Evidence map›Paper›PMID 37239128›Full record

ArticleBiomedicines2023

Myogenesis in C2C12 Cells Requires Phosphorylation of ATF6α by p38 MAPK.

Valentina Pagliara, Giuseppina Amodio, Vincenzo Vestuto, Silvia Franceschelli, Nicola Antonino Russo, Vittorio Cirillo, Giovanna Mottola, Paolo Remondelli, Ornella Moltedo

Open access · goldAbstract read
In one paragraph

Article in Biomedicines, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
3.1field-weighted citation impact, top 9% 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

9 citing papers in PubMed, 15 citations in OpenAlex.

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  9. Anticancer Therapies Based on Oxidative Damage:Antioxidants (Basel, Switzerland) · 2024
    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 3 institutions in 2 countries.

Valentina PagliaraDepartment of Medicine, Surgery and Dentistry "Scuola Medica Salernitana", University of Salerno, Via Salvador Allende, 84081 Baronissi, Italy.ORCID 0000-0001-9320-6080
Giuseppina AmodioDepartment of Medicine, Surgery and Dentistry "Scuola Medica Salernitana", University of Salerno, Via Salvador Allende, 84081 Baronissi, Italy.ORCID 0000-0001-8971-8964
Vincenzo VestutoDepartment of Pharmacy, University of Salerno, Via Giovanni Paolo II, 84084 Fisciano, Italy.ORCID 0000-0002-3603-5526
Silvia FranceschelliDepartment of Pharmacy, University of Salerno, Via Giovanni Paolo II, 84084 Fisciano, Italy.ORCID 0000-0001-7412-7918
Nicola Antonino RussoBiogem, Istituto di Biologia e Genetica Molecolare, Via Camporeale, 83031 Ariano Irpino, Italy.ORCID 0000-0001-5773-0803
Vittorio CirilloDepartment of Pharmacy, University of Salerno, Via Giovanni Paolo II, 84084 Fisciano, Italy.
Giovanna MottolaCentre de Recherche en Cardiovasculaire et Nutrition (C2VN) (AMU-INSERM 1263-INRAE 1260), Aix Marseille Université, Campus Timone, 27 Bd. Jean Moulin, 13005 Marseille, France.ORCID 0000-0002-7541-0472
Paolo RemondelliDepartment of Medicine, Surgery and Dentistry "Scuola Medica Salernitana", University of Salerno, Via Salvador Allende, 84081 Baronissi, Italy.ORCID 0000-0002-3698-3497
Ornella MoltedoDepartment of Pharmacy, University of Salerno, Via Giovanni Paolo II, 84084 Fisciano, Italy.ORCID 0000-0002-0526-2152
University of Salerno · ITBiogem · ITInserm · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Activating transcription factor 6α (ATF6α) is an endoplasmic reticulum protein known to participate in unfolded protein response (UPR) during ER stress in mammals. Herein, we show that in mouse C2C12 myoblasts induced to differentiate, ATF6α is the only pathway of the UPR activated. ATF6α stimulation is p38 MAPK-dependent, as revealed by the use of the inhibitor SB203580, which halts myotube formation and, at the same time, impairs trafficking of ATF6α, which accumulates at the cis-Golgi without being processed in the p50 transcriptional active form. To further evaluate the role of ATF6α, we knocked out the ATF6α gene, thus inhibiting the C2C12 myoblast from undergoing myogenesis, and this occurred independently from p38 MAPK activity. The expression of exogenous ATF6α in knocked-out ATF6α cells recover myogenesis, whereas the expression of an ATF6α mutant in the p38 MAPK phosphorylation site (T166) was not able to regain myogenesis. Genetic ablation of ATF6α also prevents the exit from the cell cycle, which is essential for muscle differentiation. Furthermore, when we inhibited differentiation by the use of dexamethasone in C2C12 cells, we found inactivation of p38 MAPK and, consequently, loss of ATF6α activity. All these findings suggest that the p-p38 MAPK/ATF6α axis, in pathophysiological conditions, regulates myogenesis by promoting the exit from the cell cycle, an essential step to start myoblasts differentiation.

Indexed as

activating transcription factor 6 α (ATF6α)C2C12myogenesisp38 Mitogen-Activated Protein Kinase (MAPK)unfolded protein response

Identifiers

PMID37239128
PMCPMC10216283
OpenAlexW4377041848

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.