PathWhiz

PathWhiz ID	Pathway	Meta Data
PW007843 View Pathway	metabolic Triacylglycerol Metabolism TG(18:0/18:0/18:0) Saccharomyces cerevisiae A triglyceride (TG, triacylglycerol, TAG, or triacylglyceride) is an ester derived from glycerol and three fatty acids. The biosynthesis of triacylglycerol is localized to the endoplasmic reticulum membrane and starts with glycerol 3-phosphate reacting with acyl-CoA through a glycerol-3-phosphate O-acyltransferase resulting in the release of lysophosphatidic acid (LPA). This, in turn, reacts with an acyl-CoA through a lipase complex resulting in the release of CoA and phosphatidic acid. Phosphatidic acid reacts with water through a phosphatidic acid phosphohydrolase 1 resulting in the release of a phosphate and a diacylglycerol. This reaction can be reversed through a CTP-dependent diacylglycerol kinase. The diacylglycerol reacts in the endoplasmic reticulum with an acyl-CoA through a diacylglycerol O-acyltransferase resulting in the release of coenzyme A and a triacylglycerol. Triacylglycerol metabolism begins with a reaction with water through lipase resulting in the release of a fatty acid, hydrogen ion, and a diacylglycerol. Diacylglycerol then reacts with a lipase 3 resulting in the release of a fatty acid and a monoacylglycerol. Monoacylglycerol reacts with monoglyceride lipase resulting in the release of a fatty acid in glycerol. BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Ana Marcu Created On: August 04, 2016 at 14:36 Last Updated: August 04, 2016 at 14:36
PW007880 View Pathway	metabolic Triacylglycerol Metabolism TG(18:0/18:0/20:0) Saccharomyces cerevisiae A triglyceride (TG, triacylglycerol, TAG, or triacylglyceride) is an ester derived from glycerol and three fatty acids. The biosynthesis of triacylglycerol is localized to the endoplasmic reticulum membrane and starts with glycerol 3-phosphate reacting with acyl-CoA through a glycerol-3-phosphate O-acyltransferase resulting in the release of lysophosphatidic acid (LPA). This, in turn, reacts with an acyl-CoA through a lipase complex resulting in the release of CoA and phosphatidic acid. Phosphatidic acid reacts with water through a phosphatidic acid phosphohydrolase 1 resulting in the release of a phosphate and a diacylglycerol. This reaction can be reversed through a CTP-dependent diacylglycerol kinase. The diacylglycerol reacts in the endoplasmic reticulum with an acyl-CoA through a diacylglycerol O-acyltransferase resulting in the release of coenzyme A and a triacylglycerol. Triacylglycerol metabolism begins with a reaction with water through lipase resulting in the release of a fatty acid, hydrogen ion, and a diacylglycerol. Diacylglycerol then reacts with a lipase 3 resulting in the release of a fatty acid and a monoacylglycerol. Monoacylglycerol reacts with monoglyceride lipase resulting in the release of a fatty acid in glycerol. BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Ana Marcu Created On: August 04, 2016 at 14:49 Last Updated: August 04, 2016 at 14:49
PW000341 View Pathway	drug action Triamterene Action Pathway Homo sapiens Triamterene is a diuretic that belongs to the potassium-sparing class of drugs which are commonly used to manage hypertension and edema. It acts by blocking epithelial sodium channels in the late distal convoluted tubule of the nephron. Specifically, triamterene inhibits amiloride-sensitive sodium channels which are responsible for the reabsorption of sodium in the late distal convoluted tubule in the nephron. This primarily contributes to an increase in sodium excretion and consequentially, fluid excretion which decreases blood volume and blood pressure. Potassium secretion is indirectly affected by the inhibition of sodium reabsorption due to the elimination of the electrochemical gradient that drives potassium loss. This leads to an increase in serum potassium concentration -- a common action for potassium-sparing drugs -- and has the potential to induce hyperkalemia which can potentially lead to severe heart arrhythmias. BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: WishartLab Created On: August 22, 2013 at 10:45 Last Updated: August 22, 2013 at 10:45
PW127080 View Pathway	metabolic Tricarboxylic acid cycle Homo sapiens BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Karxena Harford Created On: August 24, 2022 at 11:44 Last Updated: August 24, 2022 at 11:44
PW000339 View Pathway	drug action Trichlormethiazide Action Pathway Homo sapiens Trichlormethiazide is a pharmacologically-active small molecule that belongs to a class of drugs called thiazides. Thiazides and thiazide-like drugs are diuretics commonly employed to control hypertension. Trichloromethiazide acts by inhibiting chloride and potentially sodium reabsorption in the ascending loop of Henle, specifically at solute carrier family 12 member 3. This action results in increased fluid loss which ultimately reduces blood volume and pressure. Trichlormethiazide also acts to inhibit sodium uptake and increase potassium excretion which also serves to increase fluid loss. The long-term antihypertensive effects of thiazides and thiazide-like drugs such as trichlormethiazide are not well-characterized but may involve its action on carbonic anhydrases. BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: WishartLab Created On: August 22, 2013 at 10:45 Last Updated: August 22, 2013 at 10:45
