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E-GEOD-60477 - The oncofusion protein FUS-ERG targets key hematopoietic regulators and modulates the all-trans retinoic acid signaling pathway in t(16;21) acute myeloid leukemia

Status
Released on 23 June 2015, last updated on 27 June 2015
Organism
Homo sapiens
Samples (20)
Protocols (3)
Description
Fusion proteins involving the ETS factor ERG have been associated with multiple cancers such as Ewing's sarcoma and prostate cancer. In acute myeloid leukemias harboring t(16;21) another ERG fusion protein is expressed, FUS-ERG. Here, we found that this FUS-ERG oncofusion protein acts in the context of a heptad of proteins (ERG, FLI1, GATA2, LYL1, LNMO2, RUNX1 and TAL1) central to proper expression of genes involved in maintaining a stem cell hematopoietic phenotype. Moreover, in t(16;21) FUS-ERG co-occupies genomic regions bound by the nuclear receptor heterodimer RXR-RARA inhibiting target gene expression and interfering with hematopoietic differentiation. All-Trans Retinoic Acid treatment of t(16;21) cells as well as FUS-ERG knock down alleviate the myeloid differentiation block. Together, the results suggest that FUS-ERG acts as a transcriptional repressor of the retinoic acid signaling pathway. Cell lines were used for RNA extraction for RNA-seq and ChIP experiments for ChIP-seq.
Experiment types
ChIP-seq, RNA-seq of coding RNA 
Contacts
Joost Martens <geo@ncbi.nlm.nih.gov>, Amit Mandoli, Ana M Sotoca, Bob Reijnders, Hendrik G Stunnenberg, Joost H Martens, Koen Prange, Luan N Nguyen
MINSEQE
Exp. designProtocolsVariablesProcessedSeq. reads
Files
Investigation descriptionE-GEOD-60477.idf.txt
Sample and data relationshipE-GEOD-60477.sdrf.txt
Processed data (11)Click to browse processed data
Links