Rbm3, also known as cold-inducible protein, is an outstanding cold shock protein. It is rapidly upregulated in cold environments to maintain homeostasis and ensure cell survival, which is a crucial physiological response to cold stress [1]. Rbm3 participates in multiple cellular physiological processes such as anti-apoptosis, circadian rhythm, cell cycle, reproduction, and tumogenesis [1]. It may interact with other proteins and regulate various signaling pathways, though the exact associated pathways are yet to be fully defined. Genetic models, like KO/CKO mouse models, can be valuable in further exploring its functions.

In a KO-like study, Rbm3 deficiency was linked to transcriptome-wide pre-mRNA splicing alterations, which could be reversed by Rbm3 co-expression from a cDNA. The N-terminal part of Rbm3 with the RNA recognition motif (RRM) was sufficient to change splice site selection, suggesting a novel role of Rbm3 in RNA splicing for transcriptome integrity [3]. In an in vivo model of prion-diseased mice, an antisense oligonucleotide (ASO) targeting a poison exon in the Rbm3 gene increased RBM3 expression, leading to remarkable neuroprotection, preventing neuronal loss and spongiosis [2].

In conclusion, Rbm3 plays essential roles in maintaining cellular homeostasis, with functions in processes like RNA splicing and neuroprotection. Model-based research, especially using KO/CKO mouse models, has provided insights into its role in neurodegenerative diseases, highlighting its potential as a therapeutic target for conditions such as Alzheimer's disease and acute brain injury [2].