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Series GSE141088 Query DataSets for GSE141088
Status Public on Nov 27, 2019
Title RASSF2 knockdown in THP-1 AML cells
Organism Homo sapiens
Experiment type Expression profiling by high throughput sequencing
Summary Large-scale chromosomal translocations are frequent oncogenic drivers in acute myeloid leukemia (AML). These translocations often occur in critical transcriptional/epigenetic regulators and contribute to malignant cell growth through alteration of normal gene expression. Despite this knowledge, the specific gene expression alterations that contribute to the development of leukemia remain incompletely understood. Here, through characterization of transcriptional regulation by the RUNX1-ETO fusion protein, we have identified Ras-association domain family member 2 (RASSF2) as a critical gene that is aberrantly transcriptionally repressed in t(8;21)-associated AML. Based on this, we performed molecular and functional characterization of RASSF2 in AML cells.
Overall design RNA-seq in THP-1 AML cells transduced with two independent RASSF2-targeting shRNAs or control shRNA
Contributor(s) Stoner SA, Zhang D
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Submission date Nov 26, 2019
Last update date Dec 01, 2019
Contact name Sam Stoner
Organization name University of California, San Diego
Street address 3855 Health Sciences Dr 0815
City La Jolla
State/province CA
ZIP/Postal code 92037
Country USA
Platforms (1)
GPL24676 Illumina NovaSeq 6000 (Homo sapiens)
Samples (9)
GSM4194790 shCTRL_rep1
GSM4194791 shCTRL_rep2
GSM4194792 shCTRL_rep3
BioProject PRJNA592002
SRA SRP233387

Download family Format
SOFT formatted family file(s) SOFTHelp
MINiML formatted family file(s) MINiMLHelp
Series Matrix File(s) TXTHelp

Supplementary file Size Download File type/resource
GSE141088_THP-1_RASSF2-KD_DESeq2.xlsx 3.1 Mb (ftp)(http) XLSX
SRA Run SelectorHelp
Raw data are available in SRA
Processed data are available on Series record

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