ArticlePLoS pathogens2020
SPOP promotes ubiquitination and degradation of MyD88 to suppress the innate immune response.
Article in PLoS pathogens, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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Who cites it
22 citing papers in PubMed, 39 citations in OpenAlex.
- Not only as a Cullin3 ligase adaptor, SPOP may also act as a molecular bridge.Genes & diseases · 2027Review
- Review
- The HCMV tegument protein UL88 degrades MyD88 and reduces innate immune activation.Journal of virology · 2025Article
- Sequence rules for a long SPOP-binding degron required for protein ubiquitylation.The Biochemical journal · 2025Article
- Pathological roles of ubiquitination and deubiquitination systems in sepsis-induced myocardial dysfunction.Biomolecules & biomedicine · 2025Review
- SPOP Suppresses Hepatocellular Carcinoma Growth and Metastasis by Ubiquitination and Proteasomal Degradation of TRAF6.Cancer science · 2025Article
- Human breast milk-derived exosomes attenuate lipopolysaccharide-induced activation in microglia.Journal of neuroinflammation · 2025Article
- Cbl promotes MyD88 ubiquitin-mediated degradation in macrophages via phosphorylation and calcium mobilization.Frontiers in immunology · 2025Article
- Transcriptome-wide N6-methyladenosinem modifications analysis of chicken cecum in responding toFrontiers in immunology · 2025Article
- Cullin-Conciliated Regulation of Plant Immune Responses: Implications for Sustainable Crop Protection.Plants (Basel, Switzerland) · 2024Review
- OTUD5 promotes the inflammatory immune response by enhancing MyD88 oligomerization and Myddosome formation.Cell death and differentiation · 2024Article
- C-type lectin receptor 2d forms homodimers and heterodimers with TLR2 to negatively regulate IRF5-mediated antifungal immunity.Nature communications · 2023Article
- Article
- Transcriptome Analysis of Diffuse Large B-Cell Lymphoma Cells Inducibly Expressing MyD88 L265P Mutation Identifies Upregulated CD44, LGALS3, NFKBIZ, and BATF as Downstream Targets of Oncogenic NF-κB Signaling.International journal of molecular sciences · 2023Article
- Toxoplasma gondii microneme protein MIC3 induces macrophage TNF-α production and Ly6C expression via TLR11/MyD88 pathway.PLoS neglected tropical diseases · 2023Article
- Regulation of innate immune signaling by IRAK proteins.Frontiers in immunology · 2023Review
- USP7 Promotes deubiquitination and stabilization of MyD88 to enhance immune responses.Frontiers in immunology · 2022Article
- Counting Degrons: Lessons From Multivalent Substrates for Targeted Protein Degradation.Frontiers in physiology · 2022Review
- Association of Heterophil/Lymphocyte Ratio with Intestinal Barrier Function and Immune Response toAnimals : an open access journal from MDPI · 2021Article
- Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
As a canonical adaptor for the Toll-like receptor (TLR) family, myeloid differentiation primary response protein 88 (MyD88) has crucial roles in host defense against infection by microbial pathogens, and its dysregulation might induce autoimmune diseases. Here, we demonstrate that the chicken Cullin 3-based ubiquitin ligase adaptor Speckle-type BTB-POZ protein (chSPOP) recognizes the intermediate domain of chicken MyD88 (chMyD88) and degrades it through the proteasome pathway. Knockdown or genetic ablation of chSPOP leads to aberrant elevation of chMyD88 protein. Through this interaction, chSPOP negatively regulates NF-κB pathway activity and thus the production of IL-1β upon LPS challenge in chicken macrophages. Furthermore, Spop-deficient mice are more susceptible to infection with Salmonella typhimurium. Collectively, these findings demonstrate MyD88 as a bona fide substrate of SPOP and uncover a mechanism by which SPOP regulates MyD88 abundance and disease susceptibility.
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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.