Cardiac deletion of Smyd2 is dispensable for mouse heart development
about
SMYD proteins: key regulators in skeletal and cardiac muscle development and functionHistone methylations in heart development, congenital and adult heart diseasesCrystal Structures of Histone and p53 Methyltransferase SmyD2 Reveal a Conformational Flexibility of the Autoinhibitory C-Terminal DomainStructure of Human SMYD2 Protein Reveals the Basis of p53 Tumor Suppressor MethylationThe putative RNA helicase HELZ promotes cell proliferation, translation initiation and ribosomal protein S6 phosphorylationThe selective activation of p53 target genes regulated by SMYD2 in BIX-01294 induced autophagy-related cell deathLysine methyltransferase Smyd2 suppresses p53-dependent cardiomyocyte apoptosis.Epigenetic regulation of cardiac myocyte differentiation.Chromatin remodeling in cardiovascular development and physiology.Targeting protein lysine methylation and demethylation in cancers.LLY-507, a Cell-active, Potent, and Selective Inhibitor of Protein-lysine Methyltransferase SMYD2.Smyd2 controls cytoplasmic lysine methylation of Hsp90 and myofilament organization.RB1 methylation by SMYD2 enhances cell cycle progression through an increase of RB1 phosphorylation.Lysine Methylation of the Valosin-Containing Protein (VCP) Is Dispensable for Development and Survival of Mice.Coordination of stress signals by the lysine methyltransferase SMYD2 promotes pancreatic cancer.SET/MYND Lysine Methyltransferases Regulate Gene Transcription and Protein Activity.Understanding the language of Lys36 methylation at histone H3.Smyd2 is a Myc-regulated gene critical for MLL-AF9 induced leukemogenesis.Histone H3 lysine 4 methyltransferases and demethylases in self-renewal and differentiation of stem cells.Chromatin modifications remodel cardiac gene expression.The chromatin-binding protein Smyd1 restricts adult mammalian heart growth.Analysis of the microRNA signature in left atrium from patients with valvular heart disease reveals their implications in atrial fibrillation.Selective modulation of local linkages between active transcription and oxidative demethylation activity shapes cardiomyocyte-specific gene-body epigenetic status in mice.SMYD2 glutathionylation contributes to degradation of sarcomeric proteinsThe roles of SMYD4 in epigenetic regulation of cardiac development in zebrafish
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P2860
Cardiac deletion of Smyd2 is dispensable for mouse heart development
description
2010 թուականի Մարտին հրատարակուած գիտական յօդուած
@hyw
2010 թվականի մարտին հրատարակված գիտական հոդված
@hy
article publié dans la revue scientifique PLoS ONE
@fr
artículu científicu espublizáu en 2010
@ast
im März 2010 veröffentlichter wissenschaftlicher Artikel
@de
scientific journal article
@en
vedecký článok (publikovaný 2010/03/17)
@sk
vědecký článek publikovaný v roce 2010
@cs
wetenschappelijk artikel (gepubliceerd op 2010/03/17)
@nl
наукова стаття, опублікована в березні 2010
@uk
name
Cardiac deletion of Smyd2 is dispensable for mouse heart development
@ast
Cardiac deletion of Smyd2 is dispensable for mouse heart development
@en
Cardiac deletion of Smyd2 is dispensable for mouse heart development
@nl
type
label
Cardiac deletion of Smyd2 is dispensable for mouse heart development
@ast
Cardiac deletion of Smyd2 is dispensable for mouse heart development
@en
Cardiac deletion of Smyd2 is dispensable for mouse heart development
@nl
prefLabel
Cardiac deletion of Smyd2 is dispensable for mouse heart development
@ast
Cardiac deletion of Smyd2 is dispensable for mouse heart development
@en
Cardiac deletion of Smyd2 is dispensable for mouse heart development
@nl
P2093
P2860
P50
P1433
P1476
Cardiac deletion of Smyd2 is dispensable for mouse heart development
@en
P2093
Astrid Wietelmann
Florian Diehl
June Harriss
Machteld J van Amerongen
Mark A Brown
Philip W Tucker
Tatyana Novoyatleva
Thomas Böttger
P2860
P356
10.1371/JOURNAL.PONE.0009748
P407
P577
2010-03-17T00:00:00Z