NF-κB Inflammatory Activation
Gene co-expression module in Fibroblasts
| Category | Inflammatory |
|---|---|
| Genes | 14 |
| Annotation certainty | 4 of 5 |
| Annotation consistency | 12 of 14 genes have a known function matching the annotation |
Why this annotation
Hub genes include UBD (FAT10, NF-κB/IFN target), BIRC3 (NF-κB anti-apoptotic), TNFSF14 (TNF superfamily ligand LIGHT), CD40 (NF-κB receptor), IL32 (pro-inflammatory cytokine), STAT1, TYMP, IL15RA, CTSS, TAPBP, and DRAM1. The module is strongly upregulated in both UC and CD inflammation and suppressed in remission. The dominant program is NF-κB-driven inflammatory activation in fibroblasts, with secondary IFN-γ overlap (STAT1, TAPBP). LAP3 is IFN-inducible. This is a TNF/NF-κB inflammatory activation signature in intestinal fibroblasts, consistent with the IBD inflammatory microenvironment.
Genes
BIRC3, CD40, CTSS, DRAM1, HAPLN3, IL15RA, IL32, LAP3, STAT1, TAPBP, TLCD1, TNFSF14, TYMP, UBD
Most correlated modules
- Immunoproteasome MHC-I · correlation 0.77
- ER Stress UPR · correlation 0.74
- Inflammatory ECM Remodeling · correlation 0.71
- IFN-γ MHC-II Response · correlation 0.68
- AP-1 Inflammatory Stress · correlation 0.67
- Inflammatory Fibroblast Activation · correlation 0.65
- Cytokine Chemokine Secretion · correlation 0.63
- Inflammatory Fibroblast Activation · correlation 0.59
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.