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Vitamin C-dependent enzymes are a broad class of oxidoreductase enzymes that require vitamin C (ascorbic acid) as an essential cofactor for optimal activity[1][2][3][6]. Their key unifying feature is reliance on ascorbate’s electron-donating capability, which keeps active site metals (typically Fe^2+ or Cu^2+) in a reduced state, necessary for catalytic function[1][2]. Notable human vitamin C-dependent enzymes include: - Prolyl and lysyl hydroxylases (for collagen synthesis; crucial for connective tissue, wound healing, and vascular health) - Dopamine β-hydroxylase (neurotransmitter synthesis; converts dopamine to norepinephrine) - Peptidylglycine α-amidating monooxygenase (peptide hormone activation) - Carnitine biosynthesis enzymes (EPSILON-N-trimethyl-L-lysine hydroxylase, gamma-butyrobetaine hydroxylase; required for fatty acid oxidation) - 2-oxoglutarate-dependent dioxygenases, including hypoxia-inducible factor (HIF) hydroxylases (regulate cellular response to oxygen) and epigenetic regulators such as the TET family and Jumonji domain-containing demethylases (modulate gene expression and genome stability)[1][2][3][6][7]. This group is not a single molecule or therapeutic target but a functional class comprising multiple distinct enzymes. Thus, "Vitamin C-dependent enzyme" is too broad to be a specific target entry for most structured data systems and should refer instead to an individual enzyme with a defined gene and protein product (e.g., Prolyl 4-hydroxylase, Dopamine β-hydroxylase)[1][2][3][6]. Correction: The designation "Vitamin C-dependent enzymes" is not a canonical target but rather a descriptive group encompassing several individual enzymes each with their own canonical names and identifiers.
null (Drugs do not directly target Vitamin C-dependent enzymes, but vitamin C supplementation restores or enhances their enzymatic activity[1][2][3][6].)
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