ArticleThe Journal of biological chemistry2020
The deubiquitinase USP7 uses a distinct ubiquitin-like domain to deubiquitinate NF-ĸB subunits.
Article in The Journal of biological chemistry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 49 citations in OpenAlex.
- Thrombin concentration shapes endothelial extracellular vesicle profiles with divergent inflammatory functions.Blood advances · 2026Article
- Thrombin reprograms endothelial extracellular vesicles.Blood advances · 2026Article
- The Ubiquitin-Specific Protease Family: Master Regulators of Renal Fibrosis Pathogenesis and Therapeutic Targets.International journal of molecular sciences · 2026Review
- MLL1-pioneered H3K4me3 modification on KLF7 promoter accelerates the invasion of fibroblast-like synoviocytes in rheumatoid arthritis.In vitro cellular & developmental biology. Animal · 2026Article
- Extracellular vesicles-delivered circDB promotes ischemic muscle repair through the miR-34a/USP7/Notch1 signaling pathway.Regenerative therapy · 2025Article
- A designer polyQ fusion protein modulates NF-κB signaling by sequestering P65/RelA into aggregates.Scientific reports · 2025Article
- Ubiquitin-specific protease 7 exacerbates acute pancreatitis progression by enhancing ATF4-mediated autophagy.In vitro cellular & developmental biology. Animal · 2025Article
- Chromatin-associated cullin-RING E3 ubiquitin ligases: keeping transcriptionally active NF-κB in check.Frontiers in immunology · 2025Review
- Article
- Ubiquitin-specific protease-7 promotes expression of airway mucin MUC5AC via the NF-κB signaling pathway.Heliyon · 2024Article
- WSB1/2 target chromatin-bound lysine-methylated RelA for proteasomal degradation and NF-κB termination.Nucleic acids research · 2024Article
- CanPharmaceuticals (Basel, Switzerland) · 2024Review
- Review
- Inhibitory Effect of P22077 on Airway Inflammation in Rats with COPD and Its Mechanism.International journal of chronic obstructive pulmonary disease · 2024Article
- Ubiquitin ligase enzymes and de-ubiquitinating enzymes regulate innate immunity in the TLR, NLR, RLR, and cGAS-STING pathways.Immunologic research · 2023Review
- USP7 controls NGN3 stability and pancreatic endocrine lineage development.Nature communications · 2023Article
- Genomic signatures and prognosis of advanced stage Chinese pediatric T cell lymphoblastic lymphoma by whole exome sequencing.Frontiers in pediatrics · 2023Article
- USP7 regulates the ERK1/2 signaling pathway through deubiquitinating Raf-1 in lung adenocarcinoma.Cell death & disease · 2022Article
- RING finger 138 deregulation distorts NF-кB signaling and facilities colitis switch to aggressive malignancy.Signal transduction and targeted therapy · 2022Article
- Heparanase Blockade as a Novel Dual-Targeting Therapy for COVID-19.Journal of virology · 2022Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 3 countries.
Funding
Abstract
The transcription factor NF-ĸB is a master regulator of the innate immune response and plays a central role in inflammatory diseases by mediating the expression of pro-inflammatory cytokines. Ubiquitination-triggered proteasomal degradation of DNA-bound NF-ĸB strongly limits the expression of its target genes. Conversely, USP7 (deubiquitinase ubiquitin-specific peptidase 7) opposes the activities of E3 ligases, stabilizes DNA-bound NF-ĸB, and thereby promotes NF-ĸB-mediated transcription. Using gene expression and synthetic peptide arrays on membrane support and overlay analyses, we found here that inhibiting USP7 increases NF-ĸB ubiquitination and degradation, prevents Toll-like receptor-induced pro-inflammatory cytokine expression, and represents an effective strategy for controlling inflammation. However, the broad regulatory roles of USP7 in cell death pathways, chromatin, and DNA damage responses limit the use of catalytic inhibitors of USP7 as anti-inflammatory agents. To this end, we identified an NF-ĸB-binding site in USP7, ubiquitin-like domain 2, that selectively mediates interactions of USP7 with NF-ĸB subunits but is dispensable for interactions with other proteins. Moreover, we found that the amino acids
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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.