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Links from GEO DataSets

Items: 20

1.

ADAR1 forms a complex with Dicer to promote microRNA processing and RNA-induced gene silencing

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus; Homo sapiens
Type:
Expression profiling by high throughput sequencing; Non-coding RNA profiling by high throughput sequencing
Platforms:
GPL9115 GPL9250
8 Samples
Download data: BED, SAM, TXT, WIG
Series
Accession:
GSE43192
ID:
200043192
2.

Small RNA analysis of ADAR1-knock down HeLa cells by RNAi

(Submitter supplied) Small RNA expression was analysed in total RNA of HeLa cells treated with siRNA toward Luciferase (negative cotrol) or ADAR1.
Organism:
Homo sapiens
Type:
Non-coding RNA profiling by high throughput sequencing
Platform:
GPL9115
2 Samples
Download data: TXT
Series
Accession:
GSE43167
ID:
200043167
3.

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

(Submitter supplied) Adar1 is an essential gene for mouse embryonic development. Adar1 null mouse embryos dies around E11.5 because of massive apoptosis.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing; Non-coding RNA profiling by high throughput sequencing
Platform:
GPL9250
6 Samples
Download data: BED, SAM, TXT, WIG
Series
Accession:
GSE33473
ID:
200033473
4.

Systematic Mapping of ADAR1 Binding Reveals its Regulatory Roles in Multiple RNA Processing Pathways

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
14 Samples
Download data: TXT
Series
Accession:
GSE55363
ID:
200055363
5.

Systematic Mapping of ADAR1 Binding Reveals its Regulatory Roles in Multiple RNA Processing Pathways [small RNA-seq]

(Submitter supplied) ADARs are the primary factors underlying A-to-I editing in metazoans. We conducted the first global study of ADAR1-RNA interaction in human cells using CLIP-Seq. In contrast to the expected predominant binding of ADAR1 to Alu repeats, thousands of CLIP sites were located in non-Alu regions. This unexpectedly frequent non-Alu binding enabled discovery of transcriptome-wide functional and biophysical targets of ADAR1 in the regulation of mRNA processing including alternative 3' UTR usage and alternative splicing. more...
Organism:
Homo sapiens
Type:
Non-coding RNA profiling by high throughput sequencing
Platform:
GPL11154
12 Samples
Download data: TXT
Series
Accession:
GSE55362
ID:
200055362
6.

Systematic Mapping of ADAR1 Binding Reveals its Regulatory Roles in Multiple RNA Processing Pathways [CLIP-seq]

(Submitter supplied) ADARs are the primary factors underlying A-to-I editing in metazoans. We conducted the first global study of ADAR1-RNA interaction in human cells using CLIP-Seq. In contrast to the expected predominant binding of ADAR1 to Alu repeats, thousands of CLIP sites were located in non-Alu regions. This unexpectedly frequent non-Alu binding enabled discovery of transcriptome-wide functional and biophysical targets of ADAR1 in the regulation of mRNA processing including alternative 3' UTR usage and alternative splicing. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
2 Samples
Download data: BED
Series
Accession:
GSE55361
ID:
200055361
7.

ADAR1 is required for differentiation and neural induction by regulating microRNA processing in a catalytically independent manner (iCLIP)

(Submitter supplied) We used iCLIP to identify ADAR1 binding sites in embryonic stem cells.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
4 Samples
Download data: BED
Series
Accession:
GSE63709
ID:
200063709
8.

RNA-seq and small RNA-seq from WT and ADAR1 knockdown H9 lines and their differentiation to specific types of neurons

(Submitter supplied) Adenosine deaminases acting on RNA (ADARs) are involved in adenosine (A) to inosine (I) RNA editing and human ADARs are implicated in neurological diseases. Here we generated human embryonic stem cells (hESCs) lacking ADAR1 to investigate its role in neural development in a human context. We found that ADAR1 deficiency significantly retarded neural induction with widespread mRNA and miRNA expression changes. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Non-coding RNA profiling by high throughput sequencing
Platform:
GPL11154
24 Samples
Download data: BW, TXT
Series
Accession:
GSE56152
ID:
200056152
9.

