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Expression of the AML-1 oncogene shortens the G(1) phase of the cell cycle.

作者信息

Strom D K, Nip J, Westendorf J J, Linggi B, Lutterbach B, Downing J R, Lenny N, Hiebert S W

机构信息

Department of Biochemistry, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA.

出版信息

J Biol Chem. 2000 Feb 4;275(5):3438-45. doi: 10.1074/jbc.275.5.3438.

DOI:10.1074/jbc.275.5.3438
PMID:10652337
Abstract

The AML-1-encoded transcription factor, AML-1B, regulates numerous hematopoietic-specific genes. Inappropriate expression of AML-1-family proteins is oncogenic in cell culture systems and in mice. To understand the oncogenic functions of AML-1, we established cell lines expressing AML-1B to examine the role of AML-1 in the cell cycle. DNA content analysis and bromodeoxyuridine pulse-chase studies indicated that entry into the S phase of the cell cycle was accelerated by up to 4 h in AML-1B-expressing 32D.3 myeloid progenitor cells as compared with control cells or cells expressing E2F-1. However, AML-1B was not able to induce continued cell cycle progression in the absence of growth factors. The DNA binding and transactivation domains of AML-1B were required for altering the cell cycle. Thus, AML-1B is the first transcription factor that affects the timing of the mammalian cell cycle.

摘要

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