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1 MAP kinase activation requires generation of thromboxane A2.
2  to various prostaglandins, prostacyclin and thromboxane A2.
3 ictor response required the participation of thromboxane A2.
4 e with the metabolism of arachidonic acid to thromboxane A2.
5 abolism of microparticle arachidonic acid to thromboxane A2.
6 nase (COX) product of arachidonic acid, into thromboxane A2.
7 sphatidic acid, sphingosine-1-phosphate, and thromboxane A2.
8  soluble agonists such as thrombin, ADP, and thromboxane A2.
9 zes the isomerization of prostaglandin H2 to thromboxane A2.
10          Although the proaggregatory role of thromboxane A2, a product of the aspirin-inhibitable cyc
11 us, the autocrine and paracrine functions of thromboxane A2 act downstream of LTC4/type 2 cysLT recep
12                                              Thromboxane A2 acts via G protein-coupled receptors; two
13 inhaled NO did not reverse the effect of the thromboxane A2 agonist U-46619.
14 found that AngaD7L1 binds leukotriene C4 and thromboxane A2 analog U-46619; AngaD7L2 weakly binds leu
15 thrombin, platelet-activating factor, or the thromboxane A2 analog U46619.
16 agonists, including ADP, epinephrine and the thromboxane A2 analog, U46619, did not.
17 uced by the continuous infusion of U46619, a thromboxane A2 analog.
18 ion of the IP3-generating agonists U46619 (a thromboxane A2 analogue) and ADP.
19 induced in 8 pigs by intravenous infusion of thromboxane A2 analogue.
20 h plasma (PRP) and caused their secretion of thromboxane A2 and CXCL4.
21 s by disturbing the balance between platelet thromboxane A2 and endothelial prostacyclin.
22 logically and pathophysiologically important thromboxane A2 and endothelin-1 receptors.
23 ude that in a clinical setting in which both thromboxane A2 and iPF2alpha-III are elevated, suppressi
24 lating factor (GM-CSF), and the eiconsanoids thromboxane A2 and leukotriene B4 (LTB4).
25 ts and endothelial cells and thereby reduces thromboxane A2 and prostacyclin.
26                        The platelet products thromboxane A2 and serotonin have been shown to cause co
27 ate that this pathway requires production of thromboxane A2 and signaling through both hematopoietic
28 s for thrombin, lysophosphatidic acid (LPA), thromboxane A2, and endothelin can activate SRF in the a
29                Therefore, the thrombin, LPA, thromboxane A2, and endothelin receptors may be able to
30 E2, prostaglandin F2alpha, prostaglandin I2, thromboxane A2, and prostaglandin D2.
31 te accumulation by Gq-coupled M3-muscarinic, thromboxane-A2, and 5-HT2 receptors was desensitized in
32 edback agonists adenosine 5'-diphosphate and thromboxane A2 are mandatory for platelet aggregation.
33                       PAF, leukotrienes, and thromboxane A2 are necessary for pulmonary hypertension
34 ot release of the secondary agonists ADP and thromboxane A2, are required for full aggregation induce
35                         Prostaglandin E2 and thromboxane A2, as well as total APP levels, were found
36 bond cleavage is not a rate-limiting step in thromboxane A2 biosynthesis.
37 hed eicosanoid synthesis in platelets (e.g., thromboxane A2, control 20.5 +/- 1.4 ng/ml vs. patient 0
38                           We use carbocyclic thromboxane A2 (CTA2) to convert the TXAS heme cofactor
39 Andoh et al. demonstrate that the prostanoid thromboxane A2 elicits scratching through its TP recepto
40 -PLC and the formation of prostaglandins and thromboxane A2 from arachidonic acid through COX through
41 ate platelet aggregation, ATP secretion, and thromboxane A2 generation by low doses of collagen (<1 m
42  integrin signaling, platelet secretion, and thromboxane A2 generation.
43 n platelets, with functional implications in thromboxane A2 generation.
44 f PKCdelta dramatically blocked PAR-mediated thromboxane A2 generation.
45 with U-46619, a stable mimetic of endogenous thromboxane A2 implicated in the etiology of cerebral va
46 ction, elevated oxidant stress and increased thromboxane A2 improve perfusion-based outcomes.
47  possible to measure a urinary metabolite of thromboxane A2 in 2 of the patients as an indicator of i
48 ion of arachidonic acid for the synthesis of thromboxane A2 in human platelets.
49 H2 and the conversion of prostaglandin H2 to thromboxane A2 in intact platelets.
50 exes, suggesting a possible role of platelet thromboxane A2 in microvascular occlusion.
