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| Status |
Public on Sep 26, 2021 |
| Title |
Identification of Jmjd2a KO regulated genes in the mouse hearts |
| Organism |
Mus musculus |
| Experiment type |
Expression profiling by array
|
| Summary |
Cardiac hypertrophy and failure are accompanied by a reprogramming of gene expression that involves transcription factors and chromatin remodeling enzymes. Little is known about the role of histone methylation and demethylation in this process. To understand the role of JMJD2A, a trimethyl demethylase for histone 3 lysine 9 and 36, in cardiac hypertrophy, we generated heart specific JMJD2A deletion (JMJD2A hKO) and overexpression (JMJD2A-Tg) mouse lines. JMJD2A hKO and JMJD2A-Tg mice are viable and have no overt baseline phenotype. However, they have altered responses to cardiac stresses.
While inactivation of JMJD2A in hKO mice resulted in an attenuated hypertrophic response to transverse aortic constriction (TAC)-induced pressure overload compared to that of control littermates, JMJD2A-Tg mice have exacerbated cardiac hypertrophy after TAC.
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| Overall design |
Jmj2a KO
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| |
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| Contributor(s) |
Liu Z, Zhang Q |
| Citation missing |
Has this study been published? Please login to update or notify GEO. |
| Submission date |
Mar 25, 2021 |
| Last update date |
Sep 28, 2021 |
| Contact name |
zhi-ping liu |
| E-mail(s) |
zhi-ping.liu@utsouthwestern.edu
|
| Phone |
214-648-1485
|
| Organization name |
ut southwestern
|
| Department |
internal medicine
|
| Lab |
Liu
|
| Street address |
6000 Harry Hines Blvd
|
| City |
Dalals |
| State/province |
TX |
| ZIP/Postal code |
75390 |
| Country |
USA |
| |
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| Platforms (1) |
| GPL6887 |
Illumina MouseWG-6 v2.0 expression beadchip |
|
| Samples (6)
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| Relations |
| BioProject |
PRJNA717262 |
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