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MRNA expression of murine hematopoietic stem cells and ex vivo murine MLL-AF9 cells deficient for total PRDM16 or f-PRDM16, and AF9 cells overexpressing individual PRDM16 isoforms

ABSTRACT: mRNA expression of murine hematopoietic stem cells and ex vivo murine MLL-AF9 cells deficient for total PRDM16 or f-PRDM16, and AF9 cells overexpressing individual PRDM16 isoforms

OTHER RELATED OMICS DATASETS IN: GSE112860

PROVIDER: PRJNA449343 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6966280.fastq.gz	Fastqsanger.gz
	SRR6966290.fastq.gz	Fastqsanger.gz
	SRR6966300.fastq.gz	Fastqsanger.gz
	SRR6966310.fastq.gz	Fastqsanger.gz
	SRR6966281.fastq.gz	Fastqsanger.gz

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mRNA expression of murine hematopoietic stem cells and ex vivo murine MLL-AF9 cells deficient for total PRDM16 or f-PRDM16, and AF9 cells overexpressing individual PRDM16 isoforms

Project description:Group 1 -- WT or PRDM16-KO ex vivo murine MLL-AF9 cells, and PRDM16-KO AF9 cells overexpressing either f-PRDM16 or s-PRDM16. Group 2 -- WT or total PRDM16-KO murine HSCs isolated from adult BM. Group 3 -- WT or total PRDM16-KO murine HSCs isolated from fetal liver. Group 4 -- WT or f-PRDM16-KO murine HSCs (expressing s-PRDM16 only) isolated from fetal liver.

2018-06-08 | GSE112860 | GEO

Histone methyltransferase PRDM16 in tumor suppression

Project description:PRDM16 is highly enriched in adult stem cells and plays a crucial role in multiple developmental processes. Here we demonstrate that PRDM16 is a histone H3K4 methyltransferase and this activity is essential for PRDM16 to function as a tumor suppressor. We show that PRDM16, through its regulation of transcription factor GFI1b, antagonizes the functions of MLL fusion proteins by repressing HOXA gene expression and therefore, specifically suppresses the transformation capability of MLL-AF9, MLL-AF6 and MLL-ENL. Furthermore, overexpression of PRDM16, but not the inactive PRDM16 mutant, blocks MLL mediated leukemogenesis while PRDM16 depletion significantly shortens the disease latency in vivo. We also show that PRDM16 activity is dynamically required at the pre-leukemic stage, but not in fully transformed leukemia, depicting a little known sequence of events necessary for clonal expansion during cancer evolution. Given the importance of PRDM16 and the loss of PRDM16 methyltransferase activity in an array of human malignancies, our findings provide broad insights for PRDM16-dependent physiological and pathological processes.

2016-12-15 | GSE64218 | GEO

Genes regulated by Meis1 in murine Mll-AF9 leukemia cells

Project description:Leukemias with MLL-rearrangements are characterized by high expression of the homeo box gene MEIS1. In these studies, we knocked down Meis1 expression by shRNA lentivirus transduction in murine Mll-AF9 leukemia cells. Meis1 knockdown resulted in decreased proliferation and survival of murine Mll-AF9 leukemia cells. We also observed reduced clonogenic capacity and increased monocytic differentiation. The establishment of leukemia in transplant recipients was significantly delayed by Meis1 knockdown. Gene expression profiling of cells transduced with Meis1 shRNA showed reduced expression of genes associated with cell cycle entry and progression. shRNA mediated knockdown of MEIS1 in human MLL-fusion gene leukemia cell lines resulted in reduced cell growth. These results show that MEIS1 expression is important for MLL-rearranged leukemias and suggest that MEIS1 promotes cell cycle entry. Targeting MEIS1 may have therapeutic potential for treating leukemias expressing this transcription factor. Keywords: Gene expression

2008-12-23 | GSE14101 | GEO

Gene expression changes upon Mof knockout in MLL-AF9 transformed murine LSKs

Project description:We report Illumina next generation RNA sequencing (RNAseq) of MLL-AF9 in vitro transformed murine LSKs upon genetic deletion of Mof. These gene expression data illustrate that Mof regulates the expression of genes involved in DNA damage response and chromatin stability in MLL-AF9 transformed cells.

2017-08-30 | GSE80671 | GEO

RNA-seq profiling of murine Tet-off MLL-AF9; NRAS acute myeloid leukemia at different timepoints upon doxycycline-induced MLL-AF9 down-regulation.

