EC Number   |
Application  |
Reference |
|---|
   3.4.17.23 | medicine |
among 226000 SARSCoV-2 sequences, 1573 missense mutations are found in the spike gene, and 226 of them were within the receptor-binding domain region that directly interacts with human ACE2. Modeling shows that most of the 74 missense mutations in the receptor-binding domain region of the interaction interface have little impact on spike binding to ACE2, whereas several within the spike receptor-binding domain increase the binding affinity toward human ACE2 thus making the virus likely more contagious |
764531 |
| 3.4.17.23 | medicine |
analysis of variations in SARS-CoV-2 spike protein and hACE2 receptor protein and their interaction in the infection scale. Interactions of hACE2 variants with SARS-CoV-2 variants are very strong for G726R-G476S, R768W-V367F, Y252N-V483A, Y252N-V367F, G726R-V367F, N720D-V367F and N720DF486L, and weak for P263S-S383C, RBD-H378R, G726R-A348T |
765112 |
| 3.4.17.23 | medicine |
angiotensin converting enzyme 2 (ACE2) is the receptor of SARS-CoV-2, but only ACE2 of certain species can be utilized by SARS-CoV-2. SARS-CoV-2 tends to utilize ACE2 of various mammals, except murines, and some birds, such as pigeon. This prediction may help to screen the intermediate hosts of SARS-CoV-2. SARS-CoV-2 has a high genetic relationship with a bat coronavirus (BatCoV RaTG13) with a 96% genomic nucleotide sequence identity. The close phylogenetic relationship to Bat RaTG13 provides evidence for a bat origin of SARS-CoV-2. Direct transmission of the virus from bats to humans is unlikely due to the lack of direct contact between bats and humans (in Wuhan, China). There are probably intermediate hosts transmitting SARS-CoV-2 to humans. Combined phylogenetic analysis and critical site marking is used to predict the utilizing capability of ACE2 from different animal species by SARS-CoV-2. It is confirmed that pangolin (Manis javanica), cat (Felis catus), cow (Bos taurus), buffalo (Bubalus bubalis), goat (Capra hircus), sheep (Ovis aries) and pigeon (Columba livia) ACE2 might be utilized by SARS-CoV-2, indicating potential interspecies transmission of the virus from bats to these animals and among these animals |
754646 |
| 3.4.17.23 | medicine |
angiotensin-converting enzyme 2 (ACE2) fused to the Fc portion of immunoglobulin neutralizes SARS-CoV-2 in vitro. Provision of soluble recombinant human ACE2 protein can be beneficial as a novel biologic therapeutic to combat or limit infection progression caused by coronaviruses that utilize ACE2 as a receptor. If given in its soluble form as an appropriate recombinant ACE2 protein, a new tool may be at hand to combat the spread of coronavirus in susceptible individuals by limiting coronavirus attachment to the cell membranes, cell entry, and replication |
753315 |
| 3.4.17.23 | medicine |
angiotensin-converting enzyme 2 is a target for gene therapy for hypertension disorders |
668528 |
| 3.4.17.23 | medicine |
antibodies and small molecular inhibitors that can block the interaction of the enzyme (ACE2) with the receptor binding domain can to combat the virus SARS-CoV-2 |
752692 |
| 3.4.17.23 | medicine |
binding of SARS-CoV-2 spike protein, variant omicron B.1.1.529, to ACE2 is inhibited by caffeic acid hexoside (-6.4 kcal/mol, RMSD 2.382 A) and phloretin (-6.3 kcal/mol, RMSD 0.061 A) from Sargassum wightii, which interact with crucial residues Asn417, Ser496, Tyr501, and His505 of the spike protein. 5alpha-Cholestan-3beta-ol, 2-methylene- (-6.0 kcal/mol, RMSD 3.074 A) from Corallina officinalis shows inhibitory effect against the omicron receptor-binding domain mutated residues Leu452 and Ala484 |
765306 |
| 3.4.17.23 | medicine |
chronic treatment with the AT1R antagonist almesartan induces a fivefold increase in ACE2 mRNA in the aorta which leads to a significant increase in aortic angiotensin(1-7) protein expression. These effects are associated with significant decreases in aortic medial thickness and may represent an important protective mechanism in the prevention of cardiovascular events in hypertensive subjects |
667145 |
| 3.4.17.23 | medicine |
circulating extracellular vesicles that express ACE2 isolated from human plasma or cells neutralize SARS-CoV-2 infection by competing with cellular ACE2. Compared to vesicle-free recombinant human ACE2, ACE2 from extracellular vesicles shows a 135fold higher potency in blocking the binding of the viral spike protein receptor-binding domain, and a 60- to 80fold higher efficacy in preventing infections by both pseudotyped and authentic SARS-CoV-2. ACE2 from extracellular vesicles protects human ACE2 transgenic mice from SARS-CoV-2-induced lung injury and mortality. ACE2 from extracellular vesicles inhibits the infection of SARS-CoV-2 variants alpha, beta, and delta with equal or higher potency than for the wild-type strain |
765453 |
| 3.4.17.23 | medicine |
coexpression of intermediate filament protein vimentin with ACE2 increases SARS-CoV-2 entry in HEK-293 cells, and shRNA-mediated knockdown of vimentin significantly reduces SARS-CoV-2 infection of human endothelial cells. Incubation of A-549 cells expressing ACE2 with purified vimentin increases pseudotyped SARS-CoV-2 spike protein entry. The S-protein receptor-binding domain is sufficient for spike protein interaction with vimentin. Extracellular vimentin binds to SARS-CoV-2 spike protein and facilitates SARS-CoV-2 infection |
765690 |
