|
| Status |
Public on May 12, 2016 |
| Title |
M1-BMDMs_Keap1CKO_replicate2 |
| Sample type |
RNA |
| |
|
| Source name |
BMDMs, Keap1CKO, LPS and IFNg, 6hrs, replicate2
|
| Organism |
Mus musculus |
| Characteristics |
strain: C57BL/6
gender: Female
age: 8 weeks
cell type: BMDM
genotype/variation: Keap1 CKO
treatment: M1-stimuli (LPS and IFNg)
|
| Treatment protocol |
BMDMs are untreated, or treated with M1-stimuli (LPS and IFNg) or with M2-stimuli (IL-4) for 6 hours.
|
| Growth protocol |
Bone marrow cells were cultured in DMEM supplemented with 10% fetal bovine serum, M-CSF, and Antibiotic-Antimycotic. The cultures were incubated at 37 ºC in a humidified incubator with 5% CO2 for 7 days.
|
| Extracted molecule |
total RNA |
| Extraction protocol |
Total RNA was extracted from BMDMs using RNeasy Micro kit (Qiagen).
|
| Label |
Cy3
|
| Label protocol |
RNA samples were labeled with Cy3 using the Quick Amp Labeling kit (Agilent) according to the manufacturer's protocol.
|
| |
|
| Hybridization protocol |
Cy3-labeled cRNA were mixed and fragmented using the Agilent In Situ Hybridization Kit protocol. Hybridizations were performed for 16 hours according to the Agilent 60-mer oligo microarray processing protocol prior to washing.
|
| Scan protocol |
Slides were scanned with an Agilent DNA Microarray Scanner.
|
| Description |
Gene expression in Keap1-deficient BMDMs stimulated with LPS and IFNg for 6hrs, replicate2
|
| Data processing |
The data were normalized by percentile shift and filtered by flag, using GeneSpring GX software (Silicon Genetics).
|
| |
|
| Submission date |
Jul 23, 2015 |
| Last update date |
May 12, 2016 |
| Contact name |
Eri H Kobayashi |
| Organization name |
Tohoku University Graduate School of Medicine
|
| Department |
Medical Biochemistry
|
| Street address |
2-1 Seiryo-machi, Aobaku
|
| City |
Sendai |
| State/province |
Miyagi |
| ZIP/Postal code |
980-8575 |
| Country |
Japan |
| |
|
| Platform ID |
GPL7202 |
| Series (1) |
| GSE71263 |
Nrf2 suppresses macrophage inflammatory response by blocking proinflammatory cytokine transcription |
|
