The LMO1 and LDB1 proteins interact in human T cell acute leukaemia with the chromosomal translocation t (11; 14)(p15; q11)

V Valge-Archer, A Forster, TH Rabbitts - Oncogene, 1998 - nature.com
V Valge-Archer, A Forster, TH Rabbitts
Oncogene, 1998nature.com
The ectopic expression of LMO1 or LMO2 in T cell acute leukaemias resulting from
chromosomal translocations t (11; 14)(p15; q11) 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 …
Abstract
The ectopic expression of LMO1 or LMO2 in T cell acute leukaemias resulting from chromosomal translocations t (11; 14)(p15; q11) 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.
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