PathWhiz ID | Pathway | Meta Data |
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PW128620View Pathway |
drug action
Nomifensine Dopamine Reuptake Inhibitor Action PathwayHomo sapiens
Nomifensine, formerly known as Merital capsules, is a dopamine reuptake inhibitor drug that was removed from the market in 1986 for increased incidence of hemolytic anemia. The drug was originally used to treat depression. Nomifensine stimulates the nervous system through the reuptake of norepinephrine and dopamine, which prolongs their duration in the synapse so that they can bind more readily to the receptors. The mechanism is not fully understood, but may be similar to other dopamine reuptake inhibitors where Nomifensine would cross the blood-brain barrier through diffusion. Dopamine is synthesized in the ventral tegmental area of the brain from tyrosine being synthesized into L-dopa by the enzyme Tyrosine 3-monooxygenase . L-Dopa is then synthesized into dopamine with the enzyme aromatic-L-amino-acid decarboxylase. Dopamine then travels to the prefrontal cortex, which is released into the synapse when the neuron is stimulated and fires. Nomifensine binds to the sodium-dependent dopamine transporter, preventing dopamine from re-entering the presynaptic neuron. The dopamine then binds to Dopamine D4 receptors on the postsynaptic membrane. The dopamine D4 receptor activates the Gi protein cascade which inhibits adenylate cyclase. This prevents adenylate cyclase from catalyzing ATP into cAMP.
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Creator: Ashley Zubkowski Created On: September 06, 2023 at 17:01 Last Updated: September 06, 2023 at 17:01 |
PW147062View Pathway |
Nomifensine Drug Metabolism PathwayHomo sapiens
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Creator: Ray Kruger Created On: October 10, 2023 at 13:52 Last Updated: October 10, 2023 at 13:52 |
PW122015View Pathway |
disease
Non-Ketotic HyperglycinemiaRattus norvegicus
Non Ketotic Hyperglycinemeia (Glycine encephalopathy; Glycine cleavage system deficiency; NKH) is caused by mutations in several genes in the mitochondrial glycine cleavage system. These include the genes encoding P protein (GLDC), T protein (GCST), and, in one case, the H protein (GCSH). Most patients with GCE (Glycine Encephalopathy, or NKH) have a defect in the GLDC gene.The enzyme system for cleavage of glycine (glycine cleavage system), which is confined to the mitochondria, is composed of 4 protein components: P protein (a pyridoxal phosphate-dependent glycine decarboxylase), H protein (a lipoic acid-containing protein), T protein (a tetrahydrofolate-requiring enzyme), and L protein (a lipoamide dehydrogenase). NKH is characterized by accumulation of glycine in plasma, spinal fluid and urine. Symptoms include seizures, respiratory distress, mental retardation, chorea, visual impairment and hydrocephalus.
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Creator: Ana Marcu Created On: September 10, 2018 at 15:51 Last Updated: September 10, 2018 at 15:51 |
PW121790View Pathway |
disease
Non-Ketotic HyperglycinemiaMus musculus
Non Ketotic Hyperglycinemeia (Glycine encephalopathy; Glycine cleavage system deficiency; NKH) is caused by mutations in several genes in the mitochondrial glycine cleavage system. These include the genes encoding P protein (GLDC), T protein (GCST), and, in one case, the H protein (GCSH). Most patients with GCE (Glycine Encephalopathy, or NKH) have a defect in the GLDC gene.The enzyme system for cleavage of glycine (glycine cleavage system), which is confined to the mitochondria, is composed of 4 protein components: P protein (a pyridoxal phosphate-dependent glycine decarboxylase), H protein (a lipoic acid-containing protein), T protein (a tetrahydrofolate-requiring enzyme), and L protein (a lipoamide dehydrogenase). NKH is characterized by accumulation of glycine in plasma, spinal fluid and urine. Symptoms include seizures, respiratory distress, mental retardation, chorea, visual impairment and hydrocephalus.
