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Cobalamin metabolism pathways comprise a series of molecular processes including the absorption, transport, intracellular trafficking, and enzymatic conversion of vitamin B12 (cobalamin) to its active cofactor forms, specifically methylcobalamin and adenosylcobalamin[2][3]. These pathways involve a variety of proteins—such as transporters (intrinsic factor, transcobalamin), membrane receptors, and intracellular processing enzymes (e.g., MMACHC, MMADHC)—which collectively ensure cobalamin reaches its two known human target enzymes: methionine synthase (5-methyltetrahydrofolate-homocysteine methyltransferase, MTR) and methylmalonyl-CoA mutase (MMUT)[2][3][4]. Disruptions at any stage due to genetic, nutritional, or acquired defects can cause disease[4]. Note: "Cobalamin metabolism pathway" itself is not a single molecular target, but rather refers to an entire collection of interacting transporters, enzymes, and cofactor processing mechanisms critical for vitamin B12 homeostasis[2][3]. For structured target-level data, it would be necessary to specify an individual pathway component (such as a receptor, enzyme, or transporter).
Supplementation to correct cobalamin deficiency; Replacement of missing or dysfunctional enzymatic cofactor forms
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