ライフサイエンスコーパス: EET

1 EET analogs (10 mg/kg/d) attenuated cisplatin-induced ne

2 EET levels were measured in tissue homogenates of rat li

3 EET substrate preference for both COX-1 and COX-2 were e

4 EETs are in the third (Cytochrome P450) pathway of arach

5 EETs are produced by the cytochrome P450 (CYP) epoxygena

6 EETs are produced predominantly in the endothelium.

7 EETs formation was reversed by DNase treatment.

8 EETs may have clinical application in marrow or cord blo

9 11,12-EET and 19,20-EDP also inhibited leukocyte adherence to

10 High dietary potassium increased 11,12-EET in the isolated cortical collecting duct, an effect

11 In adult HSPCs, 11,12-EET induced transcriptional programs, including AP-1 act

12 hances the inhibitory effect of AA and 11,12-EET on ENaC by increasing CYP epoxygenase activity and d

13 ach augmented the inhibitory effect of 11,12-EET on ENaC.

14 Exogenous addition of 11,12-EET or 19,20-EDP when combined with 12-(3-adamantane-1-y

15 the developing zebrafish embryo, where 11,12-EET promoted HSPC specification by activating a unique a

16 bolite 11,12-epoxyeicosatrienoic acid (11,12-EET) can inhibit the epithelial sodium channel (ENaC) in

17 reased 11,12-epoxyeicosatrienoic acid (11,12-EET) levels in isolated rat CCD tubules.

18 entration-dependent manner by 8,9-EET, 11,12-EET, and 14,15-EET (IC(50) values of 444, 11.7, and 8.28

19 This effect seemed specific to 11,12-EET, because both 8,9- and 14,15-EET failed to stimulate

20 were estimated as 8,9-EET > 5,6-EET > 11,12-EET, whereas 14,15-EET was inactive.

21 a weak inhibitor of ENaC compared with 11,12-EET, whereas 8,9- and 14,15-DHET were not.

22 ermore, inhibition of sEH enhanced the 11,12-EET-induced inhibition of ENaC similar to high dietary p

23 ivity seemed to be responsible for the 11,12-EET-mediated enhanced inhibition of ENaC in animals on a

24 dent manner by 8,9-EET, 11,12-EET, and 14,15-EET (IC(50) values of 444, 11.7, and 8.28 nM, respective

25 were comparable (ED(50) 1.7 microM) to 14,15-EET as vasorelaxants but were approximately 10-35 times

26 6-fold more potent, respectively, than 14,15-EET as vasorelaxants; on the other hand, their ability t

27 ncer cell growth in part through (+/-)-14,15-EET biosynthesis.

28 20-I-14,15-EE8ZE-APSA and 14,15-EET displaced 20-(125)I-14,15-epoxyeicosa-5(Z)-enoic aci

29 ic to 11,12-EET, because both 8,9- and 14,15-EET failed to stimulate BK channels.

30 In polarized M1 cells, 14,15-EET inhibited amiloride-sensitive apical to basolateral

31 of 15-epi LXA4 by rapidly hydrolyzing 14,15-EET into its cognate diol, eliminating a proresolving si

32 Because 14,15-EET is chemically and metabolically labile, structurally

33 to the nucleus, suggesting that (+/-)-14,15-EET may be involved in an autocrine/paracrine pathway dr

34 dium transport effects of EGF, and its 14,15-EET metabolite rescued the knockdown phenotype.

35 The (+/-)-14,15-EET regioisomer selectively rescues breast cancer cells

36 educes nuclear Tyr(P)-705-Stat3, (+/-)-14,15-EET restores this signaling process and promotes Tyr(P)-

37 8,9-EET > 5,6-EET > 11,12-EET, whereas 14,15-EET was inactive.

38 4,15-epoxyeicosa-5,8,11-trienoic acid (14,15-EET) is a labile, vasodilatory eicosanoid generated from

39 4,15-epoxyeicosa-5,8,11-trienoic acid (14,15-EET) is a powerful endogenous autacoid that has been asc

40 sanoid 14,15-epoxyeicosatrienoic acid (14,15-EET).

