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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

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

PROVIDER: PRJNA717773 | ENA |

REPOSITORIES: ENA

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

| PRJNA717774 | ENA

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

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

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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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The megakaryocytic transcription factor ARID3A suppresses leukemia pathogenesis [ATAC-seq]

Project description:The purpose of this study was to decipher the molecular function of ARID3A. We leveraged gene expression (RNA-Seq) and chromatin profiling (ATAC-Seq and CUT&RUN) to evaluate gene expression changes upon restoring Arid3a expression in the context of the Gata1s mutation and miR-125b overexpression

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The megakaryocytic transcription factor ARID3A suppresses leukemia pathogenesis [CUT&RUN]

2022-04-20 | GSE181568 | GEO

The megakaryocytic transcription factor ARID3A suppresses leukemia pathogenesis [RNA-seq]

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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

Project description:The purpose of this study was to decipher the molecular network underlying the synergy between the GATA1s mutation and miR-125b. We used a doxycycline-regulated inducible system to determine gene expression changes associated with the expression of miR-125b.,

2022-04-20 | GSE169739 | GEO

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

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

2022-04-20 | GSE169740 | GEO

The megakaryocytic transcription factor ARID3A suppresses leukemia pathogenesis.

Project description:The megakaryocytic transcription factor ARID3A suppresses leukemia pathogenesis.

| PRJNA752569 | ENA

miR-99a/100~125b tricistrons regulate hematopoietic stem and progenitor cell homeostasis by shifting the balance between TGFM-NM-2 and Wnt signaling

Project description:Although regulation of stem cell homeostasis by miRNAs is well studied, it is unclear how individual miRNAs, genomically encoded within an organized polycistron, can interact to induce an integrated phenotype. miR-99a/100, let-7 and miR-125b paralogues are encoded in two tricistrons on human chromosome 11 and 21. They are highly expressed in hematopoietic stem cells (HSCs) and acute megakaryoblastic leukemia (AMKL), an aggressive form of leukemia with poor prognosis. Integrative analysis of global gene expression profiling, miRNA target prediction and pathway architecture revealed that miR-99a/100, let-7 and miR-125b functionally converge at the combinatorial block of the TGFM-NM-2 pathway by targeting four receptor subunits and two SMAD signaling transducers. In addition, downregulation of tumor suppressor genes APC/APC2 stabilizes active M-NM-2-Catenin and enhances Wnt signaling. By switching the balance between Wnt and TGFM-NM-2 signaling the concerted action of these tricistronic miRNAs promoted sustained expansion of murine and human HSCs in vitro or in vivo, while favoring megakaryocytic differentiation. We lentivirally transduced cord blood CD34+-hematopoietic stem and progenitor cells (CB-HSPCs) to ectopically express miR-125b-2, miR-99a, let-7c or miR-99a~125b-2 and cultured them in megakaryocytic differentiation medium for 7 days.

2014-03-28 | E-GEOD-56335 | biostudies-arrayexpress

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