The cGAS–cGAMP–STING pathway connects DNA damage to inflammation, senescence, and cancer

Detection of microbial DNA is an evolutionarily conserved mechanism that alerts the host immune system to mount a defense response to microbial infections. However, this detection mechanism also poses a challenge to the host as to how to distinguish foreign DNA from abundant self-DNA. Cyclic guanosi...

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Published in	The Journal of experimental medicine Vol. 215; no. 5; pp. 1287 - 1299
Main Authors	Li, Tuo, Chen, Zhijian J.
Format	Journal Article
Language	English
Published	United States Rockefeller University Press 07.05.2018
Subjects	Activation Adenosine monophosphate AMP Cancer Cyclic GMP Damage detection Deoxyribonucleic acid DNA DNA damage Genomic instability Guanosine Immune response Immune system Inflammation Innate immunity Microorganisms Nucleotide sequence Reviews Senescence Stability
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Abstract	Detection of microbial DNA is an evolutionarily conserved mechanism that alerts the host immune system to mount a defense response to microbial infections. However, this detection mechanism also poses a challenge to the host as to how to distinguish foreign DNA from abundant self-DNA. Cyclic guanosine monophosphate (GMP)–adenosine monophosphate (AMP) synthase (cGAS) is a DNA sensor that triggers innate immune responses through production of the second messenger cyclic GMP-AMP (cGAMP), which binds and activates the adaptor protein STING. However, cGAS can be activated by double-stranded DNA irrespective of the sequence, including self-DNA. Although how cGAS is normally kept inactive in cells is still not well understood, recent research has provided strong evidence that genomic DNA damage leads to cGAS activation to stimulate inflammatory responses. This review summarizes recent findings on how genomic instability and DNA damage trigger cGAS activation and how cGAS serves as a link from DNA damage to inflammation, cellular senescence, and cancer.
AbstractList	Detection of microbial DNA is an evolutionarily conserved mechanism that alerts the host immune system to mount a defense response to microbial infections. However, this detection mechanism also poses a challenge to the host as to how to distinguish foreign DNA from abundant self-DNA. Cyclic guanosine monophosphate (GMP)-adenosine monophosphate (AMP) synthase (cGAS) is a DNA sensor that triggers innate immune responses through production of the second messenger cyclic GMP-AMP (cGAMP), which binds and activates the adaptor protein STING. However, cGAS can be activated by double-stranded DNA irrespective of the sequence, including self-DNA. Although how cGAS is normally kept inactive in cells is still not well understood, recent research has provided strong evidence that genomic DNA damage leads to cGAS activation to stimulate inflammatory responses. This review summarizes recent findings on how genomic instability and DNA damage trigger cGAS activation and how cGAS serves as a link from DNA damage to inflammation, cellular senescence, and cancer.Detection of microbial DNA is an evolutionarily conserved mechanism that alerts the host immune system to mount a defense response to microbial infections. However, this detection mechanism also poses a challenge to the host as to how to distinguish foreign DNA from abundant self-DNA. Cyclic guanosine monophosphate (GMP)-adenosine monophosphate (AMP) synthase (cGAS) is a DNA sensor that triggers innate immune responses through production of the second messenger cyclic GMP-AMP (cGAMP), which binds and activates the adaptor protein STING. However, cGAS can be activated by double-stranded DNA irrespective of the sequence, including self-DNA. Although how cGAS is normally kept inactive in cells is still not well understood, recent research has provided strong evidence that genomic DNA damage leads to cGAS activation to stimulate inflammatory responses. This review summarizes recent findings on how genomic instability and DNA damage trigger cGAS activation and how cGAS serves as a link from DNA damage to inflammation, cellular senescence, and cancer. Detection of microbial DNA is an evolutionarily conserved mechanism that alerts the host immune system to mount a defense response to microbial infections. However, this detection mechanism also poses a challenge to the host as to how to distinguish foreign DNA from abundant self-DNA. Cyclic guanosine monophosphate (GMP)-adenosine monophosphate (AMP) synthase (cGAS) is a DNA sensor that triggers innate immune responses through production of the second messenger cyclic GMP-AMP (cGAMP), which binds and activates the adaptor protein STING. However, cGAS can be activated by double-stranded DNA irrespective of the sequence, including self-DNA. Although how cGAS is normally kept inactive