PathWhiz ID | Pathway | Meta Data |
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PW124119View Pathway |
signaling
THC on CB1Homo sapiens
The main psychoactive component in cannabis, △9-tetrahydrocannabinol (THC), acts on CB1 receptors in the brain located on synaptic terminals. THC, whose 3D structure closely resembles that of the endogenous cannabinoid anandamide, acts as a partial agonist on these receptors. Several behavioural effects of cannabis are feelings of euphoria, relaxation, lack of concentration,and altered time perception, while physiological effects range from increased appetite to rapid changes in heart rate. The mechanism of action of THC works through the activation CB1, which inhibits adenylate cyclase and lowers levels of cyclic AMP in the cell. This further inhibits protein kinase A complex, which affects regulating synaptic membrane exocytosis protein through an as yet unknown mechanism. This regulating protein is responsible for the release of GABA or ɣ-aminobutyric acid by exocytosis from the inhibitory terminal of the neuron. GABA is normally released to inhibit and regulate the release of dopamine in the brain. The binding of THC limits the exocytosis of GABA, and so dopamine is able to travel along synapses and bind to receptors. This promotes the well-known euphoric effects of cannabis. The activated CB1 receptor also interacts with its normal physiological targets, activating both MAPK and potassium channels and inhibiting calcium channels. These interactions and their physiological downstream effects are responsible for the numerous side effects associated with cannabis such as lack of concentration and impaired learning. The sustained effects of THC can be explained by the ability of CB1 receptors to influence long term plasticity in the brain.
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Creator: Alyssah Created On: August 26, 2020 at 10:12 Last Updated: August 26, 2020 at 10:12 |
PW000987View Pathway |
The Citric Acid Cycle TutorialHomo sapiens
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Creator: Guest: Anonymous Created On: July 17, 2015 at 11:43 Last Updated: July 17, 2015 at 11:43 |
PW000983View Pathway |
The Citric Acid Cycle Tutorial (2) - Pt.3 Adding LabelsHomo sapiens
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Creator: Guest: Anonymous Created On: July 16, 2015 at 15:26 Last Updated: July 16, 2015 at 15:26 |
PW000986View Pathway |
The Citric Acid Cycle Tutorial (2) - Pt.4 Adding SubPathwaysHomo sapiens
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Creator: Guest: Anonymous Created On: July 17, 2015 at 10:37 Last Updated: July 17, 2015 at 10:37 |
PW000973View Pathway |
The Citric Acid Cycle Tutorial (2) Pt.1 - Adding ReactionsHomo sapiens
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Creator: Guest: Anonymous Created On: July 14, 2015 at 11:57 Last Updated: July 14, 2015 at 11:57 |
PW000982View Pathway |
The Citric Acid Cycle Tutorial (2) Pt.2 - Adding MembranesHomo sapiens
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Creator: Guest: Anonymous Created On: July 16, 2015 at 11:53 Last Updated: July 16, 2015 at 11:53 |
PW122260View Pathway |
The MEP/DOXP pathway of PaenibacillusBacteria
Terpenoids, also known as isoprenoids, are a large class of natural products consisting of isoprene (C5) units. There are two biosynthetic pathways, the mevalonate pathway [MD:M00095] and the non-mevalonate pathway or the MEP/DOXP pathway [MD:M00096], for the terpenoid building blocks: isopentenyl diphosphate (IPP) and dimethylallyl diphosphate (DMAPP). The action of prenyltransferases then generates higher-order building blocks: geranyl diphosphate (GPP), farsenyl diphosphate (FPP), and geranylgeranyl diphosphate (GGPP), which are the precursors of monoterpenoids (C10), sesquiterpenoids (C15), and diterpenoids (C20), respectively. Condensation of these building blocks gives rise to the precursors of sterols (C30) and carotenoids (C40). The MEP/DOXP pathway is absent in higher animals and fungi, but in green plants the MEP/DOXP and mevalonate pathways co-exist in separate cellular compartments. The MEP/DOXP pathway, operating in the plastids, is responsible for the formation of essential oil monoterpenes and linalyl acetate, some sesquiterpenes, diterpenes, and carotenoids and phytol. The mevalonate pathway, operating in the cytosol, gives rise to triterpenes, sterols, and most sesquiterpenes.
