Molecular analysis of anti-apoptotic action in MALT lymphoma and its clinical application for diagnosis and treatment.

API 2-MALT 1。t（11; 18）（q21; q21）是粘膜相关淋巴组织（MALT）型淋巴瘤中的特征性染色体易位，并且该易位导致API 2（凋亡抑制剂2，也称为c-IAP 2）-MALT 1（粘膜相关淋巴瘤易位基因1）的嵌合转录物。为了鉴定结合API 2-MALT 1嵌合蛋白的蛋白，我们采用免疫共沉淀和SDS PAGE分析，然后通过液相色谱-电喷雾串联质谱。结果表明，Smac、Htra 2和TRAF 2为API 2-MALT 1结合蛋白，免疫沉淀分析表明，异位表达的API 2-MALT 1蛋白确实与这些内源性蛋白结合。此外，API 2-MALT 1蛋白显着抑制Smac促进的细胞凋亡在紫外线照射的HeLa细胞。这些数据有力地表明，API 2-MALT 1可以阻断凋亡，至少部分，通过抑制Smac介导的凋亡途径。API 2-MALT 1的分子机制及其临床应用有待进一步研究。

API2-MALT1. t(11;18)(q21;q21) is a characteristic chromosomal translocation in mucosa-associated lymphoid tissue (MALT) type lymphoma, and this translocation results in chimeric transcript of API2 (Apoptosis Inhibitor 2, also known as c-IAP2)-MALT1 (Mucosa-Associated Lymphoma Translocation gene 1). To identify proteins that bind API2-MALT1 chimeric protein, we employed coimmunoprecipitation and SDS PAGE analysis, followed by liquid chromatography-electrospray ionization tandem mass spectrometry. As a result, Smac, Htra2, and TRAF2 were identified as API2-MALT1-binding proteins.Immunoprecipitation analysis demonstrated that ectopically expressed API2-MALT1 protein indeed binds to these endogeneous proteins. Furthermore, API2-MALT1 protein significantly inhibited Smac-promoted apoptosis in UV irradiated HeLa cells. These data strongly suggest that API2-MALT1 can block apoptosis, at least in part, by inhibiting Smac-mediated apoptotic pathway. Further study is warranted to investigate the detailed molecular mechanism of API2-MALT1 and its clinical application.