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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.

Original publication




Journal article


Proc Natl Acad Sci U S A

Publication Date





7869 - 7873


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