ArticleCellular & molecular immunology2022
The membrane-associated ubiquitin ligases MARCH2 and MARCH3 target IL-5 receptor alpha to negatively regulate eosinophilic airway inflammation.
Article in Cellular & molecular immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.
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Who cites it
24 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.
- Anti-type 2 monoclonal antibody therapy for eosinophilic COPD beyond triple therapy: a systematic review and meta-analysis with strict eosinophil inclusion criteria.Frontiers in medicine · 2026Pooled it
- MARCH2/3 target FcγRI for K27-linked polyubiquitination and degradation to restrict the inflammatory response.Cellular & molecular immunology · 2026Article
- Protein Posttranslational Modifications in Immunity: Molecular Mechanisms and Therapeutic Targets.MedComm · 2026Review
- Review
- Intracellular LRG1 recruits MARCH2 to ubiquitinate and degrade endothelial VE-cadherin in septic lung injury.Acta pharmacologica Sinica · 2026Article
- How to quickly determine whether patients with chronic cough need corticosteroid treatment--construction of a predictive model for corticosteroid-responsive cough in chronic cough.NPJ primary care respiratory medicine · 2026Article
- Identifying expression and DNA methylation biomarkers for lung adenocarcinoma risk in East Asia.Journal of the National Cancer Institute · 2026Article
- Reciprocal regulation of TNF receptor 1-mediated signaling and inflammatory damages by MARCH2 and USP22.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- MARCH2 suppresses odontoblast differentiation by polyubiquitinating PTPRD.International journal of oral science · 2026Article
- MARCH E3 Ligases: Understudied Regulators of Pulmonary Immune Function.Journal of respiratory biology and translational medicine · 2026Article
- Exosomal hsa-miR-299-3p from endothelium mediates high phosphorus-induced vascular calcification in mice model of CKD via phosphorylated JAK2/STAT5 pathway.Frontiers in pharmacology · 2026Article
- Role of IL-5 in eosinophil-associated diseases and prospects for multi-target therapy.Frontiers in immunology · 2026Review
- MARCH2-mediated Lys63-linked polyubiquitination promotes metastasis by modulating the catalytic activity of TGF-β type I receptor.Cell death & disease · 2025Article
- SIRT5 Alleviated Eosinophilic Asthma Through ROS Inhibition and Nrf2/HO-1 Activation.Inflammation · 2025Article
- The Ubiquitin-Proteasome System in Asthma: Mechanisms and Therapeutic Possibilities.Clinical reviews in allergy & immunology · 2025Review
- FBXO2 Alleviates Intervertebral Disc Degeneration via Dual Mechanisms: Activating PINK1-Parkin Mitophagy and Ubiquitinating LCN2 to Suppress Ferroptosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Ubiquitination regulates allergic asthma by affecting immune cells and immune responses.Biochemistry and biophysics reports · 2025Review
- The membrane-associated ubiquitin ligases MARCH2 and MARCH3 target TIM-1 to limit Zika virus infection.Cellular & molecular immunology · 2025Article
- SIGLEC1 ubiquitination and degradation induced by MARCHF3 protects ARPE19 retinal cells from high glucose-induced oxidative stress, inflammation, and apoptosis.International ophthalmology · 2025Article
- Membrane-associated ring-CH-type finger 2 protects against metabolic dysfunction-associated fatty liver disease by targeting fatty acid synthase.Molecular metabolism · 2025Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 5 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Interleukin 5 (IL-5) plays crucial roles in type 2-high asthma by mediating eosinophil maturation, activation, chemotaxis and survival. Inhibition of IL-5 signaling is considered a strategy for asthma treatment. Here, we identified MARCH2 and MARCH3 as critical negative regulators of IL-5-triggered signaling. MARCH2 and MARCH3 associate with the IL-5 receptor α chain (IL-5Rα) and mediate its K27-linked polyubiquitination at K379 and K383, respectively, and its subsequent lysosomal degradation. Deficiency of MARCH2 or MARCH3 modestly increases the level of IL-5Rα and enhances IL-5-induced signaling, whereas double knockout of MARCH2/3 has a more dramatic effect. March2/3 double knockout markedly increases the proportions of eosinophils in the bone marrow and peripheral blood in mice. Double knockout of March2/3 aggravates ovalbumin (OVA)-induced eosinophilia and causes increased inflammatory cell infiltration, peribronchial mucus secretion and production of Th2 cytokines. Neutralization of Il-5 attenuates OVA-induced airway inflammation and the enhanced effects of March2/3 double deficiency. These findings suggest that MARCH2 and MARCH3 play redundant roles in targeting IL-5Rα for degradation and negatively regulating allergic airway inflammation.
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