ライフサイエンスコーパス: thromboxane

1 stanes) and inflammation (prostaglandins and thromboxanes).

2 s of the bioactive lipids prostaglandins and thromboxane.

3 al macrophages and increased biosynthesis of thromboxane.

4 -iso-PGF2 was diminished and that for pinane thromboxane A nonexistent when Galpha12 was the reporter

5 Pinane thromboxane A(2) (PTA(2)) activates G(q) in preference t

6 mplicated by the feedback effects of ADP and thromboxane A(2) (TxA(2)) and by the overlap with the re

7 telet PGH synthase 1-derived (PGHS1-derived) thromboxane A(2) (TxA(2)) has been implicated in its pat

8 -dose aspirin incompletely inhibits platelet thromboxane A(2) (TXA(2)) in the majority of ET patients

9 Thromboxane A(2) (TxA(2)) is a prostanoid formed by thro

10 tive cardiac sympathetic afferents, and that thromboxane A(2) (TxA(2)) is one of the mediators releas

11 Thromboxane A(2) (TXA(2)) is released during I/R injury

12 This enhanced signaling was detected as thromboxane A(2) (TxA(2)) production and granule secreti

13 c acid from glycerophospholipids, leading to thromboxane A(2) (TxA(2)) production.

14 The human thromboxane A(2) (TXA(2)) receptor (TP) is known to medi

15 s showed significantly lower agonist-induced thromboxane A(2) (TXA(2)) release through reduced extrac

16 racellular signal-regulated kinase-dependent thromboxane A(2) (TxA(2)) release.

17 release of VEGF, but not endostatin whereas, thromboxane A(2) (TXA(2)) released endostatin but not VE

18 ) receptor (TP), two critical components for thromboxane A(2) (TXA(2)) signaling, have been suggested

19 entrations of thrombin receptor agonists and thromboxane A(2) (TXA(2)), but not collagen or VWF.

20 oxygenase product, prostanglandin H(2), into thromboxane A(2) (TXA(2)), which can cause vessel constr

21 ion, Rac1 activation, and release of ADP and thromboxane A(2) (TxA(2)).

22 cted, human endothelial cells (ECs) released thromboxane A(2) (TXA(2)).

23 looxygenase-2 and catalyzes the synthesis of thromboxane A(2) (TXA(2)).

24 As reported previously, TP activation by the thromboxane A(2) analog U46619 caused inhibition of Maxi

25 d cyclooxygenase-2 expression, and increased thromboxane A(2) and prostacyclin production.

26 Macrophage-COX-2, primarily a source of thromboxane A(2) and prostaglandin (PG)E(2), promotes at

27 n the setting of PGE(2) deficiency depend on thromboxane A(2) and signaling through the T prostanoid

28 understanding of the molecular mechanism of thromboxane A(2) binding to the important receptor and i

29 ough cyclooxygenase-2 (COX-2) pathways while thromboxane A(2) formed by platelets from AA via cycloox

30 uction of PGE(2), prostacyclin (PGI(2)), and thromboxane A(2) in human coronary artery endothelial ce

31 ntractions induced by angiotensin II and the thromboxane A(2) mimetic, U46619, and had no significant

32 her IBOP or U46619, two structurally related thromboxane A(2) mimetics, significantly reduced insulin

33 In summary, the data support a role for the thromboxane A(2) pathway in the pathogenesis of bladder

34 In contrast, histamine did not stimulate thromboxane A(2) production in resting or LPS-activated

35 AYPGKF-induced thromboxane A(2) production in wild-type and P2Y(12) def

36 reas a marked inhibition of thrombin-induced thromboxane A(2) production was observed, which was foun

37 ibited by activation of the vasoconstricting thromboxane A(2) prostanoid receptor (TP), a mechanism s

38 Thromboxane synthase (TXAS) and thromboxane A(2) receptor (TP), two critical components

39 ecretion induced by arachidonic acid and the thromboxane A(2) receptor (TxA(2)R) agonist U46619 were

40 G(q) and G(13) (of the G(12) family) by the thromboxane A(2) receptor alpha (TPalpha), via agonist-e

41 Blockade of thromboxane A(2) receptor did not affect the serotonin r

42 The reduced form of the thromboxane A(2) receptor experienced a decrease in liga

43 dimensional structural model for a GPCR, the thromboxane A(2) receptor.

