TY - JOUR
AU1 - Yamaguchi, Yuko
AU2 - Kurokawa, Mineo
AU3 - Imai, Yoichi
AU4 - Izutsu, Koji
AU5 - Asai, Takashi
AU6 - Ichikawa, Motoshi
AU7 - Yamamoto, Go
AU8 - Nitta, Eriko
AU9 - Yamagata, Tetsuya
AU1 - Sasaki, Kazuki
AU1 - Mitani, Kinuko
AU1 - Ogawa, Seishi
AU1 - Chiba, Shigeru
AU1 - Hirai, Hisamaru
AU1 - 
AB - THE JOURNAL OF BIOLOGICAL CHEMISTRY Vol. 279, No. 15, Issue of April 9, pp. 15630 –15638, 2004 © 2004 by The American Society for Biochemistry and Molecular Biology, Inc. Printed in U.S.A. AML1 Is Functionally Regulated through p300-mediated Acetylation on Specific Lysine Residues* Received for publication, January 13, 2004 Published, JBC Papers in Press, January 29, 2004, DOI 10.1074/jbc.M400355200 Yuko Yamaguchi‡, Mineo Kurokawa‡ , Yoichi Imai‡, Koji Izutsu‡, Takashi Asai‡, Motoshi Ichikawa‡, Go Yamamoto‡, Eriko Nitta‡, Tetsuya Yamagata‡, Kazuki Sasaki§, Kinuko Mitani , Seishi Ogawa‡, Shigeru Chiba‡, and Hisamaru Hirai†‡ From the ‡Department of Hematology and Oncology, Graduate School of Medicine, University of Tokyo, Tokyo 113-8655, the §Growth Factor Division, National Cancer Center Research Institute, Tokyo 104-0045, and the Department of Hematology, Dokkyo University School of Medicine, Mibu, Tochigi 321-0293, Japan TG(T/c)GGT, called the PEBP2 site, through the Runt domain. AML1 (RUNX1) is one of the most frequently disrupted genes in human leukemias. AML1 encodes transcription Its affinity for DNA is markedly increased by heterodimeriza- factors, which play a pivotal role in hematopoietic dif- tion with PEBP2 (10 –13). This heterodimeric complex regu- ferentiation, and their inappropriate expression is asso- lates transcription of a large number of hematopoietic lineage- 
TI - AML1 Is Functionally Regulated through p300-mediated Acetylation on Specific Lysine Residues
JF - Journal of Biological Chemistry
DO - 10.1074/jbc.m400355200
DA - 2004-04-01
UR - https://www.deepdyve.com/lp/unpaywall/aml1-is-functionally-regulated-through-p300-mediated-acetylation-on-tjCVX8Mzv5
DP - DeepDyve
ER -