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H3K27me3 CUT&Tag - Jmjd3-scKO, Utx-scKO, Tdt-Ctrl, IgG-His

ABSTRACT: H3K27me3 CUT&Tag - Jmjd3-scKO, Utx-scKO, Tdt-Ctrl, IgG-His

PROVIDER: PRJNA776264 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16635988_1.fastq.gz	Fastqsanger.gz
	SRR16635988_2.fastq.gz	Fastqsanger.gz
	SRR16635989_1.fastq.gz	Fastqsanger.gz
	SRR16635989_2.fastq.gz	Fastqsanger.gz
	SRR16635990_1.fastq.gz	Fastqsanger.gz

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H3K4me3 CUT&Tag - Jmjd3-scKO, Utx-scKO, Tdt-Ctrl, IgG-His

Project description:H3K4me3 CUT&Tag - Jmjd3-scKO, Utx-scKO, Tdt-Ctrl, IgG-His

| PRJNA776262 | ENA

H3K27me3 CUT&Tag - Jmjd3-scKO, Utx-scKO, Tdt-Ctrl, IgG-His

Project description:Stem cells reside in specialized niches that play a critical role in modulating their fate. Supporting cells in the niche instruct fate changes to the stem cells through epigenetic enzymes that transduce cell signaling to modify gene expression. Recent studies showed that the innate immune response to muscle injury alters the muscle stem cell (MuSC) niche, it remains unknown how MuSC adapt to the modified milieu to mediate muscle repair. Here we show that the epigenetic enzyme JMJD3 coordinates MuSC adaptation to the regenerative niche in a non-cell autonomous manner where it modifies their extracellular matrix to integrate signaling that stimulates exit of quiescence. Genomics and transcriptomics approaches identified the hyaluronic acid (HA) synthesis enzyme Has2 as a key JMJD3 target gene that allows MuSCs to integrate signals from the regenerative niche. Overall, we identified a specific role for JMJD3 in regulating the expression of genes that allow MuSCs to adapt to the modified niche of regenerating muscle. We aim to determine the differential occupancy of histone H3 lysine 4 trimethyl mark muscle satellite stem cells isolated from JMJD3scKO, UTXscKO and Wild-type mice.

2022-08-04 | GSE186830 | GEO

H3K4me3 CUT&Tag - Jmjd3-scKO, Utx-scKO, Tdt-Ctrl, IgG-His

2022-08-04 | GSE186829 | GEO

Characterizing the contrasting roles of JMJD3 and UTX histone demethylases in T cell acute lymphoblastic leukemia [JMJD3_CUTLL1_ChIP-seq]

Project description:T-cell acute lymphoblastic leukemia (T-ALL) is an immature hematopoietic malignancy driven mainly by oncogenic activation of NOTCH1 signaling. In this study we assayed for genome-wide localization of JMJD3 enrichment. This piece of data was further integrated to expression changes using RNA sequencing as well as ChIP-Sequencing analysis of H3K27me3 upon genomic/genetic knock-down or chemical inhibition of JMJD3 and UTX. These results, coupled to genomic analysis of primary samples for the genomic status of the UTX gene in T-ALL, helped us to identify a hitherto unknown role of JMJD3 as an oncogenice facilitator in leukemia whereas UTX plays a tumor suppressor role. JMJD3 ChIP: 10 million cells were used for the ChIP and precipitated using 10micrograms of antibody (abgent, AP1022a) against human JMJD3.

2014-10-01 | E-GEOD-56694 | biostudies-arrayexpress

Jmjd3-Lab UTX-Lab CUT&Tag

Project description:Jmjd3-Lab UTX-Lab CUT&Tag

| PRJNA776257 | ENA

Ezh2, Utx and Jmjd3 deletion on the H3k27me3 level in mouse chondrocytes

Project description:The level of H3K27me3 were examined by conditional knockout Ezh2, Utx or Jmjd3 in mouse chondrocyte

2023-08-30 | GSE237698 | GEO

Characterizing the contrasting roles of JMJD3 and UTX histone demethylases in T cell acute lymphoblastic leukemia [GSKJ4_ChIP-seq]

