Search results for the GEO ID: GSE8199  |
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GSM ID | GPL ID |
Select for analysis |
Title |
Source name |
Description |
Characteristics |
GSM202772 | GPL1261 |
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E18.5 ERRg +/+ heart, biological rep 1
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3 ERRg WT E18.5 male cadiac ventricles
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mixed background e18.5 male cardiac ventricle
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no additional information
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GSM202773 | GPL1261 |
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E18.5 ERRg +/+ heart, biological rep 2
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3 ERRg WT E18.5 male cadiac ventricles
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mixed background e18.5 male cardiac ventricle
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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
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GSM202774 | GPL1261 |
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E18.5 ERRg +/+ heart, biological rep 3
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3 ERRg WT E18.5 male cadiac ventricles
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mixed background e18.5 male cardiac ventricle
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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
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GSM202775 | GPL1261 |
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E18.5 ERRg +/- heart, biological rep 1
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3 ERRg HET E18.5 male cadiac ventricles
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mixed background e18.5 male cardiac ventricle
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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
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GSM202776 | GPL1261 |
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E18.5 ERRg +/- heart, biological rep 2
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3 ERRg HET E18.5 male cadiac ventricles
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mixed background e18.5 male cardiac ventricle
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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
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GSM202777 | GPL1261 |
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E18.5 ERRg +/- heart, biological rep 3
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3 ERRg HET E18.5 male cadiac ventricles
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mixed background e18.5 male cardiac ventricle
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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
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GSM202778 | GPL1261 |
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E18.5 ERRg -/- heart, biological rep 1
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3 ERRg KO E18.5 male cadiac ventricles
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mixed background e18.5 male cardiac ventricle
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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
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GSM202779 | GPL1261 |
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E18.5 ERRg -/- heart, biological rep 2
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3 ERRg KO E18.5 male cadiac ventricles
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mixed background e18.5 male cardiac ventricle
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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
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GSM202780 | GPL1261 |
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E18.5 ERRg -/- heart, biological rep 3
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3 ERRg KO E18.5 male cadiac ventricles
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mixed background e18.5 male cardiac ventricle
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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
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