Expression of Non-acetylatable H2A.Z in Myoblast Cells Blocks Myoblast Differentiation through Disruption of MyoD Expression
Published 2015 View Full Article
- Home
- Publications
- Publication Search
- Publication Details
Title
Expression of Non-acetylatable H2A.Z in Myoblast Cells Blocks Myoblast Differentiation through Disruption of MyoD Expression
Authors
Keywords
-
Journal
JOURNAL OF BIOLOGICAL CHEMISTRY
Volume 290, Issue 21, Pages 13234-13249
Publisher
American Society for Biochemistry & Molecular Biology (ASBMB)
Online
2015-04-04
DOI
10.1074/jbc.m114.595462
References
Ask authors/readers for more resources
Related references
Note: Only part of the references are listed.- Chd2 interacts with H3.3 to determine myogenic cell fate
- (2012) Akihito Harada et al. EMBO JOURNAL
- A Combination of H2A.Z and H4 Acetylation Recruits Brd2 to Chromatin during Transcriptional Activation
- (2012) Ryan Draker et al. PLoS Genetics
- H2A.Z landscapes and dual modifications in pluripotent and multipotent stem cells underlie complex genome regulatory functions
- (2012) Manching Ku et al. GENOME BIOLOGY
- Sphingosine kinase/sphingosine 1-phosphate axis: a new player for insulin-like growth factor-1-induced myoblast differentiation
- (2012) Caterina Bernacchioni et al. Skeletal Muscle
- Polycomb-Repressed Genes Have Permissive Enhancers that Initiate Reprogramming
- (2011) Phillippa C. Taberlay et al. CELL
- USP10 deubiquitylates the histone variant H2A.Z and both are required for androgen receptor-mediated gene activation
- (2011) Ryan Draker et al. NUCLEIC ACIDS RESEARCH
- Essential role of p18Hamlet/SRCAP-mediated histone H2A.Z chromatin incorporation in muscle differentiation
- (2010) Ana Cuadrado et al. EMBO JOURNAL
- A unique chromatin signature uncovers early developmental enhancers in humans
- (2010) Alvaro Rada-Iglesias et al. NATURE
- Identification and characterization of the two isoforms of the vertebrate H2A.Z histone variant
- (2010) Ryo Matsuda et al. NUCLEIC ACIDS RESEARCH
- Myogenic transcriptional activation of MyoD mediated by replication-independent histone deposition
- (2010) J.-H. Yang et al. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
- Loss of human Greatwall results in G2 arrest and multiple mitotic defects due to deregulation of the cyclin B-Cdc2/PP2A balance
- (2010) Andrew Burgess et al. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
- Histone H3K27ac separates active from poised enhancers and predicts developmental state
- (2010) M. P. Creyghton et al. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
- Acetylation of Vertebrate H2A.Z and Its Effect on the Structure of the Nucleosome
- (2009) Toyotaka Ishibashi et al. BIOCHEMISTRY
- Transcriptional and epigenetic functions of histone variant H2A.ZThis paper is one of a selection of papers published in this Special Issue, entitled CSBMCB’s 51st Annual Meeting – Epigenetics and Chromatin Dynamics, and has undergone the Journal’s usual peer review process.
- (2009) Ryan Draker et al. Biochemistry and Cell Biology
- Characterization of the histone H2A.Z-1 and H2A.Z-2 isoforms in vertebrates
- (2009) Deanna Dryhurst et al. BMC BIOLOGY
- Role of the Histone Variant H2A.Z/Htz1p in TBP Recruitment, Chromatin Dynamics, and Regulated Expression of Oleate-Responsive Genes
- (2009) Y. Wan et al. MOLECULAR AND CELLULAR BIOLOGY
- H3.3/H2A.Z double variant–containing nucleosomes mark 'nucleosome-free regions' of active promoters and other regulatory regions
- (2009) Chunyuan Jin et al. NATURE GENETICS
- H2AZ Is Enriched at Polycomb Complex Target Genes in ES Cells and Is Necessary for Lineage Commitment
- (2008) Menno P. Creyghton et al. CELL
- The Genomic Distribution and Function of Histone Variant HTZ-1 during C. elegans Embryogenesis
- (2008) Christina M. Whittle et al. PLoS Genetics
Discover Peeref hubs
Discuss science. Find collaborators. Network.
Join a conversationPublish scientific posters with Peeref
Peeref publishes scientific posters from all research disciplines. Our Diamond Open Access policy means free access to content and no publication fees for authors.
Learn More