Loss of the autophagy protein Atg16L1 enhances endotoxin-induced IL-1β production

By T. Saitoh, Naonobu Fujita, M. Jang, Satoshi Uematsu, Bo-Gie Yang, T. Satoh, Hiroko Omori, Takeshi Noda, N. Yamamoto, M. Komatsu and 6 more. Nature, 2008

1,740 citations recorded by the source corpus.

Subfields: Epidemiology, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/2f7f4a3e7d4926fc845b464a165619e100590a66

How researchers see this paper

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

In Epidemiology

1. N. Mizushima
2. Beth Levine
3. V. Deretic
4. I. Slaninová
5. D. Klionsky
6. M. Komatsu
7. D. Tang
8. R. Kang

In Molecular Biology

1. N. Mizushima
2. Shizuo Akira
3. T. Kanneganti
4. M. Lamkanfi
5. V. Dixit
6. V. Deretic
7. D. Tang
8. J. Tschopp

In Physiology

1. N. Mizushima
2. V. Deretic
3. T. Yoshimori
4. M. Komatsu
5. C. Kishi
6. Sang Hun Lee
7. C. Yun
8. Herbert W. Virgin

Citations in the corpus

• Autophagy in inflammation, infection, and immunometabolism (2021, background): “In murine in vivo and ex vivo models, Atg16L1 regulates inflammasome activation (Saitoh et al., 2008) and prevents necroptosis and loss of Paneth cells (Matsuzawa-Ishimoto et al.”
• The role of pattern-recognition receptors in innate immunity: update on Toll-like receptors (2010, background): “Atg16L1-deficient mice are highly susceptible to dextran sulfate sodium–induced acute colitis, which is blocked by treatment with antibodies to IL-1β and IL-18 (ref”
• Unified Polymerization Mechanism for the Assembly of ASC-dependent Inflammasomes (2014, background): “Once formed, inflammasomesmay require active processes such as autophagy for their degradation (Saitoh et al., 2008).”
• Autophagy: Renovation of Cells and Tissues (2011, background): “Although complete systemic deletion of Atg16L1 causes neonatal lethality (Saitoh et al., 2008), Atg16L1 hypomorphic mice, which express a very low level of Atg16L1, are viable and grossly normal.”
• Reactive Oxygen Species in Inflammation and Tissue Injury (2014, positive): “In addition to direct activation by ROS, the activity of NLRP3 inflammasome is negatively regulated by autophagy/ mitophagy (310, 367).”
• The Roles of Autophagy in Cancer (2018, background): “Additionally, autophagy suppresses inflammation by inhibiting NLRP3 formation and autophagy-related protein, and ATG16L was found to modulate intestinal homeostasis and inflammation [65].”
• Colitis induced in mice with dextran sulfate sodium (DSS) is mediated by the NLRP3 inflammasome (2010, background): “Notably, Atg16L1 deficiency causes Toll/IL-1 receptor domain-containing adaptor inducing interferon β (TRIF)-dependent activation of caspase-1, and mice lacking Atg16L1 in haematopoietic cells are highly susceptible to DSS-induced acute colitis.”