Joel S Riley, Giovanni Quarato, Catherine Cloix, Jonathan Lopez, Jim O'Prey, Matthew Pearson, James Chapman, Hiromi Sesaki, Leo M Carlin, João F Passos, Ann P Wheeler, Andrew Oberst, Kevin M Ryan, Stephen Wg Tait. EMBO J 2018
Times Cited: 156
Times Cited: 156
Times Cited
Times Co-cited
Similarity
BAK/BAX macropores facilitate mitochondrial herniation and mtDNA efflux during apoptosis.
Kate McArthur, Lachlan W Whitehead, John M Heddleston, Lucy Li, Benjamin S Padman, Viola Oorschot, Niall D Geoghegan, Stephane Chappaz, Sophia Davidson, Hui San Chin,[...]. Science 2018
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Mitochondrial DNA stress primes the antiviral innate immune response.
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Apoptotic caspases suppress mtDNA-induced STING-mediated type I IFN production.
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Apoptotic caspases prevent the induction of type I interferons by mitochondrial DNA.
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VDAC oligomers form mitochondrial pores to release mtDNA fragments and promote lupus-like disease.
Jeonghan Kim, Rajeev Gupta, Luz P Blanco, Shutong Yang, Anna Shteinfer-Kuzmine, Kening Wang, Jun Zhu, Hee Eun Yoon, Xinghao Wang, Martijn Kerkhofs,[...]. Science 2019
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Autophagy proteins regulate innate immune responses by inhibiting the release of mitochondrial DNA mediated by the NALP3 inflammasome.
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Kiichi Nakahira, Jeffrey Adam Haspel, Vijay A K Rathinam, Seon-Jin Lee, Tamas Dolinay, Hilaire C Lam, Joshua A Englert, Marlene Rabinovitch, Manuela Cernadas, Hong Pyo Kim,[...]. Nat Immunol 2011
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Oxidized mitochondrial DNA activates the NLRP3 inflammasome during apoptosis.
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Mitochondrial DNA in innate immune responses and inflammatory pathology.
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Parkin and PINK1 mitigate STING-induced inflammation.
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New mitochondrial DNA synthesis enables NLRP3 inflammasome activation.
Zhenyu Zhong, Shuang Liang, Elsa Sanchez-Lopez, Feng He, Shabnam Shalapour, Xue-Jia Lin, Jerry Wong, Siyuan Ding, Ekihiro Seki, Bernd Schnabl,[...]. Nature 2018
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TDP-43 Triggers Mitochondrial DNA Release via mPTP to Activate cGAS/STING in ALS.
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A role for mitochondria in NLRP3 inflammasome activation.
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A non-death function of the mitochondrial apoptosis apparatus in immunity.
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Cyclic GMP-AMP synthase is a cytosolic DNA sensor that activates the type I interferon pathway.
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Circulating mitochondrial DAMPs cause inflammatory responses to injury.
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Limited mitochondrial permeabilization causes DNA damage and genomic instability in the absence of cell death.
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Mitochondrial DNA that escapes from autophagy causes inflammation and heart failure.
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Mitochondrial permeabilization engages NF-κB-dependent anti-tumour activity under caspase deficiency.
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Apoptotic Caspases Suppress Type I Interferon Production via the Cleavage of cGAS, MAVS, and IRF3.
Xiaohan Ning, Yutao Wang, Miao Jing, Mengyin Sha, Mengze Lv, Pengfei Gao, Rui Zhang, Xiaojun Huang, Ji-Ming Feng, Zhengfan Jiang. Mol Cell 2019
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Hepatocyte mitochondrial DNA drives nonalcoholic steatohepatitis by activation of TLR9.
Irma Garcia-Martinez, Nicola Santoro, Yonglin Chen, Rafaz Hoque, Xinshou Ouyang, Sonia Caprio, Mark J Shlomchik, Robert Lee Coffman, Albert Candia, Wajahat Zafar Mehal. J Clin Invest 2016
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Neutrophil extracellular traps enriched in oxidized mitochondrial DNA are interferogenic and contribute to lupus-like disease.
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Bax assembly into rings and arcs in apoptotic mitochondria is linked to membrane pores.
Raquel Salvador-Gallego, Markus Mund, Katia Cosentino, Jale Schneider, Joseph Unsay, Ulrich Schraermeyer, Johann Engelhardt, Jonas Ries, Ana J García-Sáez. EMBO J 2016
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cGAS surveillance of micronuclei links genome instability to innate immunity.
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Mitochondrial permeability transition triggers the release of mtDNA fragments.
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Dengue virus NS2B protein targets cGAS for degradation and prevents mitochondrial DNA sensing during infection.
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Mitochondrial double-stranded RNA triggers antiviral signalling in humans.
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cGAS produces a 2'-5'-linked cyclic dinucleotide second messenger that activates STING.
Andrea Ablasser, Marion Goldeck, Taner Cavlar, Tobias Deimling, Gregor Witte, Ingo Röhl, Karl-Peter Hopfner, Janos Ludwig, Veit Hornung. Nature 2013
Andrea Ablasser, Marion Goldeck, Taner Cavlar, Tobias Deimling, Gregor Witte, Ingo Röhl, Karl-Peter Hopfner, Janos Ludwig, Veit Hornung. Nature 2013
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Regulation and function of the cGAS-STING pathway of cytosolic DNA sensing.
Qi Chen, Lijun Sun, Zhijian J Chen. Nat Immunol 2016
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cGAS in action: Expanding roles in immunity and inflammation.
Andrea Ablasser, Zhijian J Chen. Science 2019
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Regulation of apoptosis in health and disease: the balancing act of BCL-2 family proteins.
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Mitotic progression following DNA damage enables pattern recognition within micronuclei.
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Circulating Cell-Free mtDNA Contributes to AIM2 Inflammasome-Mediated Chronic Inflammation in Patients with Type 2 Diabetes.
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Oxidized mitochondrial nucleoids released by neutrophils drive type I interferon production in human lupus.
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Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018.
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STING is an endoplasmic reticulum adaptor that facilitates innate immune signalling.
Hiroki Ishikawa, Glen N Barber. Nature 2008
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Mitochondria as multifaceted regulators of cell death.
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Structural basis of STING binding with and phosphorylation by TBK1.
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Nuclear cGAS suppresses DNA repair and promotes tumorigenesis.
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The ubiquitin kinase PINK1 recruits autophagy receptors to induce mitophagy.
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Bcl-x(L) retrotranslocates Bax from the mitochondria into the cytosol.
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Bax crystal structures reveal how BH3 domains activate Bax and nucleate its oligomerization to induce apoptosis.
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Interleukin-1β Induces mtDNA Release to Activate Innate Immune Signaling via cGAS-STING.
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Cyclic [G(2',5')pA(3',5')p] is the metazoan second messenger produced by DNA-activated cyclic GMP-AMP synthase.
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Pan-viral specificity of IFN-induced genes reveals new roles for cGAS in innate immunity.
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Targeting STING with covalent small-molecule inhibitors.
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Cyclic GMP-AMP is an endogenous second messenger in innate immune signaling by cytosolic DNA.
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DAMP-sensing receptors in sterile inflammation and inflammatory diseases.
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Co-cited is the co-citation frequency, indicating how many articles cite the article together with the query article. Similarity is the co-citation as percentage of the times cited of the query article or the article in the search results, whichever is the lowest. These numbers are calculated for the last 100 citations when articles are cited more than 100 times.