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

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

ORGANISM(S): Mus musculus

PROVIDER: GSE221626 | GEO | 2023/04/28

REPOSITORIES: GEO

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

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

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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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Specificity of ADAR1-isoforms: RIP-seq of ADAR1p150 and ADAR1p110 in HEK293 cells

Project description:Adenosine deaminase acting on RNA (ADAR) (also known as ADAR1) promotes A-to-I conversion in double-stranded and highly structured RNAs. ADAR1 has two isoforms transcribed from different promoters: ADAR1p150, which is mainly cytoplasmic and interferon-inducible, and constitutively expressed ADAR1p110 that is primarily localized in the nucleus. Mutations in ADAR1 cause Aicardi – Goutières syndrome (AGS), a severe autoinflammatory disease in humans associated with aberrant IFN production. In mice, deletion of ADAR1 or selective knockout of the p150 isoform alone leads to embryonic lethality driven by overexpression of interferon-stimulated genes. This phenotype can be rescued by concurrent deletion of cytoplasmic dsRNA-sensor MDA5. These findings indicate that the interferon-inducible p150 isoform is indispensable and cannot be rescued by the ADAR1p110 isoform. Nevertheless, editing sites uniquely targeted by ADAR1p150 but also mechanisms of isoform- specificity remain elusive. To examine in vivo interaction between ADAR1-isoforms and its substrates, we performed RNA immunoprecipitation and sequencing (RIP-seq) in HEK293 cells. RIP-seq experiment was done with overexpressed flag-tagged ADAR1 isoforms.

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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

AVA-ADR-001- a small molecular inhibitor of ADAR1 (Immuno-oncology target)

Project description:To inhibitors for ADAR1 and a strong rationale for the development of ADAR1 p150 inhibitors for cancer immunotherapy Here, we describe AVA-ADR-001, a potential first-in-class small molecule inhibitor of ADAR1 p150 targeting the Z alpha domain. AVA-ADR-001 binds specifically to the Z alpha domain of ADAR1 p150 as confirmed by fluorescence spectroscopy and showed significant interferon induction in THP1 macrophages, which have high ADAR1 p150 expression compared with monocytes. Proteomics and transcriptomics analysis revealed significant upregulation of interferon signaling upon treatment with AVA-ADR -001. Interestingly, activation of interferon signaling resulted in AVA-ADR-001 induced cell killing in ADAR1-independent cell lines. In addition, treatment with AVA-ADR -001 resulted in significant activation of PKR, which may explain the decreased cell proliferation. Finally, AVA-ADR-001 showed superior anti-tumor efficacy compared to anti-PD1 in an in vivo tumor efficacy study and has a moderately synergistic effect when combined. Overall, this study reveals that ADAR1 p150 inhibition by AVA-ADR-001 exerts a multipronged impact on anti-tumor efficacy mediated by immune cells, accumulation of interferons and activation of PKR, resulting in protein translation inhibition and cell proliferation arrest.

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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

| PRJNA915215 | ENA

ADAR1-isoforms specific editome: RNA sequencing of A-to-I editing deficient mouse embryonic fibroblast transfected with ADAR1p150 or ADAR1p110 or RFP.

Project description:Adenosine deaminase acting on RNA (ADAR) (also known as ADAR1) promotes A-to-I conversion in double-stranded and highly structured RNAs. ADAR1 has two isoforms transcribed from different promoters: ADAR1p150, which is mainly cytoplasmic and interferon-inducible, and constitutively expressed ADAR1p110 that is primarily localized in the nucleus. Mutations in ADAR1 cause Aicardi – Goutières syndrome (AGS), a severe autoinflammatory disease in humans associated with aberrant IFN production. In mice, deletion of ADAR1 or selective knockout of the p150 isoform alone leads to embryonic lethality driven by overexpression of interferon-stimulated genes. This phenotype can be rescued by concurrent deletion of cytoplasmic dsRNA-sensor MDA5. These findings indicate that the interferon-inducible p150 isoform is indispensable and cannot be rescued by the ADAR1p110 isoform. Nevertheless, editing sites uniquely targeted by ADAR1p150 but also mechanisms of isoform- specificity remain elusive. To identify ADAR1 isoform-specific ‘editome’, we transfected A-to-I editing deficient mouse embryonic fibroblasts (MEFs) with ADAR1p150- or ADAR1p110- or RFP-editing negative control. We subjected the samples to RNA sequencing and detected editing at known-editing sites.

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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 I.

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

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The RNA editing enzyme ADAR1 is a key regulatory of innate immune responses to RNA

Project description:The ADAR RNA editing enzymes deaminate adenosine bases to inosines in cellular RNAs, recoding open reading frames. Human ADAR1 mutations cause Aicardi-Goutieres Syndrome (AGS) and Adar1 mutant mice showing an aberrant interferon response and death by embryonic day E12.5 model the human disease. Searches have not identified key ADAR1 RNA editing sites recoding immune/haematopoietic proteins but editing is widespread in Alu sequences. We show that Adar1 embryonic lethality is rescued in Adar1; Mavs double mutant mice in which general antiviral responses to cytoplasmic dsRNA are prevented. We propose that inosine bases are epigenetic marks identifying cellular RNA as innate immune ÒselfÓ. Consistent with this idea we show that an editing-active cytoplasmic ADAR is required to prevent aberrant immune responses in Adar1 mutant mouse embryo fibroblasts. No dramatic increase in repetitive transcripts is observed. AGS mutations in ADAR1 affect editing by the interferon-inducible cytoplasmic ADAR1 isoform. RNA-seq expression profiling in Adar1 and Adar1/Mavs knockout mice embryos.

2014-12-19 | E-GEOD-62917 | biostudies-arrayexpress

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