44 on, localization, and functional coupling to thromboxane A(2) receptors (TPRs) during oligodendrocyte

45 Platelet phospholipase A(2) and thromboxane A(2) significantly decreased and vasodilator

46 erythrocytes blocked its ability to inhibit thromboxane A(2) synthesis and platelet aggregation.

47 Moreover, A23187-induced thromboxane A(2) synthesis, platelet aggregation, and se

48 ages with bacterial LPS increased PGI(2) and thromboxane A(2) to varied extents.

49 In contrast, production of thromboxane A(2) was significantly reduced, whereas prod

50 Neutrophil-produced thromboxane A(2) was the key eicosanoid controlling both

51 platelet aggregation induced by thrombin and thromboxane A(2) were also reversed by supplementing ADP

52 elet recruitment, platelet isoprostanes, and thromboxane A(2), and increased vasodilator-stimulated p

53 The antagonism of the thromboxane A(2), cyclooxygenase-1/cyclooxygenase-2, or

54 elet recruitment, platelet isoprostanes, and thromboxane A(2), platelet Nox2, Rac1, p47(phox), protei

55 platelets bind collagen and release ADP and thromboxane A(2), recruiting additional platelets to a g

56 To study the immunoregulatory actions of thromboxane A(2), we used mice with a targeted disruptio

57 ox2 and ultimately platelet isoprostanes and thromboxane A(2).

58 gregation induced by thrombin, collagen, and thromboxane A(2).

59 sence of exogenous adenosine diphosphate and thromboxane A(2).

60 the G(q)-coupled receptors for thrombin and thromboxane A(2).

61 We use carbocyclic thromboxane A2 (CTA2) to convert the TXAS heme cofactor

62 quantified by ELISA, and PGF2alpha (FP) and thromboxane A2 (TP) receptor expression determined by We

63 Thromboxane A2 (TxA(2)) may mediate decreases of renal b

64 X-2) and the vasoconstrictor prostaglandins, thromboxane A2 (TXA2 ) and prostaglandin F2alpha (PGF2al

65 ion of vasoconstrictive prostanoids, such as thromboxane A2 (TXA2 ), contributes to endothelial dysfu

66 ation depends on secondary mediators such as thromboxane A2 (TxA2) and ADP, which are agonists for G-

67 de-out signaling because granular secretion, Thromboxane A2 (TxA2) generation, as well as fibrinogen

68 olic phospholipase A2 (cPLA2) and consequent thromboxane A2 (TXA2) production.

69 S18886 is an orally active thromboxane A2 (TXA2) receptor (TP) antagonist in clinic

70 nduced via Gq-coupled agonist receptors, the thromboxane A2 (TXA2) receptor, and protease-activated r

71 VPC31143 increased thromboxane A2 (TXA2) release from TA of wild-type, TP-K

72 VWF-induced Erk2 phosphorylation and thromboxane A2 (TXA2) release were completely blocked by

73 olipase C (PLC) inhibitor] or furegrelate [a thromboxane A2 (TXA2) synthesis inhibitor] 5 min prior t

74 pathway is unclear but is thought to involve thromboxane A2 (TXA2) synthesis.

75 dent of Syk, adenosine diphosphate (ADP), or thromboxane A2 (TXA2), in addition to their recognized r

76 adenosine triphosphate (ATP) secretion in a thromboxane A2 (TxA2)- and Ca2+-dependent manner.

77 alphaIIbbeta3 and elicits ATP secretion in a thromboxane A2 (TxA2)-dependent manner.

78 s that produce distinct eicosanoids, such as thromboxane A2 (TXA2).

79 me processing arachidonic acid to synthesize thromboxane A2 (TxA2).

80 us, the autocrine and paracrine functions of thromboxane A2 act downstream of LTC4/type 2 cysLT recep

81 induced in 8 pigs by intravenous infusion of thromboxane A2 analogue.

82 h plasma (PRP) and caused their secretion of thromboxane A2 and CXCL4.

83 s by disturbing the balance between platelet thromboxane A2 and endothelial prostacyclin.

84 logically and pathophysiologically important thromboxane A2 and endothelin-1 receptors.

