|
| Status |
Public on Jun 29, 2019 |
| Title |
05 cKit-neg_IL-1B |
| Sample type |
RNA |
| |
|
| Source name |
PBMC
|
| Organism |
Homo sapiens |
| Characteristics |
cell type: c-kit‒ ILC2s
stimulation: IL-1β
|
| Treatment protocol |
PBMC-derived ILC2 subsets were stimulated with indicated cytokine(s)
|
| Growth protocol |
PBMC-derived ILC2s were cultured in Yssels medium containing 1% human serum at 37°C
|
| Extracted molecule |
total RNA |
| Extraction protocol |
Total RNA was isolated using Trizol (Invitrogen) and purified with RNeasy (Qiagen) according to manufacturer’s protocol,
|
| Label |
biotin
|
| Label protocol |
RNA sample integrity was checked on an Agilent 2100 Bioanalyzer (Agilent Technologies). 4 µg of total RNA was used for cRNA synthesis and fragmented. Labeling was performed with One-Cycle cDNA synthesis Kit (Affymetrix) according to manufacturer’s protocol. Sample quality was checked on a Bioanalyzer prior and after fragmentation.
|
| |
|
| Hybridization protocol |
10 µg of labeled cRNA was hybridized to Affymetrix Clariom S Assay HT arrays according to manufacturer’s protocol (Affymetrix).
|
| Scan protocol |
Arrays were scanned with a GeneChip Scanner 3000 (Affymetrix) according to manufacturer’s protoco
|
| Description |
Total RNA was isolated and analyzed on Affymetrix Clariom S Human arrayto generate expression profiles
|
| Data processing |
Expression data (cel files) were normalized with the rma_sketch algorithm (target signal = 100) using APT (Affymetrix powertools),
|
| |
|
| Submission date |
Apr 02, 2019 |
| Last update date |
Jun 30, 2019 |
| Contact name |
Richard Volckmann |
| E-mail(s) |
[email protected]
|
| Organization name |
Academic Medical Centre, University of Amsterdam
|
| Department |
Department of Oncogenomics
|
| Street address |
P.O. Box 22700
|
| City |
Amsterdam |
| ZIP/Postal code |
1100DE |
| Country |
Netherlands |
| |
|
| Platform ID |
GPL24324 |
| Series (1) |
| GSE129238 |
Differential c-Kit expression identifies two subsets of ILC2s with IL-17 producing capabilities that may contribute to IL-17 mediated pathologies |
|
