EC Number | Activating Compound | Comment | Organism | Structure |
---|---|---|---|---|
6.3.1.2 | additional information | dexamethasone increases transcription of the glutamine synthetase gene in astrocytes. The inductive effect of glucocorticoids is mediated by binding of the glucocorticoid receptor to a glucocorticoid response element in the regulatory region of the glutamine synthetase gene, and this effect is blocked by the proinflammatory cytokines interleukin 1beta and tumor necrosis factor-alpha. N-methyl-D-aspartate indces the enzyme, lipopolysaccharide and interferon-gamma inhibits the induction | Homo sapiens |
EC Number | Inhibitors | Comment | Organism | Structure |
---|---|---|---|---|
6.3.1.2 | L-methionine sulfoximine | - |
Homo sapiens | |
6.3.1.2 | additional information | elevations in c-jun may be a potential cause of the glutamine synthetase deficiency in mesial temporal lobe epilepsy, MTLE. The activity of glutamine synthetase is decreased by 38% in tissue homogenates of the sclerotic versus the nonsclerotic hippocampus. High levels of c-jun repress the glutamine synthetase gene. The inductive effect of glucocorticoids is mediated by binding of the glucocorticoi receptor to a glucocorticoid response element in the regulatory region of the glutamine synthetase gene, and this effect is blocked by the proinflammatory cytokines interleukin-1beta and tumor necrosis factor-alpha | Homo sapiens |
EC Number | Metals/Ions | Comment | Organism | Structure |
---|---|---|---|---|
6.3.1.2 | Mg2+ | - |
Homo sapiens |
EC Number | Natural Substrates | Organism | Comment (Nat. Sub.) | Natural Products | Comment (Nat. Pro.) | Rev. | Reac. |
---|---|---|---|---|---|---|---|
6.3.1.2 | ATP + L-glutamate + NH3 | Homo sapiens | extracellular glutamate, loss of the glutamate-metabolizing enzyme glutamine synthetase and proliferation of astrocytes are associated with mesial temporal lobe epilepsy, MTLE. Glial proliferation, i.e. gliosis, contributes to the epileptogenicity of the human hippocampus in MTLE, levels of extracellular glutamate are more than five-fold increased in the MTLE hippocampus, glutamate-glutamine cycle, overview | ADP + phosphate + L-glutamine | - |
? | |
6.3.1.2 | additional information | Homo sapiens | elevations in c-jun may be a potential cause of the glutamine synthetase deficiency in mesial temporal lobe epilepsy, MTLE, pathology, overview. The enzyme is also regulated by glucocorticoids and proinflammatory cytokines | ? | - |
? |
EC Number | Organism | UniProt | Comment | Textmining |
---|---|---|---|---|
6.3.1.2 | Homo sapiens | - |
- |
- |
EC Number | Source Tissue | Comment | Organism | Textmining |
---|---|---|---|---|
6.3.1.2 | astrocyte | - |
Homo sapiens | - |
6.3.1.2 | brain | neocortex | Homo sapiens | - |
6.3.1.2 | glial cell | - |
Homo sapiens | - |
6.3.1.2 | hippocampus | - |
Homo sapiens | - |
EC Number | Substrates | Comment Substrates | Organism | Products | Comment (Products) | Rev. | Reac. |
---|---|---|---|---|---|---|---|
6.3.1.2 | ATP + L-glutamate + NH3 | - |
Homo sapiens | ADP + phosphate + L-glutamine | - |
? | |
6.3.1.2 | ATP + L-glutamate + NH3 | extracellular glutamate, loss of the glutamate-metabolizing enzyme glutamine synthetase and proliferation of astrocytes are associated with mesial temporal lobe epilepsy, MTLE. Glial proliferation, i.e. gliosis, contributes to the epileptogenicity of the human hippocampus in MTLE, levels of extracellular glutamate are more than five-fold increased in the MTLE hippocampus, glutamate-glutamine cycle, overview | Homo sapiens | ADP + phosphate + L-glutamine | - |
? | |
6.3.1.2 | additional information | elevations in c-jun may be a potential cause of the glutamine synthetase deficiency in mesial temporal lobe epilepsy, MTLE, pathology, overview. The enzyme is also regulated by glucocorticoids and proinflammatory cytokines | Homo sapiens | ? | - |
? |
EC Number | Synonyms | Comment | Organism |
---|---|---|---|
6.3.1.2 | Glutamine synthetase | - |
Homo sapiens |
EC Number | Cofactor | Comment | Organism | Structure |
---|---|---|---|---|
6.3.1.2 | ATP | - |
Homo sapiens |