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ABSTRACT The transcription factor GATA-1 plays a significant role in erythroid differentiation and association with CBP stimulates its activity by acetylation. It is possible that histone
deacetylases (HDACs) repress the activity of GATA-1. In the present study, we investigated whether class I and class II HDACs interact with GATA-1 to regulate its function and indeed, GATA-1
is directly associated with HDAC3, HDAC4 and HDAC5. The expression profiling and our previous observation that GATA-2 interacts with members of the HDAC family prompted us to investigate
further the biological relevance of the interaction between GATA-1 and HDAC5. Coexpression of HDAC5 suppressed the transcriptional potential of GATA-1. Our results demonstrated that GATA-1
and HDAC5 colocalized to the nucleus of murine erythroleukemia (MEL) cells. Furthermore, a portion of HDAC5 moved to the cytoplasm concomitant with MEL cell erythroid differentiation, which
was induced by treatment with _N_,_N_′-hexamethylenebisacetamide. These observations support the suggestion that control of the HDAC5 nucleocytoplasmic distribution might be associated with
MEL cell differentiation, possibly through regulated GATA-1 transactivation. Access through your institution Buy or subscribe This is a preview of subscription content, access via your
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* Learn about institutional subscriptions * Read our FAQs * Contact customer support SIMILAR CONTENT BEING VIEWED BY OTHERS GFI1 TETHERS THE NURD COMPLEX TO OPEN AND TRANSCRIPTIONALLY ACTIVE
CHROMATIN IN MYELOID PROGENITORS Article Open access 02 December 2021 KAT7 IS A GENETIC VULNERABILITY OF ACUTE MYELOID LEUKEMIAS DRIVEN BY _MLL_ REARRANGEMENTS Article 06 August 2020
NUCLEAR INTERACTING SET DOMAIN PROTEIN 1 INACTIVATION IMPAIRS GATA1-REGULATED ERYTHROID DIFFERENTIATION AND CAUSES ERYTHROLEUKEMIA Article Open access 12 June 2020 REFERENCES * Bertos NR,
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. (2000). _Blood_, 96, 2641–2648. * Zhang Y, LeRoy G, Seelig HP, Lane WS and Reinberg D . (1998). _Cell_, 95, 279–289. Download references ACKNOWLEDGEMENTS We are grateful to S Suzuki, M
Isomura, and C Wakamatsu for technical assistance. AUTHOR INFORMATION AUTHORS AND AFFILIATIONS * Department of Molecular Medicine, Graduate School of Medicine, Nagoya University, Nagoya,
466-8550, Japan Kouichi Watamoto, Masayuki Towatari, Yukiyasu Ozawa, Yasuhiko Miyata, Mitsunori Okamoto, Akihiro Abe & Tomoki Naoe * National Nagoya Hospital, Nagoya, 460-0001, Japan
Hidehiko Saito Authors * Kouichi Watamoto View author publications You can also search for this author inPubMed Google Scholar * Masayuki Towatari View author publications You can also
search for this author inPubMed Google Scholar * Yukiyasu Ozawa View author publications You can also search for this author inPubMed Google Scholar * Yasuhiko Miyata View author
publications You can also search for this author inPubMed Google Scholar * Mitsunori Okamoto View author publications You can also search for this author inPubMed Google Scholar * Akihiro
Abe View author publications You can also search for this author inPubMed Google Scholar * Tomoki Naoe View author publications You can also search for this author inPubMed Google Scholar *
Hidehiko Saito View author publications You can also search for this author inPubMed Google Scholar CORRESPONDING AUTHOR Correspondence to Masayuki Towatari. RIGHTS AND PERMISSIONS Reprints
and permissions ABOUT THIS ARTICLE CITE THIS ARTICLE Watamoto, K., Towatari, M., Ozawa, Y. _et al._ Altered interaction of HDAC5 with GATA-1 during MEL cell differentiation. _Oncogene_ 22,
9176–9184 (2003). https://doi.org/10.1038/sj.onc.1206902 Download citation * Received: 14 April 2003 * Revised: 17 June 2003 * Accepted: 19 June 2003 * Published: 11 December 2003 * Issue
Date: 11 December 2003 * DOI: https://doi.org/10.1038/sj.onc.1206902 SHARE THIS ARTICLE Anyone you share the following link with will be able to read this content: Get shareable link Sorry,
a shareable link is not currently available for this article. Copy to clipboard Provided by the Springer Nature SharedIt content-sharing initiative KEYWORDS * GATA-1 * HDAC * differentiation
* MEL