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Gene expression profile at single cell level of tumor infiltrated Treg from the WT and the jmjd1c TregcKO mice

ABSTRACT: Gene expression profile at single cell level of tumor infiltrated Treg from the WT and the jmjd1c TregcKO mice

PROVIDER: PRJNA929058 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23262643_1.fastq.gz	Fastqsanger.gz
	SRR23262643_2.fastq.gz	Fastqsanger.gz
	SRR23262644_1.fastq.gz	Fastqsanger.gz
	SRR23262644_2.fastq.gz	Fastqsanger.gz
	SRR23262645_1.fastq.gz	Fastqsanger.gz

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Gene expression profile at single cell level of tumor infiltrated Treg from the WT and the jmjd1c TregcKO mice

Project description:Tumor infiltrated treg cells are considered to be crucial in the cancer immunotherapy. We used single cell RNA sequencing (scRNA-seq) to analyze the differences between WT and jmjd1cTreg cko mice and clarify the important function of jmjd1c.

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H3K9me2 profile of tumor infiltrated Treg from the WT and the jmjd1c TregcKO mice and chromatin accessibility profile of tumor treg and spleen treg

Project description:Tumor infiltrated treg cells are considered as a crucial in the cancer immunotherapy. We used H3K9me2 CUT&RUN to analyze the differences between WT and jmjd1cTreg cko mice and clarify the important function of jmjd1c in tumor treg. We use ATACseq to analyze the difference between tumor treg and spleen treg and characterize the epigenetic characters in tumor treg.

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H3K9me2 profile of tumor infiltrated Treg from the WT and the jmjd1c TregcKO mice and chromatin accessibility profile of tumor treg and spleen treg

Project description:H3K9me2 profile of tumor infiltrated Treg from the WT and the jmjd1c TregcKO mice and chromatin accessibility profile of tumor treg and spleen treg

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Effect of loss of Jmjd1c on H3K9me2 level across the genome

Project description:Analysis of H3K9me2 level in MLL-AF9 leukemia cells upon deletion of Jmjd1c. Jmjd1c has been shown to be a H3K9me1/2 demethylase and these results provide insight into its role in MLL-Af9 leukemia

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Jmjd1c

Project description:Jmjd1c

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Expression data from the control and Jmjd1c KD ESCs

Project description:The roles of histone demethylases (HDMs) for the establishment and maintenance of the pluripotent state are incompletely defined. Here, we show that JmjC domain-containing protein 1c (Jmjd1c), a putative histone H3 Lys 9 (H3K9) demethylase, is required for mouse embryonic stem cell (ESC) self-renewal. To understand how Jmjd1c knockdown (KD) and resultant changes in the H3K9 methylations would affect ESCs at a global gene expression level, we compared the whole genome transcriptomes between the control and Jmjd1c KD ESCs (6 samples, including 2 shNT control samples and 4 shJmjd1c samples, 2 from #3 and 2 from #4 shRNA, respectively) using affymetrix microarray. We used microarrays to identify genes affected by Jmjd1c knockdown in mouse ESCs.

2017-07-24 | GSE89709 | 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

JMJD1C knockdown (H9_CT2_JMJD1C-KD_Microarray_JW)

Project description:It has been recently reported that the pluripotency factor OCT4, the early neural inducing factor NR2F2, and the pluripotency-associated miRNA miR-302 are linked in a regulatory circuitry that critically regulate both pluripotency and neural differentiation of human embryonic stem cells (hESCs). We show here that JMJD1C, a H3K9 demethylase expressed in undifferentiated hESCs, plays a key role in the regulatory circuitry. hESCs with JMJD1C knockdown (KD) retain the state of self-renewal and pluripotency, but express lower miR-302c than control hESCs. JMJD1C directly binds to the miR-302 promoter in hESCs and reduces H3K9 methylation on the promoter. Upon withdrawal of bFGF (an inhibitor of neural initiation) from a defined culture medium, the KD, but not control, hESCs differentiate into neural progenitors within three days – the fastest ever reported, accompanied by rapid increase of NR2F2 expression. A miR-302c analogue or an inhibitor of H3K9 methylation reduces neural induction from the KD hESCs, whereas a miR-302c inhibitor promotes hESC differentiation. Together, our findings suggest that JMJD1C plays a central role in control of neural differentiation from hESCs, which involves sustained miR-302c expression, and that inhibition of JMJD1C is sufficient to rapidly induce neural progenitors from hESCs in the defined medium depleted of bFGF. This is also the first evidence, to our knowledge, for epigenetic modification of miR-302 in hESCs. 6 human ES cell lines were used in this microarray assay. Each line has two replicates.

2013-12-24 | E-GEOD-46485 | biostudies-arrayexpress

ChIP-seq of histone marks H3K36, H3K27, and H3K9 in JMJD1C knockout or mutated MLL-AF9 leukemia cells

Project description:We performed genome-wide profiling of H3K9me3, H3K9me1, H3K27me3, and H3K36me3 by ChIP-seq in JMJD1C knockout or mutated MLL-AF9 leukemia cells. For ChIP-seq in JMJD1C mutated cells, we transduced sgRNA targeting the zinc finger, jumonji domain of JMJD1C or Renilla control and sorted on day 6 for GFP (MLL-AF9) Tdtomato (sgRNA) double positive cells. For ChIP-seq in JMJD1C knockout cells, we transduced Jmjd1c flox/flox MLL-AF9 leukemia cells with CRE TdTomato and sorted on day 6 for GFP (MLL-AF9) Tdtomato (CRE) double positive cells. These cells were subjected to ChIP-seq analysis with either H3K27me3, H3K9me3, H3K9me1 (JMJD1C knockout cells) or H3K36me3 (both knockout and mutated cells) antibody. We found increased H3K36me3 level at promoters of differentially expressed genes between control and JMJD1C loss or mutated leukemia cells.

2019-04-12 | GSE129661 | GEO

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