ARHGAP24 — Rho GTPase activating protein 24
ARHGAP24 belongs to a gene co-expression module in 4 of 28 SCUBA cell types. Each module groups genes that rise and fall together in that cell type; the genes it shares a module with are its closest co-expression partners there.
ARHGAP24's module in each cell type
| Cell type | Module | Shares the module with | |
|---|---|---|---|
| CD19⁺ B cells | Adhesion/Migration migration & adhesion | ADAM28, ADAMTS6, ARHGAP5, CHPT1, CLMN, CMTR2, FCMR, JAM3 +11 more | View in SCUBA |
| Fibroblasts | CCL11 Secretory Fibroblast ECM production | ANK3, CCL11, COL16A1, COL18A1, DTX4, F11R, GABRA2, KAZN +5 more | View in SCUBA |
| Glial cells | Glial Neural Scaffolding Cytoskeletal | AKAP6, COL5A3, EIF4G2, NFIX, PPP1R12B, SCAF11, SEMA6D, USP53 | View in SCUBA |
| Neutrophils | Granulopoiesis Program Developmental | ARID1B, B4GALT5, CSGALNACT1, FLI1, IQGAP2, LYST, PDZD8, PHIP +5 more |
About the gene
| Synonyms | DKFZP564B1162, FilGAP, FLJ33877 |
|---|---|
| Chromosome | 4: 85475150-86002668 |
| Predicted location | Intracellular |
| Essential gene | No |
| Protein class | Predicted intracellular proteins |
| Molecular function | Developmental protein, GTPase activation |
| Biological process | Angiogenesis, Differentiation |
Function
Rho GTPase-activating protein involved in cell polarity, cell morphology and cytoskeletal organization. Acts as a GTPase activator for the Rac-type GTPase by converting it to an inactive GDP-bound state. Controls actin remodeling by inactivating Rac downstream of Rho leading to suppress leading edge protrusion and promotes cell retraction to achieve cellular polarity. Able to suppress RAC1 and CDC42 activity in vitro. Overexpression induces cell rounding with partial or complete disruption of actin stress fibers and formation of membrane ruffles, lamellipodia, and filopodia. Isoform 2 is a vascular cell-specific GAP involved in modulation of angiogenesis.
Human Protein Atlas · Open Targets · UniProt
Gene annotation from the Human Protein Atlas and UniProt; see sources & licences.