal spreading.
45 llagen were able to secrete contents of both alpha-granules and dense granules and generate thromboxa
46 to establish how cargos are segregated among alpha-granules and determine whether or not different al
47 n; (2) significant decreases of secretion of alpha-granules and GPIIb-IIIa activation induced by aden
48 ranules was completely ablated and that from alpha-granules and lysosomes was severely compromised.
49 2alpha inactivation have critical defects in alpha-granules and membrane structure that are associate
51 in high concentrations of TGF-beta1 in their alpha-granules and release it on platelet adhesion/activ
53 oagulation factor V (FV) from the media into alpha-granules and releases functional FV(+)CD42b(+) hum
54 FIX can be expressed and stored in platelet alpha-granules and that platelet-derived FIX can correct
55 rombocytopenia, and a deficiency of platelet alpha-granules and their cargo, including von Willebrand
56 developing megakaryocytes would be stored in alpha-granules and whether its release from circulating
59 gray platelet syndrome platelets, which lack alpha-granules, and Wiskott-Aldrich syndrome platelets,
63 uring spreading, supporting the premise that alpha-granules are heterogeneous and demonstrating that
64 arrow megakaryocytes, which store FBG in the alpha-granules, are thought not to express the FBG genes
65 S stimulates platelet secretion of dense and alpha granules as indicated by ATP release and P-selecti
66 eptolysin O-permeabilized platelets released alpha-granules, as measured by surface expression of P-s
67 e defect, demonstrating a role for VPS16B in alpha-granule biogenesis and taking us one step closer t
68 characteristics of human GPS, with defective alpha-granule biogenesis in MKs and their absence from p
77 1 indicate that TLT-1 is not simply cargo of alpha-granules but may instead regulate granule construc
78 telet factor 4 (PF4) is an abundant platelet alpha-granule C-X-C chemokine that has weak chemotactic
81 w that platelets can orient their release of alpha-granule cargo to promote spreading beyond the dot'
82 in and collagen increased exosome content of alpha-granule chemokines CXCL4 and CXCL7 and cytoplasmic
86 s on liver regeneration are unclear, because alpha-granules contain bioactive molecules with opposing
87 platelet alpha-granules, unusual stimulated alpha granule content release, abnormal lipid inclusions
88 ted that platelets selectively release their alpha-granule content dependent on the environmental sti
91 pha-granule exocytosis and deposition of the alpha-granule contents such as fibrinogen and fibronecti
93 ith syntaxin-4 and promoted the secretion of alpha-granule contents, including TGF-beta and CCL5.
94 sponsible for efficient release of dense and alpha-granule contents; thus, VAMP-8(-/-) mice are a use
96 ) platelets identified a marked reduction in alpha-granule count and the presence of small granule-li
98 platelets from patients with an inheritable alpha-granule defect, demonstrating a role for VPS16B in
101 irment in MVB maturation in MKs underlie the alpha-granule deficiency in Vps33b(fl/fl)-ER(T2) mouse a
102 for aggregation, and gray platelet syndrome alpha-granule-deficient platelets do not aggregate to 4
104 We previously showed that platelet (PLT) alpha granule-delivered urokinase plasminogen activator
105 oG(-/-) platelets was reduced secretion from alpha-granules, dense granules, and lysosomes following
107 n combination with the loss of proteins from alpha-granules drives the development of bone marrow fib
109 )](i), but it is specifically coupled to the alpha-granule exocytic pathway without concomitant effec
112 Time-lapse microscopy demonstrated that alpha-granules expressing VAMP-7 actively moved from the
114 may be caused by an abnormality in platelet alpha-granule factor V distinct from that described for
115 ith collagen and thrombin express functional alpha-granule factor V only on a subpopulation of cells.
116 vesicle trafficking pathways responsible for alpha-granule formation are beginning to be assembled as
117 nction, and they also indicate that abnormal alpha-granule formation in Nbeal2(-/-) mice has deleteri
119 s of dense granules, lysosomal granules, and alpha-granules from human platelets by S-nitrosylation o
120 pha-granule secretion that include homotypic alpha-granule fusion and the fusion of alpha-granules wi
121 -FV platelets may explain the unique role of alpha-granule FV and the hemostatic effectiveness of you
122 s express very high levels of surface-bound, alpha-granule FV on simultaneous activation with 2 agoni
123 regulates not only megakaryopoiesis but also alpha-granule generation and signaling pathways required
125 escribe cells with granules (which he called alpha-granules) having an affinity for eosin and other a
127 ltimate secretion; (2) impaired secretion of alpha granules in HPS, and to some degree of lysosomes,
133 duced platelet aggregation; and large, fused alpha-granules in 1% to 5% of circulating platelets.
