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Pathways

PathWhiz ID Pathway Meta Data

PW145399

Pw145399 View Pathway
drug action

Rasagiline Drug Metabolism Action Pathway

Homo sapiens

PW146421

Pw146421 View Pathway
drug action

Rebamipide Drug Metabolism Action Pathway

Homo sapiens

PW176516

Pw176516 View Pathway
metabolic

Rebamipide Predicted Metabolism Pathway

Homo sapiens
Metabolites of Rebamipide are predicted with biotransformer.

PW144363

Pw144363 View Pathway
drug action

Reboxetine Drug Metabolism Action Pathway

Homo sapiens

PW126100

Pw126100 View Pathway
physiological

Red Blood Cell Gas Exchange

Homo 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).

PW122010

Pw122010 View Pathway
disease

Refsum Disease

Rattus 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.

PW121785

Pw121785 View Pathway
disease

Refsum Disease

Mus 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.

PW000122

Pw000122 View Pathway
disease

Refsum Disease

Homo 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.

PW127373

Pw127373 View Pathway
disease

Refsum Disease

Homo 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.

PW132457

Pw132457 View Pathway
metabolic

Regadenoson Drug Metabolism

Homo 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.