41 ndent mechanism for ENaC inhibition by 14,15-EET, (b) point to ENaC as a proximal target for EET-acti

42 ere observed with the omega-6 epoxide, 14,15-EET, and nonoxidized DHA.

43 s, 5,6-epoxyeicosatrienoic acid (EET), 14,15-EET, and the corresponding dihydroxyeicosatrienoic acids

44 ogically inactive thiirane analogue of 14,15-EET, the opioid antagonist naloxone, the thromboxane mim

45 EGF expression is a major mechanism of 14,15-EET-induced angiogenesis.

46 nti-VEGF antibodies completely blocked 14,15-EET-induced HDMVEC migration and tube formation and Matr

47 cancer cell growth and abrogates (+/-)-14,15-EET-induced proliferation, indicating a Stat3 requiremen

48 dicating a Stat3 requirement for (+/-)-14,15-EET-mediated cell growth.

49 s with an ED(50) comparable to that of 14,15-EET.

50 acid-derived lipid mediators, such as 5',6'-EET, that activate TRPV4.

51 -1 and COX-2 were estimated as 8,9-EET > 5,6-EET > 11,12-EET, whereas 14,15-EET was inactive.

52 Levels of 5,6-EET and 15-HETE were increased in colons of mice with, b

53 inally, in vivo intrathecal injection of 5,6-EET caused mechanical allodynia in wild-type but not TRP

54 Furthermore, 5,6-EET could be metabolized to a thromboxane analog.

55 In spinal cord slices, 5,6-EET dose dependently enhanced the frequency, but not the

56 In a bioassay, 5,6-EET increased the beating rate of neonatal cardiomyocyte

57 a (DRGs) and the dorsal spinal cord, and 5,6-EET is released from activated sensory neurons in vitro.

58 We conclude that 5,6-EET is synthesized on the acute activation of nociceptor

59 t, during capsaicin-induced nociception, 5,6-EET levels increased in dorsal root ganglia (DRGs) and t

60 5,6-EET potently induced a calcium flux (100 nm) in cultured

61 shed in TRPA1-null mice, suggesting that 5,6-EET presynaptically facilitated spinal cord synaptic tra

62 nvestigated the specific contribution of 5,6-EET to transient receptor potential (TRP) channel activa

63 supernatants from IBS biopsies produced 5,6-EET via a mechanism that involved the proteinase-activat

64 Levels of the TRPV4 agonist 5,6-EET, but not levels of TRPV1 or TRPA1 agonists, were inc

65 In addition, 5,6-EET-EA inhibited the forskolin-stimulated accumulation o

66 Finally, we demonstrate that 5,6-EET-EA is more stable than anandamide in mouse brain hom

67 oxidation of anandamide by P450s to form 5,6-EET-EA represents an endocannabinoid bioactivation pathw

68 The K(i) values for the binding of 5,6-EET-EA to membranes from Chinese hamster ovary (CHO) cel

69 6-epoxyeicosatrienoic acid ethanolamide (5,6-EET-EA), is a potent and selective cannabinoid receptor

70 ed capacity for converting anandamide to 5,6-EET-EA, which correlated with increased protein expressi

71 Furthermore, 5,6-EET-induced enhancement of sEPSC frequency was abolished

72 r both COX-1 and COX-2 were estimated as 8,9-EET > 5,6-EET > 11,12-EET, whereas 14,15-EET was inactiv

73 ucture of two major products formed from 8,9-EET in this COX pathway were confirmed by chemical synth

74 (5,6-epoxyeicosatrienoic acid [EET] and 8,9-EET), and TRPA1 (PGA1, 8-iso-prostaglandin A2, and 15-de

75 d in a concentration-dependent manner by 8,9-EET, 11,12-EET, and 14,15-EET (IC(50) values of 444, 11.

