NF-κB Stress Signaling
Gene co-expression module in Endothelial
| Category | Inflammation |
|---|---|
| Genes | 13 |
| Annotation certainty | 2 of 5 |
| Annotation consistency | 8 of 13 genes have a known function matching the annotation |
Why this annotation
Hub genes include ELK4 (ETS transcription factor with vascular roles), PELI2 (Pellino E3 ubiquitin ligase in TLR/NF-κB signaling), NFAT5 (osmotic/inflammatory stress TF), METRNL (anti-inflammatory secreted factor), and AKR1C3 (prostaglandin/steroid metabolism). The module shows modest but significant upregulation in UC and CD inflammation. The combination of NF-κB pathway components (PELI2), stress-responsive TFs (NFAT5, ELK4), and metabolic genes (AKR1C3) suggests a moderate inflammatory-responsive endothelial signaling state. Compared to neighbor M75 (strong chemokine response) and M73 (ECM remodeling), this module represents a more upstream regulatory/signaling layer of the inflammatory response.
Genes
AKR1C3, ELK4, EPS15, METRNL, MYCBP2, NFAT5, PALM, PELI2, PGM5, PLXDC2, PTGFRN, SCARB2, VPS13C
Most correlated modules
- Inflammatory ECM Remodeling · correlation 0.86
- Venous EC Identity · correlation 0.82
- Actomyosin Contractility · correlation 0.76
- Arterial EC Identity · correlation 0.69
- Angiogenic Metabolic Adaptation · correlation 0.68
- Venous EC Identity · correlation 0.65
- Arterial EC Identity · correlation 0.64
- Hypoxia Stress Response · correlation 0.63
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.