mTOR Nutrient Sensing
Gene co-expression module in Dendritic cells
| Category | Vesicular traficking |
|---|---|
| Genes | 0 |
| Annotation certainty | 2 of 5 |
| Annotation consistency | 8 of 20 genes have a known function matching the annotation |
Why this annotation
This module has moderate coherence and is enriched in cDC1 and mDC subsets. The hub genes include ST3GAL1 (sialylation/glycosylation), GPX4 (glutathione peroxidase, ferroptosis defense), BMP2K (BMP2-inducible kinase, endosomal trafficking/clathrin), RRAGC (Ragulator-Rag GTPase, mTORC1 nutrient sensing), ATP6V0A2 (vacuolar ATPase, endosomal acidification), OGA (O-GlcNAcase, O-GlcNAc cycling), ABCC4 (multidrug transporter), SPPL2A (intramembrane protease involved in MHC-II processing), SAMSN1 (immune cell signaling adaptor), KRAS (RAS signaling), SMAD7 (TGF-beta inhibitory SMAD), and APC (Wnt pathway). Several genes point to endosomal/lysosomal function and mTOR nutrient sensing (RRAGC, ATP6V0A2, BMP2K, SPPL2A), with additional metabolic and stress-response components (GPX4, OGA). The module is moderately coherent and likely combines mTOR/endosomal nutrient sensing with broader metabolic regulation in mDCs. The neighbor context (M152 is MHC-II antigen presentation, M151 has RAB11A/RAB11FIP1 vesicular recycling) supports an endosomal/trafficking theme. SPPL2A is specifically known to process CD74/invariant chain fragments in MHC-II pathway. Overall, the dominant program appears to be mTOR/endosomal nutrient sensing and metabolic regulation in myeloid DCs.
Genes
Most correlated modules
- Death Receptor Signaling · correlation 0.95
- Immature DC Metabolism · correlation 0.95
- Tolerogenic mDC · correlation 0.94
- mDC Inflammatory Activation · correlation 0.94
- DC Maturation Migration · correlation 0.92
- Non-canonical NF-κB · correlation 0.90
- MHC-I Antigen Presentation · correlation 0.90
- Chromatin Remodeling · correlation 0.88
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.