Author:
Markova E. N.,Petrova N. V.,Razin S. V.,Kantidze O. L.
Subject
Structural Biology,Biophysics
Reference133 articles.
1. Miyoshi H., Shimizu K., Kozu T., Maseki N., Kaneko Y., Ohki M. 1991. t(8;21) breakpoints on chromosome 21 in acute myeloid leukemia are clustered within a limited region of a single gene, AML1. Proc. Natl. Acad. Sci. U. S. A. 88, 10431–10434.
2. Bae S.C., Ogawa E., Maruyama M., Oka H., Satake M., Shigesada K., Jenkins N.A., Gilbert D.J., Copeland N.G., Ito Y. 1994. PEBP2 alpha B/mouse AML1 consists of multiple isoforms that possess differential transactivation potentials. Mol. Cell. Biol. 14, 3242–3252.
3. Bae S.C., Yamaguchi-Iwai Y., Ogawa E., Maruyama M., Inuzuka M., Kagoshima H., Shigesada K., Satake M., Ito Y. 1993. Isolation of PEBP2 alpha B cDNA representing the mouse homolog of human acute myeloid leukemia gene, AML1. Oncogene. 8, 809–814.
4. Nucifora G., Rowley J.D. 1995. AML1 and the 8;21 and 3;21 translocations in acute and chronic myeloid leukemia. Blood. 86, 1–14.
5. Okuda T., van Deursen J., Hiebert S.W., Grosveld G., Downing J.R. 1996. AML1, the target of multiple chromosomal translocations in human leukemia, is essential for normal fetal liver hematopoiesis. Cell. 84, 321–330.
Cited by
5 articles.
订阅此论文施引文献
订阅此论文施引文献，注册后可以免费订阅5篇论文的施引文献，订阅后可以查看论文全部施引文献