Transcriptional activation by TAL1 and FUS-CHOP proteins expressed in acute malignancies as a result of chromosomal abnormalities

Proc Natl Acad Sci U S A. 1994 Aug 16;91(17):7869-73. doi: 10.1073/pnas.91.17.7869.

Abstract

Proteins that appear to participate in transcriptional control of gene expression are increasingly implicated in leukemias and malignant solid tumors. We report here that the N-terminal domains of the proteins TAL1 (ectopically activated in T-cell acute leukemias after chromosomal abnormalities caused by V-D-J recombinase error) (V, variable; D, diversity; J, joining) and FUS-CHOP (a liposarcoma tumor-specific fusion protein that is produced as a result of a chromosomal translocation) can function as transcription activators of specific responsive reporter genes. The result with TAL1 provides evidence that transcriptional activation can be mediated by a gene activated by translocation in T-cell acute leukemias. In the case of the liposarcoma, transactivation by the FUS-CHOP protein occurs because the FUS transcriptional activation domain is added to the DNA-binding CHOP protein normally lacking such activity. Therefore, the association of transcriptional activation and DNA-binding elements is a common consequence in proteins activated or newly created as fusion proteins after chromosomal translocations in acute leukemias and in malignant solid tumors.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 3T3 Cells
  • Animals
  • Base Sequence
  • Basic Helix-Loop-Helix Transcription Factors
  • Biomarkers, Tumor
  • CCAAT-Enhancer-Binding Proteins*
  • Cell Line
  • Chloramphenicol O-Acetyltransferase / biosynthesis
  • Chromosome Aberrations*
  • Chromosome Disorders*
  • DNA-Binding Proteins / biosynthesis
  • DNA-Binding Proteins / metabolism*
  • Gene Expression*
  • Helix-Loop-Helix Motifs
  • Heterogeneous-Nuclear Ribonucleoproteins
  • Humans
  • Leukemia / genetics*
  • Leukemia-Lymphoma, Adult T-Cell / genetics
  • Leukemia-Lymphoma, Adult T-Cell / metabolism
  • Liposarcoma / genetics
  • Liposarcoma / metabolism
  • Mice
  • Neoplasm Proteins / biosynthesis
  • Neoplasm Proteins / metabolism*
  • Nuclear Proteins / biosynthesis
  • Nuclear Proteins / metabolism*
  • Proto-Oncogene Proteins*
  • RNA-Binding Protein FUS
  • Ribonucleoproteins / biosynthesis
  • Ribonucleoproteins / metabolism*
  • T-Cell Acute Lymphocytic Leukemia Protein 1
  • Transcription Factor CHOP
  • Transcription Factors / metabolism
  • Transcription, Genetic*
  • Transfection
  • Translocation, Genetic

Substances

  • Basic Helix-Loop-Helix Transcription Factors
  • Biomarkers, Tumor
  • CCAAT-Enhancer-Binding Proteins
  • DDIT3 protein, human
  • DNA-Binding Proteins
  • Ddit3 protein, mouse
  • Heterogeneous-Nuclear Ribonucleoproteins
  • Neoplasm Proteins
  • Nuclear Proteins
  • Proto-Oncogene Proteins
  • RNA-Binding Protein FUS
  • Ribonucleoproteins
  • T-Cell Acute Lymphocytic Leukemia Protein 1
  • Tal1 protein, mouse
  • Transcription Factors
  • TAL1 protein, human
  • Transcription Factor CHOP
  • Chloramphenicol O-Acetyltransferase