PathWhiz ID | Pathway | Meta Data |
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PW145399View Pathway |
drug action
Rasagiline Drug Metabolism Action PathwayHomo sapiens
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Creator: Ray Kruger Created On: October 07, 2023 at 15:45 Last Updated: October 07, 2023 at 15:45 |
PW146421View Pathway |
drug action
Rebamipide Drug Metabolism Action PathwayHomo sapiens
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Creator: Ray Kruger Created On: October 07, 2023 at 18:09 Last Updated: October 07, 2023 at 18:09 |
PW176516View Pathway |
Rebamipide Predicted Metabolism PathwayHomo sapiens
Metabolites of Rebamipide are predicted with biotransformer.
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Creator: Omolola Created On: December 13, 2023 at 13:29 Last Updated: December 13, 2023 at 13:29 |
PW144363View Pathway |
drug action
Reboxetine Drug Metabolism Action PathwayHomo sapiens
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Creator: Ray Kruger Created On: October 07, 2023 at 13:28 Last Updated: October 07, 2023 at 13:28 |
PW126100View Pathway |
physiological
Red Blood Cell Gas ExchangeHomo sapiens
The primary function of erythrocytes (red blood cells) is to exchange oxygen and carbon dioxide through tiny blood vessels called capillaries. In the lungs, oxygen diffuses into the blood, hemoglobin molecules release carbon dioxide picked up from body tissues. This allows oxygen to attach to the hemoglobin molecules and it can be carried to the rest of the body. Hemoglobin is a protein that makes blood red and carries oxygen throughout the circulation. The adult form of hemoglobin contains 2 alpha chains and 2 beta chains. When CO2 is removed from tissues, a portion of it is dissolved in the plasma and converted to bicarbonate. A majority of the CO2 is taken up by the RBCs and follows one of three transport pathways. 1. The CO2 is dissolved into the RBC cytoplasm. 2. CO2 is converted, by carbonic anhydrase, into bicarbonate which is exchanged at the cell membrane for a chloride ion (involved in the Chloride shift). This bicarbonate removal increases CO2 uptake into the cell. 3. CO2 is carried by carbaminohemoglobin which can be transported to the lung for removal. After offloading of oxygen into tissues, hemoglobin has an increased affinity for carbon dioxide and hydrogen ions (Haldane effect).
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Creator: Ashley Zubkowski Created On: June 18, 2021 at 11:47 Last Updated: June 18, 2021 at 11:47 |
PW122010View Pathway |
disease
Refsum DiseaseRattus norvegicus
Adult Refsum Disease (Classic Refsum Disease; Phytanic Acid Oxidase Deficiency; Heredopathia Atactica Polyneurtiformis; Hereditary Motor and Sensory Neuropathy IV; HSMN4; Adult Refsum Disease I; Adult Refsum Disease II), can be caused by mutations in the PHYH (or PAHX) gene, which encodes Phytanoyl-CoA hydroxylase (, the first enzyme in the Phytanic Acid Peroxisomal Oxidation pathway) on chromosome 10 (adult Refsum disease I), and by mutation of the PEX7 gene. A defect in phytanoyl-CoA hydroxylase results in accumulation of phytanic acid in the plasma, as well as low levels of pristanic acid due to the inability for phytanic acid to undergo alpha and beta oxidation. Symptoms include anosmia, ataxia, nystagmus, neurological deterioration and peripheral neuropathy. Adult Refsum disease is distinctly different from Infantile Refsum disease both genetically and phenotypically. Infantile Refsum disease involves mutations of the PEX1, PEX2 and PEX26 genes.
