Inflammatory Stress Response
Gene co-expression module in Natural Killer cells
| Category | Stress |
|---|---|
| Genes | 11 |
| Annotation certainty | 2 of 5 |
| Annotation consistency | 6 of 11 genes have a known function matching the annotation |
Why this annotation
Hub genes include CCNH (Cyclin H), CLASP1 (microtubule stabilizer), and PIK3IP1 (PI3K inhibitor), alongside FKBP5 (glucocorticoid-responsive stress gene), CEBPD (acute-phase inflammatory transcription factor), AKIRIN2 (NF-κB innate immunity), and VEGFA. The module is significantly upregulated in CD inflammation and suppressed by CD treatment, consistent with a stress/inflammatory transcriptional regulatory program. FKBP5 and CEBPD together suggest glucocorticoid-mediated inflammatory regulation. The combination of PI3K inhibition (PIK3IP1), transcriptional repression (TLE1), and stress-responsive factors (FKBP5, CEBPD) points to an NK cell inflammatory stress-regulatory state active in Crohn's disease.
Genes
AKIRIN2, CCNH, CEBPD, CLASP1, FKBP5, H3C1, P2RX5, PARP8, PIK3IP1, TLE1, VEGFA
Most correlated modules
- Housekeeping Mixed · correlation 0.67
- NK/ILC Differentiation · correlation 0.64
- NK Cytotoxic Signaling · correlation 0.58
- NK Cell Identity · correlation 0.55
- Septin Cytoskeletal Assembly · correlation 0.47
- Replication-Coupled Histones · correlation 0.46
- Interferon NK Activation · correlation 0.37
- Circadian Apoptotic Priming · correlation 0.36
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.