ライフサイエンスコーパス: ACE2

1 with human angiotensin-converting enzyme 2 (ACE2).

2 or protein angiotensin-converting enzyme II (ACE2).

3 binding to angiotensin-converting enzyme 2 (ACE2).

4 ry receptor angiotensin-converting enzyme-2 (ACE2).

5 binding depends on both heparan sulfate and ACE2.

6 g ICSs also had reduced sputum expression of ACE2.

7 the open conformation of the RBD that binds ACE2.

8 2, or with overexpression of murine or human ACE2.

9 e been genetically modified to express human ACE2.

10 l species, including upregulation of IL6 and ACE2.

11 ction would affect the enzymatic activity of ACE2.

12 he SARS-CoV-2 Spike protein interaction with ACE2.

13 trimer and dissociated monomeric S1 bound to ACE2.

14 facilitate crystallization) in complex with ACE2.

15 s and affinities for the SARS-CoV-2 receptor ACE2.

16 le decrease in its ability to associate with ACE2.

17 the RBD 170-fold more tightly than wild-type ACE2.

18 at disrupt the interaction between Spike and ACE2.

19 mpetent mice with native expression of mouse ACE2.

20 respectively) and block its interaction with ACE2.

21 enhanced by the angiotensin(1-9) produced by ACE2.

22 ope to recognise and bind the human receptor ACE2.

23 lsion and forms a hydrophobic interface with ACE2.

24 of angiotensin converting enzymes (ACE)1 and ACE2 (ACE2 being the severe acute respiratory syndrome c

25 Without ACE2 acting as a guardian to inactivate the ligands of B

26 Upregulation of lung ACE2 activity in comorbid diabetes may contribute to an

27 ys, as well as a replication-competent mouse ACE2-adapted SARS-CoV-2 in BALB/c mice and native virus

28 However, we find no evidence that these ACE2-affinity-enhancing mutations have been selected in

29 in-depth structural analyses to identify key ACE2 amino acid positions including 30, 83, 90, 322, and

30 aTG13, were also found able to utilize human ACE2 and a number of animal-ACE2 orthologs for cell entr

31 ACE2 and AngII are present in many tissues but informati

32 gh the inhibition of the interaction between ACE2 and CoV-2 RBD.

33 Both ACE2 and heparin can bind independently to spike protein

34 and smokers were analyzed for expression of ACE2 and other coronavirus infection-related genes using

35 S-CoV-2 host factors, including the receptor ACE2 and protease Cathepsin L.

36 g the specificity of the interaction between ACE2 and S and for engineering high-affinity decoy recep

37 aken together, our findings define potential ACE2 and SARS-CoV-2 residues for therapeutic targeting a

38 Given the nanomolar high affinity between ACE2 and SARS-CoV-2 spike protein, we investigated how t

39 re, NIH-CoVnb-112 blocks interaction between ACE2 and several high affinity variant forms of the spik

40 e electrostatic repulsion between the low-pI ACE2 and the heparin segments not accommodated on the RB

41 ained on the noncovalent complexes formed by ACE2 and the receptor-binding domain (RBD) of the S-prot

42 oach, described a single interaction between ACE2 and the SARS-CoV-2 receptor binding domain (RBD).

43 n emerging virus that utilizes host proteins ACE2 and TMPRSS2 as entry factors.

44 We determined effects of IL-13 treatment on ACE2 and TMPRSS2 expression ex vivo in primary airway ep

45 We also examined expression of ACE2 and TMPRSS2 in 2 data sets containing gene expressi

46 ass spectrometry, we studied lung and kidney ACE2 and TMPRSS2 in diabetic mice mimicking host factors

47 use of ICS.Conclusions: Higher expression of ACE2 and TMPRSS2 in males, African Americans, and patien

48 We report that co-transcription of ACE2 and TMPRSS2 is negligible in the placenta, thus not

49 and nonbiologic, do not significantly impact ACE2 and TMPRSS2 receptor expression in the uninflamed i

50 The lower expression of ACE2 and TMPRSS2 with ICS use warrants prospective study

51 haracterize genes that are co-expressed with ACE2 and TMPRSS2, and to further explore their biologica

52 Dozens of genes are co-expressed with ACE2 and TMPRSS2, many of which have plausible links to

53 expression quantitative trait loci for both ACE2 and TMPRSS2, that vary in frequency across world po

54 us were associated with higher expression of ACE2 and TMPRSS2.

