ArticleFrontiers in immunology2020
PDLIM7 Synergizes With PDLIM2 and p62/Sqstm1 to Inhibit Inflammatory Signaling by Promoting Degradation of the p65 Subunit of NF-κB.
Article in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 46 citations in OpenAlex.
- CIDER: detecting changes in gene regulatory networks that are associated with changes in phenotype.bioRxiv : the preprint server for biology · 2026Article
- Host-directed clearance of nuclear tegument U14 terminates NF-κB signaling and supports HHV-6A replication.PLoS pathogens · 2026Article
- PDLIM4 promotes dephosphorylation of STAT transcription factors by recruiting PTP-BL and inhibits Th1, Th2, and Th17 cell differentiation.International immunology · 2026Article
- Diet-responsive proteogenomic effects following short-term restriction of animal products in humans.Nature communications · 2026Article
- PDLIM2 acts as a central regulator of ubiquitination, immune signaling, and mitochondrial metabolism in lung cancer suppression (Review).International journal of oncology · 2026Review
- Multi-omics integration and machine learning identify a novel gene signature consisting of CCDC141, CHI3L2, RIMKLB, and PDLIM7 in bronchopulmonary dysplasia associated with neutrophil-driven immune dysregulation.Clinics (Sao Paulo, Brazil) · 2026Article
- Review
- Epigenetic activation of PDLIM7 via H3K27 acetylation mitigates neuroinflammation and neurodegeneration in parkinson's disease models.Journal of bioenergetics and biomembranes · 2026Article
- Metabolic and post-translational modifications in sepsis-associated immune dysfunction: a conceptual framework.Frontiers in immunology · 2026Review
- Prognostic risk model based on cholesterol metabolism-Associated gene module for idiopathic pulmonary fibrosis.PloS one · 2026Article
- Article
- Genome-Wide Aggregated Trans-Effects Analysis Implicates Deficient Type III Interferon Signaling as a Key Cause of Inflammatory Bowel Disease.Inflammatory bowel diseases · 2025Article
- Senescent cells promote viral infection-associated inflammation and tissue damage through a robust NF-κB pathway.Cell communication and signaling : CCS · 2025Article
- Neuroprotective Terpenoids Derived fromInternational journal of molecular sciences · 2025Article
- A hybrid protein is a functional molecule to reduce the cytokine storm caused by excessively activated macrophages.Immunology and cell biology · 2025Article
- Fbxo16 mediates degradation of NF-κB p65 subunit and inhibits inflammatory response in dendritic cells.Frontiers in immunology · 2025Article
- ABLIM1: A novel oncogenic E3 ligase in colorectal cancer.Frontiers in oncology · 2025Article
- Article
- Annexin A1 binds PDZ and LIM domain 7 to inhibit adipogenesis and prevent obesity.Signal transduction and targeted therapy · 2024Article
- OGA mutant aberrantly hydrolyzes O-GlcNAc modification from PDLIM7 to modulate p53 and cytoskeleton in promoting cancer cell malignancy.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Activation of NF-κB transcription factors is critical for innate immune cells to induce inflammation and fight against microbial pathogens. On the other hand, the excessive and prolonged activation of NF-κB causes massive inflammatory damage to the host, suggesting that regulatory mechanisms to promptly terminate NF-κB activation are important to prevent immunopathology. We have previously reported that PDLIM2, a PDZ-LIM domain-containing protein, is a nuclear ubiquitin E3 ligase that targets the p65 subunit of NF-κB for degradation, thereby suppressing NF-κB activation. Here we show that PDLIM7, another member of LIM protein family, is also a ubiquitin E3 ligase that inhibits NF-κB-mediated inflammatory responses. PDLIM7 directly polyubiquitinates p65 and promotes its proteasomal degradation. Moreover, PDLIM7 heterodimerizes with PDLIM2 to promote synergistic PDLIM2-mediated degradation of p65. Mechanistically, PDLIM7 promotes K63-linked ubiquitination of PDLIM2 and then the proteasome/autophagosome cargo protein p62/Sqstm1 binds to both polyubiquitinated PDLIM2 and the proteasome, thereby facilitating the delivery of the NF-κB-PDLIM2 complex to the proteasome and subsequent p65 degradation. Consistently, double knockdown of PDLIM7 and either PDLIM2 or p62/Sqstm1 results in augmented proinflammatory cytokine production compared to control cells or single knockdown cells. These data delineate a new role for PDLIM7 and p62/Sqstm1 in the regulation of NF-κB signaling by bridging a ubiquitin E3 ligase and the proteasome.
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