Rbm8a, also known as Y14, is a component of the exon junction complex involved in mRNA splicing, transport, and nonsense-mediated decay. It plays a crucial role in multiple biological processes, such as embryonic development, hematopoiesis, and neurogenesis, and is associated with various pathways like Wnt/PCP, Notch/STAT3, and PI3K-AKT/mTOR [4,2,1,3].

In zebrafish, rbm8a perturbation leads to early hematopoietic defects via attenuated non-canonical Wnt/PCP signaling, resulting in reduced thrombocytes [4]. In mice, Rbm8a haploinsufficiency causes severe microcephaly and defective neurogenesis, disrupting radial glia proliferation and neuronal differentiation [5]. In cancer, knockdown of Rbm8a in breast cancer and glioblastoma cells inhibits cell proliferation, invasion, and promotes apoptosis, and overexpression has the opposite effects [1,2,3].

In conclusion, Rbm8a is essential for normal development and its dysregulation is associated with various diseases. Gene-knockout models in zebrafish and mice have revealed its key roles in hematopoiesis, cortical development, and cancer progression, providing valuable insights into disease mechanisms and potential therapeutic targets.