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Status |
Public on Mar 23, 2015 |
Title |
RNA-seq and small RNA-seq from WT and ADAR1 knockdown H9 lines and their differentiation to specific types of neurons |
Organism |
Homo sapiens |
Experiment type |
Expression profiling by high throughput sequencing Non-coding RNA profiling by high throughput sequencing
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Summary |
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. We have genome widely examined the changes of A-to-I editing and miRNA expression after ADAR1 knockdown. Such aberrant mRNA and miRNA expression was not due to reduced A-to-I editing after ADAR1 knockdown. We further revealed that ADAR1 regulates miRNA biogenesis independent of its editing activity.
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Overall design |
In order to study the function role of ADAR1 in neural induction, we used shRNA to stably knocked down ADAR1 in human embryonic stem cell (hESC) h9 line and then differentiated ADAR1 deficiency hESC h9 cells to specific types of neurons. We then collect total RNAs at different time points at undifferentiated stage (day 0, d0 for short), day 10 (d10), day 17 (d17) and day 35 (d35), and obtained RNA-seq and small RNA-seq datasets for further analyses.
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Contributor(s) |
Yang L, Chen T, Zhu S, Yin Q, Fang H, Chen L |
Citation(s) |
25708366 |
Submission date |
Mar 24, 2014 |
Last update date |
May 15, 2019 |
Contact name |
Li Yang |
E-mail(s) |
liyang_fudan@fudan.edu.cn
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Organization name |
Fudan University
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Department |
Institutes of Biological Sciences
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Street address |
131 Dong-An Road
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City |
Shanghai |
ZIP/Postal code |
200032 |
Country |
China |
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Platforms (1) |
GPL11154 |
Illumina HiSeq 2000 (Homo sapiens) |
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Samples (24)
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Relations |
BioProject |
PRJNA242558 |
SRA |
SRP040525 |