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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
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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.
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Overall design |
RNA-seq in THP-1 AML cells transduced with two independent RASSF2-targeting shRNAs or control shRNA
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Contributor(s) |
Stoner SA, Zhang D |
Citation missing |
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Submission date |
Nov 26, 2019 |
Last update date |
Dec 01, 2019 |
Contact name |
Sam Stoner |
E-mail(s) |
sastoner@ucsd.edu
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Organization name |
University of California, San Diego
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Street address |
3855 Health Sciences Dr 0815
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City |
La Jolla |
State/province |
CA |
ZIP/Postal code |
92037 |
Country |
USA |
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Platforms (1) |
GPL24676 |
Illumina NovaSeq 6000 (Homo sapiens) |
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Samples (9)
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Relations |
BioProject |
PRJNA592002 |
SRA |
SRP233387 |