Informatie over | Engels woord ACE2

Voorbeelden van het gebruik van ACE2 in een zin

• One study suggests that cellular heparan sulfate has a role in SARS-CoV-2 Infection, particularly when the virus attaches with ACE2.
• Mas1 proto-oncogene (MAS1, MGRA) is not to be confused with the MAS-related G-protein coupled receptor, a recently believed to be activated by the ligand alamandine (generated by catalysis of Ang A via ACE2 or directly from Ang-(1-7)).
• SARS-CoV-2 uses the SARS-CoV receptor ACE2 for entry and the serine protease TMPRSS2 for S protein priming.
• Due to the clinical similarity between MERS-CoV and SARS-CoV, it was proposed that they may use the same cellular receptor; the exopeptidase, angiotensin converting enzyme 2 (ACE2).
• All HKU5 coronaviruses have been shown to use ACE2 from their natural host species, Pipistrellus abramus, to infect their hosts.
• In 2008, Shi led a research team which studied binding of spike proteins of both natural and chimaeric SARS-like coronaviruses to ACE2 receptors in human, civet and horseshoe bat cells, to determine the mechanism by which SARS may have spilled over into humans.
• In low cholesterol ACE2 traffics the virus to TMPRSS2 which also cleaves and allows viral entry but through a putative surface mechanism that is much less efficient.
• It is confirmed by comparing infectivity of cells expressing or not expressing ACE2 that the novel coronavirus uses this same entry receptor as SARS-CoV.
• 81% had ACE2 receptor blocking antibodies capable of naturalizing the virus at 6 weeks, with the antibody titres at a level also similar to natural infection.
• Neurological complications in COVID-19 are a result of SARS-CoV-2 infection or a complication of post infection which can be due to (1) direct SARS-CoV-2 invasion on the CNS via systemic circulation or olfactory epithelium directed trans-synaptic mechanism; (2) Inflammatory mediated CNS damage due to cytokine storm and endothelitis; (3) Thrombosis mediated CNS damage due to SARS-CoV-2 interaction with host ACE2 receptor resulting in ACE2 downregulation, coagulation cascade activation, and multiple organ dysfunction; (4) Hypoxemic respiratory failures and cardiorespiratory effects due to SARS-CoV-2 invasion on brain stem.
• The CTD is responsible for the interactions of MERS-CoV with its receptor dipeptidyl peptidase-4, and those of SARS-CoV and SARS-CoV-2 with their receptor angiotensin-converting enzyme 2 (ACE2).
• The to-date unreviewed preprint finds that one mutation could result in a 'MERS-CoV-2' that, like SARS-CoV-2, can use humans' ACE2 receptor and has both a very high fatality (MERS-CoV had a mortality of around 35%) and high transmission rate, and hence represents a risk to biosafety and of potential zoonotic spillover.
• Several bat species have special cellular mechanisms to resist proinflammatory cytokines associated with Betacoronavirus virulence, for example, spike proteins in SARS-related coronaviruses coevolve with bat ACE2 receptors in an evolutionary arms race.

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