コーパス検索結果 (1語後でソート)
通し番号をクリックするとPubMedの該当ページを表示します
1 transgenic for the SARS-CoV receptor (human angiotensin-converting enzyme 2).
2 soluble forms of the receptor for the virus, angiotensin converting enzyme 2.
3 red by binding of the viral spike protein to angiotensin-converting enzyme 2.
4 n system, angiotensin-converting enzyme, and angiotensin-converting enzyme 2.
5 hin its trimeric spike glycoprotein to human angiotensin-converting enzyme 2.
6 tibodies with greater than 90% inhibition of angiotensin-converting enzyme 2.
7 a to inhibit the binding of spike protein to angiotensin-converting enzyme 2.
8 ion of the functional receptor of the virus, angiotensin-converting enzyme 2.
9 ngiotensin-aldosterone system (RAAS) through angiotensin-converting enzyme 2.
10 y be associated with whether the virus binds angiotensin-converting enzyme-2.
11 ents infected by viruses that do not bind to angiotensin-converting enzyme-2.
12 e developed transgenic mice expressing human angiotensin-converting enzyme 2, a functional receptor f
18 tudies revealed a preferential expression of angiotensin-converting enzyme 2 (ACE-2), the functional
20 virginianus), an animal species in which the angiotensin converting enzyme 2 (ACE2) - the SARS-CoV-2
22 protein to bind to the cell surface receptor angiotensin converting enzyme 2 (ACE2) glycoprotein and
26 ion occurs through binding of the virus with angiotensin converting enzyme 2 (ACE2) on the cell membr
29 pends on the binding of its Spike protein to angiotensin converting enzyme 2 (ACE2) presented on host
30 and block spike protein interaction with the angiotensin converting enzyme 2 (ACE2) with 1-5 nM affin
31 ficiently at low levels of cellular receptor angiotensin converting enzyme 2 (ACE2), and its pseudoty
34 moke causes a dose-dependent upregulation of angiotensin converting enzyme 2 (ACE2), the SARS-CoV-2 r
36 e, we developed the metallo-enzyme domain of angiotensin converting enzyme 2 (ACE2)-the cellular rece
37 ns of SARS-S with the receptor for SARS-CoV, angiotensin converting enzyme 2 (ACE2); (ii) SSAA09E1 {[
38 2, the pathogenic agent of COVID-19, employs angiotensin converting enzyme-2 (ACE2) as its cell entry
40 n in the short peptide epitope EDLFYQ of the angiotensin-converting enzyme 2 (ACE2) alpha1 helix doma
42 main (RBD) showing crucial interactions with angiotensin-converting enzyme 2 (ACE2) and cross-reactin
45 upted RBD engagement with the human receptor angiotensin-converting enzyme 2 (ACE2) and potently neut
46 ndrome coronavirus 2 (SARS-CoV-2) infection, angiotensin-converting enzyme 2 (ACE2) and transmembrane
47 ausing COVID-19, is facilitated by host cell angiotensin-converting enzyme 2 (ACE2) and transmembrane
48 s critical for SARS-CoV-2 infection, namely, angiotensin-converting enzyme 2 (ACE2) and transmembrane
49 SARS-CoV-2 and the human cellular receptor, angiotensin-converting enzyme 2 (ACE2) are both densely
50 al populations in the distal lung expressing Angiotensin-converting enzyme 2 (ACE2) are infrequent, a
51 ID-19 is a highly contagious virus that uses Angiotensin-converting enzyme 2 (ACE2) as a receptor to
53 is the only group I coronavirus known to use angiotensin-converting enzyme 2 (ACE2) as its receptor.
56 how that S2E12 and S2M11 competitively block angiotensin-converting enzyme 2 (ACE2) attachment and th
57 a trimeric spike surface protein, a dimeric angiotensin-converting enzyme 2 (ACE2) cell-surface rece
58 ke receptor-binding domain (RBD) antibodies, angiotensin-converting enzyme 2 (ACE2) competition, and
62 ity RNA in situ mapping revealed the highest angiotensin-converting enzyme 2 (ACE2) expression in the
63 coronaviruses to utilize animal orthologs of angiotensin-converting enzyme 2 (ACE2) for cell entry.
