ArticleInternational microbiology : the official journal of the Spanish Society for Microbiology2024
Mycobacterium tuberculosis Rv1043c regulates the inflammatory response by inhibiting the phosphorylation of TAK1.
Article in International microbiology : the official journal of the Spanish Society for Microbiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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
1 citing paper in PubMed, 1 citations in OpenAlex.
- MAPK signaling pathways in host immune regulation during Mycobacterium tuberculosis infection.Frontiers in immunology · 2026Review
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mycobacterium tuberculosis can manipulate the host immunity through its effectors to ensure intracellular survival and colonization. Rv1043c has been identified as an effector potentially involved in M. tuberculosis pathogenicity. To explore the function of M. tuberculosis Rv1043c during infection, we overexpressed this protein in M. smegmatis, a non-pathogenic surrogate model in tuberculosis research. Here, we reported that Rv1043c enhanced mycobacterial survival and down-regulated the release of pro-inflammatory cytokines in macrophages and mice. In addition, Rv1043c inhibited the activation of MAPK and NF-κB signaling by preventing the phosphorylation of TAK1 indirectly. In conclusion, these data suggest that Rv1043c regulates the immune response and enhances the survival of recombinant M. smegmatis in vitro and in vivo.
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