NF-κB Stress Response
Gene co-expression module in Fibroblasts
| Category | Inflammatory |
|---|---|
| Genes | 12 |
| Annotation certainty | 4 of 5 |
| Annotation consistency | 9 of 12 genes have a known function matching the annotation |
Why this annotation
Hub genes PHLDA1/PHLDA2 are stress-responsive pro-apoptotic genes induced by NF-κB and inflammatory signals. NAMPT encodes a key NAD+ biosynthesis enzyme upregulated in inflammation. TNFAIP3 (A20) is a canonical NF-κB feedback inhibitor. SOD2 is a mitochondrial antioxidant induced by cytokines. NFIL3 is a stress/inflammatory transcription factor. SAT1 is a polyamine catabolism enzyme induced by p53/stress. NCOA7 is an oxidative stress-responsive coactivator. EGR3 is an immediate-early transcription factor. The module is strongly upregulated in UC and CD inflammation and decreases with remission, consistent with a fibroblast inflammatory stress-response program driven by NF-κB and oxidative stress. All genes are core members with uniform expression across subsets.
Genes
EGR3, NAMPT, NCOA7, NFIL3, PHLDA1, PHLDA2, SAT1, SLC20A1, SOD2, TCIM, TMEM165, TNFAIP3
Most correlated modules
- Hypoxia Metabolic Stress · correlation 0.92
- Cytokine Inflammatory Response · correlation 0.88
- AP-1 Inflammatory Stress · correlation 0.84
- ER Stress UPR · correlation 0.82
- Integrated Stress Response · correlation 0.81
- Inflammatory TF Response · correlation 0.79
- Unfolded Protein Response · correlation 0.78
- NF-κB Epigenetic Reprogramming · 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.