Evidence map›Paper›PMID 39155349›Full record

ReviewMolecular biomedicine2024

METTL Family in Healthy and Disease.

Jiejie He, Fengchen Hao, Shiqi Song, Junli Zhang, Hongyu Zhou, Jun Zhang, Yan Li

Abstract readReview
In one paragraph

Review in Molecular biomedicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing 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

9 citing papers in PubMed.

  1. Review
  2. Substrate selectivity of human histidine methyltransferase METTL9.Protein science : a publication of the Protein Society · 2026
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Decreased METTL3 in atrial myocytes promotes atrial fibrillation.Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · 2025
    Article
  8. Article
  9. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Jiejie HeDepartment of Gynecologic Oncology, Affiliated Hospital of Qinghai University, Xining, 810000, Qinghai Province, China.
Fengchen HaoDepartment of Gynecologic Oncology, Affiliated Hospital of Qinghai University, Xining, 810000, Qinghai Province, China.
Shiqi SongDepartment of Gynecologic Oncology, Affiliated Hospital of Qinghai University, Xining, 810000, Qinghai Province, China.
Junli ZhangDepartment of Gynecologic Oncology, Affiliated Hospital of Qinghai University, Xining, 810000, Qinghai Province, China.
Hongyu ZhouDepartment of Radiology, Affiliated Hospital of Qinghai University, Xining, 810000, Qinghai Province, China.
Jun ZhangDepartment of Urology Surgery, Affiliated Hospital of Qinghai University, No. 29, Tongren Road, West of the City, Xining, 810000, Qinghai Province, China. zhangjun@qhuah.com.
Yan LiDepartment of Gynecologic Oncology, Affiliated Hospital of Qinghai University & Affiliated Cancer Hospital of Qinghai University, No. 29, Tongren Road, West of the City, Xining, 810000, Qinghai Province, China. liyan@qhuah.com.ORCID 0000-0002-9447-7154

Funding

National Natural Science Foundation of China 82160523
6 · The paper itself

Abstract

Transcription, RNA splicing, RNA translation, and post-translational protein modification are fundamental processes of gene expression. Epigenetic modifications, such as DNA methylation, RNA modifications, and protein modifications, play a crucial role in regulating gene expression. The methyltransferase-like protein (METTL) family, a constituent of the 7-β-strand (7BS) methyltransferase subfamily, is broadly distributed across the cell nucleus, cytoplasm, and mitochondria. Members of the METTL family, through their S-adenosyl methionine (SAM) binding domain, can transfer methyl groups to DNA, RNA, or proteins, thereby impacting processes such as DNA replication, transcription, and mRNA translation, to participate in the maintenance of normal function or promote disease development. This review primarily examines the involvement of the METTL family in normal cell differentiation, the maintenance of mitochondrial function, and its association with tumor formation, the nervous system, and cardiovascular diseases. Notably, the METTL family is intricately linked to cellular translation, particularly in its regulation of translation factors. Members represent important molecules in disease development processes and are associated with patient immunity and tolerance to radiotherapy and chemotherapy. Moreover, future research directions could include the development of drugs or antibodies targeting its structural domains, and utilizing nanomaterials to carry miRNA corresponding to METTL family mRNA. Additionally, the precise mechanisms underlying the interactions between the METTL family and cellular translation factors remain to be clarified.

Indexed as

MethyltransferasesAnimalsCardiovascular DiseasesEpigenesis, GeneticHumansMitochondriaNeoplasmsMethyltransferasesMethylationMethyltransferase-like protein (METTL) FamilyTranslationTreatment

Identifiers

PMID39155349
PMCPMC11330956

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

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 Socratic graph.