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

Davey, Helen W.; McLachlan, Michael J.; Wilkins, Richard J.; Hilton, Douglas J.; Adams, Timothy E.

doi:10.1016/s0303-7207(99)00175-6

Cited by 111 publications

(76 citation statements)

References 45 publications

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“…Using mutant IL-9Rs that selectively lost the ability to activate either STAT5 or STAT1 and STAT3, we found that CIS and SOCS-2 could be induced by IL-9 in both conditions. This contrasts with the initial paper suggesting that CIS might be specifically regulated by STAT5 [33] but is in line with the observation that GH induces CIS expression in STAT5b-deficient mice [42]. By contrast, SOCS-3 was found to be induced by IL-9 through an IL-9R mutant that activates STAT1 and STAT3, but not with a mutant receptor that activates only STAT5.…”

Section: Discussionsupporting

confidence: 62%

Interleukin 9 induces expression of three cytokine signal inhibitors: cytokine-inducible SH2-containing protein, suppressor of cytokine signalling (SOCS)-2 and SOCS-3, but only SOCS-3 overexpression suppresses interleukin 9 signalling

2000

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Interleukin 9 (IL-9) is a cytokine preferentially produced by T helper type 2 lymphocytes and active on various cell types such as T-and B-lymphocytes, mast cells and haemopoietic progenitors. The IL-9 receptor (IL-9R) belongs to the haemopoietic receptor superfamily and its signal transduction involves mainly the Janus kinase\signal transducer and activator of transcription (JAK\STAT) pathway. Here we studied the implication of a novel family of suppressors of cytokine signalling (called CIS, for cytokine-inducible SH2-containing protein, and SOCS, for suppressor of cytokine signalling) in IL-9 signal attenuation. In BW5147 T-cell lymphoma, IL-9 induced the rapid expression of CIS, SOCS-2 and SOCS-3 with a peak after 2 h of stimulation. Using IL-9R mutants, we showed that STAT activation is required for CIS\SOCS induction : CIS and SOCS-2 expression was induced either via STAT1 and\or STAT3 or via STAT5 but

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Section: Discussionsupporting

confidence: 62%

Interleukin 9 induces expression of three cytokine signal inhibitors: cytokine-inducible SH2-containing protein, suppressor of cytokine signalling (SOCS)-2 and SOCS-3, but only SOCS-3 overexpression suppresses interleukin 9 signalling

2000

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“…1). The GH regulation of the expression of IGF-I (Woelfle et al 2003) and several other genes (Bergad et al 1995, Davey et al 1999, Woelfle & Rotwein 2004 in the liver has been shown to be mediated by STAT5. To determine if GH stimulation of HNF-3 expression is also mediated by STAT5, a 967 bp promoter region of the bovine HNF-3 gene was cloned and sequenced (Fig.…”

Section: The Promoter Of Hnf-3 Contains Multiple Potential Stat5-bindmentioning

confidence: 99%

“…The signaling pathways by which GH regulates gene expression in the liver are only beginning to be understood (Herrington & Carter-Su 2001, Schwartz et al 2002, including the identification of the signal transducers and activators of transcription (STAT), especially STAT5B and STAT5A, as key transcription factors mediating GH regulation of the expression of Spi 2·1 (Bergad et al 1995), IGF-I (Woelfle et al 2003) and several other members of the GH/IGF axis in the liver (Davey et al 1999, Woelfle & Rotwein 2004. However, for most of the GHregulated genes, the signaling pathways and the transcription factors involved remain to be elucidated.…”

Section: Introductionmentioning

confidence: 99%

Growth hormone regulates the expression of hepatocyte nuclear factor-3 gamma and other liver-enriched transcription factors in the bovine liver

Eleswarapu

Jiang²

2005

Journal of Endocrinology

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“…The signaling pathways involved in induction of SOCS expression in response to GH remain to be fully characterized, but are predicted to require STAT signaling (Naka et al, 1997). In the case of SOCS-2 and SOCS-3, STAT5B is thought to mediate GH induction of their expression in liver (Davey et al, 1999a).…”

Section: Activation Of Stat Phosphorylation By Sh2-bbmentioning

confidence: 99%

The role of STAT proteins in growth hormone signaling

et al. 2000

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Growth hormone (GH) has long been known to be the body's primary regulator of body growth and a regulator of metabolism, yet the mechanisms by which GH regulates the transcription of speci®c genes required for these processes are just now being delineated. GH binding to its receptor recruits and activates the receptor-associated JAK2 that in turn phosphorylates tyrosines within itself and the GH receptor. These tyrosines form binding sites for a number of signaling proteins, including members of the family of signal transducers and activators of transcription (STAT). Among the known signaling molecules for GH, STAT proteins play a particularly prominent role in the regulation of gene transcription. This paper will review what is currently understood about which STAT proteins are regulated by GH, how they are regulated by GH, the GH-dependent genes they regulate, and discuss current theories about how GH-activated STAT signaling is regulated. Particular attention will be given to the novel role that STAT5 plays in sexually dimorphic gene expression in the liver as determined by the secretory pattern of GH and the role of STAT5 in body growth.

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

Cited by 111 publications

References 45 publications

Interleukin 9 induces expression of three cytokine signal inhibitors: cytokine-inducible SH2-containing protein, suppressor of cytokine signalling (SOCS)-2 and SOCS-3, but only SOCS-3 overexpression suppresses interleukin 9 signalling

Interleukin 9 induces expression of three cytokine signal inhibitors: cytokine-inducible SH2-containing protein, suppressor of cytokine signalling (SOCS)-2 and SOCS-3, but only SOCS-3 overexpression suppresses interleukin 9 signalling

Growth hormone regulates the expression of hepatocyte nuclear factor-3 gamma and other liver-enriched transcription factors in the bovine liver

The role of STAT proteins in growth hormone signaling

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