Evidence map›Paper›PMID 35293697›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2022

MYPT1/PP1-Mediated EZH2 Dephosphorylation at S21 Promotes Epithelial-Mesenchymal Transition in Fibrosis through Control of Multiple Families of Genes.

Lan Zhang, Ling Wang, Xue-Bin Hu, Min Hou, Yuan Xiao, Jia-Wen Xiang, Jie Xie, Zhi-Gang Chen, Tian-Heng Yang, Qian Nie and 15 more

Open access · goldAbstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

17 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
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  3. Diabetic keratopathy and nuclear proteins (Review).Molecular medicine reports · 2026
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  13. HSP90β prevents aging-related cataract formation through regulation of the charged multivesicular body protein (CHMP4B) and p53.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  14. Article
  15. Article
  16. Long Non-Coding RNACells · 2022
    Article
  17. 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

25 authors at 1 institution in 1 country.

Lan ZhangThe State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, #54 Xianlie South Road, Guangzhou, Guangdong, 510060, China.
Ling WangThe State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, #54 Xianlie South Road, Guangzhou, Guangdong, 510060, China.
Xue-Bin HuThe State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, #54 Xianlie South Road, Guangzhou, Guangdong, 510060, China.
Min HouThe State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, #54 Xianlie South Road, Guangzhou, Guangdong, 510060, China.
Yuan XiaoThe State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, #54 Xianlie South Road, Guangzhou, Guangdong, 510060, China.
Jia-Wen XiangThe State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, #54 Xianlie South Road, Guangzhou, Guangdong, 510060, China.
Jie XieThe State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, #54 Xianlie South Road, Guangzhou, Guangdong, 510060, China.
Zhi-Gang ChenThe State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, #54 Xianlie South Road, Guangzhou, Guangdong, 510060, China.
Tian-Heng YangThe State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, #54 Xianlie South Road, Guangzhou, Guangdong, 510060, China.
Qian NieThe State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, #54 Xianlie South Road, Guangzhou, Guangdong, 510060, China.
Jia-Ling FuThe State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, #54 Xianlie South Road, Guangzhou, Guangdong, 510060, China.
Yan WangThe State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, #54 Xianlie South Road, Guangzhou, Guangdong, 510060, China.
Shu-Yu ZhengThe State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, #54 Xianlie South Road, Guangzhou, Guangdong, 510060, China.
Yun-Fei LiuThe State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, #54 Xianlie South Road, Guangzhou, Guangdong, 510060, China.
Yu-Wen GanThe State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, #54 Xianlie South Road, Guangzhou, Guangdong, 510060, China.
Qian GaoThe State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, #54 Xianlie South Road, Guangzhou, Guangdong, 510060, China.
Yue-Yue BaiThe State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, #54 Xianlie South Road, Guangzhou, Guangdong, 510060, China.
Jing-Miao WangThe State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, #54 Xianlie South Road, Guangzhou, Guangdong, 510060, China.
Rui-Li QiThe State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, #54 Xianlie South Road, Guangzhou, Guangdong, 510060, China.
Ming ZouThe State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, #54 Xianlie South Road, Guangzhou, Guangdong, 510060, China.
Qin KeThe State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, #54 Xianlie South Road, Guangzhou, Guangdong, 510060, China.
Xing-Fei ZhuThe State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, #54 Xianlie South Road, Guangzhou, Guangdong, 510060, China.
Lili GongThe State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, #54 Xianlie South Road, Guangzhou, Guangdong, 510060, China.
Yizhi LiuThe State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, #54 Xianlie South Road, Guangzhou, Guangdong, 510060, China.
David Wan-Cheng LiThe State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, #54 Xianlie South Road, Guangzhou, Guangdong, 510060, China.ORCID 0000-0002-7398-7630
Sun Yat-sen University · CN

Funding

Fundamental Research Funds of the State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University 3030901010110Fundamental Research Funds of the State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University 3030901010111National Natural Science Foundation of China 81700821National Natural Science Foundation of China 81770910National Natural Science Foundation of China 81900842National Natural Science Foundation of China 81970784National Natural Science Foundation of China 81970787National Natural Science Foundation of China 82000876National Natural Science Foundation of China 82070969Natural Science Foundation of Guangdong province-Guangzhou City 2019B1515120014
6 · The paper itself

Abstract

The methyltransferase EZH2 plays an important role in regulating chromatin conformation and gene transcription. Phosphorylation of EZH2 at S21 by AKT kinase suppresses its function. However, protein phosphatases responsible for the dephosphorylation of EZH2-S21 remain elusive. Here, it is demonstrated that EZH2 is highly expressed in the ocular lens, and AKT-EZH2 axis is important in TGFβ-induced epithelial-mesenchymal transition (EMT). More importantly, it is identified that MYPT1/PP1 dephosphorylates EZH2-S21 and thus modulates its functions. MYPT1 knockout accelerates EMT, but expression of the EZH2-S21A mutant suppresses EMT through control of multiple families of genes. Furthermore, the phosphorylation status and gene expression modulation of EZH2 are implicated in control of anterior subcapsular cataracts (ASC) in human and mouse eyes. Together, the results identify the specific phosphatase for EZH2-S21 and reveal EZH2 dephosphorylation control of several families of genes implicated in lens EMT and ASC pathogenesis. These results provide important novel information in EZH2 function and regulation.

Indexed as

CataractEnhancer of Zeste Homolog 2 ProteinEpithelial-Mesenchymal TransitionLens, CrystallineAnimalsFibrosisHumansMiceMyosin-Light-Chain PhosphatasePhosphorylationProto-Oncogene Proteins c-aktEnhancer of Zeste Homolog 2 ProteinEzh2 protein, mouseMyosin-Light-Chain PhosphatasePpp1r12a protein, mouseProto-Oncogene Proteins c-aktanterior subcapsular cataract (ASC)cataractdephosphorylationenhancer of zeste homolog 2 (EZH2)epithelial-mesenchymal transition (EMT)lensMYPT1posterior subcapsular cataract (PCO)POSTNprotein phosphotase-1

Identifiers

PMID35293697
PMCPMC9108659
OpenAlexW4221102209

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.