51 e absence of Grb2 can be compensated through thromboxane A2-induced G protein-coupled receptor signal
52  with exogenous cyclic nucleotides inhibited thromboxane A2-induced MYPT1 membrane association, RhoA
53 ker indicating that secondary stimulation by thromboxane A2 induces cytosolic PLA2 phosphorylation, b
54 ory vascular reactions but is independent of thromboxane A2 levels, changes in blood pressure, or lip
55 d in part by the balance of prostacyclin and thromboxane A2, many other substances are involved in th
56 telet adhesion to collagen and generation of thromboxane A2 may further enhance expression of activat
57 serum thromboxane B2, a stable metabolite of thromboxane A2, may be implicated in post-PCI microvascu
58 andin E2, 6-keto-prostaglandin F1 alpha, and thromboxane A2 measurements were collected.
59 etion, and aggregation, but not with ADP and thromboxane A2-mediated pathways.
60 e thrombin generation plus aspirin to reduce thromboxane A2-mediated platelet activation is superior
61 ementation was associated with lower urinary thromboxane A2 metabolites at age 1 year (beta, -0.46; 9
62                                      Urinary thromboxane A2 metabolites, in contrast, were significan
63  platelet-rich plasma (PRP) treated with the thromboxane A2 mimetic U46619, collagen and thrombin in
64                                    U46619, a thromboxane A2 mimetic, but not ADP, caused activation o
65  (200 days), maximal vasoconstriction to the thromboxane A2 mimetic, U46619 (P < 0.05) and sensitivit
66 c concentrations of serotonin and the stable thromboxane A2 mimetic, U46619, injected through an IC c
67 evidence: (i) inhibition of MaxiK current by thromboxane A2 mimetic, U46619, occurs even when G-prote
68 uced by the continuous infusion of U46619, a thromboxane A2 mimetic.
69 ring elevated tone conditions induced by the thromboxane A2 mimic, U46619 (Upjohn, Kalamazoo, MI).
70 ing increased tone conditions induced by the thromboxane A2 mimic, U46619, in the pulmonary vascular
71 lar metabolism before the resulting products thromboxane A2 or LTC4 can activate their cognate recept
72             Platelet activation by thrombin, thromboxane A2, or ADP stimulates the association of 14-
73 g to RGS18 even in the presence of thrombin, thromboxane A2, or ADP.
74 ot undergo irreversible aggregation, produce thromboxane A2, or secrete adenosine diphosphate in resp
75 -based activation motif pathway, and ADP and thromboxane A2 pathways.
76 se of arachidonic acid and its conversion to thromboxane A2 play a central role in vWF-mediated [Ca2+
77                                  vWF induced thromboxane A2 production in the platelet.
78 eatment reduced interleukin-1beta-stimulated thromboxane A2 production in the pulmonary epithelial ce
79 ergic constriction combined with an elevated thromboxane A2 production may contribute to impaired fun
80                                Assessment of thromboxane A2 production showed a strong temperature de
81                               Interestingly, thromboxane A2 production was markedly increased in resp
82 lets resulting in shape change, aggregation, thromboxane A2 production, and release of granule conten
83 are more susceptible to an increase in RVSP, thromboxane A2 production, and vascular remodeling than
84 ial decrease in prostacyclin production over thromboxane A2 production, thus leading to less gastric
85 latelets, with elevated cPLA2 activation and thromboxane A2 production.
86 cteremic shock and b) selectively block PAF, thromboxane A2, prostacyclin, and leukotrienes to determ
87 vasoconstriction by way of activation of the thromboxane-A2 /prostaglandin-endoperoxide (TP) receptor
88 nce of four major prostanoids: prostacyclin, thromboxane A2, prostaglandin D2, and 12-hydroxyheptadec
89 he concentrations of leukotrienes B4 and B5, thromboxane A2, prostaglandin E2, and 6-keto-prostagland
90 ty did not significantly alter beta 2-AR and thromboxane A2/prostaglandin H2 (TP) receptor affinity.
91  beta-adrenergic (S > > R) and antagonism at thromboxane A2/prostaglandin H2 (TP; R > > S) receptors.
92                           However, neither a thromboxane A2/prostaglandin H2 receptor antagonist SQ29
93                      Furthermore, SQ29548, a thromboxane A2/prostaglandin H2 receptor antagonist, sig
94 -)- and ONOO(-)-dependent PGIS nitration and thromboxane A2/prostaglandin H2 receptor stimulation.
