ライフサイエンスコーパス: ECE

1 ECE facilities and findings indicate wide phthalate cont

2 ECE increased with annual precipitation but approached p

3 ECE of the SN metastasis is a strong predictor of NSN tu

4 ECE of the SN metastasis was present in 18 (25.7%) of th

5 ECE was determined from the final pathologic report on s

6 ECE-1 does not regulate either the resensitization of re

7 ECE-1 exists in 2 isoforms (ECE-1alpha and ECE-1beta), t

8 ECE-1 inhibition also enhanced SP-induced expression and

9 ECE-1 inhibition caused endosomal retention of the SP ne

10 ECE-1 inhibition or knockdown traps CLR/RAMP1 and beta-a

11 ECE-1 inhibition slowed ETAR recycling yet prolonged ET-

12 ECE-1 inhibitors (SM-19712, PD-069185) and the vacuolar

13 ECE-1 inhibitors also caused sustained SP-induced activa

14 ECE-1 mRNA and protein were expressed by myenteric neuro

15 ECE-1alpha and ECE-1beta immunoreactivity was present in

16 ECE-2 also degrades Abeta.

17 ECE-2 null mice develop normally, are healthy into adult

18 ECE-2 protein concentration, measured by sandwich enzyme

19 ECE-2 tolerates a wide range of amino acids in the P1-po

20 ECE-2, unlike ECE-1, exhibits restricted neuroendocrine

21 2.8+/-0.6 versus 8.4+/-1.2 pmol/mL, P<0.05), ECE-1 activity was attenuated (68+/-3% versus 32+/-8%, P

22 ified neural endothelin-converting enzyme 1 (ECE-1) as a key regulator of ET-1-induced pruritus and n

23 by endosomal endothelin-converting enzyme 1 (ECE-1) controls SSTR2A trafficking and association with

24 udes NEP and endothelin-converting enzyme 1 (ECE-1), an enzyme involved in the maintenance of vascula

25 ification of endothelin-converting enzyme-1 (ECE-1) as a novel Abeta-degrading enzyme.

26 haracterized endothelin-converting enzyme-1 (ECE-1) as an Abeta-degrading enzyme that appears to act

27 Endothelin-converting enzyme-1 (ECE-1) degrades NT in acidic conditions, and its activit

28 report that endothelin-converting enzyme-1 (ECE-1) degrades substance P (SP) in early endosomes of e

29 ors of human endothelin-converting enzyme-1 (ECE-1) have been designed as potential modulators of end

30 jor role for endothelin-converting enzyme-1 (ECE-1) in controlling substance P (SP) and the neurokini

31 hat both the endothelin-converting enzyme-1 (ECE-1) inhibitor, phosphoramidon, as well as a novel ET-

32 Endothelin-converting enzyme-1 (ECE-1) is a membrane-bound zinc-metallopeptidase that is

33 s shown that endothelin-converting enzyme-1 (ECE-1) is able to reduce amyloid beta content.

34 Endothelin-converting enzyme-1 (ECE-1) is the enzyme predominantly responsible for produ

35 Endothelin-converting enzyme-1 (ECE-1) processes big endothelin-1 (ET-1) to ET-1, a pept

36 ET converting enzyme-1 (ECE-1), however, is expressed preferentially in endothel

37 xpression of endothelin-converting enzyme-1 (ECE-1, the enzyme that converts precursor ET-1 to the ma

38 isoforms of endothelin-converting enzyme-1 (ECE-1a-d) are present in early endosomes, where they deg

39 In addition, ECE-1(-/-); ECE-2(-/-) double null embryos exhibited abnormal atriov

40 of mature ET-1 and ET-2 in whole ECE-1(-/-); ECE-2(-/-) embryos at E12.5 do not differ appreciably fr

41 ficant residual ET-1/ET-2 in the ECE-1(-/-); ECE-2(-/-) embryos indicates that proteases distinct fro

42 urthermore, these results implicate the ET-1/ECE-1/ERK1/2 pathway as a therapeutic target to treat pr