85 ude that in a clinical setting in which both thromboxane A2 and iPF2alpha-III are elevated, suppressi

86 ate that this pathway requires production of thromboxane A2 and signaling through both hematopoietic

87 edback agonists adenosine 5'-diphosphate and thromboxane A2 are mandatory for platelet aggregation.

88 Andoh et al. demonstrate that the prostanoid thromboxane A2 elicits scratching through its TP recepto

89 ate platelet aggregation, ATP secretion, and thromboxane A2 generation by low doses of collagen (<1 m

90 n platelets, with functional implications in thromboxane A2 generation.

91 f PKCdelta dramatically blocked PAR-mediated thromboxane A2 generation.

92 with U-46619, a stable mimetic of endogenous thromboxane A2 implicated in the etiology of cerebral va

93 ction, elevated oxidant stress and increased thromboxane A2 improve perfusion-based outcomes.

94 exes, suggesting a possible role of platelet thromboxane A2 in microvascular occlusion.

95 ory vascular reactions but is independent of thromboxane A2 levels, changes in blood pressure, or lip

96 Urinary thromboxane A2 metabolites, in contrast, were significan

97 platelet-rich plasma (PRP) treated with the thromboxane A2 mimetic U46619, collagen and thrombin in

98 evidence: (i) inhibition of MaxiK current by thromboxane A2 mimetic, U46619, occurs even when G-prote

99 lar metabolism before the resulting products thromboxane A2 or LTC4 can activate their cognate recept

100 -based activation motif pathway, and ADP and thromboxane A2 pathways.

101 eatment reduced interleukin-1beta-stimulated thromboxane A2 production in the pulmonary epithelial ce

102 ergic constriction combined with an elevated thromboxane A2 production may contribute to impaired fun

103 Interestingly, thromboxane A2 production was markedly increased in resp

104 are more susceptible to an increase in RVSP, thromboxane A2 production, and vascular remodeling than

105 ial decrease in prostacyclin production over thromboxane A2 production, thus leading to less gastric

106 rostaglandin F2alpha receptor (FP) (61), and thromboxane A2 receptor (TP) (11) while sparing EP2, EP3

107 structural flexibility of the purified human thromboxane A2 receptor (TP) was characterized by spectr

108 Human thromboxane A2 receptor (TP), a G protein-coupled recept

109 ted to elucidate the molecular mechanisms of thromboxane A2 receptor (TP)-induced insulin resistance

110 racterization of the signaling properties of thromboxane A2 receptor (TPalpha) -Galpha12 and -Galpha1

111 n interacting partner of the beta-isoform of thromboxane A2 receptor (TPbeta) by yeast two-hybrid scr

112 Thromboxane A2 receptor (TPr) stimulation induces cellul

113 d created by oxidative stress, activates the thromboxane A2 receptor (TXAR) and the Rho-associated ki

114 e to inhibit vasoconstriction induced by the thromboxane A2 receptor agonist U46619, which suggest a

115 We explore here, using the thromboxane A2 receptor TPalpha, the ability of G12 and

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 (S)-HETE, in addition to prostanoids such as thromboxane A2 Releasates from activated platelets cause

119 LPA1 receptor-mediated thromboxane A2 release is responsible for lysophosphatid

120 Thus, thromboxane A2 signaling within the intact cerebral vasc

121 ed the hypothesis that cyclooxygenase (COX), thromboxane A2 synthase (TxA2-S), thromboxane prostanoid

122 g that inhibits phosphodiesterase as well as thromboxane A2 synthase.

123 nd PGD2 synthase, and also between COX-1 and thromboxane A2 synthase.

124 lin, prostaglandin E2, prostaglandin D2, and thromboxane A2 were also reduced.

125 PGF2alpha and a purported antagonist (pinane thromboxane A2), was silent.

126 Prostaglandin E2 and thromboxane A2, as well as total APP levels, were found

127 hed eicosanoid synthesis in platelets (e.g., thromboxane A2, control 20.5 +/- 1.4 ng/ml vs. patient 0

128 d in part by the balance of prostacyclin and thromboxane A2, many other substances are involved in th

129 serum thromboxane B2, a stable metabolite of thromboxane A2, may be implicated in post-PCI microvascu

130 Platelet activation by thrombin, thromboxane A2, or ADP stimulates the association of 14-

131 g to RGS18 even in the presence of thrombin, thromboxane A2, or ADP.