Project description:T-cell acute lymphoblastic leukemia (T-ALL) is an immature hematopoietic malignancy driven mainly by oncogenic activation of NOTCH1 signaling. In this study we chemically inhibited the H3K27me3 demethylase JMJD3 using the GSKJ4 inhibitor and assayed for genome-wide changes in H3K27me3 and JMJD3 enrichment. This piece of data was further integrated to expression changes using RNA sequencing as well as ChIP-Sequencing analysis of H3K27me3 upon genomic knock-down of JMJD3 and UTX. These results, coupled to genomic analysis of primary samples for the genomic status of the UTX gene in T-ALL, helped us to identify a hitherto unknown role of JMJD3 as an oncogenice facilitator in leukemia whereas UTX seems to play a tumor suppressor role. Histone ChIP: Half to one million cells were treated with micrococcal nuclease (MNASE) to generate mononucleosomal particles and an adaptation of the Upstate ChIP protocol was used.

2014-10-01 | E-GEOD-56693 | biostudies-arrayexpress

Gene expression profiling in mature OT-II TCR transgenic CD4 SP thymocytes, either Jmjd3- and Utx-deficient or -sufficient.

Project description:The biological functions of histone demethylases Jmjd3 and Utx remain poorly understood. We assessed such functions in developing T cells, using conditional (CD4-Cre-mediated) gene disruption, by inactivating Kdm6a and Kdm6b, respectively encoding Utx and Jmjd3, in immature CD4+CD8+ thymocytes. We compared microarray gene expression in mature (Va2hi CD24lo) mutant and wild-type CD4+CD8- thymocytes carrying the OT-II TCR transgene. We show that Jmjd3 and Utx redundantly promote H3K27Me3 removal at, and expression of, a specific subset of genes involved in terminal thymocyte differentiation, especially S1pr1, encoding a sphingosine-phosphate receptor required for thymocyte egress. Mature (Va2hi CD24lo) CD4 thymocytes were sorted from freshly prepared single-cell suspensions OT-II TCR transgenic thymocytes deficient for Utx and Jmjd3 (dKO, CD4-Cre conditional deletion of floxed Kdm6a and Kdm6b alleles), and from Cre-negative controls (wild-type). Total RNA was extracted from sorted thymocytes using the RNeasy Plus Mini Kit (Qiagen) and processed for microarray analyses (Affymetrix Mouse Exon 1.0 ST array) at the NCI microarray facility, following the manufacturer’s recommendation. Data is generated from 3 replicates from each experiment.

2015-09-17 | E-GEOD-70363 | biostudies-arrayexpress

Characterizing the contrasting roles of JMJD3 and UTX histone demethylases in T cell acute lymphoblastic leukemia [GSKJ4_RNA-seq]

Project description:T-cell acute lymphoblastic leukemia (T-ALL) is an immature hematopoietic malignancy driven mainly by oncogenic activation of NOTCH1 signaling. In this study we chemically inhibited the H3K27me3 demethylase JMJD3 using the GSKJ4 inhibitor and assayed for genome-wide changes in H3K27me3 and JMJD3 enrichment. This piece of data was further integrated to expression changes using RNA sequencing as well as ChIP-Sequencing analysis of H3K27me3 upon genomic knock-down of JMJD3 and UTX. These results, coupled to genomic analysis of primary samples for the genomic status of the UTX gene in T-ALL, helped us to identify a hitherto unknown role of JMJD3 as an oncogenice facilitator in leukemia whereas UTX seems to play a tumor suppressor role.

2014-10-01 | GSE56691 | GEO

Characterizing the contrasting roles of JMJD3 and UTX histone demethylases in T cell acute lymphoblastic leukemia [GSKJ4_ChIP-seq]

Project description:T-cell acute lymphoblastic leukemia (T-ALL) is an immature hematopoietic malignancy driven mainly by oncogenic activation of NOTCH1 signaling. In this study we chemically inhibited the H3K27me3 demethylase JMJD3 using the GSKJ4 inhibitor and assayed for genome-wide changes in H3K27me3 and JMJD3 enrichment. This piece of data was further integrated to expression changes using RNA sequencing as well as ChIP-Sequencing analysis of H3K27me3 upon genomic knock-down of JMJD3 and UTX. These results, coupled to genomic analysis of primary samples for the genomic status of the UTX gene in T-ALL, helped us to identify a hitherto unknown role of JMJD3 as an oncogenice facilitator in leukemia whereas UTX seems to play a tumor suppressor role.

2014-10-01 | GSE56693 | GEO

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