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Molecular Biology

A. Kakizuka, W.H. Miller, K. Umesono, R.P. Warrell, et al., "Chromosomal translocation t(15;17) in human acute promyelocytic leukemia fuses RAR with a novel putative transcription factor, PML," Cell, 66:663-74, 1991. Akira Kakizuka (The Salk Institute, La Jolla, Calif.): "Our paper described the genes located at each of the breakpoints of the t(15;17) translocation associated with human acute promyelocytic leukemia (APL). In addition to the karyotype abnormality, the patients with APL can be i

The Scientist Staff

A. Kakizuka, W.H. Miller, K. Umesono, R.P. Warrell, et al., "Chromosomal translocation t(15;17) in human acute promyelocytic leukemia fuses RAR with a novel putative transcription factor, PML," Cell, 66:663-74, 1991.

Akira Kakizuka (The Salk Institute, La Jolla, Calif.): "Our paper described the genes located at each of the breakpoints of the t(15;17) translocation associated with human acute promyelocytic leukemia (APL). In addition to the karyotype abnormality, the patients with APL can be induced into complete remission with a high dose of all-trans retinoic acid (RA). The translocation fuses a previously underscribed gene, PML (for promyelocytes), on chromosome 15 to the retinoic acid receptor (RAR) gene on chromosome 17 to create the aberrant gene product, PML-RAR. The PML protein contains a cysteine-rich motif found in a variety of nuclear factors that include the recombination activating gene 1 (RAG1).

"From our structural and functional analyses, we proposed that the aberrant PML-RAR protein...

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