PathWhiz ID | Pathway | Meta Data |
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PW123577View Pathway |
signaling
ahaHomo sapiens
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Creator: Guest: Anonymous Created On: August 16, 2019 at 01:17 Last Updated: August 16, 2019 at 01:17 |
PW064763View Pathway |
protein
Ahr Signal Transduction PathwayHomo sapiens
The aryl hydrocarbon receptor, known as AHR, is a normally cytosolic transcription factor that can bind to foreign compounds such as flavonoids and indoles from foods, as well as synthetic ligands including polychlorobiphenyls (PCBs) and polychlorinated dibenzo-p-dioxins (PCDD). This includes 2,3,7,8-tetrachlorodibenzodioxin (TCDD), which is the ligand shown in this pathway.
AHR interacts with heat shock protein 90 (HSP90AA1), which acts as a chaperone for it. After this association, the ligand, in this case TCDD, can form a covalent bond with the complex in the cell's cytoplasm. This binding causes AHR and the rest of the complex to translocate into the nucleus of the cell. Once in the nucleus, the heat shock protein dissociates, leaving binding sites which the AHR nuclear translocator (ARNT) then binds to. Finally, the AHR/ARNT complex can interact, either directly or indirectly, with the DNA, in this case specifically a dioxin response element. With other ligands, the complex will bind to the equivalent DNA that corresponds to the genes that allow metabolism of the ligand.
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Creator: Hasan Badran Created On: June 13, 2018 at 14:06 Last Updated: June 13, 2018 at 14:06 |
PW109196View Pathway |
protein
Ahr Signal Transduction PathwayMus musculus
The aryl hydrocarbon receptor, known as AHR, is a normally cytosolic transcription factor that can bind to foreign compounds such as flavonoids and indoles from foods, as well as synthetic ligands including polychlorobiphenyls (PCBs) and polychlorinated dibenzo-p-dioxins (PCDD). This includes 2,3,7,8-tetrachlorodibenzodioxin (TCDD), which is the ligand shown in this pathway.
AHR interacts with heat shock protein 90 (HSP90AA1), which acts as a chaperone for it. After this association, the ligand, in this case TCDD, can form a covalent bond with the complex in the cell's cytoplasm. This binding causes AHR and the rest of the complex to translocate into the nucleus of the cell. Once in the nucleus, the heat shock protein dissociates, leaving binding sites which the AHR nuclear translocator (ARNT) then binds to. Finally, the AHR/ARNT complex can interact, either directly or indirectly, with the DNA, in this case specifically a dioxin response element. With other ligands, the complex will bind to the equivalent DNA that corresponds to the genes that allow metabolism of the ligand.
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Creator: Ana Marcu Created On: August 31, 2018 at 12:31 Last Updated: August 31, 2018 at 12:31 |
PW109244View Pathway |
protein
Ahr Signal Transduction PathwayBos taurus
The aryl hydrocarbon receptor, known as AHR, is a normally cytosolic transcription factor that can bind to foreign compounds such as flavonoids and indoles from foods, as well as synthetic ligands including polychlorobiphenyls (PCBs) and polychlorinated dibenzo-p-dioxins (PCDD). This includes 2,3,7,8-tetrachlorodibenzodioxin (TCDD), which is the ligand shown in this pathway.
AHR interacts with heat shock protein 90 (HSP90AA1), which acts as a chaperone for it. After this association, the ligand, in this case TCDD, can form a covalent bond with the complex in the cell's cytoplasm. This binding causes AHR and the rest of the complex to translocate into the nucleus of the cell. Once in the nucleus, the heat shock protein dissociates, leaving binding sites which the AHR nuclear translocator (ARNT) then binds to. Finally, the AHR/ARNT complex can interact, either directly or indirectly, with the DNA, in this case specifically a dioxin response element. With other ligands, the complex will bind to the equivalent DNA that corresponds to the genes that allow metabolism of the ligand.
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Creator: Ana Marcu Created On: August 31, 2018 at 12:40 Last Updated: August 31, 2018 at 12:40 |
PW109275View Pathway |
protein
Ahr Signal Transduction PathwayRattus norvegicus
The aryl hydrocarbon receptor, known as AHR, is a normally cytosolic transcription factor that can bind to foreign compounds such as flavonoids and indoles from foods, as well as synthetic ligands including polychlorobiphenyls (PCBs) and polychlorinated dibenzo-p-dioxins (PCDD). This includes 2,3,7,8-tetrachlorodibenzodioxin (TCDD), which is the ligand shown in this pathway.
