Grutz G, Forster A, Rabbitts T H
MRC Laboratory of Molecular Biology, Division of Protein and Nucleic Acid Chemistry, Cambridge, UK.
Oncogene. 1998 Nov 26;17(21):2799-803. doi: 10.1038/sj.onc.1202502.
The T cell oncogenes LMO1 and LMO2 are activated by distinct chromosomal translocations in childhood T cell acute leukaemias. Transgenic mouse models of this disease demonstrate that enforced expression of Lmo1 and Lmo2 cause T cell leukaemias with long latency and that Lmo2 expression leads to an inhibition of the T cell differentiation programme, prior to overt disease. These functions appear to be partly mediated by interaction of LMO1 or LMO2 with the LIM-binding protein LDB1/ NLI1. We have now identified a new member of the Lmo family, designated Lmo4, via its interaction with Ldb1. Lmo4 is widely expressed in mouse tissues, including adult thymus (mainly CD4, CD8-double positive T cells) and embryonic thymus (mainly CD4, CD8-double negative T cells). These characteristics imply that Ldb1-Lmo4 interaction may function in the T cell developmental programme and that enforced expression of LMO1 or LMO2 by chromosomal translocations or transgenesis may displace Lmo4 from this complex and thereby influence T cell differentiation prior to T cell tumour occurrence.
T细胞癌基因LMO1和LMO2在儿童T细胞急性白血病中通过不同的染色体易位而被激活。该疾病的转基因小鼠模型表明,Lmo1和Lmo2的强制表达会导致潜伏期较长的T细胞白血病,并且在明显疾病出现之前,Lmo2的表达会导致T细胞分化程序受到抑制。这些功能似乎部分是由LMO1或LMO2与LIM结合蛋白LDB1/NLI1的相互作用介导的。我们现在通过Lmo4与Ldb1的相互作用鉴定出了Lmo家族的一个新成员,命名为Lmo4。Lmo4在小鼠组织中广泛表达,包括成年胸腺(主要是CD4、CD8双阳性T细胞)和胚胎胸腺(主要是CD4、CD8双阴性T细胞)。这些特征表明,Ldb1-Lmo4相互作用可能在T细胞发育程序中发挥作用,并且通过染色体易位或转基因导致的LMO1或LMO2的强制表达可能会使Lmo4从该复合物中被取代,从而在T细胞肿瘤发生之前影响T细胞分化。