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Janne Jensen, Elisabeth D Galsgaard, Allan E Karlsen, Ying C Lee, and Jens H Nielsen

suppressor of cytokine signalling (SOCS) expression. We therefore studied possible interactions between hGH and IL-1β, IFN-γ and TNF-α on the DNA-binding activity of STAT5, STAT1 and NFκB, activation of SOCS-3 and induction of inducible nitric oxide synthase

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M Fasshauer, S Kralisch, M Klier, U Lossner, M Bluher, J Klein, and R Paschke

Various cytokines, including tumor necrosis factor (TNF) alpha, growth hormone (GH) and interleukin (IL)-6, induce insulin resistance. Recently, it was demonstrated that induction of suppressor of cytokine signaling (SOCS)-3 by TNFalpha and GH is an important mechanism by which these cytokines impair insulin sensitivity. The current study investigated in 3T3-L1 adipocytes whether TNFalpha and GH also upregulate SOCS-1 and SOCS-6, which have both been shown to inhibit insulin signaling potently, and whether IL-6 might alter synthesis of SOCS-1, -3 and -6. Interestingly, 10 ng/ml TNFalpha, 500 ng/ml GH and 30 ng/ml IL-6 induced SOCS-1 mRNA time-dependently with maximal stimulation detectable after 8 h of TNFalpha and 1 h of GH and IL-6 addition respectively. Furthermore, TNFalpha and GH caused sustained upregulation of SOCS-1 for up to 24 h, whereas stimulation by IL-6 was only transient, with SOCS-1 mRNA returning to basal levels 2 h after effector addition. Induction of SOCS-1 was dose-dependent, and significant stimulation was detectable at concentrations as low as 3 ng/ml TNFalpha, 50 ng/ml GH and 10 ng/ml IL-6. Furthermore, stimulation experiments and studies using pharmacologic inhibitors suggested that the positive effect of TNFalpha, GH and IL-6 on SOCS-1 mRNA is, at least in part, mediated by Janus kinase (Jak) 2. Finally, SOCS-3 expression was dose- and time-dependently induced by IL-6, at least in part via Jak2, but none of the cytokines affected SOCS-6 expression. Taken together, our results show a differential regulation of SOCS mRNA by insulin resistance-inducing hormones, and suggest that SOCS-1, as well as SOCS-3, may be an important intracellular mediator of insulin resistance in fat cells and a potential pharmacologic target for the treatment of impaired insulin sensitivity.

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A M Solomon and P M G Bouloux

, 5b and increases in suppressor of cytokine signalling-2 (SOCS-2; Sadowski et al. 2001 , Frost et al. 2002 ). Increasing evidence suggests that SOCS-2 is a key negative modulator of GH action ( Leroith & Nissley 2005 ). There are eight

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Raquel Barbuio, Marciane Milanski, Manoel B Bertolo, Mário J Saad, and Lício A Velloso

levels of the regulatory cytokine, IL-10, were not affected by infliximab; however, the levels of the suppressor of cytokine signaling, SOCS-3, were completely restored to basal levels. Infliximab reduces liver steatosis and

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María F Andreoli, Jose Donato Jr, Isin Cakir, and Mario Perello

pathways ( Banks et al. 2000 ). Phosphorylated Y985 also binds to the suppressor of cytokine signalling 3 (SOCS3), whose gene transcription depends on pSTAT3 and exerts an inhibitory effect on LepRb signalling ( Bjorbaek et al. 1999 ). Phosphorylated Y

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Adam Gesing, Andrzej Bartke, and Michal M Masternak

upregulation of suppressors of cytokine signaling-3 (SOCS3) – a marker of the activation of IL6 signaling (reviewed in Coelho et al . (2013) ). In turn, SOCS3, as well as SOCS1, may lead – among other effects – to impaired IRS1 and IRS2 tyrosine

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J G Miquet, A I Sotelo, F P Dominici, M S Bonkowski, A Bartke, and D Turyn

effects of suppressor of cytokine signaling (SOCS-2) on growth hormone signal transduction. FEBS Letters 453 63 –66. Frick GP , Tai LR & Goodman HM 1994 Subcellular distribution of the long and short isoforms of the

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Anna G Holmes, Jose L Mesa, Bronwyn A Neill, Jason Chung, Andrew L Carey, Gregory R Steinberg, Bruce E Kemp, Robert J Southgate, Graeme I Lancaster, Clinton R Bruce, Matthew J Watt, and Mark A Febbraio

IL-6 treatment tends to improve insulin action. This may be due to the fact that chronically elevated IL-6 results in elevated expression of suppressor of cytokine signalling-3 (SOCS3) ( Klover et al . 2003 ), which is generally thought to induce

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Cid Pitombo, Eliana P Araújo, Cláudio T De Souza, José C Pareja, Bruno Geloneze, and Lício A Velloso

actions are complex and include the activation of serine kinases ( Hotamisligil 2003 ), the induction of endoplasmic reticulum stress ( Ozcan et al. 2004 ), and the stimulation of the expression of inhibitors of signaling belonging to the suppressor of

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B T Layden, V Durai, M V Newman, A M Marinelarena, C W Ahn, G Feng, S Lin, X Zhang, D B Kaufman, N Jafari, G L Sørensen, and W L Lowe Jr

.7 <0.0005 Tac1 Tachykinin 1 2.6 <0.0005 Socs2 Suppressor of cytokine signaling 2 2.6 <0.0005 Igfbp-5 Insulin-like growth factor-binding protein-5 2.5 <0.0005 Hopx HOP homeobox 2.3 <0.0005 Enpp2 Ectonucleotide pyrophosphatase/phosphodiesterase 2 2.3 <0