76 8R-HETE and 8R,9S-eicosatrienoic acid (8R,9S-EET), plus other chiral monoepoxides and bis-allylic 10S

77 -, and (+/-)-14,15-epoxyeicosatrienoic acid (EET) (total turnover of approximately 2 pmol/pmol CYP3A4

78 ovel orally active epoxyeicosatrienoic acid (EET) analogs and investigated their prophylactic effect

79 n cirrhosis, 11,12-epoxyeicosatrienoic acid (EET) induces mesenteric arterial vasodilation, which con

80 genase and for its epoxyeicosatrienoic acid (EET) metabolites in the in vivo control of ENaC activity

81 is of the enzymes' epoxyeicosatrienoic acid (EET) substrates, so they accumulate inducing vasodilatio

82 2 metabolites, 5,6-epoxyeicosatrienoic acid (EET), 14,15-EET, and the corresponding dihydroxyeicosatr

83 ne B4), TRPV4 (5,6-epoxyeicosatrienoic acid [EET] and 8,9-EET), and TRPA1 (PGA1, 8-iso-prostaglandin

84 of proangiogenic epoxyeicosatrienoic acids (EET) by the cytochrome P450 arachidonic acid epoxygenase

85 e increased media epoxyeicosatrienoic acids (EETs) and reduced cell membrane levels of EETs.

86 Epoxyeicosatrienoic acids (EETs) are anti-inflammatory molecules synthesized by var

87 Epoxyeicosatrienoic acids (EETs) are cytochrome P450-epoxygenase-derived metabolite

88 ogenous levels of epoxyeicosatrienoic acids (EETs) are known for their analgesic, antihypertensive, a

89 Epoxyeicosatrienoic acids (EETs) are small molecules produced by cytochrome P450 ep

90 een, and identify epoxyeicosatrienoic acids (EETs) as a family of lipids that enhance HSPC engraftmen

91 verted to natural epoxyeicosatrienoic acids (EETs) by cytochrome P450 enzymes.

92 d CYP2J2 generate epoxyeicosatrienoic acids (EETs) from arachidonic acid.

93 (COX) pathway and epoxyeicosatrienoic acids (EETs) from the cytochrome P450/soluble epoxide hydrolase

94 Epoxyeicosatrienoic acids (EETs) generated from arachidonic acid by cytochrome P450

95 450 (CYP)-derived epoxyeicosatrienoic acids (EETs) possess potent anti-inflammatory effects in vitro.

96 Specifically, epoxyeicosatrienoic acids (EETs) produced from the P450 pathway are angiogenic, ind

97 450 (CYP)-derived epoxyeicosatrienoic acids (EETs) regulate sodium transport and blood pressure.

98 dothelium-derived epoxyeicosatrienoic acids (EETs) relax vascular smooth muscle by activating potassi

99 , total levels of epoxyeicosatrienoic acids (EETs), but not epoxydocosapentaenoic acids (EDPs), were

100 , and whether the epoxyeicosatrienoic acids (EETs), derived via cytochrome P450, were the predominant

101 es, including the epoxyeicosatrienoic acids (EETs), epoxidized lipids produced from arachidonic acid

102 metabolites, the epoxyeicosatrienoic acids (EETs), in ENaC activity have been identified; however, t

103 Epoxyeicosatrienoic acids (EETs), lipid mediators produced by cytochrome P450 epoxy

104 ves to inactivate epoxyeicosatrienoic acids (EETs), which are generated in the brain to couple neuron

105 n the presence of epoxyeicosatrienoic acids (EETs).

106 sis of protective epoxyeicosatrienoic acids (EETs).

107 d inactivation of epoxyeicosatrienoic acids (EETs).

108 0.01), vasoactive epoxyeicosatrienoic acids (EETs; -60%, p < 0.001) synthesis, large-conductance, cal

109 metabolites (cis-epoxyeicosatrienoic acids [EETs]) in the lung.

110 esults strongly suggest that Acsl4 activates EETs to form EET-CoAs that are incorporated into glycero

111 U937 cell membranes contain a high-affinity EET binding protein that may represent an EET receptor.

112 for close endoscopic surveillance even after EET.