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Creator: Ng Ngashangva Created On: October 18, 2018 at 02:56 Last Updated: October 18, 2018 at 02:56 |
PW002359View Pathway |
disease
The Oncogenic Action of 2-HydroxyglutarateHomo sapiens
2-Hydroxyglutarate is a compound formed from isocitric acid, a component of the TCA cycle. Isocitric acid becomes dehydrogenated by isocitrate dehydrogenase using NADP as a cofactor, and forming oxoglutaric acid. Oxoglutaric acid then forms 2-hydroxyglutarate in a reaction catalyzed by a mutant isocitrate dehydrogenase 2 enzyme, which also uses NADP as a cofactor. Normally, the isocitrate dehydrogenase 2 enzyme, encoded by the IDH2 gene, is responsible for the formation of 2-oxoglutaric acid from isocitrate. However, some gain-of-functions mutations to the IDH2 gene allow the enzyme to produce 2-hydroxyglutarate instead. This functionality is associated with several types of cancer, including glioma and acute myeloid leukemia. This is due to the buildup of 2-hydroxyglutarate, which inhibits several enzymes which rely on 2-oxoglutaric acid, such as methylcytosine dioxygenase and lysine-specific demethylase 2A. Both of these enzymes use 2-oxoglutarate to demethylate DNA, and when repressed, allow DNA to become hypermethylated. This in turn changes which genes are normally expressed, as methylation is used to suppress genes, and can lead to the expression of oncogenes or the repression of tumor-suppressing genes. This is the effect responsible for 2-hydroxyglutarate in cancer and other diseases.
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Creator: miguel ramirez Created On: November 16, 2015 at 11:41 Last Updated: November 16, 2015 at 11:41 |
PW109800View Pathway |
disease
The Oncogenic Action of 2-HydroxyglutarateMus musculus
2-Hydroxyglutarate is a compound formed from isocitric acid, a component of the TCA cycle. Isocitric acid becomes dehydrogenated by isocitrate dehydrogenase using NADP as a cofactor, and forming oxoglutaric acid. Oxoglutaric acid then forms 2-hydroxyglutarate in a reaction catalyzed by a mutant isocitrate dehydrogenase 2 enzyme, which also uses NADP as a cofactor. Normally, the isocitrate dehydrogenase 2 enzyme, encoded by the IDH2 gene, is responsible for the formation of 2-oxoglutaric acid from isocitrate. However, some gain-of-functions mutations to the IDH2 gene allow the enzyme to produce 2-hydroxyglutarate instead. This functionality is associated with several types of cancer, including glioma and acute myeloid leukemia. This is due to the buildup of 2-hydroxyglutarate, which inhibits several enzymes which rely on 2-oxoglutaric acid, such as methylcytosine dioxygenase and lysine-specific demethylase 2A. Both of these enzymes use 2-oxoglutarate to demethylate DNA, and when repressed, allow DNA to become hypermethylated. This in turn changes which genes are normally expressed, as methylation is used to suppress genes, and can lead to the expression of oncogenes or the repression of tumor-suppressing genes. This is the effect responsible for 2-hydroxyglutarate in cancer and other diseases.
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Creator: Ana Marcu Created On: August 31, 2018 at 15:50 Last Updated: August 31, 2018 at 15:50 |
PW109814View Pathway |
disease
The Oncogenic Action of 2-HydroxyglutarateRattus norvegicus
2-Hydroxyglutarate is a compound formed from isocitric acid, a component of the TCA cycle. Isocitric acid becomes dehydrogenated by isocitrate dehydrogenase using NADP as a cofactor, and forming oxoglutaric acid. Oxoglutaric acid then forms 2-hydroxyglutarate in a reaction catalyzed by a mutant isocitrate dehydrogenase 2 enzyme, which also uses NADP as a cofactor. Normally, the isocitrate dehydrogenase 2 enzyme, encoded by the IDH2 gene, is responsible for the formation of 2-oxoglutaric acid from isocitrate. However, some gain-of-functions mutations to the IDH2 gene allow the enzyme to produce 2-hydroxyglutarate instead. This functionality is associated with several types of cancer, including glioma and acute myeloid leukemia. This is due to the buildup of 2-hydroxyglutarate, which inhibits several enzymes which rely on 2-oxoglutaric acid, such as methylcytosine dioxygenase and lysine-specific demethylase 2A. Both of these enzymes use 2-oxoglutarate to demethylate DNA, and when repressed, allow DNA to become hypermethylated. This in turn changes which genes are normally expressed, as methylation is used to suppress genes, and can lead to the expression of oncogenes or the repression of tumor-suppressing genes. This is the effect responsible for 2-hydroxyglutarate in cancer and other diseases.
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Creator: Ana Marcu Created On: August 31, 2018 at 15:53 Last Updated: August 31, 2018 at 15:53 |