Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

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Davey, H.W. et al.

Davey, McLachlan, Wilkins, Hilton, Adams,

STAT5b mediates the GH- induced expression of SOCS-2 and SOCS-3 mRNA in the liver.

Suppressor of cytokine signalling ( SOCS) proteins act as part of a classical negative feedback loop regulating cytokine signal transduction. Expression of SOCS proteins is induced in response to cytokines and down-regulates the cytokine signal by inhibiting the JAK/STAT pathway. Growth hormone ( GH) was previously shown to induce strong transient expression of SOCS-3 and to a lesser extent CIS, SOCS-1 and SOCS-2 in mouse liver (Adams, T.E., Hansen, J.A., Starr, R., Nicola, N.A., Hilton, D.J., Billestrup, N., 1998. Growth hormone preferentially induces the rapid, transient expression of SOCS-3, a novel inhibitor of cytokine receptor signalling. J. Biol. Chem. 273, 1285-1287.). In this work we have compared GH- induced SOCS gene expression in wild-type and STAT5b-deficient mice, and show that STAT5b is required for the induction of SOCS-2 and SOCS-3 in liver. In contrast, the absence of STAT5b has no effect on the GH- induced expression of CIS and SOCS-2 mRNA in the mammary gland. Suprisingly, there is no activation of SOCS-3 expression in mammary glands of wild-type and STAT5b mutant mice following GH administration. These results highlight both tissue- and factor-specific differences in the regulation of SOCS gene expression by STAT5a/b.[1]

References

STAT5b mediates the GH-induced expression of SOCS-2 and SOCS-3 mRNA in the liver. Davey, H.W., McLachlan, M.J., Wilkins, R.J., Hilton, D.J., Adams, T.E. Mol. Cell. Endocrinol. (1999) [Pubmed]

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