Abstract
The mammalian-cell-entry (Mce) proteins of Mycobacterium tuberculosis enable the bacterium to acquire lipids from the host cells. Asthana et al. [IUCrJ (2021). 8, 757-774] present the first structural insights into the potential assembly of Mce1 and Mce4, advancing our understanding of lipid transport by the human pathogen that causes tuberculosis.
Highlights
Reported hexameric SBPs observed in E. coli (Ekiert et al, 2017; Isom et al, 2020; Liu et al, 2020; Coudray et al, 2020) and A. baumannii (Kamischke et al, 2019; Mann et al, 2020)
Known as Phthisis (Greek), the ‘white plague’ or consumption, tuberculosis appears as a common theme in art, music and literature, and has shaped many elements of human social history (Daniel, 2006)
One-quarter of the world’s population is estimated to carry latent infections by Mycobacterium tuberculosis, the bacterium that causes tuberculosis (Getahun et al., 2015). Why is this disease so recalcitrant to treatment? This is, in part, due to the distinctive cell envelope of M. tuberculosis, which provides a physical barrier against antibiotics (Batt et al., 2020)
Summary
Reported hexameric SBPs observed in E. coli (Ekiert et al, 2017; Isom et al, 2020; Liu et al, 2020; Coudray et al, 2020) and A. baumannii (Kamischke et al, 2019; Mann et al, 2020). Tuberculosis is a devastating disease that has afflicted humans since antiquity.
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