Genotoxic stress and viral infection induce transient expression of APOBEC3A and pro-inflammatory genes through two distinct pathways

The cytidine deaminase APOBEC3A is a main source of mutagenesis in many types of cancer. Here the authors reveal that transient up-regulation of APOBEC3A and other pro-inflammatory genes can occur due to viral infection and genotoxic stress via multiple pathways.

Bibliographic Details
Main Authors: Sunwoo Oh, Elodie Bournique, Danae Bowen, Pégah Jalili, Ambrocio Sanchez, Ian Ward, Alexandra Dananberg, Lavanya Manjunath, Genevieve P. Tran, Bert L. Semler, John Maciejowski, Marcus Seldin, Rémi Buisson
Format: Article
Language:English
Published: Nature Portfolio 2021-08-01
Series:Nature Communications
Online Access:https://doi.org/10.1038/s41467-021-25203-4
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author Sunwoo Oh
Elodie Bournique
Danae Bowen
Pégah Jalili
Ambrocio Sanchez
Ian Ward
Alexandra Dananberg
Lavanya Manjunath
Genevieve P. Tran
Bert L. Semler
John Maciejowski
Marcus Seldin
Rémi Buisson
author_facet Sunwoo Oh
Elodie Bournique
Danae Bowen
Pégah Jalili
Ambrocio Sanchez
Ian Ward
Alexandra Dananberg
Lavanya Manjunath
Genevieve P. Tran
Bert L. Semler
John Maciejowski
Marcus Seldin
Rémi Buisson
author_sort Sunwoo Oh
collection DOAJ
description The cytidine deaminase APOBEC3A is a main source of mutagenesis in many types of cancer. Here the authors reveal that transient up-regulation of APOBEC3A and other pro-inflammatory genes can occur due to viral infection and genotoxic stress via multiple pathways.
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spelling doaj.art-f03f488fd0c5499ab43ab73627e763952022-12-21T19:25:24ZengNature PortfolioNature Communications2041-17232021-08-0112111710.1038/s41467-021-25203-4Genotoxic stress and viral infection induce transient expression of APOBEC3A and pro-inflammatory genes through two distinct pathwaysSunwoo Oh0Elodie Bournique1Danae Bowen2Pégah Jalili3Ambrocio Sanchez4Ian Ward5Alexandra Dananberg6Lavanya Manjunath7Genevieve P. Tran8Bert L. Semler9John Maciejowski10Marcus Seldin11Rémi Buisson12Department of Biological Chemistry, School of Medicine, University of California IrvineDepartment of Biological Chemistry, School of Medicine, University of California IrvineDepartment of Biological Chemistry, School of Medicine, University of California IrvineDepartment of Biological Chemistry, School of Medicine, University of California IrvineDepartment of Biological Chemistry, School of Medicine, University of California IrvineDepartment of Biological Chemistry, School of Medicine, University of California IrvineMolecular Biology Program, Sloan Kettering Institute, Memorial Sloan Kettering Cancer CenterDepartment of Biological Chemistry, School of Medicine, University of California IrvineDepartment of Microbiology and Molecular Genetics, UCI Center for Virus Research, School of Medicine, University of California IrvineDepartment of Microbiology and Molecular Genetics, UCI Center for Virus Research, School of Medicine, University of California IrvineMolecular Biology Program, Sloan Kettering Institute, Memorial Sloan Kettering Cancer CenterDepartment of Biological Chemistry, School of Medicine, University of California IrvineDepartment of Biological Chemistry, School of Medicine, University of California IrvineThe cytidine deaminase APOBEC3A is a main source of mutagenesis in many types of cancer. Here the authors reveal that transient up-regulation of APOBEC3A and other pro-inflammatory genes can occur due to viral infection and genotoxic stress via multiple pathways.https://doi.org/10.1038/s41467-021-25203-4
spellingShingle Sunwoo Oh
Elodie Bournique
Danae Bowen
Pégah Jalili
Ambrocio Sanchez
Ian Ward
Alexandra Dananberg
Lavanya Manjunath
Genevieve P. Tran
Bert L. Semler
John Maciejowski
Marcus Seldin
Rémi Buisson
Genotoxic stress and viral infection induce transient expression of APOBEC3A and pro-inflammatory genes through two distinct pathways
Nature Communications
title Genotoxic stress and viral infection induce transient expression of APOBEC3A and pro-inflammatory genes through two distinct pathways
title_full Genotoxic stress and viral infection induce transient expression of APOBEC3A and pro-inflammatory genes through two distinct pathways
title_fullStr Genotoxic stress and viral infection induce transient expression of APOBEC3A and pro-inflammatory genes through two distinct pathways
title_full_unstemmed Genotoxic stress and viral infection induce transient expression of APOBEC3A and pro-inflammatory genes through two distinct pathways
title_short Genotoxic stress and viral infection induce transient expression of APOBEC3A and pro-inflammatory genes through two distinct pathways
title_sort genotoxic stress and viral infection induce transient expression of apobec3a and pro inflammatory genes through two distinct pathways
url https://doi.org/10.1038/s41467-021-25203-4
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