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Status |
Public on Jun 17, 2017 |
Title |
Role of JunB in Th17 cell effector stability [RNA-seq] |
Organism |
Mus musculus |
Experiment type |
Expression profiling by high throughput sequencing
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Summary |
Here we identify the activator protein-1 (AP-1) factor JunB as an essential regulator of Th17 cell identity. JunB activates the expression of Th17 lineage-specifying genes, and coordinately represses genes controlling Th1 and Treg fate. Through regulatory analysis, we find that JunB is a core regulator of global transcriptional programs that promote Th17 cell identity and restrict alternative CD4+ T cell potential.
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Overall design |
Examination of differential gene expression in Junb+/+CD4cre and Junbfl/flCD4cre 48 hour in vitro polarized Th17 cell cultures
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Contributor(s) |
Carr TM, Wheaton JD, Ciofani M |
Citation(s) |
28824171 |
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Submission date |
May 01, 2017 |
Last update date |
May 15, 2019 |
Contact name |
Maria Ciofani |
E-mail(s) |
maria.ciofani@duke.edu
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Organization name |
Duke University School of Medicine
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Department |
Integrative Immunobiology
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Street address |
207 Research Drive, 128 Jones Building
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City |
Durham |
State/province |
NC |
ZIP/Postal code |
27710 |
Country |
USA |
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Platforms (1) |
GPL13112 |
Illumina HiSeq 2000 (Mus musculus) |
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Samples (4)
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This SubSeries is part of SuperSeries: |
GSE98414 |
Role of JunB in Th17 cell effector stability |
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Relations |
BioProject |
PRJNA385056 |
SRA |
SRP106220 |