Evidence map›Paper›PMID 30061109›Full record

ArticleThe Journal of cell biology2018

GSK3-β promotes calpain-1-mediated desmin filament depolymerization and myofibril loss in atrophy.

Dina Aweida, Inga Rudesky, Alexandra Volodin, Eitan Shimko, Shenhav Cohen

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

42 citing papers in PubMed, 67 citations in OpenAlex.

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  5. The Approximate Subcutaneous LDMolecules (Basel, Switzerland) · 2026
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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

5 authors at 1 institution in 1 country.

Dina AweidaFaculty of Biology, Technion Institute of Technology, Haifa, Israel.
Inga RudeskyFaculty of Biology, Technion Institute of Technology, Haifa, Israel.
Alexandra VolodinFaculty of Biology, Technion Institute of Technology, Haifa, Israel.
Eitan ShimkoFaculty of Biology, Technion Institute of Technology, Haifa, Israel.ORCID 0000-0001-6812-8631
Shenhav CohenFaculty of Biology, Technion Institute of Technology, Haifa, Israel shenhavc@technion.ac.il.ORCID 0000-0001-8307-466X
Technion – Israel Institute of Technology · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myofibril breakdown is a fundamental cause of muscle wasting and inevitable sequel of aging and disease. We demonstrated that myofibril loss requires depolymerization of the desmin cytoskeleton, which is activated by phosphorylation. Here, we developed a mass spectrometry-based kinase-trap assay and identified glycogen synthase kinase 3-β (GSK3-β) as responsible for desmin phosphorylation. GSK3-β inhibition in mice prevented desmin phosphorylation and depolymerization and blocked atrophy upon fasting or denervation. Desmin was phosphorylated by GSK3-β 3 d after denervation, but depolymerized only 4 d later when cytosolic Ca

Indexed as

Down-RegulationGene Expression Regulation, DevelopmentalAnimalsCalciumCalpainDesminGlycogen Synthase Kinase 3 betaMaleMiceMuscular AtrophyMyofibrilsPhosphorylationCalciumCalpainCapn1 protein, mouseDesminGlycogen Synthase Kinase 3 betaGsk3b protein, mouse

Identifiers

PMID30061109
PMCPMC6168250
OpenAlexW2885199266

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.