55 ate of SARS-CoV-2, mice that expressed human ACE2 and were immunized with VSV-eGFP-SARS-CoV-2 show pr

56 giotensin-converting enzyme receptor type-2 (ACE2) and can be infected with virus.

57 ctions with angiotensin-converting enzyme 2 (ACE2) and cross-reacting neutralizing antibody were foun

58 on, namely, angiotensin-converting enzyme 2 (ACE2) and transmembrane protease, serine 2 (TMPRSS2), ar

59 V-2 receptors angiotensin converting enzyme (ACE2) and transmembrane protease/serine subfamily member

60 y host cell angiotensin-converting enzyme 2 (ACE2) and transmembrane serine protease 2 (TMPRSS2).

61 otein binds angiotensin-converting enzyme 2 (ACE2), and in concert with host proteases, principally t

62 mutations in each species, relative to human ACE2, and correlated these changes with COVID-19 infecti

63 ric and cell cycle-regulated localization of Ace2, and for localization of the RAM network components

64 virus cell entry, block RBD interaction with ACE2, and inhibit live virus replication.

65 e protein (S-protein) binds to its receptor, ACE2, and is then processed by TMPRSS2.

66 mulating in support of the activation of the ACE2/Ang-(1-7)/Mas receptor pathway by pharmacologic or

67 ammatory benefits of the upregulation of the ACE2/Ang1-7/Mas axis and previously demonstrated benefit

68 ACE2 (angiotensin-converting enzyme 2) and Ang 1-7 (angi

69 ACE2 (angiotensin-converting enzyme 2) and NEP (neprilys

70 S-CoV-2 infection is binding of the virus to ACE2 (angiotensin-converting enzyme 2) on the airway epi

71 ACE2 (angiotensin-converting enzyme 2), and TMPRSS2 (tra

72 ngiotensin-converting enzymes (ACEs) ACE and ACE2, angiotensin II (Ang II), Ang-(1-7), and receptors

73 with angiotensin receptor types 1 and 2 and ACE2 are components of the renin-angiotensin system (RAS

74 nding domain (RBD), and its primary receptor ACE2 are extensively glycosylated.

75 r receptor, angiotensin-converting enzyme 2 (ACE2) are both densely glycosylated.

76 CoV, strongly suggesting that 2019-nCoV uses ACE2 as its receptor.

77 me coronavirus 2 (SARS-CoV-2) utilizes human ACE2 as the receptor for entry with subsequent downregul

78 uses human angiotensin-converting enzyme 2 (ACE2) as its receptor to infect cells.

79 pointed to angiotensin-converting enzyme 2 (ACE2) as SARS-CoV-2 entry receptor.

80 at cell cycle delay is sufficient to disrupt Ace2 asymmetry.

81 In particular, through truncating ACE2 at its residue 740 but not 615, introducing a D30E

82 and 2.70 angstrom revealed a direct block of ACE2 attachment.

83 n healthy human kidneys with NEP rather than ACE2 being essential for its generation.

84 iotensin converting enzymes (ACE)1 and ACE2 (ACE2 being the severe acute respiratory syndrome coronav

85 mutations are well tolerated or even enhance ACE2 binding, including at ACE2 interface residues that

86 d that the conformation is shifted toward an ACE2 binding-competent state, which is modeled to be on

87 lized the virus by directly interfering with ACE2 binding.

88 glycans had only minor contribution to Spike-ACE2 binding.

89 on of the angiotensin I converting enzyme 2 (ACE2)-binding site.

90 ural features of SARS-CoV-2 RBD increase its ACE2-binding affinity.

