Evidence map›Paper›PMID 30174313›Full record

ArticleStem cell reports2018

The Long Noncoding RNA Lncenc1 Maintains Naive States of Mouse ESCs by Promoting the Glycolysis Pathway.

Zihao Sun, Minzhe Zhu, Pin Lv, Lu Cheng, Qianfeng Wang, Pengxiang Tian, Zixiang Yan, Bo Wen

Open access · goldAbstract read
In one paragraph

Article in Stem cell reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

28 citing papers in PubMed, 50 citations in OpenAlex.

  1. Deletion of Ybx1 results in germ cell hypoplasia in mouse embryos.The Journal of reproduction and development · 2026
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  10. A proinflammatory long noncoding RNA Lncenc1 regulates inflammasome activation in macrophage.American journal of physiology. Lung cellular and molecular physiology · 2023
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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

8 authors at 1 institution in 1 country.

Zihao SunMOE Key Laboratory of Metabolism and Molecular Medicine, School of Basic Medical Sciences, Institutes of Biomedical Sciences, Fudan University, Shanghai 200032, China.
Minzhe ZhuMOE Key Laboratory of Metabolism and Molecular Medicine, School of Basic Medical Sciences, Institutes of Biomedical Sciences, Fudan University, Shanghai 200032, China.
Pin LvMOE Key Laboratory of Metabolism and Molecular Medicine, School of Basic Medical Sciences, Institutes of Biomedical Sciences, Fudan University, Shanghai 200032, China.
Lu ChengMOE Key Laboratory of Metabolism and Molecular Medicine, School of Basic Medical Sciences, Institutes of Biomedical Sciences, Fudan University, Shanghai 200032, China.
Qianfeng WangMOE Key Laboratory of Metabolism and Molecular Medicine, School of Basic Medical Sciences, Institutes of Biomedical Sciences, Fudan University, Shanghai 200032, China.
Pengxiang TianMOE Key Laboratory of Metabolism and Molecular Medicine, School of Basic Medical Sciences, Institutes of Biomedical Sciences, Fudan University, Shanghai 200032, China.
Zixiang YanMOE Key Laboratory of Metabolism and Molecular Medicine, School of Basic Medical Sciences, Institutes of Biomedical Sciences, Fudan University, Shanghai 200032, China.
Bo WenThe Fifth People's Hospital of Shanghai, Institutes of Biomedical Sciences, Fudan University, Shanghai 200032, China; MOE Key Laboratory of Metabolism and Molecular Medicine, Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Fudan University, Shanghai 200032, China; State Key Laboratory of Genetic Engineering, Collaborative Innovation Center of Genetics and Development, Fudan University, Shanghai 200438, China. Electronic address: bowen75@fudan.edu.cn.
Fudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The naive embryonic stem cells (nESCs) display unique characteristics compared with the primed counterparts, but the underlying molecular mechanisms remain elusive. Here we investigate the functional roles of Lncenc1, a highly abundant long noncoding RNA in nESCs. Knockdown or knockout of Lncenc1 in mouse nESCs leads to a significantly decreased expression of core pluripotency genes and a significant reduction of colony formation capability. Furthermore, upon the depletion of Lncenc1, the expression of glycolysis-associated genes is significantly reduced, and the glycolytic activity is substantially impaired, as indicated by a more than 50% reduction in levels of glucose consumption, lactate production, and extracellular acidification rate. Mechanistically, Lncenc1 interacts with PTBP1 and HNRNPK, which regulate the transcription of glycolytic genes, thereby maintaining the self-renewal of nESCs. Our results demonstrate the functions of Lncenc1 in linking energy metabolism and naive state of ESCs, which may enhance our understanding of the molecular basis underlying naive pluripotency.

Indexed as

GlycolysisAnimalsCell LineGene Expression Regulation, DevelopmentalMiceMouse Embryonic Stem CellsRNA, Long NoncodingTranscriptional ActivationTranscriptomeRNA, Long Noncodingembryonic stem cellglycolysisLncenc1lncRNAmetabolismnaive pluripotencypluripotent stem cells

Identifiers

PMID30174313
PMCPMC6135739
OpenAlexW2889465314

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.