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Series GSE139329 Query DataSets for GSE139329
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
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)
GSM4138221 WT_diff T4_ATAC-seq
GSM4138222 ARID1A KO_diff T4_ATAC-seq
This SubSeries is part of SuperSeries:
GSE139343 Essential and Opposite Roles of ARID1A in Coordinating Human Cardiogenesis and Neurogenesis from Pluripotent Stem Cells
BioProject PRJNA579321
SRA SRP226829

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Supplementary file Size Download File type/resource
GSE139329_RAW.tar 8.7 Gb (http)(custom) TAR (of BW)
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Raw data are available in SRA
Processed data provided as supplementary file

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