cGAS suppresses genomic instability as a decelerator of replication forks-Reference-Cited by-同舟云学术

cGAS suppresses genomic instability as a decelerator of replication forks

Published:2020-10-16 Issue:42 Volume:6 Page:
ISSN:2375-2548
Container-title:Science Advances
language:en
Short-container-title:Sci. Adv.

Author:

Chen Hao¹²^ORCID,Chen Hao³^ORCID,Zhang Jiamin¹^ORCID,Wang Yumin¹²^ORCID,Simoneau Antoine¹⁴^ORCID,Yang Hui⁵⁶^ORCID,Levine Arthur S.³^ORCID,Zou Lee¹⁴^ORCID,Chen Zhijian⁵⁶^ORCID,Lan Li¹²^ORCID

Affiliation:

1. Massachusetts General Hospital Cancer Center, Harvard Medical School, Boston, MA 02129, USA.

2. Department of Radiation Oncology, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02115, USA.

3. UPMC Hillman Cancer Center, 5117 Centre Avenue, Pittsburgh, PA 15213, USA.

4. Department of Pathology, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02115, USA.

5. Department of Molecular Biology, Center for Inflammation Research, University of Texas Southwestern Medical Center, Dallas, TX 75390-9148, USA.

6. Howard Hughes Medical Institute, University of Texas Southwestern Medical Center, Dallas, TX 75390-9148, USA.

Abstract

cGAS controls replication dynamics and suppresses replication-associated DNA damage.

Funder

National Institutes of Health

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

Reference27 articles.

1. The DNA-damage response in human biology and disease

2. Cyclic GMP-AMP Synthase Is a Cytosolic DNA Sensor That Activates the Type I Interferon Pathway

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

4. cGAS is essential for the antitumor effect of immune checkpoint blockade

5. cGAS-STING Activation in the Tumor Microenvironment and Its Role in Cancer Immunity

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