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Chromatin binding protein PHF6 regulates activity-dependent transcription networks to promote hunger response [ChIP-Seq]

ABSTRACT: Chromatin binding protein PHF6 regulates activity-dependent transcription networks to promote hunger response [ChIP-Seq]

PROVIDER: PRJNA552959 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9648634_1.fastq.gz	Fastqsanger.gz
	SRR9648634_2.fastq.gz	Fastqsanger.gz
	SRR9648635_1.fastq.gz	Fastqsanger.gz
	SRR9648635_2.fastq.gz	Fastqsanger.gz
	SRR9648636_1.fastq.gz	Fastqsanger.gz

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Chromatin binding protein PHF6 regulates activity-dependent transcription networks to promote hunger response [RNA-Seq]

Project description:We revealed that PHF6 bound to the promoters of a subset of neuronal immediate-early genes (IEGs) and regulate their expression levels. hunger state.

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Chromatin binding protein PHF6 regulates activity-dependent transcription networks to promote hunger response [ChIP-Seq]

Project description:We revealed that PHF6 was bound to the promoters of a subset of neuronal immediate-early genes (IEGs), and this chromatin binding was dynamically regulated by hunger state.

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Chromatin binding protein PHF6 regulates activity-dependent transcription networks to promote hunger response

Project description:Chromatin binding protein PHF6 regulates activity-dependent transcription networks to promote hunger response

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Chromatin binding protein PHF6 regulates activity-dependent transcription networks to promote hunger response [RNA-Seq]

Project description:Chromatin binding protein PHF6 regulates activity-dependent transcription networks to promote hunger response [RNA-Seq]

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Chromatin binding protein PHF6 regulates activity-dependent transcription networks to promote hunger response

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

2020-03-16 | GSE139545 | GEO

PHF6 OCCUPANCYIN HUMAN T-CELL ACUTE LYMPHOBLASTIC LEUKEMIA

Project description:Here we identify the genome-wide occupancy of PHF6 in T-ALL cells. Human T-ALL cells were cross-linked with formaldehyde for 20 min. DNA was enriched by chromatin immunoprecipitation (ChIP) and analyzed by Solexa sequencing. A sample of whole cell extract (WCE) was sequenced and used as the background to determine enrichment. ChIP was performed using an antibody against total PHF6 (Bethyl A301-451A). This represents the ChIP-seq portion of this dataset.

2014-04-01 | E-GEOD-45864 | biostudies-arrayexpress

RNA sequencing of isogenic Phf6 wild type and Phf6 knockout mouse T-ALL cells

Project description:Loss-of-function mutations Phf6 occur frequently in both adult and pediatric T-cell Acute Lymphoblastic Leukemia (T-ALL). Although Phf6 is widely expressed, little is known about its proposed function as epigenetic regulator and tumor suppressor. To address the role of Phf6 in the leukemia development, here we analyze by RNAseq the gene expression profiles of isogenic Phf6 wild type and Phf6 knockout leukemia cells transformed by overexpression of an oncogenic mutant form of the NOTCH1 receptor.

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PHF6 knockdown in rat cortical neurons

Project description:E18 embryonic rat cortical neurons cultured in vitro are infected with lentivirus expressing control or PHF6shRNA-2, and harvested 5 days after infection pLL3.7 lentivirus expressing control or PHF6shRNA-2 was generated in 293T cells and concentrated using ultracentrifuge. In vitro cultured cortical neurons were infected and RNA was harvested 5 days after infection. PHF6 knockdown was validated by QPCR before sample was processed for microarray analysis.

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AgRP neuron epigenomes across hunger states reveal that IRF3 mediates leptin's effects

Project description:AgRP neurons in the arcuate nucleus of the hypothalamus (ARC) coordinate homeostatic changes in appetite associated with fluctuations in food availability and leptin signaling. Identifying the relevant transcriptional regulatory pathways in these neurons has been a priority, yet such attempts have been stymied due to their low abundance and the rich cellular diversity of the ARC. Here we generated male mouse AgRP neuron-specific transcriptomic and chromatin accessibility profiles during three distinct hunger states of satiety, fasting-induced hunger, and leptin-induced hunger suppression. Cis-regulatory analysis of these integrated datasets enabled the identification of 28 putative hunger-promoting and 29 putative hunger-suppressing transcriptional regulators in AgRP neurons, 16 of which were predicted to be transcriptional effectors of leptin. Within our dataset, Interferon regulatory factor 3 (IRF3) emerged as a leading candidate mediator of leptin-induced hunger-suppression. Gain- and loss-of-function experiments in vivo confirm the role of IRF3 in mediating the acute satiety-evoking effects of leptin in AgRP neurons, while live-cell imaging in vitro indicate that leptin can activate neuronal IRF3 in a cell autonomous manner. Finally, we employ CUT&RUN to uncover direct transcriptional targets of IRF3 in AgRP neurons in vivo. Thus, our findings identify AgRP neuron-expressed IRF3 as a key transcriptional effector of the hunger-suppressing effects of leptin.

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Transcriptomic changes in PHF6 knockout THP1 human AML cell line on rescue with PHF6 wildtype (with and without PHIP) or rescue with PHF6R274Q mutant

Project description:PHF6 is a transcriptional regulator mutated in 3-5% of acute myeloid leukemia. To understand the effect of loss and clinical mutation of PHF6 on the transcriptome of myeloid cells, we generated multiple wildtype and PHF6 knockout clones, as well as clones expressing the most common clinical mutant of the protein-PHF6R274Q. We observed that both single and double knockouts and mutation of PHF6 shifted the cells towards stemness and away from differentiation. Additionally we identified PHIP as a possible functional partner for PHF6. To investigate their common biological function, we generated multiple single knockout clones of PHIP as well as double knockout clones of PHIP and PHF6, and observed that, similar to single knockout of PHF6, PHIP knockout and double knockout also shifted cells towards stemness and away from differentiation. Collectively, our experiments show that PHF6 and PHIP, separately identified as being mutated in AML, exert similar downstream effects on the AML transcriptome.

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