Jmjd3-Lab UTX-Lab CUT&Tag
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA776257 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR16635483_1.fastq.gz | Fastqsanger.gz | |||
| SRR16635483_2.fastq.gz | Fastqsanger.gz | |||
| SRR16635485_1.fastq.gz | Fastqsanger.gz | |||
| SRR16635485_2.fastq.gz | Fastqsanger.gz | |||
| SRR16635487_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 6 |
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Project description:To understand the role of the H3K27me3 demethylases, UTX and JMJD3, in B cell differentiation. CUT&Tag for H3K27me3 was performed on CreCtrl and dKO (UTX and JMJD3-deficient) PC at day three post in vivo stimulation with LPS.
2022-02-01 | GSE185098 | GEO
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 | GSE186828 | GEO
Project description:H3K27me3 CUT&Tag - Jmjd3-scKO, Utx-scKO, Tdt-Ctrl, IgG-His
| PRJNA776264 | ENA
Project description:H3K4me3 CUT&Tag - Jmjd3-scKO, Utx-scKO, Tdt-Ctrl, IgG-His
| PRJNA776262 | ENA
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
Project description:The level of H3K27me3 were examined by conditional knockout Ezh2, Utx or Jmjd3 in mouse chondrocyte
2023-08-30 | GSE237698 | GEO
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 | GSE186829 | GEO
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
Project description:The Jumonji domain-containing protein D3 (JMJD3) is a histone demethylases that specifically demethylate di-and tri-methyl-lysine 27 on histone H3 (H3K27me2/3) to regulate correlation gene expression. JMJD3 promotes the differentiation and apoptosis of leukemia cells, and inhibits cell proliferation by regulating the methylation level of H3K27. JMJD3 promotes Zebrafish myeloid development and inhibits erythroid development. However, the function and mechanism of JMJD3 in human erythropoiesis still remains largely unknown. Here, we demonstrated that JMJD3 was expressed throughout the erythroid development process, with higher expression in the early stages. During the early erythropoiesis, JMJD3 deficiency caused cell cycle arrest in the G0/G1 phase, which impaired cell growth and erythroid progenitors differentiation, but did not result in cell apoptosis. Cut&tag sequencing and RNA sequencing analysis discovered that JMJD3 regulated the expression of cell cycle and erythrocyte differentiation associated factor lymphoid enhancer-binding factor 1(LEF1) dependently of H3K27me3 modifications. Our findings provide novel insights into understanding of the roles of JMJD3 and H3K27me3 in the regulation of erythropoiesis, and further indicates the significance of epigenetic regulation for the erythropoiesis.
2025-07-01 | GSE295820 | GEO
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