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Pathways

PathWhiz ID Pathway Meta Data

PW000519

Pw000519 View Pathway
disease

Methylenetetrahydrofolate Reductase Deficiency (MTHFRD)

Homo sapiens
Methylenetetrahydrofolate reductase deficiency (MTHFRD; Homocystinuria due to defect of n(5,10)-methylene THF deficiency) is caused by a defect in the MTHFR gene which codes for methylenetetrahydrofolate reductase. Methylenetetrahydrofolate reductase catalyzes the conversion of 5,10-methylenetetrahydrofolate to 5-methyltetrahydrofolate, a co-substrate for homocysteine remethylation to methionine. A defect in this enzyme results in accumulation of homocysteine and methionine in both plasma and urine. Some of the symptoms and signs include mental retardation, withdrawal, hallucinations, delusions, muscle weakness. Some patients remain asymptomatic until adulthood.

PW127247

Pw127247 View Pathway
disease

Methylenetetrahydrofolate Reductase Deficiency (MTHFRD)

Homo sapiens
Methylenetetrahydrofolate reductase deficiency (MTHFRD; Homocystinuria due to defect of n(5,10)-methylene THF deficiency) is caused by a defect in the MTHFR gene which codes for methylenetetrahydrofolate reductase. Methylenetetrahydrofolate reductase catalyzes the conversion of 5,10-methylenetetrahydrofolate to 5-methyltetrahydrofolate, a co-substrate for homocysteine remethylation to methionine. A defect in this enzyme results in accumulation of homocysteine and methionine in both plasma and urine. Some of the symptoms and signs include mental retardation, withdrawal, hallucinations, delusions, muscle weakness. Some patients remain asymptomatic until adulthood.

PW000104

Pw000104 View Pathway
disease

Methylenetetrahydrofolate Reductase Deficiency (MTHFRD)

Homo sapiens
Methylenetetrahydrofolate reductase deficiency (MTHFRD; Homocystinuria due to defect of n(5,10)-methylene THF deficiency) is caused by a defect in the MTHFR gene which codes for methylenetetrahydrofolate reductase. Methylenetetrahydrofolate reductase catalyzes the conversion of 5,10-methylenetetrahydrofolate to 5-methyltetrahydrofolate, a co-substrate for homocysteine remethylation to methionine. A defect in this enzyme results in accumulation of homocysteine and methionine in both plasma and urine. Some of the symptoms and signs include mental retardation, withdrawal, hallucinations, delusions, muscle weakness. Some patients remain asymptomatic until adulthood.

PW128112

Pw128112 View Pathway
drug action

Methylergometrine Mechanism of Action Action Pathway

Homo sapiens
Methylergometrine is a semisynthetic ergot alkaloid and a derivative of ergonovine. It is also known as methylergonovine. Methylergometrine acts directly on the smooth muscle of the uterus and increases the tone, rate, and amplitude of rhythmic contractions through binding and the resultant antagonism of the dopamine D1 receptor. Thus, it induces a rapid and sustained tetanic uterotonic effect which shortens the third stage of labor and reduces blood loss. It is used for the prevention and control of postpartum and post-abortion hemorrhage. In general, the effects of all the ergot alkaloids appear to results from their actions as partial agonists or antagonists at adrenergic, dopaminergic, and tryptaminergic receptors. The spectrum of effects depends on the agent, dosage, species, tissue, and experimental or physiological conditions. All of the alkaloids of ergot significantly increase the motor activity of the uterus. After small doses contractions are increased in force or frequency, or both, but are followed by a normal degree of relaxation. As the dose is increased, contractions become more forceful and prolonged, resting tonus is markedly increased, and sustained contracture can result.

PW176340

Pw176340 View Pathway
metabolic

Methylergometrine Predicted Metabolism Pathway

Homo sapiens
Metabolites of sildenafil are predicted with biotransformer.

PW146985

Pw146985 View Pathway
metabolic

Methylergonovine Drug Metabolism Pathway

Homo sapiens

PW341680

Pw341680 View Pathway
metabolic

Methylglyoxal Degradation I

Veillonella dispar ATCC 17748
The degradation of methylglyoxal starts with methylglyoxal being degraded by interacting with glutathione and a glyoxalase resulting in the release of a (R)-S-lactoylglutatione. This compound in turn reacts with a water molecule through a glyoxalase II resulting in the releas of glutathione, a hydrogen ion and an R-lactate. The R-lactate in turn reacts with an ubiquinone through a D-lactate dehydrogenase resulting in the release of an ubiquinol and a pyruvate which can then be incorporated the pyruvate metabolism

PW355819

Pw355819 View Pathway
metabolic

Methylglyoxal Degradation I

Escherichia coli O157:H7 str. EC4115
The degradation of methylglyoxal starts with methylglyoxal being degraded by interacting with glutathione and a glyoxalase resulting in the release of a (R)-S-lactoylglutatione. This compound in turn reacts with a water molecule through a glyoxalase II resulting in the releas of glutathione, a hydrogen ion and an R-lactate. The R-lactate in turn reacts with an ubiquinone through a D-lactate dehydrogenase resulting in the release of an ubiquinol and a pyruvate which can then be incorporated the pyruvate metabolism

PW355833

Pw355833 View Pathway
metabolic

Methylglyoxal Degradation I

Escherichia coli O55:H7 str. CB9615
The degradation of methylglyoxal starts with methylglyoxal being degraded by interacting with glutathione and a glyoxalase resulting in the release of a (R)-S-lactoylglutatione. This compound in turn reacts with a water molecule through a glyoxalase II resulting in the releas of glutathione, a hydrogen ion and an R-lactate. The R-lactate in turn reacts with an ubiquinone through a D-lactate dehydrogenase resulting in the release of an ubiquinol and a pyruvate which can then be incorporated the pyruvate metabolism

PW355814

Pw355814 View Pathway
metabolic

Methylglyoxal Degradation I

Escherichia coli APEC O1
The degradation of methylglyoxal starts with methylglyoxal being degraded by interacting with glutathione and a glyoxalase resulting in the release of a (R)-S-lactoylglutatione. This compound in turn reacts with a water molecule through a glyoxalase II resulting in the releas of glutathione, a hydrogen ion and an R-lactate. The R-lactate in turn reacts with an ubiquinone through a D-lactate dehydrogenase resulting in the release of an ubiquinol and a pyruvate which can then be incorporated the pyruvate metabolism