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| Status |
Public on Jan 31, 2024 |
| Title |
Mechanism of RUNX1 targeted AKT3 regulated alveolar procoagulant fibrinolytic inhibition in ARDS |
| Organism |
Rattus norvegicus |
| Experiment type |
Genome binding/occupancy profiling by high throughput sequencing
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| Summary |
Acute respiratory distress syndrome (ARDS) is an acute inflammatory lung injury and one of the serious life-threatening forms of respiratory failure. Alveolar procoagulation and fibrinolytic inhibition constitute the core part of the pathophysiology of ARDS, RUNX1 plays an important role in this pathogenesis. We screened for AKT3, the target gene of RUNX1, using CHIP-seq and verified its binding target by a dual luciferase assay.
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| Overall design |
RLE-6TN cells were transfected with LV-RUNX1 to increase the expression level of RUNX1
We screened for AKT3, the target gene of RUNX1, using CHIP-seq and verified its binding target by a dual luciferase assay.
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| Contributor(s) |
Xiao C |
| Citation(s) |
38267920 |
| |
| Submission date |
Jul 06, 2023 |
| Last update date |
Jan 31, 2024 |
| Contact name |
Tongjian Zhao |
| Organization name |
School of Pharmaceutical Sciences, Jilin University
|
| Street address |
1266 Fujin Road
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| City |
Changchun |
| ZIP/Postal code |
130021 |
| Country |
China |
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| Platforms (1) |
| GPL25947 |
Illumina NovaSeq 6000 (Rattus norvegicus) |
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| Samples (2) |
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| Relations |
| BioProject |
PRJNA992179 |
