RNA profiling of adar1-Zα mutant mouse lung
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB45231 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR6119320_1.fastq.gz | Fastqsanger.gz | |||
| ERR6119320_2.fastq.gz | Fastqsanger.gz | |||
| ERR6119312_1.fastq.gz | Fastqsanger.gz | |||
| ERR6119312_2.fastq.gz | Fastqsanger.gz | |||
| ERR6119313_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 12 |
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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
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
Project description:The purpose of this study was to examine the role of ZBP1 in the phenotype that develops when ADAR1 activity is missing, in particular when the Zα domain of ADAR1 is mutated. Mice homozygous for a Zα domain-mutant allele of Adar1 (Adar1mZα/mZα mice) were compared with control mice carrying one mZα allele and one wild type allele of Adar1 (Adar1wt/mZα mice) and with mice carrying one mZα and one null Adar1 allele (Adar1-/mZα mice). Adar1-/mZα mice were also compared with mice additionally deficient in ZBP1 (Adar1-/mZα Zbp1-/- mice). Given the early postnatal lethal phenotype that develops in Adar1-/mZα mice, comparisons were made in RNA isolated from spleen tissue from newborn mice of each genotype (5 mice per genotype).
2022-04-27 | E-MTAB-10953 | biostudies-arrayexpress
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
Project description:ADAR1-Zalpha-mutant-primary mouse lung endothelial cells
| PRJEB46161 | ENA
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
Project description:Adenosine-to-inosine (A-to-I) RNA editing catalyzed by ADAR1 plays essential roles in the regulation of diverse molecular and cellular processes both under physiological conditions and in the disease states, including cancer. However, mechanisms governing the protein abundance and activity of ADAR1, particularly of its constitutively-expressed and ubiquitous form, ADAR1p110, are largely unknown. Here, we report the E3 ubiquitin ligase SMURF2 as an essential positive regulator of ADAR1p110. We show that SMURF2 directly interacts with ADAR1p110, oligo-ubiquitinates it in an E3 ubiquitin ligase-dependent manner, and stabilizes ADAR1p110 expression by reducing its proteolysis through the proteasomal and lysosomal degradation pathways. The ability of SMURF2 to positively regulate ADAR1p110 was observed in different types of human cells and tissues, and in mouse tissues derived from Smurf2 knock-out and wild-type animals. Further investigations uncovered that SMURF2 regulates ADAR1p110 through its ubiquitination on K744 residue. Mutation of K744 to arginine (K744R), which is also linked to several human disorders, abolished SMURF2-mediated protection of ADAR1p110 from the proteolysis and inactivated its RNA editing activity. Additionally, SMURF2 showed a significant impact on ADAR1p110 protein-protein interactions, influencing its stability and functions. Altogether, these findings reveal SMURF2 as a multilayer regulator of ADAR1p110, governing its protein expression, interactions and functions.
2022-05-29 | PXD025338 | Pride
Project description:We compared gene expression in T1alpha (-/-) lungs vs wild type at dpc 18.5 when the phenotype is moderate and at term when the phenotype is more severe. Lungs present narrow and irregular alveolar spaces, thicker mesenchyme, reduced number of attenuated type I cells, normal numbers of type II cells and secreted surfactant. At term, but not a dpc 18.5, there is increased proliferation of distal cells. We compared gene expression of T1alpha null mutant lungs to wild type lungs at dpc 18.5. The mutant phenotype at this developmental stage is moderate but the alveolar sacs are narrower than normal.
2007-11-22 | E-GEOD-1363 | biostudies-arrayexpress
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.
2014-12-19 | GSE62917 | GEO
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