Srsf5, also known as serine and arginine-rich splicing factor 5, is a key regulator in pre-mRNA alternative splicing. It is involved in multiple biological processes and signaling pathways. For example, it can be regulated by various factors and in turn regulate the splicing of many genes, playing an important role in cell growth, development, and disease [1-10].

In functional studies, Srsf5-deficient mouse models have provided crucial insights. Srsf5 knockout (Srsf5-/-) mice are perinatally lethal, showing cardiac dysfunction with non-compaction of the ventricular myocardium. This indicates that Srsf5-regulated alternative splicing is critical during heart development as it affects the alternative splicing of Myom1 [2]. In influenza A virus research, conditional knockout of Srsf5 in the lung protects mice against lethal IAV challenge, suggesting Srsf5 promotes IAV replication through enhancing viral M mRNA splicing [1].

In conclusion, Srsf5 is essential for normal biological processes through its role in alternative splicing. The use of Srsf5 KO/CKO mouse models has revealed its significance in diseases such as heart development disorders and viral infections, providing a better understanding of the underlying mechanisms and potential therapeutic targets.