113 henylsulfonamide (20-I-14,15-EE8ZE-APSA), an EET analogue with a photoactive azido group.

114 2/13 cells, and in Acsl4 knockdown cells, an EET receptor antagonist partially rescued GSIS.

115 ty EET binding protein that may represent an EET receptor.

116 e synchronized presence of elevated cAMP and EET levels.

117 By considering the inter-ring distance and EET rate, we demonstrate that this group can achieve min

118 sed cortical activity and that K+ fluxes and EET signaling mediate a large part of the hemodynamic re

119 mentary and terrestrial environments, an AOM-EET niche would have implications for minimizing the net

120 cell, and isotopic experiments supported AOM-EET to the anode.

121 ificant gene expression responses to applied EET stimuli occur in only two microbial groups, Desulfob

122 There was a significant correlation between EET formation and TSLP expression (P = 0.02) as well as

123 icant negative correlation was found between EET formation and LEKTI expression (P = 0.016).

124 m was to investigate a possible link between EET formation and the presence of Staphylococcus aureus,

125 s study identifies a functional link between EETs and COX and identifies ct-8,9-E-11-HET as an angiog

126 sue regeneration via production of bioactive EETs.

127 leads to EET to both terminals, followed by EET from conventional BODIPY to the expanded version.

128 In each case, EET to the expanded dye involves initial population of t

129 dynamic community-wide response to changing EET rates.

130 othelial Cyp2c44 expression, and circulating EET levels.

131 high as 270 A/m(2) if only Ohmic-conduction EET was limiting.

132 the maximum energy loss for Ohmic-conduction EET was negligible, 0.085 mV.

133 elial EET biosynthesis or globally decreased EET hydrolysis attenuates NF-kappaB-dependent vascular i

134 Here, we demonstrate EET-dependent AOM in a biofilm anode dominated by Geobac

135 Although endothelial CYP-derived EETs are potent vasodilators, their contribution to the

136 To determine whether endothelial-derived EETs affect physiologic tissue growth in vivo, we used g

137 le of cardiomyocyte- vs. endothelial-derived EETs or compared the effects of different CYP epoxygenas

138 We show that endothelial-derived EETs play a critical role in accelerating tissue growth

139 r growth but depended on endothelium-derived EETs at the site of metastasis.

140 directly implicating CYP epoxygenase-derived EETs with the observed anti-inflammatory phenotype.

141 re of the phycobilisome supports directional EET to reaction centers with minimal losses due to therm

142 king density, achieving robust and efficient EET.

143 nic angiotensin II rat, we observed elevated EET, dihydroxyeicosatrienoic acid, and preeclamptic feat

144 pidermidis, the latter were unable to elicit EET formation and eosinophils required additional TSLP s

145 drolase inhibitors, which elevate endogenous EET levels, promote liver and lung regeneration.

146 e that metabolizes EETs, elevated endogenous EET levels and promoted primary tumor growth and metasta

147 armacological tools to manipulate endogenous EET levels.

148 d pharmacological manipulation of endogenous EET levels, we demonstrate that EETs are critical for pr

149 as sEH inhibitors, which increase endogenous EETs, stimulate primary tumor growth and metastasis.

150 CYP2C8 epoxygenases to increase endothelial EET biosynthesis.

151 d transgenic mice with increased endothelial EET biosynthesis (Tie2-CYP2C8 Tr and Tie2-CYP2J2 Tr) or

152 nase pathway by either increased endothelial EET biosynthesis or globally decreased EET hydrolysis at

153 provide evidence for a Cyp2c44 epoxygenase, EET-mediated mechanism of ENaC regulation involving an E

154 cellular ET, (2) non-Ohmic extracellular ET (EET) from an outer membrane protein to an extracellular

155 published, only a few reports have examined EET from marine strains of Shewanella.

156 ometrical arrangement that ensures excellent EET.

157 8% of the infiltrating eosinophils exhibited EETs in patients' nasal polyp tissues.

