|
| Status |
Public on Feb 06, 2013 |
| Title |
Primary human Neurons_Control M2 [miRNA] |
| Sample type |
RNA |
| |
|
| Source name |
Primary human Neurons
|
| Organism |
Homo sapiens |
| Characteristics |
cell type: Primary human Neurons
agent: untreated
|
| Treatment protocol |
Cells were treated with Tat (10 ng/ml) kindly received from NIH (AIDS reagnets Bank) for 24 hours.
|
| Growth protocol |
Primary human neurons (HN) (5 x 105) purchased from ScienCell Research Laboratories (Carlsbad, CA) were grown in DMEM + 10% FBS on MatTek glass bottom plates treated with collagen (MatTek, Ashland, MA).
|
| Extracted molecule |
total RNA |
| Extraction protocol |
Total RNA was isolated using Trizol (Invitrogen, Carlsbad, CA). 750 ng of total RNA was used for miRNA array analysis using Agilent-019118 Human miRNA Microarray 2.0 G4470B (miRNA ID version)
|
| Label |
Hy5
|
| Label protocol |
RNA was labeled using the miRCURY LNATM miRNA, Hy5 Power Labeling Kit (Exiqon) as per manufacturer’s recommendations using Maui SC Hybridization Chambers (BioMicro Systems, Salt Lake City, UT).
|
| |
|
| Hybridization protocol |
Standard Agilent protocol.
|
| Scan protocol |
Array chips were scanned using Axon GenePix Scanner (Molecular Devices, Downingtown, PA) and Genepix 4000 image capture software (Molecular Devices, Downingtown, PA).
|
| Data processing |
Quantile normalization was used using JMP Genomics (JMP, Cary, NC) at Harvard Catalyst - Laboratory for Innovative Translational Technology (HC-LITT) and differentially regulated miRNAs were determined. Untreated cells were used as control.
|
| |
|
| Submission date |
Feb 06, 2013 |
| Last update date |
Feb 12, 2013 |
| Contact name |
Bassel E Sawaya |
| E-mail(s) |
sawaya@temple.edu
|
| Phone |
2157075446
|
| Organization name |
Temple University
|
| Department |
Neurology
|
| Street address |
3307 N. Broad Street
|
| City |
Philadelphia |
| State/province |
PA |
| ZIP/Postal code |
19140 |
| Country |
USA |
| |
|
| Platform ID |
GPL8227 |
| Series (1) |
| GSE44265 |
HIV-1 Tat protein promotes neuronal dysfunction through disruption of microRNAs. |
|
