Evidence map›Paper›PMID 35509151›Full record

ArticleCell proliferation2022

CDK5RAP3, an essential regulator of checkpoint, interacts with RPL26 and maintains the stability of cell growth.

Hongchen Yan, Jun-Jie Xu, Ilyas Ali, Wei Zhang, Ming Jiang, Guiping Li, Yong Teng, Guangxun Zhu, Yafei Cai

Open access · goldAbstract read
In one paragraph

Article in Cell proliferation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.0field-weighted citation impact, top 27% 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

10 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. CDK5RAP3 Regulates Testosterone Production in Mouse Leydig Cells.International journal of molecular sciences · 2026
    Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. 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

9 authors at 3 institutions in 2 countries.

Hongchen YanCollege of Animal Science and Technology, Nanjing Agricultural University, Nanjing, China.ORCID https://orcid.org/0000-0002-2318-7707
Jun-Jie XuCollege of Animal Science and Technology, Nanjing Agricultural University, Nanjing, China.
Ilyas AliCollege of Animal Science and Technology, Nanjing Agricultural University, Nanjing, China.
Wei ZhangCollege of Animal Science and Technology, Nanjing Agricultural University, Nanjing, China.
Ming JiangDepartment of Stomatology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Guiping LiDepartment of Stomatology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Yong TengDepartment of Hematology and Medical Oncology, Winship Cancer Institute, Emory University School of Medicine, Atlanta, Georgia, USA.
Guangxun ZhuDepartment of Stomatology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Yafei CaiCollege of Animal Science and Technology, Nanjing Agricultural University, Nanjing, China.
Nanjing Agricultural University · CNTongji Hospital · CNEmory University · US

Funding

Nanjing Agricultural University 804090The National Natural Science Foundation of China 31970413
6 · The paper itself

Abstract

purpose and materialsCDK5RAP3 (CDK5 regulatory subunit associated protein 3) was originally identified as a binding protein of CDK5. It is a crucial gene controlling biological functions, such as cell proliferation, apoptosis, invasion, and metastasis. Although previous studies have also shown that CDK5RAP3 is involved in a variety of signalling pathways, however, the mechanism of CDK5RAP3 remains largely undefined. This study utilized MEFs from conditional knockout mice to inhibit CDK5RAP3 and knockdown CDK5RAP3 in MCF7 to explore the role of CDK5RAP3 in cell growth, mitosis, and cell death.

resultsCDK5RAP3 was found to be widely distributed throughout the centrosome, spindle, and endoplasmic reticulum, indicating that it is involved in regulating a variety of cellular activities. CDK5RAP3 deficiency resulted in instability of cell growth. CDK5RAP3 deficiency partly blocks the cell cycle in G

conclusionsOur experiments show that CDK5RAP3 interacts with RPL26 and maintains the stability of cell growth. It shows that CDK5RAP3 plays an important role in cell growth and can be used as the target of gene medicine.

Indexed as

Cell Cycle ProteinsTumor Suppressor ProteinsAnimalsApoptosisCell CycleCell ProliferationMiceMitosisTOR Serine-Threonine KinasesCdk5rap3 protein, mouseCell Cycle ProteinsTOR Serine-Threonine KinasesTumor Suppressor Proteins

Identifiers

PMID35509151
PMCPMC9136512
OpenAlexW4229007922

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.