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PathWhiz ID Pathway Meta Data

PW109252

Pw109252 View Pathway
protein

Ras Signaling Pathway

Bos taurus
RAS signalling pathway is one of the main pathways to transduce intracellular signals in response to mitogens to controls cell growth, survival and anti-apoptotic programs. RAS proteins are GTP-binding proteins and must be bound to GTP to be active. Active RAS binds and activates effector enzymes that control cell proliferation, survival and other cell behaviours. RAS interacts directly with the catalytic subunit of PI3K to activate lipid kinases controlling the activity of downstream enzymes. Some of these kinases have anti-apoptotic activity, playing an important role in the survival signal of RAS. PI3K is also involved in the regulation of the actin cytoskeleton and transcription factor pathways. RAS also effects exchange factors causing inhibition of transcription factors from FoxO family, part of promoting cell cycle arrest and apoptosis. Normal function of these proteins require post-transcriptional modification. Pathway mutations in activation may result in human tumours.

PW128313

Pw128313 View Pathway
drug action

Rasagiline Action Pathway

Homo sapiens
Rasagiline is a propargylamine and an irreversible monoamine oxidase inhibitor (MAOIs). It is indicated in the treatment of idiopathic Parkinson's disease as initial therapy or as adjunct therapy with levodopa. The monoamine oxidase is an enzyme that catalyzes the oxidative deamination of many amines like serotonin, norepinephrine, epinephrine, and dopamine. There are 2 isoforms of this protein: A and B. The first one is found in cells located in the periphery and breakdown serotonin, norepinephrine, epinephrine, dopamine, and tyramine. The second one, the B isoform, breakdowns phenylethylamine, norepinephrine, epinephrine, dopamine, and tyramine. This isoform is found in the extracellular tissues and mostly in the brain. The mechanism of action of the MAOIs is still not determined, it is thought that they act by increasing free serotonin and norepinephrine concentrations and/or by altering the concentrations of other amines in the CNS. MAO-A inhibition is thought to be more relevant to antidepressant activity than the inhibition caused by MAO B. Selective MAO B inhibitors have no antidepressant effects. The selectivity of rasagiline for inhibiting only MAO-B results in more dopamine in the cytosol and synapse of the neurons in the striatum. The increased dopamine level thus increases the dopaminergic activity. This helps to reduce the symptoms of Parkinson's disease that are caused by low levels of dopamine in the striatum. An overdose of this drug will result in drowsiness, faintness, hyperactivity, hallucinations, respiratory depression, convulsions, and coma. This drug is administered as an oral tablet.

PW145399

Pw145399 View Pathway
drug action

Rasagiline Drug Metabolism Action Pathway

Homo sapiens

PW123865

Pw123865 View Pathway
signaling

Rcs

Escherichia coli

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.