STAT5b mediates the GH-induced expression of SOCS-2 and SOCS-3 mRNA in the liver
- Author(s)
- Davey, HW; McLachlan, MJ; Wilkins, RJ; Hilton, DJ; Adams, TE;
- Details
- Publication Year 1999-12-20,Volume 158,Issue #1-2,Page 111-116
- Journal Title
- MOLECULAR AND CELLULAR ENDOCRINOLOGY
- Publication Type
- Journal Article
- Abstract
- 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. (C) 1999 Elsevier Science Ireland Ltd. All rights reserved.
- Publisher
- ELSEVIER SCI IRELAND LTD
- Keywords
- GROWTH-HORMONE STIMULATION; TYROSINE PHOSPHORYLATION; SIGNAL-TRANSDUCTION; GENE-EXPRESSION; PROTEIN; ACTIVATION; TRANSCRIPTION; FAMILY; CIS; RECEPTOR
- Publisher's Version
- https://doi.org/10.1016/S0303-7207(99)00175-6
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- Refer to copyright notice on published article.
Creation Date: 1999-12-20 12:00:00