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STING-mediated proton channel activity, signaling, and autoinflammatory disease require ArfGAP2 [BMDM]

ABSTRACT: STING-mediated proton channel activity, signaling, and autoinflammatory disease require ArfGAP2 [BMDM]

PROVIDER: PRJNA1193600 | ENA |

REPOSITORIES: ENA

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STING-mediated proton channel activity, signaling, and autoinflammatory disease require ArfGAP2 [BMDM]

Project description:STING transmits signals downstream of the cytosolic DNA sensor cGAS, leading to transcriptional up-regulation of cytokines. However, components of the STING signaling pathway, such as IRF3 and IFNAR1, are not essential for autoinflammatory disease in STING gain-of-function (SAVI) mice. Recent discoveries revealed that STING also functions as a proton channel that deacidifies the Golgi. Since pH impacts Golgi enzyme activity, protein maturation, and trafficking, we hypothesized that STING proton channel activity influences multiple Golgi functions. Here, we show that STING-mediated proton efflux non-transcriptionally regulates Golgi trafficking of protein cargos. This process requires the Golgi-associated protein ArfGAP2, a cell type-specific dual regulator of STING-mediated proton efflux and signaling. Deletion of ArfGAP2 in hematopoietic and endothelial cells markedly reduces STING-mediated cytokine and chemokine secretion, immune cell activation, and autoinflammatory pathology in SAVI mice. Thus, ArfGAP2 facilitates STING-mediated signaling and cytokine release in hematopoietic cells, significantly contributing to autoinflammatory disease pathogenesis.

2024-12-31 | GSE283415 | GEO

STING-mediated proton channel activity, signaling, and autoinflammatory disease require ArfGAP2 [Jurkat]

2024-12-31 | GSE283416 | GEO

STING-mediated proton channel activity, signaling, and autoinflammatory disease require ArfGAP2 [Jurkat]

Project description:STING-mediated proton channel activity, signaling, and autoinflammatory disease require ArfGAP2 [Jurkat]

| PRJNA1193602 | ENA

STING-mediated proton channel activity, signaling, and autoimmune disease require ArfGAP2

Project description:STING transmits signals downstream of the cytosolic DNA sensor cGAS, leading to transcriptional up-regulation of cytokines. However, components of the STING signaling pathway, such as IRF3 and IFNAR1, are not essential for autoinflammatory disease in STING gain-of-function (SAVI) mice. Recent findings indicate that STING can also function as a proton channel that deacidifies the Golgi. Since pH impacts Golgi enzyme activity, protein maturation, and trafficking, we hypothesized that STING proton channel activity influences multiple Golgi functions. Here, we show that STING-mediated proton efflux non-transcriptionally regulates Golgi trafficking of protein cargos. This process requires the Golgi-associated protein ArfGAP2, a cell type-specific dual regulator of STING-mediated proton efflux and signaling. Deletion of ArfGAP2 in hematopoietic and endothelial cells markedly reduces STING-mediated cytokine and chemokine secretion, immune cell activation, and autoinflammatory pathology in SAVI mice. Thus, ArfGAP2 facilitates STING-mediated signaling and cytokine release in hematopoietic cells, significantly contributing to autoinflammatory disease pathogenesis.

2024-11-30 | PXD058416 | Pride

Gene expression profiles in BMDM cells of Trex1-KO and wild-type mice after treatment of STING antagonists

Project description:Mounting evidence demonstrates that cGAS-STING signaling is the major pathway in sensing cytosolic DNAs. However, aberrant accumulation of self DNA molecules in Trex1 (a 3'-to-5' DNA exonuclease) deficient cells usually causes over-activation of cGAS-STING signaling, which is associated with the pathology of several autoimmune diseases. Here, we investigated gene expression changes in BMDM cells of Trex1 knockout mice after manipulating cGAS-STING signaling activity via treatment of two STING antagonists (SN-011 and H151) .

2021-05-26 | GSE143830 | GEO

Gene expression in murine embryonic fibroblasts stimulated with DNA or LPS

Project description:MyD88 may play a direct role in STING-dependent signaling, or alternatively that STING-dependent pro-inflammatory cytokines may require downstream MyD88-dependent signaling to exert their effect. To determine this, we treated STING or MyD88-deficient murine embryonic fibroblasts (MEFs), bone marrow derived macrophages (BMDM) or dendritic cells (BMDC) with exogenous CDN’s or cytosolic dsDNA (ISD) which triggers STING-signaling and type I IFN production.

2018-02-01 | GSE107809 | GEO

WT BMDM M2 vs RON TK- BMDM M2

Project description:WT BMDM M2 vs RON TK- BMDM M2

| PRJNA701293 | ENA

Genetics and Pathophysiology of Autoinflammatory Disorders

Project description:Genetics and Pathophysiology of Autoinflammatory Disorders

| PRJNA552920 | ENA

Genetics and Pathophysiology of Autoinflammatory Disorders

Project description:Genetics and Pathophysiology of Autoinflammatory Disorders

| PRJNA552921 | ENA

Mouse BMDM Yersinia infection

Project description:BMDM from BAL/c and C57BL/6 BMDM were stimlated with IFN-g overnight and infected with different Yersinia strains for 3 hrs. Keywords: repeat

2005-12-21 | GSE2973 | GEO

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