Tissue Residency Regulation
Gene co-expression module in Mucosal-associated invariant T cell
| Category | Tissue residence |
|---|---|
| Genes | 13 |
| Annotation certainty | 3 of 5 |
| Annotation consistency | 8 of 13 genes have a known function matching the annotation |
Why this annotation
Hub genes include ABCC1 (MRP1, multidrug resistance protein/ABC transporter mediating leukotriene C4 export and drug efflux), ANKRD28 (protein phosphatase 6 regulatory subunit), ARHGEF7 (beta-PIX, a Rac/Cdc42 GEF important for T cell motility), SPRY1 (Sprouty1, a negative regulator of RAS/MAPK signaling and T cell homeostasis — controls T cell egress and quiescence), LPIN1 (phosphatidic acid phosphatase, lipid metabolism), RGS1 (regulator of G-protein signaling, involved in lymphocyte chemotaxis desensitization), JMY (actin nucleation promoting factor), CHD7 (chromatin helicase), CYTIP (cytohesin-interacting protein, regulator of integrin-mediated adhesion), NEDD9 (focal adhesion scaffold), CA2 (carbonic anhydrase), and IL18R1 (IL-18 receptor, key for MAIT cell activation). The convergence of SPRY1 (T cell homeostasis/quiescence), RGS1 (chemotaxis desensitization/tissue residency), CYTIP and NEDD9 (adhesion/migration), ARHGEF7 (actin/migration), and IL18R1 (cytokine receptor) suggests a MAIT cell tissue residence and migration regulatory program. RGS1 in particular is a marker of tissue-resident and exhausted T cells. The ABCC1 hub could reflect efflux of inflammatory mediators in tissue-resident cells.
Genes
ABCC1, ANKRD28, ARHGEF7, CA2, CDV3, CHD7, CYTIP, IL18R1, JMY, LPIN1, NEDD9, RGS1, SPRY1
Most correlated modules
- Rho GTPase Migration · correlation 0.83
- Tissue Residency · correlation 0.81
- Splicing Regulation · correlation 0.80
- NF-κB Survival Signaling · correlation 0.77
- STAT3 Cytokine Signaling · correlation 0.73
- MAIT Cell Identity · correlation 0.71
- Apoptosis Regulation · correlation 0.69
- STAT4 T cell Identity · correlation 0.68
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.