95 evels can be increased through activation of thromboxane A2-prostanoid (TP) receptors on neurons.
96 rostaglandin F2alpha receptor (FP) (61), and thromboxane A2 receptor (TP) (11) while sparing EP2, EP3
97 rs include the PGF2 alpha receptor (FP), the thromboxane A2 receptor (TP) and the prostacyclin recept
98 structural flexibility of the purified human thromboxane A2 receptor (TP) was characterized by spectr
99                                        Human thromboxane A2 receptor (TP), a G protein-coupled recept
100 ted to elucidate the molecular mechanisms of thromboxane A2 receptor (TP)-induced insulin resistance
101 oupled receptors; two splice variants of the thromboxane A2 receptor (TPalpha and TPbeta) have been c
102 racterization of the signaling properties of thromboxane A2 receptor (TPalpha) -Galpha12 and -Galpha1
103 n interacting partner of the beta-isoform of thromboxane A2 receptor (TPbeta) by yeast two-hybrid scr
104                                              Thromboxane A2 receptor (TPr) stimulation induces cellul
105 d created by oxidative stress, activates the thromboxane A2 receptor (TXAR) and the Rho-associated ki
106 ation of human platelets by thrombin and the thromboxane A2 receptor agonist U46619 lead to phosphory
107 e to inhibit vasoconstriction induced by the thromboxane A2 receptor agonist U46619, which suggest a
108                              Aspirin and the thromboxane A2 receptor antagonist SQ29548 inhibited act
109                  After pretreatment with the thromboxane A2 receptor antagonist SQ30, 741, the vasoco
110 was immunoreactive against a polyclonal anti-thromboxane A2 receptor antibody.
111 f cyclooxygenase inhibition with aspirin and thromboxane A2 receptor blockade with ifetroban on the c
112 lts demonstrate the presence of a functional thromboxane A2 receptor in oligodendrocytes and are cons
113                           The human platelet thromboxane A2 receptor is a member of the G-protein-cou
114                   We explore here, using the thromboxane A2 receptor TPalpha, the ability of G12 and
115 he same position as the second intron of the thromboxane A2 receptor, prostaglandin D2 receptor, pros
116              Here, we show that vasopressive thromboxane A2 receptors (TP) can intimately couple with
117 in E2 (EP)1, EP4, prostaglandin F2alpha, and thromboxane A2 receptors but not anti-inflammatory EP2,
118 us observations indicating a high density of thromboxane A2 receptors in myelinated brain and spinal
119                   The presence of functional thromboxane A2 receptors in neonatal rat oligodendrocyte
120 receptors increases Galphaq association with thromboxane A2 receptors thereby shifting them to a high
121 synergism, e.g., human platelet thrombin and thromboxane A2 receptors.
122 d with a net increase in Galphaq coupling to thromboxane A2 receptors.
123 ors caused an increase in ligand affinity of thromboxane A2 receptors.
124 5 kDa) indistinguishable from human platelet thromboxane A2 receptors.
125 (S)-HETE, in addition to prostanoids such as thromboxane A2 Releasates from activated platelets cause
126                       LPA1 receptor-mediated thromboxane A2 release is responsible for lysophosphatid
127                                        Thus, thromboxane A2 signaling within the intact cerebral vasc
128 roids directly reduce hyperreactive 5-HT and thromboxane A2-stimulated Ca2+ and PKC responses of coro
129 GS in these cell lines blocked thrombin- and thromboxane A2-stimulated cell invasion.
130 ), prostacyclin synthase (PTGIS, 5.66-fold), thromboxane A2 synthase (TBXAS, 98-fold) increased signi
131 ed the hypothesis that cyclooxygenase (COX), thromboxane A2 synthase (TxA2-S), thromboxane prostanoid
132                                        Human thromboxane A2 synthase (TXAS) exhibits spectral charact
133                                              Thromboxane A2 synthase (TXAS) has been proposed to have
134 nd PGD2 synthase, and also between COX-1 and thromboxane A2 synthase.
135 g that inhibits phosphodiesterase as well as thromboxane A2 synthase.
