Cutting Edge: NF-κB Activating Pattern Recognition and Cytokine Receptors License NLRP3 Inflammasome Activation by Regulating NLRP3 Expression1

By F. Bauernfeind, Gabor L Horvath, A. Stutz, E. Alnemri, K. MacDonald, D. Speert, T. Fernandes-Alnemri, Jianghong Wu, Brian G. Monks, Katherine A. Fitzgerald and 2 more. Journal of Immunology, 2009

2,851 citations recorded by the source corpus.

Subfields: Immunology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/69ef9ef82a8df81d3069427c10f4283f75e900f3

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. T. Kanneganti
2. M. Lamkanfi
3. J. Tschopp
4. Shizuo Akira
5. G. Núñez
6. V. Dixit
7. E. Latz
8. Katherine A. Fitzgerald

In Molecular Biology

1. T. Kanneganti
2. M. Lamkanfi
3. G. Núñez
4. J. Tschopp
5. V. Dixit
6. S. Man
7. E. Latz
8. Yuan He

Citations in the corpus

• NF-κB signaling in inflammation (2017, neutral): “57, 66 However, the role of NF-κ B signaling pathway in inflammasome regulation appears to be complex, since IKK β -deficient macrophages display hyper-activation of caspase 1 and enhanced secretion of IL-1 β upon LPS stimulation, and myeloid cell-conditional IKK β knockout mice are more sensitive…”
• NLRP3 inflammasome and its inhibitors: a review (2015, background): “…PAMPs or DAMPs are recognized by TLRs, leading to activation of nuclear factor kappa B (NF-κB)-mediated signaling, which in turn up-regulates transcription of inflammasome-related components, including inactive NLRP3, proIL-1β, and proIL18 (Bauernfeind et al., 2009; Franchi et al., 2012, 2014).”
• Dopamine controls systemic inflammation through inhibition of NLRP3 inflammasome. (2015, neutral): “NLRP3 protein expression levels have been shown to be a limiting step in inflammasome activation (Bauernfeind et al., 2009; Franchi et al., 2009).”
• Cytokines in Radiobiological Responses: A Review (2012, neutral): “Pro-inflammatory NF-jB driven synthesis of high levels of IL-1 in concert with an inflammasome secretory mechanism must send a strong ‘‘danger’’ signal to the body and could mediate many auto-inflammatory disease states (82).”
• Critical role for calcium mobilization in activation of the NLRP3 inflammasome (2012, background): “Although signal 1 is important for transcriptional up-regulation of the NLRP3 subunit and is typically provided by signaling through Toll-like receptors (9), three cellular processes have been suggested to provide signal 2 (2, 3, 10).”
• The NLRP3 Inflammasome: An Overview of Mechanisms of Activation and Regulation (2019, background): “For macrophages, the presence of NLRP3 activators alone is insufficient for inducing inflammasome activation and a priming signal (signal 1) is required for its activation [33].”
• The inflammasome: an integrated view (2011, background): “the threshold of inflammasome activation by upregulating NLRP3 (12, 15).”
• Non-transcriptional Priming and Deubiquitination Regulate NLRP3 Inflammasome Activation* (2012, background): “Rapid Non-transcriptional Priming of the NLRP3 Inflammasome—We previously reported that cell priming with multipleTLR ligands for 2 ormore hours induces up-regulation of NLRP3 expression through activation of NF- B, which we identified to be an important determinant forNLRP3 activation (6).”
• Initiation and perpetuation of NLRP3 inflammasome activation and assembly (2015, background): “Priming can be accomplished by activation of receptors that signal via MyD88 (myeloid differentiation factor 88)/TRIF (TIR-domain-containing adapter-inducing interferon-b) or other NFjB (nuclear factor-jB)-activating pathways, including Toll-like receptors (TLRs), IL-1R, tumor necrosis factor recept”