Rbm25-KO Mouse

Rbm25, an RNA-binding protein, is involved in multiple biological processes such as apoptosis, inflammation, and alternative splicing regulation. It is associated with pathways like endoplasmic reticulum stress-related apoptosis and metabolism-associated inflammation pathways. Understanding its function is crucial for revealing the molecular mechanisms of related diseases [1,2].

In an ischemic heart failure (HF) rat model and oxygen-glucose deprivation (OGD) model, RBM25 was significantly upregulated, leading to cardiomyocyte apoptosis by modulating endoplasmic reticulum stress through the CHOP pathway. Inhibiting RBM25 expression improved cardiac function [1].

In RBM25-deficient mice, macrophages showed enhanced pro-inflammatory mediator production, suggesting Rbm25's role in restraining inflammation. Mechanistically, Rbm25 mediates the 14th exon skipping of Acly pre-mRNA, influencing its metabolic activity [2].

In colon cancer, RBM25 ablation suppresses cell growth both in vitro and in vivo by regulating the alternative splicing of MNK2 [3].

In conclusion, Rbm25 plays essential roles in apoptosis, inflammation, and cancer-related processes. Gene knockout or knockdown models in mice and cell-based functional studies have revealed its function in ischemic HF, rheumatoid arthritis, and colon cancer. These findings provide potential therapeutic targets for these diseases.