Evidence map›Paper›PMID 34752933›Full record

ArticleCellular signalling2022

Dyrk1b promotes autophagy during skeletal muscle differentiation by upregulating 4e-bp1.

Neha Bhat, Anand Narayanan, Mohsen Fathzadeh, Kanan Shah, Mehdi Dianatpour, Maen D Abou Ziki, Arya Mani

Open access · greenAbstract read
In one paragraph

Article in Cellular signalling, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.0field-weighted citation impact, top 21% 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

8 citing papers in PubMed, 8 citations in OpenAlex.

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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 2 institutions in 2 countries.

Neha BhatCardiovascular Research Center, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06520, USA.
Anand NarayananCardiovascular Research Center, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06520, USA.
Mohsen FathzadehCardiovascular Research Center, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06520, USA.
Kanan ShahCardiovascular Research Center, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06520, USA.
Mehdi DianatpourDepartment of Medical Genetics, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran; Stem Cells Technology Research Center, Shiraz University of Medical Sciences, Shiraz, Iran.
Maen D Abou ZikiCardiovascular Research Center, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06520, USA.
Arya ManiCardiovascular Research Center, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06520, USA; Department of Genetics, Yale School of Medicine, New Haven, CT 06511, USA. Electronic address: arya.mani@yale.edu.
Yale University · USShiraz University of Medical Sciences · IR

Funding

The Identification and characterization of genetic variants underlying cardiovascular diseasesR35HL135767 · NHLBI · YALE UNIVERSITY · PI MANI, ARYA · 2017 to 2023
$7.0M
NHLBI NIH HHS R35 HL135767
6 · The paper itself

Abstract

Rare gain of function mutations in the gene encoding Dyrk1b, a key regulator of skeletal muscle differentiation, have been associated with sarcopenic obesity (SO) and metabolic syndrome (MetS) in humans. So far, the global gene networks regulated by Dyrk1b during myofiber differentiation have remained elusive. Here, we have performed untargeted proteomics to determine Dyrk1b-dependent gene-network in differentiated C2C12 myofibers. This analysis led to identification of translational inhibitor, 4e-bp1 as a post-transcriptional target of Dyrk1b in C2C12 cells. Accordingly, CRISPR/Cas9 mediated knockout of Dyrk1b in zebrafish identified 4e-bp1 as a downstream target of Dyrk1b in-vivo. The Dyrk1b knockout zebrafish embryos exhibited markedly reduced myosin heavy chain 1 expression in poorly developed myotomes and were embryonic lethal. Using knockdown and overexpression approaches in C2C12 cells, we found that 4e-bp1 enhances autophagy and mediates the effects of Dyrk1b on skeletal muscle differentiation. Dyrk1b

Indexed as

AutophagyPhosphoproteinsProtein Serine-Threonine KinasesProtein-Tyrosine KinasesZebrafishAnimalsCell Cycle ProteinsDyrk KinasesMuscle DevelopmentMuscle, SkeletalPhosphorylationZebrafish ProteinsCell Cycle ProteinsDyrk KinasesPhosphoproteinsProtein Serine-Threonine KinasesProtein-Tyrosine KinasesZebrafish Proteins4e-bp1dyrk1bMyogenesisSarcopenic obesity

Identifiers

PMID34752933
PMCPMC8712395
OpenAlexW3213270321

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.