SOCS3 negatively regulates IL-6 signaling in vivo

By B. Croker, D. Krebs, Jian‐guo Zhang, Sam Wormald, T. Willson, E. Stanley, L. Robb, C. Greenhalgh, I. Förster, B. Clausen and 5 more. Nature Immunology, 2003

907 citations recorded by the source corpus.

Subfields: Immunology, Oncology, Pharmacology

View Paper: https://www.semanticscholar.org/paper/c516ca306ae035d173fc0d730dc65104581d3914

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Immunology

1. J. O’Shea
2. A. Laurence
3. P. Murray
4. Christopher A. Hunter
5. Rhiannon Morris
6. Bin Liu
7. J. Babon
8. N. Kershaw

In Oncology

1. J. O’Shea
2. A. Laurence
3. P. Murray
4. Christopher A. Hunter
5. Rhiannon Morris
6. Bin Liu
7. J. Babon
8. N. Kershaw

In Pharmacology

1. P. Murray
2. J. O’Shea

Citations in the corpus

• Cytokine signaling modules in inflammatory responses. (2008, background): “increases Stat3 signaling from gp130 and, surprisingly, also increases Stat1 signaling leading to an ectopic interferon response (Croker et al., 2003; Lang et al., 2003).”
• Characterization of phenotype markers and neuronotoxic potential of polarised primary microglia in vitro (2013, background): “These 3 factors are associated with a M2b-deactivating or immunomodulatory phenotype, as SOCS3 reduces aberrant IL-6 family member activation (Croker et al., 2003); SphK1 catalyses the formation of sphingolipids with potent cell survival and proliferative effects (Bryan et al.”
• The molecular details of cytokine signaling via the JAK/STAT pathway (2018, background): “Although induced by many cytokines,(170) and potent inhibitors of many cytokine signaling pathways when artificially overexpressed, knockout studies have shown that each SOCS protein is specific for only a subset of cytokines.(172,173) For example SOCS3 is induced by IL-2, IL-3, IL-4, IL-6, IL-7, IL”
• Adipocytokines: mediators linking adipose tissue, inflammation and immunity (2006, background): “Other factors involved in the regulation of insulin resistance are IL-6 and various suppressor of cytokine signalling (SOCS) protein”
• Should we stimulate or suppress immune responses in COVID-19? Cytokine and anti-cytokine interventions (2020, neutral): “T cell exhaustion, characterizing severe COVID-19, may stem from increased PD-1 or Tim-3 expression, from elevated levels of inhibitory IL-10 [60] or from increased IL-6-induced expression of SOCS3 [69] [70] [71] .”
• The STAT3 isoforms α and β have unique and specific functions (2004, background): “The suppressor of cytokine signaling 3 gene ( Socs3 ) is a good candidate for this, because it is involved in negative regulation of IL-6 signalin”
• Regulation of JAK–STAT signalling in the immune system (2003, background): “Conditional Socs3 gene-targeting studies have shown an important role for SOCS3 in the negative regulation of interleukin-6 (IL-6) signalling in macrophage”
• The JAK-STAT Signaling Pathway: Input and Output Integration1 (2007, neutral): “At the same time however, STAT1 phosphorylation is also induced, leading to a dominant IFN-like gene expression signature (35, 36).”