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Creator: Ana Marcu Created On: September 10, 2018 at 15:51 Last Updated: September 10, 2018 at 15:51 |
PW121785View Pathway |
disease
Refsum DiseaseMus musculus
Adult Refsum Disease (Classic Refsum Disease; Phytanic Acid Oxidase Deficiency; Heredopathia Atactica Polyneurtiformis; Hereditary Motor and Sensory Neuropathy IV; HSMN4; Adult Refsum Disease I; Adult Refsum Disease II), can be caused by mutations in the PHYH (or PAHX) gene, which encodes Phytanoyl-CoA hydroxylase (, the first enzyme in the Phytanic Acid Peroxisomal Oxidation pathway) on chromosome 10 (adult Refsum disease I), and by mutation of the PEX7 gene. A defect in phytanoyl-CoA hydroxylase results in accumulation of phytanic acid in the plasma, as well as low levels of pristanic acid due to the inability for phytanic acid to undergo alpha and beta oxidation. Symptoms include anosmia, ataxia, nystagmus, neurological deterioration and peripheral neuropathy. Adult Refsum disease is distinctly different from Infantile Refsum disease both genetically and phenotypically. Infantile Refsum disease involves mutations of the PEX1, PEX2 and PEX26 genes.
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Creator: Ana Marcu Created On: September 10, 2018 at 15:49 Last Updated: September 10, 2018 at 15:49 |
PW000122View Pathway |
disease
Refsum DiseaseHomo sapiens
Adult Refsum Disease (Classic Refsum Disease; Phytanic Acid Oxidase Deficiency; Heredopathia Atactica Polyneurtiformis; Hereditary Motor and Sensory Neuropathy IV; HSMN4; Adult Refsum Disease I; Adult Refsum Disease II), can be caused by mutations in the PHYH (or PAHX) gene, which encodes Phytanoyl-CoA hydroxylase (, the first enzyme in the Phytanic Acid Peroxisomal Oxidation pathway) on chromosome 10 (adult Refsum disease I), and by mutation of the PEX7 gene. A defect in phytanoyl-CoA hydroxylase results in accumulation of phytanic acid in the plasma, as well as low levels of pristanic acid due to the inability for phytanic acid to undergo alpha and beta oxidation. Symptoms include anosmia, ataxia, nystagmus, neurological deterioration and peripheral neuropathy. Adult Refsum disease is distinctly different from Infantile Refsum disease both genetically and phenotypically. Infantile Refsum disease involves mutations of the PEX1, PEX2 and PEX26 genes.
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Creator: WishartLab Created On: August 01, 2013 at 15:52 Last Updated: August 01, 2013 at 15:52 |
PW127373View Pathway |
disease
Refsum DiseaseHomo sapiens
Adult Refsum Disease (Classic Refsum Disease; Phytanic Acid Oxidase Deficiency; Heredopathia Atactica Polyneurtiformis; Hereditary Motor and Sensory Neuropathy IV; HSMN4; Adult Refsum Disease I; Adult Refsum Disease II), can be caused by mutations in the PHYH (or PAHX) gene, which encodes Phytanoyl-CoA hydroxylase (, the first enzyme in the Phytanic Acid Peroxisomal Oxidation pathway) on chromosome 10 (adult Refsum disease I), and by mutation of the PEX7 gene. A defect in phytanoyl-CoA hydroxylase results in accumulation of phytanic acid in the plasma, as well as low levels of pristanic acid due to the inability for phytanic acid to undergo alpha and beta oxidation. Symptoms include anosmia, ataxia, nystagmus, neurological deterioration and peripheral neuropathy. Adult Refsum disease is distinctly different from Infantile Refsum disease both genetically and phenotypically. Infantile Refsum disease involves mutations of the PEX1, PEX2 and PEX26 genes.
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Creator: Ray Kruger Created On: December 19, 2022 at 17:59 Last Updated: December 19, 2022 at 17:59 |
PW132457View Pathway |
Regadenoson Drug MetabolismHomo sapiens
Regadenoson is a drug that is not metabolized by the human body as determined by current research and biotransformer analysis. Regadenoson passes through the liver and is then excreted from the body mainly through the kidney.
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Creator: Ray Kruger Created On: September 21, 2023 at 21:53 Last Updated: September 21, 2023 at 21:53 |