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    Role of post-translational modifications in the acquisition of drug resistance in Mycobacterium tuberculosis

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    Authors
    Arora, G.
    Bothra, A.
    Prosser, Gareth
    Arora, K.
    Sajid, A.
    Affiliation
    Yale School of Medicine, Yale University, New Haven, CT, 06519, USA.
    Issue Date
    2020
    
    Metadata
    Show full item record
    Abstract
    Tuberculosis (TB) is one of the primary causes of deaths due to infectious diseases. The current TB regimen is long and complex, failing of which leads to relapse and/or the emergence of drug resistance. There is a critical need to understand the mechanisms of resistance development. With increasing drug pressure, Mycobacterium tuberculosis (Mtb) activates various pathways to counter drug-related toxicity. Signaling modules steer the evolution of Mtb to a variant that can survive, persist, adapt, and emerge as a form that is resistant to one or more drugs. Recent studies reveal that about 1/3rd of the annotated Mtb proteome is modified post-translationally, with a large number of these proteins being essential for mycobacterial survival. Post-translational modifications (PTMs) such as phosphorylation, acetylation, and pupylation play a salient role in mycobacterial virulence, pathogenesis, and metabolism. The role of many other PTMs is still emerging. Understanding the signaling pathways and PTMs may assist clinical strategies and drug development for Mtb. In this review, we explore the contribution of PTMs to mycobacterial physiology, describe the related cellular processes, and discuss how these processes are linked to drug resistance. A significant number of drug targets, InhA, RpoB, EmbR, and KatG, are modified at multiple residues via PTMs. A better understanding of drug-resistance regulons and associated PTMs will aid in developing effective drugs against TB.
    Citation
    Arora G, Bothra A, Prosser G, Arora K, Sajid A. Role of post-translational modifications in the acquisition of drug resistance in Mycobacterium tuberculosis. FEBS J. 2020.
    Journal
    FEBS Journal
    URI
    http://hdl.handle.net/10541/623354
    DOI
    10.1111/febs.15582
    PubMed ID
    33021056
    Additional Links
    https://dx.doi.org/10.1111/febs.15582
    Type
    Article
    Language
    en
    ae974a485f413a2113503eed53cd6c53
    10.1111/febs.15582
    Scopus Count
    Collections
    All Paterson Institute for Cancer Research

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