Vesicle Trafficking Secretion
Gene co-expression module in Mast cells
| Category | Degranulation |
|---|---|
| Genes | 0 |
| Annotation certainty | 2 of 5 |
| Annotation consistency | 10 of 23 genes have a known function matching the annotation |
Why this annotation
This module has lower mean expression (0.508) and detection rate (31.1%), suggesting a more restricted or state-specific program. Hub genes include SCIN (scinderin/adseverin, actin-severing protein expressed in secretory cells), SELENOM (selenoprotein M, ER-localized antioxidant), GCSAML (germinal center-associated signaling and motility-like), DBNDD2 (dysbindin domain-containing, vesicle trafficking), BMERB1 (Rab effector), VWC2 (von Willebrand factor C domain), NAV1 (neuron navigator, cytoskeletal/migration), SLC25A4 (ANT1, mitochondrial ADP/ATP translocase), CYB5R1 (cytochrome b5 reductase), TIMP3 (tissue inhibitor of metalloproteinases 3, ECM regulation), PRXL2A (peroxiredoxin-like), GOLGA4 (Golgi apparatus), ASAH1 (acid ceramidase, sphingolipid metabolism), ATG5 (autophagy), CYTH4 (cytohesin-4, ARF GTPase activator, immune cell signaling), LYPLAL1 (lipase-like), CAVIN2 (caveolae-associated). The module shows increased expression in UC remission (delta_remission_UC = 0.454). SCIN is a key hub — it is highly expressed in mast cells and involved in regulated exocytosis/degranulation. Combined with ASAH1 (sphingolipid processing relevant to degranulation), GOLGA4 (Golgi, secretory pathway), CYTH4 (immune signaling), ATG5 (autophagy/membrane trafficking), and TIMP3 (ECM remodeling), this module likely reflects a mast cell secretory/vesicle trafficking program, possibly linked to regulated degranulation or autophagy-related secretion. The remission association may reflect resolution-phase mast cell activity.
Genes
Most correlated modules
- Mitochondrial Protein Import · correlation 0.84
- Mast Cell Activation · correlation 0.81
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.