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Chromosome 21-encoded miR-125b cooperates with GATA1s in trisomy 21-associated megakaryoblastic leukemia by targeting the megakaryocytic transcription factor ARID3A I

ABSTRACT: Chromosome 21-encoded miR-125b cooperates with GATA1s in trisomy 21-associated megakaryoblastic leukemia by targeting the megakaryocytic transcription factor ARID3A I

PROVIDER: PRJNA717774 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14083344_1.fastq.gz	Fastqsanger.gz
	SRR14083344_2.fastq.gz	Fastqsanger.gz
	SRR14083345_1.fastq.gz	Fastqsanger.gz
	SRR14083345_2.fastq.gz	Fastqsanger.gz
	SRR14083346_1.fastq.gz	Fastqsanger.gz

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Chromosome 21-encoded miR-125b cooperates with GATA1s in trisomy 21-associated megakaryoblastic leukemia by targeting the megakaryocytic transcription factor ARID3A I

Project description:The purpose of this study was to decipher the molecular network underlying the synergy between the GATA1s mutation and loss of Arid3a. We used gene expression profiling (RNA-Seq) to evaluate gene expression changes upon gain and loss of Arid3a in the context of the Gata1s mutation

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Chromosome 21-encoded miR-125b cooperates with GATA1s in trisomy 21-associated megakaryoblastic leukemia by targeting the megakaryocytic transcription factor ARID3A II

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Project description:The purpose of this study was to decipher the gene expression changes in the ML-DS cell line CMK upon overexpression of ARID3A. For that, we used a doxycycline-inducible gene expression system to overexpress ARID3A

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Expression data from transgenic ERG, GATA1s KI and ERG/GATA1s fetal livers

Project description:DS children have a 500-fold increased risk for developing acute megakaryoblastic leukemia (AMKL). Around 10% of DS newborns have a transient myeloproliferative disorder (TMD) that resolves spontaneously. Somatic mutations acquired during fetal hematopoiesis in the GATA1 transcription factor are detected in megakaryoblasts from all the DS TMDs or AMKLs. GATA1 is an X chromosome transcription factor essential for the development of multiple hematopoietic lineages. Loss of GATA1 results in embryonic lethality due to severe anemia. The GATA1 mutations result in the expression of a shorter isoform, GATA1s. Replacement of GATA1 with GATA1s causes transient proliferation of immature fetal megakaryocytic progenitors. The Hsa21 ETS transcription factor, ERG, is expressed in megakaryocytes and erythrocytes and is involved in several types of cancer. Mutation in GATA1 gene leading to expression of the short isoform (GATA1s) that occurs on the background of trisomy 21 is regarded as one of the driving forces for megakaryocytic expansion observed in DS fetal livers. ERG, which is located on chromosome 21, is considered one of the leading candidates to cooperate with GATA1 mutation in the generation of DS AMKL. To study the in vivo cooperation between ERG and GATA1 isoforms, we crossed the ERG transgenic mice with the GATA1s Knock-in mice (GATA null background). We found that males expressing both ERG and the short isoform of GATA1(GATA1s) died in uterus between embryonic days E121/2 and E141/2.We studied erythropoiesis and megakaryopoiesis in fetal livers from the different genotypes generated from our cross.

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