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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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HEMATOPOIESIS AND STEM CELLS

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

Hideaki Nakajima1, Toshiki Tamura2,*, Miyuki Ito1,*, Fumi Shibata3,*, Kana Kuroda4, Yumi Fukuchi4, Naohide Watanabe5, Toshio Kitamura3, Yasuo Ikeda4, and Makoto Handa5

1 Center of Excellence, The Institute of Medical Science, The University of Tokyo, Tokyo; 2 Department of Microbiology, Leprosy Research Center, National Institute of Infectious Diseases, Tokyo; 3 Division of Cellular Therapy, Advanced Clinical Research Center, The Institute of Medical Science, The University of Tokyo, Tokyo; 4 Division of Hematology, Department of Internal Medicine, Keio University School of Medicine, Tokyo; and 5 Department of Transfusion and Cell Therapy, Keio University School of Medicine, Tokyo, Japan

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-2 (IL-2), or IL-3. SHD1 interacted specifically with STAT5A and STAT5B, 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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