Evidence map›Paper›PMID 30717351›Full record

ArticleInternational journal of molecular sciences2019

The Possible Role of Complete Loss of Myostatin in Limiting Excessive Proliferation of Muscle Cells (C2C12) via Activation of MicroRNAs.

Peixuan Huang, Daxin Pang, Kankan Wang, Aishi Xu, Chaogang Yao, Mengjing Li, Wenni You, Qiushuang Wang, Hao Yu

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.6field-weighted citation impact, top 34% 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

7 citing papers in PubMed, 10 citations in OpenAlex.

  1. Polymorphism of Genes and Their Impact on Beef Quality.Current issues in molecular biology · 2023
    Review
  2. RNA Regulatory Networks 2.0.International journal of molecular sciences · 2023
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. EffectiveInternational journal of molecular sciences · 2020
    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

9 authors at 1 institution in 1 country.

Peixuan HuangJilin Provincial Key Laboratory of Animal Embryo Engineering, College of Animal Sciences, Jilin University, Changchun 130062, China. huangpx16@mails.jlu.edu.cn.
Daxin PangJilin Provincial Key Laboratory of Animal Embryo Engineering, College of Animal Sciences, Jilin University, Changchun 130062, China. pdx@jlu.edu.cn.
Kankan WangJilin Provincial Key Laboratory of Animal Embryo Engineering, College of Animal Sciences, Jilin University, Changchun 130062, China. wang4196@purdue.edu.
Aishi XuJilin Provincial Key Laboratory of Animal Embryo Engineering, College of Animal Sciences, Jilin University, Changchun 130062, China. xuas14@mails.jlu.edu.cn.
Chaogang YaoJilin Provincial Key Laboratory of Animal Embryo Engineering, College of Animal Sciences, Jilin University, Changchun 130062, China. yaocg13@mails.jlu.edu.cn.ORCID 0000-0003-3855-9056
Mengjing LiJilin Provincial Key Laboratory of Animal Embryo Engineering, College of Animal Sciences, Jilin University, Changchun 130062, China. mjli18@mails.jlu.edu.cn.
Wenni YouJilin Provincial Key Laboratory of Animal Embryo Engineering, College of Animal Sciences, Jilin University, Changchun 130062, China. youwn18@mails.jlu.edu.cn.
Qiushuang WangPublic Computer Education and Research Center, Jilin University, Changchun 130062, China. wqs@jlu.edu.cn.
Hao YuJilin Provincial Key Laboratory of Animal Embryo Engineering, College of Animal Sciences, Jilin University, Changchun 130062, China. yu_hao@jlu.edu.cn.ORCID 0000-0002-2833-6441
Jilin University · CN

Funding

the Program for "Changjiang Scholars" and Innovative Research Team in University No.IRT_16R32the Program for JLU Science and Technology Innovative Research Team 2017TD-28This work was supported by Special Funds for Cultivation and Breeding of New Transgenic Organisms No.2016ZX08006001
6 · The paper itself

Abstract

Myostatin (MSTN) is a member of the TGF-β superfamily that negatively regulates skeletal muscle growth and differentiation. However, the mechanism by which complete MSTN deletion limits excessive proliferation of muscle cells remains unclear. In this study, we knocked out MSTN in mouse myoblast lines using a Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR/Cas9) system and sequenced the mRNA and miRNA transcriptomes. The results show that complete loss of MSTN upregulates seven miRNAs targeting an interaction network composed of 28 downregulated genes, including

Indexed as

AnimalsCell LineComputational BiologyGene Expression ProfilingGene Expression RegulationGene Knockout TechniquesGene OrderGene Regulatory NetworksGenetic VectorsMiceMicroRNAsMolecular Sequence AnnotationMuscle CellsMyostatinReproducibility of ResultsRNA InterferenceMicroRNAsMyostatinRNA, MessengerC2C12miRNA-seqMSTNRMSRNA-seqtranscriptomics

Identifiers

PMID30717351
PMCPMC6386905
OpenAlexW2914594322

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.