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mtDNA cGAS Sting

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https://www.readbyqxmd.com/read/27500737/the-mechanism-for-type-i-interferon-induction-by-mycobacterium-tuberculosis-is-bacterial-strain-dependent
#1
Kirsten E Wiens, Joel D Ernst
Type I interferons (including IFNαβ) are innate cytokines that may contribute to pathogenesis during Mycobacterium tuberculosis (Mtb) infection. To induce IFNβ, Mtb must gain access to the host cytosol and trigger stimulator of interferon genes (STING) signaling. A recently proposed model suggests that Mtb triggers STING signaling through bacterial DNA binding cyclic GMP-AMP synthase (cGAS) in the cytosol. The aim of this study was to test the generalizability of this model using phylogenetically distinct strains of the Mtb complex (MTBC)...
August 2016: PLoS Pathogens
https://www.readbyqxmd.com/read/26939583/mitochondrial-dna-sensing-by-sting-signaling-participates-in-inflammation-cancer-and-beyond
#2
REVIEW
Song Liu, Min Feng, Wenxian Guan
Recent studies have revealed the diverse pathophysiological functions of mitochondria beyond traditional energetic metabolism in cells. Mitochondria-released damage-associated molecular patterns, particularly mitochondrial deoxyribonucleic acid (mtDNA), play a central role in host immune defenses against foreign pathogens. Newly discovered cGAS-STING signaling is responsible for microbial DNA recognition, and potentially participates in mitochondrial DNA sensing. Inappropriate inflammatory signaling mediated by mtDNA is implicated in various human diseases, especially infectious/inflammatory disease and cancer...
August 15, 2016: International Journal of Cancer. Journal International du Cancer
https://www.readbyqxmd.com/read/26039443/innate-immune-recognition-of-mtdna-an-undercover-signal
#3
COMMENT
Thirumala-Devi Kanneganti, Mondira Kundu, Douglas R Green
In addition to their roles in cellular metabolism and apoptosis, mitochondria function as signaling platforms in the innate immune response. In Nature, West et al. (2015) demonstrate that mitochondrial stress triggers a type I interferon response and confers viral resistance via release of mtDNA and activation of the cGAS-STING pathway.
June 2, 2015: Cell Metabolism
https://www.readbyqxmd.com/read/25642965/mitochondrial-dna-stress-primes-the-antiviral-innate-immune-response
#4
A Phillip West, William Khoury-Hanold, Matthew Staron, Michal C Tal, Cristiana M Pineda, Sabine M Lang, Megan Bestwick, Brett A Duguay, Nuno Raimundo, Donna A MacDuff, Susan M Kaech, James R Smiley, Robert E Means, Akiko Iwasaki, Gerald S Shadel
Mitochondrial DNA (mtDNA) is normally present at thousands of copies per cell and is packaged into several hundred higher-order structures termed nucleoids. The abundant mtDNA-binding protein TFAM (transcription factor A, mitochondrial) regulates nucleoid architecture, abundance and segregation. Complete mtDNA depletion profoundly impairs oxidative phosphorylation, triggering calcium-dependent stress signalling and adaptive metabolic responses. However, the cellular responses to mtDNA instability, a physiologically relevant stress observed in many human diseases and ageing, remain poorly defined...
April 23, 2015: Nature
https://www.readbyqxmd.com/read/25525874/apoptotic-caspases-suppress-mtdna-induced-sting-mediated-type-i-ifn-production
#5
Michael J White, Kate McArthur, Donald Metcalf, Rachael M Lane, John C Cambier, Marco J Herold, Mark F van Delft, Sammy Bedoui, Guillaume Lessene, Matthew E Ritchie, David C S Huang, Benjamin T Kile
Activated caspases are a hallmark of apoptosis induced by the intrinsic pathway, but they are dispensable for cell death and the apoptotic clearance of cells in vivo. This has led to the suggestion that caspases are activated not just to kill but to prevent dying cells from triggering a host immune response. Here, we show that the caspase cascade suppresses type I interferon (IFN) production by cells undergoing Bak/Bax-mediated apoptosis. Bak and Bax trigger the release of mitochondrial DNA. This is recognized by the cGAS/STING-dependent DNA sensing pathway, which initiates IFN production...
December 18, 2014: Cell
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