PathWhiz

PathWhiz ID	Pathway	Meta Data
PW132375 View Pathway	metabolic 2-mercaptobenzothiazole Drug Metabolism Homo sapiens 2-mercaptobenzothiazole is a drug that is not metabolized by the human body as determined by current research and biotransformer analysis. 2-mercaptobenzothiazole passes through the liver and is then excreted from the body mainly through the kidney. BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Ray Kruger Created On: September 21, 2023 at 21:19 Last Updated: September 21, 2023 at 21:19
PW000525 View Pathway	disease 2-Ketoglutarate Dehydrogenase Complex Deficiency Homo sapiens 2-Ketoglutarate dehydrogenase complex deficiency, also known as alpha-ketoglutarate dehydrogenase deficiency or oxoglutaric aciduria, is an autosomal recessive disorder of the Krebs cycle caused by a defective oxoglutarate dehydrogenase complex (OGDC). OGDC catalyzes the conversion of 2-ketoglutarate into succinyl-CoA. This disorder is characterized by a large accumulation of 2-ketoglutarate in the urine. Symptoms of the disorder include opisthotonus, ataxia, developmental delay, and seizures. BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: WishartLab Created On: August 29, 2013 at 10:39 Last Updated: August 29, 2013 at 10:39
PW122093 View Pathway	disease 2-Ketoglutarate Dehydrogenase Complex Deficiency Rattus norvegicus 2-Ketoglutarate dehydrogenase complex deficiency, also known as alpha-ketoglutarate dehydrogenase deficiency or oxoglutaric aciduria, is an autosomal recessive disorder of the Krebs cycle caused by a defective oxoglutarate dehydrogenase complex (OGDC). OGDC catalyzes the conversion of 2-ketoglutarate into succinyl-CoA. This disorder is characterized by a large accumulation of 2-ketoglutarate in the urine. Symptoms of the disorder include opisthotonus, ataxia, developmental delay, and seizures. 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
PW127322 View Pathway	disease 2-Ketoglutarate Dehydrogenase Complex Deficiency Homo sapiens 2-Ketoglutarate dehydrogenase complex deficiency, also known as alpha-ketoglutarate dehydrogenase deficiency or oxoglutaric aciduria, is an autosomal recessive disorder of the Krebs cycle caused by a defective oxoglutarate dehydrogenase complex (OGDC). OGDC catalyzes the conversion of 2-ketoglutarate into succinyl-CoA. This disorder is characterized by a large accumulation of 2-ketoglutarate in the urine. Symptoms of the disorder include opisthotonus, ataxia, developmental delay, and seizures. BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Ray Kruger Created On: December 08, 2022 at 17:05 Last Updated: December 08, 2022 at 17:05
PW121869 View Pathway	disease 2-Ketoglutarate Dehydrogenase Complex Deficiency Mus musculus 2-Ketoglutarate dehydrogenase complex deficiency, also known as alpha-ketoglutarate dehydrogenase deficiency or oxoglutaric aciduria, is an autosomal recessive disorder of the Krebs cycle caused by a defective oxoglutarate dehydrogenase complex (OGDC). OGDC catalyzes the conversion of 2-ketoglutarate into succinyl-CoA. This disorder is characterized by a large accumulation of 2-ketoglutarate in the urine. Symptoms of the disorder include opisthotonus, ataxia, developmental delay, and seizures. 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
PW121689 View Pathway	disease 2-Hydroxyglutric Aciduria (D and L Form) Mus musculus L-2-Hydroxyglutaric Aciduria (D-2-Hydroxyglutaric Aciduria ) is an autosomal recessive disease caused by a mutation in the L2HGDH gene which codes for L-2-Hydroxygluarate dehydrogenase. A deficiency in this enzyme results in accumulation of L-2-Hydroxyglutaric acid in plasma, spinal fluid, and urine; and L-lysine in plasma and spinal fluid. Symptoms, which present at birth, include ataxia, hypotonia, mental retardation, and seizures. Premature death often results. D-2-Hydroxyglutaric Aciduria is an autosomal recessive disease caused by a mutation in the D2HGDH gene which does for D-2-Hydroxygluarate dehydrogenase. A deficiency in this enzyme results in accumulation of D-2-Hydroxyglutaric acid in plasma, spinal fluid, and urine; oxoglutaric acid in urine; and gabba-aminobutyric acid in spinal fluid. Symptoms, which present at birth, include ataxia, hypotonia, mental retardation, and seizures. Premature death often results. BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Ana Marcu Created On: September 10, 2018 at 15:49 Last Updated: September 10, 2018 at 15:49