132 e absence of Grb2 can be compensated through thromboxane A2-induced G protein-coupled receptor signal

133 with exogenous cyclic nucleotides inhibited thromboxane A2-induced MYPT1 membrane association, RhoA

134 etion, and aggregation, but not with ADP and thromboxane A2-mediated pathways.

135 evels can be increased through activation of thromboxane A2-prostanoid (TP) receptors on neurons.

136 GS in these cell lines blocked thrombin- and thromboxane A2-stimulated cell invasion.

137 sphatidic acid, sphingosine-1-phosphate, and thromboxane A2.

138 soluble agonists such as thrombin, ADP, and thromboxane A2.

139 Furthermore, SQ29548, a thromboxane A2/prostaglandin H2 receptor antagonist, sig

140 -)- and ONOO(-)-dependent PGIS nitration and thromboxane A2/prostaglandin H2 receptor stimulation.

141 vasoconstriction by way of activation of the thromboxane-A2 /prostaglandin-endoperoxide (TP) receptor

142 te accumulation by Gq-coupled M3-muscarinic, thromboxane-A2, and 5-HT2 receptors was desensitized in

143 uced vasoconstriction was dependent on a non-thromboxane agonist of the thromboxane receptor, whereas

144 tometry, without and with stimulation by the thromboxane analog U46619 or ADP.

145 han the predominantly Galpha(12/13)-mediated thromboxane analog U46619.

146 induced only by 5 muM ADP and 10 muM of the thromboxane analog, U46619.

147 rthermore, 5,6-EET could be metabolized to a thromboxane analog.

148 ated the constriction with serotonin and the thromboxane-analog U-46619 in arteries +E.

149 In awake, instrumented lambs, the thromboxane analogue U-46619 was intravenously administe

150 is stimulated by agonists such as thrombin, thromboxane and collagen, is a major mechanism of platel

151 kg; i.v.) inhibited COX-1, measured as blood thromboxane and COX-2, measured as lung PGE2.

152 identified that the cyclooxygenase products thromboxane and PGF2alpha are released from coronary art

153 e-2 inhibitors create an 'imbalance' between thromboxane and prostacyclin (reduction of prostacyclin)

154 coronary vasoconstrictor after stenting, and thromboxane and TNFalpha somewhat potentiate the seroton

155 M, and the effect was not altered by a DP(2)/thromboxane antagonist or by a peroxisome proliferator-a

156 Thromboxane appears to mediate the PVAT-induced contract

157 Prostaglandins (PGs) and thromboxanes are produced in vivo both from the omega 6

158 f prostanoids, made up of prostaglandins and thromboxanes, are generated via COX-mediated metabolism

159 ion risk score, clopidogrel use), both serum thromboxane B(2) >3.1 ng/mL and PFA-100 collagen-ADP CT

160 (PFA)-100, and levels of urinary 11-dehydro-thromboxane B(2) (11-dh-TxB(2)).

161 ns PGD(2) and PGE(2) from RAW264.7 cells and thromboxane B(2) (TXB(2)) from human alveolar macrophage

162 Thromboxane B(2) (TXB(2)) production was detected by enz

163 surface expression and release of CD40L and thromboxane B(2) (TXB(2)).

164 California), and urine levels of 11-dehydro-thromboxane B(2) (UTXB(2)).

165 al platelet COX-1 function measured by serum thromboxane B(2) and COX-1-independent platelet function

166 l as their products PGE(2), PGF(2alpha), and thromboxane B(2) and their receptors following stimulati

167 sis, COX-1-dependent assays, including serum thromboxane B(2) level, were not associated with adverse

168 icantly increased and prostaglandin E(2) and thromboxane B(2) significantly decreased in the airways,

169 injury, produced more prostaglandin E(2) and thromboxane B(2), and had greater expression of prostagl

170 Serotonin, thromboxane B(2), and TNFalpha release into aspirate pla

171 se of catecholamines, endothelin, serotonin, thromboxane B(2), and tumor necrosis factor (TNF)alpha w

172 taglandin (PG)E(2), PGD(2), PGF(2alpha), and thromboxane B(2), as well as the expression of proinflam

173 rations at dosages that did not affect serum thromboxane B(2), consistent with a selective COX-2 effe

