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 Blood, 29 January 2009, Vol. 113, No. 5, pp. 1027-1036.
Prepublished online as a Blood First Edition Paper on October 6, 2008; DOI 10.1182/blood-2008-01-133405.

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Submitted January 10, 2008
Accepted September 14, 2008

SHD1 is a novel cytokine-inducible, negative feedback regulator of STAT5-dependent transcription

Hideaki Nakajima*, Toshiki Tamura, Miyuki Ito, Fumi Shibata, Kana Kuroda, Yumi Fukuchi, Naohide Watanabe, Toshio Kitamura, Yasuo Ikeda, and Makoto Handa

Center of Excellence, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan
Department of Microbiology, Leprosy Research Center, National Institute of Infectious Diseases, Tokyo, Japan
Division of Cellular Therapy, Advanced Clinical Research Center, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan
Division of Hematology, Department of Internal Medicine, Keio University School of Medicine, Tokyo, Japan
Department of Transfusion and Cell Therapy, Keio University School of Medicine, Tokyo, Japan

* Corresponding author; email: hnakajim{at}sc.itc.keio.ac.jp.

STAT5 is a critical mediator of a variety of cytokine signaling whose transcriptional activity is regulated by associating with various proteins. During a search for STAT5-interacting proteins, we identified SHD1, a mammalian homologue of yeast gene Sac3, as a potential interacter. SHD1 was localized in the nucleus, and induced by cytokines that activate STAT5, such as erythropoietin, interleukin (IL)-2, or IL-3. SHD1 interacted specifically with STAT5A and 5B, and interestingly, it specifically repressed STAT5-dependent transcription in vitro without affecting the stability or phosphorylation of STAT5 protein. Gene disruption study revealed that T, B, or bone marrow cells from mice lacking SHD1 were hyperresponsive to T-cell receptor engagement, or stimulation with various STAT5-activating cytokines. These results suggest that SHD1 is a novel cytokine-inducible negative feedback regulator of STAT5.


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