ArticleJournal of virology2025
A conserved cysteine in the DNA-binding domain of MmuPV1 E2 is required for replication
Article in Journal of virology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
3 citing papers in PubMed.
- E2 Tyrosine 102 Regulates MmuPV1 Pathogenesis In Vivo.Pathogens (Basel, Switzerland) · 2025Article
- Structural and functional roles of conserved residues of human papillomavirus (HPV) E2 protein and biological consequences.Virology journal · 2025Article
- A Conserved Di-Lysine Motif in the E2 Transactivation Domain Regulates MmuPV1 Replication and Disease Progression.Pathogens (Basel, Switzerland) · 2025Article
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
The papillomavirus (PV) E2 protein is highly conserved, consisting of an N-terminal transactivation domain linked to a C-terminal DNA binding and dimerization domain (DBD) by a flexible hinge region. The E2 DBD exhibits a helix-turn-helix structure that dimerizes into a beta barrel prior to binding DNA; the first helix, α1, is responsible for recognition of the palindromic E2 binding site. The DNA recognition helix consists of a tract of basic amino acids with a highly conserved central cysteine residue. Previous mutational analysis studies on this conserved cysteine have found that it is not required for viral replication or DNA binding. To investigate the function of this conserved cysteine IMPORTANCE: Papillomaviruses are the etiological agents of cancers of the oropharynx and anogenital tract. Understanding the mechanisms underlying PV pathogenesis is complicated by the strict species tropism displayed by the virus. The research presented here is significant because it links
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Registered trials
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