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PathWhiz ID Pathway Meta Data

PW012878

Pw012878 View Pathway
metabolic

5-Deoxystrigol Biosynthesis

Arabidopsis 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.

PW147006

Pw147006 View Pathway
metabolic

5-Aminolevulinic acid Drug Metabolism Pathway

Homo sapiens

PW246846

Pw246846 View Pathway
metabolic

4-Hydroxyphthalate degradation

Comamonas testosteroni
Bacteria such as Comamonas testosteroni plays a crucial role in degradation of 4-hydroxyphthalate, an environmental pollutant. 4-hydroxyphthalate is degraded by Comamonas testosterone, yielding precursors used in the benzoate degradation pathway to yield carbon and energy, which is vital for the bacteria's growth and survival. Although the precise mechanisms of 4-hydroxyphthalate uptake, potentially facilitated by MFS transporters, are not fully understood, the subsequent enzymatic breakdown within the cell yields 4-Carboxy-2-hydroxymuconate semialdehyde, an essential intermediate for the benzoate degradation pathway.

PW127351

Pw127351 View Pathway
disease

4-Hydroxybutyric Aciduria/Succinic Semialdehyde Dehydrogenase Deficiency

Homo 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.

PW121696

Pw121696 View Pathway
disease

4-Hydroxybutyric Aciduria/Succinic Semialdehyde Dehydrogenase Deficiency

Mus 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.

PW000070

Pw000070 View Pathway
disease

4-Hydroxybutyric Aciduria/Succinic Semialdehyde Dehydrogenase Deficiency

Homo 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.

PW121922

Pw121922 View Pathway
disease

4-Hydroxybutyric Aciduria/Succinic Semialdehyde Dehydrogenase Deficiency

Rattus 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.

PW147022

Pw147022 View Pathway
metabolic

4-Hydroxybutyric acid Drug Metabolism Pathway

Homo sapiens

PW251361

Pw251361 View Pathway
metabolic

4-Chlorobiphenyl degradation

Pseudoxanthomonas spadix
4-chlorobiphenyl, a PCB and environmental pollutant, is degraded by bacteria e.g., Pseudoxanthomonas spadix a source of carbon and energy. 4-Chlorobiphenyl degradation in Pseudoxanthomonas spadix begins with the oxidation of 4-chlorobiphenyl by biphenyl 2,3-dioxygenase small subunit (BphA2) to form an intermediate compound, cis-2,3-Dihydro-2,3-dihydroxy-4'-chlorobiphenyl. This intermediate is then dehydrogenated to 2,3-Dihydroxy-4'-chlorobiphenyl, by 2,3-dihydroxy-2,3-dihydrophenylpropionate dehydrogenase. Subsequently, the compound is converted by 2,3-dihydroxybiphenyl-1,2-dioxygenase to form 2-Hydroxy-6-oxo-6-(4'-chlorophenyl)-hexa-2,4-dienoate, that is further degraded to produce compounds such as pyruvate and acetyl-COA which are essential for glycolysis and citrate cycle.

PW146983

Pw146983 View Pathway
metabolic

4-Aminohippuric acid Drug Metabolism Pathway

Homo sapiens