158 Further, exogenous EETs reduced GSIS in INS 832/13 cells, and in Acsl4 knoc

159 Finally, EET may be the physical mechanism underlying many cases

160 de the multiheme cytochromes responsible for EET, rather than pilin-based structures as previously th

161 , (b) point to ENaC as a proximal target for EET-activated ERK1/2 mitogenic kinases, (c) characterize

162 d Cyp2J2, the principal Cyps responsible for EETs synthesis, as well as soluble epoxide hydrolase (sE

163 and in vitro studies demonstrate a role for EETs in limiting cisplatin-induced renal apoptosis.

164 our observations indicate a central role for EETs in organ and tissue regeneration and their contribu

165 Thus, our data indicate a central role for EETs in tumorigenesis, offering a mechanistic link betwe

166 ly suggest that Acsl4 activates EETs to form EET-CoAs that are incorporated into glycerophospholipids

167 s and possibly other microorganisms and form EETs at sites of airway epithelial damage to protect the

168 ted with eosinophil granule proteins forming EETs and the expression of filaggrin, the protease inhib

169 p could be identified, they may benefit from EET, whereas, the majority may be managed conservatively

170 gate whether eosinophils generate functional EETs as a direct response to TSLP, and further to study

171 Furthermore, EET/dihydroxy-epoxyeicosatrienoic acid isomer ratios wer

172 sulation of the conjugated backbone improves EET, increasing the fraction of CPs possessing epsilon =

173 atment with MS-PPOH reversed the increase in EET levels.

174 These data suggest that an increase in EETs due to sEH-gene knockout leads to an increase in th

175 Two stimuli were employed: to increase EET and to stop EET.

176 and mask the beneficial effects of increased EET production following I/R.

177 ng soluble epoxide hydrolase (sEH) increased EET concentration and mildly promoted tumor growth.

178 trong transcriptional responses to increased EET rates, with one responding positively and the other

179 strogen loss decreased the anti-inflammatory EETs in the cardiovascular system.

180 Inhibitors of these anti-inflammatory EETs reversed TGA inhibition.

181 oss would reduce levels of anti-inflammatory EETs.

182 metabolically channels arachidonic acid into EETs, whereas in failing hearts, increased iPLA2gamma ac

183 ditions where both inter- and intramolecular EET operate.

184 OS production and degranulation and involves EET formation.

185 While extensive studies involving EET from a fresh water Shewanella microbe (S. oneidensis

186 ecapitulated these results, whereas lowering EET levels, either genetically or pharmacologically, del

187 owever, the effect of increased CYP-mediated EET biosynthesis and decreased soluble epoxide hydrolase

188 uble epoxide hydrolase (sEH, Ephx2)-mediated EET hydrolysis on vascular inflammation in vivo has not

189 hydrolase (sEH), the enzyme that metabolizes EETs, elevated endogenous EET levels and promoted primar

190 de hydrolase (sEH, EPHX2), which metabolizes EETs to their less active diols.

191 primitive unaltered Antarctic CR meteorites EET 92042 and QUE 99177.

192 ex vivo human mucosal disease tissue model, EET formation was induced (4.2 +/- 0.9-fold) on exposure

193 ty led to a complete inhibition (P < .05) of EET formation by S aureus.

194 ted in vitro that the protective activity of EET analogs does not compromise the anticancer effects o

195 t study demonstrating a direct comparison of EET and EDP on vascular inflammatory endpoints, and we h

196 paper, the spatial and temporal dynamics of EET through the FMO complex at physiological temperature

197 mportance of considering possible effects of EET-modulating drugs on cancer.

198 cell can reduce or remove the frustration of EET rates across the photosynthetic network.

199 A new generation of EET mimics incorporating modifications to the carboxylat

200 , P < 0.05) was reversed after inhibition of EET production (-6.388 +/- 0.263, P < 0.05).

201 hemodynamic effects of in vivo inhibition of EET production in experimental cirrhosis.

