ライフサイエンスコーパス: ACE2

1 an receptor angiotensin-converting enzyme 2 (ACE2).

2 ARS) CoV is angiotensin-converting enzyme 2 (ACE2).

3 t receptor, angiotensin-converting enzyme 2 (ACE2).

4 s with either human (hACE2) or civet (cACE2) ACE2.

5 oronavirus isolated from bats appears to use ACE2.

6 h TMPRSS2-mediated proteolysis of both S and ACE2.

7 gely because of a "virus-binding hotspot" on ACE2.

8 nuous receptor-binding motifs (RBMs) to bind ACE2.

9 or-binding domain (RBD) complexed with human ACE2.

10 SARS-CoV spike (S) protein and its receptor ACE2.

11 ation by Ace2 and asymmetric distribution of Ace2.

12 ruct has the same receptor activity as civet ACE2.

13 nimal level of synergy between DC/L-SIGN and ACE2.

14 ralizing antibodies capable of out-competing ACE2.

15 affinities between their RBDs and the mouse ACE2.

16 try by inhibiting the repressor functions of Ace2.

17 HO is normally activated by Swi5 but not by Ace2.

18 Both ace2Delta and ace2-35 show defects in cell separation, and both can re

19 SIN mutant sid2-250, we isolated a mutation, ace2-35, in the transcription factor Ace2p.

20 very of the angiotensin-converting enzyme 2 (ACE2), a protective axis of RAS namely ACE2/Ang-(1-7)/Ma

21 near the start of mitosis, here we show that Ace2 accumulates in the nucleus and binds DNA about 10 m

22 We show that in the rts1 mutant, Ace2 accumulation in mother cells results in Ash1 expres

23 Our work suggests that the precise timing of Ace2 accumulation in the nucleus involves both a nuclear

24 growth is accomplished by enzymes encoded by Ace2 activated genes expressed in G(1).

25 ACE2 expression was lower, and ACE2 activators xanthenone and diminazine aceturate were

26 the development of hypertension and restored ACE2 activity and baroreflex function.

27 sfunction, as well as decreased hypothalamic ACE2 activity and expression, although these changes wer

28 mal tubules and cortical collecting tubules, ACE2 activity had a strong positive correlation with ACE

29 ACE2 activity in renal cortex correlated positively with

30 We also observed an increase in ACE2 activity in the cerebrospinal fluid of hypertensive

31 ivity in the brain paralleled an increase in ACE2 activity in the cerebrospinal fluid of nontransgeni

32 for the concurrent determination of ACE and ACE2 activity in tissue samples.

33 Soluble ACE2 activity is increased in patients with HF and corre

34 assay for concurrent measurement of ACE and ACE2 activity should be helpful in the evaluation of kid

35 In renal cortex, ACE2 activity was increased in both models of diabetes (

36 ibed in experimental models of diabetes, but ACE2 activity was not assessed in previous studies.

37 Whereas loss of ACE2 activity worsens liver fibrosis in chronic liver in

38 infected with an adenovirus expressing human ACE2 (Ad-hACE2-eGFP) or the control virus (Ad-eGFP) via

39 f a diploid reference strain with two mutant ace2 alleles led to complete reconstruction of the multi

40 However, ACE2 also converts AngI to Ang1-9, a poorly characterise

41 ssary for both transcriptional activation by Ace2 and asymmetric distribution of Ace2.

42 metazoan hippo signaling pathways, activates Ace2 and drives its accumulation in daughter cell nuclei

43 We show that convergent regulation of Ace2 and Efg1 defines the transcriptional program of cel

44 Apelin is a second catalytic substrate for ACE2 and functions as an inotropic and cardioprotective

45 show that generation of angiotensin-(1-7) by ACE2 and its binding to the Mas receptor (MasR) improves

46 a highlight the compensatory role of central ACE2 and its potential benefits as a therapeutic target

47 Levels of ACE2 and MasR were increased in splanchnic vessels from

48 a downstream component of the regulation of Ace2 and morphogenesis (RAM) signaling network.

