PathWhiz ID | Pathway | Meta Data |
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PW123551View Pathway |
4-Aminobutanoate Degradation IPseudomonas aeruginosa
Putrescine is an organic chemical produced when amino acids are broken down in organsisms, both living and dead. It can be used as a carbon and nitrogen source in E. coli, and is broken down into gamma-aminobutyric acid (GABA). In this pathway, GABA from putrescine degradation reacts with oxoglutaric acid in a reversible reaction catalyzed by 4-aminobutyrate aminotransferase. This reaction forms succinic acid semialdehyde, as well as L-glutamic acid as a byproduct. Succinic acid semialdehyde is then converted to succinic acid in a reaction catalyzed by succinate-semialdehyde dehydrogenase, using NAD as a cofactor. Succinic acid can then be used by the bacteria in the TCA cycle.
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Creator: Ana Marcu Created On: August 12, 2019 at 22:31 Last Updated: August 12, 2019 at 22:31 |
PW146983View Pathway |
4-Aminohippuric acid Drug Metabolism PathwayHomo sapiens
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Creator: Ray Kruger Created On: October 10, 2023 at 13:35 Last Updated: October 10, 2023 at 13:35 |
PW147022View Pathway |
4-Hydroxybutyric acid Drug Metabolism PathwayHomo sapiens
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Creator: Ray Kruger Created On: October 10, 2023 at 13:40 Last Updated: October 10, 2023 at 13:40 |
PW127351View Pathway |
disease
4-Hydroxybutyric Aciduria/Succinic Semialdehyde Dehydrogenase DeficiencyHomo sapiens
4-Hydroxybutyric Aciduria/Succinic Semialdehyde Dehydrogenase Deficiency (SSADH; Gamma-hydroxybutyric acidemia) inhibits the formation of succinate from GABA. This deficiency results in urinary excretion of 4-hydroxybutyric acid. In vivo proton MR also indicates elevated GABA levels as compared with an age-matched control. Symptoms include ataxia, chorea or athetosis, motor retardation, seizures, macrocephaly and delayed or abnormal speech development.
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Creator: Ray Kruger Created On: December 14, 2022 at 13:57 Last Updated: December 14, 2022 at 13:57 |
PW121696View Pathway |
disease
4-Hydroxybutyric Aciduria/Succinic Semialdehyde Dehydrogenase DeficiencyMus musculus
4-Hydroxybutyric Aciduria/Succinic Semialdehyde Dehydrogenase Deficiency (SSADH; Gamma-hydroxybutyric acidemia) inhibits the formation of succinate from GABA. This deficiency results in urinary excretion of 4-hydroxybutyric acid. In vivo proton MR also indicates elevated GABA levels as compared with an age-matched control. Symptoms include ataxia, chorea or athetosis, motor retardation, seizures, macrocephaly and delayed or abnormal speech development.
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Creator: Ana Marcu Created On: September 10, 2018 at 15:49 Last Updated: September 10, 2018 at 15:49 |
PW000070View Pathway |
disease
4-Hydroxybutyric Aciduria/Succinic Semialdehyde Dehydrogenase DeficiencyHomo sapiens
4-Hydroxybutyric Aciduria/Succinic Semialdehyde Dehydrogenase Deficiency (SSADH; Gamma-hydroxybutyric acidemia) inhibits the formation of succinate from GABA. This deficiency results in urinary excretion of 4-hydroxybutyric acid. In vivo proton MR also indicates elevated GABA levels as compared with an age-matched control. Symptoms include ataxia, chorea or athetosis, motor retardation, seizures, macrocephaly and delayed or abnormal speech development.
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Creator: WishartLab Created On: August 01, 2013 at 15:52 Last Updated: August 01, 2013 at 15:52 |
PW121922View Pathway |
disease
4-Hydroxybutyric Aciduria/Succinic Semialdehyde Dehydrogenase DeficiencyRattus norvegicus
4-Hydroxybutyric Aciduria/Succinic Semialdehyde Dehydrogenase Deficiency (SSADH; Gamma-hydroxybutyric acidemia) inhibits the formation of succinate from GABA. This deficiency results in urinary excretion of 4-hydroxybutyric acid. In vivo proton MR also indicates elevated GABA levels as compared with an age-matched control. Symptoms include ataxia, chorea or athetosis, motor retardation, seizures, macrocephaly and delayed or abnormal speech development.
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Creator: Ana Marcu Created On: September 10, 2018 at 15:51 Last Updated: September 10, 2018 at 15:51 |
PW147006View Pathway |
5-Aminolevulinic acid Drug Metabolism PathwayHomo sapiens
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Creator: Ray Kruger Created On: October 10, 2023 at 13:38 Last Updated: October 10, 2023 at 13:38 |
PW012878View Pathway |
5-Deoxystrigol BiosynthesisArabidopsis thaliana
5-Deoxystrigol Biosynthesis is a pathway that has not yet become fully elucidated. Beginning in the chloroplast and potentially finishing in the cytosol, the pathway follows the synthesis of 5-deoxystrigol from beta-carotene. 5-Deoxystrigol is a strigolactone, a plant hormone that stimulates the branching and growth of symbiotic arbuscular mycorrhizal fungi and inhibits plant shoot branching. Strigolactones share a common C19 structure composed of a tricyclic lactone (A, B, and C rings) connected to a second lactone (D ring) by an enol ether bridge. 5-deoxystrigol is the precursor of other beta-oriented C-ring strigolactones (strigol-configured strigolactones) (PMID: 25425668). First, beta-carotene isomerase catalyzes the conversion of beta-carotene into 9-cis-beta-carotene with the help of an iron cofactor. Second, 9-cis-beta-carotene 9',10'-cleavage dioxygenase converts 9-cis-beta-carotene and oxygen to 9-cis-10'-apo-beta-carotenal and beta-ionone with the help of an Fe2+ cofactor. Third, carlactone synthase converts 9-cis-10'-apo-beta-carotenal and oxygen to carlactone and (2E,4E,6E)-7-hydroxy-4-methylhepta-2,4,6-trienal with the help of an Fe2+ cofactor. The final two reactions are not completely understood and may occur in the cytosol. Cytochrome P450 monooxygenase is theorized to catalyze the fourth reaction whereby carlactone is conveted into carlactone carboxylate. It requires heme as a cofactor. This same enzyme could possibly also catalyze the fifth reaction in which 5-deoxystrigol is made.
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Creator: Carin Li Created On: February 08, 2017 at 12:54 Last Updated: February 08, 2017 at 12:54 |
PW147030View Pathway |
5-Hydroxy-L-tryptophan Drug Metabolism PathwayHomo sapiens
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Creator: Ray Kruger Created On: October 10, 2023 at 13:41 Last Updated: October 10, 2023 at 13:41 |