GLUL — Glutamate-ammonia ligase
GLUL belongs to a gene co-expression module in 9 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.
GLUL's module in each cell type
About the gene
| Synonyms | GLNS |
|---|---|
| Chromosome | 1: 182378098-182392206 |
| Predicted location | Intracellular |
| Essential gene | No |
| Protein class | Disease related genes, Enzymes, Human disease related genes, Metabolic proteins, Plasma proteins, Potential drug targets, Predicted intracellular proteins |
| Molecular function | Ligase, Transferase |
| Biological process | Angiogenesis |
Function
Glutamine synthetase that catalyzes the ATP-dependent conversion of glutamate and ammonia to glutamine. Its role depends on tissue localization: in the brain, it regulates the levels of toxic ammonia and converts neurotoxic glutamate to harmless glutamine, whereas in the liver, it is one of the enzymes responsible for the removal of ammonia (By similarity). Plays a key role in ammonium detoxification during erythropoiesis: the glutamine synthetase activity is required to remove ammonium generated by porphobilinogen deaminase (HMBS) during heme biosynthesis to prevent ammonium accumulation and oxidative stress (By similarity). Essential for proliferation of fetal skin fibroblasts. Independently of its glutamine synthetase activity, required for endothelial cell migration during vascular development: acts by regulating membrane localization and activation of the GTPase RHOJ, possibly by promoting RHOJ palmitoylation. May act as a palmitoyltransferase for RHOJ: able to autopalmitoylate and then transfer the palmitoyl group to RHOJ. Plays a role in ribosomal 40S subunit biogenesis. Through the interaction with BEST2, inhibits BEST2 channel activity by affecting the gating at the aperture in the absence of intracellular L-glutamate, but sensitizes BEST2 to intracellular L-glutamate, which promotes the opening of BEST2 and thus relieves its inhibitory effect on BEST2.
Human Protein Atlas · Open Targets · UniProt
Gene annotation from the Human Protein Atlas and UniProt; see sources & licences.