49 rthologue and component of the Regulation of Ace2 and Morphogenesis signaling network.

50 Ace2 and Swi5 also showed differences in prevalence duri

51 Ace2 and Swi5 are cell cycle-regulated transcription fac

52 Yeast Ace2 and Swi5 are such activators, with targets we class

53 Ace2 and Swi5 both bind in vitro to Swi5-only genes such

54 In contrast, Ace2 and Swi5 both bind in vivo to Ace2-only genes, such

55 d we recently showed that phosphorylation of Ace2 and Swi5 is altered in an rts1 mutant.

56 Here we examine expression of Ace2 and Swi5 target genes and find that an rts1 mutatio

57 arallels in the cell cycle regulation of the Ace2 and Swi5 transcription factors.

58 s that all Ace2-only genes are bound by both Ace2 and Swi5, and also by Fkh1/2.

59 proteins serve as receptors independently of ACE2 and that there is a minimal level of synergy betwee

60 ACE2 and TMPRSS2 colocalized on cell surfaces and enhanc

61 ion of angiotensin-converting enzyme type 2 (ACE2) and an increase in a disintegrin and metalloprotea

62 Angiotensin-converting enzyme 2 (ACE2) and its product, angiotensin 1-7 (Ang-[1-7]), are

63 ractions with two virus-binding hot spots on ACE2, and by doing so, they enhance viral interactions w

64 Levels of Swi5, Ace2, and the SCF(Grr1) targets Cln1 and Cln2 are elevat

65 The autocrine regulation of the AngII/AT1-ACE2-Ang(1-7)/Mas axis upon adipogenesis has also been r

66 ptidase A-Ang III-Ang II type 2 receptor and ACE2-Ang-(1 to 7)-Mas receptor arms, paving the way for

67 ept study suggests that activation of ocular ACE2/Ang-(1-7)/Mas axis with AAV gene transfer modulates

68 me 2 (ACE2), a protective axis of RAS namely ACE2/Ang-(1-7)/Mas that counteracts the deleterious ACE/

69 Thus, ACE2/Ang-(1-7)\Mas pathway activation corrects existing

70 system, the angiotensin-converting enzyme 2 (ACE2)/angiotensin-(1-7) [Ang-(1-7)]/Mas receptor axis, c

71 adding a conceptual framework for the apelin-ACE2-angiotensin 1-7 axis as a therapeutic target for ca

72 diator of beneficial effects ascribed to the ACE2/angiotensin-(1-7)/MasR axis.

73 and rats with cirrhosis, increased levels of ACE2 appear to increase production of Ang-(1-7), which l

74 ome duplication and a frameshift mutation in ACE2 are sufficient to generate a fast-sedimenting, mult

75 ding angiotensin-converting enzymes (Ace and Ace2) are essential for heart function regulation.

76 These findings identify ACE2 as a novel target for the prevention of beta-cell d

77 ty studies indicated that this virus can use ACE2 as a receptor and infect animal and human cell line

78 fusions to identify the N-terminal region of Ace2 as responsible for the delay, and this same region

79 mass spectrometry-based assay, we identified ACE2 as the main enzyme converting angiotensin II into a

80 cycle and requires the transcription factor Ace2 as well as all RAM network components.

81 nown to use angiotensin-converting enzyme 2 (ACE2) as its receptor.

82 us utilizes angiotensin-converting enzyme 2 (ACE2) as the primary receptor.

83 artmentalization of the nucleoplasm promoted Ace2 asymmetry in anaphase nuclei.

84 We show that Ace2 asymmetry is initiated in the elongated, but undivi

85 Treatment with recombinant ACE2 attenuated experimental fibrosis in the course of c

86 In this study a chimeric ACE2 bearing the critical N-terminal helix from civet an

87 mutations in the spike protein on 80R versus ACE2 binding, including escape mutants, which should fac

88 699, which are distinct from residues of the ACE2-binding domain (amino acids 318 to 510).

89 rotruding beta6-beta7 loop with two putative ACE2-binding hotspot residues (Ile-489 and Tyr-491).

