PathWhiz

PathWhiz ID	Pathway	Meta Data
PW002096 View Pathway	metabolic 2-O-alpha-Mannosyl-D-glycerate Degradation Escherichia coli 2-O-α-Mannosyl-D-glycerate (MG; also named as Alpha-Mannosylglycerate) is an organic compound that will affect the osmosis in hyperthermophilic archaea and bacteria. In E.coli, 2-O-α-mannosyl-D-glycerate PTS permease (mngA) import MG into cell, and then phosphorylate MG to 2-O-(6-phospho-α-mannosyl)-D-glycerate by phosphocarrier protein HPr. 2-O-(6-phospho-α-mannosyl)-D-glycerate is converted to glyceric acid as well as mannose 6-phosphate by alpha-mannosidase mngB. Finally, glyceric acid is catalyzed to 2-Phospho-D-glyceric acid with ATP as energy source by Glycerate kinase 2. E.coli can't use MG as osmotic stress protection, but it can use MG as a carbon source. BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Ana Marcu Created On: October 13, 2015 at 17:28 Last Updated: October 13, 2015 at 17:28
PW000061 View Pathway	disease 2-Methyl-3-hydroxybutyryl-CoA Dehydrogenase Deficiency Homo sapiens 2-Methyl-3-hydroxybutyryl CoA dehydrogenase deficiency (Hydroxyl-CoA dehydrogenase deficiency; MHBD) is a rare inborn disease of metabolism caused by a mutation in the HSD17B10 gene which codes for 3-hydroxyacyl-CoA dehydrogenase type-2. A deficiency in this enzyme results in accumulation of L-lactic acid in blood, spinal fluid, and urine; 2-ethylhydracrylic acid, 2-methyl-3-hydroxybutyric acid, and tiglylglycine in urine. Symptoms include cerebal atrophy, motor and mental retardation, overactivity and behavior issues, seizures and progressive neurological defects leading to early death. Treatment includes a high carbohydrate and low protein diet. BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: WishartLab Created On: August 01, 2013 at 15:52 Last Updated: August 01, 2013 at 15:52
PW127223 View Pathway	disease 2-Methyl-3-hydroxybutyryl-CoA Dehydrogenase Deficiency Homo sapiens 2-Methyl-3-hydroxybutyryl CoA dehydrogenase deficiency (Hydroxyl-CoA dehydrogenase deficiency; MHBD) is a rare inborn disease of metabolism caused by a mutation in the HSD17B10 gene which codes for 3-hydroxyacyl-CoA dehydrogenase type-2. A deficiency in this enzyme results in accumulation of L-lactic acid in blood, spinal fluid, and urine; 2-ethylhydracrylic acid, 2-methyl-3-hydroxybutyric acid, and tiglylglycine in urine. Symptoms include cerebal atrophy, motor and mental retardation, overactivity and behavior issues, seizures and progressive neurological defects leading to early death. Treatment includes a high carbohydrate and low protein diet. BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Ray Kruger Created On: November 15, 2022 at 11:02 Last Updated: November 15, 2022 at 11:02
PW121916 View Pathway	disease 2-Methyl-3-hydroxybutryl-CoA Dehydrogenase Deficiency Rattus norvegicus 2-Methyl-3-hydroxybutyryl CoA dehydrogenase deficiency (Hydroxyl-CoA dehydrogenase deficiency; MHBD) is a rare inborn disease of metabolism caused by a mutation in the HSD17B10 gene which codes for 3-hydroxyacyl-CoA dehydrogenase type-2. A deficiency in this enzyme results in accumulation of L-lactic acid in blood, spinal fluid, and urine; 2-ethylhydracrylic acid, 2-methyl-3-hydroxybutyric acid, and tiglylglycine in urine. Symptoms include cerebal atrophy, motor and mental retardation, overactivity and behavior issues, seizures and progressive neurological defects leading to early death. Treatment includes a high carbohydrate and low protein diet. 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
PW121690 View Pathway	disease 2-Methyl-3-hydroxybutryl-CoA Dehydrogenase Deficiency Mus musculus 2-Methyl-3-hydroxybutyryl CoA dehydrogenase deficiency (Hydroxyl-CoA dehydrogenase deficiency; MHBD) is a rare inborn disease of metabolism caused by a mutation in the HSD17B10 gene which codes for 3-hydroxyacyl-CoA dehydrogenase type-2. A deficiency in this enzyme results in accumulation of L-lactic acid in blood, spinal fluid, and urine; 2-ethylhydracrylic acid, 2-methyl-3-hydroxybutyric acid, and tiglylglycine in urine. Symptoms include cerebal atrophy, motor and mental retardation, overactivity and behavior issues, seizures and progressive neurological defects leading to early death. Treatment includes a high carbohydrate and low protein diet. 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
PW146374 View Pathway	drug action 2-mercaptobenzothiazole Drug Metabolism Action Pathway Homo sapiens BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Ray Kruger Created On: October 07, 2023 at 18:03 Last Updated: October 07, 2023 at 18:03
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