ArticleNature communications2021
MAEA is an E3 ubiquitin ligase promoting autophagy and maintenance of haematopoietic stem cells.
Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 50 citations in OpenAlex.
- The CTLH ubiquitin ligase substrates ZMYND19 and MKLN1 negatively regulate mTORC1 at the lysosomal membrane.Nature communications · 2025Article
- The many faces of the GID/CTLH E3 ligase complex.Biochemical Society transactions · 2025Review
- SRAS1.1 E3 ligase mediates DSK2A degradation to regulate autophagy and drought tolerance in Arabidopsis.EMBO reports · 2025Article
- Integrating single-cell RNA sequencing and spatial transcriptomics reveals the therapeutic effect of nitazoxanide in head and neck squamous cell carcinoma.Discover oncology · 2025Article
- The E3 ubiquitin ligase MAEA promotes macrophage phagocytosis and inhibits gastrointestinal cancer progression by mediating PARP1 ubiquitination and degradation.International journal of biological sciences · 2025Article
- Identification of MAEA protein as a potential target for chemoresistance in osteosarcoma using bioinformatics and proteomic analysis.Frontiers in oncology · 2025Article
- Essential role of Dhx16-mediated ribosome assembly in maintenance of hematopoietic stem cells.Leukemia · 2024Article
- Genome-wide screen of Mycobacterium tuberculosis-infected macrophages revealed GID/CTLH complex-mediated modulation of bacterial growth.Nature communications · 2024Article
- Trim47 prevents hematopoietic stem cell exhaustion during stress by regulating MAVS-mediated innate immune pathway.Nature communications · 2024Article
- The E3 ubiquitin ligase Nedd4L preserves skeletal muscle stem cell quiescence by inhibiting their activation.iScience · 2024Article
- mTORC1-CTLH E3 ligase regulates the degradation of HMG-CoA synthase 1 through the Pro/N-degron pathway.Molecular cell · 2024Article
- Ventromedial hypothalamic nucleus subset stimulates tissue thermogenesis via preoptic area outputs.Molecular metabolism · 2024Article
- Multisite phosphorylation dictates selective E2-E3 pairing as revealed by Ubc8/UBE2H-GID/CTLH assemblies.Molecular cell · 2024Article
- LAD1 promotes malignant progression by diminishing ubiquitin-dependent degradation of vimentin in gastric cancer.Journal of translational medicine · 2023Article
- Identifying E3 Ligase Substrates With Quantitative Degradation Proteomics.Chembiochem : a European journal of chemical biology · 2023Article
- Evaluation of obstructive sleep apnea: an analysis based on aberrant genes.Sleep & breathing = Schlaf & Atmung · 2023Article
- Genome-wide CRISPR-Cas9 screen analyzed by SLIDER identifies network of repressor complexes that regulate TRIM24.iScience · 2023Article
- Review
- E3 ubiquitin ligase on the biological properties of hematopoietic stem cell.Journal of molecular medicine (Berlin, Germany) · 2023Review
- Regulation of adult stem cell quiescence and its functions in the maintenance of tissue integrity.Nature reviews. Molecular cell biology · 2023Review
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 3 countries.
Funding
Abstract
Haematopoietic stem cells (HSCs) tightly regulate their quiescence, proliferation, and differentiation to generate blood cells during the entire lifetime. The mechanisms by which these critical activities are balanced are still unclear. Here, we report that Macrophage-Erythroblast Attacher (MAEA, also known as EMP), a receptor thus far only identified in erythroblastic island, is a membrane-associated E3 ubiquitin ligase subunit essential for HSC maintenance and lymphoid potential. Maea is highly expressed in HSCs and its deletion in mice severely impairs HSC quiescence and leads to a lethal myeloproliferative syndrome. Mechanistically, we have found that the surface expression of several haematopoietic cytokine receptors (e.g. MPL, FLT3) is stabilised in the absence of Maea, thereby prolonging their intracellular signalling. This is associated with impaired autophagy flux in HSCs but not in mature haematopoietic cells. Administration of receptor kinase inhibitor or autophagy-inducing compounds rescues the functional defects of Maea-deficient HSCs. Our results suggest that MAEA provides E3 ubiquitin ligase activity, guarding HSC function by restricting cytokine receptor signalling via autophagy.
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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.