90 cell entry, angiotensin-converting enzyme 2 (ACE2), but it is largely unclear whether ACE2 interactio

91 We hypothesize that control of Ace2 by PP2A(Rts1) plays a role in mechanisms that link

92 1) phosphorylation of CDK consensus sites in Ace2 by the G1 CDKs Pho85 and Cdc28/CDK1 and 2) an unkno

93 Once exported, Ace2 cannot re-enter nuclei for the remainder of the cel

94 generated an adenovirus expressing the human ACE2 cDNA upstream of an enhanced green fluorescent prot

95 ACE2 co-localized with glomerular epithelial cell (podoc

96 that ADAM17-mediated shedding impairs brain ACE2 compensatory activity, thus contributing to the dev

97 ce infected with the wild-type or Deltaace2::ace2-complemented strains.

98 addition, crystal structures of the chimeric ACE2 complexed with RBDs from various human and civet SA

99 h a previously determined structure of human ACE2 complexed with the RBD from a human SARS-CoV strain

100 D8 and D22 virus RBDs contained mutations in ACE2 contact residues, Y442F and L472F, that remodeled S

101 We hypothesized that ACE2 could play a pivotal role in the central regulation

102 These data demonstrate that ACE2 couples the RAS to the apelin system, adding a conc

103 Moreover, ACE2 deficiency aggravated RSV-associated disease pathog

104 On the C57BL/6 background, ACE2 deficiency was associated with a modest increase in

105 nd normal cardiac dimensions and function in ACE2-deficient animals with mixed or inbred genetic back

106 of Ang II increased almost 3-fold higher in ACE2-deficient mice than in controls.

107 d pressures were substantially higher in the ACE2-deficient mice than in WT.

108 ACE2-deficient mice were viable, fertile, and lacked any

109 We also observed an ACE2-dependent increase in Ang-(1-7) production.

110 on cohort: untreated diabetic, 24.2 +/- 6.7; ACE2 diabetic, 2.5 +/- 1.6 per mm(2); reversal cohort: u

111 al cohort: untreated diabetic, 56.8 +/- 5.2; ACE2 diabetic, 5.6 +/- 2.3 per mm(2)).

112 on cohort: untreated diabetic, 11.3 +/- 1.4; ACE2 diabetic, 6.4 +/- 0.9 per mm(2)) and partially reve

113 al cohort: untreated diabetic, 15.7 +/- 1.9; ACE2 diabetic, 6.5 +/- 1.2 per mm(2)) the diabetes-assoc

114 Loss of ACE2 disrupts the balance of the renin-angiotensin syste

115 rtension showed marked ACE up-regulation and ACE2 down-regulation in both hypertensive cardiopathy an

116 denovirus was able to abolish Ang II-induced ACE2 down-regulation in human kidney tubular cells.

117 Recombinant human ACE2 effectively metabolized Ang-(1-10) and Ang II into

118 poral regulation of the transcription factor Ace2 ensures that it acts only once in a cell's lifetime

119 We hypothesize that loss of ACE2 exacerbates cardiovascular complications induced by

120 several groups have reported decreased brain ACE2 expression and activity during the development of h

121 In addition, reduction of ACE2 expression and activity in the brain paralleled an

122 cities of infection), exhibit dose-dependent ACE2 expression and activity.

123 Our studies demonstrated that increased ACE2 expression exerts protective effects on inflammatio

124 Alterations in renal ACE and ACE2 expression have been described in experimental mode

125 2 promoter activity in vitro and upregulated ACE2 expression in failing hearts in vivo.