174 derivatization method allows prostaglandins, thromboxane B(2), leukotriene B(4), hydroxyeicosatetraen

175 Platelet function was tested by (1) serum thromboxane B(2); (2) arachidonic acid-stimulated platel

176 ionship between PCSK9 and urinary 11-dehydro-thromboxane B2 (11-dh-TxB2), a marker of platelet activa

177 F=3.64; P=0.01334) and correlated with serum thromboxane B2 (rho=0.31; P=0.0413) in control but not i

178 Levels of PGF2alpha and thromboxane B2 (TXB2 ) were quantified by ELISA, and PGF

179 etter understand aspirin "resistance," serum thromboxane B2 (TXB2) and flow cytometric measures of ar

180 y the rate and extent of inhibition of serum thromboxane B2 (TXB2) generation.

181 e P-selectin, soluble CD40 ligand, and serum thromboxane B2 (TxB2) were measured.

182 lipopolysaccharide: prostaglandin E2 (PGE2)>thromboxane B2 (TxB2)>6-keto prostaglandin F1alpha (PGF1

183 yl leukotrienes, leukotriene B4 , 11-dehydro-thromboxane B2 , and prostaglandins E2 , D2 , and F2alph

184 Levels of thromboxane B2 and 12-hydroxyeicosatetraenoic acid produ

185 ines (TNF-alpha, IL-6, CXCL8), IL-12, CCL11, thromboxane B2 and immunoglobulin E at 24 h after local

186 and isofuranes, markers of oxidative stress, thromboxane B2 and immunoglobulin E were measured in bro

187 lush grade=3 exhibited lower values of serum thromboxane B2 compared with those with myocardial blush

188 looxygenase metabolites prostaglandin E2 and thromboxane B2 differed at baseline.

189 assay for the clopidogrel response and serum thromboxane B2 for the aspirin response) and aggregation

190 serum hemolytic activity and increase plasma thromboxane B2 levels in rats.

191 VerifyNow Aspirin assays and serum thromboxane B2 measurements were performed.

192 ted arachidonic acid-induced aggregation and thromboxane B2 production by > or = 99% (P<0.0001).

193 erent eicosanoids, both prostaglandin E2 and thromboxane B2 significantly enhanced serum-induced germ

194 Serum thromboxane B2 significantly increased after 120 minutes

195 din E2, 11-hydroxyeicosatetraenoic acid, and thromboxane B2 were identified as differentiating metabo

196 -VI,2,3-dinor-6-keto-PGF1alpha and 2,3-dinor-thromboxane B2 were increased in GhOEs, reflecting incre

197 creases in concentrations of prostaglandins, thromboxane B2, 15-HETE and 11-HETE in cerebellar sample

198 helial cell adhesion molecule-1, P-selectin, thromboxane B2, 6-ketoprostaglandin F1a, vascular cell a

199 We analyzed whether serum thromboxane B2, a stable metabolite of thromboxane A2, m

200 flammatory leukotriene B4 and procoagulating thromboxane B2, as well as lower specialized proresolvin

201 , M1 and M2 phenotypes were distinguished by thromboxane B2, prostaglandin (PG) E2, and PGD2 producti

202 Serum levels of thromboxane B2, reperfusion indexes (corrected Thromboly

203 537 on leukotriene, HETE, prostaglandin, and thromboxane biosynthesis in stimulated whole blood.

204 nted PGI(2) expression, and had no effect on thromboxane biosynthesis in vivo.

205 rin 100 mg/day seems insufficient to inhibit thromboxane biosynthesis.

206 Inhibition of urinary thromboxane excretion and platelet activation in pathway

207 ast, inhibition of connexins, P2Y12, P2Y1 or thromboxane formation had no effect on synchrony or ball

208 ion can be explained by a greater release of thromboxane from PVAT from female animals and greater se

209 The rate and extent of serum thromboxane generation and aspirin pharmacokinetics were

210 which inhibits cyclooxygenase-1 activity and thromboxane generation in platelets, reduces early SVG o

211 Aspirin-insensitive thromboxane generation measured by UTXB(2) and shear-dep

212 ation of G(i) plus G(z) pathways also caused thromboxane generation that was dependent on outside-in

213 ad no affect on ADP-induced aggregation when thromboxane generation was blocked.

