Disruption of NBS1/MRN Complex Formation by E4orf3 Supports NF-κB That Licenses E1B55K-Deleted Adenovirus-Infected Cells to Accumulate DNA>4n-Reference-Cited by-同舟云学术

Disruption of NBS1/MRN Complex Formation by E4orf3 Supports NF-κB That Licenses E1B55K-Deleted Adenovirus-Infected Cells to Accumulate DNA>4n

Published:2022-02-23 Issue:1 Volume:10 Page:
ISSN:2165-0497
Container-title:Microbiology Spectrum
language:en
Short-container-title:Microbiol Spectr

Author:

Almuzaini Nujud¹,Moore Madison¹,Robert-Guroff Marjorie²^ORCID,Thomas Michael A.¹^ORCID

Affiliation:

1. Department of Biology, College of Arts and Sciences, Howard University, Washington, D.C., USA

2. Section on Immune Biology of Retroviral Infection, Vaccine Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA

Abstract

Genome instability, a hallmark of cancer, exists as part of a cycle that leads to DNA damage and DNA > 4n that further enhances genome instability. Ad E4orf3 is a viral oncogene. Here, we describe E4orf3 mediated signaling events that support DNA > 4n in Δ E1B Ad-infected cells. These signaling events may be linked to the oncogenic potential of E4orf3 and may provide a basis for how some cells survive with DNA > 4n.

Funder

HHS | NIH | National Institute of Allergy and Infectious Diseases

Publisher

American Society for Microbiology

Subject

Infectious Diseases,Cell Biology,Microbiology (medical),Genetics,General Immunology and Microbiology,Ecology,Physiology

Link

https://journals.asm.org/doi/pdf/10.1128/spectrum.01881-21

Reference85 articles.

1. The Causes and Consequences of Polyploidy in Normal Development and Cancer

2. When bigger is better: the role of polyploidy in organogenesis

3. Endoreplication and polyploidy: insights into development and disease