Atg9a controls dsDNA-driven dynamic translocation of STING and the innate immune response

By T. Saitoh, Naonobu Fujita, Takafumi Hayashi, Keigo Takahara, T. Satoh, Hanna Lee, K. Matsunaga, S. Kageyama, Hiroko Omori, Takeshi Noda and 6 more. Proceedings of the National Academy of Sciences of the United States of America, 2009

815 citations recorded by the source corpus.

Subfields: Immunology, Infectious Diseases

View Paper: https://www.semanticscholar.org/paper/fbc6522c5404017c314739f53d67afa25e887074

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Citations in the corpus

Pattern recognition receptors and inflammation. (2010, background): “In response to transfection of dsDNA, STING translocates from the ER to the Golgi apparatus and subsequently to cytoplasmic punctate structures where it colocalizes with TBK1 (Ishikawa et al., 2009).”
The origin of the autophagosomal membrane (2010, background): “So far there is no known function for yeast or mAtg9, but mAtg9 knockout mice are unable to survive after birt”
Autophagy-deficient mice develop multiple liver tumors. (2011, background): “However, because systemic deletion of Atg3, Atg5, Atg7, Atg9, and Atg16L1 causes neonatal lethality (Kuma et al. 2004; Komatsu et al. 2005; Saitoh et al. 2008, 2009; Sou et al. 2008), the long-term effects of defects in autophagy have not been analyzed.”
The cGAS–cGAMP–STING pathway connects DNA damage to inflammation, senescence, and cancer (2018, background): “…second messengers c-di-GMP and c-di-AMP (Burdette et al., 2011; Wu et al., 2013). cGAMP binding induces a conformational change in STI NG (Gao et al., 2013b; Zhang et al., 2013), which subsequently translocates from the ER to the Golgi apparatus (Ishikawa and Barber, 2008; Saitoh et al., 2009).”
cGAS in action: Expanding roles in immunity and inflammation (2019, background): “After initiation of downstream signaling, STING is degraded in endolysosomes (21, 25).”
PAMPs and DAMPs: Signal 0s that Spur Autophagy and Immunity (2012, background): “However, Atg9a, but not Atg7, controls dsDNA-driven dynamic translocation of stimulator of IFN genes (STING) from the ER to the Golgi (142).”
STING Specifies IRF3 phosphorylation by TBK1 in the Cytosolic DNA Signaling Pathway (2012, background): “Furthermore, in response to stimulation with dsDNA, STING relocalizes from the ER to Golgi and assembles into punctate structures that contain the kinase TANK-binding kinase 1 (TBK1) (21, 22).”
Activation of STING requires palmitoylation at the Golgi (2016, neutral): “After DNA and/or CDN binding, STING translocates from the ER to perinuclear compartments that include the Golgi, endosomes and autophagy-related compartments 6,22 .”
Autophagy and the integrated stress response (2010, neutral): “The PRRs include families of TLRs that recognize PAMPS to activate proinflammatory cytokines and type I interferon production via NF-kB-, MAPK-, and interferon-regulatory pathways; NOD-like receptors (NLRs) that primarily activate signaling via NF-kBandMAPKand components of the inflammasome; RIG-I l”
Autophagy in malignant transformation and cancer progression (2015, neutral): “…pro-inflammatory NF-j B signaling (Paul et al , 2012); (4) they are connected to the inhibition of transmembrane protein 173 (TM173, best known as STING), a pattern recognition receptor involved in the delivery of pro-inflammatory cues in response to cytosolic nucleic acids (Saitoh et al , 2009).”
Molecular definitions of autophagy and related processes (2017, neutral): “…the macroautophagy machinery at the whole-body level (Qu et al , 2003; Yue et al , 2003; Kuma et al , 2004; Komatsu et al , 2005; Gan et al , 2006; Saitoh et al , 2008, 2009; Sou et al , 2008), which is likely to reflect the key role of macroautophagy in development and adult tissue homeostasis…”