Hypoxia-IFN Endothelial
Gene co-expression module in Endothelial
| Category | Endothelial cell development |
|---|---|
| Genes | 17 |
| Annotation certainty | 3 of 5 |
| Annotation consistency | 14 of 17 genes have a known function matching the annotation |
Why this annotation
Hub genes EPAS1 (HIF-2α), NOS3 (eNOS), MMRN2 (endothelial ECM), HEG1 (endothelial heart development), BCAM, RNASE1, and CRIP2 define a quiescent/homeostatic endothelial state with hypoxia sensing. IFI27 and IFITM1 indicate basal interferon signaling. ORAI1 mediates Ca2+ entry for eNOS activation. Downregulation in inflammation (delta ~-0.10 for both UC and CD) supports a homeostatic program lost during active disease. Neighbor context: complements M43 as a quiescent endothelial identity module but with a hypoxia/IFN overlay distinct from M43's angiogenic focus.
Genes
BCAM, CRIP2, EPAS1, FES, HEG1, IFI27, IFITM1, LIMA1, LIMS2, MALL, MMRN2, NOS3, NPDC1, ORAI1, PPA1, RNASE1, STOM
Most correlated modules
- EC Barrier Integrity · correlation 0.86
- Endothelial Angiogenic Identity · correlation 0.84
- EC Quiescence Identity · correlation 0.84
- Arterial EC Identity · correlation 0.83
- Vascular EC Identity · correlation 0.81
- Endothelial Junction Identity · correlation 0.79
- Cytoskeletal Scaffolding · correlation 0.77
- Vascular Homeostasis · correlation 0.74
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.