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Blood, 1 December 2006, Vol. 108, No. 12, pp. 3736-3738. Prepublished online as a Blood First Edition Paper on August 3, 2006; DOI 10.1182/blood-2006-07-032847. This Article Full Text Full Text (PDF) Supplemental Methods and Figures All Versions of this Article: blood-2006-07-032847v1 108/12/3736    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Lamonica, J. M. Articles by Blobel, G. A. Search for Related Content PubMed PubMed Citation Articles by Lamonica, J. M. Articles by Blobel, G. A. Related Collections Hematopoiesis and Stem Cells Gene Expression Brief Reports Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  HEMATOPOIESIS Brief report Acetylation of GATA-1 is required for chromatin occupancy Janine M. Lamonica, Christopher R. Vakoc, and Gerd A. Blobel From the Division of Hematology, the Children's Hospital of Philadelphia, PA; and the University of Pennsylvania School of Medicine, Philadelphia. All 3 hematopoietic GATA transcription factors, GATA-1, GATA-2, and GATA-3, are acetylated, although the in vivo role of this modification remains unclear. We examined the functions of an acetylation-defective mutant of GATA-1 in maturing erythroid cells. We found that removal of the acetylation sites in GATA-1 does not impair its nuclear localization, steady-state protein levels, or its ability to bind naked GATA elements in vitro. However, chromatin immunoprecipitation (ChIP) experiments revealed that mutant GATA-1 was dramatically impaired in binding to all examined cellular target sites in vivo, including genes that are normally activated and repressed by GATA-1. Together, these results suggest that acetylation regulates chromatin occupancy of GATA-1. These findings point to a novel function for transcription factor acetylation, perhaps by facilitating protein interactions required for stable association with chromatin templates in vivo. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: I. Qamar, E. Park, E.-Y. Gong, H. J. Lee, and K. Lee ARR19 (Androgen Receptor Corepressor of 19 kDa), an Antisteroidogenic Factor, Is Regulated by GATA-1 in Testicular Leydig Cells J. Biol. Chem., July 3, 2009; 284(27): 18021 - 18032. [Abstract] [Full Text] [PDF] T. Takaya, T. Kawamura, T. Morimoto, K. Ono, T. Kita, A. Shimatsu, and K. Hasegawa Identification of p300-targeted Acetylated Residues in GATA4 during Hypertrophic Responses in Cardiac Myocytes J. Biol. Chem., April 11, 2008; 283(15): 9828 - 9835. [Abstract] [Full Text] [PDF] R. Shimizu, C. D. Trainor, K. Nishikawa, M. Kobayashi, K. Ohneda, and M. Yamamoto GATA-1 Self-association Controls Erythroid Development in Vivo J. Biol. Chem., May 25, 2007; 282(21): 15862 - 15871. [Abstract] [Full Text] [PDF] N. Wiper-Bergeron, H. A. Salem, J. J. Tomlinson, D. Wu, and R. J. G. Hache Glucocorticoid-stimulated preadipocyte differentiation is mediated through acetylation of C/EBPbeta by GCN5 PNAS, February 20, 2007; 104(8): 2703 - 2708. [Abstract] [Full Text] [PDF]

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