NF-κB Endothelial Activation
Gene co-expression module in Endothelial
| Category | Inflammation |
|---|---|
| Genes | 14 |
| Annotation certainty | 4 of 5 |
| Annotation consistency | 10 of 14 genes have a known function matching the annotation |
Why this annotation
Hub genes LITAF (LPS-induced TNF activating factor), RELB and NFKB2 (non-canonical NF-κB subunits), SELE (E-selectin, canonical endothelial activation marker), ZC3H12A (Regnase-1/MCPIP1, post-transcriptional NF-κB regulator), TNFRSF10B (TRAIL receptor 2), SBNO2 (NF-κB modulator), and NAMPT (PBEF/visfatin, pro-inflammatory cytokine) define a tight NF-κB activation program. UGCG (ceramide glycosylation, sphingolipid signaling downstream of TNF) and NUAK2 (stress kinase) further support inflammatory signaling. Strongly upregulated in IBD inflammation and reversed in remission. This is the most coherent NF-κB-driven endothelial activation module in the batch, with M108 representing its downstream cytokine/adhesion effectors.
Genes
LITAF, NAMPT, NFKB2, NUAK2, RELB, SBNO2, SELE, SLC35F2, SRGAP1, TNFRSF10B, UGCG, YPEL2, ZC3H12A, ZNF267
Most correlated modules
- Wnt Angiogenic Remodeling · correlation 0.86
- Procoagulant TGF-β Response · correlation 0.82
- Stress RNA Processing · correlation 0.82
- Leukocyte Recruitment Signaling · correlation 0.80
- NF-κB Activation · correlation 0.76
- Complement Innate Immune · correlation 0.73
- Inflammatory Angiogenesis · correlation 0.73
- Myeloid Contamination · correlation 0.67
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.