64 SARS-CoV-2), which causes COVID-19, utilizes angiotensin-converting enzyme 2 (ACE2) for entry into ta
65 the ligand and key binding-site residues of angiotensin-converting enzyme 2 (ACE2) from its homologu
71 locked S conformation, resulting in reduced angiotensin-converting enzyme 2 (ACE2) interaction in vi
80 The membrane-associated carboxypeptidase angiotensin-converting enzyme 2 (ACE2) is an essential r
89 2 (TMPRSS2) mRNA expression while decreasing angiotensin-converting enzyme 2 (ACE2) mRNA and protein
90 ent study showed that directed expression of angiotensin-converting enzyme 2 (ACE2) on cells previous
93 ry syndrome coronavirus 2 (SARS-CoV-2) binds angiotensin-converting enzyme 2 (ACE2) on host cells to
94 can efficiently bind to and use specific bat angiotensin-converting enzyme 2 (ACE2) orthologues and,
96 as recently reported that the human receptor angiotensin-converting enzyme 2 (ACE2) plays a key role
97 case studies were demonstrated, one being on angiotensin-converting enzyme 2 (ACE2) protein which is
99 e novel coronavirus canonically utilizes the angiotensin-converting enzyme 2 (ACE2) receptor and the
100 RBD) of the spike protein binds to the human angiotensin-converting enzyme 2 (ACE2) receptor as a pre
101 ining region (CDR) H3, and competes with the angiotensin-converting enzyme 2 (ACE2) receptor because
103 arly transmission phase and increasing human angiotensin-converting enzyme 2 (ACE2) receptor binding
104 rotein), which binds with not only the human angiotensin-converting enzyme 2 (ACE2) receptor but also
106 SARS-CoV-2 spike protein and blocking to the Angiotensin-converting enzyme 2 (ACE2) receptor in a sin
107 furthered our understanding of spike protein-angiotensin-converting enzyme 2 (ACE2) receptor interact
108 s 2 (SARS-CoV-2) spike protein and the human angiotensin-converting enzyme 2 (ACE2) receptor is a pro
109 n S likely increase recognition of the mouse angiotensin-converting enzyme 2 (ACE2) receptor not only
110 OCs had a greater affinity towards the human angiotensin-converting enzyme 2 (ACE2) receptor than tha
111 the spike protein of SARS-CoV-2 to the human angiotensin-converting enzyme 2 (ACE2) receptor triggers
112 tible host species based on variation in the angiotensin-converting enzyme 2 (ACE2) receptor used for
113 domain (RBD), the hexapeptide YKYRYL on the angiotensin-converting enzyme 2 (ACE2) receptor, and its
114 were engineered to stably express the human angiotensin-converting enzyme 2 (ACE2) receptor, but sta
116 oprotein (S400-600), which overlaps with the angiotensin-converting enzyme 2 (ACE2) receptor-binding
124 ycoprotein receptor binding domain (RBD) and angiotensin-converting enzyme 2 (ACE2) stand in as proxi
125 stantially higher affinity for host receptor angiotensin-converting enzyme 2 (ACE2) than BA.5 and oth
126 racts with both cellular heparan sulfate and angiotensin-converting enzyme 2 (ACE2) through its recep
127 by adipocytes, can be catabolized by adipose angiotensin-converting enzyme 2 (ACE2) to form Ang(1-7).
128 ry syndrome (SARS-CoV) utilizes the receptor angiotensin-converting enzyme 2 (ACE2) to infect cells.
130 clade 3 sarbecovirus PRD-0038 S has a broad angiotensin-converting enzyme 2 (ACE2) usage and that re
131 -CoVs), while recent studies have identified angiotensin-converting enzyme 2 (ACE2) usage in multiple
134 evidence that the 2019-nCoV S protein binds angiotensin-converting enzyme 2 (ACE2) with higher affin
139 l host binding via the cell surface receptor angiotensin-converting enzyme 2 (ACE2), as well as the s
140 mploy the same receptor for host cell entry, angiotensin-converting enzyme 2 (ACE2), but it is largel
141 2) virus enters host cells by binding to the angiotensin-converting enzyme 2 (ACE2), but whether or n
142 of the viral Spike protein to host receptor angiotensin-converting enzyme 2 (ACE2), followed by fusi
143 - SARS-CoV-2 - gains entry to host cells via angiotensin-converting enzyme 2 (ACE2), highlighting the
144 species of the SARS-CoV-2 host receptor, the angiotensin-converting enzyme 2 (ACE2), in patients at d
145 d binding to the human cell-surface receptor angiotensin-converting enzyme 2 (ACE2), increased replic
146 re acute respiratory syndrome coronavirus 2, angiotensin-converting enzyme 2 (ACE2), is highly expres
148 onavirus 2 (SARS-CoV-2) viral association to angiotensin-converting enzyme 2 (ACE2), its main host re
149 in is a candidate vaccine antigen that binds angiotensin-converting enzyme 2 (ACE2), leading to virus
150 S-CoV-2 for entry and replication, including angiotensin-converting enzyme 2 (ACE2), may disrupt SARS
153 lity to infection by modifying expression of angiotensin-converting enzyme 2 (ACE2), the cell entry r
154 involved in SARS-CoV-2 infection, including angiotensin-converting enzyme 2 (ACE2), the receptor for
155 s, we demonstrate that, in addition to human angiotensin-converting enzyme 2 (ACE2), the Spike glycop
156 demic in 2002 and 2003, binds to a receptor, angiotensin-converting enzyme 2 (ACE2), through the rece
157 interface between the RBD and its receptor, angiotensin-converting enzyme 2 (ACE2), to assess their
158 eloped by tethering the SARS-CoV-2 receptor, angiotensin-converting enzyme 2 (ACE2), to known non-neu
160 r-binding domain (RBD) and its host receptor angiotensin-converting enzyme 2 (ACE2), which regulate b
161 SARS-CoV spike protein and its host receptor angiotensin-converting enzyme 2 (ACE2), which regulate b
162 lar localization of the SARS-CoV-2 receptor, angiotensin-converting enzyme 2 (ACE2), within the upper
163 d 489) overlapping a critical portion of the angiotensin-converting enzyme 2 (ACE2)-binding surface.
