ArticleCellular & molecular immunology2021
SPOP negatively regulates Toll-like receptor-induced inflammation by disrupting MyD88 self-association.
Article in Cellular & molecular immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 49 citations in OpenAlex.
- Not only as a Cullin3 ligase adaptor, SPOP may also act as a molecular bridge.Genes & diseases · 2027Review
- Rab43 mitigates the inflammatory response in acute lung injury via MyD88 ubiquitination.Scientific reports · 2026Article
- Glial activation and increase in cerebral pro-inflammatory cytokine expression in a female animal post-COVID model.Brain, behavior, & immunity - health · 2025Article
- 9H-carbazole derivatives from a Streptomyces species under potassium iodide stress and their anti-inflammatory properties.Archives of pharmacal research · 2025Article
- Sequence rules for a long SPOP-binding degron required for protein ubiquitylation.The Biochemical journal · 2025Article
- SPOP Suppresses Hepatocellular Carcinoma Growth and Metastasis by Ubiquitination and Proteasomal Degradation of TRAF6.Cancer science · 2025Article
- Screening necroptosis genes influencing osteoarthritis development based on machine learning.Scientific reports · 2025Article
- Integrative Multi-Omics Analysis and Experimental Validation Identify SPOP as a Prognostic Biomarker and Immune Regulator in Lung Adenocarcinoma.Journal of Cancer · 2025Article
- A Chimeric Peptide Derived from a Bacterial Effector Protein Attenuates TLR-2/4-Mediated Production of Pro-Inflammatory Cytokines and Enhances the Cellular Availability of Gentamicin.Journal of inflammation research · 2025Article
- Somatic USP8 alteration affects the immune landscape of corticotroph pituitary adenomas- a pilot study.Hormones (Athens, Greece) · 2024Article
- Adipsin inhibits Irak2 mitochondrial translocation and improves fatty acid β-oxidation to alleviate diabetic cardiomyopathy.Military Medical Research · 2023Article
- Gastric protective effect ofPharmaceutical biology · 2023Article
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- Interrogating bromodomain inhibitor resistance in KMT2A-rearranged leukemia through combinatorial CRISPR screens.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
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- T Lymphocyte Subsets Profile and Toll-Like Receptors Responses in Patients with Herpes Zoster.Journal of pain research · 2023Article
- Regulation of inflammation and immunity in sepsis by E3 ligases.Frontiers in endocrinology · 2023Review
- Review
- Peste Des Petits Ruminants Virus N Protein Is a Critical Proinflammation Factor That Promotes MyD88 and NLRP3 Complex Assembly.Journal of virology · 2022Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Toll-like receptor (TLR) signaling pathways need to be tightly controlled to avoid excessive inflammation and unwanted damage to the host. Myeloid differentiation primary response gene 88 (MyD88) is a critical adaptor of TLR signaling. Here, we identified the speckle-type POZ protein (SPOP) as a MyD88-associated protein. SPOP was recruited to MyD88 following TLR4 activation. TLR4 activation also caused the translocation of SPOP from the nucleus to the cytoplasm. SPOP depletion promoted the aggregation of MyD88 and recruitment of the downstream signaling kinases IRAK4, IRAK1 and IRAK2. Consistently, overexpression of SPOP inhibited the TLR4-mediated activation of NF-κB and production of inflammatory cytokines, whereas SPOP depletion had the opposite effects. Furthermore, knockdown of SPOP increased MyD88 aggregation and inflammatory cytokine production upon TLR2, TLR7 and TLR9 activation. Our findings reveal a mechanism by which MyD88 is regulated and highlight a role for SPOP in limiting inflammatory responses.
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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.