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A pan-family screen of Nuclear Receptors in immunocytes reveals ligand-dependent inflammasome control

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE254573 | GEO | 2024/12/16

REPOSITORIES: GEO

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A pan-family screen of Nuclear Receptors in immunocytes reveals ligand-dependent inflammasome control [ChIPmentation]

Project description:We profiled RXRα binding to genomic loci in peritoneal macrophages using ChIPmentation.

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A pan-family screen of Nuclear Receptors in immunocytes reveals ligand-dependent inflammasome control [scRNA-seq]

Project description:To examine more closely the varied effects of RA receptor deletions on peritoneal MFs, and determine whether inactivation of RXRα and RARγ elicited superimposable effects on different LPM clusters (as predicted if they operate as a heterodimer, a known propensity of RXR proteins), we performed single-cell RNA sequencing (scRNAseq) analyses on total CD11b+CD115+ peritoneal cells from BMC mice edited for several RA receptors, 17 days after reconstitution.

2024-12-16 | GSE254572 | GEO

A pan-family screen of Nuclear Receptors in immunocytes reveals ligand-dependent inflammasome control [RNA-seq 2]

Project description:We performed RNAseq profiling of sorted LYVE1+CD206+ MFs from WT, RARγ mutant and RXRα mutant converting macrophages (Conv.MF).

2024-12-16 | GSE273340 | GEO

A pan-family screen of Nuclear Receptors in immunocytes reveals ligand-dependent inflammasome control [RNA-seq 1]

Project description:We profiled the transcriptional effects of NR deficiencies on peritoneal macrophages.

2024-12-16 | GSE254406 | GEO

A pan-family screen of Nuclear Receptors in immunocytes reveals ligand-dependent inflammasome control

Project description:A pan-family screen of Nuclear Receptors in immunocytes reveals ligand-dependent inflammasome control

| PRJNA1071064 | ENA

A pan-family screen of Nuclear Receptors in immunocytes reveals ligand-dependent inflammasome control [ChIPmentation]

Project description:A pan-family screen of Nuclear Receptors in immunocytes reveals ligand-dependent inflammasome control [ChIPmentation]

| PRJNA1070328 | ENA

A pan-family screen of Nuclear Receptors in immunocytes reveals ligand-dependent inflammasome control [scRNA-seq]

Project description:A pan-family screen of Nuclear Receptors in immunocytes reveals ligand-dependent inflammasome control [scRNA-seq]

| PRJNA1071071 | ENA

A pan-family screen of Nuclear Receptors in immunocytes reveals ligand-dependent inflammasome control [RNA-seq 1]

Project description:A pan-family screen of Nuclear Receptors in immunocytes reveals ligand-dependent inflammasome control [RNA-seq 1]

| PRJNA1070322 | ENA

A pan-family screen of Nuclear Receptors in immunocytes reveals ligand-dependent inflammasome control [RNA-seq 2]

Project description:A pan-family screen of Nuclear Receptors in immunocytes reveals ligand-dependent inflammasome control [RNA-seq 2]

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Histone methylation-dependent mechanisms impose ligand dependency for gene activation by nuclear receptors.

Project description:Nuclear receptors undergo ligand-dependent conformational changes that are required for corepressor-coactivator exchange, but whether there is an actual requirement for specific epigenetic landmarks to impose ligand dependency for gene activation remains unknown. Here we report an unexpected and general strategy that is based on the requirement for specific cohorts of inhibitory histone methyltransferases (HMTs) to impose gene-specific gatekeeper functions that prevent unliganded nuclear receptors and other classes of regulated transcription factors from binding to their target gene promoters and causing constitutive gene activation in the absence of stimulating signals. This strategy, based at least in part on an HMT-dependent inhibitory histone code, imposes a requirement for specific histone demethylases, including LSD1, to permit ligand- and signal-dependent activation of regulated gene expression. These events link an inhibitory methylation component of the histone code to a broadly used strategy that circumvents pathological constitutive gene induction by physiologically regulated transcription factors.

| S-EPMC1994663 | biostudies-literature

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