PathWhiz

PathWhiz ID	Pathway	Meta Data
PW002490 View Pathway	metabolic Leucine Degradation Saccharomyces cerevisiae The degradation of L-leucine starts either in the mitochondria or the cytosol. L-leucine reacts with 2-oxoglutarate through a branch-chain amino acid aminotransferase resulting in the release of ketoleucine and glutamate. The latter compound reacts with ketoisocaproate decarboxylase resulting in the release of carbon dioxide and 3-methylbutanal. The latter compound can then be turned into 3-methylbutanol through a alcohol dehydrogenase BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: miguel ramirez Created On: February 29, 2016 at 14:20 Last Updated: February 29, 2016 at 14:20
PW013301 View Pathway	metabolic Leucine degradation Bacteria I would like to test Pathwhiz BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Guest: Anonymous Created On: April 27, 2017 at 06:57 Last Updated: April 27, 2017 at 06:57
PW002541 View Pathway	metabolic Leucine Degradation Arabidopsis thaliana The degradation of L-leucine starts either in the mitochondria, the cytosol or the chloroplast. L-leucine reacts with 2-oxoglutarate through a branch-chain amino acid aminotransferase resulting in the release of ketoleucine and glutamate. Ketoleucine reacts with coenzyme a through a NAD dependent branched chain keto-acid dehydrogenase complex resulting in the release of NADH, carbon dioxide and isovaleryl-CoA. Isovaleryl-CoA reacts with an oxidized electron flavoprotein resulting in the release of a reduced flavoprotein and a methylcrotonyl-CoA. The latter reacts with ATP and hydrogen carbonate through a 3-methylcrotonyl-CoA carboxylase resulting in the release of phosphate, ADP, hydrogen ion and 3-methylglutaconyl-CoA. The latter compound reacts with water through a methylglutaconyl-CoA hydratase resulting in the release of hydroxy-3-methylglutaryl-CoA. The latter reacts with a hydroxymethylglutaryl-CoA lyase resulting in the release of acetyl-CoA and acetoacetate. BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: miguel ramirez Created On: May 05, 2016 at 16:47 Last Updated: May 05, 2016 at 16:47
PW109051 View Pathway	signaling Leucine Stimulation on Insulin Signaling Rattus norvegicus The branched chain amino acid (BCAA) leucine is able to signal transduction pathways that modulate translation initiation for protein synthesis in skeleton muscles. In the presence of leucine, hyperphosphorylation of 4E-BP1 causes its affinity for eIF4E to be lowered. This allows eIF4F protein complexes to recognize, unfold and guide the mRNA to the 43S preinitiation complex thereby increasing translation initiation. In addition, leucine has a transient affect on the release of insulin and/or enhances sensitivity of muscle cells to insulin. A culmination of both signals at the mammalian target of rapamycin (mTOR) and perhaps other signaling, such as PKCδ, are needed for maximum translation initiation to occur. BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Ana Marcu Created On: August 31, 2018 at 11:46 Last Updated: August 31, 2018 at 11:46
PW109041 View Pathway	signaling Leucine Stimulation on Insulin Signaling Bos taurus The branched chain amino acid (BCAA) leucine is able to signal transduction pathways that modulate translation initiation for protein synthesis in skeleton muscles. In the presence of leucine, hyperphosphorylation of 4E-BP1 causes its affinity for eIF4E to be lowered. This allows eIF4F protein complexes to recognize, unfold and guide the mRNA to the 43S preinitiation complex thereby increasing translation initiation. In addition, leucine has a transient affect on the release of insulin and/or enhances sensitivity of muscle cells to insulin. A culmination of both signals at the mammalian target of rapamycin (mTOR) and perhaps other signaling, such as PKCδ, are needed for maximum translation initiation to occur. BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Ana Marcu Created On: August 31, 2018 at 11:45 Last Updated: August 31, 2018 at 11:45
