Learn / Metabolism
Metabolic pathways
Every FMK pathway as a clickable map. Pick one pathway to hammer it — next step, enzyme, regulator, cofactor, and the facts that get tested (NADPH and who needs it, rate-limiting steps, deficiencies) — or set it to all pathways for a mixed drill. Every answer says which enzyme and which pathway.
Catecholamines, serotonin & the tyrosine tree
Dopaquinone
Made from L-DOPA by TYROSINASE (copper-dependent) — DOPA → melanin branch
TYROSINASE (copper-dependent) — DOPA → melanin branch — Catecholamines, serotonin & the tyrosine tree
Cofactors: Cu²⁺, O₂
Inhibited by: Excess phenylalanine (competitive) — the PKU mechanism
Deficiency: Oculocutaneous ALBINISM — here the melanin pathway itself is broken. OCA1, the most severe form, is absent or defective COPPER-REQUIRING TYROSINASE. Contrast with PKU's hypopigmentation, which is competitive inhibition of a working enzyme
The melanin branch leaves the pathway at L-DOPA, not at tyrosine — the same L-DOPA node the catecholamine spine runs through. Tyrosinase is the rate-limiting enzyme of melanin synthesis and is bifunctional: in the melanocyte it can also make L-DOPA from tyrosine directly (monophenolase activity), so a melanocyte does not need tyrosine hydroxylase. In classic PKU the melanin pathway is entirely INTACT — the fair hair, light skin and blue eyes come from excess phenylalanine COMPETITIVELY INHIBITING tyrosinase. Substrate excess poisoning an unrelated pathway, not a defect in it.
Condition cards:Albinism (oculocutaneous albinism type 1, OCA1) →
Becomes MELANIN via DOPA oxidase → eumelanin / pheomelanin
DOPA oxidase → eumelanin / pheomelanin — Catecholamines, serotonin & the tyrosine tree
DOPA oxidase activity is tyrosinase's own second activity (diphenolase). Many diagrams collapse DOPA → melanin into a single tyrosinase arrow; the dopaquinone step is what sits inside it.