Effects of ADARs on small RNA processing pathways in C. elegans

(Submitter supplied) Adenosine deaminases that act on RNA (ADARs) are RNA editing enzymes that convert adenosine to inosine in double-stranded RNA (dsRNA). To evaluate effects of ADARs on small RNAs that derive from dsRNA precursors, we performed deep-sequencing, comparing small RNAs from wildtype and ADAR mutant C. elegans. While editing in small RNAs was rare, at least 40% of microRNAs had altered levels in at least one ADAR mutant strain, and miRNAs with significantly altered levels had mRNA targets with correspondingly affected levels. more...
Organism:
Caenorhabditis elegans
Type:
Non-coding RNA profiling by high throughput sequencing
Platform:
GPL9269
5 Samples
Download data: TAR
Series
Accession:
GSE28888
ID:
200028888
10.

RNA Sequencing Quantitative Analysis and identification of RNA editing sites of Wild Type and ADAR1 editing deficient (ADAR1E861A) murine fetal liver RNA

(Submitter supplied) Purpose: RNA editing by ADAR1 is essential for hematopoietic development. The goals of this study were firstly, to identify ADAR1-specific RNA-editing sites by indentifying A-to-I (G) mismatches in RNA-seq data compared to mm9 reference genome in wild type mice that were not edited or reduced in editing frequency in ADAR1E861A editing deficient mice. Secondly, to determine the transcriptional consequence of an absence of ADAR1-mediated A-to-I editing. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL13112
6 Samples
Download data: TXT
Series
Accession:
GSE58917
ID:
200058917
11.

Regulation of miRNA biogenesis by MCPIP1

(Submitter supplied) Effect of MCPIP1 knockdown on miRNA expression profile.
Organism:
Homo sapiens; Human alphaherpesvirus 1; Human betaherpesvirus 5; Macaca mulatta polyomavirus 1; Mus musculus; Rattus norvegicus; Murid betaherpesvirus 1; Human gammaherpesvirus 4; JC polyomavirus; Human immunodeficiency virus 1; Human gammaherpesvirus 8; Murid gammaherpesvirus 4; Human polyomavirus 1
Type:
Non-coding RNA profiling by array
Platform:
GPL7723
2 Samples
Download data: TXT
Series
Accession:
GSE31091
ID:
200031091
12.

ADAR1-mediated A-to-I RNA editing is essential for erythropoiesis

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by array; Expression profiling by high throughput sequencing
Platforms:
GPL13112 GPL6246
17 Samples
Download data: CEL
Series
Accession:
GSE71047
ID:
200071047
13.

ADAR1-mediated A-to-I RNA editing is essential for erythropoiesis [RNA-seq]

(Submitter supplied) Purpose: RNA editing by ADAR1 is essential for hematopoietic development. The goals of this study were firstly, to identify ADAR1-specific RNA-editing sites by indentifying A-to-I (G) RNA editing sites in wild type mice that were not edited or reduced in editing frequency in ADAR1 deficient murine erythroid cells. Secondly, to determine the transcription consequence of an absence of ADAR1-mediated A-to-I editing. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL13112
4 Samples
Download data: GCT, TXT, XLS
Series
Accession:
GSE71042
ID:
200071042
14.

RNA editing by ADAR1 is essential for erythropoiesis [array]

(Submitter supplied) Erythroid progenitors purified from EpoRCreR26eYFPADAR1fl/- and EpoRCreR26eYFPADAR1fl/+ control mice were compared for global gene array profiles
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6246
13 Samples
Download data: CEL
Series
Accession:
GSE59664
ID:
200059664
15.