126 ude that in renal cortex from diabetic mice, ACE2 expression is increased at the posttranscriptional

127 ere, we show that, although endogenous islet ACE2 expression is sparse, its inhibition abrogates angi

128 is able to up-regulate ACE and down-regulate ACE2 expression levels under hypertensive conditions bot

129 ACE2 expression was lower, and ACE2 activators xanthenon

130 The inhibition of ACE2 expression was shown to be associated with ACE up-r

131 Ace and repress Ace2, tipping the balance to Ace2 expression with enhanced angiotensin II production,

132 on of the significance of reduced glomerular ACE2 expression, db/db mice were treated for 16 wk with

133 key mechanism by which Ang II down-regulates ACE2 expression, implicating an ACE/ACE2 imbalance in hy

134 Angiotensin-converting enzyme 2 (ACE2) expression has been shown to be altered in renal t

135 Cardiac stress enhances Ace, but suppresses Ace2, expression in the heart, leading to a net producti

136 noclonal antibody, m396, which competes with ACE2 for binding to RBD, and determined the crystal stru

137 oonotic SARS-CoV was completely dependent on ACE2 for entry.

138 require the ancillary protein collectrin or ACE2 for plasma membrane expression.

139 ibodies competed with the SARS-CoV receptor, ACE2, for binding to the receptor-binding domain (RBD),

140 residues of angiotensin-converting enzyme 2 (ACE2) from its homologue ACE, which is not possible via

141 DK phosphorylations that block both Cbk1 and Ace2 function.

142 s of recurrent positive selection in the bat ACE2 gene map almost perfectly to known SARS-CoV interac

143 nerated mice with targeted disruption of the Ace2 gene.

144 Delta19) or reduce binding to soluble human ACE2 (hACE2).

145 se in blood pressure, whereas the absence of ACE2 had no effect on baseline blood pressures in 129/Sv

146 ace1 encodes the synaptic enzyme and ace2 has other essential actions in many insect species,

147 Angiotensin-converting-enzyme-2 (ACE2) has been described as a crucial enzymatic player i

148 ion of angiotensin-converting enzyme type 2 (ACE2) has been shown to be beneficial in reducing hypert

149 giotensin-converting-enzyme 1 (ACE1), termed ACE2, has been identified that appears to be a negative

150 r SARS-CoV, angiotensin converting enzyme 2 (ACE2); (ii) SSAA09E1 {[(Z)-1-thiophen-2-ylethylideneamin

151 egulates ACE2 expression, implicating an ACE/ACE2 imbalance in hypertensive cardiovascular and renal

152 ACE2 immunoprecipitation captured transmembrane protease

153 of ACE2 in the liver, to define the role of ACE2 in acute and chronic liver disease, and to characte

154 Diabetic state was associated with increased ACE2 in Akita mice, whereas additional loss of ACE2 in t

155 ardiovascular function; however, the role of ACE2 in blood pressure regulation remains unclear becaus

156 as able to up-regulate ACE and down-regulate ACE2 in human kidney tubular cells, which were blocked b

157 transgenic and syn-hACE2 mice overexpressing ACE2 in neurons.

158 We studied the role of ACE2 in obesity-mediated cardiac dysfunction.

159 In this review, we focus on ACE2 in relation to pulmonary hypertension and provide p

160 Disrupting the transcription factor ACE2 in Saccharomyces cerevisiae prevents mother-daughte

161 shedding results in decreased membrane-bound ACE2 in the brain, thus promoting the development of neu

162 ze the long-term effects of gene deletion of ACE2 in the liver, to define the role of ACE2 in acute a

163 E2 in Akita mice, whereas additional loss of ACE2 in these mice leads to increased plasma and tissue

164 ffect of enhancing the enzymatic activity of ACE2 in vitro.

165 es that the SCV entry may not be mediated by ACE2-induced conformational changes in the RBD but may i

166 The finding that chronic ACE2 inhibition increases UAE suggests that ACE2, likely

167 mice and the effect of chronic pharmacologic ACE2 inhibition.

168 nted the increase in UAE associated with the ACE2 inhibitor (161 +/- 56; P < 0.05).

169 mice were treated for 16 wk with a specific ACE2 inhibitor (MLN-4760) alone or combined with telmisa

170 eneficial effects were abolished by C-16, an ACE2 inhibitor.

171 that involves interference with the SARS-CoV-ACE2 interaction.