91 In comparison with the SARS-CoV RBD, an ACE2-binding ridge in SARS-CoV-2 RBD has a more compact

92 heparan sulfate-binding site adjacent to the ACE2-binding site.

93 tools available for further understanding of ACE2 biology and for the investigation of ACE2 in the pa

94 c antibodies show more potent S1 binding, S1/ACE2 blocking, and SARS-CoV-2 pseudovirus neutralization

95 in for fusion activation and dissociation of ACE2-bound S1 monomers.

96 unbound, closed spike trimer, the fully open ACE2-bound trimer and dissociated monomeric S1 bound to

97 Here we showed that ACE2, but not TMPRSS2 or Furin, has a higher level of se

98 -CoV-2) is initiated by virus binding to the ACE2 cell-surface receptors(1-4), followed by fusion of

99 As a carboxypeptidase, ACE2 cleaves many biological substrates besides angioten

100 With the addition of the natural ACE2 collectrin domain and fusion to a human immunoglobu

101 edict infection risks, we modelled S-protein:ACE2 complexes from 215 vertebrate species, calculated c

102 ntributes to the viral host range, S-protein:ACE2 complexes from other animals have not been investig

103 on, and adopting an antibody-like tetrameric-ACE2 configuration, we generated an ACE2-Ig variant that

104 3) provide favorable interactions with human ACE2, consistent with 2019-nCoV's capacity for human cel

105 for entry with subsequent downregulation of ACE2, corneal inflammation in Ace2(-/-) mice may have a

106 hypothesis that during this process, reduced ACE2 could result in clinical deterioration in COVID-19

107 epithelial debridement experiments in young ACE2-deficient mice showed normal appearing corneas, dev

108 Cell surface expression of ACE2 determines the tissue susceptibility for coronaviru

109 served that mice deficient in the Ace2 gene (Ace2(-/-) ), developed a cloudy cornea phenotype as they

110 In contrast, deglycosylation of ACE2 did not influence SARS-CoV-2 binding.

111 As a result of SARS-CoV-2 binding, ACE2 downregulation enhances the angiotensin II receptor

112 ine enterocytes among coronavirus receptors (ACE2, DPP4, ANPEP).

113 On the other hand, identifying ACE2 dysregulation in patients with comorbidities may of

114 The enhancement in ACE2 enzymatic function was mediated by the binding of S

115 ensine dramatically reduced viral entry into ACE2 expressing HEK293T cells.

116 rt here pseudoviruses carrying S(G614) enter ACE2-expressing cells more efficiently than those with S

117 We show that HMGB1 regulates ACE2 expression and is critical for entry of SARS-CoV-2,

118 individuals of African descent may regulate ACE2 expression and may be associated with increased sus

119 We also discuss ACE2 expression and potential role in the context of com

120 Treatment with antiandrogenic drugs reduced ACE2 expression and protected hESC-derived lung organoid

121 RS-CoV-2 infection or the loss of functional ACE2 expression as a result of viral internalization.

122 d VAQWRTKYETDAIQRTEELEEAKKK, which increased ACE2 expression by 0.52-0.84 folds, respectively, were i

123 2/interleukin-23 treatment on SB and colonic ACE2 expression in 3 clinical trials.

124 needed to elucidate whether upregulation of ACE2 expression in airways and lungs has consequences on

125 s to identify factors influencing intestinal ACE2 expression in Crohn's disease (CD), ulcerative coli

126 We compared sputum ACE2 expression in patients with COPD stratified accordi

127 ls, no study has systematically assessed the ACE2 expression in the lungs of patients with these dise

128 We further determine whether ciliary ACE2 expression in the upper airway is influenced by pat

129 he effect of ICS administration on pulmonary ACE2 expression in vitro in human airway epithelial cell

130 In contrast, canonical ACE2 expression is unresponsive to IFN stimulation.

131 Thus, interferon-induced variability in ACE2 expression levels could be important for susceptibi

132 n host tissues and the factors that regulate ACE2 expression remain unknown.

133 ACE2 expression was significantly negatively associated

134 L-13 and virus infection mediated effects on ACE2 expression were also observed at the protein level

135 ional role of type-I interferon signaling in ACE2 expression.

