Evidence map›Paper›PMID 30894510›Full record

ArticleCell death & disease2019

Absence of cyclin-dependent kinase inhibitor p27 or p18 increases efficiency of iPSC generation without induction of iPSC genomic instability.

Zhiyan Zhan, Lili Song, Weiwei Zhang, Haihui Gu, Haizi Cheng, Yingwen Zhang, Yi Yang, Guangzhen Ji, Haizhong Feng, Tao Cheng and 1 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.9field-weighted citation impact, top 28% 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

12 citing papers in PubMed, 16 citations in OpenAlex.

  1. SEC Mediates mAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  2. Coupling of stemness maintenance with cell cycle control in stem cells.Frontiers in cell and developmental biology · 2025
    Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 6 institutions in 2 countries.

Zhiyan ZhanKey Laboratory of Pediatric Hematology and Oncology Ministry of Health, Department of Hematology & Oncology, Pediatric Translational Medicine Institute, Shanghai Children's Medical Center, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200127, China.
Lili SongKey Laboratory of Pediatric Hematology and Oncology Ministry of Health, Department of Hematology & Oncology, Pediatric Translational Medicine Institute, Shanghai Children's Medical Center, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200127, China.
Weiwei ZhangState Key Laboratory of Oncogenes and Related Genes, Renji-Med X Clinical Stem Cell Research Center, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200127, China.
Haihui GuDepartment of Blood Transfusion, Changhai Hospital, Shanghai, 200433, China.
Haizi ChengDepartment of Radiation Oncology, University of Pittsburgh School of Medicine, University of Pittsburgh Cancer Institute, 5117 Center Avenue, Pittsburgh, PA, 15213, USA.
Yingwen ZhangKey Laboratory of Pediatric Hematology and Oncology Ministry of Health, Department of Hematology & Oncology, Pediatric Translational Medicine Institute, Shanghai Children's Medical Center, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200127, China.
Yi YangKey Laboratory of Pediatric Hematology and Oncology Ministry of Health, Department of Hematology & Oncology, Pediatric Translational Medicine Institute, Shanghai Children's Medical Center, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200127, China.
Guangzhen JiState Key Laboratory of Experimental Hematology, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Tianjin, China.
Haizhong FengState Key Laboratory of Oncogenes and Related Genes, Renji-Med X Clinical Stem Cell Research Center, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200127, China. fenghaizhong@sjtu.edu.cn.
Tao ChengState Key Laboratory of Experimental Hematology, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Tianjin, China. chengtao@ihcams.ac.cn.
Yanxin LiKey Laboratory of Pediatric Hematology and Oncology Ministry of Health, Department of Hematology & Oncology, Pediatric Translational Medicine Institute, Shanghai Children's Medical Center, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200127, China. liyanxin@scmc.com.cn.
Shanghai Children's Medical Center · CNChinese Academy of Medical Sciences & Peking Union Medical College · CNShanghai Jiao Tong University · CNState Key Laboratory of Oncogene and Related Genes · CNSecond Military Medical University · CNUPMC Hillman Cancer Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mechanisms underlying the generation of induced pluripotent stem cells (iPSC) and keeping iPSC stability remain to be further defined. Accumulated evidences showed that iPSC reprogramming may be controlled by the cell-division-rate-dependent model. Here we reported effects of absence of mouse p27 or p18 on iPSC generation efficiency and genomic stability. Expression levels of cyclin-dependent kinases inhibitors (CDKIs), p21, p27, and p18 decreased during iPSC reprogramming. Like p21 loss, p27 or p18 deficiency significantly promoted efficiency of iPSC generation, whereas ectopic expression of p27, p18, or treatment with CDK2 or CDK4 inhibitors repressed the reprogramming rate, suggesting that CDKIs-regulated iPSC reprogramming is directly related with their functions as CDK inhibitors. However, unlike p21 deletion, absence of p27 or p18 did not increase DNA damage or chromosomal aberrations during iPSC reprogramming and at iPSC stage. Our data not only support that cell cycle regulation is critical for iPSC reprogramming, but also reveal the distinction of CDKIs in somatic cell reprogramming.

Indexed as

AnimalsCell DivisionCellular ReprogrammingChromosome AberrationsCyclin-Dependent Kinase 2Cyclin-Dependent Kinase 4Cyclin-Dependent Kinase Inhibitor p18Cyclin-Dependent Kinase Inhibitor p21Cyclin-Dependent Kinase Inhibitor p27FibroblastsGenomic InstabilityInduced Pluripotent Stem CellsMiceMice, Inbred C57BLMice, Inbred NODMice, KnockoutCdk2 protein, mouseCdk4 protein, mouseCyclin-Dependent Kinase 2Cyclin-Dependent Kinase 4Cyclin-Dependent Kinase Inhibitor p18Cyclin-Dependent Kinase Inhibitor p21Cyclin-Dependent Kinase Inhibitor p27

Identifiers

PMID30894510
PMCPMC6426969
OpenAlexW2924355397

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.