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Overexpression of ADAR1 in mice does not initiate or accelerate cancer formation in vivo II.

ABSTRACT: RNAseq of Osteosarcoma model from ADAR1 knock in mice generated by deep sequencing.

ORGANISM(S): Mus musculus

PROVIDER: GSE221627 | GEO | 2023/04/28

REPOSITORIES: GEO

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Overexpression of ADAR1 in mice does not initiate or accelerate cancer formation in vivo I.

Project description:RNAseq of Adult Liver in ADAR1 E861A, ADARp110, ADAR p150, ADAR1 knock in mice generated by deep sequencing.

2023-04-28 | GSE221626 | GEO

Overexpression of ADAR1 in mice does not initiate or accelerate cancer formation in vivo II.

Project description:Overexpression of ADAR1 in mice does not initiate or accelerate cancer formation in vivo II.

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Overexpression of ADAR1 in mice does not initiate or accelerate cancer formation in vivo

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

2023-04-26 | GSE221628 | GEO

Overexpression of ADAR1 in mice does not initiate or accelerate cancer formation in vivo

Project description:Overexpression of ADAR1 in mice does not initiate or accelerate cancer formation in vivo

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Overexpression of ADAR1 in mice does not initiate or accelerate cancer formation in vivo I.

Project description:Overexpression of ADAR1 in mice does not initiate or accelerate cancer formation in vivo I.

| PRJNA915218 | ENA

ADAR1-editing in HeLa, p150-KO and ADAR1-KO transcriptomes

Project description:RNAseq analysis of cell lines with ADAR1-p150 and ADAR1-p110 knock-outs and primary human tissue samples (from GSE57353 and GSE99392 data sets) to identify sites of ADAR1 editing

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Microrna expression profile in ADAR1 p110 overexpression

Project description:The change in Microrna expression profile in ADAR1 p110 overexpression.

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ADAR1 mutation causes ZBP1-dependent immunopathology II

Project description:The RNA editing enzyme ADAR1 is essential for suppression of innate immune activation and pathology caused by aberrant recognition of self-RNA, a role it carries out by disrupting the duplex structure of endogenous double-stranded RNA species. A point mutation in the Z-nucleic-acid binding domain (ZBD) of ADAR1 is associated with severe autoinflammatory disease. ZBP1 is the only other ZBD-containing mammalian protein and its activation can trigger both cell death and transcriptional responses via the kinases RIPK1 and RIPK3, and the protease caspase-8. Here, we show that the pathology caused by ADAR1 ZBD mutation is driven by activation of ZBP1. We found that ablation of ZBP1 fully rescued the overt pathology caused by ADAR1 mutation, without reversing the underlying inflammatory program caused by this mutation. While loss of RIPK3 partially phenocopied the protective effects of ZBP1 ablation, combined deletion of caspase-8 and RIPK3, or of caspase-8 and MLKL, unexpectedly exacerbated the pathogenic effects of ADAR1 mutation. These findings indicate that ADAR1 is a negative regulator of sterile ZBP1 activation, and that ZBP1-dependent signaling underlies the autoinflammatory pathology caused by mutation of ADAR1.

2022-08-10 | GSE200986 | GEO

ADAR1 regulates melanoma progression via miRNAs biogenesis

Project description:Aberrant RNA-editing was observed in several human tumors, but its significance is mostly unknown. Here we show that ADAR1, a ubiquitous RNA-editing enzyme, is commonly lost in metastatic melanoma cells and specimens. Experimental ADAR1 silencing significantly alters melanoma cell morphology, facilitates proliferation and cell-cycle, and increases the tumorigenicity in-vivo. A series of ADAR1 truncation mutants establishes a novel RNA-editing-independent role for ADAR1 in controlling the nuclear and cytoplasmic processing steps of miRNA biogenesis. Altered expression of ADAR1-controled miRNAs accounts for the observed phenotype. We show that the oncogenic miR-17-5p endogenously regulates ADAR1 expression and that its genomic sequence is frequently amplified in melanoma to overexpress the mature miR-17-5p form. ADAR1 and miR-17-5p are ubiquitously expressed, suggesting the generality of this mechanism. Melanoma cell line expressing low ADAR1 levels (ADAR1-Knockdown) using shRNA technique were selected for RNA extraction and hybridization on Affymetrix microarrays. We sought to examine the alterations in the genes and microRNA expression profile in the manipulated cell system, due to ADAR1 possible involvement cancer development. To that end, we selected ADAR1-knockdown (ADAR1-KD) cells that demonstrated an enhanced aggressive phenotype both in vivo and in vitro as compared to the control cells (Control).

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Irf7 orchestrates the immunological reaction in cardiomyocytes upon Adar1 deletion

Project description:Adenosine deaminases acting on RNA (Adar1 and Adar2) catalyze I-to-A RNA editing, a post-transcriptional mechanism involved in multiple cellular functions. The role of Adar1-dependent RNA editing in cardiomyocytes (CMs) remains unclear. Here we show that conditional deletion of Adar1 in CMs results in myocarditis progressively evolving into dilated cardiomyopathy and heart failure at only 6 months of age. Adar1 depletion drives activation of interferon signaling genes (ISGs) in the absence of apoptosis and cytokine activation, and reduces the hypertrophic response of CMs upon pressure overload. Interestingly, ablation of the cytosolic sensor MDA5 prevents cardiac ISG activation and delays disease onset, but does not rescue the long-term lethal phenotype elicited by conditional deletion of Adar1. Retention of a single catalytically inactive Adar1 allele in CMs, in combination with MDA5 depletion, however, completely restores the cardiac function and prevents heart failure. Finally, ablation of interferon regulatory factor 7 (Irf7) attenuates the phenotype of Adar1-deficient CMs to a similar extent as MDA5 depletion, highlighting Irf7 as the main regulator of the immune response triggered by lack of Adar1 in CMs.

2022-08-24 | PXD024974 | Pride

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