COVID-19: A novel holistic systems biology approach to predict its molecular mechanisms (in vitro) and repurpose drugs.

Purpose: COVID-19 strangely kills some youth with no history of physical weakness, and in addition to the lungs, it may even directly harm other organs. Its complex mechanism has led to the loss of any significantly effective drug, and some patients with severe forms still die daily. Common methods for identifying disease mechanisms and drug design are often time-consuming or reductionist.

Deciphering crucial genes in multiple sclerosis pathogenesis and drug repurposing: A systems biology approach.

This study employed systems biology and high-throughput technologies to analyze complex molecular components of MS pathophysiology, combining data from multiple omics sources to identify potential biomarkers and propose therapeutic targets and repurposed drugs for MS treatment. This study analyzed GEO microarray datasets and MS proteomics data using geWorkbench, CTD, and COREMINE to identify differentially expressed genes associated with MS disease. Protein-protein interaction networks were constructed using Cytoscape and its plugins, and functional enrichment analysis was performed to identify crucial molecules.

Specific Regulatory Motifs Network in SARS-CoV-2-Infected Caco-2 Cell Line, as a Model of Gastrointestinal Infections.

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) was primarily noted as a respiratory pathogen, but later clinical reports highlighted its extrapulmonary effects particularly on the gastrointestinal (GI) tract. The aim of the current study was the prediction of crucial genes associated with the regulatory network motifs, probably responsible for the SARS-CoV-2 effects on the GI tract. The data were obtained from a published study on the effect of SARS-CoV-2 on the Caco-2 (colon carcinoma) cell line.

Investigating the efficacy of UVSE protein at repairing CPD and 6-4 pp DNA damages in human cells.

UV exposure could induce carcinogenic mutation in human cells, including CPD (Cyclobutane pyrimidine dimer), and 6-4 pp (6-4 photoproduct) DNA damages. Spiting the active BER (Base Excision Repair) system of human cells, it lacks initiator glycosylase, rendering these damages to be only repaired through NER (Nucleotide Excision Repair) system. Some microorganisms such as Deinococcus radiodurans bacteria have a BER system for repairing these damages with an enzyme coded by the uvsE gene.