Evidence map›Paper›PMID 28803986›Full record

ArticleBiochemical and biophysical research communications2017

Ubiquitin C-Terminal Hydrolase L1 regulates myoblast proliferation and differentiation.

Hongbo Gao, Sigurd Hartnett, Yifan Li

Abstract read
In one paragraph

Article in Biochemical and biophysical research communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

16 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Blockage of UCHL1 activity attenuates cardiac remodeling in spontaneously hypertensive rats.Hypertension research : official journal of the Japanese Society of Hypertension · 2020
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Skeletal muscle secretion of IL-6 is muscle type specific: Ex vivo evidence.Biochemical and biophysical research communications · 2018
    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

3 authors at 1 institution in 1 country.

Hongbo GaoDivision of Basic Biomedical Sciences, Sanford School of Medicine, University of South Dakota, 414 East Clark Street, Lee Med Building, Vermillion, SD 57069, USA.
Sigurd HartnettDivision of Basic Biomedical Sciences, Sanford School of Medicine, University of South Dakota, 414 East Clark Street, Lee Med Building, Vermillion, SD 57069, USA.
Yifan LiDivision of Basic Biomedical Sciences, Sanford School of Medicine, University of South Dakota, 414 East Clark Street, Lee Med Building, Vermillion, SD 57069, USA. Electronic address: yifan.li@usd.edu.
University of South Dakota · US

Funding

PARASYMPATHETIC DYSFUNCTION IN OBESITY: EFFECT OF CHOLESTEROL ON VAChTR15HL118696 · NHLBI · UNIVERSITY OF SOUTH DAKOTA · PI LI, YIFAN · 2013 to 2013
$409k
Induction of ACE2 expression in skeletal muscles in aged mice by transcutaneous electrical stimulationR03AG051926 · NIA · UNIVERSITY OF SOUTH DAKOTA · PI LI, YIFAN · 2016 to 2017
$145k
NHLBI NIH HHS R15 HL118696NIA NIH HHS R03 AG051926
6 · The paper itself

Abstract

Skeletal muscles are dynamic tissues that possess regenerative abilities, which require multiple processes and regulatory factors. Ubiquitin C-Terminal Hydrolase L1 (UCHL1), which is primarily expressed in neuronal tissues, was upregulated in skeletal muscles in disease conditions but its functional role in skeletal muscles is unknown. Using mouse myoblast cells C2C12 as an in vitro model, this study reported that UCHL1 elicits different regulation in myoblast cell proliferation and differentiation. We first observed that UCHL1 protein level was continuously declined during cell differentiation. Gene knockdown of UCHL1 by siRNA resulted in a significant decrease in cell proliferation but marked acceleration of cell differentiation and myotube formation. Meanwhile, UCHL1 gene knockdown upregulated myogenic factors myoD and Myogenin (MyoG). In mice, UCHL1 was significantly upregulated in denervated skeletal muscle. Overall, these novel data suggest that UCHL1 may play a role in myogenesis by promoting myoblast proliferation and inhibiting differentiation.

Indexed as

Cell DifferentiationCell ProliferationAnimalsCells, CulturedMiceMyoblastsUbiquitin ThiolesteraseUbiquitin ThiolesteraseUchl1 protein, mouseDifferentiationMyoblastMyogeninProliferationUbiquitin C-Terminal Hydrolase L1

Identifiers

PMID28803986
PMCPMC5584584
OpenAlexW2744683708

What OpenQuestion holds

Textmetadata
LicenceTDM
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.