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Series GSE207466 Query DataSets for GSE207466
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
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.
 
Overall design RNA-Seq analysis was performed to identify key transcriptomic differences between exon 2 -/- and CTR neurons.
 
Contributor(s) Marco F, Noel B
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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
Organization name University of Oxford
Department Department of Psychiatry, Warneford Ln, Headington
Street address Department of Psychiatry, Warneford Ln, Headington
City Oxford
ZIP/Postal code OX3 7JX
Country United Kingdom
 
Platforms (1)
GPL24676 Illumina NovaSeq 6000 (Homo sapiens)
Samples (18)
GSM6288206 A4 [WTCHG_823226_70965072]
GSM6288207 A4 [WTCHG_823226_70015073]
GSM6288208 A4 [WTCHG_823226_70065078]
Relations
BioProject PRJNA855866

Download family Format
SOFT formatted family file(s) SOFTHelp
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Series Matrix File(s) TXTHelp

Supplementary file Size Download File type/resource
GSE207466_normalized_counts.txt.gz 3.6 Mb (ftp)(http) TXT
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Raw data are available in SRA
Processed data are available on Series record

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