Evidence map›Paper›PMID 30850672›Full record

ArticleScientific reports2019

Carboxyl-terminal modulator protein regulates Akt signaling during skeletal muscle atrophy in vitro and a mouse model of amyotrophic lateral sclerosis.

Junmei Wang, Colin M E Fry, Chandler L Walker

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

12 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
  2. Review
  3. Skeletal muscle dysfunction in amyotrophic lateral sclerosis: a mitochondrial perspective and therapeutic approaches.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2024
    Review
  4. Roles of THEM4 in the Akt pathway: a double-edged sword.Journal of Zhejiang University. Science. B · 2024
    Review
  5. Targeting mitochondrial CaThe Journal of physiology · 2024
    Review
  6. Review
  7. Article
  8. Article
  9. Article
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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

3 authors at 3 institutions in 1 country.

Junmei WangDepartment of Biomedical and Applied Sciences, Indiana University School of Dentistry, Indianapolis, IN, 46202, USA.
Colin M E FryDepartment of Anatomy and Cell Biology, Indiana University School of Medicine, Indianapolis, IN, 46202, USA.
Chandler L WalkerDepartment of Biomedical and Applied Sciences, Indiana University School of Dentistry, Indianapolis, IN, 46202, USA. chalwalk@iu.edu.ORCID 0000-0002-8616-8263
Indiana University – Purdue University Indianapolis · USIndiana University School of MedicineRichard L. Roudebush VA Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Amyotrophic lateral sclerosis (ALS) is a progressive neuromuscular disease involving motor neuron death, paralysis and, ultimately, respiratory failure. Motor neuron dysfunction leads to target skeletal muscle atrophy involving dysregulation of downstream cell survival, growth and metabolic signaling. Decreased Akt activity is linked to muscle atrophy in ALS and is associated with increased atrophy gene expression. Unfortunately, the regulating mechanism of Akt activity in atrophic muscle remains unclear. Recent research indicates a role of carboxyl-terminal modulator protein (CTMP) in Akt-signaling related neurologic dysfunction and skeletal muscle metabolism. CTMP is known to bind and reduce Akt phosphorylation and activation. We hypothesized that CTMP expression might progressively increase in ALS skeletal muscle as the disease progresses, downregulating Akt activity. We found that CTMP protein expression significantly increased in hindlimb skeletal muscle in the mSOD1

Indexed as

Amyotrophic Lateral SclerosisAnimalsCarrier ProteinsCell LineDisease Models, AnimalGene Knockdown TechniquesHumansIn Vitro TechniquesMiceMice, Mutant StrainsModels, BiologicalMuscle, SkeletalMuscular AtrophyMutant ProteinsPalmitoyl-CoA HydrolasePhosphorylationCarrier ProteinsCTMP protein, mouseMutant ProteinsPalmitoyl-CoA HydrolaseProto-Oncogene Proteins c-aktRNA, Small InterferingSOD1 G93A proteinSod1 protein, mouseSuperoxide DismutaseSuperoxide Dismutase-1

Identifiers

PMID30850672
PMCPMC6408440
OpenAlexW2919981977

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.