Loader

Pathways

PathWhiz ID Pathway Meta Data

PW002382

Pw002382 View Pathway
metabolic

4-Aminobutanoate Degradation

Saccharomyces cerevisiae
GABA(γ-aminobutyric acid) is a non-protein amino acid that can be accumulated via permease-mediated uptake by Uga4p, Put4p, and Gap1p. GABA can also be produced via glutamate degradation by the glutamate decarboxylase, this variant of the pathway includes a 2-oxoglutarate-dependent 4-aminobutyrate transaminase and an NAD+-dependent dehydrogenase. This combination of enzymes has been documented in bacteria and animals and in some plants. Regarding the hydrogenase, NAD-specific variants have been studied from many bacteria, plant and animals.

PW002068

Pw002068 View Pathway
metabolic

4-Aminobutanoate Degradation I

Escherichia coli
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.

PW123551

Pw123551 View Pathway
metabolic

4-Aminobutanoate Degradation I

Pseudomonas 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.

PW146983

Pw146983 View Pathway
metabolic

4-Aminohippuric acid Drug Metabolism Pathway

Homo sapiens

PW147022

Pw147022 View Pathway
metabolic

4-Hydroxybutyric acid Drug Metabolism Pathway

Homo sapiens

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.

PW246846

Pw246846 View Pathway
metabolic

4-Hydroxyphthalate degradation

Comamonas testosteroni