Evidence map›Paper›PMID 33104214›Full record

ArticleJournal of molecular cell biology2020

RNF219 interacts with CCR4-NOT in regulating stem cell differentiation.

Hao Du, Chen Chen, Yan Wang, Yang Yang, Zhuanzhuan Che, Xiaoxu Liu, Siyan Meng, Chenghao Guo, Manman Xu, Haitong Fang and 3 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of molecular cell biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.6field-weighted citation impact, top 34% 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

14 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Poly(A) tail regulation in stem cells and early development.Cell regeneration (London, England) · 2025
    Review
  5. Article
  6. Review
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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

13 authors at 4 institutions in 2 countries.

Hao DuSchool of Life Science and Technology, The Key Laboratory of Developmental Genes and Human Disease, Southeast University, Nanjing 210096, China.
Chen ChenSchool of Life Science and Technology, The Key Laboratory of Developmental Genes and Human Disease, Southeast University, Nanjing 210096, China.
Yan WangSchool of Life Science and Technology, The Key Laboratory of Developmental Genes and Human Disease, Southeast University, Nanjing 210096, China.
Yang YangDepartment of Biological Sciences, Center for Systems Biology, the University of Texas at Dallas, Richardson, TX 75080, USA.
Zhuanzhuan CheSchool of Life Science and Technology, The Key Laboratory of Developmental Genes and Human Disease, Southeast University, Nanjing 210096, China.
Xiaoxu LiuSchool of Life Science and Technology, The Key Laboratory of Developmental Genes and Human Disease, Southeast University, Nanjing 210096, China.
Siyan MengSchool of Life Science and Technology, The Key Laboratory of Developmental Genes and Human Disease, Southeast University, Nanjing 210096, China.
Chenghao GuoSchool of Life Science and Technology, The Key Laboratory of Developmental Genes and Human Disease, Southeast University, Nanjing 210096, China.
Manman XuSchool of Life Science and Technology, The Key Laboratory of Developmental Genes and Human Disease, Southeast University, Nanjing 210096, China.
Haitong FangSchool of Life Science and Technology, The Key Laboratory of Developmental Genes and Human Disease, Southeast University, Nanjing 210096, China.
Fengchao WangInstitute of Combined Injury of PLA, State Key Laboratory of Trauma, Burns and Combined Injury, Army Medical University, Chongqing 400038, China.
Chengqi LinSchool of Life Science and Technology, The Key Laboratory of Developmental Genes and Human Disease, Southeast University, Nanjing 210096, China.
Zhuojuan LuoSchool of Life Science and Technology, The Key Laboratory of Developmental Genes and Human Disease, Southeast University, Nanjing 210096, China.
Southeast University · CNNantong University · CNArmy Medical University · CNThe University of Texas at Dallas · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Regulation of RNA stability plays a crucial role in gene expression control. Deadenylation is the initial rate-limiting step for the majority of RNA decay events. Here, we show that RING finger protein 219 (RNF219) interacts with the CCR4-NOT deadenylase complex. RNF219-CCR4-NOT exhibits deadenylation activity in vitro. RNA-seq analyses identify some of the 2-cell-specific genes and the neuronal genes significantly downregulated upon RNF219 knockdown, while upregulated after depletion of the CCR4-NOT subunit CNOT10 in mouse embryonic stem (ES) cells. RNF219 depletion leads to impaired neuronal lineage commitment during ES cell differentiation. Our study suggests that RNF219 is a novel interacting partner of CCR4-NOT and required for maintenance of ES cell pluripotency.

Indexed as

Cell DifferentiationAnimalsGene Expression RegulationHEK293 CellsHumansMiceMicroRNAsMouse Embryonic Stem CellsNeuronsPolycomb Repressive Complex 1Protein BindingTranscription FactorsUbiquitin-Protein LigasesCnot10 protein, mouseMicroRNAsPolycomb Repressive Complex 1Rnf2 protein, mouseTranscription FactorsUbiquitin-Protein LigasesCCR4–NOTdeadenylationprotein complexRNF219stem cell differentiation

Identifiers

PMID33104214
PMCPMC7883825
OpenAlexW3093885064

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.