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JMJD1C facilitates long distance genomic interactions by promoting condensates formation of key leukemic transcription factors in multiple AML cells [ChIP-seq]

ABSTRACT: JMJD1C facilitates long distance genomic interactions by promoting condensates formation of key leukemic transcription factors in multiple AML cells [ChIP-seq]

PROVIDER: PRJNA1055125 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27308267_1.fastq.gz	Fastqsanger.gz
	SRR27308267_2.fastq.gz	Fastqsanger.gz
	SRR27308268_1.fastq.gz	Fastqsanger.gz
	SRR27308268_2.fastq.gz	Fastqsanger.gz
	SRR27308269_1.fastq.gz	Fastqsanger.gz

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JMJD1C facilitates long distance genomic interactions by promoting condensates formation of key leukemic transcription factors in multiple AML cells [RNA-seq]

Project description:Dysregulation of transcriptional programs that establish and maintain specific cell identities can lead to various diseases, especially cancer. Acute myeloid leukemia (AML) is an extremely heterogeneous malignancy with frequent genetic mutations such as transcription factors (TFs) and epigenetic factors, resulting in gene dysregulation, differentiation blockade and aberrant proliferation of immature clonal myeloid cells. Various AML subtypes usually involve in distinct genetic alterations, and most studies and therapeutic drugs are focused on specific AML genetic abnormalities. However, whether these seemingly different AML subtypes share a universal transcriptional programs and regulation mechanism is not clear. Identification of such program could help finding of common vulnerabilities and thus future therapeutics against multiple AML subtypes. In this study, we set out to elucidate the underlying mechanism that explains the general dependency towards JMJD1C by AML with different genetic backgrounds. Towards this goal, we first identify RUNX1 as a transcription factor that recruits JMJD1C to chromatin in multiple types of leukemia. Second, we show that JMJD1C directly interacts with RUNX1 at the N-terminus and they co-regulate a set of genes required by leukemic cells. Finally, we found that the N-terminus of JMJD1C could form liquid-like biomolecular RUNX1-containing condensates that are independent of its enzymatic activity, to mediate promoter-enhancer interactions to activate downstream gene expression.

2025-06-04 | GSE251728 | GEO

JMJD1C facilitates long distance genomic interactions by promoting condensates formation of key leukemic transcription factors in multiple AML cells [ChIP-seq]

2025-06-04 | GSE251726 | GEO

JMJD1C facilitates long distance genomic interactions by promoting condensates formation of key leukemic transcription factors in multiple AML cells [4C-seq]

2025-06-04 | GSE251725 | GEO

JMJD1C facilitates long distance genomic interactions by promoting condensates formation of key leukemic transcription factors in multiple AML cells

Project description:JMJD1C facilitates long distance genomic interactions by promoting condensates formation of key leukemic transcription factors in multiple AML cells

| PRJNA1055129 | ENA

JMJD1C facilitates long distance genomic interactions by promoting condensates formation of key leukemic transcription factors in multiple AML cells [4C-seq]

Project description:JMJD1C facilitates long distance genomic interactions by promoting condensates formation of key leukemic transcription factors in multiple AML cells [4C-seq]

| PRJNA1055123 | ENA

JMJD1C facilitates long distance genomic interactions by promoting condensates formation of key leukemic transcription factors in multiple AML cells [RNA-seq]

Project description:JMJD1C facilitates long distance genomic interactions by promoting condensates formation of key leukemic transcription factors in multiple AML cells [RNA-seq]

| PRJNA1055138 | ENA

Gene expression profiling of Hox-driven AML overexpressing JMJD1C

Project description:JMJD1C, a Jumonji C (JmjC) domain-containing histone demethylase, has been reported as a direct cofactor of oncogenic transcription factor HOXA9. To identify JMJD1C downstream effectors, we performed a genome-wide gene expression profiling experiment. Our microarray analysis identified a new role for JMJD1C in regulating a cancer metabolic program in HOX-driven AML. GFP+ HOXA9/MEIS1-mediated pre-leukemic stem cells were transduced with retroviruses carrying JMJD1C or empty vector for the microarray experiment. Each group has 4 samples.

2018-12-30 | E-MTAB-5760 | biostudies-arrayexpress

JMJD1C facilitates long distance genomic interactions by promoting condensates formation of key leukemic transcription factors in multiple AML cells

Project description:This SuperSeries is composed of the SubSeries listed below.

2025-06-04 | GSE251729 | GEO

RNA expression analysis upon JMJD1C depletion

Project description:The AML1-ETO fusion protein, a transcription factor generated by the t(8;21) translocation in acute myeloid leukaemia (AML), dictates a leukemic program by increasing self-renewal and inhibiting differentiation. Here we demonstrate that the histone demethylase JMJD1C functions as a co-activator for AML1-ETO and is required for its transcriptional program. JMJD1C is directly recruited by AML1-ETO to its target genes and regulates their expression by maintaining low H3K9me2 levels. Analyses in JMJD1C knockout mice also establish a JMJD1C requirement for AML1-ETOâs ability to increase proliferation. We also show a critical role for JMJD1C in the survival of multiple human AML cell lines, suggesting that it is required for leukemic programs in different AML cell types through its association with key transcription factors. Examination of RNA expression when Kasumi-1 cells are treated with control shRNA or two different JMJD1C shRNAs; in duplicate. Please note that the 'shAML1_ETO_vs_shControl.all_gene_exp.tb.txtl' was generated comparing control and shRNA treated RNA abundance-using previously published data [GSE43834; GSM1071857 and GSM1071852].

2015-11-02 | E-GEOD-63485 | biostudies-arrayexpress

RNA expression analysis upon JMJD1C depletion

Project description:The AML1-ETO fusion protein, a transcription factor generated by the t(8;21) translocation in acute myeloid leukaemia (AML), dictates a leukemic program by increasing self-renewal and inhibiting differentiation. Here we demonstrate that the histone demethylase JMJD1C functions as a co-activator for AML1-ETO and is required for its transcriptional program. JMJD1C is directly recruited by AML1-ETO to its target genes and regulates their expression by maintaining low H3K9me2 levels. Analyses in JMJD1C knockout mice also establish a JMJD1C requirement for AML1-ETO’s ability to increase proliferation. We also show a critical role for JMJD1C in the survival of multiple human AML cell lines, suggesting that it is required for leukemic programs in different AML cell types through its association with key transcription factors.

2015-11-02 | GSE63485 | GEO

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