The RAG2 gene encodes a protein that, together with the RAG1 protein, forms the RAG complex, which plays a crucial role in V(D)J recombination during the maturation of B and T cells. During V(D)J recombination, the RAG complex attaches to the recombination signal sequences (RSS) on the DNA, located next to the V, D, or J segments. The RAG complex cuts the DNA between the signal sequences and the segments, allowing the segments to separate and move to different regions of the genome. This process is repeated multiple times in B and T cells, resulting in various combinations of V, D, and J segments. The resulting protein diversity provides a broader range of recognition for foreign invaders, enabling the body to combat infections effectively. RAG2 not only participates in the catalytic reaction but also regulates the reaction by controlling access to specific loci ^[1].

The SD-Rag2 KO rat is an immunodeficient model with the Rag2 gene knocked out, and it can be used for extensive research in oncology and immunology. Studies have shown that the absence of functional RAG2 protein can lead to severe combined immunodeficiency (SCID). The deletion of the Rag2 gene in rats results in the absence of V(D)J recombination, blocking the differentiation, development, and maturation of T cells and B cells. This manifests as severe thymic hypoplasia, with no mature T and B cells, but a compensatory increase in NK cells ^[2-3]. In addition, Cyagen also offers the SDRG rat (Product Number: IR1023) with a double knockout of the Il2rg and Rag2 genes. Compared to the Rag2 gene knockout rats, the Il2rg and Rag2 double knockout rats exhibit a more severe phenotype of severe combined immunodeficiency.