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Menin orchestrates macrophage reprogramming to maintain the pulmonary immune homeostasis

ABSTRACT: Menin orchestrates macrophage reprogramming to maintain the pulmonary immune homeostasis

PROVIDER: PRJNA1005936 | ENA |

REPOSITORIES: ENA

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Menin orchestrates macrophage reprogramming to maintain the pulmonary immune homeostasis

Project description:The potential importance of menin in immune regulation remains unclear. Here, we report that myeloid deletion of Men1 results in the development of spontaneous pulmonary alveolar proteinosis (PAP). This is strongly correlated with impaired development of alveolar macrophages (AM) and epigenetic inactivation of the GM-CSF pathway caused by Men1 deficiency. Mechanistically, menin directly interacts with SETD2 and collectively maintain GM-CSF expression through H3K36me3, which orchestrates AM reprogramming and pulmonary immune homeostasis.

2024-12-25 | GSE240958 | GEO

Menin orchestrates macrophage reprogramming to maintain the pulmonary immune homeostasis [RNA-seq]

Project description:Menin is a scaffold protein encoded by the Men1 gene, and it interacts with a variety of chromatin regulators to activate or repress cellular processes. The potential importance of menin in immune regulation remains unclear. Here, we report that myeloid deletion of Men1 results in the development of spontaneous pulmonary alveolar proteinosis (PAP). This is strongly correlated with impaired development of alveolar macrophages (AM) and epigenetic inactivation of the GM-CSF pathway caused by Men1 deficiency. Mechanistically, menin directly interacts with SETD2 through the NTD and Palm domains to maintain protein stability and chromatin recruitment. SETD2 and menin collectively maintain GM-CSF expression through H3K36me3, which orchestrates AM reprogramming and pulmonary immune homeostasis.

2024-08-31 | GSE265805 | GEO

Menin orchestrates macrophage reprogramming to maintain the pulmonary immune homeostasis [RNA-seq]

Project description:Menin orchestrates macrophage reprogramming to maintain the pulmonary immune homeostasis [RNA-seq]

| PRJNA1104231 | ENA

The Menin–Bach2 axis is critical for regulating CD4 T cell senescence and homeostasis

Project description:Although CD4 T cell senescence plays an important role in immunosenescence, the mechanisms remain unclear. We found that T cell-specific Menin deficiency results in the premature senescence of CD4 T cells, accompanied by the senescence-associated secretory phenotype (SASP) after antigenic stimulation. TH1 and TH2 differentiation was dysregulated in Menin-knockout CD4 T cells. Bach2, which regulates SASP and TH differentiation, was identified as a Menin target. Menin binds to the Bach2 locus, and controls its expression through maintenance of histone acetylation. These findings reveal a critical role of the Menin-Bach2 pathway in regulating CD4 T cell senescence and homeostasis, thus indicating the involvement of this pathway in the inhibition of age-associated development of inflammatory diseases, which are induced by immunosenescence. Examination of transcriptional factor Menin binding and histone modefications in Menin WT and KO CD4 T cells

2014-03-27 | E-GEOD-53831 | biostudies-arrayexpress

The Menin-Bach2 axis is critical for regulating CD4 T cell senescence and cytokine homeostasis

Project description:Although CD4 T cell senescence plays an important role in immunosenescence, the mechanism behind this process remains unclear. Here we show that T cell-specific Menin deficiency results in the premature senescence of CD4 T cells, which is accompanied by the senescence-associated secretory phenotype after antigenic stimulation and dysregulated cytokine production. Menin is required for the expansion and survival of antigen-stimulated CD4 T cells in vivo and acts by targeting Bach2, which is known to regulate immune homeostasis and cytokine production. Menin binds to the Bach2 locus, and controls its expression through maintenance of histone acetylation. Menin binding at the Bach2 locus and the Bach2 expression are decreased in the senescent CD4 T cells. These findings reveal a critical role of the Menin-Bach2 pathway in regulating CD4 T cell senescence and cytokine homeostasis, thus indicating the involvement of this pathway in the inhibition of immunosenescence. Gene expression in Menin WT-TH and Menin KO-TH

2014-03-27 | E-GEOD-49968 | biostudies-arrayexpress

Oxidative phosphorylation selectively orchestrates tissue macrophage homeostasis

Project description:Oxidative phosphorylation selectively orchestrates tissue macrophage homeostasis

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NHGRI Menin ChIP-Chip

Project description:Multiple endocrine neoplasia type I (MEN1) is a familial cancer syndrome characterized primarily by tumors of multiple endocrine glands. The gene for MEN1 encodes a ubiquitously expressed tumor suppressor protein called menin. Menin was recently shown to interact with several components of a trithorax family histone methyltransferase complex including ASH2, Rbbp5, WDR5, and the leukemia proto-oncoprotein MLL. To elucidate menin's role as a tumor suppressor and gain insights into the endocrine-specific tumor phenotype in MEN1, we mapped the genomic binding sites of menin, MLL1, and Rbbp5, to approximately 20,000 promoters in HeLa S3, HepG2, and pancreatic islet cells using the strategy of chromatin-immunoprecipitation coupled with microarray analysis. We found that menin, MLL1, and Rbbp5 localize to the promoters of thousands of human genes but do not always bind together. These data suggest that menin functions as a general regulator of transcription. Keywords: ChIP/chip NHGRI Menin ChIP-Chip

2006-07-24 | E-GEOD-5357 | biostudies-arrayexpress

BMPR2 Regulates Hypoxic Exosome Signaling to Maintain Vascular Homeostasis

Project description:Endothelial cells (EC) sense stimuli in the circulation and release responsive signaling molecules to coordinate the multicellular adaptations required to maintain vascular homeostasis. The goal of this study were to analyze the transcriptional changes induced by hypoxia in control donor pulmonary arterial endothelial cells and the effect of loss of BMPR2 that is associated with pulmonary arterial hypertension.

2020-09-01 | GSE157231 | GEO

The Menin–Bach2 axis is critical for regulating CD4 T cell senescence and homeostasis

2014-03-27 | GSE53831 | GEO

MLL-Menin inhibition reverses pre-leukemic progenitor self-renewal induced by NPM1c mutations [RNA-Seq]

Project description:Menin binding to MLL1 is required to maintain self-renewal properties of NPM1c progenitors at different stages of leukemia development

2020-02-11 | GSE129637 | GEO

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