Evidence map›Paper›PMID 32988975›Full record

ArticleDevelopment (Cambridge, England)2020

The Gridlock transcriptional repressor impedes vertebrate heart regeneration by restricting expression of lysine methyltransferase.

Peilu She, Huifang Zhang, Xiangwen Peng, Jianjian Sun, Bangjun Gao, Yating Zhou, Xuejiao Zhu, Xueli Hu, Kaa Seng Lai, Jiemin Wong and 3 more

Open access · hybridAbstract read
In one paragraph

Article in Development (Cambridge, England), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
0.7field-weighted citation impact, top 32% 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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.

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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 1 country.

Peilu SheState Key Laboratory of Genetic Engineering, School of Life Sciences, Zhongshan Hospital, Fudan University, Shanghai, 200438, China.
Huifang ZhangShanghai Key Laboratory of Regulatory Biology, Institute of Molecular Medicine, School of Life Sciences, East China Normal University, Shanghai, 200241, China.
Xiangwen PengState Key Laboratory of Genetic Engineering, School of Life Sciences, Zhongshan Hospital, Fudan University, Shanghai, 200438, China.
Jianjian SunShanghai Key Laboratory of Regulatory Biology, Institute of Molecular Medicine, School of Life Sciences, East China Normal University, Shanghai, 200241, China.
Bangjun GaoShanghai Key Laboratory of Regulatory Biology, Institute of Molecular Medicine, School of Life Sciences, East China Normal University, Shanghai, 200241, China.
Yating ZhouShanghai Key Laboratory of Regulatory Biology, Institute of Molecular Medicine, School of Life Sciences, East China Normal University, Shanghai, 200241, China.
Xuejiao ZhuShanghai Key Laboratory of Regulatory Biology, Institute of Molecular Medicine, School of Life Sciences, East China Normal University, Shanghai, 200241, China.
Xueli HuShanghai Key Laboratory of Regulatory Biology, Institute of Molecular Medicine, School of Life Sciences, East China Normal University, Shanghai, 200241, China.
Kaa Seng LaiShanghai Key Laboratory of Regulatory Biology, Institute of Molecular Medicine, School of Life Sciences, East China Normal University, Shanghai, 200241, China.
Jiemin WongShanghai Key Laboratory of Regulatory Biology, Institute of Molecular Medicine, School of Life Sciences, East China Normal University, Shanghai, 200241, China.
Bin ZhouInstitute of Biochemistry and Cell Biology, Chinese Academy of Sciences, Shanghai, 200031, China.
Linhui WangDepartment of Urology, Shanghai Changzheng Hospital, Shanghai, 200003, China.
Tao P ZhongShanghai Key Laboratory of Regulatory Biology, Institute of Molecular Medicine, School of Life Sciences, East China Normal University, Shanghai, 200241, China tzhong@bio.ecnu.edu.cn.ORCID 0000-0003-1159-5487
East China Normal University · CNFudan University · CNChinese Academy of Sciences · CNShanghai Changzheng Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Teleost zebrafish and neonatal mammalian hearts exhibit the remarkable capacity to regenerate through dedifferentiation and proliferation of pre-existing cardiomyocytes (CMs). Although many mitogenic signals that stimulate zebrafish heart regeneration have been identified, transcriptional programs that restrain injury-induced CM renewal are incompletely understood. Here, we report that mutations in

Indexed as

AnimalsAnimals, NewbornBasic Helix-Loop-Helix ProteinsCell DifferentiationCell ProliferationHeartLysineMethyltransferasesMyocardiumMyocytes, CardiacPhosphorylationRegenerationSignal TransductionSTAT3 Transcription FactorTranscription, GeneticVertebratesBasic Helix-Loop-Helix Proteinshey2 protein, zebrafishLysineMethyltransferasesSTAT3 Transcription FactorZebrafish ProteinsCardiomyocyte proliferationGrlHeart regenerationHey2Lysine methyltransferaseZebrafish

Identifiers

PMID32988975
PMCPMC7541343
OpenAlexW3088692926

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.