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Mus musculus

ABSTRACT: Expression profiling of murine monosomal karyotype p53-/- shPU.1 AML cells following gradual PU.1 restoration

PROVIDER: PRJNA308836 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR3101930.fastq.gz	Fastqsanger.gz
	SRR3101931.fastq.gz	Fastqsanger.gz
	SRR3101932.fastq.gz	Fastqsanger.gz
	SRR3101933.fastq.gz	Fastqsanger.gz
	SRR3101934.fastq.gz	Fastqsanger.gz

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Mus musculus

Project description:Expression profiling of murine cytogenetic normal p53-/- shPU.1 AML cells following gradual PU.1 restoration

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PU.1 ChIP-seq in p53-/- shPU.1 AML cells following acute PU.1 restoration

Project description:We have utilized advanced RNAi technology to dynamically restore endogenous PU.1 expression and perform PU.1 ChIP-seq in p53-deficient shPU.1 AML cells in vivo. This causes rapid cell cycle shutdown and myeloid differentiation. PU.1 restoration results in regression and clearance and prolongs survival.

2019-05-13 | GSE76933 | GEO

Single cell expression profiling of murine p53-/- shPU.1 AML cells following PU.1 restoration

Project description:Single cell expression profiling of murine p53-/- shPU.1 AML cells following PU.1 restoration

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Project description:PU.1 ChIP-seq in p53-/- shPU.1 AML cells following acute PU.1 restoration

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Expression profiling of p53-/- shPU.1 AML cells single cell clones

Project description:We have utilized advanced RNAi technology to dynamically restore endogenous PU.1 expression in p53-deficient shPU.1 AML single cell clones in vitro. This causes rapid cell cycle shutdown and reversible myeloid differentiation.

2019-05-13 | GSE76879 | GEO

Expression profiling of murine monosomal karyotype p53-/- shPU.1 AML cells following gradual PU.1 restoration

Project description:We have utilized advanced RNAi technology to dynamically restore endogenous PU.1 expression in p53-deficient AML cells. This causes rapid cell cycle shutdown and myeloid differentiation. PU.1 restoration results in regression and clearance and prolongs survival.

2019-05-13 | GSE76875 | GEO

Expression profiling of murine cytogenetic normal p53-/- shPU.1 AML cells following gradual PU.1 restoration

Project description:We have utilized advanced RNAi technology to dynamically restore endogenous PU.1 expression in p53-deficient AML cells . This causes rapid cell cycle shutdown and myeloid differentiation. PU.1 restoration results in regression and clearance and prolongs survival.

2019-05-13 | GSE76874 | GEO

Mus musculus

Project description:Expression profiling of p53-/- shPU.1 AML cells single cell clones

| PRJNA308840 | ENA

Transcription profiling of hematopoietic stem cells in the preleukemic phase from wiltype mice and mice deficient in transcription factor PU.1 to identify transcriptional changes preceding malignant transformation

Project description:Knockdown of the transcription factor PU.1 (Spi1) leads to acute myeloid leukemia (AML) in mice. We examined the transcriptome of PU.1 knockdown hematopoietic stem cells (HSC) in the preleukemic phase by linear amplification and genome-wide array analysis to identify transcriptional changes preceding malignant transformation. Hierarchical cluster analysis and principal component analysis clearly distinguished PU.1 knockdown from wildtype HSC. Jun family transcription factors c-Jun and JunB were among the top downregulated targets. Retroviral restoration of c-Jun expression in bone marrow cells of preleukemic mice partially rescued the PU.1-initiated myelomonocytic differentiation block. Lentiviral restoration of JunB at the leukemic stage led to reduced clonogenic growth, loss of leukemic self-renewal capacity, and prevented leukemia in transplanted NOD-SCID mice. Examination of 305 AML patients confirmed the correlation between PU.1 and JunB downregulation and suggests its relevance in human disease. These results delineate a transcriptional pattern that precedes the leukemic transformation in PU.1 knockdown HSC and demonstrate that decreased levels of c-Jun and JunB contribute to the development of PU.1-induced AML by blocking differentiation (c-Jun) and increasing self-renewal (JunB). Therefore, examination of disturbed gene expression in HSC can identify genes whose dysregulation is essential for leukemic stem cell function and are targets for therapeutic interventions. Experiment Overall Design: Total RNA of HSC of PU.1 knockdown or wildtype animals (3 pools of 3 animals each) was amplified by two rounds of RT and T7 promoter-based in-vitro transcription and the resultant biotinylated cRNA was then hybridized to Affymetrix Mouse Genome 430 2.0 arrays.

2007-11-22 | E-GEOD-5654 | biostudies-arrayexpress

Transcriptional profiling of lung tumour cell lines with distinct p53 mutations in the absence or presence of WT p53

Project description:Microarray expression data generated to determine the impact of defined p53 mutations on lung cancer cell phenotypes, and on the tumour supressive responses induced by WT p53 restoration. In murine models of lung cancer, the therapeutic benefit of WT p53 restoration has been demonstrated in p53-deficient tumours (Juntilla et al, 2010; Feldser et al, 2010). However, it remains unknown if the restoration of WT p53 function is beneficial in p53 mutant tumours. Thus, to determine the impact of p53-targeted therapy in mutant p53 lung cancer, we analysed cells from murine lung tumours of distinct p53 genotypes. Utilising the well characterised p53-ER allele (Christophorou et al, 2005; Martins et al, 2006; Juntilla et al, 2010) we carried out transcriptional profiling of KrasG12D/+ cell lines isolated from advanced lung tumours with defined p53 status: p53Fx/ER (null), p53R270H/ER and p53R172H/ER in the absence (p53 WT OFF) or presence (p53 WT ON) of 4-hydroxytamoxifen (4-OHT). The temporal specificity of p53-ER restoration allowed us to utilised two timepoints to determine both the immediate (2hr) and sustained (8hr) impact of WT p53 function.

2017-08-09 | GSE94758 | GEO

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