Cytokine signaling modules in inflammatory responses.
By J. O’Shea, P. Murray. Immunity, 2008
832 citations recorded by the source corpus.
Subfields: Cancer Research, Immunology, Oncology
View Paper: https://www.semanticscholar.org/paper/9ee605f3c1929f917a78f50dda74682f0ec84c4a
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In Cancer Research
In Immunology
In Oncology
- M. Karin
- S. Grivennikov
- R. Flavell
- D. Mosser
- K. Garcia
- P. Murray
- Christopher A. Hunter
- Charles G. Drake
Citations in the corpus
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- The composition and signaling of the IL-35 receptor are unconventional (2012, background): “Two well-known activators of STAT1 and STAT4 are IFN-γ and IL-12, respectivel”
- The role of JAK-STAT signaling pathway and its regulators in the fate of T helper cells (2017, background): “If phosphorylation of STATs (On) and STAT dimerization occur upon activation of JAKs [9], phosphorylated STATs abandon docking sites on the receptors.”
- Interleukin-10: new perspectives on an old cytokine (2008, background): “3 (SOCS3), which controls the quality and quantity of STAT activation (20, 21).”
- Anti- and Pro-inflammatory Roles of TGF-β, IL-10, and IL-22 In Immunity and Autoimmunity (2009, background): “Ligation of IL-10 activates Jak1 and Tyk2 followed by Stat3 phosphorylation [29].”
- Dangerous liaisons: STAT3 and NF-κB collaboration and crosstalk in cancer (2009, background): “a broad impact on cytokine production, including other activators of NF-kB and STAT3, such as IL-6 and TNF-a [109] (Fig.”
- Macrophages, Foreign Body Giant Cells and Their Response to Implantable Biomaterials (2015, background): “The presence of interferon-γ (INFγ) and tumor necrosis factor (TNF), or lipopolysaccharide (LPS) creates a macrophage population that secretes pro-inflammatory cytokines [32,33].”