Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The circular RNA circ_ATP8B regulates ROS production and antiviral immunity

ABSTRACT: The circular RNA circ_ATP8B regulates ROS production and antiviral immunity

PROVIDER: PRJNA1045534 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

The circular RNA circ_ATP8B regulates ROS production and antiviral immunity [circRNA-Seq]

Project description:The circular RNA circ_ATP8B regulates ROS production and antiviral immunity [circRNA-Seq]

| PRJNA1045541 | ENA

The circular RNA circ_ATP8B regulates ROS production and antiviral immunity [RNA-Seq]

Project description:The circular RNA circ_ATP8B regulates ROS production and antiviral immunity [RNA-Seq]

| PRJNA1045542 | ENA

The circular RNA circ_ATP8B regulates ROS production and antiviral immunity [circRNA-Seq]

Project description:Circular RNAs (circRNAs) are widely expressed in eukaryotes. However, only a subset has been functionally characterized. We have identified and validated a collection of circular RNAs in Drosophila melanogaster. We show that the circular RNA circ_ATP8B is induced by viral infection and that depletion of circ_ATP8B, but not its linear sibling, compromises viral infection both in cultured cells and in vivo. In addition, our analyses reveal that circ_ATP8B is enriched in the fly gut and that gut-specific depletion of circ_ATP8B attenuates viral replication in an oral infection model. Furthermore, we find circ_ATP8B-depletion resulted in increased levels of reactive oxygen species (ROS) and enhanced expression of Duox (Dual oxidase), which produces ROS. Genetic and pharmacological manipulation of circ_ATP8B-depleted flies that reduce ROS levels rescue the viral replication defects elicited by circ_ATP8B depletion. Notably, circ_ATP8B and Duox associate with each other, and that expression of various versions of circ_ATP8B that are competent in binding Duox, but not a mutant circ_ATP8B that is incapable of binding Duox, restores physiological levels of ROS in circ_ATP8B-depleted cells. Lastly, our data show that Gaq, a subunit of G protein required for optimal Duox activity, acts downstream of circ_ATP8B to regulate Duox activity. We conclude that circ_ATP8B regulates anti-viral immunity by modulating Duox-dependent ROS production.

2024-05-15 | GSE248666 | GEO

The circular RNA circ_ATP8B regulates ROS production and antiviral immunity [RNA-Seq]

2024-05-15 | GSE248665 | GEO

The circular RNA circ_ATP8B regulates ROS production and antiviral immunity

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

2024-05-15 | GSE248667 | GEO

IFN-inducible phospholipid levels govern endosomal antiviral immunity

Project description:Untargeted lipidomics of 3 cell lines at baseline with focus on phospholipids to understand the role of these lipids in endosomal antiviral immunity

2022-12-16 | ST002413 | MetabolomicsWorkbench

Exercise Activates Interferon Immune Response of the Liver via Gpld1 to Enhance Antiviral Innate Immunity

Project description:<p>Healthy behavioral patterns could modulate organ functions to enhance the body’s immunity. However, whether exercise regulates antiviral innate immunity remains elusive. Here, we found that exercise promotes type-I IFN (IFN-I) production in the liver and enhances IFN-I immune activity of the body. Despite the possibility that many exercise-induced factors could regulate IFN-I production, we identified Gpld1 as a crucial molecule and the liver as the major organ to promote IFN-I production after exercise. Exercise largely loses the efficiency to induce IFN-I in Gpld1-/- mice. Further studies demonstrated that exercise-produced 3-hydroxybutanoic acid (3-HB) critically induces Gpld1 expression in the liver. Gpld1 blocks the PP2A-IRF3 interaction and therefore enhances IRF3 activation and IFN-I production, and improves the body’s antiviral ability. This study reveals that the exercise behavior improves antiviral innate immunity by linking the liver metabolism to systemic IFN-I activity, and uncovers an unknown function of liver cells in innate immunity.</p>

2024-04-24 | MTBLS7972 | MetaboLights

Chromatin remodeler ARID1A binds IRF3 to selectively induce antiviral interferon production in macrophages

Project description:Transcription factor IRF3 is critical for the induction of antiviral type I interferon (IFN-I). The epigenetic regulation of IFN-I production in antiviral innate immunity need to be further identified. Here, we report that epigenetic remodeler ARID1A, a critical component of the mSWI/SNF complex, could bind IRF3 and then was recruited to the Ifn-I promoter by IRF3, thus selectively promoting IFN-I but not TNF-α, IL-6 production in macrophages upon viral infection. Myeloid cell-specific deficiency of Arid1a rendered mice more susceptible to viral infection, accompanied with less IFN-I production. Mechanistically, ARID1A facilitates chromatin accessibility of IRF3 at the Ifn-I promoter by interacting with histone methyltransferase NSD2, which methylates H3K4 and H3K36 of promoter region. Our findings demonstrate the new roles of ARID1A and NSD2 in innate immunity, providing insight to the crosstalks of chromatin remodeling, histone modification and transcription factor in the epigenetic regulation of antiviral innate immunity.

2022-07-01 | GSE176452 | GEO