Corpus overview


MeSH Disease

HGNC Genes

SARS-CoV-2 proteins

ProteinN (1)

ProteinS (1)


SARS-CoV-2 Proteins
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    Zinc supplement augments the suppressive effects of repurposed drugs of NF-kappa B inhibitor on ACE2 HGNC expression in human lung cell lines in vitro.

    Authors: Ming Cheng Lee; Yin-Kai Chen; Yih-Jen Hsu; Bor-Ru Lin; Balqis Afifah; Lestari Dewi; Andra Kusuma Putra; Arif Nur Muhammad Ansori; Muhammad Khaliim Jati Kusala; Mohammad Yusuf Alamudi; Chairul Anwar Nidom

    doi:10.1101/2021.01.27.428372 Date: 2021-01-27 Source: bioRxiv

    Severe acute respiratory syndrome coronavirus 2 MESHD (SARS-CoV-2) causes a vast number of infections and fatalities worldwide. As the development and safety validation of effective vaccines are ongoing, drug repurposing is most efficient approach to search FDA approved agents against coronavirus disease 2019 MESHD ( COVID-19 MESHD). In the present study, we found that endogenous ACE2 HGNC expressions could be detected in H322M and Calu-3 cell lines, as well as their ACE2 HGNC mRNA and protein expressions were suppressed by pyrrolidine dithiocarbamate (PDTC), a NF-kappa B inhibitor, in dose- and time-dependent manners. Moreover, N-acetyl-cysteine ( NAC HGNC) pretreatment reversed PDTC-induced ACE2 HGNC suppression, as well as the combined treatment of hydrogen peroxide and knockdown of p50 subunit of NF-kappa B by siRNA reduced ACE2 HGNC expression in H322M cells. In addition, anthelmintic drug triclabendazole and antiprotozoal drug emetine, repurposed drugs of NF-kappa B inhibitor, also inhibited ACE2 HGNC mRNA and protein expressions in H322M cells. Moreover, zinc supplement augmented the suppressive effects of triclabendazole and emetine on ACE2 HGNC suppression in H322M and Calu-3 cells. Taken together, these results indicate that ACE2 HGNC expression is modulated by reactive oxygen species (ROS) and NF-kappa B HGNC signal in human lung cell lines, and zinc combination with triclabendazole or emetine has the clinical potential for the prevention and treatment of COVID-19 MESHD.

    A Network-Biology led Computational Drug repurposing Strategy to prioritize therapeutic options for COVID-19 MESHD

    Authors: Pankaj Khurana; Rajeev Varshney; Aporv gupta

    doi:10.21203/ Date: 2021-01-06 Source: ResearchSquare

    The alarming pandemic situation of novel Severe Acute Respiratory Syndrome Coronavirus 2 (nSARS-CoV-2) infection MESHD, high drug development cost and slow process of drug discovery have made repositioning of existing drugs for therapeutics a popular alternative. It involves the repurposing of existing safe compounds which results in low overall development costs and shorter development timeline. In the present study, a computational network-biology approach has been used for comparing three candidate drugs i.e. quercetin, N-acetyl cysteine ( NAC HGNC), and 2-deoxy-glucose (2-DG) to be effectively repurposed against COVID-19 MESHD. For this, the associations between these drugs and genes of Severe Acute Respiratory Syndrome MESHD (SARS) and the Middle East Respiratory Syndrome MESHD ( MERS MESHD) diseases were retrieved and a directed drug-gene-gene-disease interaction network was constructed. Further, to quantify the associations between a target gene and a disease gene, the shortest paths from the target gene to the disease genes were identified. A vector DV was calculated to represent the extent to which a disease gene was influenced by these drugs. Quercetin was quantified as the best among the three drugs,  suited for repurposing with DV of -70.19, followed by NAC HGNC with DV of -39.99 and 2-DG with DV of -13.71. The drugs were also assessed for their safety and efficacy balance (in terms of therapeutic index) using network properties. It was found that quercetin was a forerunner than other two drugs. 

    In Silico studies of Natural compounds that inhibit SARS-CoV-2 Nucleocapsid Nsp1 HGNC/ Nsp3 HGNC proteins mediated Viral Replication and Pathogenesis

    Authors: Hemanth Kumar Manikyam

    doi:10.21203/ Date: 2020-11-05 Source: ResearchSquare

    Highly Transmissible and pathogenic coronavirus that emerged in late December of 2019 caused Severe acute respiratory syndrome MESHD (SARS-CoV-2), which challenged human health and public safety. Severity of the disease depends on the viral load and the type of mutation that occurred in the coronavirus. Nonstructural proteins like, Nsp1 HGNC, Nsp3 HGNC, Nsp12 and Nsp13 including other viral proteins plays important role during viral replication life cycle. Viral Replication initiated by hacking the host cellular mechanism either by synergy or by suppression using nucleocapsid proteins PROTEIN of the virus. Spike (S) protein PROTEIN of the SARS-CoV-2 uses angiotensin-converting enzyme II ( ACE2 HGNC) and TRMPSS as a cell entry. Once virus enters host cell, nucleocapsid proteins PROTEIN along with its genome is releases from endosomes into cytosol of the host cell. Ca2+/ CaM HGNC ( Calmodulin HGNC)/Calcineurin complex of the host cell plays important role during viral replication which is mediated by nucleocapsid proteins PROTEIN of the virus. Nsp1 HGNC/ Nsp3 HGNC nonstructural proteins triggers synergetic activity with CD147 HGNC/ CyPA HGNC/ HSPG HGNC pathway and TRMP2/ADPr/Ca+2 mediated Ca2+/CaM ( Calmodulin HGNC)/Calcineurin synthesis and free radicle generation in mitochondria leading to viral replication and severe chemokine activation pathways. Docking studies were carried out to inhibit Cyclophilin A and TRMP2 proteins as drug targets. Natural compounds like Withanolide A, Columbin, Cucurbitacin E, Boswellic acid along with Cyclosporines, Vitamin E and N-Acetyl cysteine ( NAC HGNC) were selected as ligands to study docking studies. Withanolide A and Cyclosporines had shown good inhibition activity against Cyclophilin A, whereas Columbin, Boswellic acid, Cucurbitacin E, Vitamin E and N-Acetyl cysteine ( NAC HGNC) had shown inhibitory activity against TRMP2. Thus, we suggest conducting further studies to conclude above pathways mechanism and inhibitory effect of natural compounds against the Nsp1 HGNC/ Nsp3 HGNC mediated pathways Invitro and In vivo.

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MeSH Disease
HGNC Genes
SARS-CoV-2 Proteins

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