Tra2b, also known as SFRS10, is an RNA binding protein that plays well - established roles in developmentally regulated alternative splicing, especially during Drosophila sexual differentiation. In mammals, it is essential for embryogenesis. It is involved in multiple biological processes such as neurogenesis, T - cell fate determination, and myogenic differentiation [2,3,5].

In murine cortical neurogenesis, TRA2B is expressed in neural progenitors and cortical projection neurons. Depletion of TRA2B in cortex - specific Tra2b mutant mice leads to apoptosis of neural progenitor cells and disorganization of the cortical plate, indicating its essential role in proper cerebral cortex development [2]. Predicted loss - of - function variants in the 5' portion of TRA2B in humans cause a new neurodevelopmental syndrome. These variants decrease the expression of the canonical Tra2β - 1 isoform and increase the expression of the Tra2β - 3 isoform, which interferes with the incorporation of CHEK1 exon 3 [4].

In endometrial carcinoma, overexpression of TRA2B promotes cell viability, proliferation, invasion, and inhibits apoptosis, while knockdown has the opposite effects, suggesting its role in the pathogenesis of endometrial carcinoma [1]. In osteosarcoma, overexpression of TRA2B is associated with tumor progression, and bone marrow mesenchymal stem cell - derived exosomal miR - 206 can inhibit tumor progression by targeting TRA2B [6].

In conclusion, Tra2b is crucial for processes like neural development, T - cell function, and myogenesis. Research on Tra2b, especially through gene - knockout models in mice, has revealed its significant roles in neurodevelopmental syndromes and various cancers. Understanding Tra2b's functions provides insights into the underlying mechanisms of these diseases, potentially leading to new therapeutic strategies.