in cells is still not well understood, recent research has provided strong evidence that genomic DNA damage leads to cGAS activation to stimulate inflammatory responses. This review summarizes recent findings on how genomic instability and DNA damage trigger cGAS activation and how cGAS serves as a link from DNA damage to inflammation, cellular senescence, and cancer. The cGAS–cGAMP–STING pathway mediates immune and inflammatory responses to cytosolic DNA. This review summarizes recent findings on how genomic instability leads to cGAS activation and how this pathway critically connects DNA damage to autoinflammatory diseases, cellular senescence, and cancer. Detection of microbial DNA is an evolutionarily conserved mechanism that alerts the host immune system to mount a defense response to microbial infections. However, this detection mechanism also poses a challenge to the host as to how to distinguish foreign DNA from abundant self-DNA. Cyclic guanosine monophosphate (GMP)–adenosine monophosphate (AMP) synthase (cGAS) is a DNA sensor that triggers innate immune responses through production of the second messenger cyclic GMP-AMP (cGAMP), which binds and activates the adaptor protein STING. However, cGAS can be activated by double-stranded DNA irrespective of the sequence, including self-DNA. Although how cGAS is normally kept inactive in cells is still not well understood, recent research has provided strong evidence that genomic DNA damage leads to cGAS activation to stimulate inflammatory responses. This review summarizes recent findings on how genomic instability and DNA damage trigger cGAS activation and how cGAS serves as a link from DNA damage to inflammation, cellular senescence, and cancer. The cGAS–cGAMP–STING pathway mediates immune and inflammatory responses to cytosolic DNA. This review summarizes recent findings on how genomic instability leads to cGAS activation and how this pathway critically connects DNA damage to autoinflammatory diseases, cellular senescence, and cancer.Detection of microbial DNA is an evolutionarily conserved mechanism that alerts the host immune system to mount a defense response to microbial infections. However, this detection mechanism also poses a challenge to the host as to how to distinguish foreign DNA from abundant self-DNA. Cyclic guanosine monophosphate (GMP)–adenosine monophosphate (AMP) synthase (cGAS) is a DNA sensor that triggers innate immune responses through production of the second messenger cyclic GMP-AMP (cGAMP), which binds and activates the adaptor protein STING. However, cGAS can be activated by double-stranded DNA irrespective of the sequence, including self-DNA. Although how cGAS is normally kept inactive in cells is still not well understood, recent research has provided strong evidence that genomic DNA damage leads to cGAS activation to stimulate inflammatory responses. This review summarizes recent findings on how genomic instability and DNA damage trigger cGAS activation and how cGAS serves as a link from DNA damage to inflammation, cellular senescence, and cancer.
Author	Chen, Zhijian J. Li, Tuo
AuthorAffiliation	1 Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 2 Center for Inflammation Research, University of Texas Southwestern Medical Center, Dallas, TX 3 Howard Hughes Medical Institute, Chevy Chase, MD
AuthorAffiliation_xml	– name: 3 Howard Hughes Medical Institute, Chevy Chase, MD – name: 1 Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX – name: 2 Center for Inflammation Research, University of Texas Southwestern Medical Center, Dallas, TX
Author_xml	– sequence: 1 givenname: Tuo surname: Li fullname: Li, Tuo – sequence: 2 givenname: Zhijian J. orcidid: 0000-0002-8475-8251 surname: Chen fullname: Chen, Zhijian J.
BackLink	https://www.ncbi.nlm.nih.gov/pubmed/29622565$$D View this record in MEDLINE/PubMed
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Snippet	Detection of microbial DNA is an evolutionarily conserved mechanism that alerts the host immune system to mount a defense response to microbial infections.... The cGAS–cGAMP–STING pathway mediates immune and inflammatory responses to cytosolic DNA. This review summarizes recent findings on how genomic instability...
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SubjectTerms	Activation Adenosine monophosphate AMP Cancer Cyclic GMP Damage detection Deoxyribonucleic acid DNA DNA damage Genomic instability Guanosine Immune response Immune system Inflammation Innate immunity Microorganisms Nucleotide sequence Reviews Senescence Stability
Title	The cGAS–cGAMP–STING pathway connects DNA damage to inflammation, senescence, and cancer
URI	https://www.ncbi.nlm.nih.gov/pubmed/29622565 https://www.proquest.com/docview/2035235653 https://www.proquest.com/docview/2022996279 https://pubmed.ncbi.nlm.nih.gov/PMC5940270
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