ArticlePLoS pathogens2017
ALPK1 controls TIFA/TRAF6-dependent innate immunity against heptose-1,7-bisphosphate of gram-negative bacteria.
Article in PLoS pathogens, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.
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Who cites it
68 citing papers in PubMed, 130 citations in OpenAlex.
- Variants of ALPK1 with ABCG2, SLC2A9, and SLC22A12 increased the positive predictive value for gout.Journal of human genetics · 2018Trial
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- Host response to bacteria induces a shift towards the enteroendocrine cell lineage in the murine enteroid model.PLoS pathogens · 2026Article
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- Enhanced ADP-heptose-dependent NF-κB activation bymicroLife · 2026Article
- TIFA: a signaling hub linking inflammation, innate immunity, and human disease.Frontiers in immunology · 2026Review
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- Discovery of a selective alpha-kinase 1 inhibitor for the rare genetic disease ROSAH syndrome.Nature communications · 2025Article
- TRAF2 binds to TIFA via a novel motif and contributes to its autophagic degradation.FEBS letters · 2025Article
- The importance of ALPK1 kinase functionality as a potential biomarker for inflammatory diseases.Molecular biology reports · 2025Review
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- Proximity biotinylation at the host-bioRxiv : the preprint server for biology · 2025Article
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- Patterns of Klebsiella pneumoniae bacteremic dissemination from the lung.Nature communications · 2025Article
- Anaerobic gut bacteria and their potential role in the initiation, exacerbation, and development of human colorectal cancer: a narrative review.Frontiers in cellular and infection microbiology · 2025Review
- The relationship of ALPK1, hyaluronic acid and M1 macrophage polarization in the temporomandibular joint synovitis.Journal of cellular and molecular medicine · 2024Article
- TIFAB regulates the TIFA-TRAF6 signaling pathway involved in innate immunity by forming a heterodimer complex with TIFA.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- TIFA contributes to periodontitis in diabetic mice via activating the NF‑κB signaling pathway.Molecular medicine reports · 2024Article
8 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
During infection by invasive bacteria, epithelial cells contribute to innate immunity via the local secretion of inflammatory cytokines. These are directly produced by infected cells or by uninfected bystanders via connexin-dependent cell-cell communication. However, the cellular pathways underlying this process remain largely unknown. Here we perform a genome-wide RNA interference screen and identify TIFA and TRAF6 as central players of Shigella flexneri and Salmonella typhimurium-induced interleukin-8 expression. We show that threonine 9 and the forkhead-associated domain of TIFA are necessary for the oligomerization of TIFA in both infected and bystander cells. Subsequently, this process triggers TRAF6 oligomerization and NF-κB activation. We demonstrate that TIFA/TRAF6-dependent cytokine expression is induced by the bacterial metabolite heptose-1,7-bisphosphate (HBP). In addition, we identify alpha-kinase 1 (ALPK1) as the critical kinase responsible for TIFA oligomerization and IL-8 expression in response to infection with S. flexneri and S. typhimurium but also to Neisseria meningitidis. Altogether, these results clearly show that ALPK1 is a master regulator of innate immunity against both invasive and extracellular gram-negative bacteria.
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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.