172 2 (ACE2), but it is largely unclear whether ACE2 interactions are sufficient to allow HCoV-NL63 bind

173 Our data suggest that ACE2 is a functional component of the renin-angiotensin

174 ACE2 is a key negative regulator of the RAS and function

175 ng RSV-induced lung injury, and suggest that ACE2 is a promising potential therapeutic target in the

176 ACE2 is abundantly expressed in the lung tissue and emer

177 Incidentally, ACE2 is also used by group II SARS coronavirus (SARS-CoV

178 One of the genes activated by Ace2 is ASH1, a protein that normally accumulates mostly

179 ce2 levels throughout the cell cycle suggest Ace2 is exported from the nucleus.

180 ssue sampling, little is known about whether ACE2 is involved in the pathophysiology of HF in humans.

181 Therefore, Ace2 is not only a downstream target of Cbk1 but also re

182 However, in an rts1 mutant, Ace2 is present in both mother and daughter cells.

183 dy explored the signaling mechanism by which ACE2 is regulated under hypertensive conditions.

184 Angiotensin-converting enzyme-2 (ACE2) is a negative regulator of the renin-angiotensin s

185 Angiotensin converting enzyme 2 (ACE2) is a negative regulator of the renin-angiotensin s

186 Angiotensin-converting enzyme 2 (ACE2) is an integral membrane protein that antagonizes t

187 , and generated double-mutant mice using the ACE2 knockout (KO) mice (Akita/ACE2(-/y)).

188 Ace2 knockout (KO) mice and wild-type (wt) littermates u

189 protein(-1) . h(-1)) was examined in ACE and ACE2 knockout mice and in two rodent models of diabetes,

190 Ace2 KO mice showed increased liver fibrosis following b

191 One-year-old ace2 KO mice spontaneously developed an inflammatory cel

192 In contrast, ace2 KO mice subjected to acute liver injury models did

193 nsin metabolites in the kidney and plasma of ACE2 KO mice surprisingly revealed an increase in Ang-(1

194 ent also increased cardiac contractility and ACE2 levels in AT1R-deficient mice.

195 d soon after nuclear entry, whereas constant Ace2 levels throughout the cell cycle suggest Ace2 is ex

196 ells, and loss of Grr1 causes an increase in Ace2 levels.

197 tant mice, which was accompanied by restored ACE2 levels.

198 12 proteins, including 3 new markers of IM (ACE2, LGALS4, AKR1B10) and 3 of SPEM (OLFM4, LYZ, DPCR1)

199 ACE2 inhibition increases UAE suggests that ACE2, likely by modulating the levels of glomerular angi

200 te glycemic control had higher expression of ACE2/Mas mRNA than patients with diabetes with microvasc

201 blockade by D-Ala(7)-Ang-(1-7) prevented the ACE2-mediated improvements in intraperitoneal glucose to

202 ptors or as enhancer factors that facilitate ACE2-mediated virus infection.

203 The ACE homologue ACE2 metabolises AngII to Ang1-7, decreasing AngII and i

204 trol mice (r = 0.621, P < 0.05) but not with ACE2 mRNA (r = -0.468 and r = -0.522, respectively).

205 ime PCR and immunohistochemistry showed that ACE2 mRNA and protein expression levels were high, where

206 Introduction of the two ace2 mutant alleles into the haploid parental strain led

207 t is significantly restored by an additional ace2 mutation, a surprising result because HO is normall

208 The nature of the ace2 mutations and their occurrence in two independent e

209 eart disease associated with obesity wherein ACE2 negatively regulates obesity-induced EAT inflammati

210 ders; angiotensin (Ang)-converting enzyme 2 (ACE2) negatively regulates RAS by metabolizing Ang II in

211 Ace2 normally accumulates only in daughter cells, and on

212 ACE2 null (ACE2KO) and wild-type (WT) mice were fed a hi

213 pression of angiotensin-converting enzyme 2 (ACE2) on cells previously resistant to HCoV-NL63 renders

214 Global analysis shows that all Ace2-only genes are bound by both Ace2 and Swi5, and als

215 d by either Ace2 or Swi5 can be converted to Ace2-only genes by the insertion of Fkh-binding sites.