202 n rats with cirrhosis, in vivo inhibition of EET production normalizes the response of mesenteric art

203 The relative partitioning of EET from the spacer to each terminal is somewhat sensiti

204 hy/mass spectrometry showed that the rate of EET conversion to dihydroxyeicosatrienoic acids (DHET) w

205 Overall, the rate of EET falls by only a factor of 4-fold on moving from the

206 The rate of EET from spacer to conventional BODIPY dye, as measured

207 The availability of EETs is limited primarily by the soluble epoxide hydrola

208 growth, suggesting that the contribution of EETs to angiogenesis and subsequent tumor growth may be

209 investigate the presence and distribution of EETs in esophageal tissues from EoE patients and their a

210 The pro-haematopoietic effects of EETs were conserved in the developing zebrafish embryo,

211 This study explores the fate of EETs with COX, the angiogenic activity of the primary me

212 ophil survival, but induced the formation of EETs consisting of mitochondrial DNA in association with

213 The formation of EETs could serve as a firewall against the invasion of p

214 Formation of EETs was associated with increased IL-5 (P < .05) and pe

215 s spectrometry was used to measure levels of EETs and their metabolites, dihydroxyeicosatrienoic acid

216 easured in plasma or aortic tissue levels of EETs.

217 s (EETs) and reduced cell membrane levels of EETs.

218 Since the metabolism of EETs by sEH reduces or eliminates their bioactivity, inh

219 a physiological role for COX metabolites of EETs.

220 g in vivo that pharmacological modulation of EETs can affect cancer growth.

221 nstrating that pharmacological modulation of EETs can affect normal organ and tissue growth.

222 slides were investigated for the presence of EETs and S aureus by using immunofluorescent staining an

223 immunoblotting and linked to the presence of EETs.

224 Active EoE exhibits the presence of EETs.

225 To address the role of EETs in regulating glucose homeostasis and insulin signa

226 hesis (Tie2-CYP2C8 Tr and Tie2-CYP2J2 Tr) or EET hydrolysis (Tie2-sEH Tr).

227 n directly stimulates eosinophils to produce EETs.

228 This attenuation was inhibited by a putative EET receptor antagonist and CYP epoxygenase inhibitor, d

229 As a result, drugs that raise EET levels are in clinical trials for the treatment of h

230 bacterial nanowires that mediate long-range EET by the previously proposed multistep redox hopping m

231 PY dye and is followed by slower, long-range EET to the opposite terminal.

232 Here, rapid EET occurs from pyrene to the BODIPY dye and is followed

233 lyngbya ohadii strain identified (i) reduced EET between phycobilisome components, (ii) shorter fluor

234 The resulting EET path will exhibit increased coupling to the environm

235 o glycerophospholipids, thereby sequestering EETs.

236 Here we identify specific EET-active microbes and genes in a diverse biofilm using

237 i were employed: to increase EET and to stop EET.

238 These data also suggest EETs contribute to about half of the EDHF response.

239 rofiling revealed that MCF7 cells synthesize EETs in a CYP3A4-dependent manner.

240 Administration of synthetic EETs recapitulated these results, whereas lowering EET l

241 Administration of synthetic EETs recapitulated these results, while EET antagonists

242 lphaMHC-CYP2J2 Tr) or treated with synthetic EETs have increased functional recovery after ischemia/r

243 In the central nervous system, EETs are thought to play a role in the regulation of loc

244 employed a novel endogenous epitope tagging (EET) approach, which revealed that endogenous PTEN inter

245 It is demonstrated that EET between tryptophan or tyrosine and a disulfide bond

246 Collectively, our data provide evidence that EET analogs attenuate cisplatin-induced nephrotoxicity b

247 It is noted that EET could occur in many systems, making measured entropi

248 Here we experimentally show that EET in single antennas can be characterized by 2D polari

249 f endogenous EET levels, we demonstrate that EETs are critical for primary tumor growth and metastasi

250 Here we demonstrate that EETs or inhibition of sEH lead to antihyperalgesia by at

251 Remarkably, we found that EETs stimulated extensive multiorgan metastasis and esca

252 In this study, we tested the hypothesis that EETs are involved in glucose regulation and in retarding

253 Recent evidence suggests that EETs act via a membrane binding site or receptor.

254 The EET analogue relaxed preconstricted bovine coronary arte

255 The EET effects were associated with increased threonine pho

256 secreted by C. marina were facilitating the EET process.

