Magoh, also known as mago homolog, exon junction complex subunit, is a core component of the exon junction complex (EJC) along with EIF4A3 and RBM8A [1]. The EJC is crucial for mRNA splicing, export, translation, and nonsense-mediated mRNA decay (NMD). MAGOH is essential for embryonic development and normal cellular functioning [1].

In mouse models, conditional Magoh ablation from interneuron progenitors depletes cortical interneuron number through adulthood, with increased severity in homozygotes. Magoh deficiency delays progenitor mitotic progression in a dosage-sensitive fashion, indicating its requirement in progenitors for both generation and survival of newborn progeny [5].

In cancer research, abnormally increased MAGOH expression is associated with poor prognosis in several tumors like lower-grade glioma, gastric cancer, and melanoma [2,3,4]. In lower-grade glioma, increased MAGOH expression is an independent prognostic biomarker and is essential for cell proliferation [2]. In gastric cancer, MAGOH promotes cancer progression via a specific signaling pathway [3]. In melanoma, knockdown of MAGOH and MAGOHB decreases NMD activity and promotes apoptosis [4].

In conclusion, Magoh plays multifaceted roles in mRNA processing, embryonic development, and normal cellular function. Studies using gene knockout or conditional knockout mouse models have revealed its significance in neurodevelopmental pathologies and cancer. Understanding Magoh's functions provides potential therapeutic targets for treating diseases related to abnormal cell proliferation and development.