ArticleThe Journal of biological chemistry2019
The E3 ubiquitin ligase MIB2 enhances inflammation by degrading the deubiquitinating enzyme CYLD.
Article in The Journal of biological chemistry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
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Who cites it
20 citing papers in PubMed, 33 citations in OpenAlex.
- Ubiquitin Ligases in pro-atrophic and antiatrophic signaling cascades in muscles.Molecular biology reports · 2026Review
- 25 Years of Ebola Virus VP35 Research.Journal of molecular biology · 2025Review
- Ebola virus VP35 NNLNS motif modulates viral RNA synthesis and MIB2-mediated signaling.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Spatial and Single-Cell Transcriptomics Reveals the Regional Division of the Spatial Structure of MASH Fibrosis.Liver international : official journal of the International Association for the Study of the Liver · 2025Article
- New insights into the role of ubiquitination in angiogenesis (Review).International journal of molecular medicine · 2025Review
- Friend or foe? Reciprocal regulation between E3 ubiquitin ligases and deubiquitinases.Biochemical Society transactions · 2024Review
- Mind bomb 2 limits inflammatory dermatitis inPNAS nexus · 2024Article
- Mechanisms underlying linear ubiquitination and implications in tumorigenesis and drug discovery.Cell communication and signaling : CCS · 2023Review
- MIB2 promotes the progression of non-small cell lung cancer by regulating cell cycle control pathways.Genes & genomics · 2023Article
- Endothelial FAT1 inhibits angiogenesis by controlling YAP/TAZ protein degradation via E3 ligase MIB2.Nature communications · 2023Article
- MALT1-dependent cleavage of CYLD promotes NF-κB signaling and growth of aggressive B-cell receptor-dependent lymphomas.Blood cancer journal · 2023Article
- CF-PPiD technology based on cell-free protein array and proximity biotinylation enzyme for in vitro direct interactome analysis.Scientific reports · 2022Article
- 6-O-angeloylplenolin inhibits anti-IgE-stimulated human mast cell activation via suppressing calcium influx and ERK phosphorylation.Iranian journal of basic medical sciences · 2022Article
- Deubiquitinase CYLD acts as a negative regulator of dopamine neuron survival in Parkinson's disease.Science advances · 2022Article
- Genotoxicity-Stimulated and CYLD-Driven Malignant Transformation.Cancer management and research · 2022Article
- Selenite Inhibits Notch Signaling in Cells and Mice.International journal of molecular sciences · 2021Article
- MIND bomb 2 prevents RIPK1 kinase activity-dependent and -independent apoptosis through ubiquitylation of cFLIPCommunications biology · 2021Article
- Comprehensive Analysis of Differentially Expressed lncRNA, circRNA and mRNA and Their ceRNA Networks in Mice With Severe Acute Pancreatitis.Frontiers in genetics · 2021Article
- Linear Ubiquitin Code: Its Writer, Erasers, Decoders, Inhibitors, and Implications in Disorders.International journal of molecular sciences · 2020Review
- UBE2I promotes metastasis and correlates with poor prognosis in hepatocellular carcinoma.Cancer cell international · 2020Article
Corrections and comments
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Authors and funding
15 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The tumor suppressor CYLD is a deubiquitinating enzyme that suppresses polyubiquitin-dependent signaling pathways, including the proinflammatory and cell growth-promoting NF-κB pathway. Missense mutations in the
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What OpenQuestion holds
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.