43 ght to demonstrate the distribution of the 2 ECE-1 isoforms in experimental atherosclerosis, to deter

44 Endothelin-converting enzyme-1 and -2 (ECE-1 and -2) are membrane-bound metalloproteases that c

45 Among them, endothelin-converting enzyme-2 (ECE-2) is a good candidate because it exhibits a neuroen

46 Endothelin-converting enzyme-2 (ECE-2), a member of M13 family of zinc metallopeptidases

47 Endothelin-converting enzyme-2 (ECE-2), which is expressed in neural tissues, cleaves 'b

48 lthough ECE-1 regulates both pools of Abeta, ECE-2 regulates mainly the intracellular pool of the pep

49 Hs <3 kDa may act as dual vasopeptidase (ACE/ECE) or as single ECE inhibitors with different antivaso

50 eporter assays indicated that E2F2 activates ECE-1b transcription.

51 o the plasma membrane, which required active ECE-1 and an intact Golgi.

52 hibit endothelin-converting enzyme activity (ECE) and decrease endothelin-1 synthesis.

53 In addition, ECE-1(-/-); ECE-2(-/-) double null embryos exhibited abn

54 Also, ECE-2 processes proenkephalin-derived bovine adrenal med

55 Although ECE-1 rapidly degraded SST-14, SST-28 was resistant to d

56 Although ECE-1 regulates both pools of Abeta, ECE-2 regulates mai

57 Although ECE-1 was once thought to be specific for the processing

58 nd beta-arrestins that were stabilized by an ECE-1 inhibitor.

59 However, when they are bred into an ECE-1-null background, defects in cardiac outflow struct

60 sk (i) does the intensity of stressors of an ECE vary across a landscape?

61 t work, we show that levels of both ET-1 and ECE-1 are increased in gestational tissues in E16.5 mice

62 mediated coexpression of both preproET-1 and ECE-1 in the embryonic myocardium induces myocytes to ex

63 cates that proteases distinct from ECE-1 and ECE-2 can carry out ET-1 activation in vivo.

64 for a physiological role for both ECE-1 and ECE-2 in limiting Abeta accumulation in the brain and al

65 tablished Abeta degrading enzymes, ECE-1 and ECE-2, we tested whether impairments in their catalytic

66 We show here that ETAR, ET-1, and ECE-1 are expressed and colocalize in murine dorsal root

67 ECE-1alpha and ECE-1beta immunoreactivity was present in the aortas of

68 ECE-1 exists in 2 isoforms (ECE-1alpha and ECE-1beta), the result of alternative splicing of a comm

69 e transmembrane metallopeptidases ECE-1c and ECE-1d.

70 fying protein 1 (RAMP1), beta-arrestin2, and ECE-1 to early endosomes, where ECE-1 degrades CGRP.

71 in and mRNA expressions of ET(A), ET(B), and ECE-1 were detected in retinal arterioles.

72 Thus, the primary function of betaARRs and ECE-1 in SP-dependent inflammatory signaling is to promo

73 lonic epithelial cells involves betaARRs and ECE-1, respectively.

74 Our results also indicate that betaARRs and ECE-1-dependent recycling regulate MAP kinase and NF-kap

75 tion, ET(A) receptor antagonism (BQ123), and ECE inhibition (phosphoramidon, SM19712) or by inhibitin

76 14, SST-28 was resistant to degradation, and ECE-1 did not degrade SST analogs.

77 Expression of preproET-1 mRNA and ECE-1 mRNA were increased in aged compared to young endo

78 receptors predominantly in smooth muscle and ECE-1 predominantly in endothelium and smooth muscle.

79 Therapeutic SST analogs are ECE-1-resistant and retain SSTR2A in endosomes, which ma

80 criticality of the system and the associated ECE enhancement.

81 outdoor air (n = 40 and 14, respectively) at ECE facilities in Northern California.