136 ell population and a concomitant increase in ACE2 expression.

137 the highest angiotensin-converting enzyme 2 (ACE2) expression in the nose with decreasing expression

138 alizing activities of various antibodies and ACE2-Fc soluble decoy protein in both assays revealed a

139 ntibody, IgG1 ab1, which competed with human ACE2 for binding to RBD.

140 identified the distinct viral entry factors ACE2 (for SARS-CoV-2), aminopeptidase N (for 229E), and

141 rthologs of angiotensin-converting enzyme 2 (ACE2) for cell entry.

142 translation product is a truncated, unstable ACE2 form, lacking domains required for SARS-CoV-2 bindi

143 -nCoV, 2019-nCoV also potentially recognizes ACE2 from a diversity of animal species (except mice and

144 t need to be addressed to fully characterize ACE2 function in SARS-CoV-2 infection and associated pat

145 We observed that mice deficient in the Ace2 gene (Ace2(-/-) ), developed a cloudy cornea phenot

146 dy compares angiotensin-converting enzyme 2 (ACE2) gene expression, which has been associated with SA

147 ed transcripts, we describe a new isoform of ACE2, generated by co-option of intronic retroelements a

148 ce receptor angiotensin converting enzyme 2 (ACE2) glycoprotein and facilitate host cell entry.

149 SARS-CoV-2 spike binds to its receptor human ACE2 (hACE2) through its receptor-binding domain (RBD) a

150 ACE2 has been proposed as an interferon-stimulated gene

151 ACE2 has recently been proposed to be interferon (IFN) i

152 Angiotensin-converting enzyme 2 (ACE2) has been identified as the host entry receptor for

153 ation within bronchoalveolar lavage cells of ACE2-high subjects was reciprocally increased.

154 t cells via angiotensin-converting enzyme 2 (ACE2), highlighting the need to understand the relations

155 binding of the spike trimer to more than one ACE2 homodimer and suggests a mechanical contribution of

156 s flexibility translates into an ensemble of ACE2 homodimer conformations that could sterically accom

157 embrane helix while still not disrupting the ACE2 homodimer or ACE2-RBD interfaces.

158 trameric-ACE2 configuration, we generated an ACE2-Ig variant that neutralizes SARS-CoV-2 at picomolar

159 These data demonstrate that the improved ACE2-Ig variants developed in this study could potential

160 vestigate whether the glycosylation state of ACE2 impacts the interaction with SARS-CoV-2 viral spike

161 ICS administration attenuated expression of ACE2 in airway epithelial cell cultures from patients wi

162 The identification of ACE2 in as many as 72 tissues suggests that extrapulmona

163 respiratory syndrome coronavirus 2 receptor ACE2 in bronchial epithelium.

164 ression of ENaC-alpha and the viral receptor ACE2 in cell types linked to the cardiovascular-renal-pu

165 Neonatal hyperoxia stimulated expression of ACE2 in Club cells and in AT2 cells by 2 months of age.

166 on the assembly process of the CoV-2 RBD to ACE2 in long-time enhanced correlation guided MD simulat

167 s virus binds to the extracellular domain of ACE2 in nasal, lung, and gut epithelial cells through it

168 Furthermore, by examining the disruption of ACE2 in several comorbid diseases, we offer insight into

169 e was to gain insight into the expression of ACE2 in the human airway epithelium.Methods: Airway epit

170 alyses revealed many potential regulators of ACE2 in the human lung, including genes related to histo

171 of ACE2 biology and for the investigation of ACE2 in the pathogenesis and treatment of COVID-19.

172 ral and functional insights into the role of ACE2 in viral infection that can potentially be exploite

173 me receptor-angiotensin-converting enzyme 2 (ACE2)-in humans(3,4).

174 on of interferon-responsive genes, including ACE2, increased as a function of viral load, while trans

175 erlaps with angiotensin-converting enzyme 2 (ACE2)-interacting sites on the CoV-2 RBD.

