Absence of autophagy results in reactive oxygen species-dependent amplification of RLR signaling

By M. C. Tal, Miwa Sasai, H. Lee, Brian Yordy, G. Shadel, A. Iwasaki. Proceedings of the National Academy of Sciences of the United States of America, 2009

596 citations recorded by the source corpus.

Subfields: Cancer Research, Immunology

View Paper: https://www.semanticscholar.org/paper/eb02796899bee6175d028f0d8a66fe0b4d553378

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. D. Tang
3. Beth Levine
4. R. Kang
5. O. Takeuchi
6. Michael Schieber
7. Navdeep S. Chandel
8. Taro Kawai

In Immunology

1. Shizuo Akira
2. O. Takeuchi
3. H. J. Zeh
4. V. Deretic
5. D. Tang
6. R. Kang
7. Beth Levine
8. Michael Lotze

Citations in the corpus

• Autophagy in inflammation, infection, and immunometabolism (2021, background): “Peroxisomes are also an alternative location for MAVS (in a continuum with mitochondrial location of MAVS) specializing in rapid anti-viral innate Immunity.”
• Autophagy, Immunity, and Microbial Adaptations (2009, background): “…immunity functions identified to date encompass both effector outputs (Delgado et al., 2008; Sanjuan et al., 2007; Shelly et al., 2009; Xu et al., 2007) and regulatory roles, some of which are in conjunction with PRRs (Jounai et al., 2007; Lee et al., 2007; Saitoh et al., 2008; Tal et al., 2009).”
• Mitochondria in the regulation of innate and adaptive immunity (2015, unknown): “…importance of fatty-acid oxidation for Tm cells is bolstered by the observations that diminishing or enhancing AMPK, a positive regulator of fatty-acid oxidation, decreases or increases formation of memory T cells (MacIver et al., 2011; Pearce et al., 2009; Rolf et al., 2013; Tamás et al., 2010).”
• Pattern recognition receptors and inflammation. (2010, background): “In contrast to pDCs, autophagy negatively regulates IFN responses in fibroblasts and cDCs by suppressing RLR signaling (Jounai et al., 2007; Tal et al., 2009).”
• Virus-Plus-Susceptibility Gene Interaction Determines Crohn’s Disease Gene Atg16L1 Phenotypes in Intestine (2010, background): “Since Atg16L1 and its binding partner Atg5 can limit cytokine production (Saitoh et al., 2008; Jounai et al., 2007; Tal et al., 2009), viral infection may trigger an altered cytokine response in Atg16L1 mutant mice.”
• ROS Function in Redox Signaling and Oxidative Stress (2014, background): “RLRs also signal through mitochondrial ROS [83], which might not be surprising since the outer mitochondrial membrane serves as a platform for formation of the RLR signaling complex [84].”
• Autophagy is required to maintain muscle mass. (2009, unknown): “It is unclear whether our data of oxidative stress in Atg7 / muscle is mainly caused by accumulation of dysfunctional mitochondria due to a defect in mitophagy, as recently described in autophagy-deficient cells (Tal et al., 2009), or whether it is secondary to p62 aggregates (Mathew et al., 2009).”
• Mitochondria are required for antigen-specific T cell activation through reactive oxygen species signaling (2013, unknown): “Other studies have identified a critical role for mROS in RIG-1-like receptor signaling (Tal et al., 2009) and NLRP3 inflammasome activation (Zhou et al.”
• PAMPs and DAMPs: Signal 0s that Spur Autophagy and Immunity (2012, background): “Further analysis reveals that ROS play a key role in autophagy-mediated RLR signaling (44).”