PathWhiz

PathWhiz ID	Pathway	Meta Data
PW121921 View Pathway	disease 3-Methylglutaconic Aciduria Type IV Rattus norvegicus 3-Methylglutaconic Aciduria Type IV, also called MGA, Type IV and MGA4, is a rare inborn error of metabolism (IEM) and autosomal recessive disorder and caused by a defective methylglutaconyl-CoA hydratase. Methylglutaconyl-CoA hydratase catalyzes the conversion of 3-Methylglutaconyl-CoA into 3-Hydroxy-3-methylglutaryl-CoA which is the substrate of hydroxymethylglutaryl-CoA lyase. This disorder is characterized by increased urinary excretion of 3-methylglutaconic acid. Symptoms of the disorder include poor growth and neurological degression. Currently, there is no effective treatment for 3-MGA type IV. BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Ana Marcu Created On: September 10, 2018 at 15:51 Last Updated: September 10, 2018 at 15:51
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. BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: WishartLab Created On: April 21, 2014 at 07:15 Last Updated: April 21, 2014 at 07:15
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. BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Karxena Harford Created On: January 09, 2022 at 21:08 Last Updated: January 09, 2022 at 21:08
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. BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Ana Marcu Created On: September 10, 2018 at 15:50 Last Updated: September 10, 2018 at 15:50
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. BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: WishartLab Created On: June 23, 2014 at 02:39 Last Updated: June 23, 2014 at 02:39
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. BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Ana Marcu Created On: September 10, 2018 at 15:52 Last Updated: September 10, 2018 at 15:52
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. BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Ray Kruger Created On: October 24, 2022 at 18:18 Last Updated: October 24, 2022 at 18:18
PW146791 View Pathway	drug action 4-(Isopropylamino)diphenylamine Drug Metabolism Action Pathway Homo sapiens BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Ray Kruger Created On: October 07, 2023 at 19:03 Last Updated: October 07, 2023 at 19:03
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. BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: miguel ramirez Created On: December 10, 2015 at 12:00 Last Updated: December 10, 2015 at 12:00
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. BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Ana Marcu Created On: October 09, 2015 at 15:50 Last Updated: October 09, 2015 at 15:50