Essential function for the kinase TAK1 in innate and adaptive immune responses

By Shintaro Sato, H. Sanjo, K. Takeda, J. Ninomiya-Tsuji, Masahiro Yamamoto, Taro Kawai, K. Matsumoto, O. Takeuchi, Shizuo Akira. Nature Immunology, 2005

1,010 citations recorded by the source corpus.

Subfields: Cancer Research, Immunology

View Paper: https://www.semanticscholar.org/paper/c0ee715525a83293ea3270a857b786b59019f169

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. S. Ghosh
2. M. Hayden
3. Shizuo Akira
4. M. Karin
5. T. Mogensen
6. A. West
7. O. Takeuchi
8. V. Dixit

In Immunology

1. Shizuo Akira
2. S. Ghosh
3. M. Hayden
4. T. Mogensen
5. M. Karin
6. O. Takeuchi
7. T. Kanneganti
8. A. West

Citations in the corpus

• Innate Immunity to Virus Infection (2009, background): “Deletion of TAK1 and UBC13 in mice revealed that these molecules play a critical role in TLR-mediated cytokine production, in addition to their role in embryonic development (70, 71).”
• A critical role of RICK/RIP2 polyubiquitination in Nod‐induced NF‐κB activation (2008, background): “Polyubiquitination of RICK is required for the recruitment of TAK1 Recent studies showed that a TAK1 complex containing TAK1, TAB1, TAB2 and/or TAB3 is a general mediator of NF-kB activation induced by various inflammatory stimuli (Ishitani et al, 2003; Sato et al, 2005; Shim et al, 2005).”
• Pathogen Recognition and Inflammatory Signaling in Innate Immune Defenses (2009, background): “The essential and nonredundant role played by TAK1 is strongly suggested by significantly reduced NF- B, JNK, and p38 responses to various TLR ligands in cells derived from mice deficient in this kinase (317, 332).”
• ZBP1 and TAK1: Master Regulators of NLRP3 Inflammasome/Pyroptosis, Apoptosis, and Necroptosis (PAN-optosis) (2019, background): “In support of this concept, genetic deletion of TAK1 in mice was shown to result in spontaneous cell death and embryonic lethality (Sato et al., 2005; Shim et al., 2005).”
• Regulation and Function of IKK and IKK-Related Kinases (2006, methodology): “(81, 82), and both TAK1- and MEKK3-deficient fibroblasts exhibit defective NF-κB activation in response to IL-1 (83, 85).”
• Regulation of NF-κB by TNF Family Cytokines (2014, background): “However, such a model does not account for the requirement for TAK1, for TNF induced IKK activation [72, 73].”