ArticleBMC biology2019
Role of self-organising myddosome oligomers in inflammatory signalling by Toll-like receptors.
Article in BMC biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed.
- RNA Binding Proteins that Mediate LPS-induced Alternative Splicing of the MyD88 Innate Immune Regulator.Journal of molecular biology · 2024Article
- The Role of TRL7/8 Agonists in Cancer Therapy, with Special Emphasis on Hematologic Malignancies.Vaccines · 2023Review
- Supramolecular organizing centers at the interface of inflammation and neurodegeneration.Frontiers in immunology · 2022Review
- Toll-Like Receptors as a Therapeutic Target in the Era of Immunotherapies.Frontiers in cell and developmental biology · 2021Review
- Identification of candidate biomarkers correlated with pathogenesis of postoperative peritoneal adhesion by using microarray analysis.World journal of gastrointestinal oncology · 2020Article
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Abstract
A paper published in BMC Biology characterises biophysically oligomeric and filamentous structures formed spontaneously by the Toll-like receptor signalling adaptor MyD88. Naturally occurring mutants of MyD88 that cause immunodeficiency are unable to form these structures. By contrast a somatic mutant that promotes the survival of tumour cells forms oligomers much more readily than the wild-type protein. These findings suggest that assembly of oligomeric MyD88 is critical for the regulation of inflammatory signalling.
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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.