TAL2, a helix-loop-helix gene activated by the (7;9)(q34;q32) translocation in human T-cell leukemia.

Ying Xia(The University of Texas Southwestern Medical Center), J. Lesley Brown(The University of Texas Southwestern Medical Center), C Y Yang(The University of Texas Southwestern Medical Center), Julia Tsou Tsan(The University of Texas Southwestern Medical Center), Michael J. Siciliano(The University of Texas Southwestern Medical Center), R Espinosa(The University of Texas Southwestern Medical Center), Michelle M. Le Beau(The University of Texas Southwestern Medical Center), Richard Baer(The University of Texas Southwestern Medical Center)
Proceedings of the National Academy of Sciences
December 15, 1991
Cited by 206Open Access

Abstract

Tumor-specific alteration of the TAL1 gene occurs in almost 25% of patients with T-cell acute lymphoblastic leukemia (T-ALL). We now report the identification of TAL2, a distinct gene that was isolated on the basis of its sequence homology with TAL1. The TAL2 gene is located 33 kilobase pairs from the chromosome 9 breakpoint of t(7;9)(q34;q32), a recurring translocation specifically associated with T-ALL. As a consequence of t(7;9)(q34;q32), TAL2 is juxtaposed with sequences from the T-cell receptor beta-chain gene on chromosome 7. TAL2 sequences are actively transcribed in SUP-T3, a T-ALL cell line that harbors the t(7;9)(q34;q32). The TAL2 gene product includes a helix-loop-helix protein dimerization and DNA binding domain that is especially homologous to those encoded by the TAL1 and LYL1 protooncogenes. Hence, TAL2, TAL1, and LYL1 constitute a discrete subgroup of helix-loop-helix proteins, each of which can potentially contribute to the development of T-ALL.


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