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| Status |
Public on Jan 17, 2020 |
| Title |
Knocking out C9ORF72 exacerbates axonal trafficking defects associated with hexanucleotide repeat expansion and reduces levels of heat shock proteins I |
| Organism |
Homo sapiens |
| Experiment type |
Expression profiling by high throughput sequencing
|
| Summary |
iPSCs with mutant C9ORF72 were edited using CRISPR/Cas9 (1) to knockout C9ORF72 or, alternatively, (2) to correct the ALS mutation, followed by differentiation into motor neurons.
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| Overall design |
We tested the effects of mutations in C9ORF72 on iPSC-derived MNs by comparing to isogenic gene-corrected controls. In addition, we generated a knockout in MNs containing mutant C9ORF72 to test if this would exacerbate MN degeneration.
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| Contributor(s) |
Sterneckert J, Abo-Rady M |
| Citation(s) |
32084385 |
| |
| Submission date |
Jan 15, 2020 |
| Last update date |
Apr 21, 2020 |
| Contact name |
Jared Sterneckert |
| E-mail(s) |
Jared.Sterneckert@tu-dresden.de
|
| Organization name |
TU Dresden
|
| Department |
Center for Molecular and Cellular Bioengineering (CMCB)
|
| Lab |
iPS Cells and Neurodegenerative Disease
|
| Street address |
Fetscherstraße 105
|
| City |
Dresden |
| State/province |
Saxony |
| ZIP/Postal code |
01307 |
| Country |
Germany |
| |
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| Platforms (1) |
| GPL18573 |
Illumina NextSeq 500 (Homo sapiens) |
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| Samples (9)
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| Relations |
| BioProject |
PRJNA601468 |
| SRA |
SRP242090 |
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