The suppressors of cytokine signaling (SOCS) proteins

Nicola, Nicos A.; Greenhalgh, Christopher J.

doi:10.1016/s0301-472x(00)00525-7

Cited by 67 publications

(9 citation statements)

References 59 publications

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“…Interestingly, the gene with the greatest increase in expression was a suppressor gene, suppressor of cytokine signaling (SOCS‐1). SOCS‐1 is an intracellular protein able to block the signaling response to at least 8 cytokines, including interferon‐γ 14,15 . Mice lacking SOCS‐1 develop a lethal neonatal phenotype characterized by diffuse granulocyte and macrophage infiltration of most solid organs, including skin.…”

Section: Resultsmentioning

confidence: 99%

Early gene expression profile of human skin to injury using high‐density cDNA microarrays

Cole

Tsou

Wallace

et al. 2001

Wound Repair Regeneration

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Disturbances in normal wound healing may be traced to perturbations in gene expression following injury. To decipher normal and abnormal genetic responses to cutaneous injury, baseline gene expression of uninjured skin and injured skin must be better defined. Our aim for this study was to determine the gene expression profile of human skin immediately following injury using cDNA microarrays. Samples of normal and injured skin were obtained from 5 healthy females undergoing breast reduction surgery. Specimens of the epidermis and dermis were obtained at 30 minutes and 1 hour after the initial injury. RNA was extracted, reverse transcribed into cDNA and hybridized onto high-density cDNA microarray membranes of 4,000 genes. At 30 minutes, injury resulted in a consistent increase (> 2x) in gene expression of 124 out of 4,000 genes (3%). These genes were primarily involved in transcription and signaling. None of the 4,000 genes were decreased (< 2x) at 30 minutes. At 1 hour only 46 out of the 4,000 genes were increased in expression (1.15%) but 264 out of 4,000 (6.6%) genes were decreased greater than 2 fold, indicating a silencing of many structural genes. We have identified several genes, namely, suppressor of cytokine signaling-1, rho HP1, and BB1, that are highly expressed after injury and may have an unappreciated role in regulating the initial inflammatory response. These data provide an initial high-throughput analysis of gene expression immediately following human skin injury and show the utility and future importance of high-throughput analysis in skin biology and wound repair.

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Section: Resultsmentioning

confidence: 99%

Early gene expression profile of human skin to injury using high‐density cDNA microarrays

Cole

Tsou

Wallace

et al. 2001

Wound Repair Regeneration

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“…So we next focused on SOCSs as negative regulators of the action of IFN␣/␤. Eight isoforms of SOCS were earlier identified as a family of intracellular proteins controlling the magnitude and/or duration of signals propagated by diverse cytokine receptors by suppressing their signal transduction process (37). We examined the effect of sRANKL on the expression of SOCS-1 and -3 mRNAs in osteoclast progenitors by semiquantitative RT-PCR.…”

Section: Induction Of Socs-1 and -3 By Srankl Inmentioning

confidence: 99%

“…These results imply a protein inhibitors of activated STATs-independent mechanism. SOCS, also called JAKbinding protein and cytokine-inducible SH2 protein, was originally discovered as the product of an immediate early gene induced by stimulation with IL-3 and erythropoietin; so far eight isoforms have been cloned (37). Among these SOCSs, SOCS-1 and SOCS-3 have been extensively studied for their actions and are considered to be potent negative feedback regulators of a number of cytokines and growth factors whose signals are mediated by the JAK/STAT system (38).…”

Section: Figmentioning

confidence: 99%

Regulation of Receptor Activator of NF-κB Ligand-induced Osteoclastogenesis by Endogenous Interferon-β (INF-β) and Suppressors of Cytokine Signaling (SOCS)

Hayashi

Kaneda

Toyama

et al. 2002

Journal of Biological Chemistry

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“…These include the SOCS proteins, such as the pathway target gene SOCS3 , which act to negatively regulate the stimulated receptor/JAK complex forming negative feedback loops that reduce the duration and intensity of pathway activation 11 . In addition, the PIAS proteins and the SHP1/2 tyrosine phosphatases also act as negative regulators of pathway activity 12 .…”

Section: Introductionmentioning

confidence: 99%

Modulation of human JAK-STAT pathway signaling by functionally conserved regulators

2012

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Both the core JAK-STAT pathway components and their in vivo roles have been widely conserved between vertebrates and invertebrate models such as Drosophila melanogaster. Misregulation of JAK-STAT pathway activity has also been identified as a key factor in the development of multiple human malignancies. Recently, whole genome RNA interference (RNAi) screens in cultured Drosophila cells have identified both positively and negatively acting JAK-STAT pathway regulators. Here, we describe the analysis of 73 human genes representing homologs of 56 Drosophila genes originally identified by genome-wide RNAi screening as regulators of JAK-STAT signaling. Using assays for human STAT1 and STAT3 protein levels and phosphorylation status, as well as assays measuring the expression of endogenous STAT1 and STAT3 transcriptional targets, we have tested siRNAs targeting these 73 human genes and have identified potential JAK-STAT pathway regulatory roles in 69 (95%) of these. The genes identified represent a wide range of human JAK-STAT pathway regulators and include genes not previously known to modulate this signaling cascade. These results underline the value of model system based approaches for the identification of pathway regulators and have led to the identification of loci whose misregulation may ultimately be implicated in JAK-STAT pathway-mediated human disease.

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The suppressors of cytokine signaling (SOCS) proteins

Cited by 67 publications

References 59 publications

Early gene expression profile of human skin to injury using high‐density cDNA microarrays

Early gene expression profile of human skin to injury using high‐density cDNA microarrays

Regulation of Receptor Activator of NF-κB Ligand-induced Osteoclastogenesis by Endogenous Interferon-β (INF-β) and Suppressors of Cytokine Signaling (SOCS)

Modulation of human JAK-STAT pathway signaling by functionally conserved regulators

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