PW127471 View Pathway	drug action Trifluridine Action Pathway Homo sapiens Trifluridine is a fluorinated pyrimidine nucleoside that is structurally related to idoxuridine and an active antiviral agent in ophthalmic solutions that is mainly used in the treatment of primary keratoxonjunctivitis and recurrent epithelial keratitis due to herpes simplex virus. It displays effective antiviral activity against Herpes simplex virus type 1 and 2. The mechanism of action of trifluridine as an antiviral agent has not been fully elucidated, but appears to involve the inhibition of viral replication. Trifluridine gets incorporated into viral DNA during replication in replacement of thymidine, which leads to the formation of defective proteins and an increased mutation rate. Less Viral DNA is transported into the nucleus, therefore, less viral DNA is integrated into the host DNA. Less viral proteins produced, fewer viruses can form. Trifluridine also mediates antineoplastic activities via this mechanism; following uptake into cancer cells, trifluridine is rapidly phosphorylated by thymidine kinase to its active monophosphate form. It is further phosphorylated into trifluridine triphosphate, which is readily incorporated into the DNA of tumour cells in place of thymidine bases to perturb DNA function, DNA synthesis, and tumour cell proliferation. BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Ray Kruger Created On: March 07, 2023 at 14:17 Last Updated: March 07, 2023 at 14:17
PW121865 View Pathway	disease Trifunctional Protein Deficiency Mus musculus Trifunctional protein deficiency is a condition caused by mutations in the genes HADHA and HADHB. The enzyme affected is required to metabolize long-chain fatty acids, which makes a patients ability to convert fats to energy very difficult. This is exacerbated by periods without food. The symptoms associated with this disorder differ depending on when they appear in a patient. In infancy, symptoms would include lethargy, hypoglycaemia and hypotonia. Infants are also at higher risk for sudden death and heart problems. Later onset trifunctional protein deficiency symptoms also include hypotonia, but also include breakdown of muscle tissue and peripheral neuropathy. Treatment includes a low-fat, high-carbohydrate diet and avoiding fasting, as this can induce symptoms of this condition. 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
PW122089 View Pathway	disease Trifunctional Protein Deficiency Rattus norvegicus Trifunctional protein deficiency is a condition caused by mutations in the genes HADHA and HADHB. The enzyme affected is required to metabolize long-chain fatty acids, which makes a patients ability to convert fats to energy very difficult. This is exacerbated by periods without food. The symptoms associated with this disorder differ depending on when they appear in a patient. In infancy, symptoms would include lethargy, hypoglycaemia and hypotonia. Infants are also at higher risk for sudden death and heart problems. Later onset trifunctional protein deficiency symptoms also include hypotonia, but also include breakdown of muscle tissue and peripheral neuropathy. Treatment includes a low-fat, high-carbohydrate diet and avoiding fasting, as this can induce symptoms of this condition. 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
PW127311 View Pathway	disease Trifunctional Protein Deficiency Homo sapiens Trifunctional protein deficiency is a condition caused by mutations in the genes HADHA and HADHB. The enzyme affected is required to metabolize long-chain fatty acids, which makes a patients ability to convert fats to energy very difficult. This is exacerbated by periods without food. The symptoms associated with this disorder differ depending on when they appear in a patient. In infancy, symptoms would include lethargy, hypoglycaemia and hypotonia. Infants are also at higher risk for sudden death and heart problems. Later onset trifunctional protein deficiency symptoms also include hypotonia, but also include breakdown of muscle tissue and peripheral neuropathy. Treatment includes a low-fat, high-carbohydrate diet and avoiding fasting, as this can induce symptoms of this condition. BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Ray Kruger Created On: December 06, 2022 at 17:02 Last Updated: December 06, 2022 at 17:02
PW000521 View Pathway	disease Trifunctional Protein Deficiency Homo sapiens Trifunctional protein deficiency is a condition caused by mutations in the genes HADHA and HADHB. The enzyme affected is required to metabolize long-chain fatty acids, which makes a patients ability to convert fats to energy very difficult. This is exacerbated by periods without food. The symptoms associated with this disorder differ depending on when they appear in a patient. In infancy, symptoms would include lethargy, hypoglycaemia and hypotonia. Infants are also at higher risk for sudden death and heart problems. Later onset trifunctional protein deficiency symptoms also include hypotonia, but also include breakdown of muscle tissue and peripheral neuropathy. Treatment includes a low-fat, high-carbohydrate diet and avoiding fasting, as this can induce symptoms of this condition. 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