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Chromatin immunoprecipitation sequencing (ChIP-Seq) for Bhlhe40 from naïve and IL-4c-stimulated large peritoneal macrophages (LPMs)

ABSTRACT: Chromatin immunoprecipitation sequencing (ChIP-Seq) for Bhlhe40 from naïve and IL-4c-stimulated large peritoneal macrophages (LPMs)

PROVIDER: PRJNA517407 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8494734.fastq.gz	Fastqsanger.gz
	SRR8494735.fastq.gz	Fastqsanger.gz
	SRR8494736.fastq.gz	Fastqsanger.gz
	SRR8494737.fastq.gz	Fastqsanger.gz

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Chromatin immunoprecipitation sequencing (ChIP-Seq) for Bhlhe40 from naïve and IL-4c-stimulated large peritoneal macrophages (LPMs)

Project description:Most tissue-resident macrophage populations develop during embryogenesis, self-renew in the steady state, and can expand during type 2 immunity. Whether shared mechanisms regulate macrophage proliferation in homeostasis and disease is unclear. We found that the transcription factor Bhlhe40 was cell-intrinsically required in large peritoneal macrophages (LPMs) for self-renewal and maintenance, but was not required in other resident macrophages. Bhlhe40 was selectively necessary in LPMs for proliferation, but not polarization, in response to IL-4. During a helminth infection, Bhlhe40 was required for normal LPM cell cycling. Bhlhe40 repressed the expression of Maf and Mafb and directly promoted expression of cell cycle-related transcripts to enable proliferation of LPMs. Genomic sites bound by Bhlhe40 in LPMs included some co-bound by the macrophage lineage-determining factor PU.1 and others uniquely bound by Bhlhe40, including Maf and cell cycle-related loci. Our findings demonstrate a tissue-specific control mechanism regulating resident macrophage proliferation in homeostasis and type 2 immunity.

2019-04-30 | GSE125729 | GEO

Expression data from mouse differentiated Bhlhe40-GFPneg and Bhlhe40-GFPpos TH17 cells

Project description:Microarray data on TH17 cells from Bhlhe40-GFP reporter mice We used microarrays to detail the global programme of gene expression in polarized Bhlhe40-GFPneg and Bhlhe40-GFPpos TH17 cells Purified naÃ¯ve CD4 T cells from spleen were polarized under TH17 condition in vitro. On day 4, cells were stimulated with PMA and ionomycin, and sorted by their Bhlhe40-GFP expression prior to microarray analysis

2016-01-04 | E-GEOD-75407 | biostudies-arrayexpress

Role of BHLHE40 in shaping macrophage inflammatory response

Project description:BHLHE40 is a member of basic helix-loop-helix family transcription factors and highly conserved across mammalian species. Structurally, BHLHE40 consists of an N-terminal basic DNA binding domain, a helix-loop-helix dimerization domain, and a protein interacting orange domain. BHLHE40 is known to regulate a wide variety of essential cellular processes, including cell cycle, cellular proliferation, programmed cell death, cellular development and differentiation, and circadian rhythm. Here we isolated thioglycollate-elicited peritoneal macrophages (PMs) from 3 mice per group (Lyz2cre and Lyz2cre:BHLHE40Fl/Fl). These cells were stimulated with 100ng/ml LPS for 4 hours. Total RNA was isolated and subjected to RNAseq analyses.

2021-09-24 | GSE176174 | GEO

Microarray data for Bhlhe40-sufficient and -deficient resident macrophages

2019-04-30 | GSE125727 | GEO

Expression data from mouse differentiated Bhlhe40-GFPneg and Bhlhe40-GFPpos TH17 cells

2016-01-04 | GSE75407 | GEO

Molecular subtypes of malignant peritoneal mesothelioma

Project description:Malignant Peritoneal Mesothelioma (PeM) is a rare but frequently fatal cancer that originates from the peritoneal lining of the abdomen. Standard treatment of PeM is limited to cytoreductive surgery and/or chemotherapy, and no targeted therapies for PeM yet exist. This study performs comprehensive integrative analysis of genome, transcriptome, and proteome of treatment-naïve PeM tumors with the aim of identifying mesothelioma-related molecular alterations and potentially identifying novel treatment strategies.

