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首页> 外文期刊>Oncogene >AID and RAG1 do not contribute to lymphomagenesis in E|[mu]| c-myc transgenic mice
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AID and RAG1 do not contribute to lymphomagenesis in E|[mu]| c-myc transgenic mice

机译：AID和RAG1在E |μ|中无助于淋巴瘤发生。 c-myc转基因小鼠

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DNA breaks caused by recombination-activating gene 1 (RAG1) and activation-induced cytidine deaminase (AID) induce c-myc/immunoglobulin (Ig) heavy chain chromosomal translocations and thereby stimulate lymphomagenesis. However, constitutive expression of c-myc alone is not sufficient to induce lymphomas. Because RAG1 and AID activity occurs outside of Ig genes, we assessed whether these enzymes provide the secondary genetic lesions in Eμ c-myc transgenic mice to promote lymphoma development. We found that the tumor incidence and tumor phenotype in Eμ c-myc transgenic mice is similar in AID+/+, AID+/? and AID?/? backgrounds in both specific pathogen-free and conventional animal facilities, indicating that AID does not contribute to lymphoma development in Eμ c-myc transgenic mice. To examine the role of RAG proteins in Eμ c-myc mice, we examined Eμ c-myc transgenic mice that harbor the Ig-HEL heavy- and light-chain transgenes, and thus have reduced RAG expression in B cells. We found that tumor incidence was not affected by these Ig transgenes. However, we found that RAG1?/? Eμ c-myc mice exhibited accelerated tumor development compared to controls. This data combined with our finding that Eμ c-myc mice lived longer in the conventional facility than in the specific pathogen-free facility suggest an immune-mediated activity that suppresses lymphoma development.
机译：重组激活基因1（RAG1）和激活诱导的胞苷脱氨酶（AID）引起的DNA断裂诱导c-myc /免疫球蛋白（Ig）重链染色体易位，从而刺激淋巴瘤的发生。然而，仅c-myc的组成型表达不足以诱导淋巴瘤。由于RAG1和AID活性发生在Ig基因之外，因此我们评估了这些酶是否在Eμc-myc转基因小鼠中提供了继发性遗传损伤，从而促进了淋巴瘤的发展。我们发现Eμc-myc转基因小鼠的肿瘤发生率和肿瘤表型在AID + / +，AID + /？中相似。和AID？/？特定的无病原体和常规动物设施的背景，表明AID对Eμc-myc转基因小鼠的淋巴瘤发展无贡献。为了检查RAG蛋白在Eμc-myc小鼠中的作用，我们检查了具有Ig-HEL重链和轻链转基因并因此降低了B细胞中RAG表达的Eμc-myc转基因小鼠。我们发现肿瘤发生率不受这些Ig转基因的影响。但是，我们发现RAG1？/？与对照组相比，Eμc-myc小鼠表现出加速的肿瘤发展。该数据与我们的发现相结合，即Eμc-myc小鼠在常规设备中的寿命比在无特定病原体的设备中寿命更长，这表明免疫介导的活性可抑制淋巴瘤的发展。

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