Ben-Neriah Y, Daley G Q, Mes-Masson A M, Witte O N, Baltimore D
Science. 1986 Jul 11;233(4760):212-4. doi: 10.1126/science.3460176.
Chronic myelogenous leukemia (CML) is a human disease associated with a consistent chromosomal translocation that results in sequences from the c-abl locus on chromosome 9 being fused to sequences in a breakpoint cluster region (bcr) on chromosome 22. CML cells have two novel products: an 8.5-kilobase RNA transcript containing both abl and bcr and a 210-kilodalton phosphoprotein (P210) recognized by v-abl-specific antisera. To test whether the P210 is the product of the novel 8.5-kilobase bcr/abl fusion transcript, antibodies were prepared against c-abl and bcr determinants. By using these reagents and v-abl-specific antisera, it was demonstrated that the P210 in CML cells is indeed the protein product of the 8.5-kilobase transcript. By analogy to the gag/abl fusion protein of Abelson murine leukemia virus, the replacement of amino terminal c-abl sequences by bcr sequences in P210 may create a transforming protein involved in CML. A 190-kilodalton phosphoprotein that is a candidate for the normal bcr protein was identified in both HeLa and K562 cells.
慢性粒细胞白血病(CML)是一种与持续染色体易位相关的人类疾病,该易位导致9号染色体上c-abl基因座的序列与22号染色体上断裂点簇区域(bcr)的序列融合。CML细胞有两种新产物:一种包含abl和bcr的8.5千碱基RNA转录本,以及一种可被v-abl特异性抗血清识别的210千道尔顿磷蛋白(P210)。为了检测P210是否是新的8.5千碱基bcr/abl融合转录本的产物,制备了针对c-abl和bcr决定簇的抗体。通过使用这些试剂和v-abl特异性抗血清,证明CML细胞中的P210确实是8.5千碱基转录本的蛋白质产物。与阿贝尔森鼠白血病病毒的gag/abl融合蛋白类似,P210中bcr序列取代氨基末端c-abl序列可能产生一种参与CML的转化蛋白。在HeLa和K562细胞中均鉴定出一种190千道尔顿磷蛋白,它是正常bcr蛋白的候选物。