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GPR174 signals via Gαs to control a CD86-containing gene expression program in B cells [0h and 4h culture]

ABSTRACT: GPR174 signals via Gαs to control a CD86-containing gene expression program in B cells [0h and 4h culture]

PROVIDER: PRJNA826840 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18753136.fastq.gz	Fastqsanger.gz
	SRR18753137.fastq.gz	Fastqsanger.gz
	SRR18753138.fastq.gz	Fastqsanger.gz
	SRR18753139.fastq.gz	Fastqsanger.gz
	SRR18753140.fastq.gz	Fastqsanger.gz

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Similar Datasets

GPR174 signals via Gαs to control a CD86-containing gene expression program in B cells [0h and 4h culture]

Project description:GPR174 is abundantly expressed in B and T lymphocytes and has a role in restraining T cell responses, but the function of GPR174 in B cells is less clear. Here we report that upon in vitro culture B cells undergo a spontaneous GPR174-dependent activation process that is associated with marked changes in gene expression, including upregulation of Cd86, Nr4a1, Ccr7 and phosphodiesterases. B cells lacking Gas show a block in induction of the GPR174-dependent program. Spontaneous upregulation of CD86 in cultured B cells is dependent on protein kinase A. Both GPR174- and Gas-deficient B cells show enhanced survival in culture. In vivo, GPR174 contributes to NUR77 expression in follicular B cells and is needed for establishing a marginal zone compartment of normal size. Treatment of mice with lysophosphatidylserine (lysoPS), a GPR174 ligand, is sufficient to promote CD86 upregulation by follicular B cells. These findings demonstrate that GPR174 can signal via Gas to modulate B cell gene expression and show this can occur in vivo in response to lysoPS. Additionally, the findings illuminate a pathway that might be targeted to improve systems for the in vitro study of B cell responses.

2022-05-16 | GSE200797 | GEO

GPR174 signals via Gαs to control a CD86-containing gene expression program in B cells [GNAS KO]

2022-05-16 | GSE200799 | GEO

GPR174 signals via Gαs to control a CD86-containing gene expression program in B cells [1 hour culture]

2022-05-16 | GSE200798 | GEO

GPR174 signals via Gαs to control a CD86-containing gene expression program in B cells

Project description:GPR174 signals via Gαs to control a CD86-containing gene expression program in B cells

| PRJNA826839 | ENA

GPR174 signals via Gαs to control a CD86-containing gene expression program in B cells [GNAS KO]

Project description:GPR174 signals via Gαs to control a CD86-containing gene expression program in B cells [GNAS KO]

| PRJNA826847 | ENA

GPR174 signals via Gαs to control a CD86-containing gene expression program in B cells [1 hour culture]

Project description:GPR174 signals via Gαs to control a CD86-containing gene expression program in B cells [1 hour culture]

| PRJNA826848 | ENA

GPR174 Knockdown Enhances Blood Flow Recovery in Hindlimb Ischemia Mice Model by Upregulating AREG Expression

Project description:Regulatory T cells (Tregs) are critically involved in neovascularization, an important compensatory mechanism in peripheral artery disease (PAD). The contribution of G protein coupled receptor 174 (GPR174), which is a regulator of Treg function and development, in neovascularization remains elusive. Here, we reveal that genetic deletion of GPR174 in Tregs potentiated blood flow recovery in mice after hindlimb ischemia (HLI). GPR174 deficiency upregulates amphiregulin (AREG) expression in Tregs, thereby enhancing endothelial cell functions and reducing pro-inflammatory macrophage polarization and endothelial cell apoptosis. Mechanically, GPR174 regulates AREG expression by inhibiting the nuclear accumulation of early growth response protein 1 (EGR1) via Gαs/cAMP/PKA signal pathway activation. Collectively, these findings demonstrate that GPR174 negatively regulates angiogenesis and vascular remodeling in response to ischemic injury and that GPR174 may be a potential molecular target for therapeutic interventions of ischemic vascular diseases.

2022-10-03 | GSE214684 | GEO

GPR174 signals via Gαs to control a CD86-containing gene expression program in B cells

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

2022-05-16 | GSE200800 | GEO

Clostridioides difficile CD86

Project description:Clostridioides difficile CD86 Genome sequencing and assembly

| PRJNA85725 | ENA

β2-adrenergic receptor transcriptional response in HEK293 wild type, β-arrestin1/2 KO and Gαs KO cells upon isoproterenol stimulation.

Project description:The role of nuclear signaling by β2-adrenergic receptor (β2AR) through β-arrestins in the absence of a functional Gαs protein has not been evaluated. This has prevented a comprehensive understanding of the relative contribution of Gαs and β-arrestins to the overall β2AR signaling, thereby limiting our appreciation of how β-arrestin- or Gαs-biased ligands may affect their therapeutic outcomes. To explore the role of Gαs and β-arrestin in nuclear transcriptional programs in a global unbiased approach, we performed RNA sequencing studies in cells lacking either of these two signaling arms downstream from β2AR, followed by detailed bioinformatics analysis of gene expression signatures. We noticed multiple genes whose individual expression levels were distinct in β-arrestin1/2 and Gαs KO cells. Rather than focusing on the individual gene level, we performed a detailed analysis of gene signatures taking advantage of large datasets that were recently compiled as part of the Molecular Signatures Database (MSigDB). This approach supported that β-arrestins are not required for the activation of PKA gene signatures, including prior datasets of forskolin and CREB1 targets, while Gαs is essential. β2AR activation also led to significant changes in multiple MAPK signatures, which clearly support the activation of MAPK nuclear transcriptional programs by these receptors. Although individual variations do exist reflecting the complexities of β-arrestin- and Gαs-mediated signaling events, stimulation of these MAPK regulated gene signatures was not significantly reduced in β-arrestin1/2 KO cells but abolished in Gαs KO cells.

2023-10-17 | GSE245270 | GEO

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