Asymmetry of STAT action in driving IL-27 and IL-6 transcriptional outputs and cytokine specificity
Transcriptomics Dataset
FAIR Metrics
0 evaluations
General Information
| Accession | GSE65621 |
| Title | Asymmetry of STAT action in driving IL-27 and IL-6 transcriptional outputs and cytokine specificity |
| Description | IL-6 and IL-27 have antagonistic and overlapping functions, signal through a shared receptor subunit and employ the same downstream STAT proteins. To evaluate the degree of specificity and redundancy for these cytokines, we quantified global transcriptomic changes induced by the two cytokines and determined the relative contributions of STAT1 and STAT3 using genetic models and ChIP-seq. We found a high degree of overlap of the transcriptomes induced by IL-6 and IL-27 and extremely few examples in which the cytokines acted in opposition. Using STAT deficient cells and T cells from patients with gain-of-function STAT1 mutations, we show that STAT3 was responsible for the overall transcriptional output driven by both cytokines, whereas STAT1 was the driver of cytokine specificity. STAT1 did not compensate for the lack STAT3; on the contrary, much of STAT1 binding to chromatin was STAT3 dependent. Thus, STAT1 shapes the specific cytokine signature superimposed upon STAT3s action. |
| Landing Page | https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE65621 |
| Repository | Gene Expression Omnibus |
Related Datasets
GSE37646
Distinct STAT5 concentrations uniquely control establishment and differentiation of mammary epithelium during pregnancy
1
GSE48970
Contribution of the STAT1alpha and STAT1beta isoforms to IFN-gamma mediated innate immunity
21
Tools
used to analyze the dataset
Canned Analyses
generated with the dataset
FAIR Evaluation
Sorry, you must be signed in to evaluate this object.
