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

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.
Authors	I Sánchez-García, T H Rabbitts
Journal	Proceedings of the National Academy of Sciences of the United States of America (Proc Natl Acad Sci U S A) Vol. 91 Issue 17 Pg. 7869-73 (Aug 16 1994) ISSN: 0027-8424 [Print] United States
PMID	8058726 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References	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
Topics	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, metabolism) Gene Expression Helix-Loop-Helix Motifs Heterogeneous-Nuclear Ribonucleoproteins Humans Leukemia (genetics) Leukemia-Lymphoma, Adult T-Cell (genetics, metabolism) Liposarcoma (genetics, metabolism) Mice Neoplasm Proteins (biosynthesis, metabolism) Nuclear Proteins (biosynthesis, metabolism) Proto-Oncogene Proteins RNA-Binding Protein FUS Ribonucleoproteins (biosynthesis, metabolism) T-Cell Acute Lymphocytic Leukemia Protein 1 Transcription Factor CHOP Transcription Factors (metabolism) Transcription, Genetic Transfection Translocation, Genetic

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