Evidence map›Paper›PMID 32170063›Full record

ArticleNature communications2020

A signaling hub of insulin receptor, dystrophin glycoprotein complex and plakoglobin regulates muscle size.

Yara Eid Mutlak, Dina Aweida, Alexandra Volodin, Bar Ayalon, Nitsan Dahan, Anna Parnis, Shenhav Cohen

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.8field-weighted citation impact, top 5% 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

31 citing papers in PubMed, 47 citations in OpenAlex.

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  19. MicroRNAs in Dystrophinopathy.International journal of molecular sciences · 2022
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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

7 authors at 1 institution in 1 country.

Yara Eid Mutlak *Faculty of Biology, Technion Institute of Technology, Haifa, Israel.
Dina Aweida *Faculty of Biology, Technion Institute of Technology, Haifa, Israel.
Alexandra VolodinFaculty of Biology, Technion Institute of Technology, Haifa, Israel.
Bar AyalonFaculty of Biology, Technion Institute of Technology, Haifa, Israel.
Nitsan DahanFaculty of Biology, Technion Institute of Technology, Haifa, Israel.ORCID http://orcid.org/0000-0003-2021-050X
Anna ParnisFaculty of Biology, Technion Institute of Technology, Haifa, Israel.
Shenhav CohenFaculty of Biology, Technion Institute of Technology, Haifa, Israel. shenhavc@technion.ac.il.
Technion – Israel Institute of Technology · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Signaling through the insulin receptor governs central physiological functions related to cell growth and metabolism. Here we show by tandem native protein complex purification approach and super-resolution STED microscopy that insulin receptor activity requires association with the fundamental structural module in muscle, the dystrophin glycoprotein complex (DGC), and the desmosomal component plakoglobin (γ-catenin). The integrity of this high-molecular-mass assembly renders skeletal muscle susceptibility to insulin, because DGC-insulin receptor dissociation by plakoglobin downregulation reduces insulin signaling and causes atrophy. Furthermore, low insulin receptor activity in muscles from transgenic or fasted mice decreases plakoglobin-DGC-insulin receptor content on the plasma membrane, but not when plakoglobin is overexpressed. By masking β-dystroglycan LIR domains, plakoglobin prevents autophagic clearance of plakoglobin-DGC-insulin receptor co-assemblies and maintains their function. Our findings establish DGC as a signaling hub, and provide a possible mechanism for the insulin resistance in Duchenne Muscular Dystrophy, and for the cardiomyopathies seen with plakoglobin mutations.

Indexed as

Signal TransductionAnimalsAutophagyCell MembraneDisease Models, AnimalDystroglycansDystrophingamma CateninGlycoproteinsMaleMiceMice, TransgenicMuscle, SkeletalMuscular Dystrophy, DuchenneProtein DomainsReceptor, InsulinDystroglycansDystrophingamma CateninGlycoproteinsReceptor, Insulin

Identifiers

PMID32170063
PMCPMC7070008
OpenAlexW3012370260

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.