PW109030 View Pathway	signaling Leucine Stimulation on Insulin Signaling Mus musculus The branched chain amino acid (BCAA) leucine is able to signal transduction pathways that modulate translation initiation for protein synthesis in skeleton muscles. In the presence of leucine, hyperphosphorylation of 4E-BP1 causes its affinity for eIF4E to be lowered. This allows eIF4F protein complexes to recognize, unfold and guide the mRNA to the 43S preinitiation complex thereby increasing translation initiation. In addition, leucine has a transient affect on the release of insulin and/or enhances sensitivity of muscle cells to insulin. A culmination of both signals at the mammalian target of rapamycin (mTOR) and perhaps other signaling, such as PKCδ, are needed for maximum translation initiation to occur. BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Ana Marcu Created On: August 31, 2018 at 11:43 Last Updated: August 31, 2018 at 11:43
PW000659 View Pathway	signaling Leucine Stimulation on Insulin Signaling Homo sapiens The branched chain amino acid (BCAA) leucine is able to signal transduction pathways that modulate translation initiation for protein synthesis in skeleton muscles. In the presence of leucine, hyperphosphorylation of 4E-BP1 causes its affinity for eIF4E to be lowered. This allows eIF4F protein complexes to recognize, unfold and guide the mRNA to the 43S preinitiation complex thereby increasing translation initiation. In addition, leucine has a transient affect on the release of insulin and/or enhances sensitivity of muscle cells to insulin. A culmination of both signals at the mammalian target of rapamycin (mTOR) and perhaps other signaling, such as PKCδ, are needed for maximum translation initiation to occur. BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: WishartLab Created On: April 25, 2014 at 23:15 Last Updated: April 25, 2014 at 23:15
PW121764 View Pathway	disease Leukotriene C4 Synthesis Deficiency Mus musculus Leukotriene C4 synthetase deficiency is caused by a defect in the enzyme leukotriene C4 synthetase (LTC4S). This enzyme catalyzes the synthesis of leukotriene C4 (LTC4) through conjugation of LTA4 with reduced glutathione (GSH), which is synthesized by glutathione synthetase. Leukotriene C4 and its receptor-binding metabolites LTD4 and LTE4 are cysteinyl leukotrienes that are potent lipid mediators of tissue inflammation. In general, leukotrienes are potent proinflammatory mediators synthesized from membrane-derived arachidonic acid after activation of certain granulocytes. A defect in LTC4 results in decreased concentrations of cysteinyl leukotrienes LTC4, LTD4 and LTE4 in plasma, spinal fluid and urine. Symptoms include early death, failure to thrive, motor retardation, microcephaly, and progressive neurological defect. 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
PW000118 View Pathway	disease Leukotriene C4 Synthesis Deficiency Homo sapiens Leukotriene C4 synthetase deficiency is caused by a defect in the enzyme leukotriene C4 synthetase (LTC4S). This enzyme catalyzes the synthesis of leukotriene C4 (LTC4) through conjugation of LTA4 with reduced glutathione (GSH), which is synthesized by glutathione synthetase. Leukotriene C4 and its receptor-binding metabolites LTD4 and LTE4 are cysteinyl leukotrienes that are potent lipid mediators of tissue inflammation. In general, leukotrienes are potent proinflammatory mediators synthesized from membrane-derived arachidonic acid after activation of certain granulocytes. A defect in LTC4 results in decreased concentrations of cysteinyl leukotrienes LTC4, LTD4 and LTE4 in plasma, spinal fluid and urine. Symptoms include early death, failure to thrive, motor retardation, microcephaly, and progressive neurological defect. 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
PW121989 View Pathway	disease Leukotriene C4 Synthesis Deficiency Rattus norvegicus Leukotriene C4 synthetase deficiency is caused by a defect in the enzyme leukotriene C4 synthetase (LTC4S). This enzyme catalyzes the synthesis of leukotriene C4 (LTC4) through conjugation of LTA4 with reduced glutathione (GSH), which is synthesized by glutathione synthetase. Leukotriene C4 and its receptor-binding metabolites LTD4 and LTE4 are cysteinyl leukotrienes that are potent lipid mediators of tissue inflammation. In general, leukotrienes are potent proinflammatory mediators synthesized from membrane-derived arachidonic acid after activation of certain granulocytes. A defect in LTC4 results in decreased concentrations of cysteinyl leukotrienes LTC4, LTD4 and LTE4 in plasma, spinal fluid and urine. Symptoms include early death, failure to thrive, motor retardation, microcephaly, and progressive neurological defect. 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