AHR interacts with heat shock protein 90 (HSP90AA1), which acts as a chaperone for it. After this association, the ligand, in this case TCDD, can form a covalent bond with the complex in the cell's cytoplasm. This binding causes AHR and the rest of the complex to translocate into the nucleus of the cell. Once in the nucleus, the heat shock protein dissociates, leaving binding sites which the AHR nuclear translocator (ARNT) then binds to. Finally, the AHR/ARNT complex can interact, either directly or indirectly, with the DNA, in this case specifically a dioxin response element. With other ligands, the complex will bind to the equivalent DNA that corresponds to the genes that allow metabolism of the ligand.
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Creator: Ana Marcu Created On: August 31, 2018 at 12:48 Last Updated: August 31, 2018 at 12:48 |
PW121703View Pathway |
disease
AICA-RibosiduriaMus musculus
AICA-ribosiduria is a metabolic disease caused by a defect in final steps of purine de novo biosynthesis. This defect is caused by a mutation in the ATIC which codes for bifunctional purine biosynthesis protein PURH. A deficiency in this enzyme results in accumulation of 5-aminoimidazole-4-carboxamide in urine. Symptoms include mental retardation, epilepsy, dysmorphic features, and congenital blindness.
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Creator: Ana Marcu Created On: September 10, 2018 at 15:49 Last Updated: September 10, 2018 at 15:49 |
PW121929View Pathway |
disease
AICA-RibosiduriaRattus norvegicus
AICA-ribosiduria is a metabolic disease caused by a defect in final steps of purine de novo biosynthesis. This defect is caused by a mutation in the ATIC which codes for bifunctional purine biosynthesis protein PURH. A deficiency in this enzyme results in accumulation of 5-aminoimidazole-4-carboxamide in urine. Symptoms include mental retardation, epilepsy, dysmorphic features, and congenital blindness.
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Creator: Ana Marcu Created On: September 10, 2018 at 15:51 Last Updated: September 10, 2018 at 15:51 |
PW000082View Pathway |
disease
AICA-RibosiduriaHomo sapiens
AICA-ribosiduria is a metabolic disease caused by a defect in final steps of purine de novo biosynthesis. This defect is caused by a mutation in the ATIC which codes for bifunctional purine biosynthesis protein PURH. A deficiency in this enzyme results in accumulation of 5-aminoimidazole-4-carboxamide in urine. Symptoms include mental retardation, epilepsy, dysmorphic features, and congenital blindness.
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Creator: WishartLab Created On: August 01, 2013 at 15:52 Last Updated: August 01, 2013 at 15:52 |
PW127297View Pathway |
disease
AICA-RibosiduriaHomo sapiens
AICA-ribosiduria is a metabolic disease caused by a defect in final steps of purine de novo biosynthesis. This defect is caused by a mutation in the ATIC which codes for bifunctional purine biosynthesis protein PURH. A deficiency in this enzyme results in accumulation of 5-aminoimidazole-4-carboxamide in urine. Symptoms include mental retardation, epilepsy, dysmorphic features, and congenital blindness.
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Creator: Ray Kruger Created On: December 02, 2022 at 15:31 Last Updated: December 02, 2022 at 15:31 |
PW127860View Pathway |
drug action
Ajmaline Action PathwayHomo sapiens
Ajmaline is an antiarrhythmic used to manage a variety of forms of tachycardias. It can be found under the brand names Gilurytmal, Ritmos, and Aritmina. An alkaloid found in the root of Rauwolfia serpentina, among other plant sources. It is a class Ia antiarrhythmic agent that apparently acts by changing the shape and threshold of cardiac action potentials. Ajmaline produces potent sodium channel blocking effects and a very short half-life which makes it a very useful drug for acute intravenous treatments. The drug has been very popular in some countries for the treatment of atrial fibrillation in patients with the Wolff–Parkinson–White syndrome and in well tolerated monomorphic ventricular tachycardias. It has also been used for many years as a drug to challenge the conduction system of the heart in cases of bundle branch block and syncope. In these cases, abnormal prolongation of the HV interval has been taken as a proof for infrahisian conduction defects tributary for permanent pacemaker implantation. The class I antiarrhythmic agents interfere with the sodium channel. A class IA agent lengthens the action potential (right shift) which brings about improvement in abnormal heart rhythms. This drug in particular has a high affinity for the Nav 1.5 sodium channel. Some side effects of using ajmaline may include warm flushes, tingling skin, vertigo, and eye twitches.
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Creator: Hayley Created On: June 12, 2023 at 08:41 Last Updated: June 12, 2023 at 08:41 |