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Pathways

PathWhiz ID Pathway Meta Data

PW013090

Pw013090 View Pathway
metabolic

TG Test

Arabidopsis thaliana
In higher plants, the primary seed storage reserve is triacylglycerol rather than carbohydrates. Thus, triacylglycerol degradation is an important pathway from which plants obtain energy for growth. First, triacylglycerol lipase, an enzyme localized to the oil body (storage vacuole) membrane, catalyzes the conversion of a triglyceride into a 1,2-diglyceride. Second, the predicted enzyme diglyceride lipase (coloured orange in the image) is theorized to catalyze the conversion of a 1,2-diglyceride iinto a 2-acylglycerol. Third, a 2-acylglycerol is spontaneously converted into a 1-monoglyceride. Fourth, acylhydrolase catalyzes the conversion of a 1-monoglyceride into glycerol. Fifth, glycerol kinase catalyzes the conversion of glycerol into glycerol 3-phosphate. Sixth, glycerol-3-phosphate dehydrogenase (coloured dark green in the image), localized to the mitochondrial inner membrane, catalyzes the conversion of glycerol 3-phosphate into glycerone phosphate.

PW123678

Pw123678 View Pathway
metabolic

TG Test

Saccharomyces cerevisiae
A triglyceride (TG, triacylglycerol, TAG, or triacylglyceride) is an ester derived from glycerol and three fatty acids. The biosynthesis of triacylglycerol is localized to the endoplasmic reticulum membrane and starts with glycerol 3-phosphate reacting with acyl-CoA through a glycerol-3-phosphate O-acyltransferase resulting in the release of lysophosphatidic acid (LPA). This, in turn, reacts with an acyl-CoA through a lipase complex resulting in the release of CoA and phosphatidic acid. Phosphatidic acid reacts with water through a phosphatidic acid phosphohydrolase 1 resulting in the release of a phosphate and a diacylglycerol. This reaction can be reversed through a CTP-dependent diacylglycerol kinase. The diacylglycerol reacts in the endoplasmic reticulum with an acyl-CoA through a diacylglycerol O-acyltransferase resulting in the release of coenzyme A and a triacylglycerol. Triacylglycerol metabolism begins with a reaction with water through lipase resulting in the release of a fatty acid, hydrogen ion, and a diacylglycerol. Diacylglycerol then reacts with a lipase 3 resulting in the release of a fatty acid and a monoacylglycerol. Monoacylglycerol reacts with monoglyceride lipase resulting in the release of a fatty acid in glycerol.

PW092100

Pw092100 View Pathway
signaling

TGF-Beta and Cav1

Mus musculus

PW002525

Pw002525 View Pathway
disease

TGFB

Homo sapiens

PW002362

Pw002362 View Pathway
signaling

TGFbcoreandaltered

Homo sapiens

PW145135

Pw145135 View Pathway
drug action

Thalidomide Drug Metabolism Action Pathway

Homo sapiens

PW176528

Pw176528 View Pathway
metabolic

Thalidomide Predicted Metabolism Pathway

Homo sapiens
Metabolites of Thalidomide are predicted with biotransformer.

PW146083

Pw146083 View Pathway
drug action

Thallous chloride Drug Metabolism Action Pathway

Homo sapiens

PW146963

Pw146963 View Pathway
drug action

Thallous chloride Tl-201 Drug Metabolism Action Pathway

Homo sapiens

PW124119

Pw124119 View Pathway
signaling

THC on CB1

Homo 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.