Valge-Archer V, Forster A, Rabbitts T H
MRC Laboratory of Molecular Biology, Division of Protein and Nucleic Acid Chemistry, Cambridge, UK.
Oncogene. 1998 Dec 17;17(24):3199-202. doi: 10.1038/sj.onc.1202353.
The ectopic expression of LMO1 or LMO2 in T cell acute leukaemias resulting from chromosomal translocations t(11;14)(p15;qll) or t(11;14)(p13;q11) respectively in a causal factor in tumorigenesis. LMO1 has been found as a heterodimer with a 46 Kd protein in a T cell line derived from a childhood T-acute leukaemia. This 46 Kd protein is the LIM-binding protein LDB1/NLI. The latter is a phosphoprotein and binds to LMO1 in its phosphorylated state and essentially all the LMO1 and LDB1 protein in the T cell line is part of the complex. Therefore, the LMO1-LDB1 interaction is likely to be involved in tumorigenesis after LMO1 is ectopically expressed following chromosomal translocation in T cells prior to development of acute leukaemias.
分别由染色体易位t(11;14)(p15;q11)或t(11;14)(p13;q11)导致的T细胞急性白血病中LMO1或LMO2的异位表达是肿瘤发生的一个致病因素。在一个源自儿童T细胞急性白血病的T细胞系中，LMO1被发现与一种46 Kd的蛋白质形成异二聚体。这种46 Kd的蛋白质是LIM结合蛋白LDB1/NLI。后者是一种磷蛋白，在其磷酸化状态下与LMO1结合，并且该T细胞系中基本上所有的LMO1和LDB1蛋白都是复合物的一部分。因此，在急性白血病发生之前，T细胞染色体易位后LMO1异位表达，LMO1-LDB1相互作用可能参与肿瘤发生。
