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Pathways

PathWhiz ID Pathway Meta Data

PW145851

Pw145851 View Pathway
drug action

Tauroursodeoxycholic acid Drug Metabolism Action Pathway

Homo sapiens

PW127415

Pw127415 View Pathway
drug action

Tavaborole Action Pathway

Homo sapiens
Tavaborole is an antifungal agent used to treat onychomycosis, a fungal infection of the nail and nail bed due to Trichophyton rubrum or Trichophyton mentagrophytes infection. Tavaborole functions by inhibiting Leucyl-tRNA synthetase, or LeuRS, an essential fungal enzyme required for protein synthesis and for the catalysis of ATP-dependent ligation of L-leucine to tRNA(Leu). This blocks the protein synthesis in the fungal cell which leads to cell degradation and death.

PW132330

Pw132330 View Pathway
metabolic

Tavaborole Drug Metabolism

Homo sapiens
Tavaborole is a drug that is not metabolized by the human body as determined by current research and biotransformer analysis. Tavaborole passes through the liver and is then excreted from the body mainly through the kidney.

PW145933

Pw145933 View Pathway
drug action

Tavaborole Drug Metabolism Action Pathway

Homo sapiens

PW127282

Pw127282 View Pathway
disease

Tay-Sachs Disease

Homo sapiens
Tay-Sachs Disease (TSD; GM2-Gangliosidosis, type I; B-Variant GM2-Gangliosidosis; Hexosaminidase A Deficiency; HEXA Deficiency; Tay-Sachs Disease Variant B1), is an autosomal recessive lysosomal storage disease. TSD is caused by a mutation in the alpha subunit of the hexosaminidase A gene (HEXA), which codes for the enzyme hexosaminidase A. HEXA degrades GM2 gangliosides and other molecules with terminal N-acetyl hexosamines in the brain and other tissues. A defect in this enzyme causes accumulation of oligosaccharides in urine. The most lethal variant of this disease is the classical infantile Tay-Sachs disease, in which children exhibit developmental retardation, dementia and blindness, finally ending in death by the second or third years. Tay-Sachs disease also has debilitating juvenile and adult forms. The majority of cases of TSD are found among (but not limited to) the Ashkenazi Jews and French Canadians in Eastern Quebec. Symptoms include ataxia, visual impairment and loss, cherry-red spot on retinal macula, dystosis multiplex, mental retardation, myoclonus, encephalopathy and psychosis.

PW000215

Pw000215 View Pathway
disease

Tay-Sachs Disease

Homo sapiens
Tay-Sachs Disease (TSD; GM2-Gangliosidosis, type I; B-Variant GM2-Gangliosidosis; Hexosaminidase A Deficiency; HEXA Deficiency; Tay-Sachs Disease Variant B1), is an autosomal recessive lysosomal storage disease. TSD is caused by a mutation in the alpha subunit of the hexosaminidase A gene (HEXA), which codes for the enzyme hexosaminidase A. HEXA degrades GM2 gangliosides and other molecules with terminal N-acetyl hexosamines in the brain and other tissues. A defect in this enzyme causes accumulation of oligosaccharides in urine. The most lethal variant of this disease is the classical infantile Tay-Sachs disease, in which children exhibit developmental retardation, dementia and blindness, finally ending in death by the second or third years. Tay-Sachs disease also has debilitating juvenile and adult forms. The majority of cases of TSD are found among (but not limited to) the Ashkenazi Jews and French Canadians in Eastern Quebec. Symptoms include ataxia, visual impairment and loss, cherry-red spot on retinal macula, dystosis multiplex, mental retardation, myoclonus, encephalopathy and psychosis.

PW121801

Pw121801 View Pathway
disease

Tay-Sachs Disease

Mus musculus
Tay-Sachs Disease (TSD; GM2-Gangliosidosis, type I; B-Variant GM2-Gangliosidosis; Hexosaminidase A Deficiency; HEXA Deficiency; Tay-Sachs Disease Variant B1), is an autosomal recessive lysosomal storage disease. TSD is caused by a mutation in the alpha subunit of the hexosaminidase A gene (HEXA), which codes for the enzyme hexosaminidase A. HEXA degrades GM2 gangliosides and other molecules with terminal N-acetyl hexosamines in the brain and other tissues. A defect in this enzyme causes accumulation of oligosaccharides in urine. The most lethal variant of this disease is the classical infantile Tay-Sachs disease, in which children exhibit developmental retardation, dementia and blindness, finally ending in death by the second or third years. Tay-Sachs disease also has debilitating juvenile and adult forms. The majority of cases of TSD are found among (but not limited to) the Ashkenazi Jews and French Canadians in Eastern Quebec. Symptoms include ataxia, visual impairment and loss, cherry-red spot on retinal macula, dystosis multiplex, mental retardation, myoclonus, encephalopathy and psychosis.

PW122026

Pw122026 View Pathway
disease

Tay-Sachs Disease

Rattus norvegicus
Tay-Sachs Disease (TSD; GM2-Gangliosidosis, type I; B-Variant GM2-Gangliosidosis; Hexosaminidase A Deficiency; HEXA Deficiency; Tay-Sachs Disease Variant B1), is an autosomal recessive lysosomal storage disease. TSD is caused by a mutation in the alpha subunit of the hexosaminidase A gene (HEXA), which codes for the enzyme hexosaminidase A. HEXA degrades GM2 gangliosides and other molecules with terminal N-acetyl hexosamines in the brain and other tissues. A defect in this enzyme causes accumulation of oligosaccharides in urine. The most lethal variant of this disease is the classical infantile Tay-Sachs disease, in which children exhibit developmental retardation, dementia and blindness, finally ending in death by the second or third years. Tay-Sachs disease also has debilitating juvenile and adult forms. The majority of cases of TSD are found among (but not limited to) the Ashkenazi Jews and French Canadians in Eastern Quebec. Symptoms include ataxia, visual impairment and loss, cherry-red spot on retinal macula, dystosis multiplex, mental retardation, myoclonus, encephalopathy and psychosis.

PW144906

Pw144906 View Pathway
drug action

Tazarotene Drug Metabolism Action Pathway

Homo sapiens

PW146565

Pw146565 View Pathway
drug action

Tazemetostat Drug Metabolism Action Pathway

Homo sapiens