|
| Status |
Public on Jul 10, 2007 |
| Title |
E18.5 ERRg +/- heart, biological rep 2 |
| Sample type |
RNA |
| |
|
| Source name |
3 ERRg HET E18.5 male cadiac ventricles
|
| Organism |
Mus musculus |
| Characteristics |
mixed background e18.5 male cardiac ventricle
|
| Treatment protocol |
Stored -20degrees C in RNALater (Qiagen)
|
| Growth protocol |
E18.5 male mouse cardiac ventricle
|
| Extracted molecule |
total RNA |
| Extraction protocol |
RNeasy of total RNA was performed according to the manufacturer's instructions (Qiagen). Disrupted by passage through hypedermic needle.
|
| Label |
biotin
|
| Label protocol |
Biotinylated cRNA were prepared according to the standard Affymetrix protocol from 6 ug total RNA (Expression Analysis Technical Manual, 2001, Affymetrix).
|
| |
|
| Hybridization protocol |
Following fragmentation, 10 ug of cRNA were hybridized for 16 hr at 45C on GeneChip Mouse Genome 430 2.0 Array. GeneChips were washed and stained in the Affymetrix Fluidics Station 400.
|
| Scan protocol |
GeneChips were scanned using the Hewlett-Packard GeneArray Scanner G2500A.
|
| Description |
Title: ERRγ Directs and Maintains the Transition to Oxidative Metabolism in the Post-Natal Heart
Abstract: At birth the heart undergoes a critical metabolic switch to transition from a predominant dependence on carbohydrates during fetal life to a greater dependence on postnatal oxidative metabolism. This remains the principle metabolic state throughout life; although pathologic conditions such as heart failure and cardiac hypertrophy reactivate components of the fetal genetic program to increase carbohydrate utilization. Disruption of the ERRγ gene, which is expressed at high levels in the fetal and postnatal mouse heart, blocks this switch resulting in lactatemia, electrocardiographic (ECG) abnormalities and death during the first week of life. Genomic ChIP-on-chip and expression analysis at E18.5 clearly identifies ERRγ as both a direct and indirect regulator of a nuclear-encoded mitochondrial genetic network that coordinates the postnatal metabolic transition. These findings reveal an unexpected and essential molecular genetic component of the oxidative metabolic gene program in the heart and highlight ERRγ in the study of cardiac hypertrophy and failure.
Key Words: ChIP-on-chip, electrocardiography, fetal gene program, OXPHOS, PGC-1α, sodium current
|
| Data processing |
The data were analyzed with Microarray Suite version 5.0 (MAS 5.0) using Affymetrix default analysis settings and global scaling as normalization method. The trimmed mean target intensity of each array was arbitrarily set to 100.
|
| |
|
| Submission date |
Jun 20, 2007 |
| Last update date |
Aug 28, 2018 |
| Contact name |
Ronald M Evans |
| E-mail(s) |
evans@salk.edu
|
| Phone |
858-453-4100
|
| Organization name |
The Salk Institute for Biological Studies
|
| Department |
Howard Hughes Medical Institute
|
| Lab |
Gene Expression Laboratory
|
| Street address |
10010 North Torrey Pines
|
| City |
La Jolla |
| State/province |
CA |
| ZIP/Postal code |
92037 |
| Country |
USA |
| |
|
| Platform ID |
GPL1261 |
| Series (1) |
| GSE8199 |
E18.5 Estrogen-related Receptor gamma Knockout Mouse Heart |
|
| Relations |
| Reanalyzed by |
GSE119085 |
