ReviewPLoS biology2025
Why does the m6A writer complex require so many proteins?
Review in PLoS biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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
8 citing papers in PubMed.
- RBM15 in leukemogenesis: an emerging regulator at the interface of RNA biology and hematopoiesis.Trends in cancer · 2026Review
- Epigenetic mechanisms in traumatic brain injury: a focus on astrocytes and therapeutic implications.Journal of neuroinflammation · 2026Review
- Pancreatic β-cell aging in physiology and diabetes: emerging roles of m6A mRNA methylation.Journal of molecular endocrinology · 2026Review
- N6-methyladenosine modification in the context of viral infection: from molecular mechanism to therapeutic potential.Virus research · 2026Review
- Pharmacological METTL3 inhibition attenuates HIV-1 latency reversal in CD4Antimicrobial agents and chemotherapy · 2026Article
- Pharmacological METTL3 inhibition attenuates HIV-1 latency reversal in CD4bioRxiv : the preprint server for biology · 2026Article
- The regulatory role of mFrontiers in cell and developmental biology · 2026Review
- Impact of NbioRxiv : the preprint server for biology · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
The conversion of adenosine to N6-methyladenosine (m6A) is the most common internal modification made to eukaryotic mRNA and is involved in post-transcriptional control of gene expression. When dysregulated, m6A has been linked to a variety of diseases, including cancer. Unlike other RNA methyltransferases, m6A conversion is catalyzed by a multi-protein writer complex with only one catalytic subunit. So why is the m6A writer complex composed of so many proteins? This Unsolved Mystery explores the possible functions of the proteins of the m6A writer complex and discusses why it might require multiple subunits. Understanding the roles of these proteins could provide insight into how m6A is regulated and reveal new strategies for targeting diseases linked to m6A dysregulation.
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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.