Evidence map›Paper›PMID 34382339›Full record

ArticleJournal of cellular and molecular medicine2021

The effects of NCBP3 on METTL3-mediated m6A RNA methylation to enhance translation process in hypoxic cardiomyocytes.

Fei Ye, Xiaoyan Wang, San Tu, Lixiong Zeng, Xu Deng, Wenzhi Luo, Zhihui Zhang

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.0field-weighted citation impact, top 25% of its field
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

18 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. METTL3: a multifunctional regulator in diseases.Molecular and cellular biochemistry · 2025
    Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Multilevel regulation of NGenes & diseases · 2023
    Review
  12. Critical roles of mFrontiers in cardiovascular medicine · 2023
    Review
  13. Article
  14. Review
  15. Review
  16. mCurrent opinion in physiology · 2022
    Article
  17. Review
  18. 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 at 1 institution in 1 country.

Fei YeDepartment of Cardiology, The Third Xiangya Hospital of Central South University, Changsha, China.
Xiaoyan WangDepartment of Cardiology, The Third Xiangya Hospital of Central South University, Changsha, China.
San TuDepartment of Cardiology, The Third Xiangya Hospital of Central South University, Changsha, China.
Lixiong ZengDepartment of Cardiology, The Third Xiangya Hospital of Central South University, Changsha, China.
Xu DengDepartment of Cardiology, The Third Xiangya Hospital of Central South University, Changsha, China.
Wenzhi LuoDepartment of Cardiology, The Third Xiangya Hospital of Central South University, Changsha, China.
Zhihui ZhangDepartment of Cardiology, The Third Xiangya Hospital of Central South University, Changsha, China.ORCID 0000-0002-3569-5856
Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hypoxia as a crucial pathogenesis factor usually results in huge harmful effects on cardiac injury and dysfunction. Our previous study has uncovered the global transcriptome and translatome profiles of cardiomyocytes in vitro and in vivo to response to hypoxia by RNA sequencing and ribosome profiling sequencing. We observe a series of differential expressed genes between transcription and translation, which may be attributed to the hypoxia-specific binding affinity of nuclear cap-binding subunit 3 (NCBP3) at 5' untranslation region of target genes. Although we observe that NCBP3 can facilitate translational process in myocardium under hypoxia stress, the underlying molecular mechanism of NCBP3 for gene translation modulation remains unclear. In this study, we performed NCBP3 immunoprecipitation for mass spectrum and found that METTL3 and eIF4A2 particularly interacted with NCBP3 in hypoxic rat H9C2 cardiomyocytes. Furthermore, we observed that METTL3-mediated N6-methyladenosine (m6A) methylation was elevated in hypoxia, but compromised by NCBP3 or METTL3 knockdown. Finally, we also demonstrated that NCBP3/METTL3/eIF4A2 regulatory axis plays a specific role in cardiomyocytes undergoing hypoxic stress. Taken together, we unmasked NCBP3, a novel hypoxia-specific response protein functions as a scaffold to coordinate METTL3 and eIF4A2 for enhancing gene translation by m6A RNA methylation in cardiomyocytes upon hypoxic stress.

Indexed as

Cell HypoxiaAnimalsCell Line, TumorMethylationMethyltransferasesMyocytes, CardiacNuclear Cap-Binding Protein ComplexRatsRNA, MessengerMethyltransferasesMETTL3 protein, humanNuclear Cap-Binding Protein ComplexRNA, MessengercardiomyocyteseIF4A2hypoxiam6A RNA methylationMETTL3NCBP3translation

Identifiers

PMID34382339
PMCPMC8435433
OpenAlexW3191624517

What OpenQuestion 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 OpenQuestion graph.