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Small RNA analysis of wildtype Mouse embryo and Adar1 null mouse embryo at E11.0 and E11.5 together with mRNA-seq results of E11.5

ABSTRACT: Adar1 is an essential gene for mouse embryonic development. Adar1 null mouse embryos dies around E11.5 because of massive apoptosis.

ORGANISM(S): Mus musculus

PROVIDER: GSE33473 | GEO | 2013/05/01

SECONDARY ACCESSION(S): PRJNA148757

REPOSITORIES: GEO

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Small RNA analysis of wildtype Mouse embryo and Adar1 null mouse embryo at E11.0 and E11.5 together with mRNA-seq results of E11.5

Project description:Adar1 is an essential gene for mouse embryonic development. Adar1 null mouse embryos dies around E11.5 because of massive apoptosis. Small RNA: 4 samples examined: wild type E11.0, ADAR1 null E11.0, wild type E11.5, ADAR1 null E11.5, mRNA-seq: wild type E11.5, ADAR1 null E11.5.

2013-05-01 | E-GEOD-33473 | biostudies-arrayexpress

Transcriptome profile of wildtype and Ret homozygote null mouse guts at E11.5 and E12.5

Project description:Total mRNA seq was perfomed on widtype and Ret null mouse embryonic gut at 2 stages of devlopment- E11.5 and E12.5

2016-09-30 | GSE84145 | 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

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

2018-12-04 | GSE115127 | GEO

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

RNA-seq of mouse alveolar macrophages (ADAR1 deficient and WT)

Project description:Whole RNA was isolated from CD11c-Cre ADAR1-deficient and WT alveolar macrophages.

2018-12-11 | E-MTAB-6477 | biostudies-arrayexpress

Complete embryonic E11.5 metanephric kidney analysis of wild type and Hoxa11, Hoxd11 null targeted mice

Project description:E11.5 metanephric mesenchyme and ureteric bud were dissected from the E11.5 kidney rudiment using fine manual microdissection (ureteric bud only) or both fine manual microdissection and laser capture microdissection (metanephric mesenchyme) to define the gene expression profiles of these structures. Additionally, HoxA11, HoxD11 compound null E11.5 metanephric mesenchyme was obtained through laser capture microdissection allowing analysis of possible Hox targets in kidney development. Targets from multiple biological replicates of each were generated and the expression profiles were determined using Affymetrix MOE430_v2 arrays. Keywords: embryonic metanephric kidney, kidney development, Hoxa11, Hoxd11, compound null targeted mice

2006-05-01 | GSE3822 | GEO

ADAR1 suppression in human astrocytes

Project description:ADAR1 regulates the accumulation of endeognouse double-stranded RNA (dsRNA), a pro-inflammatory/innate immune activator. The purpose of this study was to measure the effects of ADAR1 suppression in human astrocytes and determine RNAs regulated by ADAR1. Primary human astrocytes were culture and transfected with a scramble or ADAR1 siRNA. RNA was isolated from these cells for total RNA-seq to analyze changes in gene/repetitive element expression and RNA editing.

2023-09-07 | GSE225369 | GEO

ADAR1-mediated RNA editing promotes B cell lymphomagenesis.

Project description:The project aims to evaluate the contribution of ADAR1 RNA editing to B cell lymphomagenesis, specifically in diffuse large B cell lymphoma (DLBCL). Within our DLBCL cohort, RNA editing targets transcripts within known lymphoma-driving pathways such as apoptosis, p53 and NF-kB signaling, as well as the previously unrecognized RIG-I-like pathway. In the latter context, we show that ADAR1-mediated editing in the MAVS transcript correlates with increased MAVS protein expression levels, associating with increased interferon/NF-kB signaling and increased T cell exhaustion. To confirm this mechanism, we have performed LC-MSMS analysis on a DLBCL cell line (RCK8) in the presence or absence of ADAR1 (Figure S11D ). Additionally, using targeted RNA base editing tools to restore editing within MAVS 3'UTR in ADAR1-deficient cells, we demonstrate that editing is likely to be causal to an increase in downstream signaling in the absence of activation by canonical nucleic acid receptor sensing. To confirm that this signaling increase depends on an increase of MAVS protein upon specific editing, we have performed LC-MSMS analysis on the same samples (Figure 4G).

2023-07-20 | PXD041549 | Pride

HyperTRIBE assay of VSV-GFP-infected HEK293T cells overexpressing ADAR1-CD, PTENα-N(WT)-ADAR1-CD, or PTENα-N(6R/D)-ADAR1-CD fusion protein

Project description:To explore the binding sites of PTENα on viral or host RNAs, we performed HyperTRIBE assay of HEK293T cells overexpressing ADAR1-CD, PTENα-N(WT)-ADAR1-CD, or PTENα-N(6R/D)-ADAR1-CD fusion protein under VSV-GFP (green fluorescent protein-expressing vesicular stomatitis virus) infection.

2024-02-19 | GSE237910 | GEO

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