164 .617.2 (Delta) on binding, neutralizing, and angiotensin-converting enzyme 2 (ACE2)-competing antibod
165 V-2 and SARS-CoV recognize the same receptor-angiotensin-converting enzyme 2 (ACE2)-in humans(3,4).
166 he scarcity of the SARS-CoV-2 receptor-human angiotensin-converting enzyme 2 (ACE2)-in the respirator
167 izes an epitope that partially overlaps with angiotensin-converting enzyme 2 (ACE2)-interacting sites
168 ternative receptor for SARS-CoV-2 entry into angiotensin-converting enzyme 2 (ACE2)-negative cells. S
188 ive arm of the renin angiotensin system, the angiotensin-converting enzyme 2 (ACE2)/angiotensin-(1-7)
189 ment of the antibody to block RBD binding to angiotensin-converting enzyme 2 (ACE2; hereafter referre
190 ment of the antibody to block RBD binding to angiotensin-converting enzyme 2 (ACE2; hereafter referre
191 nt parameters to identify factors related to angiotensin-converting enzyme-2 (ACE2) expression within
201 duced hyperuricaemia and increased levels of angiotensin-converting enzyme 2 and angiotensin (1-7).
205 zed that trophoblasts at term do not express angiotensin-converting enzyme 2 and transmembrane protea
208 us-specific capture agent (in this instance, angiotensin-converting enzyme 2), and finally quantifies
210 on with enhanced BP, decreased expression of angiotensin converting enzyme 2, and increased expressio
211 eptapeptide generated by catalytic action of angiotensin-converting enzyme-2 angiotensin A or directl
213 ) exchanger 3, agonists of components of the angiotensin-converting enzyme 2/angiotensin(1-7)/Mas rec
214 is brief perspective, we examine the role of angiotensin converting enzyme 2 as the receptor for seve
215 han SARS-CoV according to computed S protein-angiotensin-converting enzyme 2 binding free energy chan
216 nity binding to the receptor-binding domain, angiotensin-converting enzyme 2 binding inhibition, and
218 protein with approximately 50% homology with angiotensin converting enzyme 2, but without a catalytic
219 BD, infected cells expressing human receptor angiotensin-converting enzyme 2, but with 90 to 95% less
220 rease in angiotensin 2 after inactivation of angiotensin-converting enzyme 2 by severe acute respirat
224 part, could be attributable to a decrease in angiotensin-converting enzyme 2 expression observed in H
225 55 in oral cavity is predicted to upregulate angiotensin-converting enzyme 2 expression, essential SA
226 an alternate viral illness; (3) investigate angiotensin-converting enzyme 2 expression; and (4) prov
227 g their affinity for a viral receptor, human angiotensin-converting enzyme 2 (hACE-2), and their sens
228 Alpha, Beta, and Delta VoC in the K18 human angiotensin converting enzyme 2 (hACE2) transgenic mouse
229 at binds to its receptor glycoprotein, human angiotensin converting enzyme 2 (hACE2), and mediates vi
232 ted coronavirus (SARS-CoV-2) that uses human angiotensin-converting enzyme 2 (hACE2) as the entry rec
233 e show that transgenic mice expressing human angiotensin-converting enzyme 2 (hACE2) by the human cyt
234 alidation, and optimization of de novo human angiotensin-converting enzyme 2 (hACE2) decoys to neutra
235 s the SARS-coronavirus entry receptor, human angiotensin-converting enzyme 2 (hACE2) driven by the ke
236 ed conformational capacity for binding human angiotensin-converting enzyme 2 (hACE2) for at least a w
237 ) with the extracellular domain of the human angiotensin-converting enzyme 2 (hACE2) receptor detects
238 ne responses and better protection for human angiotensin-converting enzyme 2 (hACE2) transgenic mice
239 tion in HEK293T cells that overexpress human angiotensin-converting enzyme 2 (hACE2) without triggeri
240 complexed with their common receptor, human angiotensin-converting enzyme 2 (hACE2), and proposed th
242 umented interaction with its receptor, human angiotensin-converting enzyme 2 (hACE2), SGP has been fo
