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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.

Original publication




Journal article



Publication Date





2799 - 2803


Adaptor Proteins, Signal Transducing, Amino Acid Sequence, Animals, Base Sequence, Cell Differentiation, Cell Transformation, Neoplastic, DNA-Binding Proteins, Gene Expression Regulation, Developmental, Genes, Homeodomain Proteins, LIM Domain Proteins, Leukemia-Lymphoma, Adult T-Cell, Metalloproteins, Mice, Molecular Sequence Data, Multigene Family, Nuclear Proteins, Oncogene Proteins, Organ Specificity, Sequence Alignment, Sequence Homology, Amino Acid, T-Lymphocyte Subsets, Thymus Gland, Transcription Factors, Translocation, Genetic