The Atg5–Atg12 conjugate associates with innate antiviral immune responses
By N. Jounai, F. Takeshita, K. Kobiyama, A. Sawano, A. Miyawaki, K. Xin, K. Ishii, Taro Kawai, Shizuo Akira, Koichi Suzuki and 1 more. Proceedings of the National Academy of Sciences of the United States of America, 2007
599 citations recorded by the source corpus.
Subfields: Epidemiology, Immunology, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/a75101c5ba61f649ec9ae2f019397468149629f6
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Citations in the corpus
- MDA5/RIG-I and virus recognition. (2008, background): “Recently, IPS-1 and RIG-I were found to associate with Atg5–Atg12 conjugates, which are essential components for autophagy [27].”
- RNA recognition and signal transduction by RIG‐I‐like receptors (2009, background): “Atg5–Atg12 conjugate, an essential regulator of autophagic machinery, directly associates with the CARD of RIG-I and IPS-1 and inhibits the interaction between them (101).”
- Autophagy during viral infection — a double-edged sword (2018, background): “The ATG5-ATG12 complex and its binding protein (elongation factor Tu, mitochondrial (TUFM)) suppress dsRNA-induced production of IFN by disrupting RIG-I signalling 22 (FIg.”
- Immune signaling by RIG-I-like receptors (2011, background): “Moreover, the Atg5-Atg12 conjugate previously implicated in the induction of autophagic responses directly associates with RIG-I and IPS-1 CARDs to suppress virus-induced signaling (Jounai et al., 2007; Takeshita et al., 2008).”
- 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.”
- Nod1 and Nod2 direct autophagy by recruiting ATG16L1 to the plasma membrane at the site of bacterial entry (2010, methodology): “After treatment and/or infection, cells were lysed and extracts were separated by 10% (wt/vol) SDS-PAGE, transferred to nitrocellulose membranes and subjected to immunodetection by standard procedure”
- TBK-1 promotes autophagy-mediated antimicrobial defense by controlling autophagosome maturation (2012, unknown): “Specific autophagic factors, such as Atg5-Atg12, have been shown to inhibit RIG-I receptor signaling (Jounai et al., 2007), whereas Atg9 has been reported to regulate negatively trafficking, assembly, and activation of TBK-1 (TANK-binding kinase 1), which, among its key functions, controls type I…”
- Mitochondria in innate immune responses (2011, background): “demonstrated that Atg5 −/− cells accumulate dysfunctional mitochondria and exhibit increased mROS levels and increased type I IFN production in response to polyI:C stimulatio”
- Autophagy in malignant transformation and cancer progression (2015, unknown): “…(2) they are linked to the inhibition of pro-inflammatory signals delivered by some pattern recognition receptors, such as RIG-I-like receptors (Jounai et al , 2007); (3) they limit the abundance of B-cell CLL/ lymphoma 10 (BCL10), a protein involved in pro-inflammatory NF-j B signaling (Paul…”
- 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).”
- Absence of autophagy results in reactive oxygen species-dependent amplification of RLR signaling (2009, background): “The authors further demonstrated that the Atg5-Atg12 conjugate directly associates with RIG-I, MDA-5 and the adaptor protein IFN- promoter stimulator 1 (IPS-1) (17–20)—also known as mitochondrial antiviral signaling (19), Cardif (21), or virusinduced signaling adaptor (20)—through the caspase recrui”