ArticleNature immunology2015
Mycobacterium tuberculosis suppresses innate immunity by coopting the host ubiquitin system.
Article in Nature immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 108 papers.
What it found
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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
108 citing papers in PubMed, 181 citations in OpenAlex.
- Rab14 restricts pathogens by promoting V-ATPase lysosomal delivery to drive lysosomal acidification.Nature communications · 2026Article
- A bacterial YopJ-family acetyltransferase suppresses host immune response by Nε-acetylation of JAK1.Nature communications · 2026Article
- A Key Metabolic Protein in Active Mycobacterium tuberculosis: Insights into Carbon, Nitrogen, and Sulfur Metabolism.Advances in experimental medicine and biology · 2026Review
- Structure and mechanism of an actin-dependent bacterial phosphoryl AMPylase.Nature chemical biology · 2026Article
- Review
- Secreted proteins ofFrontiers in tuberculosis · 2026Review
- Cell death pathways in response toInfection and immunity · 2025Review
- Mycobacterial Tyrosine Phosphatase PtpB Affects Host Cytokine Expression by Dephosphorylating ERK1/2 and STAT3.Molecular & cellular proteomics : MCP · 2025Article
- Spatiotemporal Regulation of STING Activity by Linear Ubiquitination Governs Antiviral Immunity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Characterization of the Biological Effect Mediated by Mycobacterial Kinase PknG on Protein Phosphorylation and Acetylation.ACS omega · 2025Article
- Coexisting Lung Cancer and Pulmonary Tuberculosis: A Comprehensive Review From Incidence to Management.Cancer reports (Hoboken, N.J.) · 2025Review
- Mycobacterial PstP impairs host RNA alternative splicing by dephosphorylation of spliceosome RBMX at S189.iMetaOmics · 2025Article
- Article
- Rheumatic diseases and latent tuberculosis infection in children: diagnostic and therapeutic challenges.Frontiers in cellular and infection microbiology · 2025Review
- Research progress on protein tyrosine phosphatase A from Mycobacterium tuberculosis.Frontiers in immunology · 2025Review
- Dysregulation of the JNK signaling pathway in tuberculosis: mechanisms and therapeutic strategies.Frontiers in cellular and infection microbiology · 2025Review
- Selective Autophagy Mediated by Protein Ubiquitination in Major Prevalent Zoonoses.Transboundary and emerging diseases · 2025Review
- Article
- Mycobacterium tuberculosis protein Rv2652c enhances intracellular survival by inhibiting host immune responses.Immunity, inflammation and disease · 2024Article
- Suppression of host gene expression is associated with latent TB infection: a possible diagnostic biomarker.Scientific reports · 2024Article
48 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mycobacterium tuberculosis PtpA, a secreted tyrosine phosphatase essential for tuberculosis pathogenicity, could be an ideal target for a drug against tuberculosis, but its active-site inhibitors lack selectivity over human phosphatases. Here we found that PtpA suppressed innate immunity dependent on pathways of the kinases Jnk and p38 and the transcription factor NF-κB by exploiting host ubiquitin. Binding of PtpA to ubiquitin via a region with no homology to human proteins activated it to dephosphorylate phosphorylated Jnk and p38, leading to suppression of innate immunity. Furthermore, the host adaptor TAB3 mediated NF-κB signaling by sensing ubiquitin chains, and PtpA blocked this process by competitively binding the ubiquitin-interacting domain of TAB3. Our findings reveal how pathogens subvert innate immunity by coopting host ubiquitin and suggest a potential tuberculosis treatment via targeting of ubiquitin-PtpA interfaces.
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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.