ArticleCell death & disease2023
The ubiquitin ligase TRIM32 promotes the autophagic response to Mycobacterium tuberculosis infection in macrophages.
Article in Cell death & disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 30 citations in OpenAlex.
- The role of E3 ubiquitin ligases in selective types of macroautophagy.EMBO reports · 2026Review
- TRIM28 and TRIM32: multifaceted regulators of innate immunity and antiviral defence.Immunologic research · 2026Review
- EliminateJournal of medical microbiology · 2026Article
- Tissue-specific transcriptional epistasis between Prkn and Lrrk2 during mycobacterial infection.Mammalian genome : official journal of the International Mammalian Genome Society · 2026Article
- TRIM32 promotes anoikis resistance and metastasis in NSCLC by degrading CHEK2 to enhance IL-6 secretion.Cell death and differentiation · 2026Article
- The role of TRIM proteins in the pathogenesis of mycobacterium tuberculosis.Biology direct · 2025Review
- Deciphering macrophage dynamics and immune evasion strategies by the intracellular bacteria.Immunologic research · 2025Review
- The pathway of autophagy in the epigenetic landscape ofAutophagy · 2025Review
- SMURF2 inhibits autophagic control ofbioRxiv : the preprint server for biology · 2025Article
- Inducible antibacterial responses in macrophages.Nature reviews. Immunology · 2025Review
- Exploring the multilayered response of TB bacterium Mycobacterial tuberculosis to lysosomal injury.FEMS microbiology reviews · 2025Review
- Development of a four autophagy-related gene signature for active tuberculosis diagnosis.Frontiers in cellular and infection microbiology · 2025Article
- Selective Autophagy Mediated by Protein Ubiquitination in Major Prevalent Zoonoses.Transboundary and emerging diseases · 2025Review
- Mitophagy: A Potential Therapeutic Target for Tuberculosis Immunotherapy.ImmunoTargets and therapy · 2025Review
- Autophagy in mycobacterial infections: molecular mechanisms, host-pathogen interactions, and therapeutic opportunities.Frontiers in cellular and infection microbiology · 2025Review
- Insights into the protein ubiquitinome in the host‒pathogen interplay duringFrontiers in molecular biosciences · 2025Article
- Ubiquitination in macrophage plasticity: from inflammatory to immunometabolic pathways.Frontiers in immunology · 2025Review
- Emerging discoveries on the role of TRIM14: from diseases to immune regulation.Cell death discovery · 2024Review
- Role of AMBRA1 in mitophagy regulation: emerging evidence in aging-related diseases.Autophagy · 2024Review
- Review
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Authors and funding
12 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mycobacterium tuberculosis (Mtb) is known to evade host immune responses and persist in macrophages for long periods. A mechanism that the host uses to combat Mtb is xenophagy, a selective form of autophagy that targets intracellular pathogens for degradation. Ubiquitination of Mtb or Mtb-containing compartments is a key event to recruit the autophagy machinery and mediate the bacterial delivery to the lysosome. This event relies on the coordinated and complementary activity of different ubiquitin ligases, including PARKIN, SMURF1, and TRIM16. Because each of these factors is responsible for the ubiquitination of a subset of the Mtb population, it is likely that additional ubiquitin ligases are employed by macrophages to trigger a full xenophagic response during Mtb infection. In this study, we investigated the role TRIM proteins whose expression is modulated in response to Mtb or BCG infection of primary macrophages. These TRIMs were ectopically expressed in THP1 macrophage cell line to assess their impact on Mtb replication. This screening identified TRIM32 as a novel player involved in the intracellular response to Mtb infection, which promotes autophagy-mediated Mtb degradation. The role of TRIM32 in xenophagy was further confirmed by silencing TRIM32 expression in THP1 cells, which causes increased intracellular growth of Mtb associated to impaired Mtb ubiquitination, reduced recruitment of the autophagy proteins NDP52/CALCOCO2 and BECLIN 1/BECN1 to Mtb and autophagosome formation. Overall, these findings suggest that TRIM32 plays an important role in the host response to Mtb infection through the induction of autophagy, representing a promising target for host-directed tuberculosis therapies.
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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.