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Genome-wide binding profiles of JUNB in unstimulated HoxER-PU.1 WT and PU.1 KO neutrophils

ABSTRACT: Genome-wide binding profiles of JUNB in unstimulated HoxER-PU.1 WT and PU.1 KO neutrophils

PROVIDER: PRJNA434708 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6751050_1.fastq.gz	Fastqsanger.gz
	SRR6751050_2.fastq.gz	Fastqsanger.gz
	SRR6751051_1.fastq.gz	Fastqsanger.gz
	SRR6751051_2.fastq.gz	Fastqsanger.gz
	SRR6751052_1.fastq.gz	Fastqsanger.gz

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Genome-wide binding profiles of JUNB in unstimulated HoxER-PU.1 WT and PU.1 KO neutrophils

Project description:Neutrophils are essential first line defense cells against invading pathogens, yet their inappropriate activation contributes to immunological diseases and can cause collateral tissue damage. However, neutrophil-intrinsic mechanisms adjusting an appropriate inflammatory response are unknown. Herein, we conditionally deleted PU.1, a key myeloid transcription factor, from the neutrophils of mice undergoing fungal infection, and then performed comprehensive epigenomic profiling. We find that a major function of PU.1 is to restrain the neutrophils’ immune response by broadly suppressing genomic enhancer outputs via recruiting histone deacetylase activity, thereby limiting the immune-stimulatory AP1-transcription factor JUNB from entering chromatin. Thus, PU.1 acts as rheostat of the inflammatory chromatin state, safeguarding the neutrophil epigenome from undergoing uncontrolled activation prior to pathogenic stimulation.

2019-03-19 | GSE110862 | GEO

Transcritpional profiling of unstimulated and Candida albicans stimulated HoxER-PU.1 WT and HoxER-PU.1 KO neutrophils

Project description:Transcritpional profiling of unstimulated and Candida albicans stimulated HoxER-PU.1 WT and HoxER-PU.1 KO neutrophils

| PRJNA434710 | ENA

Genome-wide maps of chromatin state in unstimulated HoxER-PU.1 WT and HoxER-PU.1 KO neutrophils

Project description:Genome-wide maps of chromatin state in unstimulated HoxER-PU.1 WT and HoxER-PU.1 KO neutrophils

| PRJNA434712 | ENA

Transcritpional profiling of unstimulated and Candida albicans stimulated HoxER-PU.1 WT and HoxER-PU.1 KO neutrophils

Project description:Neutrophils are essential first line defense cells against invading pathogens, yet their inappropriate activation contributes to immunological diseases and can cause collateral tissue damage. However, if and how neutrophils cell-intrinsically titrate their inflammatory response remains unknown. Here, we conditionally deleted PU.1, a key myeloid transcription factor, from the neutrophils of mice undergoing fungal infection, and then performed comprehensive epigenomic profiling. We find that a major function of PU.1 is to restrain the neutrophils’ immune response by broadly suppressing genomic enhancer outputs via recruiting histone deacetylase activity, thereby limiting the immune-stimulatory AP1-transcription factor JUNB from entering chromatin. Thus, neutrophils rely on a direct PU.1 repressor function as rheostat of the inflammatory chromatin state, safeguarding their epigenome from undergoing uncontrolled activation prior to pathogenic stimulation.

2019-03-19 | GSE110864 | GEO

Genome-wide maps of chromatin state in unstimulated HoxER-PU.1 WT and HoxER-PU.1 KO neutrophils

Project description:Neutrophils are essential first line defense cells against invading pathogens, yet their inappropriate activation contributes to immunological diseases and can cause collateral tissue damage. However, if and how neutrophils cell-intrinsically titrate their inflammatory response remains unknown. Here, we conditionally deleted PU.1, a key myeloid transcription factor, from the neutrophils of mice undergoing fungal infection, and then performed comprehensive epigenomic profiling. We find that a major function of PU.1 is to restrain the neutrophils’ immune response by broadly suppressing genomic enhancer outputs via recruiting histone deacetylase activity, thereby limiting the immune-stimulatory AP1-transcription factor JUNB from entering chromatin. Thus, neutrophils rely on a direct PU.1 repressor function as rheostat of the inflammatory chromatin state, safeguarding their epigenome from undergoing uncontrolled activation prior to pathogenic stimulation.

