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t(14;18)(q32;q21)涉及14q32上的IgH基因和18q21上的bcl-2基因,易位结果形成bcl-2/IgH融合基因。bcl-2的断裂区在3′端的非翻译区内,该区对bcl-2的表达起调节作用。融合基因仍能编码完整的bcl-2蛋白,由于失去了3′端的调节,使bcl-2过度表达、细胞寿命延长、凋亡减少,起到癌基因作用。转染bcl-2/IgH的转基因鼠,淋巴瘤的发生率明显高于对照组。在bcl-2的断裂区和IgH的D区和J区均有chi样序列,在IgH发生重排时,DNA重组酶对chi样序列的误认可能是发生易位的原因。
The t (14; 18) (q32; q21) relates to the IgH gene on 14q32 and the bcl-2 gene on 18q21, resulting in the bcl-2 / IgH fusion gene. The cleavage site of bcl-2 is in the 3 ’untranslated region, which regulates bcl-2 expression. The fusion gene can still encode the complete bcl-2 protein. Due to the loss of regulation of 3 ’end, bcl-2 overexpression, prolonged cell life span, decreased apoptosis, play an oncogene effect. Transgenic mice transfected with bcl-2 / IgH, the incidence of lymphoma was significantly higher than the control group. There are chi-like sequences in the cleavage site of bcl-2 and D and J regions of IgH. The misidentification of chi-like sequences by DNA recombinase may be responsible for the translocation when IgH is rearranged.