257 e moieties resulting in the cessation of the EET (electronic energy transfer) process from borane to

258 e lattice for the global optimization of the EET network.

259 Quantification of the EET processes operating in this planktonic system assist

260 ts into the expression and regulation of the EET receptor.

261 In this study, the EET activity of the photosynthetic marine raphidophyte,

262 ave been made to develop drugs targeting the EET pathway.

263 Furthermore, we demonstrate that the EET effects on enhancing HSPC homing and engraftment are

264 Through its metabolism of the EETs and other lipid mediators, sEH contributes to the r

265 on various endoscopic eradication therapies (EET) specifically in this patient population are limited

266 This EET photoaffinity labeling method with a high signal-to-

267 Three EET regioisomers were found to be substrates for COX, ba

268 Less attention has been given to EET by planktonic organisms in oxic environments where e

269 tanding of the synergetic effects leading to EET optimization of light-harvesting antenna systems whi

270 ect illumination of the spacer unit leads to EET to both terminals, followed by EET from conventional

271 of functional microbes and genes related to EET activity in a diverse community, representing the ne

272 k and the associated short-term responses to EET stimuli that induce changes to metabolic flow and co

273 unknown genes that are highly responsive to EET stimuli and associated with our identified draft gen

274 that we term entropy-enthalpy transduction (EET), in which the thermodynamic character of a local pe

275 Shewanella extracellular electron transfer (EET) are highly conserved.

276 interest in extracellular electron transfer (EET) from organisms to receptors, particularly in anaero

277 iration via extracellular electron transfer (EET) is a ubiquitous reaction that occurs throughout ano

278 ior support extracellular electron transfer (EET) through a solid conductive matrix - the first such

279 current via extracellular electron transfer (EET) to a solid electrode surface.

280 oupled with extracellular electron transfer (EET) to conductive solids is relatively insufficient.

281 is rapid singlet excitation energy transfer (EET) from the macrocycle to the hexayne (tau = 3.0 ps),

282 ghly efficacious electronic energy transfer (EET) occurs from the first-excited singlet state localiz

283 and compare the excitation energy transfer (EET) properties of various natural and artificial antenn

284 try that enables excitation energy transfer (EET) to be accurately measured via action spectroscopy o

285 he efficiency of excitation energy transfer (EET) to fit light energy supply to biochemical demands.

286 f photosynthetic electronic energy transfer (EET), although the data were acquired at cryogenic tempe

287 a intramolecular excitation energy transfer (EET).

288 otion of maximum excitation energy transfer (EET).

289 ms of electronic excitation energy transfer (EET).

290 P-to-chromophore excitation energy transfer (EET).

291 s offer an extracellular electron transport (EET) pathway for linking the respiratory chain of bacter

292 < 0.0001) or eosinophil extracellular trap (EET) formation (P = 0.048).

293 so-called extracellular eosinophilic traps (EETs) under similar pathologic conditions.

294 ils generate eosinophil extracellular traps (EETs) able to kill bacteria.

295 would induce eosinophil extracellular traps (EETs) in bronchoalveolar lavage fluid and lung tissue.

296 By releasing eosinophil extracellular traps (EETs), eosinophils achieve an efficient extracellular ba

297 eas in the rhenium-rotaxane there is triplet EET, from the macrocycle complex (3)MLCT state to the he

298 SIS by regulating the levels of unesterified EETs and that arachidonate controls the expression of it

299 The structurally unrelated EET ligands miconazole, MS-PPOH, and ketoconazole also i

300 etic EETs recapitulated these results, while EET antagonists suppressed tumor growth and metastasis,

301 Lastly, MCs incubated with EET and challenged through FcepsilonRI had a significant