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Article

Cardiac deletion of Smyd2 is dispensable for mouse heart development.

PloS one - 17 Mar 2010

Diehl Florian, Brown Mark A, van Amerongen Machteld J, Novoyatleva Tatyana, Wietelmann Astrid, Harriss June, Ferrazzi Fulvia, Böttger Thomas, Harvey Richard P, Tucker Philip W, Engel Felix B

Abstract excerpt

Chromatin modifying enzymes play a critical role in cardiac differentiation. Previously, it has been shown that the targeted deletion of the histone methyltransferase, Smyd1, the founding member of the SET and MYND domain containing (Smyd) family, interferes with cardiomyocyte maturation and proper formation of the right heart ventricle. The highly related paralogue, Smyd2 is a histone 3 lysine 4- and lysine...

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Share to Gene Deletion
Share to Gene Expression Regulation, Developmental

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Histone-Lysine N-Methyltransferase

Share to Myocardium

Share to Rats, Sprague-Dawley

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Source

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Identifiers

PMID: 20305823
DOI: 10.1371/journal.pone.0009748
PMCID: PMC2840034

Genes

HELZ
SET

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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