Srsf12-flox Mouse

Srsf12, a member of the serine-arginine rich splicing factor (SRSF) family, is involved in regulating RNA splicing processes [3,4,5]. It has been associated with various biological functions and pathways, and its dysregulation may impact different biological processes and disease states [1-3,7]. Genetic models, such as gene knockout or conditional knockout mouse models, can be valuable in further exploring its functions.

In a study on pancreatic cancer, Srsf12 knockout in Kras-mutated mice (KrasG12DSrsf12fl/fl and Srsf12fl/flPdx1cre mice) led to accelerated Kras-driven pancreatic tumorigenesis and enhanced tumor innervation. Mechanistically, SRSF12 inhibits neurite outgrowth by generating a LAMA3 splice isoform lacking the fourth and fifth LG (G45) domains, and G45 promotes tumor innervation by activating ITGB1 and FAK in neurons [2]. In acute myeloid leukemia (AML), SRSF12 is highly expressed and is an independent predictor of favorable prognosis. Enrichment analysis showed its involvement in pathways like PI3K-AKT and Jak-STAT, and its expression is correlated with immune cell infiltration [1].

In conclusion, Srsf12 plays crucial roles in regulating RNA splicing and is involved in important biological processes. Its functions have been revealed through in vivo studies, especially in the context of pancreatic cancer and AML. The use of KO/CKO mouse models has provided valuable insights into its role in tumorigenesis and immune-related processes in these disease areas.