SOCS-1 participates in negative regulation of LPS responses.

By Reiko Nakagawa, T. Naka, H. Tsutsui, M. Fujimoto, A. Kimura, Tatsuo Abe, E. Seki, Shintaro Sato, O. Takeuchi, K. Takeda and 5 more. Immunity, 2002

708 citations recorded by the source corpus.

Subfields: Cancer Research, Immunology, Oncology

View Paper: https://www.semanticscholar.org/paper/f6feec86c012af87f2dc7e21995bcc2712db6e74

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In Cancer Research

1. Shizuo Akira
2. S. Ghosh
3. M. Hayden
4. K. Takeda
5. Luke A. O'Neill
6. A. West
7. Aly Karsan
8. S. Dauphinee

In Immunology

1. S. Ghosh
2. Shizuo Akira
3. M. Hayden
4. Luke A. O'Neill
5. K. Takeda
6. A. West
7. P. Murray
8. Aly Karsan

In Oncology

1. Shizuo Akira
2. K. Takeda
3. S. Ghosh
4. M. Hayden
5. J. O’Shea
6. D. Iliopoulos
7. Masato Kubo
8. A. Yoshimura

Citations in the corpus

• 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].”
• Cytokine signaling modules in inflammatory responses. (2008, background): “…majority of pro-inflammatory effects of excessive IFN-g signaling caused by loss of Socs1 can be rescued by removal of IFN-g or its signaling components (IFN-gR and Stat1), Socs1 / ; Ifng / mice remain extremely sensitive to systemic challenge with LPS (Kinjyo et al., 2002; Nakagawa et al., 2002).”
• Tolerogenic dendritic cells and the quest for transplant tolerance (2007, background): “Changes in the expression or function of the LPS receptor complex, alterations in TLR-driven signalling pathways or feedback inhibition, and/or primary effects on transcription, mRNA stability and translational efficiency have all been implicated in endotoxin toleranc”
• TAM receptor tyrosine kinases: biologic functions, signaling, and potential therapeutic targeting in human cancer. (2008, background): “E.1.b), including attenuation of proinflammatory cytokine production following exposure to LPS, a potential role for Axl SOCS‐1 signaling as SOCS‐1 is implicated in negative regulation of LPS‐induced signaling (Kinjyo et al., 2002; Nakagawa et al., 2002).”
• Akt1 controls macrophage response to LPS by regulating microRNAs (2009, background): “Mutations that interfere with these negative regulatory loops 220 Immunity 31, 220–231, August 21, 2009 ª2009 Elsevier Inc. promote hyperresponsiveness to LPS and inhibit the development of endotoxin tolerance (Kinjyo et al., 2002; Nakagawa et al., 2002; Kobayashi 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”
• SOCS proteins, cytokine signalling and immune regulation (2007, background): “SOCS1-deficient mice are hypersensitive to LPS, leading to an increase in tumour-necrosis factor ( TNF ) and IL-12 productio”
• Lipopolysaccharide signaling in endothelial cells (2006, background): “157 LPS-induced upregulation of the SOCS1 protein has been observed in a macrophage cell line and SOCS−s− mice are hyperresponsive to LPS, showing increased serum TNF α levels and increased lethality”
• NF-κB and the immune response (2006, background): “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).”
• 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”