Corpus overview


MeSH Disease

HGNC Genes

SARS-CoV-2 proteins

ProteinS (1)


SARS-CoV-2 Proteins
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    Fatty Acid Synthase inhibition prevents palmitoylation of SARS-CoV2 SpikeProtein MESHD and improves survival of mice infected with murine hepatitis virus MESHD.

    Authors: Minhyoung Lee; Katrina Mekhail; Michael Sugiyama; Elyse Latreille; Costin N Antonescu; Greg D Fairn

    doi:10.1101/2020.12.20.423603 Date: 2020-12-21 Source: bioRxiv

    Severe acute respiratory syndrome coronavirus 2 MESHD ( SARS-CoV2 MESHD) is the causative agent of COVID19 MESHD that has infected >76M people and caused >1.68M deaths. The SARS-CoV2 MESHD Spike glycoprotein PROTEIN is responsible for the attachment and infection of target cells. The viral Spike protein PROTEIN serves the basis for many putative therapeutic countermeasures including vaccines, blocking and neutralizing antibodies, and decoy receptors. Here we investigated the cytosolic domain of Spike and its interaction with the protein palmitoyltransferase ZDHHC5. The Spike protein PROTEIN is palmitoylated on multiple juxtamembrane cysteine residues conserved among coronavirus. Increased abundance of ZDHHC5 HGNC resulted in hyper-palmitoylation MESHD, while silencing of ZDHHC5 HGNC reduced the ability of the human CoV 229E to form viral plaques in cell monolayers. Inhibition of fatty acid synthase using the pharmacological inhibitor TVB-3166 eliminated palmitoylation of SARS-CoV2 Spike MESHD. Additionally, TVB-3166 attenuated plaque formation and promoted the survival of mice from a lethal murine CoV infection MESHD. Thus, inhibition of the Spike protein PROTEIN palmitoylation has the potential to treat SARS-CoV-2 and other CoV infections MESHD.

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MeSH Disease
HGNC Genes
SARS-CoV-2 Proteins

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