82 t evidence for a physiological role for both ECE-1 and ECE-2 in limiting Abeta accumulation in the br

83 Thus, both ECE-1 and betaARRs mediate the resensitization of NK1R C

84 Big endothelin-1 is activated by ECE-1, and mRNA levels of ECE-1b, the repressive ECE-1 i

85 After activation by ECE-1-resistant SST-28 and analogs, SSTR2A remains in en

86 cumulation in AD is unlikely to be caused by ECE-2 deficiency.

87 ut is hydrolyzed 10-fold more efficiently by ECE-1, making this substrate selective for ECE-1.

88 than 90% and their performance evaluated by ECE was satisfactory.

89 he-Lys(2, 4-dinitrophenyl), is hydrolyzed by ECE-1 with a k(cat)/K(m) value of 1.9 x 10(7) M(-1) s(-1

90 ly 10 of these 42 peptides were processed by ECE-2.

91 availability in endosomes, here regulated by ECE-1, controls beta-arrestin-dependent signaling of end

92 stin interactions that were not regulated by ECE-1.

93 e endosomal ERK pathway but is suppressed by ECE-1 inhibition or betaARR2 knockdown.

94 t carbon uptake of ecosystems is affected by ECEs under future elevated atmospheric CO2 concentration

95 e existence of Abeta clearance mechanisms by ECEs at intracellular sites of production.

96 dicate that 82-89% of children in California ECE had DBP exposure estimates exceeding reproductive he

97 me, populated by cardiac neural crest cells, ECE-1 expression is localized to the outermost ectoderma

98 This complex, {[ECE]Ni acetylide --> CuBr} contains both nickel and copp

99 Under these conditions, ECE inhibition produced significantly higher elevations

100 e that both water and N availability control ECE and the effects of future precipitation changes and

101 apy can help identify tumor sites and depict ECE and SVI with reasonable accuracy in patients with re

102 e, ECE-1a, -1c, and -1d), and to deregulated ECE-1 activity.

103 portant influence on children's development, ECE experiences have both short- and long-term impacts o

104 Here, we report direct ECE measurements performed on MPB tuned NBT-06BT bulk ce

105 nd long duration of action in vivo, the dual ECE-1 and neutral endopeptidase 24.11 (NEP) inhibitor, C

106 s of another signaling pathway (EDNRB, EDN3, ECE-1); and the transcription factor, SOX10, have been i

107 childhood years in early care and education (ECE) settings.

108 pend some time in early childhood education (ECE) facilities where they may be exposed to potentially

109 cooling, based on the electrocaloric effect (ECE), is a significant contender for efficient new solid

110 c coefficient and the electrocaloric effect (ECE), it was determined that a large ECE can be realized

111 display a pronounced electrocaloric effect (ECE).

112 e hamster ovary cells, which lack endogenous ECE activity, reduces extracellular Abeta concentration

113 and pharmacological inhibition of endogenous ECE activity, we found that ECEs participate in the degr

114 We show that treatment of endogenous ECE-expressing cell lines with the metalloprotease inhib

115 Thus, endosomal ECE-1 attenuates ERK2-mediated SP signaling in the nucle

116 We propose a mechanism by which endosomal ECE-1 degrades neuropeptides in endosomes to disrupt the

117 as evaluated by the Empirical cross entropy (ECE) approach.

118 us to mammalian endothelin-converting enzyme ECE-1.

119 Members of the endothelin-converting enzyme (ECE) family are considered good candidate enzymes becaus

120 prilysin (NEP)/endothelin-converting enzyme (ECE) family of metalloproteases contains a highly conser

121 novel putative endothelin-converting enzyme (ECE) has been cloned from hydra, a freshwater invertebra

122 bitors towards endothelin-converting enzyme (ECE), both LFHs <3 kDa exerted in vitro inhibitory effec

123 ceptors and of endothelin-converting enzyme (ECE)-1 in ET-1-induced vasomotor responses of single ret

124 orphism in the endothelin-converting enzyme (ECE)-1b promoter (-338C/A) that is strongly associated w

125 T(A), and the ET-specific converting enzyme, ECE-1, in the pharyngeal arches and great vessels of the

126 ient for ECE-1 and a closely related enzyme, ECE-2.

