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AuthorKeerthana, G.
AuthorVasudevan, Karthick
AuthorDey, Hrituraj
AuthorKausar, Tasmia
AuthorUdhaya Kumar, S.
AuthorThirumal Kumar, D.
AuthorZayed, Hatem
AuthorGeorge Priya Doss, C.
Available date2023-03-28T11:06:49Z
Publication Date2023-12-31
Publication NameAdvances in Protein Chemistry and Structural Biology
Identifierhttp://dx.doi.org/10.1016/bs.apcsb.2022.11.017
CitationDonev, R. (Ed.). (2022). Protein Interaction Networks. Academic Press.
ISBN9780443131813
ISSN1876-1623
URIhttps://www.sciencedirect.com/science/article/pii/S1876162322001067
URIhttp://hdl.handle.net/10576/41401
AbstractAntimicrobial resistance (AMR) in microorganisms is an urgent global health threat. AMR of Mycobacterium tuberculosis is associated with significant morbidity and mortality. It is of great importance to underpin the resistance pathways involved in the mechanisms of AMR and identify the genes that are directly involved in AMR. The focus of the current study was the bacteria M. tuberculosis, which carries AMR genes that give resistance that lead to multidrug resistance. We, therefore, built a network of 43 genes and examined for potential gene-gene interactions. Then we performed a clustering analysis and identified three closely related clusters that could be involved in multidrug resistance mechanisms. Through the bioinformatics pipeline, we consistently identified six-hub genes (dnaN, polA, ftsZ, alr, ftsQ, and murC) that demonstrated the highest number of interactions within the clustering analysis. This study sheds light on the multidrug resistance of MTB and provides a protocol for discovering genes that might be involved in multidrug resistance, which will improve the treatment of resistant strains of TB.
Languageen
PublisherElsevier
SubjectAMR
M. tuberculosis
Antimicrobial resistance
Gene interaction network
Cytoscape
Enrichment analysis
TitleChapter Three Elucidating the mechanism of antimicrobial resistance in Mycobacterium tuberculosis using gene interaction networks
TypeBook chapter
Pagination53 - 74
Volume Number134
ESSN1876-1631
dc.accessType Abstract Only


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