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SD-Rag2 KO
製品ID :
CR005
系統:
SD
状況:
説明:
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.
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.
SDRG
製品ID :
IR1023
系統:
SD
状況:
説明:
The IL2RG gene, also known as CD132, encodes the interleukin-2 receptor gamma chain (IL-2Rγ), an essential signaling component in multiple interleukin receptors and a common receptor subunit for various critical immune factors, including IL-2, IL-4, IL-7, IL-9, IL-15, and IL-21. These interleukin receptors are located on the surface of immune cells, and when any of these interleukins binds to its receptor, it triggers a cascade of intracellular reactions that promote cell growth and division. Consequently, IL-2Rγ is also called the common gamma chain (γc). In humans, mutations in IL2RG can lead to X-linked severe combined immunodeficiency (X-SCID), a condition characterized by the absence of T cells and natural killer (NK) cells, along with impaired B cell function, leaving patients highly susceptible to recurrent infections and rarely surviving beyond infancy [1]. Studies have shown that Il2rg knockout rats exhibit a severe immunodeficient phenotype, with markedly reduced T and B cells, absent NK cells, and intact macrophages [2].
The RAG2 gene encodes a protein that, together with RAG1, forms the RAG complex, which is crucial for V(D)J recombination during B and T cell maturation. In V(D)J recombination, the RAG complex binds to the recombination signal sequence (RSS) adjacent to DNA's V, D, or J segments. The complex cleaves DNA between the signal sequence and segments, allowing segments to rearrange to different gene regions. This process occurs repeatedly in B and T cells, rearranging V, D, and J segments into various combinations. The resulting protein diversity enables a broader recognition of foreign invaders and allows the body to defend effectively against infections. RAG2 is involved not only in catalysis but also in regulating the reaction by controlling access to specific loci [3]. Lack of functional RAG2 protein can also cause SCID. In rats, Rag2 gene knockout leads to an absence of V(D)J recombination, blocking T and B cell differentiation, development, and maturation, resulting in severe thymic hypoplasia, a lack of mature T and B cells, and a compensatory increase in NK cells [4-5].
SDRG rats are an immunodeficient model with both Il2rg and Rag2 genes knocked out. Research indicates that compared with rats with a single Il2rg or Rag2 gene knockout, rats with a dual knockout of Il2rg and Rag2 exhibit a more severe SCID phenotype. Compared to Il2rg and Rag2 double-knockout mice, Il2rg and Rag2 double-knockout rats show higher engraftment rates for human tumor cells or xenografts in the construction of CDX and PDX models, retaining better characteristics of primary tumors [6]. Data suggest that SDRG rats, characterized by the complete absence of mature T cells, B cells, and circulating NK cells, can be widely applied in oncology and immunology research.
The IL2RG gene, also known as CD132, encodes the interleukin-2 receptor gamma chain (IL-2Rγ), an essential signaling component in multiple interleukin receptors and a common receptor subunit for various critical immune factors, including IL-2, IL-4, IL-7, IL-9, IL-15, and IL-21. These interleukin receptors are located on the surface of immune cells, and when any of these interleukins binds to its receptor, it triggers a cascade of intracellular reactions that promote cell growth and division. Consequently, IL-2Rγ is also called the common gamma chain (γc). In humans, mutations in IL2RG can lead to X-linked severe combined immunodeficiency (X-SCID), a condition characterized by the absence of T cells and natural killer (NK) cells, along with impaired B cell function, leaving patients highly susceptible to recurrent infections and rarely surviving beyond infancy [1]. Studies have shown that Il2rg knockout rats exhibit a severe immunodeficient phenotype, with markedly reduced T and B cells, absent NK cells, and intact macrophages [2].
The RAG2 gene encodes a protein that, together with RAG1, forms the RAG complex, which is crucial for V(D)J recombination during B and T cell maturation. In V(D)J recombination, the RAG complex binds to the recombination signal sequence (RSS) adjacent to DNA's V, D, or J segments. The complex cleaves DNA between the signal sequence and segments, allowing segments to rearrange to different gene regions. This process occurs repeatedly in B and T cells, rearranging V, D, and J segments into various combinations. The resulting protein diversity enables a broader recognition of foreign invaders and allows the body to defend effectively against infections. RAG2 is involved not only in catalysis but also in regulating the reaction by controlling access to specific loci [3]. Lack of functional RAG2 protein can also cause SCID. In rats, Rag2 gene knockout leads to an absence of V(D)J recombination, blocking T and B cell differentiation, development, and maturation, resulting in severe thymic hypoplasia, a lack of mature T and B cells, and a compensatory increase in NK cells [4-5].
SDRG rats are an immunodeficient model with both Il2rg and Rag2 genes knocked out. Research indicates that compared with rats with a single Il2rg or Rag2 gene knockout, rats with a dual knockout of Il2rg and Rag2 exhibit a more severe SCID phenotype. Compared to Il2rg and Rag2 double-knockout mice, Il2rg and Rag2 double-knockout rats show higher engraftment rates for human tumor cells or xenografts in the construction of CDX and PDX models, retaining better characteristics of primary tumors [6]. Data suggest that SDRG rats, characterized by the complete absence of mature T cells, B cells, and circulating NK cells, can be widely applied in oncology and immunology research.
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