Rbm14, an RNA-binding protein, is involved in multiple essential biological processes. It plays a role in maintaining genome integrity, regulating alternative splicing, and is associated with pathways like homologous recombination repair, DNA damage response, and cellular O-GlcNAcylation. It also has significance in embryonic development, oocyte maturation, and cancer-related processes [1,3,4,6].

In gene knockout studies, Rbm14 knockout in mice leads to apoptosis and cell proliferation defects in early post-implantation epiblast cells, causing gastrulation disruption and embryonic lethality. This indicates its crucial role in maintaining genome integrity during early mouse embryogenesis by regulating alternative splicing of DNA damage response (DDR)-related genes [4]. Rbm14 depletion in mouse embryonic stem cells (mESCs) alters gene expression profiles, downregulating pluripotency-associated genes and genes in the Wnt and TGF-β signaling pathways, showing its importance in maintaining pluripotency and mesoderm development [6]. In mouse oocytes, Rbm14 knockdown results in spindle defects and chromosome abnormalities due to α-tubulin hyperacetylation, highlighting its role in oocyte meiotic maturation [3].

In conclusion, Rbm14 is essential for multiple biological functions including genome integrity maintenance, pluripotency, and oocyte maturation. Studies using gene knockout mouse models have revealed its significance in early embryonic development and provided insights into its potential as a therapeutic target in diseases such as cancer where its dysregulation is observed [2,4,5].