|
| Status |
Public on Sep 11, 2018 |
| Title |
Coronary artery disease genes SMAD3 and TCF21 promote opposing interactive genetic programs that regulate smooth muscle cell differentiation and disease risk |
| Organism |
Homo sapiens |
| Experiment type |
Expression profiling by high throughput sequencing
Genome binding/occupancy profiling by high throughput sequencing
Third-party reanalysis
|
| Summary |
This SuperSeries is composed of the SubSeries listed below.
|
| |
|
| Overall design |
Refer to individual Series
|
| |
|
| Citation(s) |
30307970 |
| |
| Submission date |
Jun 04, 2018 |
| Last update date |
May 01, 2023 |
| Contact name |
Thomas Quertermous |
| E-mail(s) |
tomq1@stanford.edu
|
| Phone |
650-723-5012
|
| Organization name |
Stanford University
|
| Department |
Medicine Cardiology
|
| Lab |
Quertermous
|
| Street address |
300 Pasteur Drive
|
| City |
Stanford |
| State/province |
CA |
| ZIP/Postal code |
94305 |
| Country |
USA |
| |
|
| Platforms (2) |
|
| Samples (8)
|
|
| This SuperSeries is composed of the following SubSeries: |
| GSE115317 |
Coronary artery disease genes SMAD3 and TCF21 promote opposing interactive genetic programs that regulate smooth muscle cell differentiation and disease risk [ChIP-seq] |
| GSE115318 |
Coronary artery disease genes SMAD3 and TCF21 promote opposing interactive genetic programs that regulate smooth muscle cell differentiation and disease risk [RNA-seq] |
|
| Relations |
| BioProject |
PRJNA474525 |
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