ArticleCell communication and signaling : CCS2024
MyD88 protein destabilization mitigates NF-κB-dependent protection against macrophage apoptosis.
Article in Cell communication and signaling : CCS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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
3 citing papers in PubMed.
- Identification MYD88 as a candidate molecule of sodium overload-induced cell death in myocardial ischemia-reperfusion injury.Journal of cardiothoracic surgery · 2026Article
- Dysregulation of myddosome complex genes its related to alendronate treatment failure in osteoporosis postmenopausal patients.Genetics and molecular biology · 2026Article
- Inhibition of Farnesoid-x-receptor signaling during abdominal sepsis by dysbiosis exacerbates gut barrier dysfunction.Cell communication and signaling : CCS · 2025Article
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Various signaling pathways are essential for both the innate immune response and the maintenance of cell homeostasis, requiring coordinated interactions among them. In this study, a mutation in the caspase-1 recognition site within MyD88 abolished inflammasome-dependent negative regulation, causing phenotypic changes in mice with some similarities to human NEMO-deficiencies. The MyD88
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Registered trials
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