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

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

PROVIDER: PRJNA826847 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18753162.fastq.gz	Fastqsanger.gz
	SRR18753163.fastq.gz	Fastqsanger.gz
	SRR18753164.fastq.gz	Fastqsanger.gz
	SRR18753165.fastq.gz	Fastqsanger.gz
	SRR18753166.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 [GNAS KO]

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 | 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 [0h and 4h culture]

2022-05-16 | GSE200797 | 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 [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 signals via Gαs to control a CD86-containing gene expression program in B cells [0h and 4h culture]

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

| PRJNA826840 | 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

Oncogene addiction to GNAS in GNASR201 mutant tumors

Project description:The GNASR201 gain-of-function mutation is the single most frequent cancer-causing mutation across all heterotrimeric G proteins, driving oncogenesis in various low-grade/benign gastrointestinal and pancreatic tumors. In this study, we investigated the role of GNAS and its product Gαs in tumor progression using peritoneal models of colorectal cancer (CRC). GNAS was knocked out in multiple CRC cell lines harboring GNASR201C/H mutations (KM12, SNU175, SKCO1), leading to decreased cell-growth in 2D and 3D organoid models. Nude mice were peritoneally injected with GNAS-knockout KM12 cells, leading to a decrease in tumor growth and drastically improved survival at 7 weeks. Supporting these findings, GNAS overexpression in LS174T cells led to increased cell-growth in 2D and 3D organoid models, and increased tumor growth in PDX mouse models. GNAS knockout decreased levels of cyclic AMP in KM12 cells, and molecular profiling identified phosphorylation of β-catenin and activation of its targets as critical downstream effects of mutant GNAS signaling. Supporting these findings, chemical inhibition of both PKA and β-catenin reduced growth of GNAS mutant organoids. Our findings demonstrate oncogene addiction to GNAS in peritoneal models of GNASR201C/H tumors, which signal through the cAMP/PKA and Wnt/β-catenin pathways. Thus, GNAS and its downstream mediators are promising therapeutic targets for GNAS mutant tumors.

2022-07-19 | GSE208278 | GEO

A Reciprocal Regulatory Loop Between TAZ/YAP and G protein Gαs Regulates Schwann Cell Proliferation and Differentiation

Project description:Schwann cell (SC) myelination in the peripheral nervous system is essential for motor function, and uncontrolled SC proliferation occurs in cancer. Here, we show that a dual direct role for Hippo effectors TAZ and YAP in regulation of SC proliferation and myelination through modulating G protein expression and interacting with SOX10, respectively. Developmentally-regulated mutagenesis indicates that TAZ/YAP are critical for SC proliferation yet also required for their differentiation and myelination. Genome-wide occupancy mapping and transcriptome profiling reveal that nuclear TAZ and YAP promote SC proliferation by activating cell cycle regulators, while targeting critical differentiation regulators in cooperation with SOX10 for myelination. We further identified that TAZ targets and represses Gnas, encoding Gαs-protein, which opposes TAZ/YAP activities to decelerate proliferation. Gnas deletion expands SC precursor pools and blocks myelination in the sciatic nerve. Thus, our study revealed that the Hippo/TAZ/YAP and Gαs-protein feedback circuit functions as a fulcrum balancing SC proliferation and differentiation, providing insights into molecular programming of SC lineage progression and homeostasis.

2017-04-26 | GSE94990 | GEO

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