Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

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IGR_MEGAKARYOCYTE_STUDY_TM


ABSTRACT: The OTT1-MAL fusion oncogene is specifically associated with human infant acute megakaryoblastic leukemia. In a murine model of OTT-MAL expression, leukemic cells expressing OTT-MAL present an aberrant activation of the Notch pathway target genes. IKZF1 was proposed to interact with the Notch signaling pathway during T-cell development and leukemogenesis. IKZF1-deficient animals present thrombocytosis with increased number of megkaryocytes indicating that it plays a role during megakaryocyte development. To assess the interaction betweeen the Notch signaling pathway and Ikaros in the context of acute megakaryoblastic leukemia, we expressed full-length IKZF1 in a cell line expressing the fusion OTT-MAL (6133 cells). To identify the target gene of IKZF1 we performed a global expression analysis as follow: i) 6133 cells were infected with the following retroviruses :1-empty retrovirus (MIE) 2-retrovirus allowing the expression of the full-length IKZF1 (IK1) and 3- a retrovirus allowing the expression of an alternatively spliced form of IKZF1 (IK7). Ii) Infected cells were sorted by flow cytometry 24 hours after infection and RNA was extracted with the Qiagen Rneasy kit with DNase treatment. After quantification biological replicates of RNA were hybridized on Agilent arrays with dye-swap as indicated below.

ORGANISM(S): Mus musculus

SUBMITTER: Philippe DESSEN 

PROVIDER: E-MTAB-897 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications


The transcription factor Ikaros regulates the development of hematopoietic cells. Ikaros-deficient animals fail to develop B cells and display a T-cell malignancy, which is correlated with altered Notch signaling. Recently, loss of Ikaros was associated with progression of myeloproliferative neoplasms to acute myeloid leukemia and increasing evidence shows that Ikaros is also critical for the regulation of myeloid development. Previous studies showed that Ikaros-deficient mice have increased meg  ...[more]

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