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Hydroxychloroquine deglycosylates ACE2. 32 / 32
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"2, 3 Hydroxychloroquine is thought to impair the terminal glycosylation of the angiotensin-converting-enzyme 2 (ACE2) receptor, which is the binding site for the envelope spike glycoprotein and has been shown to inhibit endolysosome function."
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"The antimalarial drugs chloroquine phosphate (CQ) and hydroxychloroquine (HCQ) impair in vitro the terminal glycosylation of ACE2 without significant change of cell-surface ACE2 and, therefore, might be potent inhibitors of SARS-CoV-2 infections."
| DOI
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"Hydroxychloroquine inhibits glycosylation of angiotensin-converting enzyme-2 (ACE2), a cell surface receptor thought to facilitate entry of SARS-nCoV-2 into cells [1, 3]."
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"However, Hydroxychloroquine increase in human organelles raises their pH, thereby inhibiting antigen processing, preventing the alpha and beta chains of the major histocompatibility complex (MHC) class II from dimerizing, inhibiting antigen presentation of the cell, and reducing the inflammatory response.10 Hydroxychloroquine prevents terminal glycosylation of ACE2, the receptor that SARS-CoV and SARS-CoV-2 target for cell pass."
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"In vitro data suggest that hydroxychloroquine can reduce glycosylation of the ACE2 receptor and also can lower blood glucose concentrations, both which could be possible mechanisms of antiviral activity."
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"4 Hydroxychloroquine effectively inhibited the entry step, as well as the post-entry stages of SARS-CoV-2 infection, by changing the glycosylation of the ACE2 receptor and the spike protein."
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"In addition to endosomal pH increase mentioned above, HCQ is also said to inhibit terminal glycosylation of ACE2 receptor, which is considered to be the target of SARS-CoV and SARS-CoV-2 cell entry."
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"Chloroquine and hydroxychloroquine may reduce glycosylation of the ACE2 receptor which prevents the virus binding to and entering the new cells."
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"HCQ inhibits the glycosylation of ACE2 receptors and increases the pH to prevent the fusion of viral and endosomal membrane treatment may increase the risk of different neurodegenerative disorders in older individuals and aggravate protein aggregation in patients with PD, DLB, MSA, AD, PSP, FTD, or HD(Fig. 3c)."
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"Hydroxychloroquine inhibits glycosylation of angiotensin converting enzyme-2 (ACE2), a cell surface receptor thought to facilitate entry of SARS-nCoV-2 into cells [XREF_BIBR, XREF_BIBR]."
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"By contrast, hydroxychloroquine, which inhibits viral entry by increasing endosomal pH and affecting terminal glycosylation of the ACE2 receptor (19) , is predicted by the model to be less likely to be effective since drugs that act on viral entry would require exceptionally high suppression to achieve appreciable effects on viral production."
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"The antimalarial drugs chloroquine phosphate (CQ) and hydroxychloroquine (HCQ) impair in vitro the terminal glycosylation of ACE2 without significant change of cell-surface ACE2 and, therefore, might be potent inhibitors of SARS-CoV-2 infections."
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"Moreover, HCQ might reduce glycosylation of ACE2, interfering with SARS-CoV-2 to bind effectively to the host cell [51]."
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"Hydroxychloroquine (HCQ) inhibits terminal glycosylation of ACE2 receptor, which may reduce the efficiency of its interaction with SARS-CoV spike protein."
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"Chloroquine and hydroxychloroquine (CQ/HCQ) are thought to alter endosomal pH and reduce glycosylation of the ACE2 receptor, thus preventing viral entry [60,61]."
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"There are many ongoing clinical trials which may provide more information on this issue.At the beginning of COVID-19 pandemic, scientists discovered in in-vitro studies that Chloroquine (CQ) and Hydroxychloroquine (HCQ) can inhibit glycosylation of ACE2 receptors [77] and block SARS-CoV-2 transfer from primary endosomes to intracellular lysosomes, thus potentially preventing the release of viral genome [78]."
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"10 Hydroxychloroquine prevents terminal glycosylation of ACE2, the receptor that SARS-CoV and SARS-CoV-2 target for cell pass."
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"At the beginning of COVID-19 pandemic, scientists discovered in in-vitro studies that Chloroquine (CQ) and Hydroxychloroquine (HCQ) can inhibit glycosylation of ACE2 receptors [77] and block SARS-CoV-2 transfer from primary endosomes to intracellular lysosomes, thus potentially preventing the release of viral genome [78] ."
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"The terminal glycosylation of ACE2 is inhibited by hydroxychloroquine, prevents the interaction of ACE2 with SARS-CoV-2 “spike” protein, and hence inhibits the entry of the virus."
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"Although HCQ mediated inhibition of ACE2 receptor glycosylation and the action of nicotine exerts control over ACE2 s SARS-CoV-2 binding, a recent clinical meta-analysis data denied association of latter with disease severity [157]."
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"Hydroxychloroquine is also shown to inhibit the terminal glycosylation of the ACE2 receptor, which in turn inhibits SARS-CoV-2 entry, infection, and disease progression [XREF_BIBR]."
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"HCQ inhibits terminal glycosylation of ACE2 receptor, the main portal of entry for SARS-CoV and SARS-CoV-2."
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"The antimalarial drugs chloroquine phosphate (CQ) and hydroxychloroquine (HCQ) impair in vitro the terminal glycosylation of ACE2 without significant change of cell-surface ACE2 and, therefore, might be potent inhibitors of SARS-CoV-2 infections."
| PMC
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"HCQ was reported to inhibit the viral infection by glycosylating the ACE2 receptor of SARS-CoV-1 and increases the endosomal pH, rendering the membrane fusion [XREF_BIBR, XREF_BIBR]."
| PMC
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"XREF_BIBR, XREF_BIBR Hydroxychloroquine is thought to impair the terminal glycosylation of the angiotensin-converting-enzyme 2 (ACE2) receptor, which is the binding site for the envelope spike glycoprotein and has been shown to inhibit endolysosome function."
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"However, HCQ treatment inhibits glycosylation of ACE2 receptors and thereby prevents COVID-19 from binding to the receptor and its entry into host cells (Fig. 2) ."
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"XREF_BIBR Hydroxychloroquine is found to reduce the entry of coronavirus into a cell through interference with the terminal glycosylation of the angiotensin converting enzyme 2 (ACE2) receptor, which inhibits viral replication."
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"Implications of HCQ Mediated Inhibition of ACE-2 Glycosylation in People with Hypertension and Obesity."
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"Although debatable, this mechanism also suggests that HCQ may have a prophylactic effect since it would reduce the chances of COVID-19 infection.Implications of HCQ-Mediated Inhibition of ACE-2 Glycosylation in People with Hypertension and Obesity While HCQ inhibits the entry of COVID-19 into host cells via suppressing the glycosylation and membrane attachment of ACE2, the most important function of ACE2 is to convert a physiological vasoconstrictor (AngII) to a vasodilator (Ang1-7) (Fig. 3a) ."
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"On the other hand, HCQ might reduce glycosylation of ACE2, interfering with SARS-CoV-2 to bind effectively to the host cell [27]."
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"It has been posited that the antimalaric drugs chloroquine and hydroxychloroquine reduce glycosylation of ACE2, thus preventing SARS-CoV-2 from binding to host cells."
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"However, recent studies indicate that Hydroxychloroquine may also reduce glycosylation of ACE2, therefore inhibiting virus/ACE2 interaction (Devaux et al., 2020)."
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