216 contrast, Ace2 and Swi5 both bind in vivo to Ace2-only genes, such as CTS1, but promoter-bound Swi5 f

217 tors, with targets we classify as Swi5-only, Ace2-only, or both.

218 Genes normally activated by either Ace2 or Swi5 can be converted to Ace2-only genes by the

219 does not affect interactions of SARS-S with ACE2 or the enzymatic functions of cathepsin L but preve

220 Brain-targeted ACE2 overexpression attenuated the development of neurog

221 ACE2 overexpression attenuates the development of neurog

222 Furthermore, subfornical organ-targeted ACE2 overexpression dramatically reduced the Ang II-medi

223 ACE2 overexpression had no effect on insulin sensitivity

224 These data suggest that ACE2 overexpression in the subfornical organ impairs Ang

225 ACE2 overexpression resulted in increased NOS and NO lev

226 Interestingly, ACE2 overexpression was associated with downregulation o

227 This prevention of hypertension by ACE2 overexpression was reversed by blockade of the Ang-

228 These findings demonstrate that ACE2 plays a critical role in preventing RSV-induced lun

229 In conclusion, ACE2 plays a novel role in heart disease associated with

230 Taken together, our results show that ACE2 plays a pivotal role in the central regulation of b

231 Overexpression of ACE2 prevented (prevention cohort: untreated diabetic, 1

232 verexpression of adenoassociated virus (AAV)-ACE2 prevents or reverses diabetic retinopathy.

233 a activation of its receptor, APJ, increased ACE2 promoter activity in vitro and upregulated ACE2 exp

234 and FoxM1 form a protein complex on Ace and Ace2 promoters to concurrently activate Ace and repress

235 report that angiotensin-converting enzyme-2 (ACE2) protected against severe lung injury induced by RS

236 -NL63 renders them susceptible, showing that ACE2 protein acts as a functional receptor and that its

237 Furthermore, administration of a recombinant ACE2 protein alleviated the severity of RSV-induced lung

238 ivity had a strong positive correlation with ACE2 protein expression (90-kDa band) in both knockout m

239 cted expression or selective scission of the ACE2 protein had no measurable effect on virus adhesion.

240 y in renal cortex correlated positively with ACE2 protein in db/db and db/m mice (r = 0.666, P < 0.00

241 Here, we show that the ACE2 protein is required for viral entry but that it is

242 ACE2 protein was proposed as a receptor for HCoV-NL63 al

243 d an endothelial mechanism of modulating Ace/Ace2 ratio for heart failure therapy.

244 ssion levels correlate strongly with the ACE/ACE2 ratio, suggesting a conserved mechanism.

245 -S, MBL did not affect interactions with the ACE2 receptor or cathepsin L-mediated activation of SARS

246 me animals experienced downregulation of the ACE2 receptor.

247 s the human angiotensin-converting enzyme 2 (ACE2) receptor for cellular entry, no coronavirus isolat

248 f the mouse angiotensin-converting enzyme 2 (ACE2) receptor not only in MA15 but also in two addition

249 or RBMs; yet the 2 viruses recognize common ACE2 regions, largely because of a "virus-binding hotspo

250 We find that Sfg1 represses early G(1), Swi5/Ace2-regulated genes involved in mother-daughter cell se

251 ptor human angiotensin converting enzyme II (ACE2), replicate efficiently in primary human airway cel

252 are determined by interactions between four ACE2 residues (residues 31, 35, 38, and 353) and two RBD

253 Loss of ACE2 resulted in decreased weight gain but increased glu

254 and therapeutic effects of recombinant human ACE2 (rhACE2) on peptide metabolism was evaluated in hum

255 of CDK consensus sites is not necessary for Ace2's cytoplasmic retention, indicating that these mech

256 Two separate mechanisms enforce Ace2's cytoplasmic sequestration: 1) phosphorylation of

257 We found that Ace2's nuclear localization is maintained by continuous

258 Our study demonstrates that ACE2 serves as a protective mechanism against diabetes-i

259 e clinical relevance of this ADAM17-mediated ACE2 shedding in hypertensive patients and further ident

260 II type 1 receptors promote ADAM17-mediated ACE2 shedding in the brain of hypertensive patients, lea

261 We hypothesized that ADAM17-mediated ACE2 shedding results in decreased membrane-bound ACE2 i

262 injury models, administration of recombinant ACE2 shows therapeutic potential.

