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Status |
Public on Oct 10, 2018 |
Title |
Histone deacetylase 3 deletion in the embryonic heart at day E9.5 |
Organism |
Mus musculus |
Experiment type |
Expression profiling by array
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Summary |
Analysis of whole hearts from e9.5 embryos from Nkx2.5Cre; Hdac3f/f embryos and littermate controls. Results provide insight into gene programs regulated by Hdac3 in cardiac development. Progenitor cells require coordinated expression of lineage-specific genes to regulate differentiation into daughter cell types. Epigenetic regulators are ideally positioned to synchronize transcription of disparate genomic loci. Using cardiac development to model progenitor cell behavior, we demonstrate that Histone deacetylase 3 (Hdac3) functions in a deacetylase-independent manner to repress cardiac differentiation. Loss of Hdac3 promotes differentiation into cardiomyocytes by de-repressing a myocyte gene program.
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Overall design |
4 biological replicates of mutant vs 4 biological replicates of wild-type E9.5 microdissected hearts (3 pooled hearts per biological replicate)
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Contributor(s) |
Epstein JA, Gupta M, Morley MP |
Citation missing |
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Submission date |
Dec 12, 2014 |
Last update date |
Oct 10, 2018 |
Contact name |
Michael Patrick Morley |
E-mail(s) |
[email protected]
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Phone |
215-898-2026
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Organization name |
Perelman School of Medicine at the University of Pennsylvania
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Department |
Penn Cardiovascular Institute
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Street address |
3400 Civic Center Blvd, Bldg 421
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City |
Philadelphia |
State/province |
PA |
ZIP/Postal code |
19104 |
Country |
USA |
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Platforms (1) |
GPL10333 |
Agilent-026655 Whole Mouse Genome Microarray 4x44K v2 (Feature Number version) |
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Samples (4)
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This SubSeries is part of SuperSeries: |
GSE64149 |
Genome-nuclear lamina interactions regulate progenitor cell behavior during cardiac development |
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Relations |
BioProject |
PRJNA270256 |