2019-03-19 | GSE110861 | GEO

Genome-wide binding profiles of PU.1 in unstimulated and Candida albicans stimulated HoxER-PU.1 WT neutrophils

Project description:Neutrophils are essential first line defense cells against invading pathogens, yet their inappropriate activation contributes to immunological diseases and can cause collateral tissue damage. However, if and how neutrophils cell-intrinsically titrate their inflammatory response remains unknown. Here, we conditionally deleted PU.1, a key myeloid transcription factor, from the neutrophils of mice undergoing fungal infection, and then performed comprehensive epigenomic profiling. We find that a major function of PU.1 is to restrain the neutrophils’ immune response by broadly suppressing genomic enhancer outputs via recruiting histone deacetylase activity, thereby limiting the immune-stimulatory AP1-transcription factor JUNB from entering chromatin. Thus, neutrophils rely on a direct PU.1 repressor function as rheostat of the inflammatory chromatin state, safeguarding their epigenome from undergoing uncontrolled activation prior to pathogenic stimulation.

2019-03-19 | GSE110863 | GEO

Chromatin accessibility in C. albicans stimulated HoxER-PU.1 WT and HoxER-PU.1 KO neutrophils and DMSO, TSA or Entinostat treated HoxER-PU.1 WT neutrophils

Project description:Neutrophils are essential first line defense cells against invading pathogens, yet their inappropriate activation contributes to immunological diseases and can cause collateral tissue damage. However, if and how neutrophils cell-intrinsically titrate their inflammatory response remains unknown. Here, we conditionally deleted PU.1, a key myeloid transcription factor, from the neutrophils of mice undergoing fungal infection, and then performed comprehensive epigenomic profiling. We find that a major function of PU.1 is to restrain the neutrophils’ immune response by broadly suppressing genomic enhancer outputs via recruiting histone deacetylase activity, thereby limiting the immune-stimulatory AP1-transcription factor JUNB from entering chromatin. Thus, neutrophils rely on a direct PU.1 repressor function as rheostat of the inflammatory chromatin state, safeguarding their epigenome from undergoing uncontrolled activation prior to pathogenic stimulation.

2019-03-19 | GSE110860 | GEO

Genome-wide binding profiles of PU.1 in unstimulated and Candida albicans stimulated HoxER-PU.1 WT neutrophils

Project description:Genome-wide binding profiles of PU.1 in unstimulated and Candida albicans stimulated HoxER-PU.1 WT neutrophils

| PRJNA434711 | ENA

Chromatin accessibility in C. albicans stimulated HoxER-PU.1 WT and HoxER-PU.1 KO neutrophils and DMSO, TSA or Entinostat treated HoxER-PU.1 WT neutrophils

Project description:Chromatin accessibility in C. albicans stimulated HoxER-PU.1 WT and HoxER-PU.1 KO neutrophils and DMSO, TSA or Entinostat treated HoxER-PU.1 WT neutrophils

| PRJNA434709 | ENA

ChIP-Seq analysis of PU.1, BATF, and JunB in murine BMDCs

Project description:Purpose: The purpose of this study is to identify the genome-wide binding sites for IRF4 interaction partners PU.1, BATF, and JunB in dendritic cells. These ChIP-seq data were integrated with gene expression analysis in IRF4-sufficient and -deficient BMDCs in order to assemble an IRF4 gene regulatory network. Hematopoietic bone marrow progenitors from C57BL/6 mice were differentiated with GM-CSF and IL-4 for 5 days. On day 6, BMDCs were stimulated for 6 hours with 100ng/ml LPS. Fixed chromatin was immunoprecipitated with anti-PU.1, BATF, and JunB antibodies and subjected to high-throughput sequencing. The sequencing data for the input DNA was previously submitted as GSM999807.

2013-12-22 | E-GEOD-52772 | biostudies-arrayexpress

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