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H3K27me3 localization in UTX deficient Plasma cells by ChIP-seq

ABSTRACT: H3K27me3 localization in UTX deficient Plasma cells by ChIP-seq

PROVIDER: PRJNA767651 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16130903_1.fastq.gz	Fastqsanger.gz
	SRR16130903_2.fastq.gz	Fastqsanger.gz
	SRR16130904_1.fastq.gz	Fastqsanger.gz
	SRR16130904_2.fastq.gz	Fastqsanger.gz
	SRR16130905_1.fastq.gz	Fastqsanger.gz

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H3K27me3 localization in UTX deficient Plasma cells by ChIP-seq

Project description:To evalute how deletion of H3K27me3 demethylases, UTX and JMJD3, affect H3K27me3 enrichment in plasma cells. ChIP-seq for H3K27me3 was performed on CreCtrl and dKO (UTX and JMJD3-deficient) PC at day three post in vivo stimulation with LPS.

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H3K27me3 localization in UTX deficient Plasma cells by CUT&Tag

Project description:H3K27me3 localization in UTX deficient Plasma cells by CUT&Tag

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H3K27me3 localization in UTX deficient Plasma cells by CUT&Tag

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.

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HNF1A, UTX, H3K27me3 and H3K27ac ChIP-seq in wild-type and UTX- or HNF1A-deficient mouse pancreas

Project description:HNF1A and UTX are putative tumor suppressors in pancreatic cancer. In this study, we have combined mouse genetics, transcriptomics and genome binding studies to link HNF1A and UTX in a molecular mechanism that suppresses pancreatic cancer. In this session, we have profiled UTX, HNF1A, H3K27me3 and H3K27ac in normal and UTX- or HNF1A-deficient mouse pancreas by ChIP-seq experiments. We show that HNF1A recruits UTX to its genomic targets in pancreatic acinar cells, which results in remodeling of the chromatin landscape and activation of a broad transcriptional program of differentiated acinar cells, which in turn indirectly suppresses tumor suppressor pathways.

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Project description:HNF1A, UTX, H3K27me3 and H3K27ac ChIP-seq in wild-type and UTX- or HNF1A-deficient mouse pancreas

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X-linked H3K27me3 demethylase Utx is required for embryonic development in a sex-specific manner [ChIP-Seq data]

Project description:Embryogenesis requires the timely and coordinated activation of developmental regulators. It has been suggested that the recently discovered class of histone demethylases (UTX and JMJD3) that specifically target the repressive H3K27me3 modification play an important role in the activation of M-bM-^@M-^\bivalentM-bM-^@M-^] genes in response to specific developmental cues. To determine the requirements for UTX in pluripotency and development, we have generated Utx null ES cells and mutant mice. The loss of UTX had a profound effect during embryogenesis. Utx null embryos had reduced somite counts, neural tube closure defects and heart malformation which presented between E9.5 and E13.5. Unexpectedly, homozygous mutant female embryos were more severely affected than hemizygous mutant male embryos. In fact, we observed the survival of a subset of UTX-deficient males which were smaller in size and had reduced life-span. Interestingly, these animals were fertile with normal spermatogenesis. Consistent with a mid-gestation lethality, UTX null male and female ES cells gave rise to all three germ layers in teratoma assays although sex-specific differences could be observed in the activation of developmental regulators in embryoid body assays. Lastly, ChIP-seq analysis revealed an increase in H3K27me3 in Utx null male ES cells. In summary, our data demonstrate sex-specific requirements for this X-linked gene while suggesting a role for UTY during development. Examination of H3K27me3 and H3K4me3 in UtxKO ES cells (V6.5 background) vs UtxFlx (V6.5 background) ES cells grown in LIF containing ES cell media or treated with retinoic acid without LIF.

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The X-linked H3K27me3 demethylase Utx is required for embryonic development in a sex specific manner [Agilent array data]

Project description:Embryogenesis requires the timely and coordinated activation of developmental regulators. It has been suggested that the recently discovered class of histone demethylases (UTX and JMJD3) that specifically target the repressive H3K27me3 modification play an important role in the activation of M-bM-^@M-^\bivalentM-bM-^@M-^] genes in response to specific developmental cues. To determine the requirements for UTX in pluripotency and development, we have generated Utx null ES cells and mutant mice. The loss of UTX had a profound effect during embryogenesis. Utx null embryos had reduced somite counts, neural tube closure defects and heart malformation which presented between E9.5 and E13.5. Unexpectedly, homozygous mutant female embryos were more severely affected than hemizygous mutant male embryos. In fact, we observed the survival of a subset of UTX-deficient males which were smaller in size and had reduced life-span. Interestingly, these animals were fertile with normal spermatogenesis. Consistent with a mid-gestation lethality, UTX null male and female ES cells gave rise to all three germ layers in teratoma assays although sex-specific differences could be observed in the activation of developmental regulators in embryoid body assays. Lastly, ChIP-seq analysis revealed an increase in H3K27me3 in Utx null male ES cells. In summary, our data demonstrate sex-specific requirements for this X-linked gene while suggesting a role for UTY during development. Keywords: Expression profiling by array Four-condition experiment, Wt (V6.5) ES vs. RA-treated Wt (V6.5) ES cells; UtxKO ES vs RA-treated UtxKO ES cells. This Series represents the Agilent microarray data only (not ChIP-Seq).

2012-07-31 | E-GEOD-39473 | biostudies-arrayexpress

The X-linked H3K27me3 demethylase Utx is required for embryonic development in a sex specific manner

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2012-07-31 | E-GEOD-39222 | biostudies-arrayexpress

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Project description:To understand the role of the H3K27me3 demethylases, UTX and JMJD3, in regulating chromatin accessibility. ATAC-seq was performed on the following populations from control (CreCtrl) and double knockout (dKO) mice: naïve marginal zone B cells and follicular B cells as well plasma cell generated at three days post in vivo stimulation with LPS.

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