UDP glucuronic acid is a sugar used in the creation of polysaccharides and is an intermediate in the biosynthesis of ascorbic acid (except in primates and guinea pigs).
It is made from UDP-glucose by UDP-glucose 6-dehydrogenase (EC 1.1.1.22) using NAD+ as a cofactor. It is the source of the glucuronosyl group in glucuronosyltransferase reactions.
UDP-glucose consists of the pyrophosphate group, the pentose sugar ribose, glucose, and the nucleobase uracil.
It is used in nucleotide sugars metabolism as an activated form of glucose as a substrate for enzymes called glucosyltransferases.[1]
It is a precursor of glycogen and can be converted into UDP-galactose and UDP-glucuronic acid, which can then be used as substrates by the enzymes that make polysaccharides containing galactose and glucuronic acid.
UDP-glucose can also be used as a precursor of sucrose lipopolysaccharides, and glycosphingolipids.
Uridine diphosphate glucose (uracil-diphosphate glucose, UDP-glucose) is a nucleotide sugar. It is involved in glycosyltransferase reactions in metabolism.
Uridine diphosphate galactose (UDP-galactose) is an intermediate in the production of polysaccharides. It is important in nucleotide sugars metabolism.
UDP-N-acetylglucosamine or UDP-GlcNAc is a nucleotide sugar and a coenzyme in metabolism. It is used by glycosyltransferases to transfer N-acetylglucosamine residues to substrates. D-Glucosamine is made naturally in the form of glucosamine-6-phosphate, and is the biochemical precursor of all nitrogen-containing sugars.[1] Specifically, glucosamine-6-phosphate is synthesized from fructose-6-phosphate and glutamine[2] as the first step of the hexosamine biosynthesis pathway.[3] The end-product of this pathway is UDP-N-acetylglucosamine (UDP-GlcNAc), which is then used for making glycosaminoglycans, proteoglycans, and glycolipids.[4
Tiglyl-CoA is an intermediate in the metabolism of isoleucine.
N-Formylmethanofuran donates the C1 group to the N5 site of the pterin to give the formylH4MPT.[2] The formyl group subsequently condenses intramolecularly to give methenylH4MPT+, which is then reduced to methyleneH4MPT.[3] MethyleneMPT is subsequently converted, using H2F420 as the electron source, to methylH4MPT, catalyzed by F420-dependent methylene-H4MPT reductase. MethylH4MPT is the methyl donor to coenzyme M, a conversion mediated by methyl-H4MPT:coenzyme M methyl-transferase.[1]
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Comparison with tetrahydrofolate
H4MPT is related to the better known tetrahydrofolate (H4F). The differences are indicated in red and blue in the figure. The most important difference between H4MPT and H4F is that H4F has an electron-withdrawing carbonyl group on the phenyl ring. As a consequence, methenyl-H4MPT is more difficult to reduce than methenyl-H4F. Reduction is effected by a so-called Iron-sulfur cluster free hydrogenase.[3] The cumbersome name distinguishes this hydrogenase from the so-called Fe-only hydrogenases that do contain Fe-S cluster.
Tetrahydromethanopterin, abbreviated H4MPT, is a coenzyme in methanogenesis. It is the carrier of the C1 group as it is reduced to the methyl level, before transferring to the coenzyme M.[1]
Tetrahydrosarcinapterin (H4SPT) is a modified form of H4MPT, wherein a glutamyl group linked to the 2-hydroxyglutaric acid terminus.
It is a coenzyme in many reactions, especially in the metabolism of amino acids and nucleic acids. It acts as a donor of a group with one carbon atom. It gets this carbon atom by sequestering formaldehyde produced in other processes. A shortage in THF can cause anemia.
Tetrahydrofolic acid is reduced by the drug methotrexate, which is used to impair nucleotide synthesis. This drug is a potent chemotherapy and anti rheumatic.