Maea, also known as macrophage erythroblast attacher or EMP, is an E3 ubiquitin ligase. It plays crucial roles in multiple biological processes, including regulation of canonical Wnt signalling via β -catenin degradation, maintenance of haematopoietic stem cells (HSCs) by promoting autophagy and cytokine receptor regulation, and formation and maintenance of erythroblastic islands. It is also involved in pathways related to tumour progression and embryogenesis [2,3,4].

In glioblastoma, knocking down Maea in xenograft models inhibited tumour growth, as Maea promotes proliferation, invasion, stemness, and temozolomide resistance by targeting PHD3 for ubiquitination and degradation, enhancing HIF-1α stability [1]. In mice, deletion of Maea in macrophages (using Csf1r -Cre or CD169 -Cre for conditional knockout) led to severe reductions in bone marrow macrophages, erythroblasts, and in vivo island formation, highlighting its role in postnatal murine bone marrow erythropoiesis [4].

In summary, Maea is essential for multiple biological functions such as embryonic development, haematopoiesis, and erythropoiesis. Gene knockout and conditional knockout mouse models have revealed its significance in diseases like glioblastoma and in maintaining proper erythropoiesis, providing insights into potential therapeutic targets for related disorders.