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2022_de Reuver_ADAR1 +/+ vs ADAR1 Za/Za HEK293 cells (deep-seq)

ABSTRACT: ADAR1 +/+ vs ADAR1 Za/Za HEK293 cells (deep-seq)

PROVIDER: PRJEB52618 | ENA |

REPOSITORIES: ENA

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RNA-sequencing of lung RNA from mice with compound mutations in ADAR1 and MAVS, ZBP1 or RIPK3.

Project description:The purpose of this study was to examine the role of MAVS, ZBP1 and RIPK3 in the phenotype that develops when ADAR1 activity is impaired, in particular when the Za domain of ADAR1 is mutated. Mice homozygous for a Za domain-mutant allele of Adar1 (Adar1mZa/mZa mice) and mice carrying one mZa and one null Adar1 allele (Adar1-/mZa mice) were compared with control mice that were either wild type or heterozygous for the Adar1 mZa allele (Adar1wt/mZa mice). The effects of MAVS deficiency, RIPK3 deficiency, ZBP1 deficiency or ZBP1 Za domain mutations were assessed by analysing compound mutant mice. Given the early postnatal lethal phenotype that develops in Adar1-/mZa mice, comparisons were made in RNA isolated from lung tissue from newborn mice of each genotype (5 mice per genotype). As Adar1-/mZa mice additionally lacking Mavs or Zbp1 are viable, adult mice (15-20 weeks of age) were also used for several compound mutations as donors of lung tissue.

2022-06-09 | E-MTAB-11540 | biostudies-arrayexpress

RNA-sequencing of brain RNA from mice with compound mutations in ADAR1 and MAVS or ZBP1

Project description:The purpose of this study was to examine the role of MAVS and ZBP1 in the phenotype that develops when ADAR1 activity is missing, in particular when the Za domain of ADAR1 is mutated. Mice homozygous for a Za domain-mutant allele of Adar1 (Adar1mZa/mZa mice) were compared with control mice carrying one mZa allele and one wild type allele of Adar1 (Adar1wt/mZa mice) and with mice carrying one mZa and one null Adar1 allele (Adar1-/mZa mice). Adar1-/mZa mice were also compared with mice additionally deficient in ZBP1 (Adar1-/mZa Zbp1-/- mice) or MAVS (Adar1-/mZa Mavs-/- mice). Given the early postnatal lethal phenotype that develops in Adar1-/mZa mice, comparisons were made in RNA isolated from brain tissue from newborn mice of each genotype (4 mice per genotype).

2022-04-27 | E-MTAB-11537 | biostudies-arrayexpress

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.

2021-11-19 | GSE188937 | GEO

RNA sequencing quantitative analysis of RNA editing levels in ADAR1, ADAR2, AIMP2 overexpression and wild type HEK293 cells

Project description:We overexpressed ADAR1, ADAR2 and AIMP2 in HEK293 cells and examined editing using RNA-seq.

2017-10-01 | GSE87198 | GEO

2022_de Reuver_ADAR1 +/- vs ADAR1 Za/- primary lung fibroblasts

Project description:Adar +/- vs Adar Za/- primary lung fibroblasts

| PRJEB52610 | ENA

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

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

| PRJNA780821 | ENA

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

In vivo atlas of RNA secondary structures recognized by ADARs [irCLASH-seq&hiCLIP-seq]

Project description:We performed irCLASH and HiCLIP for ADAR1-3 in HEK293 cells. In addition, we performed mRNA-seq in ADAR1-3 overexpressed HEK293 cells and control HEK293 cells

2020-03-26 | GSE136325 | GEO

In vivo atlas of RNA secondary structures recognized by ADARs [RNA-Seq]

Project description:We performed irCLASH and HiCLIP for ADAR1-3 in HEK293 cells. In addition, we performed mRNA-seq in ADAR1-3 overexpressed HEK293 cells and control HEK293 cells

2020-03-26 | GSE136326 | 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).

2012-08-31 | E-GEOD-31963 | biostudies-arrayexpress

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