134 and morphologically distinct populations of alpha-granules in megakaryocytes and platelets may provi
139 REM-like transcript-1, which is localized to alpha-granules in resting platelets, binds fibrinogen, a
144 odel of GPS and demonstrate that the lack of alpha-granules is due to their loss from platelets/matur
146 red PDI secretion and impaired exocytosis of alpha granules, lysosomes, and T granules due to decreas
147 rder characterized by deficiency of platelet alpha-granules, macrothrombocytopenia and marrow fibrosi
148 number, as well as maximal secretion of the alpha-granule marker P-selectin; however, their capacity
149 s), and with S12 antibody (to P-selectin, an alpha-granule membrane protein expressed on the platelet
152 , we investigated the pattern of circulating alpha-granule molecules during liver regeneration in 157
154 al platelet counts, platelet morphology, and alpha-granule number, as well as maximal secretion of th
155 Deficiency of COMMD3/CCDC22 causes reduced alpha-granule numbers and overall levels of alpha-granul
156 olipase A2 (sPLA2) is an enzyme found in the alpha granules of platelets and at inflammatory sites.
157 ke growth factor-1 (IGF-1) is present in the alpha granules of platelets and its receptor is expresse
159 id not affect the sorting of P-selectin into alpha-granules of platelets but severely compromised the
160 This indispensable cofactor is stored in alpha-granules of platelets via a poorly understood endo
161 FVIII in megakaryocytes, with storage in the alpha-granules of platelets, has the advantage of delive
162 e most abundant protein contained within the alpha-granules of platelets, is a broad-spectrum inhibit
163 In this study, we show that ATX is stored in alpha-granules of resting human platelets and released u
164 the effects of factors derived from platelet alpha-granules on liver regeneration are unclear, becaus
165 studies, whereas STX8 was not essential for alpha-granule or lysosome secretion, Stx8(-/-) platelets
166 T (dense core granules), platelet factor IV (alpha granules), or hexosaminidase (lysosomes) between n
168 V is highly concentrated within the platelet alpha-granule, previous analysis of human bone marrow an
169 he structure, function, and formation of the alpha-granule protein "coat." Confocal microscopy reveal
171 phosphatidylserine (PS) surface expression, alpha-granule protein retention, and lack of active inte
172 latelet factor 4 (PF4), an abundant platelet alpha-granule protein, accelerates in vitro generation o
176 are characterized by high surface levels of alpha-granule proteins and phosphatidylserine, which sup
177 adequate packaging and secretion of selected alpha-granule proteins and reduced secretion of dense gr
179 r-wise comparisons of 15 angiogenic-relevant alpha-granule proteins displayed little, if any, pattern
180 -1 is stabilized by its packaging with other alpha-granule proteins in a calcium-dependent manner.
182 ceptionally strong retention of procoagulant alpha-granule proteins on the surface of COAT platelets.
184 taining revealed 25-nm diameter complexes of alpha-granule proteins under the electron microscope.
185 approximately 65% to 75% was observed in the alpha-granule proteins von Willebrand factor and P-selec
188 alpha-granule numbers and overall levels of alpha-granule proteins, establishing the COMMD3/CCC comp
189 riety of monoclonal antibodies show that the alpha-granule proteins, fibrinogen, von Willebrand facto
190 high levels of phosphatidylserine and retain alpha-granule proteins, including fibrinogen, on their s
191 rred to as 'COAT-platelets', bind additional alpha-granule proteins, including fibrinogen, von Willeb
194 uent plasmin-mediated degradation of diverse alpha-granule proteins; and platelet-dependent, accelera
196 dy to syntaxin 4 also inhibited Ca2+-induced alpha-granule release by approximately 75% in this syste
198 lets showed enhanced integrin activation and alpha-granule release in response to stimulation of (hem
199 sembles with activation and demonstrate that alpha-granule release is dependent on vesicle SNAP recep
200 Patients with an unfavorable postoperative alpha-granule release profile (high TSP-1/low VEGF) show
202 isoform, the Pro(33) variant showed greater alpha-granule release, clot retraction, and adhesion to
208 en recent controversy as to whether platelet alpha-granules represent a single granule population or
209 acrothrombocytopenia and absence of platelet alpha-granules resulting in typical gray platelets on pe
212 rt a mechanism whereby the reported enhanced alpha granule secretion in the Pro(33)-positive platelet
213 surface expression of P-selectin (reflecting alpha granule secretion); (ii) exposure of the fibrinoge
214 global, because other activation responses, alpha granule secretion, shape change, and aggregation w
215 enosine 5'-diphosphate (ADP) restored normal alpha granule secretion, suggesting that the impairment
217 ly inhibits thrombin peptide (SFLLR)-induced alpha-granule secretion (IC(50) = 20 microM) during the
219 ma2, leading to downstream responses such as alpha-granule secretion and activation of integrin alpha
220 show that PtdIns(4,5)P(2) mediates platelet alpha-granule secretion and that PtdIns(4,5)P(2) synthes
221 8220 completely inhibited platelet dense and alpha-granule secretion at a concentration of 20 microM