136 e data demonstrate the beneficial effects of thromboxane A2 synthesis inhibition in the setting of is
137  particularly in inhibiting the synthesis of thromboxane A2, the prostaglandin that causes platelet a
138  quantified by ELISA, and PGF2alpha (FP) and thromboxane A2 (TP) receptor expression determined by We
139 coupled receptors [EP1, EP3, PGF2alpha (FP), thromboxane A2 (TP)] suggests that prostaglandin recepto
140                                              Thromboxane A2 (TxA(2)) may mediate decreases of renal b
141 X-2) and the vasoconstrictor prostaglandins, thromboxane A2 (TXA2 ) and prostaglandin F2alpha (PGF2al
142 ion of vasoconstrictive prostanoids, such as thromboxane A2 (TXA2 ), contributes to endothelial dysfu
143                                     In lung, thromboxane A2 (TXA2) activates the TP receptor to induc
144 ation depends on secondary mediators such as thromboxane A2 (TxA2) and ADP, which are agonists for G-
145 de-out signaling because granular secretion, Thromboxane A2 (TxA2) generation, as well as fibrinogen
146                                              Thromboxane A2 (TXA2) is a labile metabolite of arachido
147                                              Thromboxane A2 (TXA2) is a potent inducer of vasoconstri
148                                              Thromboxane A2 (TxA2) is a potent vasoconstrictor and pl
149                           Here, we show that thromboxane A2 (TXA2) is one of several eicosanoid produ
150 yze either an isomerization reaction to form thromboxane A2 (TXA2) or a fragmentation reaction to for
151 py, and dependent on inhibition of the COX-1/thromboxane A2 (TXA2) pathway.
152                                              Thromboxane A2 (TXA2) potently stimulates platelet aggre
153 iated outside-in signaling, granule release, thromboxane A2 (TxA2) production, and aggregation.
154 olic phospholipase A2 (cPLA2) and consequent thromboxane A2 (TXA2) production.
155                   S18886 is an orally active thromboxane A2 (TXA2) receptor (TP) antagonist in clinic
156                          Two subtypes of the thromboxane A2 (TxA2) receptor (TxA2R-E and TxA2R-P), wh
157 nduced via Gq-coupled agonist receptors, the thromboxane A2 (TXA2) receptor, and protease-activated r
158 phy can be used to purify the human platelet thromboxane A2 (TXA2) receptor-Galphaq complex.
159                                              Thromboxane A2 (TxA2) receptors belong to the class of G
160                           VPC31143 increased thromboxane A2 (TXA2) release from TA of wild-type, TP-K
161         VWF-induced Erk2 phosphorylation and thromboxane A2 (TXA2) release were completely blocked by
162                            ADP, thrombin, or thromboxane A2 (TxA2) signaling through their respective
163 olipase C (PLC) inhibitor] or furegrelate [a thromboxane A2 (TXA2) synthesis inhibitor] 5 min prior t
164 pathway is unclear but is thought to involve thromboxane A2 (TXA2) synthesis.
165                                              Thromboxane A2 (TXA2) was the prostanoid product of COX-
166 on of prostaglandin endoperoxide (PGH2) into thromboxane A2 (TxA2) which plays a crucial role in hemo
167 pha-granules and dense granules and generate thromboxane A2 (TXA2), but platelets adhering to acid so
168  antibodies and complement released PGE2 and thromboxane A2 (TXA2), in addition to increased amounts
169 dent of Syk, adenosine diphosphate (ADP), or thromboxane A2 (TXA2), in addition to their recognized r
170 acids in desensitization of the receptor for thromboxane A2 (TxA2), we created a mutant TxA2 receptor
171  platelets release both serotonin (5-HT) and thromboxane A2 (TXA2), we examined whether 5-HT and TXA2
172  adenosine triphosphate (ATP) secretion in a thromboxane A2 (TxA2)- and Ca2+-dependent manner.
173 alphaIIbbeta3 and elicits ATP secretion in a thromboxane A2 (TxA2)-dependent manner.
174                                              Thromboxane A2 (TXA2)-mediated platelet secretion and ag
175 me processing arachidonic acid to synthesize thromboxane A2 (TxA2).
176 on for several important agonists, including thromboxane A2 (TXA2).
177 eneration of the vasoconstricting prostanoid thromboxane A2 (TXA2).
178 s that produce distinct eicosanoids, such as thromboxane A2 (TXA2).
179  (prostacyclin [PGI2]) and vasoconstricting (thromboxane A2 [TxA2]) eicosanoids may be important in p
180  intracoronary (IC) injections of serotonin, thromboxane A2 (U46619), endothelin 1 or angiotensin II
181 DP must be generating an agonist, other than thromboxane A2, via an aspirin-sensitive pathway, which
182 PGF2alpha and a purported antagonist (pinane thromboxane A2), was silent.
183 lin, prostaglandin E2, prostaglandin D2, and thromboxane A2 were also reduced.
184 ereas concentrations of prostaglandin E2 and thromboxane A2 were similar in the aspirin-treated group

 
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