A retrotransposon-driven Dicer variant enhances endogenous RNAi in mouse oocytes

(Submitter supplied) Mammals have one Dicer gene required for biogenesis of small RNAs in microRNA (miRNA) and RNA interference (RNAi) pathways. Yet, endogenous RNAi is highly active in oocytes but not in somatic cells. Here, we provide a mechanistical explanation for high RNAi activity in mouse oocytes. The main Dicer isoform in oocytes is transcribed from an intronic MT-C retrotransposon, which functions as a promoter of an oocyte-specific Dicer isoform (denoted DicerO). more...
Organism:
Mus musculus
Type:
Non-coding RNA profiling by high throughput sequencing
Platform:
GPL14602
19 Samples
Download data: BED
Series
Accession:
GSE41207
ID:
200041207
16.

Combinatory RNA sequencing analyses reveal RNA editing-dependent and -independent gene regulation by ADAR1 in gastric cancer

(Submitter supplied) To investigate the role of ADAR1 in gastric carcinogenesis, RNA sequencing and small RNA sequencing were performed in AGS and MKN-45 cells with stable ADAR1 knock-down. Changed frequencies of editing and messenger RNA (mRNA) and microRNA (miRNA) expression were then identified by bioinformatic analyses.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Non-coding RNA profiling by high throughput sequencing
Platform:
GPL16791
8 Samples
Download data: TXT
Series
Accession:
GSE106874
ID:
200106874
17.

secondary structure based on icSHAPE of pre-let-7 and hDicer-TRBP bound pre-let-7

(Submitter supplied) we resolved precusor let7 (pre-let-7) and human Dicer-TRBP complex bound precusor let7 (hDicer-TRBP-pre-let-7) secondary structure based on in vivo click selective 2'-hydroxyl acylation and profiling experiment (icSHAPE). We found the free pre-let-7 RNA is more flexible comparing with hDicer-TRBP-pre-7 in the double strand region [10-20nt and 50- 60 nt].
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL20795
4 Samples
Download data: TXT
Series
Accession:
GSE110516
ID:
200110516
18.

Transcriptome analysis of C. elegans embryos lacking ADARs and the 26G pathway

(Submitter supplied) Adenosine deaminases that act on RNA (ADARs) catalyze the conversion of adenosine to inosine in dsRNA. C. elegans ADARs, ADR-1 and ADR-2, promote the expression of genes containing dsRNA structures by preventing their processing into siRNAs and silencing by RNAi. The 26G endogenous siRNA (endo-siRNA) pathway generates a subset of siRNAs distinct from those made in adr-1;adr-2 mutants, but using many of the same factors. more...
Organism:
Caenorhabditis elegans
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18245
24 Samples
Download data: TXT
Series
Accession:
GSE106647
ID:
200106647
19.

Gene regulation by small RNAs and ADAR RNA editing

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Caenorhabditis elegans
Type:
Expression profiling by high throughput sequencing; Third-party reanalysis; Non-coding RNA profiling by high throughput sequencing
Platforms:
GPL13657 GPL18245
32 Samples
Download data
Series
Accession:
GSE89890
ID:
200089890
20.

ADARs regulate small RNAs mapped to edited sequences

(Submitter supplied) Cellular RNAs containing double-stranded RNA (dsRNA) structures are subject to A-to-I RNA editing by the adenosine deaminases that act on RNA (ADARs). While A-to-I editing can alter mRNA coding potential, most editing is observed in non-coding sequences, the function of which remains poorly characterized. To correlate small RNA population with expression patterns of ADARs and hyperedited RNAs (editing-enriched regions: EERs) defined and characterized in a separate RNAseq analysis, we re-analyzed existing smallRNAseq datasets of a wildtype strain and a strain lacking ADARs (adr-1;adr-2). more...
Organism:
Caenorhabditis elegans
Type:
Non-coding RNA profiling by high throughput sequencing; Third-party reanalysis
Download data: TXT, XLS
Series
Accession:
GSE89765
ID:
200089765
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