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HGNC Genes

SARS-CoV-2 proteins

ProteinN (1)


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    Direct activation of endothelial cells by SARS-CoV-2 nucleocapsid protein PROTEIN is blocked by Simvastatin

    Authors: Yisong Qian; Tianhua Lei; Parth Patel; Chi Lee; Paula Monaghan-Nichols; Hong-Bo Xin; Jianming Qiu; Mingui Fu

    doi:10.1101/2021.02.14.431174 Date: 2021-02-15 Source: bioRxiv

    Emerging evidence suggests that endothelial activation plays a central role in the pathogenesis of acute respiratory distress syndrome MESHD ( ARDS MESHD) and multi-organ failure MESHD in patients with COVID-19 MESHD. However, the molecular mechanisms underlying endothelial activation in COVID-19 MESHD patients remain unclear. In this study, the SARS-CoV-2 viral proteins that potently activate human endothelial cells were screened to elucidate the molecular mechanisms involved with endothelial activation. It was found that nucleocapsid protein PROTEIN (NP) of SARS-CoV-2 significantly activated human endothelial cells through TLR2 HGNC/ NF-{kappa}B HGNC and MAPK signaling pathways. Moreover, by screening a natural microbial compound library containing 154 natural compounds, simvastatin was identified as a potent inhibitor of NP-induced endothelial activation. Remarkablely, though the protein sequences of N proteins PROTEIN from coronaviruses are highly conserved, only NP from SARS-CoV-2 induced endothelial activation. The NPs from other coronaviruses such as SARS-CoV, MERS-CoV, HUB1-CoV MESHD and influenza virus H1N1 did not affect endothelial activation. These findings are well consistent with the results from clinical investigations showing broad endotheliitis and organ injury MESHD in severe COVID-19 MESHD patients. In conclusion, the study provides insights on SARS-CoV-2-induced vasculopathy and coagulopathy MESHD, and suggests that simvastatin, an FDA-approved lipid-lowering drug, may benefit to prevent the pathogenesis and improve the outcome of COVID-19 MESHD patients.

    Perversely expressed long noncoding RNAs can alter host response and viral proliferation in SARS-CoV-2 infection MESHD

    Authors: Rafeed Rahman Turjya; Md. Abdullah-Al-Kamran Khan; Abul B.M.M.K. Islam

    doi:10.1101/2020.06.29.177204 Date: 2020-06-29 Source: bioRxiv

    BackgroundSince December 2019, the world is experiencing an unprecedented crisis due to a novel coronavirus, SARS-CoV-2. Owing to poor understanding of pathogenicity, the virus is eluding treatment and complicating recovery. Regulatory roles of long non-coding RNAs (lncRNAs) during viral infection MESHD and associated antagonism of host antiviral immune responses has become more evident in last decade. To elucidate possible functions of lncRNAs in the COVID-19 MESHD pathobiology, we have utilized RNA-seq dataset of SARS-CoV-2 infected MESHD lung epithelial cells. ResultsOur analyses uncover 21 differentially expressed lncRNAs whose functions are broadly involved in cell survival and regulation of gene expression. By network enrichment analysis we find that these lncRNAs can directly interact with differentially expressed protein-coding genes ADAR HGNC, EDN1 HGNC, KYNU HGNC, MALL HGNC, TLR2 HGNC and YWHAG HGNC; and also AKAP8L HGNC, EXOSC5 HGNC, GDF15 HGNC, HECTD1 HGNC, LARP4B HGNC, LARP7 HGNC, MIPOL1 HGNC, UPF1 HGNC, MOV10 HGNC and PRKAR2A HGNC, host genes that interact with SARS-CoV-2 proteins. These genes are involved in cellular signaling, metabolism, immune response and RNA homeostasis. Since lncRNAs have been known to sponge microRNAs and protect expression of upregulated genes, we also identified 9 microRNAs that are induced in viral infections; however, some lncRNAs are able to block their usual suppressive effect on overexpressed genes and consequently contribute to host defense and cell survival. ConclusionsOur investigation determines that deregulated lncRNAs in SARS-CoV-2 infection MESHD are involved in viral proliferation, cellular survival, and immune response, ultimately determining disease outcome and this information could drive the search for novel RNA therapeutics as a treatment option.

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MeSH Disease
HGNC Genes
SARS-CoV-2 Proteins


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