Severe impairment of interleukin-1 and Toll-like receptor signalling in mice lacking IRAK-4

By N. Suzuki, Shinobu Suzuki, G. Duncan, D. Millar, T. Wada, C. Mirtsos, H. Takada, A. Wakeham, A. Itié, Shyun Li and 5 more. Nature, 2002

938 citations recorded by the source corpus.

Subfields: Cancer Research, Immunology

View Paper: https://www.semanticscholar.org/paper/89b7bdb23f944a8f19fedada73183b7180c70d3f

How researchers see this paper

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

In Cancer Research

1. Shizuo Akira
2. T. Mogensen
3. R. Medzhitov
4. Luke A. O'Neill
5. K. Takeda
6. M. Karin
7. B. Beutler
8. T. Lawrence

In Immunology

1. Shizuo Akira
2. R. Medzhitov
3. Taro Kawai
4. T. Mogensen
5. B. Beutler
6. Luke A. O'Neill
7. M. Karin
8. K. Takeda

Citations in the corpus

• Pathogen Recognition and Inflammatory Signaling in Innate Immune Defenses (2009, background): “sponse to IL-1 and various TLR ligands (348).”
• Identification of Lps2 as a key transducer of MyD88-independent TIR signalling (2003, background): “MyD88 signals by way of IRAK-4, a serine kinase required for the effective production of inflammatory cytokines induced by all of the TLR”
• Innate immunity gone awry: linking microbial infections to chronic inflammation and cancer. (2006, background): “Here, we outline this mechanistic framework and briefly review how alteration of innate immune response genes in murine models can provide insights into the potential microbial origins of diverse conditions including Crohn’s disease, psoriasis, atherosclerosis, diabetes, and liver cancer.”
• The Interleukin-1 Receptor/Toll-Like Receptor Superfamily: Signal Transduction During Inflammation and Host Defense (2000, background): “IRAK-4-knockout mice are completely resistant to LPS, CpG-DNA, peptidoglycan, and polyI:C, indicating that IRAK-4 plays an essential role in innate immunity (130).”
• TLR signaling pathways. (2004, background): “TIRAP/Mal knockout mice showed normal responses to the TLR3, TLR5, TLR7, and TLR9 ligands, but were defective in TLR2 ligand-induced inflammatory cytokine production.”
• Regulation and Function of IKK and IKK-Related Kinases (2006, background): “Nonetheless, MEKK3-deficient fibroblasts exhibit defects in IL-1 and TNFα-induced activation of IKK (and of JNK1 or JNK2), a phenotype similar to that of RIP1-deficient cells (71, 72, 83).”