ArticlemBio2026
Differentiation-dependent proximity proteomics identifies novel host factors linked to HPV16 E2 function.
Article in mBio, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
- Update of
Authors and funding
13 authors.
Funding
Abstract
Human papillomavirus 16 (HPV16) is a causative agent of oropharyngeal, cervical, and anogenital cancers. The viral E2 protein is essential for viral genome replication, transcriptional regulation, episome maintenance, and activation of the host DNA damage response. Despite its central role, the full network of HPV16 E2 interactions with host proteins remains incompletely defined, particularly under differentiating conditions, which support the complete viral life cycle. In this study, we used TurboID-based proximity labeling to characterize the interactome of HPV16 E2 and its known host partner protein TOPBP1 in both undifferentiated monolayer and differentiating keratinocytes. We generated stable keratinocyte lines expressing doxycycline-inducible TurboID-tagged HPV16 E2 and confirmed that the tagged protein retained transcriptional, replicative, and DNA damage-inducing functions. Mass spectrometry analysis of streptavidin-enriched proteins identified both known and novel E2-associated host factors, including chromatin regulators, DNA repair proteins, and nucleolar components. Comparative analysis revealed substantial overlap between E2 and TOPBP1 interactomes, and IMPORTANCE: Human papillomaviruses (HPVs) establish persistent infections in stratified epithelia and rely on host DNA damage and repair factors to support their replication. The E2 protein is central to viral genome replication and maintenance and depends heavily on its interaction with the host factor TOPBP1 for these functions. Here, we define the E2 and TOPBP1 interactomes in differentiating keratinocytes and identify nucleolin (NCL) as a critical differentiation- and TOPBP1-dependent E2 partner required for episomal genome stability. These findings expand the understanding of how HPV16 coordinates viral replication with host chromatin and DNA repair networks, uncovering a cooperative E2-TOPBP1-NCL axis that may represent a new target for antiviral intervention.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.