ATL3 — Atlastin GTPase 3
ATL3 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.
ATL3's module in each cell type
| Cell type | Module | Shares the module with | |
|---|---|---|---|
| Endothelial | ER-Golgi Trafficking Protein processing & ER | DIAPH2, ECE1, EID1, GOLIM4, KTN1, MAGT1, PGK1, SHISA5 +4 more | View in SCUBA |
| Gamma-delta T cells | ER Antigen Processing Protein processing & ER | ACLY, ATR, CANX, DCTN1, DDB1, ERAP1, FOXJ3, ITCH +9 more | |
| Macrophages | ER Morphology Stress Stress | ARMC1, ARPP19, CMPK1, CYB5B, EIF2AK1, ELAVL1, ERGIC2, HDAC2 +8 more | View in SCUBA |
| Mucosal-associated invariant T cell | SWI/SNF Chromatin Remodeling DNA/chromatin regulation | ARCN1, CASP8, CYFIP2, DENND4C, DIDO1, DPP4, ERAP1, NFATC3 +8 more |
About the gene
| Synonyms | DKFZP564J0863 |
|---|---|
| Chromosome | 11: 63624087-63671921 |
| Predicted location | Intracellular, Membrane |
| Essential gene | No |
| Protein class | Disease related genes, Human disease related genes, Potential drug targets, Predicted intracellular proteins, Predicted membrane proteins, Transporters |
| Molecular function | Hydrolase |
Function
Atlastin-3 (ATL3) is a membrane-anchored GTPase that mediates the GTP-dependent fusion of endoplasmic reticulum (ER) membranes, maintaining the continuous ER network. It facilitates the formation of three-way junctions where ER tubules intersect. Two atlastin-3 on neighboring ER tubules bind GTP and form loose homodimers through the GB1/RHD3-type G domains and 3HB regions. Upon GTP hydrolysis, the 3HB regions tighten, pulling the membranes together to drive their fusion. After fusion, the homodimer disassembles upon release of inorganic phosphate (Pi). Subsequently, GDP dissociates, resetting the monomers to a conformation ready for a new fusion cycle (By similarity).
Human Protein Atlas · Open Targets · UniProt
Gene annotation from the Human Protein Atlas and UniProt; see sources & licences.