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Pathways

PathWhiz ID Pathway Meta Data

PW000656

Pw000656 View Pathway
drug action

3-Methylthiofentanyl Action Pathway

Homo sapiens
Methadyl Acetate (also known as Acetylmethadol) is analgesic that can bind to mu-type opioid receptor to activate associated G-protein in the sensory neurons of central nervous system (CNS), which will reduce the level of intracellular cAMP by inhibiting adenylate cyclase. The binding of methadyl acetate will eventually lead to reduced pain because of decreased nerve conduction and release of neurotransmitter. Hyperpolarization of neuron is caused by inactivation of calcium channels and activation of potassium channels via facilitated by G-protein.

PW121695

Pw121695 View Pathway
disease

3-Methylglutaconic Aciduria Type IV

Mus musculus
3-Methylglutaconic Aciduria Type IV, also called MGA, Type IV and MGA4, is a rare inborn error of metabolism (IEM) and autosomal recessive disorder and caused by a defective methylglutaconyl-CoA hydratase. Methylglutaconyl-CoA hydratase catalyzes the conversion of 3-Methylglutaconyl-CoA into 3-Hydroxy-3-methylglutaryl-CoA which is the substrate of hydroxymethylglutaryl-CoA lyase. This disorder is characterized by increased urinary excretion of 3-methylglutaconic acid. Symptoms of the disorder include poor growth and neurological degression. Currently, there is no effective treatment for 3-MGA type IV.

PW000214

Pw000214 View Pathway
disease

3-Methylglutaconic Aciduria Type IV

Homo sapiens
3-Methylglutaconic Aciduria Type IV, also called MGA, Type IV and MGA4, is a rare inborn error of metabolism (IEM) and autosomal recessive disorder and caused by a defective methylglutaconyl-CoA hydratase. Methylglutaconyl-CoA hydratase catalyzes the conversion of 3-Methylglutaconyl-CoA into 3-Hydroxy-3-methylglutaryl-CoA which is the substrate of hydroxymethylglutaryl-CoA lyase. This disorder is characterized by increased urinary excretion of 3-methylglutaconic acid. Symptoms of the disorder include poor growth and neurological degression. Currently, there is no effective treatment for 3-MGA type IV.

PW127237

Pw127237 View Pathway
disease

3-Methylglutaconic Aciduria Type IV

Homo sapiens
3-Methylglutaconic Aciduria Type IV, also called MGA, Type IV and MGA4, is a rare inborn error of metabolism (IEM) and autosomal recessive disorder and caused by a defective methylglutaconyl-CoA hydratase. Methylglutaconyl-CoA hydratase catalyzes the conversion of 3-Methylglutaconyl-CoA into 3-Hydroxy-3-methylglutaryl-CoA which is the substrate of hydroxymethylglutaryl-CoA lyase. This disorder is characterized by increased urinary excretion of 3-methylglutaconic acid. Symptoms of the disorder include poor growth and neurological degression. Currently, there is no effective treatment for 3-MGA type IV.

PW121921

Pw121921 View Pathway
disease

3-Methylglutaconic Aciduria Type IV

Rattus norvegicus
3-Methylglutaconic Aciduria Type IV, also called MGA, Type IV and MGA4, is a rare inborn error of metabolism (IEM) and autosomal recessive disorder and caused by a defective methylglutaconyl-CoA hydratase. Methylglutaconyl-CoA hydratase catalyzes the conversion of 3-Methylglutaconyl-CoA into 3-Hydroxy-3-methylglutaryl-CoA which is the substrate of hydroxymethylglutaryl-CoA lyase. This disorder is characterized by increased urinary excretion of 3-methylglutaconic acid. Symptoms of the disorder include poor growth and neurological degression. Currently, there is no effective treatment for 3-MGA type IV.

PW121694

Pw121694 View Pathway
disease

3-Methylglutaconic Aciduria Type III

Mus musculus
3-Methylglutaconic aciduria type 3 (Costeff syndrome; Optic atrophy plus syndrome) is an autosomal recessive disease caused by a deficiency in the OPA3 code which does for optic atrophy 3 protein. A deficiency of this enzyme results in accumulation of 3-methylglutaconic acid and methylglutaric acid. Symptoms include ataxia, dysarthria, optic atrophy, and neurological deterioration.

PW000067

Pw000067 View Pathway
disease

3-Methylglutaconic Aciduria Type III

Homo sapiens
3-Methylglutaconic aciduria type 3 (Costeff syndrome; Optic atrophy plus syndrome) is an autosomal recessive disease caused by a deficiency in the OPA3 code which does for optic atrophy 3 protein. A deficiency of this enzyme results in accumulation of 3-methylglutaconic acid and methylglutaric acid. Symptoms include ataxia, dysarthria, optic atrophy, and neurological deterioration.

PW127232

Pw127232 View Pathway
disease

3-Methylglutaconic Aciduria Type III

Homo sapiens
3-Methylglutaconic aciduria type 3 (Costeff syndrome; Optic atrophy plus syndrome) is an autosomal recessive disease caused by a deficiency in the OPA3 code which does for optic atrophy 3 protein. A deficiency of this enzyme results in accumulation of 3-methylglutaconic acid and methylglutaric acid. Symptoms include ataxia, dysarthria, optic atrophy, and neurological deterioration.

PW121920

Pw121920 View Pathway
disease

3-Methylglutaconic Aciduria Type III

Rattus norvegicus
3-Methylglutaconic aciduria type 3 (Costeff syndrome; Optic atrophy plus syndrome) is an autosomal recessive disease caused by a deficiency in the OPA3 code which does for optic atrophy 3 protein. A deficiency of this enzyme results in accumulation of 3-methylglutaconic acid and methylglutaric acid. Symptoms include ataxia, dysarthria, optic atrophy, and neurological deterioration.

PW000066

Pw000066 View Pathway
disease

3-Methylglutaconic Aciduria Type I

Homo sapiens
3-Methylglutaconic aciduria type 1 (3-Methylglutaconicaciduria; Aciduria, 3-methylglutaconic type I) is an autosomal recessive disease caused by a mutation in the AUH gene which codes for methylglutaconyl-CoA hydratase. A deficiency in this enzyme results in accumulation of 3-hydroxyisovaleric acid, 3-methylglutaconic acid, and methylglutaric acid in urine. Symptoms include hypoglycemia, low birth weight, coma, seizures, and mental retardation. Treatment includes a low protein diet.