214 nPKCeta positively regulates agonist-induced thromboxane generation with no effects on platelet aggre

215 inhibitor of nPKCeta, inhibited ADP-induced thromboxane generation.

216 lphaIIbbeta3 signaling, which contributes to thromboxane generation.

217 OX-2-derived PGI2 and COX-1-derived platelet thromboxane is misplaced.

218 anoids such as prostaglandins, leukotrienes, thromboxanes, isoprostanes, resolvins, hydroxides, hydro

219 ic acid-derived eicosanoids (prostaglandins, thromboxanes, leukotrienes, and other oxidized derivativ

220 D prostanoid receptor 1 (DP(1)) or the thromboxane-like prostanoid (TP) receptor did not play a

221 duction induced by PGD2, while the selective thromboxane-like prostanoid receptor antagonist SQ29548

222 Ramatroban, a dual CRTH2/thromboxane-like prostanoid receptor antagonist, markedl

223 /- 0.8 pmol/mg creatinine [Cr], P < .05) and thromboxane metabolite (TX-M; 1.4 +/- 0.3 vs 0.9 +/- 0.1

224 e demonstrated that exogenously-administered thromboxane mimetic stimulates ACTH secretion in fetal s

225 ,15-EET, the opioid antagonist naloxone, the thromboxane mimetic U46619, or the cannabinoid antagonis

226 h an H2S donor, after preconstriction with a thromboxane mimetic, resulted in dose-dependent vasorela

227 sheep, and that the endogenous production of thromboxane modifies the HPA response to cardiovascular

228 elet factor 4, beta-thromboglobulin, RANTES, thromboxane, or serotonin) in the pathogenesis of allerg

229 e sensitive at characterizing defects in the thromboxane pathway, which presented with normal respons

230 improved graft survival and decreased plasma thromboxane, platelet factor 4 (CXCL4), and IFN-gamma.

231 when activated, which then induces platelet thromboxane production by signaling through platelet-exp

232 olished VWF-induced platelet aggregation and thromboxane production in non-aspirin-treated washed pla

233 mg/d are adequate to fully inhibit platelet thromboxane production, dosages as high as 1300 mg/d are

234 family kinases in GPIIb/IIIa activation and thromboxane production.

235 dium arachidonate or ADP; 3) agonist-induced thromboxane production; and 4) NO production, cGMP synth

236 l concentrations of ADP, collagen, thrombin, thromboxane, prostacyclin, and nitric oxide.

237 cyclooxygenase-1 [COX1 knockout (KO)] or the thromboxane prostanoid (TP) receptor (TP KO).

238 ase (COX), thromboxane A2 synthase (TxA2-S), thromboxane prostanoid receptors (TP-Rs), or superoxide

239 targeted disruption of the gene encoding the thromboxane-prostanoid (TP) receptor.

240 effect of 8-iso-PGF2alpha was mimicked by a thromboxane receptor (TP) agonist (U46619) and blocked b

241 aglandin E(2) receptor subtype 4 (EP(4)) and thromboxane receptor (TP).

242 TXA2 and isoprostanes) which act through the thromboxane receptor (TP).

243 L receptor-deficient mice) by activating the thromboxane receptor (TP).

244 selectively blocked both ADP-stimulated and thromboxane receptor agonist U46619-stimulated platelet

245 amine, antioxidant treatment with Tempol and thromboxane receptor antagonism with SQ-29548) were show

246 oxygenase inhibitor, or SQ29548, a selective thromboxane receptor antagonist.

247 tease-activated receptor-1) antagonists, and thromboxane receptor antagonists.

248 with little further antagonism by additional thromboxane receptor blockade.

249 ipase A2, cyclooxygenase, or blockade of the thromboxane receptor markedly reduced the effects of H2S

250 n potential.(1) Their studies reveal a novel thromboxane receptor mutation (TP-V241G) in humans that

251 Inhibition of the thromboxane receptor or cyclooxygenase-2 dramatically at

252 nocytes and macrophages depends on autocrine thromboxane receptor signaling and that under normal con

253 d LDL-mediated PGIS nitration and associated thromboxane receptor stimulation might be important in t

254 cement by activating PGF(2alpha) receptor or thromboxane receptor, or approximately 15% enhancement b

255 ependent on a non-thromboxane agonist of the thromboxane receptor, whereas vasodilatory mechanisms of

256 h is mediated, in part, by activation of the thromboxane receptor.

