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Glutamine synthetase !

Glutamine synthetase traps free ammonia by joining it to glutamate. This protects the brain and carries nitrogen safely in the blood.

Updated 2026-11-01

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Key facts

  • Glutamate + NH₄⁺ + ATP → glutamine + ADP + Pi.
  • In the brain it sits in astrocytes and is the main route for removing ammonia.
  • In the liver it sits in hepatocytes around the central vein: it traps ammonia that escaped the urea cycle.
  • It is a decamer: two rings of five subunits with the active sites between them.
EC number
6.3.1.2
Genes
GLUL
Structure (PDB)
2QC8

Structure

  • 2QC8: human glutamine synthetase with ADP and methionine sulfoximine phosphate, an inhibitor that mimics the intermediate.

Regulation

  • Glucocorticoids induce it; excess glutamine speeds its breakdown.

Inhibitors and toxins

  • Methionine sulfoximine (experimental)
  • Glufosinate (herbicide)

Clinical notes

  • In hyperammonaemia, astrocytes pile up glutamine, swell, and cerebral oedema follows.
  • Its very rare congenital deficiency leaves glutamine almost undetectable and causes severe brain damage.

Test yourself

Think of the answer, then tap the question to see it.

Which brain cells clear ammonia with glutamine synthetase?

Astrocytes; that is why they swell when ammonia rises.

What is its job in the liver if the urea cycle already exists?

Perivenous cells trap as glutamine the ammonia that was not turned into urea in the periportal zone.

How much energy does the reaction cost?

One ATP per glutamine made.

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Educational information, not medical advice. For any symptom, see a health professional.

Sources: GLUL: Glutamine synthetase (human) (UniProt, 2026); Glutamate and glutamine metabolism (Reactome, 2026); 2QC8: Crystal structure of human glutamine synthetase in complex with ADP and methionine sulfoximine phosphate (RCSB Protein Data Bank, 2026).

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Representative model, for educational purposes only.