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Pathways

PathWhiz ID Pathway Meta Data

PW145511

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drug action

Vorinostat Drug Metabolism Action Pathway

Homo sapiens

PW145949

Pw145949 View Pathway
drug action

Vortioxetine Drug Metabolism Action Pathway

Homo sapiens

PW176166

Pw176166 View Pathway
metabolic

Vortioxetine Predicted Metabolism Pathway new

Homo sapiens
Metabolites of Vortioxetine are predicted with biotransformer.

PW128392

Pw128392 View Pathway
drug action

Vortioxetine Serotonin Action Action Pathway

Homo sapiens
Vortioxetine is classified as a serotonin modulator and simulator (SMS) as it has a multimodal mechanism of action towards the serotonin neurotransmitter system whereby it simultaneously modulates one or more serotonin receptors and inhibits the reuptake of serotonin. More specifically, vortioxetine acts via the following biological mechanisms: as a serotonin reuptake inhibitor (SRI) through inhibition of the serotonin transporter, while also acting as a partial agonist of the 5-HT1B receptor, an agonist of 5-HT1A, and antagonist of the 5-HT3, 5-HT1D, and 5-HT7 receptors

PW146901

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drug action

Voxelotor Drug Metabolism Action Pathway

Homo sapiens

PW127535

Pw127535 View Pathway
drug action

Voxilaprevir Action Pathway

Homo sapiens
Voxilaprevir is a nonstructural protein 3 and 4a protease inhibitor used to treat Hepatitis C infections. Hepatitis C virus lipoviroparticles enter target hepatocytes via receptor-mediated endocytosis. The lipoviroparticles attach to LDL-R and SR-B1, and then the virus binds to CD81 and subsequently claudin-1 and occludin, which mediate the late steps of viral entry. The virus is internalized by clathrin-dependent endocytosis. RNA is released from the mature Hepatitis C virion and translated at the rough endoplasmic reticulum into a single Genome polyprotein. Voxilaprevir accumulates in the liver after uptake into hepatocytes via solute carrier organic anion transporter family member 1B1. Voxilaprevir inhibits NS3/4A protease, which is an enzyme that cleaves the heptatitis C virus polyprotein downstream of the NS3 proteolytic site, which generates nonstructural proteins NS3, NS4A, NS4B, NS5A, and NS5B. These proteins are required in viral RNA replication, therefore because of the inhibition of their formation, RNA replication cannot occur. Because RNA replication does not occur, the mature virion is unable to form.

PW146489

Pw146489 View Pathway
drug action

Voxilaprevir Drug Metabolism Action Pathway

Homo sapiens

PW064795

Pw064795 View Pathway
metabolic

Warburg Effec

Homo sapiens

PW088439

Pw088439 View Pathway
metabolic

Warburg Effect

Drosophila melanogaster
The Warburg Effect refers to the phenomenon that occurs in most cancer cells where instead of generating energy with a low rate of glycolysis followed by oxidizing pyruvate via the Krebs cycle in the mitochondria, the pyruvate from a high rate of glycolysis undergoes lactic acid fermentation in the cytosol. As the Krebs cycle is an aerobic process, in normal cells lactate production is reserved for anaerobic conditions. However, cancer cells preferentially utilize glucose for lactate production via this “aerobic glycolysis”, even when oxygen is plentiful. The Warburg Effect is thought to be the result of mutations to oncogenes and tumour suppressor genes. It may be an adaptation to low-oxygen environments within tumors, the result of cancer genes shutting down the mitochondria, or a mechanism to aid cell proliferation via increased glycolysis. The Warburg Effect involves numerous pathways, including growth factor stimulation, transcriptional activation, and glycolysis promotion.

PW087949

Pw087949 View Pathway
metabolic

Warburg Effect

Mus musculus
The Warburg Effect refers to the phenomenon that occurs in most cancer cells where instead of generating energy with a low rate of glycolysis followed by oxidizing pyruvate via the Krebs cycle in the mitochondria, the pyruvate from a high rate of glycolysis undergoes lactic acid fermentation in the cytosol. As the Krebs cycle is an aerobic process, in normal cells lactate production is reserved for anaerobic conditions. However, cancer cells preferentially utilize glucose for lactate production via this “aerobic glycolysis”, even when oxygen is plentiful. The Warburg Effect is thought to be the result of mutations to oncogenes and tumour suppressor genes. It may be an adaptation to low-oxygen environments within tumors, the result of cancer genes shutting down the mitochondria, or a mechanism to aid cell proliferation via increased glycolysis. The Warburg Effect involves numerous pathways, including growth factor stimulation, transcriptional activation, and glycolysis promotion.