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

Oncogene. 1998 Dec 17;17(24):3199-202. doi: 10.1038/sj.onc.1202353.

Abstract

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Chromosomes, Human, Pair 11*
  • Chromosomes, Human, Pair 14*
  • DNA-Binding Proteins / biosynthesis
  • DNA-Binding Proteins / genetics*
  • Humans
  • LIM Domain Proteins
  • Leukemia-Lymphoma, Adult T-Cell / genetics*
  • Metalloproteins / biosynthesis
  • Metalloproteins / genetics*
  • Oncogene Proteins*
  • Transcription Factors
  • Translocation, Genetic*
  • Tumor Cells, Cultured

Substances

  • DNA-Binding Proteins
  • LDB1 protein, human
  • LIM Domain Proteins
  • LMO1 protein, human
  • Metalloproteins
  • Oncogene Proteins
  • Transcription Factors