Evidence map›Paper›PMID 21071677›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2010

skNAC, a Smyd1-interacting transcription factor, is involved in cardiac development and skeletal muscle growth and regeneration.

Chong Yon Park, Stephanie A Pierce, Morgan von Drehle, Kathryn N Ivey, Jayson A Morgan, Helen M Blau, Deepak Srivastava

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed, 1 pooled it
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

52 citing papers in PubMed, 1 synthesis or guideline pooled it, 83 citations in OpenAlex.

  1. Pooled it
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  8. The molecular mechanisms of cardiac development and related diseases.Signal transduction and targeted therapy · 2024
    Review
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  16. Skeletal Muscle Regeneration in Cardiotoxin-Induced Muscle Injury Models.International journal of molecular sciences · 2022
    Review
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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 3 institutions in 1 country.

Chong Yon ParkDepartment of Pediatrics, Gladstone Institute of Cardiovascular Disease, University of California, San Francisco, CA 94158, USA.
Stephanie A Pierce
Morgan von Drehle
Kathryn N Ivey
Jayson A Morgan
Helen M Blau
Deepak Srivastava
University of California, San Francisco · USStanford University · USThe University of Texas Southwestern Medical Center · US

Funding

Basic and Translational Research iPSC-based hematologic and vascular therapiesU01HL100397 · NHLBI · STANFORD UNIVERSITY · PI COOKE, JOHN P · 2009 to 2015
$7.4M
Stem Cells for Brain and BrawnR01AG020961 · NIA · STANFORD UNIVERSITY · PI BLAU, HELEN M · 2002 to 2019
$5.0M
ACTIVATORS OF MUSCLE GENESR01AG009521 · NIA · STANFORD UNIVERSITY · PI BLAU, HELEN M · 1990 to 2014
$4.7M
EXTRAMULAR RESEARCH FACILITIES CONSTRUCTIONC06RR018928 · NCRR · J. DAVID GLADSTONE INSTITUTES · PI MAHLEY, ROBERT W. · 2003 to 2003
$2.1M
NCRR NIH HHS C06 RR018928NHLBI NIH HHS U01 HL100397NIA NIH HHS R01 AG009521NIA NIH HHS R01 AG020961
6 · The paper itself

Abstract

Cardiac and skeletal muscle development and maintenance require complex interactions between DNA-binding proteins and chromatin remodeling factors. We previously reported that Smyd1, a muscle-restricted histone methyltransferase, is essential for cardiogenesis and functions with a network of cardiac regulatory proteins. Here we show that the muscle-specific transcription factor skNAC is the major binding partner for Smyd1 in the developing heart. Targeted deletion of skNAC in mice resulted in partial embryonic lethality by embryonic day 12.5, with ventricular hypoplasia and decreased cardiomyocyte proliferation that were similar but less severe than in Smyd1 mutants. Expression of Irx4, a ventricle-specific transcription factor down-regulated in hearts lacking Smyd1, also depended on the presence of skNAC. Viable skNAC(-/-) adult mice had reduced postnatal skeletal muscle growth and impaired regenerative capacity after cardiotoxin-induced injury. Satellite cells isolated from skNAC(-/-) mice had impaired survival compared with wild-type littermate satellite cells. Our results indicate that skNAC plays a critical role in ventricular cardiomyocyte expansion and regulates postnatal skeletal muscle growth and regeneration in mice.

Indexed as

AnimalsAnimals, NewbornBody PatterningCell ProliferationDNA-Binding ProteinsEmbryo, MammalianGene Expression Regulation, DevelopmentalGene TargetingHeartHeart VentriclesMiceMolecular ChaperonesMuscle DevelopmentMuscle Fibers, SkeletalMuscle ProteinsMuscle, SkeletalDNA-Binding ProteinsMolecular ChaperonesMuscle Proteinsnascent-polypeptide-associated complexSmyd1 protein, mouseTranscription Factors

Identifiers

PMID21071677
PMCPMC2996447
OpenAlexW2168027209

What OpenQuestion holds

Textmetadata
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.