ArticleThe Journal of experimental medicine2018
USP38 critically promotes asthmatic pathogenesis by stabilizing JunB protein.
Article in The Journal of experimental medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 50 citations in OpenAlex.
- USP38 promotes breast cancer immune evasion and malignant progression by deubiquitinating and stabilizing PD-L1.Mammalian genome : official journal of the International Mammalian Genome Society · 2026Article
- OTUD6A in Airway Epithelial Cells Exacerbates Allergic Asthma by Promoting Airway Inflammation and Airway Remodeling Through Deubiquitination of hResistin/mRELMα.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- USP18 confers protection against allergic asthma by suppressing CCL8 production in alveolar type II epithelial cells.Respiratory research · 2025Article
- The Ubiquitin-Proteasome System in Asthma: Mechanisms and Therapeutic Possibilities.Clinical reviews in allergy & immunology · 2025Review
- Ubiquitination regulates allergic asthma by affecting immune cells and immune responses.Biochemistry and biophysics reports · 2025Review
- Inhibition of Mitochondrial Succinate Dehydrogenase with Dimethyl Malonate Promotes M2 Macrophage Polarization by Enhancing STAT6 Activation.Inflammation · 2025Article
- The Role of Ubiquitin-Proteasome System (UPS) in Asthma Pathology.Journal of asthma and allergy · 2025Review
- USP38: an important regulatory factor in tumor malignant progression.Frontiers in immunology · 2025Review
- The role of ubiquitination in health and disease.MedComm · 2024Review
- Article
- Anti-CD20 treatment attenuates Th2 cell responses: implications for the role of lung follicular mature B cells in the asthmatic mice.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024Article
- Review
- USP38 promotes deubiquitination of K11-linked polyubiquitination of HIF1α at Lys769 to enhance hypoxia signaling.The Journal of biological chemistry · 2024Article
- Ubiquitin specific protease 38 aggravates pathological cardiac remodeling by stabilizing phospho-TBK1.International journal of biological sciences · 2024Article
- USP38 exacerbates atrial inflammation, fibrosis, and susceptibility to atrial fibrillation after myocardial infarction in mice.Molecular medicine (Cambridge, Mass.) · 2023Article
- JunB: a paradigm for Jun family in immune response and cancer.Frontiers in cellular and infection microbiology · 2023Review
- Neutrophil activation and NETosis are the predominant drivers of airway inflammation in an OVA/CFA/LPS induced murine model.Respiratory research · 2022Article
- The feedback loop of METTL14 and USP38 regulates cell migration, invasion and EMT as well as metastasis in bladder cancer.PLoS genetics · 2022Article
- Long-term effects of wildfire smoke exposure during early life on the nasal epigenome in rhesus macaques.Environment international · 2022Article
- Ubiquitin specific peptidase 38 promotes the progression of gastric cancer through upregulation of fatty acid synthase.American journal of cancer research · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Th2 immune response is critical for allergic asthma pathogenesis. Molecular mechanisms for regulating Th2 immunity are still not well understood. Here we report that the ubiquitin-specific protease USP38 is crucial for Th2-mediated allergic asthma. TCR stimulation up-regulated the USP38 level, and USP38 in turn mediated the protein stabilization of JunB, a transcription factor specific for Th2 development. Consequently, USP38 was specifically required for TCR-induced production of Th2 cytokines and Th2 development both in vitro and in vivo, and USP38-deficient mice were resistant to asthma pathogenesis induced by OVA or HDM. Mechanistically, USP38 directly associated with JunB, deubiquitinated Lys-48-linked poly-ubiquitination of JunB, and consequently blocked TCR-induced JunB turnover. USP38 represents the first identified deubiquitinase specifically for Th2 immunity and the associated asthma.
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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.