176 Consequently, antibodies targeting the ACE2-interacting surface (ACE2IS) located in the recepto

177 Antibodies that disrupt the SARS-CoV-2 S-ACE2 interaction can potently neutralize the virus witho

178 eely adopted "up" conformations required for ACE2 interaction, primarily through RBD movement combine

179 in reduced angiotensin-converting enzyme 2 (ACE2) interaction in vitro.

180 ptide epitopes and directly modulating Spike-ACE2 interactions.

181 d or even enhance ACE2 binding, including at ACE2 interface residues that vary across SARS-related co

182 bilize two virus-binding hotspots at the RBD-ACE2 interface.

183 Strikingly, we discovered that ACE2 is a human interferon-stimulated gene (ISG) in vitr

184 2 upregulation in the SAE of smokers; and 5) ACE2 is expressed in airway epithelium differentiated in

185 lower expression in the SAE; 2) in the SAE, ACE2 is expressed in basal, intermediate, club, mucus, a

186 d microRNA.Measurements and Main Results: 1) ACE2 is expressed similarly in the trachea and LAE, with

187 try into human cells, and confirm that human ACE2 is the receptor for the recently emerging SARS-CoV-

188 mediate, club, mucus, and ciliated cells; 3) ACE2 is upregulated in the SAE by smoking, significantly

189 binding to angiotensin-converting enzyme 2 (ACE2) is critical for viral cell entry and infection.

190 Although angiotensin-converting enzyme 2 (ACE2) is crucial for SARS-CoV-2 to bind and enter host c

191 vity of the angiotensin-converting enzyme 2 (ACE2) is dysregulated in cardiovascular disease, and thi

192 Angiotensin-converting enzyme 2 (ACE2) is the canonical cell surface receptor for SARS-Co

193 r-binding motif (RBM) that directly contacts ACE2, is similar to that of SARS-CoV, strongly suggestin

194 ociation to angiotensin-converting enzyme 2 (ACE2), its main host receptor, and host cell entry.

195 ent of the viral entry to the host cell, and ACE2, its docking site on the host cell surface, are ext

196 that binds angiotensin-converting enzyme 2 (ACE2), leading to virus entry.

197 s that SARS-CoV-2 infection may downregulate ACE2, leading to toxic overaccumulation of angiotensin I

198 ening strategy to identify drugs that reduce ACE2 levels in human embryonic stem cell (hESC)-derived

199 ACE2 levels were consistently reduced in SB CD and eleva

200 nregulation of ACE2, corneal inflammation in Ace2(-/-) mice may have a similar mechanism with that in

201 We therefore studied ACE2 mRNA and protein expression in lung tissue samples

202 Pulmonary ACE2 mRNA expression was not different between subjects

203 Two ACE2 noncoding variants (rs4646118 and rs143185769) pres

204 hat SARS-CoV-2 is nearly optimal for binding ACE2 of humans compared to other animals, which may unde

205 rganoids with apical-out polarity to present ACE2 on the exposed external surface, facilitating infec

206 A striking expression of ACE2 on the small bowel enterocyte brush border supports

207 ccumulating evidence points to activation of ACE2 or Mas receptor as a promising approach for restori

208 ed permissive by ectopic expression of human ACE2 or of ACE2 orthologs from various mammals, includin

209 blocker telmisartan affected lung or kidney ACE2 or TMPRSS2, except for a small increase in kidney A

210 with systemic or organ-specific deletion of ACE2, or with overexpression of murine or human ACE2.

211 tigated the structural properties of several ACE2 orthologs bound to the SARS-CoV-2 spike protein.

