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Showing 51 - 60 of 605359 pathways
SMPDB ID Pathway Name and Description Pathway Class Chemical Compounds Proteins

SMP0125672

Pw127237 View Pathway

3-Methylglutaconic Aciduria Type IV

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.
Disease

SMP0000679

Pw000656 View Pathway

3-Methylthiofentanyl Action Pathway

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.
Drug Action

SMP0125012

Pw126542 View Pathway

3-Methylthiofentanyl Opioid Agonist Action Pathway

3-Methyl-thiofentanyl is a fentanyl analog and an opioid analgesic that works by inducing central nervous system (CNS) depression. 3-Methylthiofentanyl binds to the mu, delta, and kappa opioid receptors. These ultimately lead to decreased pain sensation as well as a number of side effects, such as euphoria, sedation, depressed breathing. In neurons, 3-methyl-thiofentanyl binds to mu opioid receptors, stimulating the exchange of GTP for GDP on the G-protein complex. As the effector system is adenylate cyclase and cAMP located at the inner surface of the plasma membrane, opioids decrease intracellular cAMP by inhibiting adenylate cyclase. Subsequently, the release of nociceptive neurotransmitters such as GABA is inhibited. Opioids close N-type voltage-operated calcium channels (OP2-receptor agonist) and open calcium-dependent inwardly rectifying potassium channels (OP3 and OP1 receptor agonist). This results in hyperpolarization and reduced neuronal excitability. 3-Methyl-thiofentanyl acts at A delta and C pain fibres in the dorsal horn of the spinal cord. By decreasing neurotransmitter action there is less pain transmittance into the spinal cord. This leads to less pain perception.
Drug Action

SMP0000721

Pw000698 View Pathway

3-Phosphoglycerate Dehydrogenase Deficiency

3-Phosphoglycerate dehydrogenase deficiency is a disorder of L-serine biosynthesis that is characterized by congenital microcephaly, psychomotor retardation, and seizures.The disorder is caused by homozygous or compound heterozygous or homozygous mutation in the gene encoding phosphoglycerate dehydrogenase on chromosome 1p12. Defects in the gene lead to a decrease of Glycine and Serine.
Disease

SMP0125581

Pw127145 View Pathway

3-Phosphoglycerate Dehydrogenase Deficiency

3-Phosphoglycerate dehydrogenase deficiency is a disorder of L-serine biosynthesis that is characterized by congenital microcephaly, psychomotor retardation, and seizures.The disorder is caused by homozygous or compound heterozygous or homozygous mutation in the gene encoding phosphoglycerate dehydrogenase on chromosome 1p12. Defects in the gene lead to a decrease of Glycine and Serine.
Disease

SMP0145123

Pw146791 View Pathway

4-(Isopropylamino)diphenylamine Drug Metabolism Action Pathway

Drug Action
  • 4-(Isopropylamino)diphenylamine

SMP0145315

Pw146983 View Pathway

4-Aminohippuric acid Drug Metabolism Pathway

Metabolic

SMP0145354

Pw147022 View Pathway

4-Hydroxybutyric acid Drug Metabolism Pathway

Metabolic

SMP0125784

Pw127351 View Pathway

4-Hydroxybutyric Aciduria/Succinic Semialdehyde Dehydrogenase Deficiency

4-Hydroxybutyric Aciduria/Succinic Semialdehyde Dehydrogenase Deficiency (SSADH; Gamma-hydroxybutyric acidemia) inhibits the formation of succinate from GABA. This deficiency results in urinary excretion of 4-hydroxybutyric acid. In vivo proton MR also indicates elevated GABA levels as compared with an age-matched control. Symptoms include ataxia, chorea or athetosis, motor retardation, seizures, macrocephaly and delayed or abnormal speech development.
Disease

SMP0000243

Pw000070 View Pathway

4-Hydroxybutyric Aciduria/Succinic Semialdehyde Dehydrogenase Deficiency

4-Hydroxybutyric Aciduria/Succinic Semialdehyde Dehydrogenase Deficiency (SSADH; Gamma-hydroxybutyric acidemia) inhibits the formation of succinate from GABA. This deficiency results in urinary excretion of 4-hydroxybutyric acid. In vivo proton MR also indicates elevated GABA levels as compared with an age-matched control. Symptoms include ataxia, chorea or athetosis, motor retardation, seizures, macrocephaly and delayed or abnormal speech development.
Disease
Showing 51 - 60 of 65005 pathways