Project description:Using an acute myeloid leukemia (AML) mouse model driven by tet-regulated MLL-AF9 (fusion between the gene MLL1 (KMT2A/MLL) and MLLT3 (AF9)) co-expressed with oncogenic NRASG12D (Tet-off MLL-AF9), we investigated the effect of modulating the expression of the MLL-AF9 fusion oncogene on the transcriptome and proteome of established murine AML. Treatment in vitro or in vivo of these Tet-off MLL-AF9 AMLs with doxycycline (DOX) results in the efficient down-regulation of the expression of the driver oncogene MLL-AF9. RNA sequencing analysis was performed on primary Tet-Off MLL-AF9 AML cells obtained from the spleen of leukemic animals and cultured in vitro for either 2 or 4 days in the presence of doxycycline (1μg/ml) (DOX= down-regulation of MLL-AF9) or left untreated (UT).

2021-12-31 | GSE108326 | GEO

Prdm16 newborn mouse (ventricular zone) VZ cells microarray

Project description:As Prdm16 deficiency reduces self-renewal potential and depletes neural stem cells in culture we decided to investigate the underlying molecular mechanisms of the neural stem cells depletion in the Prdm16 deficient animals. For the experiment we used Prdm16Gt(OST67423)Lex (Prdm16LacZ) genetrap mice obtained from the NIH Mutant Mouse Regional Resource Center (http://www.mmrrc.org/). We compared the gene expression profiles of uncultured ventricular zone cells from newborn Prdm16LacZ/LacZ (KO), Prdm16LacZ/+(HET), and Prdm16+/+ (WT) mice. The uncultured ventricular zone cells from newborn Prdm16LacZ/LacZ, Prdm16LacZ/+, and Prdm16+/+ mice were dissected from the brains and placed into the Trizol reagent. Purified RNA was reverse transcribed and amplified using the WT-Ovation™ Applause WT/Amp RNA amplification system (NuGEN Technologies,) following the manufacturer’s instructions. Sense strand cDNA was fragmented and labeled using the FL-Ovation™ cDNA Biotin Module V2 (NuGEN). 2.5µg of labeled cDNA were hybridized to Affymetrix Mouse Gene ST 1.0 microarrays.

2010-09-09 | E-GEOD-23406 | biostudies-arrayexpress

Eed inactivation in Cdkn2a-null MLL-AF9 transformed cells

Project description:We sequenced mRNA from MLL-AF9 transformed Cdkn2ako murine LSK-cells with and without a functional Eed locus

2015-07-15 | GSE70904 | GEO

Prdm16 Knockout Brown Adipose Tissue

Project description:Gene expression profile from brown adipose tissues of Prdm16 knockout and wile type mice. Prdm16 is a transcription factor that regulates the thermogenic gene program in brown and beige adipocytes. However, whether Prdm16 is required for the development or physiological function of brown adipose tissue (BAT) in vivo has been unclear. By analyzing mice that selectively lacked Prdm16 in the brown adipose lineage, we found that Prdm16 was dispensable for embryonic BAT development. Brown adipose tissues were collected from Prdm16 knockout and wiletype mice with 4 biological replicates per condition. Experiment was done in two separate batch for 6-week-old and 11-month-old. Extracted RNA was hybridized to Agilent two-color arrays.

2014-04-09 | E-GEOD-55080 | biostudies-arrayexpress

Expression changes after loss of Dot1l in murine MLL-AF9 leukemia cells

Project description:MLL-fusions may induce leukemogenic gene expression programs by recruiting the histone H3K79 methyltransferase to MLL-target promoters. We evaluated gene expression changes after cre-mediated loss of Dot1l in leukemia cells obtained from mice injected with MLL-9 transformed lineage negative bone marrow cells. MLL-AF9 murine leukemia cells carrying two conditional Dot1l alleles were retrovirally transduced with Cre or empty control vector, and gene expression changes were monitored on day 3, 5, and 7 after transduction.

2011-09-12 | E-GEOD-25911 | biostudies-arrayexpress

Gene expression profiles of control versus Prdm16-overexpressing cells

Project description:Embryonic neocortical cells were isolated from E14.5 WT mice, followed by TrypLE Express treatment and trituration to generate a single-cell suspension. Plasmid DNA was introduced into primary neocortical cells using Neon Transfection System. Next, neocortical neurospheres were cultured in serum-free media containing, then control and Prdm16-overexpressing cells were corrected after GFP sorting of 1 day cultures. We found that marked upregulation of modulators of mitochondrial metabolism and ROS balance in Prdm16 GOF cells

2017-04-03 | E-MTAB-5646 | biostudies-arrayexpress

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