Open AccessDisruption of NBS1/MRN Complex Formation by E4orf3 Supports NF-κB That Licenses E1B55K-Deleted Adenovirus-Infected Cells to Accumulate DNA>4n
Author(s) -
Nujud Almuzaini,
Madison Moore,
Marjorie Robert-Guroff,
Michael A. Thomas
Publication year - 2022
Publication title -
microbiology spectrum
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.502
H-Index - 51
ISSN - 2165-0497
DOI - 10.1128/spectrum.01881-21
Subject(s) - biology , dna damage , dna , cell cycle , apoptosis , dna repair , oncolytic virus , microbiology and biotechnology , cell cycle checkpoint , cancer research , cancer , genetics
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 ΔE1B 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.
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