SOCS1/JAB is a negative regulator of LPS-induced macrophage activation.

By I. Kinjyo, Toshikatsu Hanada, K. Inagaki-Ohara, H. Mori, Daisuke Aki, M. Ohishi, H. Yoshida, Masato Kubo, A. Yoshimura. Immunity, 2002

627 citations recorded by the source corpus.

Subfields: Immunology, Oncology

View Paper: https://www.semanticscholar.org/paper/1b63f6c8e6e2238a09368f01a870d362d5196bb0

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. Shizuo Akira
2. S. Ghosh
3. M. Hayden
4. Luke A. O'Neill
5. K. Takeda
6. T. Hirano
7. A. Bowie
8. P. Murray

In Oncology

1. Shizuo Akira
2. K. Takeda
3. T. Hirano
4. A. Yoshimura
5. S. Ghosh
6. M. Hayden
7. Luke A. O'Neill
8. J. O’Shea

Citations in the corpus

• The family of five: TIR-domain-containing adaptors in Toll-like receptor signalling (2007, background): “These data provide an explanation for why SOCS1-deficient cells are hyper-responsive to LP”
• IL-6 induces an anti-inflammatory response in the absence of SOCS3 in macrophages (2003, methodology): “We determined the concentrations of TNF and IL-12 in the culture supernatant”
• New regulators of NF-κB in inflammation (2008, background): “Suppressor of cytokine signalling-1 ( SOCS1 ) participates in the formation of the ECS ubiquitin ligase complex and thereby decreases NF-κB transcriptional activit”
• Toll-like receptors in innate immunity. (2004, positive): “SOCS1-deficient mice were hyper-sensitive to LPS-induced endotoxin shock and showed defective induction of LPS tolerance (114,115).”
• Regulation of NF-κB by TNF Family Cytokines (2014, background): “Suppressor of cytokine signalling-1 (SOCS1) recruits protein substrates to ubiquitin ligase elongin-B–elongin-C– cullin-2–SOCS1 protein (ECS) complex [144] and decreases p65 stability [145, 146] and transcriptional activity when overexpressed [147, 148].”
• NF-κB and the immune response (2006, neutral): “Finally, suppressor of cytokine signaling-1 (SOCS-1) has been reported to negatively regulate LPS signaling to NF-kB and socs1 / mice exhibit an inflammatory phenotype that is consistent with this prediction (Kinjyo et al., 2002; Nakagawa et al., 2002).”
• Toll-like receptor signalling (2004, background): “, and SOCS1-deficient mice have been shown to be hypersensitive to LPS-induced endotoxic shock (that is, to show increased production of inflammatory cytokines”
• Cytokine signaling modules in inflammatory responses. (2008, background): “However, enforced expression of Socs1 has no effect on LTA signaling via TLR2 and LPS signaling via TLR4, and as noted above, loss of Socs1 has no obvious effects on LPS signaling (Baetz et al., 2004; Gingras et al., 2004).”