257 ndertaken to determine the potential role of thromboxane receptors (TP) in bladder cancer.

258 menon by demonstrating that H1 histamine and thromboxane receptors utilize the same mechanism to augm

259 ion activated trapped platelets (assessed by thromboxane release).

260 ce of adenosine = 20-HETE > angiotensin II > thromboxane = superoxide > renal nerves > ATP.

261 Thromboxane synthase (TXAS) and thromboxane A(2) recepto

262 ntly, we reported prognostic significance of thromboxane synthase (TXAS) gene expression in invasive

263 ance Raman (RR) spectra of recombinant human thromboxane synthase (TXAS) in both the presence and the

264 Thromboxane synthase (TXAS) is one of the enzymes downst

265 Thromboxane synthase (TxS) metabolizes the cyclooxygenas

266 Cardiomyocyte expression of COX-2, thromboxane synthase (TxS), and the receptors for TxA2 (

267 xpression of nuclear factor-kappaB-dependent thromboxane synthase and microsomal PGE(2) synthase was

268 xane A(2) (TxA(2)) is a prostanoid formed by thromboxane synthase using the cyclooxygenase product pr

269 Previously, increased expression of thromboxane synthase was found in prostate tumors, and t

270 ell motility was attenuated by inhibitors of thromboxane synthase.

271 nhibitor, and is enhanced by an inhibitor of thromboxane synthase.

272 feres with the aspirin-induced inhibition of thromboxane synthesis and/or activation of the nitric ox

273 Blocking thromboxane synthesis reversed that finding and also nor

274 not modify the aspirin-induced inhibition of thromboxane synthesis, and inhibits the aspirin-induced

275 l role in the catalysis of prostaglandin and thromboxane synthesis.

276 d not modify the L-ASA-induced inhibition of thromboxane synthesis; and 3) prevented the L-ASA-induce

277 oxygenase pathway forming prostaglandins and thromboxanes, the lipoxygenase pathway generating leukot

278 plaque-like deposits, this was blocked by a thromboxane (TP) receptor antagonist, suggesting that TP

279 ation (EDH) is lost following stimulation of thromboxane (TP) receptors, an effect that may contribut

280 Platelet thromboxane (Tx) A(2) (P < 0.001) was inhibited in all a

281 Suppression of thromboxane (Tx) A(2) biosynthesis retards atherogenesis

282 The thromboxane (TX) A(2) receptor (TP) encompasses two alte

283 pha1-adrenergic agonist phenylephrine or the thromboxane (TX) A2 analog U-46619 were similar between

284 In smokers, the biosynthesis of both thromboxane (Tx) A2 and prostacyclin is increased.

285 Thromboxane (TX) A2 is released from multiple cell types

286 Thromboxane (TX) A2 is released from multiple cell types

287 aspirin leads to long-lasting suppression of thromboxane (TX) A2 production and TXA2-mediated platele

288 ro through the inhibition of COX-1-dependent thromboxane (TX) A2.

289 We investigated in vivo thromboxane (TX) and prostacyclin (PGI2) biosynthesis an

290 d human platelets, coincident with increased thromboxane (Tx) formation.

291 COX-1-mediated platelet thromboxane (TX) production has been proposed to promote

292 expression of both prostacyclin (PGI(2)) and thromboxane (Tx) synthases in endothelial cells, and VSM

293 This is coupled with enhanced levels of thromboxane (TX), an eicosanoid that facilitates platele

294 omitant inhibition of platelet COX-1-derived thromboxane (Tx)A(2).

295 Generation of both thromboxane (Tx)A2 and the isoprostane, 8, 12 -iso iPF(2

296 the TP) for the cyclooxygenase (COX) product thromboxane (Tx)A2, retards atherogenesis in apolipoprot

297 Plasma thromboxane (TX)B2, an indicator of platelet reactivity,

298 Prostacyclin (PGI(2)) and thromboxane (TxA(2)) are biological opposites; PGI(2), a

299 en shown that ADP-, but not thrombin-induced thromboxane (TxA2) generation depends on integrin signal

300 therogenic mediators CD40 ligand (CD40L) and thromboxanes (TXs).

301 olved in the synthesis of prostaglandins and thromboxanes, which are regulators of biologic processes