222 GPVI and PAR-induced aggregation, dense and alpha-granule secretion at low agonist concentrations.
223 s of latrunculin A inhibited agonist-induced alpha-granule secretion but stimulated dense granule sec
229 osphate 4-kinase augmented SFLLRN-stimulated alpha-granule secretion from SL-O-permeabilized platelet
230 membrane protein and inhibited Ca2+-induced alpha-granule secretion from streptolysin O-permeabilize
231 Inhibition of actin polymerization prevented alpha-granule secretion in this system, and purified pla
232 ctin cytoskeleton by latrunculin A inhibited alpha-granule secretion induced by several different pla
233 5)P(2) synthesis required for Ca(2+)-induced alpha-granule secretion involves the type II phosphatidy
234 the possibility that morphologic features of alpha-granule secretion may be influenced by the subcell
237 vides a basis for several characteristics of alpha-granule secretion that include homotypic alpha-gra
239 Phorbol 12-myristate 13-acetate-stimulated alpha-granule secretion was inhibited by anti-type II Pt
242 leration and augmentation of agonist-induced alpha-granule secretion with comparatively modest effect
243 ed integrin alpha(IIb)beta(3) activation and alpha-granule secretion, (ii) synergistic enhancement of
244 tion of the matrix itself regulates platelet alpha-granule secretion, a key component of platelet act
245 asured by integrin alphaIIbbeta3 activation, alpha-granule secretion, and procoagulant activity.
246 sure of platelet factor XI is independent of alpha-granule secretion, because ADP and collagen expose
248 bserved that platelet DREAM is important for alpha-granule secretion, Ca(2+) mobilization, and aggreg
249 platelets fail to spread and have decreased alpha-granule secretion, integrin alphaIIbbeta3 activati
250 ulated through GPVI, resulting in defects in alpha-granule secretion, integrin alphaIIbbeta3 activati
251 ying platelet aggregation, dense granule and alpha-granule secretion, P-selectin expression, micropar
252 dIns 3-kinase did not inhibit Ca(2+)-induced alpha-granule secretion, suggesting that PtdIns 3-kinase
253 rmine whether these proteins are involved in alpha-granule secretion, we developed a streptolysin O-p
254 Exogenously added PtdIns(4,5)P(2) inhibited alpha-granule secretion, with 80% inhibition at 50 micro
269 te SEPT5 levels in the maintenance of normal alpha-granule size and may explain the variant granules
270 y bleeding symptoms, the absence of platelet alpha-granules, splenomegaly, and bone marrow (BM) fibro
274 Individuals whose platelets lack dense or alpha-granules suffer various degrees of abnormal bleedi
275 pecifically accumulated fibronectin in their alpha-granules, suggesting that fibronectin could be the
276 s more evenly distributed among membranes of alpha-granules, the open canalicular system, and plasma
277 openia with large platelets and a paucity of alpha-granules; these abnormalities cause mostly moderat
278 ation of HYAL2 from a distinct population of alpha-granules to platelet surfaces where it exerts its
280 zed platelet abnormalities (reduced platelet alpha-granules, unusual stimulated alpha granule content
283 wed similar ultra-structure characteristics (alpha granules, vacuoles and dense tubular system) as PL
285 y of PAI-1 in both platelets and in isolated alpha-granules was prolonged in comparison to the rapid
286 ibodies derived from a rabbit immunized with alpha-granules, was subcloned into the prokaryotic expre
289 count and P-selectin (a ubiquitous cargo of alpha-granules) were not associated with postoperative l
291 on microscopy revealed a complete absence of alpha-granules, whereas delta-granules were observed.
292 h isoforms are expressed in resting platelet alpha-granules, which are up-regulated to the cell surfa
294 ombospondin-1 (TSP-1) purified from platelet alpha-granules with an apparent K(D) of approximately 7.
295 duced by a GP Ibbeta(Null) genotype revealed alpha-granules with increased size as compared with the
296 ity of PAI-1 activity, whereas incubation of alpha-granules with the calcium ionophore A23187 reduced
297 typic alpha-granule fusion and the fusion of alpha-granules with the open canalicular system and plas
299 bleeding disorder characterized by a lack of alpha-granules within blood platelets and progressive bo
300 as associated with uptake of fibrinogen into alpha-granules without surface binding despite pretreatm