127 he well established Abeta degrading enzymes, ECE-1 and ECE-2, we tested whether impairments in their

128 d by caffeic acid, punicalagin, epicatechin, ECE and PPE during storage.

129 s confirmed an upregulation of the ET-1/ETAR/ECE-1/ERK1/2 axis in patients with chronic itch.

130 (NAO), particularly in East-Central Europe (ECE).

131 ncy and intensity of extreme climate events (ECEs).

132 o the importance of extreme climatic events (ECEs) in determining changes in species populations.

133 Extreme climatic events (ECEs) such as droughts and heat waves are predicted to i

134 We have examined ECE-2 expression in the temporal cortex of brain tissue

135 gnificant effects on ecosystem CO2 exchange (ECE), which includes net ecosystem productivity (NEP), e

136 ation of myocardial extracellular expansion (ECE), which has been related to interstitial fibrosis in

137 oprenoid precursors in cell lines expressing ECE-1.

138 rs hypothesize that extracapsular extension (ECE) of the SN metastasis is highly predictive of NSN tu

139 the likelihoods of extracapsular extension (ECE), seminal vesicle invasion (SVI), and adjacent organ

140 SM negative) and no extracapsular extension (ECE).

141 Finally, ECE-2 processes PEN-LEN, an endogenous inhibitor of proh

142 The first [ECE]Ni(II) pincer complexes with E = Si(II) and E = Ge(I

143 a levels in the brains of mice deficient for ECE-1 and a closely related enzyme, ECE-2.

144 e most sensitive substrate yet described for ECE-1.

145 ts are consistent with an important role for ECE-2 in the processing of regulatory peptides at noncla

146 y ECE-1, making this substrate selective for ECE-1.

147 high affinity and exhibited specificity for ECE-2 compared to neprilysin.

148 bryos indicates that proteases distinct from ECE-1 and ECE-2 can carry out ET-1 activation in vivo.

149 Furthermore, ECE-2 was detected in autophagic vesicles in cells treat

150 Greater ECE is associated with reduced LV end-diastolic volume i

151 In addition, greater ECE is associated with reduced circumferential shortenin

152 n fraction in women, whereas in men, greater ECE is associated with greater LV dysfunction manifested

153 er postcontrast T1 times, reflecting greater ECE, were associated with lower circumferential shorteni

154 In the developing mouse heart, ECE-2 mRNA is expressed in the endocardial cushion mesen

155 Some of the highest ECE performances reported are found in compounds close t

156 However, ECE-2 expression is up-regulated, perhaps to minimize Ab

157 trongly resembles a prenylation motif, human ECE-1 did not appear to be prenylated when labeled in vi

158 strate that a CpG-CA repeat within the human ECE-1c promoter is highly polymorphic, harbors transcrip

159 This is the first study to identify ECE-1 as a target for APA, a regulatory mechanism aberra

160 levels of the membranous ECE-1 isoforms (ie, ECE-1a, -1c, and -1d), and to deregulated ECE-1 activity

161 Alterations in ECE activity may be considered as a cause for increased

162 r downregulation of E2F2 led to a decline in ECE-1b levels, to higher levels of the membranous ECE-1

163 ic Abeta(1-42) caused an initial decrease in ECE-2 mRNA at 4 hours, but a marked increase by 24 hours

164 ) The quality of adult-child interactions in ECE settings is the most potent source of variation in c

165 served cysteine residue of the CXAW motif in ECE-1, Cys(755), is critical for proper folding of the e

166 nt, we have now generated a null mutation in ECE-2 by homologous recombination.

167 r valve formation, a phenotype never seen in ECE-1 single knockout embryos.

168 structures become more severe than those in ECE-1 single knockout embryos.

169 h arteries, and the cardiac outflow tract in ECE-1 knockout mice.