212 to utilize human ACE2 and a number of animal-ACE2 orthologs for cell entry, indicating risks of spill

213 ve by ectopic expression of human ACE2 or of ACE2 orthologs from various mammals, including Chinese r

214 We found that ACE2 orthologs of a wide range of domestic and wild mamm

215 Genes highly correlated with ACE2 overlapped with type 1 and 2 IFN signatures, normal

216 Angiotensin converting enzyme 2 (ACE2) plays an important role in inflammation, which is

217 t loss of angiotensin-I converting enzyme 2 (ACE2) promotes the ACE/angiotensin-II (Ang-II)/angiotens

218 PRSS2, except for a small increase in kidney ACE2 protein with ramipril.

219 sm for any of the 3 genetically distinct bat ACE2 proteins we examined indicates that SARS-CoV-2 rece

220 SARS-CoV-2 trimeric spike protein increased ACE2 proteolytic activity ~3-10 fold against model pepti

221 e still not disrupting the ACE2 homodimer or ACE2-RBD interfaces.

222 echanistic information on attenuation of the ACE2/RBD association by heparin, the study demonstrates

223 ows the role of heparin in destabilizing the ACE2/RBD association to be studied, providing critical i

224 luc infection of A549 cells expressing human ACE2 receptor (A549-hACE2), we show that the assay can b

225 ke glycoprotein mediates viral attachment to ACE2 receptor and is a major determinant of host range a

226 ARS-CoV-2 Spike proteins in complex with the ACE2 receptor and showed that the SARS-CoV-2 Spike glyco

227 r-binding domains (RBDs) to engage the human ACE2 receptor and to facilitate virus entry, which can o

228 s to an epitope that overlaps with the human ACE2 receptor binding motif providing a structural basis

229 the highly conserved epitope, away from the ACE2 receptor binding site.

230 pike complex revealed an epitope that blocks ACE2 receptor binding.

231 eralocorticoid receptor antagonists increase ACE2 receptor expression, it has been tacitly believed t

232 CoV-2 spike protein, which engages with host ACE2 receptor for entry.

233 well as the influence of natural variants on ACE2 receptor glycosylation.

234 In addition, given the key role of the ACE2 receptor in the early stages of viral entry, we sho

235 AB7A reduces viral entry by sequestering the ACE2 receptor inside cells.

236 major antigen and its engagement with human ACE2 receptor plays an essential role in viral entry int

237 can measure competition and blocking of the ACE2 receptor to the SARS-CoV-2 spike protein with antis

238 stabilization and avidity, the most optimal ACE2 receptor traps neutralized SARS-CoV-2-pseudotyped l

239 Engineered ACE2 receptor traps offer a promising route to fighting

240 ction and block Spike protein binding to the ACE2 receptor, and biodistribution of SARS-CoV-2 targeti

241 in, and block the interaction with the human ACE2 receptor.

242 through enhancing the expression of ciliary ACE2 receptor.

243 o the human angiotensin-converting enzyme 2 (ACE2) receptor as a prelude to viral entry into the cell

244 the human angiotensin I-converting enzyme 2 (ACE2) receptor driven by the cytokeratin-18 (K18) gene p

245 king to the Angiotensin-converting enzyme 2 (ACE2) receptor in a single experiment.

246 s the human angiotensin-converting enzyme 2 (ACE2) receptor, but stably introducing an additional cop

247 (RBD) with angiotensin-converting enzyme 2 (ACE2) receptor.

248 ed out given the expression of low levels of ACE2 receptors in the brain.

249 ng motif, important for specificity to human ACE2 receptors, appears to be an ancestral trait shared

250 the oral mucosa and salivary gland ducts via ACE2 receptors.

251 es in their angiotensin-converting enzyme 2 (ACE2) receptors.

252 ces among SARS-CoV-2, SARS-CoV and RaTG13 in ACE2 recognition shed light on the potential animal-to-h

253 ome analysis, with associated examination of ACE2-related microRNA.Measurements and Main Results: 1)

254 on of immune responses, and maladaptation of ACE2-related pathways might all contribute to these extr

255 In the absence of ACE2, single-RBD-up conformations dominated at pH 5.5, r

256 sense variants from genomic databases within ACE2/SLC6A19/transmembrane serine protease 2 (TMPRSS2),

257 ct that this protein only weakly attaches to ACE2 so that the activation of CoV-2 RBD might be inhibi

258 with the angiotensin I-converting enzyme 2 (ACE2)-solute carrier family 6 member 19 (SLC6A19) dimer.