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Creator: Ana Marcu Created On: September 10, 2018 at 15:49 Last Updated: September 10, 2018 at 15:49 |
PW127144View Pathway |
disease
Non-Ketotic HyperglycinemiaHomo sapiens
Non Ketotic Hyperglycinemeia (Glycine encephalopathy; Glycine cleavage system deficiency; NKH) is caused by mutations in several genes in the mitochondrial glycine cleavage system. These include the genes encoding P protein (GLDC), T protein (GCST), and, in one case, the H protein (GCSH). Most patients with GCE (Glycine Encephalopathy, or NKH) have a defect in the GLDC gene.The enzyme system for cleavage of glycine (glycine cleavage system), which is confined to the mitochondria, is composed of 4 protein components: P protein (a pyridoxal phosphate-dependent glycine decarboxylase), H protein (a lipoic acid-containing protein), T protein (a tetrahydrofolate-requiring enzyme), and L protein (a lipoamide dehydrogenase). NKH is characterized by accumulation of glycine in plasma, spinal fluid and urine. Symptoms include seizures, respiratory distress, mental retardation, chorea, visual impairment and hydrocephalus.
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Creator: Ray Kruger Created On: October 24, 2022 at 17:23 Last Updated: October 24, 2022 at 17:23 |
PW000209View Pathway |
disease
Non-Ketotic HyperglycinemiaHomo sapiens
Non Ketotic Hyperglycinemeia (Glycine encephalopathy; Glycine cleavage system deficiency; NKH) is caused by mutations in several genes in the mitochondrial glycine cleavage system. These include the genes encoding P protein (GLDC), T protein (GCST), and, in one case, the H protein (GCSH). Most patients with GCE (Glycine Encephalopathy, or NKH) have a defect in the GLDC gene.The enzyme system for cleavage of glycine (glycine cleavage system), which is confined to the mitochondria, is composed of 4 protein components: P protein (a pyridoxal phosphate-dependent glycine decarboxylase), H protein (a lipoic acid-containing protein), T protein (a tetrahydrofolate-requiring enzyme), and L protein (a lipoamide dehydrogenase). NKH is characterized by accumulation of glycine in plasma, spinal fluid and urine. Symptoms include seizures, respiratory distress, mental retardation, chorea, visual impairment and hydrocephalus.
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Creator: WishartLab Created On: August 19, 2013 at 12:05 Last Updated: August 19, 2013 at 12:05 |
PW145808View Pathway |
drug action
Nonoxynol-9 Drug Metabolism Action PathwayHomo sapiens
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Creator: Ray Kruger Created On: October 07, 2023 at 16:42 Last Updated: October 07, 2023 at 16:42 |
PW128139View Pathway |
drug action
Norelgestromin Action PathwayHomo sapiens
Norelgestromin is a synthetic progestational hormone indicated in women to prevent pregnancy. This drug is also used in menopausal hormonal therapy. This drug is administered as a contraceptive pill or as a transdermal patch. This drug is also available in combination with ethinyl estradiol as a vaginal ring. Norelgestromin acts on the hypothalamic–pituitary–gonadal axis (HPG axis) where it binds to the progesterone receptor. This binding inhibits the release of gonadotropin-releasing hormone (GnRH) from the hypothalamus. GnRH secretion is required to activate a luteinizing hormone (LH) surge that leads to ovulation. By its inhibition, the absence of LH results in no release of a viable egg from the ovaries. The thickening of the mucus interferes with sperm migration into the uterus for fertilization.
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Creator: Daphnee Created On: July 21, 2023 at 14:46 Last Updated: July 21, 2023 at 14:46 |
PW132526View Pathway |
Norelgestromin Drug MetabolismHomo sapiens
Norelgestromin is a drug that is not metabolized by the human body as determined by current research and biotransformer analysis. Norelgestromin passes through the liver and is then excreted from the body mainly through the kidney.
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Creator: Ray Kruger Created On: September 21, 2023 at 22:16 Last Updated: September 21, 2023 at 22:16 |
PW145754View Pathway |
drug action
Norelgestromin Drug Metabolism Action PathwayHomo sapiens
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Creator: Ray Kruger Created On: October 07, 2023 at 16:34 Last Updated: October 07, 2023 at 16:34 |