ArticleCell reports2026
N(6)-methyladenosine modification of RNA is regulated by senataxin and E6 to control HPV replication.
Article in Cell reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
The levels of N6-methyladenosine (m6A)-modified RNAs are reduced within cells with high-risk human papillomaviruses (HPVs) in comparison to normal cells. These reduced m6A levels stabilize RNA:DNA hybrids (R-loops), whose regulation is critical for viral replication. HPV E6 induces the degradation of the m6A methyltransferases, Mettl3 and Mettl14, in an E6AP-dependent manner to reduce m6A levels, while the RNA helicase senataxin (SETX) counteracts this by activating the expression of m6A regulators. Maintenance of the residual m6A levels in undifferentiated cells is also critical for viral replication. A subset of early viral transcripts is m6A modified, and the inhibition of Mettl3 impairs viral gene expression. Upon differentiation, the levels of SETX and m6A are increased by over 8-fold, which is necessary for the productive replication of HPVs. These studies identify a role for SETX and E6 in regulating m6A deposition to control HPV pathogenesis in a differentiation-dependent manner.
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.