|
Status |
Public on Jun 19, 2020 |
Title |
Assay for Transposase Accessible Chromatin with high-throughput sequencing (ATAC-seq) revealed genomic chromatin accessibilities change induced by loss of ARID1A in differentiated (day 4) H9 hESCs |
Organism |
Homo sapiens |
Experiment type |
Genome binding/occupancy profiling by high throughput sequencing
|
Summary |
We reported loss of ARID1A promoted neurogenesis and inhibited cardiogenesis. Under microscopy, we observed that spontaneously differentiated cells were induced in ARID1A KO H9 hESCs cultured in mTesR medium. We did not know what cells types were. Here ATAC-seq were used to investigate chromatin accessibilities change in differentiated (day 4) WT H9 hESCs and ARID1A KO hESC cells.
|
|
|
Overall design |
Identification of genomic chromatin accessibilities change induced by loss of ARID1A in H9 hESCs.
|
|
|
Contributor(s) |
Yang L, Liu J |
Citation(s) |
32646524 |
Submission date |
Oct 24, 2019 |
Last update date |
Jul 16, 2020 |
Contact name |
Lei Yang |
E-mail(s) |
lyang7@iu.edu
|
Phone |
(317) 278-5233
|
Organization name |
Indiana University School of Medicine
|
Department |
Department of Pediatrics
|
Street address |
1044 W. Walnut St.
|
City |
Indianapolis |
State/province |
Indiana |
ZIP/Postal code |
46202 |
Country |
USA |
|
|
Platforms (1) |
GPL24676 |
Illumina NovaSeq 6000 (Homo sapiens) |
|
Samples (2) |
|
This SubSeries is part of SuperSeries: |
GSE139343 |
Essential and Opposite Roles of ARID1A in Coordinating Human Cardiogenesis and Neurogenesis from Pluripotent Stem Cells |
|
Relations |
BioProject |
PRJNA579321 |
SRA |
SRP226829 |