243 d that transgenic (Tg) mice expressing human angiotensin-converting enzyme 2 (hACE2), the receptor fo
244 ed infection by selectively expressing human angiotensin-converting enzyme 2 (hACE2), the SARS-CoV-2
247 a set of six human mAbs that bind the human angiotensin-converting enzyme-2 (hACE2) receptor, rather
248 ce that express the SARS-CoV receptor (human angiotensin-converting enzyme 2 [hACE2]) in airway and o
251 essing a functional SARS-CoV receptor (human angiotensin-converting enzyme 2) in a dose-dependent man
253 ose receptor binding domain (RBD) recognizes angiotensin-converting enzyme 2, initiating conformation
254 t cells by disrupting the spike glycoprotein-angiotensin-converting enzyme 2 interaction has already
256 r by adsorptive transcytosis and that murine angiotensin-converting enzyme 2 is involved in brain and
259 was lower in fetal growth restriction in an angiotensin-converting enzyme 2 knockout mouse model cha
260 /vegetable glycerin aerosols increased ACE2 (angiotensin converting enzyme 2) levels, the SARS-CoV-2
262 inent effects on host proteins, most notably angiotensin-converting enzyme 2, might also provide wort
263 gainst SARS-CoV-2 infection in the K18-human angiotensin-converting enzyme 2 mouse model, using both
265 tor-binding domain of the spike protein with angiotensin-converting enzyme 2 on the host cell surface
266 2 infection is binding of the virus to ACE2 (angiotensin-converting enzyme 2) on the airway epitheliu
267 h other respiratory viruses that do not bind angiotensin-converting enzyme-2 (p < 0.001) experienced
268 nts with other respiratory viruses that bind angiotensin-converting enzyme-2 (p = 0.061) and 12% (95%
270 Heavily glycosylated S trimers bind to the angiotensin-converting enzyme 2 receptor and mediate ent
271 s the interplay between virus binding to the angiotensin-converting enzyme 2 receptor and the impact
272 capable of blocking interactions between the angiotensin-converting enzyme 2 receptor and the spike p
273 oV-2 spike glycoprotein (S protein) and host angiotensin-converting enzyme 2 receptor following mutat
274 f its spike protein S1 to attach to the host angiotensin-converting enzyme 2 receptor in lung and air
275 the respiratory tract, the expression of the angiotensin-converting enzyme 2 receptor in other tissue
276 quilibrium constant for binding to the human angiotensin-converting enzyme 2 receptor more than 3.5-f
278 l, and inhaled corticosteroids decreased the angiotensin-converting enzyme 2 receptor, an important r
279 18 of 69 (26.1%) of individuals did not have angiotensin-converting enzyme 2 receptor-blocking Abs, w
283 nalysis demonstrates that it binds the human angiotensin-converting enzyme-2 receptor with a 4-fold h
284 etails of prefusion spike protein binding to angiotensin-converting enzyme 2 remain elusive at the mo
285 izing the protease activity of its receptor, angiotensin-converting enzyme 2, S protein induces an in
286 ght to determine whether circulating soluble angiotensin-converting enzyme 2 (sACE2) is increased in
287 ally, NETs triggered by SARS-CoV-2 depend on angiotensin-converting enzyme 2, serine protease, virus
289 renin-angiotensin system and is a homolog of angiotensin-converting enzyme 2, sharing approximately 5
290 ke protein trimer immunoglobulin G inhibited angiotensin-converting enzyme 2-spike protein binding to
291 mAbs significantly blocked RBD-Fc binding to angiotensin-converting enzyme 2, suggesting that their e
293 omain (RBD), which mediates virus binding to angiotensin-converting enzyme 2, the functional receptor
294 dicate that endothelial cells do not express angiotensin-converting enzyme 2, the receptor that SARS-
295 onsists of angiotensin 1-7, angiotensin 1-9, angiotensin-converting enzyme 2, the type 2 angiotensin
296 n culture, and conferred protection in human angiotensin-converting enzyme 2-transgenic (ACE2-transge
300 CoV-2 to invade endothelial cells via ACE-2 (angiotensin-converting enzyme 2), which is expressed on