ArticleNucleic acids research2011
The FANC pathway is activated by adenovirus infection and promotes viral replication-dependent recombination.
Article in Nucleic acids research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 16 citations in OpenAlex.
- TRIM21 induces selective autophagy of viruses and bacteria.Molecular cell · 2026Article
- Human cytomegalovirus regulates host DNA repair machinery for viral genome integrity.Nucleic acids research · 2026Article
- ARGLU1 is a negative regulator of the adenoviral replicative cycle.Journal of virology · 2025Article
- Review
- Human Papillomavirus and the DNA Damage Response: Exploiting Host Repair Pathways for Viral Replication.Viruses · 2017Review
- Article
- Transcriptional modules related to hepatocellular carcinoma survival: coexpression network analysis.Frontiers of medicine · 2016Article
- Co-opting the Fanconi anemia genomic stability pathway enables herpesvirus DNA synthesis and productive growth.Molecular cell · 2014Article
- E1B and E4 oncoproteins of adenovirus antagonize the effect of apoptosis inducing factor.Virology · 2014Article
- Sugar and chromosome stability: clastogenic effects of sugars in vitamin B6-deficient cells.PLoS genetics · 2014Article
- Replication-uncoupled histone deposition during adenovirus DNA replication.Journal of virology · 2012Article
- Changing the ubiquitin landscape during viral manipulation of the DNA damage response.FEBS letters · 2011Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Deciphering the crosstalk between a host cell and a virus during infection is important not only to better define viral biology but also to improve our understanding of cellular processes. We identified the FANC pathway as a helper of viral replication and recombination by searching for cellular targets that are modified by adenovirus (Ad) infection and are involved in its outcome. This pathway, which is involved in the DNA damage response and checkpoint control, is altered in Fanconi anaemia, a rare cancer predisposition syndrome. We show here that Ad5 infection activates the FANC pathway independent of the classical DNA damage response. Infection with a non-replicating Ad shows that the presence of viral DNA is not sufficient to induce the monoubiquitination of FANCD2 but still activates the DNA damage response coordinated by phospho-NBS1 and phospho-CHK1. E1A expression alone fails to induce FANCD2 monoubiquitination, indicating that a productive viral infection and/or replication is required for FANC pathway activation. Our data indicate that Ad5 infection induces FANCD2 activation to promote its own replication. Specifically, we show that FANCD2 is involved in the recombination process that accompanies viral DNA replication. This study provides evidence of a DNA damage-independent function of the FANC pathway and identifies a cellular system involved in Ad5 recombination.
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