Evidence map›Paper›PMID 42532042›Full record

ArticleCell genomics2026

PUS7 mRNA pseudouridylation is driven by RNA sequence, structure, and cell-type-specific features.

Rebecca Rodell, Ronit Jain, Hossein Shenasa, Matias Montes, Nicolas Robalin, Stefan Prodic, Eduardo Eyras, Nicole M Martinez

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Article in Cell genomics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors.

Rebecca RodellDepartment of Chemical and Systems Biology, Stanford University, Stanford, CA 94305, USA.
Ronit JainDepartment of Genetics, Stanford University, Stanford, CA 94305, USA.
Hossein ShenasaDepartment of Chemical and Systems Biology, Stanford University, Stanford, CA 94305, USA.
Matias MontesDepartment of Chemical and Systems Biology, Stanford University, Stanford, CA 94305, USA.
Nicolas RobalinDepartment of Chemistry, Stanford University, Stanford, CA 94305, USA.
Stefan ProdicEMBL Australia Partner Laboratory Network, the Australian National University, Canberra, ACT 2601, Australia; The Shine-Dalgarno Centre for RNA Innovation, The John Curtin School of Medical Research, the Australian National University, Canberra, ACT 2601, Australia; The Centre for Computational Biomedical Science, The John Curtin School of Medical Research, the Australian National University, Canberra, ACT 2601, Australia.
Eduardo EyrasEMBL Australia Partner Laboratory Network, the Australian National University, Canberra, ACT 2601, Australia; The Shine-Dalgarno Centre for RNA Innovation, The John Curtin School of Medical Research, the Australian National University, Canberra, ACT 2601, Australia; The Centre for Computational Biomedical Science, The John Curtin School of Medical Research, the Australian National University, Canberra, ACT 2601, Australia.
Nicole M MartinezDepartment of Chemical and Systems Biology, Stanford University, Stanford, CA 94305, USA; Department of Developmental Biology, Stanford University, Stanford, CA 94305, USA; Sarafan ChEM-H Institute, Stanford University, Stanford, CA 94305, USA; Biohub, San Francisco, CA 94158, USA. Electronic address: nicolemm@stanford.edu.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

PUS7 is a major mRNA pseudouridine synthase that influences gene expression and is dysregulated in neurodevelopmental disorders and cancer. PUS7 recognizes a prevalent and degenerate UNUAR sequence, but the mechanisms underlying PUS7's specificity remain unknown. We developed Nano-Mod-Amp, a targeted Nanopore high-throughput pseudouridine detection method, to interrogate PUS7 regulatory features. We established that USUAG, accessibility of the target uridine, and RNA structure are drivers of mRNA modification by PUS7. Perturbing structure through mutations or antisense oligos modulates pseudouridine levels. In cells, pseudouridines are responsive to PUS7 levels, demonstrating the regulatory potential of varying PUS7 levels across cell states. Conversely, PUS7 activity varies across cell types independently of expression levels, suggesting a potential regulatory role for RNA-binding proteins, RNA structure, or other cellular factors. We uncovered principles guiding PUS7 activity, enabling site-specific modulation of pseudouridines. These epitranscriptomic mechanisms provide molecular insight into the regulation and dysregulation of PUS7.

Indexed as

antisense oligocell type regulationepitranscriptomenanopore sequencingpseudouridinePUS7RNA modificationRNA structure

Identifiers

PMID42532042

What OpenQuestion holds

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Registered trials

None linked

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.