The role of suppressors of cytokine signaling (SOCS) proteins in regulation of the immune response.

By Warren S. Alexander, D. Hilton. Annual Review of Immunology, 2004

764 citations recorded by the source corpus.

Subfields: Immunology, Oncology, Pharmacology

View Paper: https://www.semanticscholar.org/paper/81479b3dc5a3019a44d08e71eebc9fb44ccf43d8

How researchers see this paper

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In Immunology

1. Alexander Y. Rudensky
2. J. O’Shea
3. M. Karin
4. T. Lawrence
5. J. P. Rasmussen
6. J. Fontenot
7. V. Nizet
8. A. Yoshimura

In Oncology

1. J. O’Shea
2. Alexander Y. Rudensky
3. M. Karin
4. T. Lawrence
5. V. Nizet
6. A. Laurence
7. P. Murray
8. Christopher A. Hunter

In Pharmacology

1. M. Karin
2. P. Murray
3. J. O’Shea
4. R. Ransohoff

Citations in the corpus

• Human tyrosine kinase 2 deficiency reveals its requisite roles in multiple cytokine signals involved in innate and acquired immunity. (2006, background): “…that several inhibitory mechanisms are involved in the regulation of the Jak-STAT pathway to prevent it from overactivation, including SOCS (suppressor of cytokine signaling) proteins that are induced through the Jak-STAT pathway to make a negative feedback loop (Alexander and Hilton, 2004).”
• Cytokine signaling modules in inflammatory responses. (2008, methodology): “) Subsequent extensive genetic analysis using Socs1 / mice or Socs1 conditionally deficient mice crossed to deficiencies in immune and inflammatory pathways has revealed that whereas the IFN-gR is the primary target of Socs1, other cytokine receptors also respond to the negative effects of Socs1 inc”
• Interferons at age 50: past, current and future impact on biomedicine (2007, background): “SoCS inhibit receptor signalling both by directly inhibiting JAKs and by targeting the receptor complex for proteasomal degradation 71 .”
• Innate immunity gone awry: linking microbial infections to chronic inflammation and cancer. (2006, background): “Inducible suppressors of cytokine signaling (SOCS), which function as ubiquitin ligases, are responsible for the negative feedback control of JAK-STAT signaling (Alexander and Hilton, 2004).”
• The JAK-STAT Signaling Pathway: Input and Output Integration1 (2007, neutral): “Mice lacking SOCS1 die rapidly from excessive IFN- signaling: a phenotype that can be rescued in multiple ways that reduce the amounts of IFN- or IFN- signaling (47).”
• A function for interleukin 2 in Foxp3-expressing regulatory T cells (2005, background): “The decrease in Socs2 is also not likely to affect T reg cell function, because the only documented in vivo function for the protein encoded by Socs2 has been the regulation of growth hormone and potentially insulin-like growth factor I signaling, and no defect in lymphocyte development or fu”
• Interleukin 27 negatively regulates the development of interleukin 17–producing T helper cells during chronic inflammation of the central nervous system (2006, background): “One of the direct consequences of signaling by many type I cytokines is the 'downstream' activation of SOCS proteins, which leads to the suppression of T cell responses through a negative regulatory feedback loo”
• Seeded Bayesian Networks: Constructing genetic networks from microarray data (2008, background): “The up-regulation of SOCS3 represents a classical negative feedback loop required to regulate the magnitude and duration of signalling downstream of the IFNG receptor signalling, in addition to limiting the response to any subsequent cytokine stimulus [29,30].”