2018-12-11 | PXD008873 | Pride

STAT4 promotes Bhlhe40 induction to drive protective IFN-g from natural killer cells during viral infection [BHLHE40 CUT&RUN]

Project description:NK cells represent a cellular component of the mammalian innate immune system, and mount rapid responses against viral infection, including the secretion of the potent anti-viral effector cytokine IFN-g. Following mouse cytomegalovirus (MCMV) infection, Bhlhe40 was the most highly induced transcription factor in NK cells among the basic helix-loop-helix family. Bhlhe40 upregulation in NK cells depended upon IL-12 and IL-18 signals, with the promoter of Bhlhe40 enriched for STAT4 and the permissive histone H3K4me3, and STAT4-deficient NK cells showing an impairment of Bhlhe40 induction and diminished H3K4me3. Transcriptomic and protein analysis of Bhlhe40-deficient NK cells revealed a defect in IFN-g production during MCMV infection, resulting in diminished protective immunity following viral challenge. Finally, we provide evidence that Bhlhe40 directly promotes IFN-g by binding throughout the Ifng loci in activated NK cells. Thus, our study reveals how STAT4-mediated control of Bhlhe40 drives protective IFN-g secretion by NK cells during viral infection.

2023-09-13 | GSE242900 | GEO

BHLHE40 is key hypoxia-induced transcriptional repressor in beta cells

Project description:To assess the impact of hypoxia on global gene expression of beta cells, we performed bulk RNA-seq on mouse islets, human islets and MIN6 cells. Bhlhe40 was transcriptional repressor which was highly induced by hypoxia in beta cells. Thus, we established Bhlhe40 overexpressing MIN6 cells and performed RNA-seq to identify the targets of Bhlhe40.

2023-05-01 | GSE202603 | GEO

Impact of BHLHE40-AS1 over expression in MCF10A cells

Project description:BHLHE40-AS1 was cloned into pBABE-Puro. Empty vector and pBABE-BHLHE40-AS1 were used to generate retrovirus and infect MCF10A cells. Transduced cells were selected with 1ug/mL puromycin for 2 weeks.

2020-06-10 | GSE136579 | GEO

BHLHE40 regulates myeloid cell polarization through IL-10-dependent and independent mechanisms

Project description:Better understanding of the host responses to Mycobacterium tuberculosis (Mtb) infections is required to prevent tuberculosis and develop new therapeutic interventions. The host transcription factor BHLHE40 is essential for controlling Mtb infection, in part by repressing Il10 expression, where excess IL-10 contributes to the early susceptibility of Bhlhe40-/- mice to Mtb infection. Deletion of Bhlhe40 in lung macrophages and dendritic cells is sufficient to increase the susceptibility of mice to Mtb infection, but how BHLHE40 impacts macrophage and dendritic cell responses to Mtb is unknown. Here we report that BHLHE40 is required in myeloid cells exposed to GM-CSF, an abundant cytokine in the lung, to promote the expression of genes associated with a pro-inflammatory state and better control of Mtb infection. Loss of Bhlhe40 expression in murine bone marrow derived myeloid cells cultured in the presence of GM-CSF results in lower levels of pro-inflammatory associated signaling molecules IL-1b, IL-6, IL-12, TNFα, iNOS, IL-2, KC, and RANTES, as well as higher levels of the anti-inflammatory associated molecules MCP-1 and IL-10 following exposure to heat-killed Mtb. Deletion of Il10 in Bhlhe40-/- myeloid cells restored some, but not all, pro-inflammatory signals, demonstrating that BHLHE40 promotes pro-inflammatory responses via both IL-10-dependent and independent mechanisms. In addition, we show that macrophages and neutrophils within the lungs of Mtb-infected Bhlhe40-/- mice exhibit defects in iNOS production compared to infected WT mice, supporting that BHLHE40 promotes pro-inflammatory responses in innate immune cells, which may contribute to the essential role for BHLHE40 during Mtb infection in vivo.

2024-07-02 | GSE265840 | GEO

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