Rbm24, an RNA-binding protein, is a critical post-transcriptional regulator of gene expression. It binds to a wide range of target mRNAs and is involved in multiple post-transcriptional events such as pre-mRNA splicing, mRNA stability, polyadenylation, and translation. It plays essential roles in promoting cellular differentiation during organogenesis and tissue regeneration, and is implicated in various physiological and pathological processes [1,2].

In Rbm24 knockout mouse models, impaired S181 phosphorylation of Rbm24 leads to cardiac contractile dysfunction, atrial fibrillation, dyslipidemia, reduced muscle strength, behavioral abnormalities, and sudden death under acute and chronic psychological stressors, as it inhibits cardiac translation including APOE translation [3]. Rbm24 knockout also significantly impairs neural stem/progenitor cell (NSPC) proliferation in the adult subventricular zone (SVZ), resulting in collapsed neurogenesis in the olfactory bulb, highlighting its role in maintaining Notch1 mRNA stability in adult NSPCs [4]. In RBM24 knockout mice, there is an aberrant shift of CaMKIIδ towards the δ-C isoform, marked alteration in Ca2+ handling, prolongation of the ventricular cardiac action potential and QT interval [5].

In conclusion, Rbm24 is a multifunctional regulator crucial for processes like embryonic lineage differentiation, cellular homeostasis, and organ development. Model-based research, especially through Rbm24 KO mouse models, has revealed its significant roles in psychological stress-induced cardiovascular disease, Parkinson-associated olfactory dysfunction, and cardiac rhythm regulation, enhancing our understanding of related disease mechanisms.