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C200450200v1
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Papers In Press, published online ahead of print September 2, 2002
J. Biol. Chem, 10.1074/jbc.C200450200
Submitted on August 9, 2002
Revised on September 2, 2002
Accepted on September 2, 2002

Biological evidence that SOCS-2 can act either as an enhancer or suppressor of growth hormone signaling

Christopher J. Greenhalgh, Donald Metcalf, Anne L. Thaus, Jason E. Corbin, Rachel T. Uren, Phillip O. Morgan, Louis J. Fabri, Jian-Guo Zhang, Helene M. Martin, Tracy A. Willson, Nils Billestrup, Nicos A. Nicola, Manuel Baca, Warren S. Alexander, and Douglas J. Hilton

Department of Cancer and Haematology Division, The Walter and Eliza Hall Institute of Medical Research, Melbourne, Victoria 3050

Corresponding Author: greenhalgh{at}wehi.edu.au

Suppressor of cytokine signaling (SOCS)-2 is a member of a family of intracellular proteins implicated in the negative regulation of cytokine signaling. The generation of SOCS-2 deficient mice, which grow to one and a half times the size of their wild-type littermates, suggests that SOCS-2 may attenuate growth hormone (GH) signaling. In vitro studies indicate that, while SOCS-2 can inhibit growth hormone action at low concentrations, at higher concentrations it may potentiate signaling. To determine whether a similar enhancement of signaling is observed in vivo or alternatively whether increased SOCS-2 levels repress growth in vivo we generated and analyzed transgenic mice that overexpress SOCS-2 from a human ubiquitin C promoter. These mice are not growth deficient and are, in fact, significantly larger than wild-type mice. The overexpressed SOCS-2 was found to bind to endogenous GH receptors in a number of mouse organs, while phosphopeptide binding studies with recombinant SOCS-2 defined phosphorylated tyrosine 595 on the GH receptor as the site of interaction. Together, the data implicate SOCS-2 as having dual effects on GH signaling in vivo.


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