ArticleNature communications2026
Mycobacterium tuberculosis modulates phosphorylation of host ATP6V1E1 to promote intracellular survival.
Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- Carrier-free nanoparticles in microneedles disrupt endosomal acidification suppress ferroptosis in radiation-induced oral mucositis.Materials today. Bio · 2026Article
- Multi-Omics Reveals Dysregulation of the Endosome-Lysosome-Autophagy Axis and Immune-Inflammatory Imbalance in Elderly Sepsis.Clinical interventions in aging · 2026Article
Corrections and comments
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Authors and funding
23 authors.
Funding
Abstract
Intracellular pathogens such as Mycobacterium tuberculosis (Mtb) can promote their survival within infected cells by preventing lysosomal acidification. Here, we report that Mtb secretes a protein (Rv1184, or acyltransferase Chp2) that inhibits lysosomal acidification by targeting the host vacuolar ATPase (V-ATPase). We show that phosphorylation of the V-ATPase E1 subunit (ATP6V1E1) at Tyr56/57 suppresses lysosomal acidification through inhibition of V-ATPase assembly. Further investigation reveals that tyrosine kinase BMX promotes phosphorylation of ATP6V1E1. Strikingly, Chp2 increases BMX-dependent phosphorylation of ATP6V1E1, apparently by directly binding ATP6V1E1 and facilitating its interaction with BMX. Furthermore, inhibition of BMX impairs Mtb growth within macrophages and in mice. Thus, our work reveals a mechanism for the regulation of lysosomal acidification and suggests lysosomal acidification modulation as a potential approach for host-directed therapy against Mtb.
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Registered trials
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