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The effects of expression of mutant ASXL1 and HHEX on hematopoietic cells

ABSTRACT: To identify target genes of mutant ASXL1 (ASXL1-MT) and HHEX in hematopoietic cells, we performed RNA-seq using RUNX1-ETO expressing cord blood cells transduced with vector or ASXL1-MT together with vector or HHEX.

ORGANISM(S): Homo sapiens

PROVIDER: GSE147654 | GEO | 2020/06/09

REPOSITORIES: GEO

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The effects of mutant ASXL1 and BAP1 expression on hematopoietic cells

Project description:To identify target genes of mutant ASXL1 and BAP1 in hematopoietic cells, we performed RNA-seq using murine c-kit positive cells transduced with ASXL1-MT (MT) or ASXL1-MT-K351R (KR) together with vector or BAP1. Method：Murine c-kit positive bone marrow cells were transduced with ASXL1-MT (MT) or ASXL1-MT-K351R (KR) (coexpressing blastcidin resistant gene) together with vector or BAP1 (coexpressing puromycin resistant gene). After the selection with blasticidin and puromycin for three days, colony-forming cells were collected to extract RNA for RNA-seq analysis.

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Functional study on the cooperation of ASXL1 and RUNX1 mutations for myeloid leukemia transformation

Project description:BACKGROUND: Our previous studies showed that RUNX1 and ASXL1 mutations were frequently co-existed in chronic myelomonocytic leukemia (CMML) and clonal evolution of RUNX1 and/or ASXL1 occurred most frequently in chronic myeloid leukemia (CML) with myeloid blastic crisis. The molecular pathogenesis of cooperation of RUNX1 and ASXL1 mutations has not been reported yet. METHODS: Lentiviral-mediated stable transduction of RUNX1-WT/MT (R135T) in K562 cells which harboring ASXL1-MT (Y591X). RNA was extracted from stable cell line and used for gene-expression microarray analysis. RESULTS: For in vitro study, we overexpressed RUNX1-WT/MT (R135T) in K562 cells which harboring ASXL1-MT (Y591X). We found that RUNX1-MT augmented cell proliferation, colony formation, HOXA gene expression and inhibited megakaryocytic differentiation in ASXL1-MT K562 cells compared to RUNX1-WT or empty vector control. We performed gene expression profile of K562 cells overexpressed with EV, RUNX1-WT and RUNX1-R135T mutation. Gene expression microarray data revealed that 147 genes upregulated more than 2-fold in RUNX1-R135T expressing K562 cells compared to EV control cells. From gene expression data analysis, we found that inhibitor of DNA binding 1 (ID1), a key transcriptional regulator of hematopoietic stem cell (HSC) lineage commitment, is upregulated in RUNX1-R135T-transduced K562 cells compared to EV and RUNX1-WT-expressing cells.

2018-06-01 | GSE99640 | GEO

ASXL1 Knock Down in Normal CD34+ Cord Blood and UKE1 Cell Lines

Project description:Gene expression analysis of Normal CD34+ Cord Blood and UKE1 cell lines treated with hairpins targeting ASXL1. Two independent studies where 1) CD34+ cord blood from normal donors were treated with either A) GFP Vector or B) ASXL1 specific short hairpin and 2) UKE1 cell lines treated with either A) GFP Vector or B) ASXL1 specific short hairpin.

2012-08-21 | E-GEOD-38692 | biostudies-arrayexpress

Gene expression profiles of mutant ASXL1 knock-in HSPCs

Project description:To assess the effect of mutant ASXL1 (ASXL1-MT) on gene expression and RNA splicing in hematopoietic cells, we performed RNA-seq using HSPCs (bone marrow lineage-, c-Kit+ cells) derived from control or ASXL1-MT-KI mice.

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AML1-ETO target genes

Project description:human CD34 cells isolated from cord blood or peripheral blood transduced with AML1-ETO or Empty vector (MIGR1) Keywords = AML1-ETO Leukemia Keywords: repeat sample

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Clonal Haematopoiesis-related Mutant ASXL1 Promotes Atherosclerosis in Mice via Dysregulated Innate Immunity

Project description:Certain somatic mutations confer a fitness advantage in hematopoietic stem cells, resulting in the clonal expansion of mutant blood cells, known as clonal haematopoiesis (CH). Among the top 3 CH mutations, ASXL1 mutations present the highest risk for developing cardiovascular diseases (CVDs). However, how ASXL1 mutations induce CVDs remains totally elusive. Here we show that haematopoietic cells harbouring C-terminally truncated form of ASXL1 mutant (ASXL1-MT) accelerated development of atherosclerosis in Ldlr–/– mice. Transcriptome analyses of plaque-cells showed inflammatory signatures of monocytes and macrophages expressing ASXL1-MT. Mechanistically, wild-type ASXL1 inhibited innate immune signalling through the inhibition of IRAK1-TAK1 interaction in the cytoplasm, indicating an unexpected non-epigenetic role of ASXL1. In contrast, ASXL1-MT lost this regulatory function, leading to NF-κB activation. Intriguingly, IRAK1/4 inhibition decreased inflammatory monocytes and atherosclerosis driven by ASXL1-MT. The present work connects ASXL1 mutations with inflammation and CVDs, giving a clue to prevent CVDs in ASXL1-CH.

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Clonal Haematopoiesis-related Mutant ASXL1 Promotes Atherosclerosis in Mice via Dysregulated Innate Immunity [scRNA-seq]

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E-MTAB-3466

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Mutant ASXL1 induces age-related expansion of phenotypic hematopoietic stem cells through activation of Akt/mTOR pathway

Project description:Somatic mutations of ASXL1 are frequently detected in age-related clonal hematopoiesis (CH). However, how ASXL1 mutations drive CH remains elusive. Using knockin (KI) mice expressing a C-terminally truncated form of ASXL1-mutant (ASXL1-MT), we examined the influence of ASXL1-MT on physiological aging in hematopoietic stem cells (HSCs). HSCs expressing ASXL1-MT display competitive disadvantage after transplantation. Nevertheless, in genetic mosaic mouse model, they acquire clonal advantage during aging, recapitulating CH in humans. Mechanistically, ASXL1-MT cooperates with BAP1 to deubiquitinate and activate AKT. Overactive Akt/mTOR signaling induced by ASXL1-MT results in aberrant proliferation and dysfunction of HSCs associated with age-related accumulation of DNA damage. Treatment with an mTOR inhibitor rapamycin ameliorates aberrant expansion of the HSC compartment as well as dysregulated hematopoiesis in aged ASXL1-MT KI mice. Our findings suggest that ASXL1-MT provokes dysfunction of HSCs, whereas it confers clonal advantage on HSCs over time, leading to the development of CH.

2021-02-08 | MSV000086816 | MassIVE

Transcription profiling of mouse bone marrow cells expressing NUP98/HHEX or NUP98/HOXA9 a new oncogenic fusion with acute myeloid leukemia

Project description:We have cloned and characterized a fusion gene NUP98/HHEX1 resulting from t(7;10) from a patient with acute myeloid leukemia (AML). As NUP98/HHEX acts as an aberrant transcriptional activator, putative targets were searched upon transient expression of the fusion in primary murine bone marrow cells. Experiment Overall Design: Murine bone marrow cells were transduced with a retrovirus (MSCV-IRES-GFP, MIG) expressing either NUP98/HHEX or NUP98/HOXA9 (or the empty vector), mRNA was isolated after 72h. Each experiment was performed in triplicates.

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