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    Cell wall peptidoglycan in Mycobacterium Tuberculosis: an Achilles’ heel for the TB-causing pathogen

    Maitra, Arundhati and Munshi, Tulika and Healy, J. and Martin, L.T. and Vollmer, W. and Keep, Nicholas and Bhakta, Sanjib (2019) Cell wall peptidoglycan in Mycobacterium Tuberculosis: an Achilles’ heel for the TB-causing pathogen. FEMS Microbiology Reviews , ISSN 1574-6976. (In Press)

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    Abstract

    Tuberculosis (TB), caused by the intracellular pathogen Mycobacterium tuberculosis, remains one of the leading causes of mortality across the world. There is an urgent requirement to build a robust arsenal of effective antimicrobials, targeting novel molecular mechanisms to overcome the challenges posed by the increase of antibiotic resistance in TB. M. tuberculosis has a unique cell envelope structure and composition, containing a peptidoglycan layer that is essential for maintaining cellular integrity and for virulence. The enzymes involved in the biosynthesis, degradation, remodelling and recycling of peptidoglycan have resurfaced as attractive targets for anti-infective drug discovery. Here we review the importance of peptidoglycan, including the structure, function and regulation of key enzymes involved in its metabolism. We also discuss known inhibitors against ATP-dependent Mur ligases, and discuss the potential for the development of pan-enzyme inhibitors targeting multiple Mur ligases.

    Metadata

    Item Type: Article
    Additional Information: This is a pre-copyedited, author-produced PDF of an article accepted for publication following peer review. The version of record is available online at the link above.
    Keyword(s) / Subject(s): Tuberculosis (TB), cell envelope, peptidoglycan, metabolism, drug-target validation, 21 antibiotic resistance, antibacterial
    School: Birkbeck Schools and Departments > School of Science > Biological Sciences
    Depositing User: Administrator
    Date Deposited: 05 Jun 2019 12:46
    Last Modified: 09 Dec 2019 02:33
    URI: http://eprints.bbk.ac.uk/id/eprint/27730

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