Evidence map›Paper›PMID 32483152›Full record

ArticleNature communications2020

Long noncoding RNA SAM promotes myoblast proliferation through stabilizing Sugt1 and facilitating kinetochore assembly.

Yuying Li, Jie Yuan, Fengyuan Chen, Suyang Zhang, Yu Zhao, Xiaona Chen, Leina Lu, Liang Zhou, Ching Yan Chu, Hao Sun and 1 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.9field-weighted citation impact, top 13% 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

24 citing papers in PubMed, 41 citations in OpenAlex.

  1. A Myocyte-Enriched Long Non-Coding RNA NRMLncR Enhances Myogenesis in Mouse.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
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  4. bioRxiv : the preprint server for biology · 2026
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  18. An Emerging Role for Epigenetics in Cerebral Palsy.Journal of personalized medicine · 2021
    Review
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  20. 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

11 authors at 2 institutions in 3 countries.

Yuying LiDepartment of Chemical Pathology, The Chinese University of Hong Kong, Hong Kong, China.
Jie YuanDepartment of Chemical Pathology, The Chinese University of Hong Kong, Hong Kong, China.
Fengyuan ChenDepartment of Orthaepedics and Traumatology, The Chinese University of Hong Kong, Hong Kong, China.
Suyang ZhangDepartment of Orthaepedics and Traumatology, The Chinese University of Hong Kong, Hong Kong, China.
Yu ZhaoDepartment of Orthaepedics and Traumatology, The Chinese University of Hong Kong, Hong Kong, China.ORCID http://orcid.org/0000-0002-0349-7206
Xiaona ChenDepartment of Orthaepedics and Traumatology, The Chinese University of Hong Kong, Hong Kong, China.
Leina LuDepartment of Chemical Pathology, The Chinese University of Hong Kong, Hong Kong, China.
Liang ZhouDepartment of Toxicology, School of Public Health, Southern Medical University, Guangzhou, China.ORCID http://orcid.org/0000-0001-5973-7873
Ching Yan ChuDepartment of Obstetrics and Gynaecology, Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Hong Kong, China.
Hao SunDepartment of Chemical Pathology, The Chinese University of Hong Kong, Hong Kong, China. haosun@cuhk.edu.hk.ORCID http://orcid.org/0000-0002-5547-9501
Huating WangDepartment of Orthaepedics and Traumatology, The Chinese University of Hong Kong, Hong Kong, China. huating.wang@cuhk.edu.hk.
Chinese University of Hong Kong · HKSouthern Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The functional study of lncRNAs in skeletal muscle satellite cells (SCs) remains at the infancy stage. Here we identify SAM (Sugt1 asssociated muscle) lncRNA that is enriched in the proliferating myoblasts. Global deletion of SAM has no overt effect on mice but impairs adult muscle regeneration following acute damage; it also exacerbates the chronic injury-induced dystrophic phenotype in mdx mice. Consistently, inducible deletion of SAM in SCs leads to deficiency in muscle regeneration. Further examination reveals that SAM loss results in a cell-autonomous defect in the proliferative expansion of myoblasts. Mechanistically, we find SAM interacts and stabilizes Sugt1, a co-chaperon protein key to kinetochore assembly during cell division. Loss of SAM or Sugt1 both disrupts kinetochore assembly in mitotic cells due to the mislocalization of two components: Dsn1 and Hec1. Altogether, our findings identify SAM as a regulator of SC proliferation through facilitating Sugt1 mediated kinetochore assembly during cell division.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsCell Cycle ProteinsCell LineCell ProliferationCells, CulturedChromosomal Proteins, Non-HistoneGene Expression RegulationKinetochoresMice, Inbred C57BLMice, Inbred mdxMice, KnockoutMicrotubule-Associated ProteinsMyoblastsProtein StabilityRNA, Long NoncodingAdaptor Proteins, Signal TransducingCell Cycle ProteinsChromosomal Proteins, Non-HistoneHec1 protein, mouseMicrotubule-Associated ProteinsRNA, Long NoncodingSugt1 protein, mouse

Identifiers

PMID32483152
PMCPMC7264179
OpenAlexW3032438672

What OpenQuestion holds

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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.