TGF-β Antagonism
Gene co-expression module in Natural Killer cells
| Category | Immune regulation |
|---|---|
| Genes | 10 |
| Annotation certainty | 2 of 5 |
| Annotation consistency | 8 of 10 genes have a known function matching the annotation |
Why this annotation
Hub genes include SRSF5 (serine/arginine-rich splicing factor), ZBTB1 (zinc finger transcription factor, involved in DNA damage response and lymphocyte development), IFRD1 (interferon-related developmental regulator, modulates NF-κB and inflammatory responses), STK17B (DRAK2, serine/threonine kinase involved in T/NK cell apoptosis and activation), SMAD7 (inhibitory SMAD, antagonizes TGF-β signaling), SBDS (ribosome assembly factor), IRS2 (insulin receptor substrate 2, PI3K/Akt signaling), ZFAND5 (zinc finger AN1-type, stress response/ubiquitin), MOB3A (Mps one binder kinase activator), and RBM39 (RNA-binding protein, splicing regulation). The module is significantly upregulated in CD inflammation and significantly downregulated with CD treatment. SMAD7 is a canonical TGF-β antagonist upregulated in IBD. IFRD1 modulates inflammatory gene expression. STK17B regulates NK/T cell survival. IRS2 links cytokine/growth factor signaling to PI3K. This module reflects TGF-β pathway antagonism and inflammatory kinase signaling in NK cells during CD inflammation.
Genes
IFRD1, IRS2, MOB3A, RBM39, SBDS, SMAD7, SRSF5, STK17B, ZBTB1, ZFAND5
Most correlated modules
- MAPK/AP-1 Signaling · correlation 0.81
- NK Activation Response · correlation 0.81
- Glucocorticoid Response · correlation 0.80
- Autophagy-Inflammation Stress · correlation 0.79
- ER Stress Response · correlation 0.78
- NK Cell Activation · correlation 0.76
- NRF2 Stress Response · correlation 0.76
- NF-κB Activation · correlation 0.76
Module annotations were drafted by a large language model from the module's genes, then reviewed and approved by a domain expert. See sources & licences.