ArticleFrontiers in genetics2022
METTL16 regulates m
Article in Frontiers in genetics, 2022. 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, 14 citations in OpenAlex.
- Targeting METTL16 attenuates mesangial cell viability and fibrosis in a high-glucose state by suppressing m6A modification and the expression of RAP1B.BMC molecular and cell biology · 2025Article
- m6A RNA modification pathway: orchestrating fibrotic mechanisms across multiple organs.Briefings in functional genomics · 2025Review
- N6-methyladenosine (m6A) RNA modification in fibrosis and collagen-related diseases.Clinical epigenetics · 2024Review
- Genetic variants in the 6p21.3 region influence hepatitis B virus clearance and chronic hepatitis B risk in the Han Chinese population.Liver research (Beijing, China) · 2024Article
- mInternational journal of biological sciences · 2024Article
- Changes in m6A in Steatotic Liver Disease.Genes · 2023Review
- RNA methylations in hepatic fibrosis, a gradually emerging new treatment strategy.Cell & bioscience · 2023Review
- METTL16 in human diseases: What should we do next?Open medicine (Warsaw, Poland) · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The role of genetic factors in the occurrence and progression of CHB (CHB) is still not fully explored. In recent years, genome-wide association studies on CHB patients have demonstrated that a large number of CHB-associated single nucleotide polymorphisms exist in the gene intron, which may regulate expression at the transcriptional level. Modification of RNA m
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.