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Homo sapiens

ABSTRACT: Breaching self-tolerance to Alu duplex RNA underlies MDA5-mediated inflammation [WT HEK293T and mutant MDA5]

PROVIDER: PRJNA401809 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6008900_1.fastq.gz	Fastqsanger.gz
	SRR6008900_2.fastq.gz	Fastqsanger.gz
	SRR6008896_1.fastq.gz	Fastqsanger.gz
	SRR6008896_2.fastq.gz	Fastqsanger.gz
	SRR6008897_1.fastq.gz	Fastqsanger.gz

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Breaching self-tolerance to Alu duplex RNA underlies MDA5-mediated inflammation [ADAR1KO HEK293T and WT MDA5]

Project description:Breaching self-tolerance to Alu duplex RNA underlies MDA5-mediated inflammation [ADAR1KO HEK293T and WT MDA5]

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Breaching self-tolerance to Alu duplex RNA underlies MDA5-mediated inflammation

Project description:Breaching self-tolerance to Alu duplex RNA underlies MDA5-mediated inflammation

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Breaching self-tolerance to Alu duplex RNA underlies MDA5-mediated inflammation [WT HEK293T and mutant MDA5]

Project description:Aberrant activation of innate immune receptors can cause a spectrum of immune disorders, such as Aicardi-Goutières syndrome (AGS). One such receptor is MDA5, a viral double-stranded RNA (dsRNA) sensor that induces antiviral immune response. We here demonstrate that constitutive activation of MDA5 in AGS results from the loss of tolerance to cellular dsRNAs formed by Alu retroelements. While wild-type MDA5 cannot efficiently recognize Alu-dsRNA because its filament formation on dsRNA is impaired by the imperfect duplex structure, AGS-variants of MDA5 display reduced sensitivity to duplex structural irregularities, assembling signaling-competent filaments on Alu-dsRNA. Moreover, we identified an unexpected role of RNA-rich cellular environment in suppressing aberrant MDA5 oligomerization, highlighting context-dependence of self vs. non-self discrimination. Overall, our work demonstrates that the increased efficiency of MDA5 to recognize dsRNA comes at a cost of self-recognition, and implicates a unique role of Alu RNAs as virus-like elements that shape the primate immune system.

2018-01-29 | GSE103539 | GEO

Breaching self-tolerance to Alu duplex RNA underlies MDA5-mediated inflammation [ADAR1KO HEK293T and WT MDA5]

2018-01-29 | GSE104864 | GEO

Hepatocyte-macrophage crosstalk via the PGRN-EGFR axis modulates ADAR1-mediated immunity in the liver -bulk RNA-seq

Project description:ADAR1 is thought to be an immune suppressor maintaining self-tolerance to endogenous nucleic acids. Lack of ADAR1 results in MDA5 (Ifih1) activation and MDA5 deletion rescues ADAR1 null embryonic lethality. We generated liver specific ADAR1; MDA5 double KO mice and performed high throughput sequencing to investigate hepatic inflammation in these mice. Bulk RNA was sequenced on the HiSeq X platform. Over 100 million pairs of mappable reads for each sample were obtained.

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Hepatocyte-macrophage crosstalk via the PGRN-EGFR axis modulates ADAR1-mediated immunity in the liver -Spatial Transcriptomics

Project description:ADAR1 is thought to be an immune suppressor maintaining self-tolerance to endogenous nucleic acids. Lack of ADAR1 results in MDA5 (Ifih1) activation and MDA5 deletion rescues ADAR1 null embryonic lethality. We generated liver specific ADAR1; MDA5 double KO mice and performed high throughput sequencing to investigate hepatic inflammation in these mice. Spatial transcriptomics (Visium, 10x Genomics) was performed on FFPE mice liver tissues. Constructed libraries were sequenced on the Novaseq 6000 platform. Over 250 million pairs of mappable reads for each sample were obtained.

2024-05-28 | GSE228195 | GEO

Hepatocyte-macrophage crosstalk via the PGRN-EGFR axis modulates ADAR1-mediated immunity in the liver -scRNAseq

Project description:ADAR1 is thought to be an immune suppressor maintaining self-tolerance to endogenous nucleic acids. Lack of ADAR1 results in MDA5 (Ifih1) activation and MDA5 deletion rescues ADAR1 null embryonic lethality. We generated liver specific ADAR1; MDA5 double KO mice and performed high throughput sequencing to investigate hepatic inflammation in these mice. Single cell RNA sequencing was performed on cells isolated from mice livers. Constructed libraries were sequenced on the HiSeq X platform. Over 100 million pairs of mappable reads for each sample were obtained.

2024-05-28 | GSE227092 | GEO

Post-transcriptional regulation by Alu within mRNA

Project description:An extrachromosomal replication system was established to examine the perturbation of Alu-carrying genes in response to elevated Alu RNAs in the opposite direction. The null hypothesis is that the Alu-carrying RNA duplex cannot trigger subsequent post-transcriptional regulation, manifesting a random perturbation of expression levels. Comparing HEK293 cells transfected and not-transfected with pDR2-Alu vectors.

2013-05-13 | E-GEOD-39822 | biostudies-arrayexpress

Post-transcriptional regulation by Alu within mRNA

2013-05-13 | GSE39822 | GEO

Splenic CD43- B cells exhibit DNA hypomethylation specifically at repetitive elements compared to CD43+ cells

Project description:EZH2 is a histone methyltransferase that deposits H3K27me2/3 in heterochromatin and it is misregulated in tumorigenesis. Inhibition of heterochromatin can induce viral mimicry in cancer cells, where upregulated repetitive elements are detected by cytosolic pattern recognition receptors (PRRs) to activate inflammatory signaling. Here we demonstrate that EZH2 inhibitors stimulate inflammation and immune self-recognition of resting splenic B cells. We generated a PRR loss-of-function mouse model called RIC with mutations in Rigi, Ifih1 (MDA5), and Cgas. In both WT and RIC mutant B cells, EZH2 inhibition caused loss of H3K27me3 at repetitive elements and upregulated their expression. However, expression of inflammatory chemokines in B cells was interrupted by the RIC mutations. Furthermore, recruitment of cytotoxic T cells and neutrophils in response to EZH2 inhibition was blocked in RIC mutants preserving viability of B cells. This study demonstrates a pharmacologically induced mechanism of inflammation that causes self-recognition and B cell death.

2023-10-18 | GSE229684 | GEO

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