PW000212 View Pathway	disease 2-Hydroxyglutric Aciduria (D and L Form) Homo sapiens L-2-Hydroxyglutaric Aciduria (D-2-Hydroxyglutaric Aciduria ) is an autosomal recessive disease caused by a mutation in the L2HGDH gene which codes for L-2-Hydroxygluarate dehydrogenase. A deficiency in this enzyme results in accumulation of L-2-Hydroxyglutaric acid in plasma, spinal fluid, and urine; and L-lysine in plasma and spinal fluid. Symptoms, which present at birth, include ataxia, hypotonia, mental retardation, and seizures. Premature death often results. D-2-Hydroxyglutaric Aciduria is an autosomal recessive disease caused by a mutation in the D2HGDH gene which does for D-2-Hydroxygluarate dehydrogenase. A deficiency in this enzyme results in accumulation of D-2-Hydroxyglutaric acid in plasma, spinal fluid, and urine; oxoglutaric acid in urine; and gabba-aminobutyric acid in spinal fluid. Symptoms, which present at birth, include ataxia, hypotonia, mental retardation, and seizures. Premature death often results. BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: WishartLab Created On: August 20, 2013 at 13:00 Last Updated: August 20, 2013 at 13:00
PW121915 View Pathway	disease 2-Hydroxyglutric Aciduria (D and L Form) Rattus norvegicus L-2-Hydroxyglutaric Aciduria (D-2-Hydroxyglutaric Aciduria ) is an autosomal recessive disease caused by a mutation in the L2HGDH gene which codes for L-2-Hydroxygluarate dehydrogenase. A deficiency in this enzyme results in accumulation of L-2-Hydroxyglutaric acid in plasma, spinal fluid, and urine; and L-lysine in plasma and spinal fluid. Symptoms, which present at birth, include ataxia, hypotonia, mental retardation, and seizures. Premature death often results. D-2-Hydroxyglutaric Aciduria is an autosomal recessive disease caused by a mutation in the D2HGDH gene which does for D-2-Hydroxygluarate dehydrogenase. A deficiency in this enzyme results in accumulation of D-2-Hydroxyglutaric acid in plasma, spinal fluid, and urine; oxoglutaric acid in urine; and gabba-aminobutyric acid in spinal fluid. Symptoms, which present at birth, include ataxia, hypotonia, mental retardation, and seizures. Premature death often results. 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
PW127064 View Pathway	disease 2-HG (updated) Homo sapiens BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Nitya Khetarpal Created On: August 04, 2022 at 13:04 Last Updated: August 04, 2022 at 13:04
PW248313 View Pathway	metabolic 2-Heptyl-3-hydroxy-quinolone (PQS) biosynthesis Pseudomonas aeruginosa 2-Heptyl-3-hydroxy-4-quinolone (PQS) is key to quorum sensing and virulence in bacteria like Pseudomonas aeruginosa PAO1. This biosynthesis begins with the precursor chorismate, which is derived from the shikimate pathway during the biosynthesis of aromatic amino acids e.g., phenylalanine, tyrosine and tryptophan. Chorismate is converted into anthranilate by anthranilate synthase, then into Anthraniloyl-CoA. The subsequent steps involve the action of enzymes 3-oxoacyl-ACP synthase, thioesterase PqsE, and 2-heptyl-4(1H)-quinolone synthase, which facilitate the conversion of Anthraniloyl-CoA to 2-heptyl-4(1H)-quinolone (HHQ), the direct precursor of PQS. Finally, 2-heptyl-3-hydroxy-4(1H)-quinolone synthase hydroxylates HHQ to produce PQS thus linking primary metabolism to secondary metanolism, significant to microbial communication and adaptation. BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Julia Wakoli Created On: May 17, 2024 at 16:32 Last Updated: May 17, 2024 at 16:32