Endothelial Quiescence
Gene co-expression module in Endothelial
| Category | Endothelial cell development |
|---|---|
| Genes | 16 |
| Annotation certainty | 3 of 5 |
| Annotation consistency | 11 of 16 genes have a known function matching the annotation |
Why this annotation
ID1, ID3, and HES5 are canonical BMP/Notch inhibitors of differentiation that maintain endothelial quiescence. SMAD7 and SMURF2 are negative regulators of TGF-β signaling. SAV1 is a Hippo pathway component that restricts proliferation. KLF7 is a vascular transcription factor. CGAS indicates innate immune DNA sensing. CDC42EP3 links to cytoskeletal remodeling. The module is significantly upregulated in both UC and CD inflammation, suggesting an anti-proliferative/quiescence program activated in inflamed endothelium to restrain angiogenesis. The TGF-β negative feedback (SMAD7/SMURF2) and Notch/BMP quiescence signals (ID1/ID3/HES5) define this as an endothelial quiescence program.
Genes
CCRL2, CDC42EP3, CGAS, CHSY1, CYTH1, HES5, HIPK3, ID1, ID3, INPP1, KLF7, SAV1, SMAD7, SMURF2, SRSF4, STK17A
Most correlated modules
- Inflammatory Stress Response · correlation 0.81
- Stress RNA Processing · correlation 0.80
- NF-κB Early Response · correlation 0.79
- Notch Ligand Signaling · correlation 0.76
- Chronic Inflammatory Activation · correlation 0.67
- Heat Shock Response · correlation 0.66
- NF-κB Endothelial Activation · correlation 0.64
- NF-κB Activation · 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.