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PathWhiz ID Pathway Meta Data

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.

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.

PW175957

Pw175957 View Pathway
metabolic

4-(Isopropylamino)diphenylamine Predicted Metabolism Pathway new

Homo sapiens
Metabolites of 4-(Isopropylamino)diphenylamine are predicted with biotransformer.

PW146791

Pw146791 View Pathway
drug action

4-(Isopropylamino)diphenylamine Drug Metabolism Action Pathway

Homo sapiens

PW000698

Pw000698 View Pathway
disease

3-Phosphoglycerate Dehydrogenase Deficiency

Homo sapiens
3-Phosphoglycerate dehydrogenase deficiency is a disorder of L-serine biosynthesis that is characterized by congenital microcephaly, psychomotor retardation, and seizures.The disorder is caused by homozygous or compound heterozygous or homozygous mutation in the gene encoding phosphoglycerate dehydrogenase on chromosome 1p12. Defects in the gene lead to a decrease of Glycine and Serine.

PW121909

Pw121909 View Pathway
disease

3-Phosphoglycerate Dehydrogenase Deficiency

Mus musculus
3-Phosphoglycerate dehydrogenase deficiency is a disorder of L-serine biosynthesis that is characterized by congenital microcephaly, psychomotor retardation, and seizures.The disorder is caused by homozygous or compound heterozygous or homozygous mutation in the gene encoding phosphoglycerate dehydrogenase on chromosome 1p12. Defects in the gene lead to a decrease of Glycine and Serine.

PW122133

Pw122133 View Pathway
disease

3-Phosphoglycerate Dehydrogenase Deficiency

Rattus norvegicus
3-Phosphoglycerate dehydrogenase deficiency is a disorder of L-serine biosynthesis that is characterized by congenital microcephaly, psychomotor retardation, and seizures.The disorder is caused by homozygous or compound heterozygous or homozygous mutation in the gene encoding phosphoglycerate dehydrogenase on chromosome 1p12. Defects in the gene lead to a decrease of Glycine and Serine.

PW127145

Pw127145 View Pathway
disease

3-Phosphoglycerate Dehydrogenase Deficiency

Homo sapiens
3-Phosphoglycerate dehydrogenase deficiency is a disorder of L-serine biosynthesis that is characterized by congenital microcephaly, psychomotor retardation, and seizures.The disorder is caused by homozygous or compound heterozygous or homozygous mutation in the gene encoding phosphoglycerate dehydrogenase on chromosome 1p12. Defects in the gene lead to a decrease of Glycine and Serine.

PW126542

Pw126542 View Pathway
drug action

3-Methylthiofentanyl Opioid Agonist Action Pathway

Homo sapiens
3-Methyl-thiofentanyl is a fentanyl analog and an opioid analgesic that works by inducing central nervous system (CNS) depression. 3-Methylthiofentanyl binds to the mu, delta, and kappa opioid receptors. These ultimately lead to decreased pain sensation as well as a number of side effects, such as euphoria, sedation, depressed breathing. In neurons, 3-methyl-thiofentanyl binds to mu opioid receptors, stimulating the exchange of GTP for GDP on the G-protein complex. As the effector system is adenylate cyclase and cAMP located at the inner surface of the plasma membrane, opioids decrease intracellular cAMP by inhibiting adenylate cyclase. Subsequently, the release of nociceptive neurotransmitters such as GABA is inhibited. Opioids close N-type voltage-operated calcium channels (OP2-receptor agonist) and open calcium-dependent inwardly rectifying potassium channels (OP3 and OP1 receptor agonist). This results in hyperpolarization and reduced neuronal excitability. 3-Methyl-thiofentanyl acts at A delta and C pain fibres in the dorsal horn of the spinal cord. By decreasing neurotransmitter action there is less pain transmittance into the spinal cord. This leads to less pain perception.

PW000656

Pw000656 View Pathway
drug action

3-Methylthiofentanyl Action Pathway

Homo sapiens
Methadyl Acetate (also known as Acetylmethadol) is analgesic that can bind to mu-type opioid receptor to activate associated G-protein in the sensory neurons of central nervous system (CNS), which will reduce the level of intracellular cAMP by inhibiting adenylate cyclase. The binding of methadyl acetate will eventually lead to reduced pain because of decreased nerve conduction and release of neurotransmitter. Hyperpolarization of neuron is caused by inactivation of calcium channels and activation of potassium channels via facilitated by G-protein.