170 e intent of reconstructing past variation in ECE hydroclimate and examine NAO impacts on winter preci

171 ue to ECE-1 mRNA stabilization and increased ECE-1 expression in stellate cells, which in turn was a

172 How water and N availability influence ECE in arid and semiarid grasslands is still uncertain.

173 coring compounds three were found to inhibit ECE-2 with high affinity and exhibited specificity for E

174 sociation with augmented cGMP, would inhibit ECE-1 conversion of big ET-1 to active ET-1, thus reduci

175 bitory effects on ECE activity and inhibited ECE-dependent vasoconstriction.

176 Superoxide inhibits ECE but hydrogen peroxide and nitric oxide do not.

177 Superoxide inhibits ECE by ejecting zinc from the enzyme, and the addition o

178 Although additional gains in intrinsic ECE-1 inhibitory potency could occasionally be achieved

179 ECE-1 exists in 2 isoforms (ECE-1alpha and ECE-1beta), the result of alternative spl

180 o synthesis of the identified 56- and 62-kDa ECE-1 3' UTR mRNA binding proteins.

181 demonstrate up-regulation of 56- and 62-kDa ECE-1 3'-untranslated region (UTR) mRNA binding proteins

182 transition and minimized hysteresis, a large ECE becomes accessible with high cooling efficiency over

183 effect (ECE), it was determined that a large ECE can be realized in the ferroelectric poly(vinylidene

184 ir (0.45, 0.52, and 0.47 for tumor location, ECE, and SVI, respectively).

185 oprecipitation), and repressed E2F2-mediated ECE-1b promoter activity (promoter-reporter assays).

186 b levels, to higher levels of the membranous ECE-1 isoforms (ie, ECE-1a, -1c, and -1d), and to deregu

187 nd 2 and the transmembrane metallopeptidases ECE-1c and ECE-1d.

188 w that human and chimpanzee [CpG](m)-[CA](n) ECE-1c promoter repeats are genetically and functionally

189 50) = 22 nM) and selective (104-fold vs NEP) ECE-1 inhibition.

190 a subset of patients with SM negative and no ECE (n = 10,870).

191 with resected LAHNC with SM negative and no ECE is common.

192 with resected LAHNC with SM negative and no ECE, 47% received adjuvant CRT.

193 ation of receptors for peptides that are not ECE-1 substrates (e.g., angiotensin II), or the recyclin

194 e significantly associated with detection of ECE in both groups of readers (P <.05).

195 are significant predictors for detection of ECE when MR images are interpreted by genitourinary radi

196 ging in tumor detection and determination of ECE and SVI.

197 The mechanisms regulating the expression of ECE-1 in cancer cells are poorly understood, hampering t

198 e we provide evidence that the expression of ECE-1 is markedly inhibited by its 3'UTR, and that alter

199 These results suggest that expression of ECE-1 plays a key role in defining an active site of ET

200 cursor peptides, and increased expression of ECE-1.

201 in contrast to the endocardial expression of ECE-1.

202 The frontiers of ECE research are addressing individual differences in ch

203 A major in vivo function of ECE-1 is the proteolytic conversion of big endothelin-1

204 ntifying the short- and long-term impacts of ECE experiences has a long history, the results of which

205 his study, producing sustained inhibition of ECE-1 activity in rats, as measured by their ability to

206 Inhibition of ECE-1 by NEP-I represents a novel approach to interrupti

207 We further showed that a similar level of ECE near room temperature can be achieved by working wit

208 Elevated levels of ECE-1 have been observed in a range of malignancies, wit

209 -1 is activated by ECE-1, and mRNA levels of ECE-1b, the repressive ECE-1 isoform, were significantly

210 Likelihood of ECE described in MR imaging reports was compared with cl

211 The likelihood of ECE was scored retrospectively on the basis of MR imagin

212 a three-dimensional (3D) molecular model of ECE-2 using the crystal structure of neprilysin (EC 3.4.

