ArticleCell reports2017
Mycobacterium tuberculosis Controls Phagosomal Acidification by Targeting CISH-Mediated Signaling.
Article in Cell reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 86 citations in OpenAlex.
- Molecular Interplay of Brucellosis and Tuberculosis: Insights into Telomere Biology, Oxidative Stress, and Drug Resistance Mechanisms.Diseases (Basel, Switzerland) · 2026Review
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- Mycobacterium tuberculosis modulates phosphorylation of host ATP6V1E1 to promote intracellular survival.Nature communications · 2026Article
- Mitochondria beyond boundaries: from cellular powerhouses to intercellular messengers in health and disease.Science China. Life sciences · 2026Review
- Mycobacterial α-glucans hijack dectin-1 to facilitate intracellular bacterial survival.Science immunology · 2026Article
- Cytokine inducible SH2-containing protein: a versatile negative regulator of cytokine receptor signaling.Frontiers in immunology · 2026Review
- Excessive Kynurenine Metabolism Impairs Lysosomal acidification and Triggers mtDNA Release via the AHR/CISH/ATP6V1A Axis in Decidual Macrophages Associated with Unexplained Recurrent Pregnancy Loss.International journal of biological sciences · 2026Article
- Endogenous hepcidin plays an essential role inEmerging microbes & infections · 2025Article
- Proton-activated chloride channel governs phagosome-mediated antibacterial immunity in peritoneal macrophages.The Journal of experimental medicine · 2025Article
- Host-directed therapeutic targets in macrophages and their ligands against mycobacteria tuberculosis.Infection and immunity · 2025Review
- Unraveling Mycobacterium tuberculosis acid resistance and pH homeostasis mechanisms.FEBS letters · 2025Review
- Functionalized Polydopamine Nanoparticles: A Promising Drug Delivery Platform for the Treatment of Tuberculosis.Drug development research · 2025Review
- Phagosome-mediated anti-bacterial immunity is governed by the proton-activated chloride channel in peritoneal macrophages.bioRxiv : the preprint server for biology · 2025Article
- The tryptophan-aspartate (WD) repeat domain of bovine Coronin-1A promotes mycobacterial survival by inhibiting calcium signaling-mediated phagosome-lysosome fusion.Veterinary research · 2025Article
- Host Immune Response toJournal of inflammation research · 2025Review
- High throughput screening assay for the identification of ATF4 and TFEB activating compounds.Autophagy reports · 2025Article
- Dual single-cell and bulk RNA sequencing reveal transcriptional profiles underlying heterogenous host-parasite interactions in human peripheral blood mononuclear cells.Frontiers in immunology · 2025Article
- Reprogramming the host: Mycobacterium tuberculosis as a silent architect of the immuno-tumoral.Frontiers in cellular and infection microbiology · 2025Review
- Advancements in Green Nanoparticle Technology: Focusing on the Treatment of Clinical Phytopathogens.Biomolecules · 2024Review
- Characterisation of sRNAs enriched in outer membrane vesicles of pathogenicJournal of extracellular biology · 2024Article
Corrections and comments
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Authors and funding
18 authors at 8 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pathogens have evolved a range of mechanisms to counteract host defenses, notably to survive harsh acidic conditions in phagosomes. In the case of Mycobacterium tuberculosis, it has been shown that regulation of phagosome acidification could be achieved by interfering with the retention of the V-ATPase complexes at the vacuole. Here, we present evidence that M. tuberculosis resorts to yet another strategy to control phagosomal acidification, interfering with host suppressor of cytokine signaling (SOCS) protein functions. More precisely, we show that infection of macrophages with M. tuberculosis leads to granulocyte-macrophage colony-stimulating factor (GM-CSF) secretion, inducing STAT5-mediated expression of cytokine-inducible SH2-containing protein (CISH), which selectively targets the V-ATPase catalytic subunit A for ubiquitination and degradation by the proteasome. Consistently, we show that inhibition of CISH expression leads to reduced replication of M. tuberculosis in macrophages. Our findings further broaden the molecular understanding of mechanisms deployed by bacteria to survive.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.