259 at transgenic animal models expressing human ACE2, such as the hACE2 transgenic mouse, are also likel

260 A hypothesis-free profiling of ACE2 suggests tongue keratinocytes, olfactory epithelial

261 system based on the strong expression of the ACE2 target throughout the brain.

262 By using deep mutagenesis, mutations in ACE2 that increase S binding are found across the intera

263 SARS-CoV-2 enters the cell via ACE2 that next to its role in RAAS is needed to inactiva

264 Given that ACE2, the entry receptor for the causative coronavirus S

265 derived from healthy nonsmokers.Conclusions: ACE2, the gene encoding the receptor for SARS-CoV-2, is

266 First, ACE2, the severe acute respiratory syndrome coronavirus

267 sulfate and angiotensin-converting enzyme 2 (ACE2) through its receptor-binding domain (RBD).

268 ACE2 together with angiotensin receptor types 1 and 2 an

269 K18 ACE2 transgenic mice produced a modest TH1/2/17 cytokine

270 relevant phenotypes than those seen in Hfh4-ACE2 transgenic mice, which express human ACE2 under the

271 Moreover, the MIRb-ACE2 translation product is a truncated, unstable ACE2 f

272 h4-ACE2 transgenic mice, which express human ACE2 under the control of the Hfh4 (also known as Foxj1)

273 of miR-1246 expression could play a role in ACE2 upregulation in the SAE of smokers; and 5) ACE2 is

274 fighting infections by SARS-CoV-2 and other ACE2-using coronaviruses, with the key advantage that vi

275 ffinity optimized, enzymatically inactivated ACE2 variants that potently block SARS-CoV-2 infection o

276 Combining mutations gives ACE2 variants with affinities that rival those of monocl

277 Within UC, colonic ACE2 was elevated in active disease and in patients subs

278 sociated with severe COVID-19 and found that ACE2 was highly expressed in these patients compared to

279 mRNA expression of ACE2 was measured by quantitative RT-PCR.

280 SARS-CoV-2 particles, but D614G affinity for ACE2 was reduced due to a faster dissociation rate.

281 Within CD, SB ACE2 was reduced in patients subsequently developing com

282 ACE2 was similarly upregulated in the kidneys of mice wi

283 Human angiotensin-converting enzyme 2(ACE2) was identified as the entry receptor for SARS-CoV-

284 -2 binding, angiotensin-converting enzyme 2 (ACE2), was not detected by messenger RNA (mRNA) or prote

285 In contrast, protein levels of ACE2 were significantly increased in both alveolar tissu

286 Protein levels of ACE2 were visualized by immunohistochemistry on paraffin

287 st receptor angiotensin-converting enzyme 2 (ACE2), which regulate both the cross-species and human-t

288 st receptor angiotensin-converting enzyme 2 (ACE2), which regulate both the cross-species and human-t

289 The entry point for the virus is ACE2, which is a component of the counteracting hypotens

290 blockers may promote COVID-19 by increasing ACE2, which severe acute respiratory syndrome coronaviru

291 riptionally independent truncated isoform of ACE2, which we designate as deltaACE2 (dACE2).

292 the binding interface between CoV-2 RBD and ACE2, which we investigate using 20 independent equilibr

293 SARS-CoV-2 unbalances RAS functionality via ACE2 will help design therapies to attenuate a COVID-19-

294 is difficulty by exogenous delivery of human ACE2 with a replication-deficient adenovirus (Ad5-hACE2)

295 s infection of HEK293 cells expressing human ACE2 with an EC(50) of 0.3 ug/mL.

296 glycoprotein is compatible to bind the human ACE2 with high specificity.

297 Viral entry mediated by the interaction of ACE2 with spike protein largely determines host range an

298 ons, we find that CoV-2 RBD does not bind to ACE2 with the binding motif shown in experiments, but it

299 on with the angiotensin converting enzyme 2 (ACE2) with 1-5 nM affinity.

300 2 receptor, angiotensin-converting enzyme 2 (ACE2), within the upper (nasal) and lower (pulmonary) re