Suppressor of cytokine signaling (SOCS) 2, a protein with multiple functions

Rico-Bautista, Elizabeth; Flores‐Morales, Amilcar; Fernández-Pérez, Leandro

doi:10.1016/j.cytogfr.2006.09.008

Cited by 181 publications

(171 citation statements)

References 83 publications

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“…Confirming earlier reports, it was found that the mRNA signal encoding PRLR is significantly upregulated during pregnancy [16], indicating the presence of a positive feedback loop by which initial stimulation of PRLR by PL leads to reinforcement of the signalling axis. On the other hand, the feed-forward signal is counterbalanced by upregulation of two transcripts encoding suppressors of cytokine signalling, CISH [20] and SOCS2 [21]. In addition, in a mouse model of PRLR deficiency we have shown that expression of this receptor is required for the induction of many of the pregnancy-related mRNA changes in mouse islets of Langerhans [14].…”

Section: Introductionmentioning

confidence: 85%

Serotonin competence of mouse beta cells during pregnancy

2016

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Pregnancy is a key mammalian reproductive event in which growth and differentiation of the fetus imposes extra metabolic and hormonal demands on the mother. Its successful outcome depends on major changes in maternal blood circulation, metabolism and endocrine function. One example is the endocrine pancreas, where beta cells undergo a number of changes in pregnancy that result in enhanced functional beta cell mass in order to compensate for the rising metabolic needs for maternal insulin. During the last 5 years, a series of studies have increased our understanding of the molecular events involved in this functional adaptation. In the mouse, a prominent functional change during pregnancy is the capacity of some beta cells to produce serotonin. In this review we will discuss the mechanism and potential effects of pregnancyrelated serotonin production in beta cells, considering functional consequences at the local intra-islet and systemic level.

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Section: Introductionmentioning

confidence: 85%

Serotonin competence of mouse beta cells during pregnancy

2016

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“…(22,23) In addition, the suppressors of cytokine signaling (SOCS) family of proteins are generated in response to ORIGINAL ARTICLE J JBMR cytokines including GH and through their SH2 domains can bind to phosphorylated tyrosine residues within the cytokine receptor-JAK complex, inhibiting JAK signaling and downstream STAT activation. (24)(25)(26) There are eight identified SOCS proteins, CIS and SOCS1-7, all of which are involved in negatively regulating cytokine signaling. SOCS proteins consist of a central SH2 domain, a conserved C-terminal motif named the SOCS box, and a variable N-terminal domain.…”

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confidence: 99%

SOCS2 is the critical regulator of GH action in murine growth plate chondrogenesis

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Huesa

et al. 2012

Journal of Bone and Mineral Research

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Suppressor of Cytokine Signaling-2 (SOCS2) is a negative regulator of growth hormone (GH) signaling and bone growth via inhibition of the Janus kinase/signal transducers and activators of transcription (JAK/STAT) pathway. This has been classically demonstrated by the overgrowth phenotype of SOCS2 À/À mice, which has normal systemic insulin-like growth factor 1 (IGF-1) levels. The local effects of GH on bone growth are equivocal, and therefore this study aimed to understand better the SOCS2 signaling mechanisms mediating the local actions of GH on epiphyseal chondrocytes and bone growth. SOCS2, in contrast to SOCS1 and SOCS3 expression, was increased in cultured chondrocytes after GH challenge. Gain-and loss-of-function studies indicated that GH-stimulated chondrocyte STATs-1, -3, and -5 phosphorylation was increased in SOCS2 À/À chondrocytes but not in cells overexpressing SOCS2. This increased chondrocyte STAT signaling in the absence of SOCS2 is likely to explain the observed GH stimulation of longitudinal growth of cultured SOCS2À/À embryonic metatarsals and the proliferation of chondrocytes within. Consistent with this metatarsal data, bone growth rates, growth plate widths, and chondrocyte proliferation were all increased in SOCS2 À/À 6-week-old mice as was the number of phosphorylated STAT-5-positive hypertrophic chondrocytes. The SOCS2 À/À mouse represents a valid model for studying the local effects of GH on bone growth. ß

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“…Evidence also indicates that growth factors (e.g., insulin, chemokines), xenobiotics, and steroid hormones, including estrogens, can induce SOCS expression (RicoBautista et al, 2006). Consequently, regulation of SOCS protein expression provides a mechanism for cross-talk where multiple factors can regulate the activity of specific cytokines (Greenhalgh and Alexander, 2004;Leung et al, 2004;Rico-Bautista et al, 2006). Particularly, SOCS2 may be a physiological mechanism by which estrogen signaling pathways influence GH activity: estrogen suppresses GH-dependent JAK2 phosphorylation by increasing the expression of SOCS2 (Leung et al, 2004).…”

Section: Positive and Negative Regulation Of Gh Signalingmentioning

confidence: 99%

“…Finally, SOCS proteins have been shown key components of negative regulators of GHR-JAK-STAT signaling pathway. The SOCS family comprises at least eight proteins: CIS and SOCS-1 to -7 (Flores- Rico-Bautista et al, 2006). SOCS proteins have been shown to modify cytokine actions through a classic negative feedback loop.…”

Section: Positive and Negative Regulation Of Gh Signalingmentioning

confidence: 99%