263 By contrast, strong ACE2 staining in glomeruli from diabetic mice was less f

264 hich function initially to activate SWI5 and ACE2, subsequently function as Swi5-specific antiactivat

265 mentally confirm our prediction that for the Ace2/Swi5 paralogs, Cbk1 regulated localization was lost

266 and show that for the Rck1/Rck2, Fkh1/Fkh2, Ace2/Swi5 paralogs, they are associated with previously

267 DEM1 and TOS1, and the mediating TF complex Ace2/Swi5.

268 also displays preferential association with Ace2 target gene promoters during hyphal growth.

269 1 (hypha-specific G(1) cyclin) downregulates Ace2 target genes during hyphal growth in G(1).

270 ylation is not sufficient for Cbk1 to act on Ace2: the kinase is also negatively regulated prior to c

271 ers to concurrently activate Ace and repress Ace2, tipping the balance to Ace2 expression with enhanc

272 obese db/db mice, we examined the ability of ACE2 to alter pancreatic beta-cell function and thereby

273 Yet, the relative contribution of ACE2 to Ang-(1-7) formation in vivo has not been elucida

274 I is cleaved by the Ang-converting enzyme-2 (ACE2) to Ang-(1-7), which activates the G-protein-couple

275 by adipose angiotensin-converting enzyme 2 (ACE2) to form Ang(1-7).

276 s receptor, angiotensin-converting enzyme 2 (ACE2), to assess their cross-neutralization activities a

277 athologically stressed hearts to trigger the Ace2-to-Ace enzyme switch, angiotensin I-to-II conversio

278 The regulatory mechanism that underlies the Ace2-to-Ace pathological switch, however, is unknown.

279 bition of FoxM1 abolishes the stress-induced Ace2-to-Ace switch and protects the heart from pathologi

280 sly unrecognized levels of regulation of the Ace2 transcription factor and the cyclin-dependent prote

281 A(Rts1) in these pathways, we focused on the Ace2 transcription factor, which is thought to delay cel

282 thelial cells leads to the activation of the Ace2 transcription factor, which regulates cell wall deg

283 gene cluster, which is regulated by Swi5 and Ace2 transcription factors, is induced in CDC34(tm) cell

284 Ace2 transcription factors, which are present in many fu

285 Furthermore, when C-terminally fused to an ACE2 transmembrane anchor, the secretory N-terminal cata

286 Cbk1 cannot phosphorylate Ace2 until after mitotic exit network (MEN)-initiated re

287 Thus, islet ACE2 upregulation is viewed as a desirable therapeutic g

288 Our data indicate that ACE2 utilization preceded the emergence of SARS-CoV-like

289 AS by subretinal delivery of an AAV8 (Y733F)-ACE2 vector would protect against the ocular inflammatio

290 Here we found that ACE2 was downregulated in apelin-deficient mice.

291 sible for the delay, and this same region of Ace2 was required for interaction with Cbk1, a kinase ne

292 of the RAS, angiotensin converting enzyme 2 (ACE2), was discovered.

293 To clarify the physiological roles of ACE2, we generated mice with targeted disruption of the

294 metrically inherits the transcription factor Ace2, which activates daughter-specific transcriptional

295 utations in a stretch of eight adenosines in ACE2, which encodes a transcriptional regulator involved

296 mutant that lacked the transcription factor Ace2, which influences virulence in other fungi.

297 tion are induced by the transcription factor Ace2, which is activated by the kinase Cbk1, an Ndr/LATS

298 the expression of ANG-(1-7) receptor Mas and ACE2, which were responsible for vascular complications.

299 s study examined the localization of ACE and ACE2 within the glomerulus of kidneys from control (db/m

300 ice using the ACE2 knockout (KO) mice (Akita/ACE2(-/y)).