213 Furthermore, we show that overexpression of ECE-1 in Chinese hamster ovary cells, which lack endogen

214 The AUC values for prediction of ECE were 0.87 (95% CI: 0.80, 0.94) for reader 1 and 0.76

215 s add incremental value in the prediction of ECE.

216 nd P <.001, respectively) were predictors of ECE.

217 enylation (APA) results in the production of ECE-1 transcripts with truncated 3'UTRs which promote el

218 thereby simplifying both the purification of ECE-1 and the characterization of its inhibitors.

219 re vulnerable to variation in the quality of ECE settings than do other children.

220 ex-associated differences in the relation of ECE to left ventricular (LV) remodeling and myocardial s

221 ogical tools useful in assessing the role of ECE-1 in pathological conditions.

222 To examine the role of ECE-2 in cardiovascular development, we have now generat

223 new useful tool to probe the active site of ECE-2 and design additional selective inhibitors of this

224 To characterize the substrate specificity of ECE-2, we used mass spectrometry with a panel of 42 pept

225 ated knowledge gained from recent studies of ECE-1 substrate specificity to aid the design of interna

226 that is related to but distinct from that of ECE-1.

227 12.5 do not differ appreciably from those of ECE-1(-/-) embryos.

228 is the first study to examine the effects of ECEs at the site level across all life stages of a butte

229 This study examined the impact of ECEs on the resident UK butterfly species (n = 41) over

230 ok distribution patterns when the passage of ECEs is most likely to occur from 2012 to 2016 using pas

231 ation level effects following the passage of ECEs.

232 3 kDa exerted in vitro inhibitory effects on ECE activity and inhibited ECE-dependent vasoconstrictio

233 Both exerted in vitro inhibitory effects on ECE activity.

234 and N was conducted to test their effects on ECE in a semiarid temperate steppe of northern China for

235 ition, had significantly positive effects on ECE in years when the natural precipitation was normal o

236 erted non-significant or negative effects on ECE when precipitation was low but switched to a positiv

237 However, only ECE of the SN metastasis was associated with NSN tumor i

238 ined (stage pT2) disease; 29 (18%) patients, ECE (stage pT3a); two (1%) patients, SVI (stage pT3b); a

239 ther, our data identify the neural peptidase ECE-1 as a negative regulator of itch on sensory nerves

240 s substantially augmented by pharmacological ECE-1 inhibition and abrogated by treatment with an ERK1

241 )' and P(2)' positions were also very potent ECE-1 inhibitors, albeit lacking the desired selectivity

242 ocalized to a CC-rich region in the proximal ECE-1 3' UTR base pairs (the 56-kDa protein) and to a re

243 Purified ECE-2 efficiently processes big endothelin-1 to endothel

244 1, and mRNA levels of ECE-1b, the repressive ECE-1 isoform, were significantly lower in E2F2(-/-) mic

245 s and recycles via the Golgi, which requires ECE-1 degradation of SST-14 and receptor dissociation fr

246 Consistent with this result, ECE-2 was found to co-localize with markers of the endos

247 group led to more potent and more selective ECE-1 inhibitors, such as the tetrazole 27.

248 stochemistry with specific antibodies showed ECE-2 to be abundant within pyramidal neurons in both th

249 Quantitative real-time PCR showed ECE-2 mRNA to be markedly elevated in AD but not in vasc

250 SP and destabilizing endosomal signalosomes, ECE-1 has a dual role in controlling endocytic signallin

251 as dual vasopeptidase (ACE/ECE) or as single ECE inhibitors with different antivasoconstrictor effect

252 Finally, we show that recombinant soluble ECE-1 is capable of hydrolyzing synthetic Abeta40 and Ab

253 idues around the cleavage site revealed that ECE-2 exhibits a unique cleavage site selectivity that i

254 These studies suggest that ECE-1 is present and functionally active in the vascular

255 on of endogenous ECE activity, we found that ECEs participate in the degradation of at least two dist

256 ECE but also enhances its recovery after the ECE, as mediated by increases of root growth and plant n

257 itation assays confirmed that E2F2 binds the ECE-1b promoter, and promoter-reporter assays indicated

258 on over 20 minutes, which was blocked by the ECE-1 inhibitor phosphoramidon.

