Skip to content
MS
unreviewed

Methionine synthase (MTR)

2 reactions · 2 pathways

Clinical / pharmacological. B12-dependent; deficiency causes megaloblastic anaemia and the methyl-folate trap

What it does, reaction by reaction

2 reactions

Methionine Cycle / Transmethylation (SAM Cycle, homocysteine) Amino Acid & Nitrogen Metabolism · Cytosol

step 4 Irreversible/directional

Homocysteine + 5-methyl-THF → methionine + THF

Converts Homocysteine 5-Methyl-THF into Methionine Tetrahydrofolate (THF)

Notes

Methionine synthase (MTR) requires methylcobalamin (vitamin B12) and links the methionine cycle to the folate cycle. Reductive reactivation of oxidized cobalamin requires methionine synthase reductase, NADPH, FAD, FMN, and SAM; remethylation is the principal methionine-conserving route in most tissues.

One-Carbon Metabolism (Folate Cycle) Amino Acid & Nitrogen Metabolism · Cytosol + mitochondrion

step 10 Irreversible/directional

5-Methyl-THF + homocysteine → THF + methionine

Converts 5-Methyl-THF Homocysteine into Tetrahydrofolate (THF) Methionine

Notes

Methionine synthase (5-methyltetrahydrofolate–homocysteine methyltransferase) requires methylcobalamin (vitamin B12) and transfers the methyl group through a cobalamin intermediate. The reaction regenerates THF and prevents trapping of cellular folate as 5-methyl-THF.

Showing all 2 reactions.

What accelerates and inhibits it

Regulation is pathway-specific, so each context is listed separately

1 entries

Methionine Cycle / Transmethylation (SAM Cycle, homocysteine)

Listed there as: Methionine synthase

Accelerated by

5-methyl-THF, homocysteine, and functional B12 availability

Inhibited by

B12 deficiency/inactivation; nitrous oxide oxidizes cobalamin and inhibits function

Hormonal control

Mainly controlled by vitamin status and substrate flux

Recent literature

Nothing is fetched until you ask, so the page stays fast and the request is yours rather than automatic.

Europe PMC · ten most recent, newest first