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Status |
Public on Jul 05, 2022 |
Title |
Glycosylated clusterin species facilitate amyloid beta toxicity in human neurons. |
Organism |
Homo sapiens |
Experiment type |
Expression profiling by high throughput sequencing
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Summary |
Clusterin (CLU) is one of the most significant genetic risk factors for late onset Alzheimer’s disease. Numerous studies have now demonstrated that CLU-AD mutations and amyloid-β (Aβ) treatment alter the trafficking and localisation of glycosylated CLU. iPSCs with altered CLU trafficking were generated following the removal of CLU exon 2 by CRISPR/Cas9 gene editing. Neurons were generated from control, unedited and exon 2 -/- iPSCs and were incubated with aggregated Aβ peptides. Changes in cell death and neurite length were quantified to determine if altered CLU protein trafficking influenced neuronal sensitivity to Aβ.
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Overall design |
RNA-Seq analysis was performed to identify key transcriptomic differences between exon 2 -/- and CTR neurons.
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Contributor(s) |
Marco F, Noel B |
Citation missing |
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Submission date |
Jul 05, 2022 |
Last update date |
Jul 05, 2022 |
Contact name |
Marco Fernandes |
E-mail(s) |
marco.fernandes@psych.ox.ac.uk
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Organization name |
University of Oxford
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Department |
Department of Psychiatry, Warneford Ln, Headington
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Street address |
Department of Psychiatry, Warneford Ln, Headington
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City |
Oxford |
ZIP/Postal code |
OX3 7JX |
Country |
United Kingdom |
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Platforms (1) |
GPL24676 |
Illumina NovaSeq 6000 (Homo sapiens) |
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Samples (18)
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Relations |
BioProject |
PRJNA855866 |