259 wth and plant nitrogen uptake induced by the ECE.

260 ecline of ecosystem carbon uptake during the ECE but also enhances its recovery after the ECE, as med

261 , these data support a critical role for the ECE-1/ET-1 system in inflammation-associated premature d

262 there are three major copies of "CYC" in the ECE clade, and that duplications leading to these copies

263 region between 60 and 193 base pairs in the ECE-1 3' UTR mRNA (62 kDa).

264 The significant residual ET-1/ET-2 in the ECE-1(-/-); ECE-2(-/-) embryos indicates that proteases

265 The increase in Abeta levels in the ECE-deficient mice provides the first direct evidence fo

266 coimmunoprecipitated with E2F2, occupied the ECE-1b promoter (chromatin immunoprecipitation), and rep

267 Abolition of the ECE-1 APA sites reduced protein expression from a report

268 re delivery by antagonizing or silencing the ECE-1/ET-1 system offers a novel approach to an unmet cl

269 erated quinone of fluorone black (1) via the ECE mechanism is reported.

270 yOH under acidic conditions proceeds via the ECE mechanism to a diquinonepyrene, which shows reversib

271 Pretreatment of NCM460 cells with the ECE-1 inhibitor SM19712 or gene silencing of betaARR1 or

272 etic placement of major duplications in the "ECE" (CYC/TB1) clade of TCP transcription factors.

273 ructural features, DFT calculations of the {[ECE]Ni acetylide --> CuBr} intermediates revealed an unu

274 PYFGY) were chemically synthesized and their ECE-inhibitory activity was tested.

275 This effect was due to ECE-1 mRNA stabilization and increased ECE-1 expression

276 d the hepatic wound healing response lead to ECE-1 mRNA stabilization in stellate cells via binding o

277 information about the mechanisms leading to ECE-1 overexpression in malignant cells.

278 rafficked by a dynamin-mediated mechanism to ECE-1-containing early endosomes, where ECE-1 can degrad

279 that S. parasanguis PepO is more similar to ECE-1 than to NEP.

280 istory traits play in species sensitivity to ECEs.

281 ile species influence their vulnerability to ECEs?

282 ransfer-chemical reaction-electron transfer (ECE) mechanism to generate new chemical species that are

283 ECE-2, unlike ECE-1, exhibits restricted neuroendocrine distribution a

284 Endogenous production of ET-1 from vascular ECE-1 is sufficient to evoke ET(A) receptor-dependent co

285 mponent of the endothelin system, vertebrate ECE functions in the activation of endothelin (ET) pepti

286 on plasma cGMP concentrations, vascular wall ECE-1 activity, and ET-1 concentration, and to correlate

287 etaARRs deliver the SP-NK1R endosomes, where ECE-1 associates with the complex, degrades SP, and allo

288 m to ECE-1-containing early endosomes, where ECE-1 can degrade SP.

289 restin2, and ECE-1 to early endosomes, where ECE-1 degrades CGRP.

290 tivation in the cytosol and nucleus, whereas ECE-1 overexpression attenuated ERK2 activation.

291 RAMP1 recycling and resensitization, whereas ECE-1 overexpression has the opposite effect.

292 Levels of mature ET-1 and ET-2 in whole ECE-1(-/-); ECE-2(-/-) embryos at E12.5 do not differ ap

293 analysis, all variables were associated with ECE.

294 nalization of SSTR2A, which colocalized with ECE-1 in endosomes and the Golgi.

295 y hydrodynamic transfection of E15 mice with ECE-1 RNAi.

296 All patients with ECE of the SN metastasis should undergo mandatory comple

297 Patients with ECE of the SN metastasis were more likely to have NSN tu

298 ignificantly more negative associations with ECEs than specialists.

299 ET-1 induced internalization of ETAR within ECE-1-containing endosomes.

300 f tumor-involved nodes than patients without ECE of the SN metastasis.