Evidence map›Paper›PMID 34329593›Full record

ArticleStem cell reports2021

A BMP4-p38 MAPK signaling axis controls ISL1 protein stability and activity during cardiogenesis.

Yanyan Jing, Yonggang Ren, Hagen Roland Witzel, Gergana Dobreva

Open access · goldAbstract read
In one paragraph

Article in Stem cell reports, 2021. 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
1.2field-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

9 citing papers in PubMed, 13 citations in OpenAlex.

  1. Review
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  8. Review
  9. Spotlight on Isl1: A Key Player in Cardiovascular Development and Diseases.Frontiers in cell and developmental biology · 2021
    Review
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

4 authors at 2 institutions in 1 country.

Yanyan JingDepartment of Anatomy and Developmental Biology, European Center for Angioscience (ECAS), Medical Faculty Mannheim, Heidelberg University, Ludolf-Krehl-Street 7-11, 68167 Mannheim, Germany; Max-Planck-Institute for Heart and Lung Research, Bad Nauheim, Germany.
Yonggang RenDepartment of Anatomy and Developmental Biology, European Center for Angioscience (ECAS), Medical Faculty Mannheim, Heidelberg University, Ludolf-Krehl-Street 7-11, 68167 Mannheim, Germany; Max-Planck-Institute for Heart and Lung Research, Bad Nauheim, Germany; German Centre for Cardiovascular Research (DZHK), Partner Site Heidelberg/Mannheim, Mannheim, Germany.
Hagen Roland WitzelMax-Planck-Institute for Heart and Lung Research, Bad Nauheim, Germany; Present address: Institute of Pathology, University Medical Center Mainz, Mainz, Germany.
Gergana DobrevaDepartment of Anatomy and Developmental Biology, European Center for Angioscience (ECAS), Medical Faculty Mannheim, Heidelberg University, Ludolf-Krehl-Street 7-11, 68167 Mannheim, Germany; Max-Planck-Institute for Heart and Lung Research, Bad Nauheim, Germany; German Centre for Cardiovascular Research (DZHK), Partner Site Heidelberg/Mannheim, Mannheim, Germany. Electronic address: gergana.dobreva@medma.uni-heidelberg.de.
Heidelberg University · DEJohannes Gutenberg University Mainz · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

During development, cells respond rapidly to intra- and intercellular signals, which induce signaling cascades regulating the activity of transcription factors at the transcriptional and/or post-translational level. The transcription factor ISL1 plays a key role in second heart field development and cardiac differentiation, and its mRNA levels are tightly regulated during cardiogenesis. Here, we show that a BMP-p38 MAPK signaling axis controls ISL1 protein function at the post-translational level. BMP-mediated activation of p38 MAPK leads to ISL1 phosphorylation at S269 by p38, which prevents ISL1 degradation and ensures its transcriptional activity during cardiogenesis. Interfering with p38 MAPK signaling leads to the degradation of ISL1 by the proteasome, resulting in defects in cardiomyocyte differentiation and impaired zebrafish and mouse heart morphogenesis and function. Given the critical role of the tight control of ISL1 activity during cardiac lineage diversification, modulation of BMP4-p38 MAPK signaling could direct differentiation into specific cardiac cell subpopulations.

Indexed as

Signal TransductionAnimalsAnimals, Genetically ModifiedBone Morphogenetic Protein 4Cell DifferentiationGene Expression Regulation, DevelopmentalHeartLIM-Homeodomain ProteinsMiceMice, KnockoutMyocardiumNIH 3T3 CellsOrganogenesisp38 Mitogen-Activated Protein KinasesProtein StabilityStem CellsBone Morphogenetic Protein 4insulin gene enhancer binding protein Isl-1LIM-Homeodomain Proteinsp38 Mitogen-Activated Protein KinasesTranscription FactorsBMP signalingcardiac progenitor cellscardiomyocyte differentiationheart developmentISL1p38 MAPKprotein phosphorylation

Identifiers

PMID34329593
PMCPMC8365108
OpenAlexW3185269065

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.