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Literature summary for 6.3.1.2 extracted from

  • Eid, T.; Williamson, A.; Lee, T.S.; Petroff, O.A.; de Lanerolle, N.C.
    Glutamate and astrocytes - key players in human mesial temporal lobe epilepsy? (2008), Epilepsia, 49 Suppl. 2, 42-52.
    View publication on PubMed

Activating Compound

Activating Compound Comment Organism Structure
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

Inhibitors

Inhibitors Comment Organism Structure
L-methionine sulfoximine
-
Homo sapiens
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

Metals/Ions

Metals/Ions Comment Organism Structure
Mg2+
-
Homo sapiens

Natural Substrates/ Products (Substrates)

Natural Substrates Organism Comment (Nat. Sub.) Natural Products Comment (Nat. Pro.) Rev. Reac.
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
-
?
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 ?
-
?

Organism

Organism UniProt Comment Textmining
Homo sapiens
-
-
-

Source Tissue

Source Tissue Comment Organism Textmining
astrocyte
-
Homo sapiens
-
brain neocortex Homo sapiens
-
glial cell
-
Homo sapiens
-
hippocampus
-
Homo sapiens
-

Substrates and Products (Substrate)

Substrates Comment Substrates Organism Products Comment (Products) Rev. Reac.
ATP + L-glutamate + NH3
-
Homo sapiens ADP + phosphate + L-glutamine
-
?
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
-
?
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 ?
-
?

Synonyms

Synonyms Comment Organism
Glutamine synthetase
-
Homo sapiens

Cofactor

Cofactor Comment Organism Structure
ATP
-
Homo sapiens