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Argonaute3-SF3B3 complex controls pre-mRNA splicing to restrain Type-2 immunity

ABSTRACT: Argonaute3-SF3B3 complex controls pre-mRNA splicing to restrain Type-2 immunity

PROVIDER: PRJNA1020566 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26158100.fastq.gz	Fastqsanger.gz
	SRR26187100_1.fastq.gz	Fastqsanger.gz
	SRR26187100_2.fastq.gz	Fastqsanger.gz
	SRR26158101.fastq.gz	Fastqsanger.gz
	SRR26187101_1.fastq.gz	Fastqsanger.gz

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Argonaute3-SF3B3 complex controls pre-mRNA splicing to restrain Type-2 immunity [miRNA-seq]

Project description:Argonaute3-SF3B3 complex controls pre-mRNA splicing to restrain Type-2 immunity [miRNA-seq]

| PRJNA1020567 | ENA

Argonaute3-SF3B3 complex controls pre-mRNA splicing to restrain Type-2 immunity [miRNA-seq]

Project description:Argonaute (AGO) proteins execute Micro-RNA (miRNA) mediated gene silencing. However it is currently debated whether all 4 mammalian AGO proteins (AGO1, AGO2, AGO3 and AGO4) are required for miRNA activity. To address this, we generated a mouse with deleted Ago1, Ago3 and Ago4 genes (Ago134), and found that these Argonaute proteins are completely redundant for miRNA biogenesis, miRNA homeostasis or miRNA function, a role that is carried out exclusively by AGO2. Instead, AGO1/3/4 are required to curtail the expansion of Type-2 adaptive immunity in mice via regulation of precursor-mRNA (pre-mRNA) splicing in CD4+ TH lymphocytes. Gain- and loss-of-function experiments demonstrate that nuclear AGO3 interacts directly with SF3B3, a component of the U2 spliceosome complex, to aid global mRNA splicing. Our work uncouples AGO1, AGO3 and AGO4 from miRNA-mediated RNAi, discovers a new AGO3:SF3B3 complex in the cellular nucleus, and reveals an underappreciated mechanism by which AGO proteins prevent hyper-inflammatory disease.

2024-10-31 | GSE243916 | GEO

Argonaute3-SF3B3 complex controls pre-mRNA splicing to restrain Type-2 immunity [RNA-seq: dissected tissues]

2024-10-31 | GSE244066 | GEO

Argonaute3-SF3B3 complex controls pre-mRNA splicing to restrain Type-2 immunity [RNA-seq: cultured cells]

2024-10-31 | GSE243700 | GEO

Argonaute3-SF3B3 complex controls pre-mRNA splicing to restrain Type-2 immunity [RNA-seq: dissected tissues]

Project description:Argonaute3-SF3B3 complex controls pre-mRNA splicing to restrain Type-2 immunity [RNA-seq: dissected tissues]

| PRJNA1021190 | ENA

Argonaute3-SF3B3 complex controls pre-mRNA splicing to restrain Type-2 immunity [RNA-seq: cultured cells]

Project description:Argonaute3-SF3B3 complex controls pre-mRNA splicing to restrain Type-2 immunity [RNA-seq: cultured cells]

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FXR splicing by SF3B3 promotes MYC-driven hepatocarcinogenesis

Project description:BACKGROUND AND AIMS: Dysregulation of the MYC oncogene is a major genetic event in hepatocellular carcinoma (HCC). Farnesoid X receptor (FXR), a bile acid (BA) receptor, has emerged as a promising therapeutic target for various liver diseases. Both BA composition and FXR isoforms have been shown to be significantly altered in human HCCs. This study aimed to investigate their potential roles in MYC-driven hepatocarcinogenesis. APPROACH AND RESULTS: HCC was induced in mice by hydrodynamic injection with MYC and MCL1 oncogenes. UPLC-MS/MS analysis revealed elevated BA levels, particularly primary conjugated BAs, in both serum and livers of MYC-driven HCC mice. qPCR and western blot analyses demonstrated suppression of BSEP and dysregulation of FXR splicing in the livers of these mice. Using RNA antisense purification coupled with mass spectrometry (RAP-MS), the splicing factor SF3B3 was identified as a regulator of FXR splicing. Both in silico and in vitro studies confirmed that SF3B3 is a direct downstream target of MYC in mice and humans. Functionally, overexpression of Fxrα2 and Fxrα4 or deletion of Sf3b3 significantly impeded MYC-driven hepatocarcinogenesis in mice. Moreover, combination treatment with a SF3B inhibitor and an FXR agonist synergistically suppressed proliferation of HCC cells. Analysis of clinical HCC samples revealed a positive correlation between SF3B3 and the relative expression of FXRα2. Conclusions: SF3B3 is a key downstream effector of MYC-driven hepatocarcinogenesis and a critical regulator of FXR splicing. Both SF3B3 and FXR represent druggable vulnerabilities in MYC-amplified HCC.

2025-10-02 | GSE309158 | GEO

Argonaute3-SF3B3 complex controls pre-mRNA splicing to restrain Type-2 immunity

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

2024-10-31 | GSE243918 | GEO

FXR splicing by SF3B3 promotes MYC-driven hepatocarcinogenesis

Project description:FXR splicing by SF3B3 promotes MYC-driven hepatocarcinogenesis

| PRJNA1334243 | ENA

SFRS8 regulates memory by modulating pre-mRNA splicing of synaptic genes in mice

Project description:SFRS8 is a member of SR family protein. It is also a known splicing factor that is highly expressed in the brain. However, its function in the brain remains elusive. Here, we find that SFRS8 is required to maintain normal synaptic protein levels as well as synaptic densities. Mechanistically, we demonstrate that SFRS8 interacts with SF3B3, a major component of U2 snRNP complex, and regulates the RNA alternative splicing process. Specifically, SFRS8 regulates the levels of PSD95, through enhancing the loading of Psd95 mRNA on the U2 snRNP complex and increasing the skipping of exon18 of Psd95. We further demonstrate that SFRS8 knockdown in the hippocampus leads to reduced synaptic protein expression, decreased spine density, consequently defective memory in mice. Similar reduction in synaptic protein expression and synaptic density are also evident in cultured neurons. Taken together, SFRS8 regulates memory function in mice through altering the alternative splicing and expression of synaptic genes via SFRS8-SF3B3 interaction.

2025-06-06 | GSE273869 | GEO

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