PathWhiz ID | Pathway | Meta Data |
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PW122269View Pathway |
physiological
charlieHomo sapiens
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Creator: Guest: Anonymous Created On: October 27, 2018 at 13:13 Last Updated: October 27, 2018 at 13:13 |
PW145785View Pathway |
drug action
Chenodeoxycholic acid Drug Metabolism Action PathwayHomo sapiens
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Creator: Ray Kruger Created On: October 07, 2023 at 16:39 Last Updated: October 07, 2023 at 16:39 |
PW121715View Pathway |
disease
CHILD SyndromeMus musculus
CHILD Syndrome, (Congenital Hemidysplasia with Icthyosiform Erythroderma and Limb Defects; Ichthyosiform Eruthroderma, Unilateral, with Epsilateral Malformations, Especially Absence Deformity of Limbs) is caused by a mutation in the gene encoding NADH steroid dehydrogenase-like protein (NSDHL). A defect in sterol-4 alpha-carboxylate 3-dehydrogenase, which normally catalyzes the reaction 3-beta-hydroxy-4-beta-methyl-5-alpha-cholest-7-ene-4-alpha-carboxylate + NAD+ = 4-alpha-methyl-5-alpha-cholest-7-en-3-one + CO2 + NADH, causes accumulation of 8(9)cholestenol and 8-dehydrocholesterol in plasma. Symptoms of CHILD syndrome include hearing defects, hemidysplasia, unilateral hypomelia, ichthyosiform nevi, limb abnormalities, lung hypoplasia, and punctate calcifications.
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Creator: Ana Marcu Created On: September 10, 2018 at 15:49 Last Updated: September 10, 2018 at 15:49 |
PW127201View Pathway |
disease
CHILD SyndromeHomo sapiens
CHILD Syndrome, (Congenital Hemidysplasia with Icthyosiform Erythroderma and Limb Defects; Ichthyosiform Eruthroderma, Unilateral, with Epsilateral Malformations, Especially Absence Deformity of Limbs) is caused by a mutation in the gene encoding NADH steroid dehydrogenase-like protein (NSDHL). A defect in sterol-4 alpha-carboxylate 3-dehydrogenase, which normally catalyzes the reaction 3-beta-hydroxy-4-beta-methyl-5-alpha-cholest-7-ene-4-alpha-carboxylate + NAD+ = 4-alpha-methyl-5-alpha-cholest-7-en-3-one + CO2 + NADH, causes accumulation of 8(9)cholestenol and 8-dehydrocholesterol in plasma. Symptoms of CHILD syndrome include hearing defects, hemidysplasia, unilateral hypomelia, ichthyosiform nevi, limb abnormalities, lung hypoplasia, and punctate calcifications.
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Creator: Ray Kruger Created On: November 08, 2022 at 08:57 Last Updated: November 08, 2022 at 08:57 |
PW121940View Pathway |
disease
CHILD SyndromeRattus norvegicus
CHILD Syndrome, (Congenital Hemidysplasia with Icthyosiform Erythroderma and Limb Defects; Ichthyosiform Eruthroderma, Unilateral, with Epsilateral Malformations, Especially Absence Deformity of Limbs) is caused by a mutation in the gene encoding NADH steroid dehydrogenase-like protein (NSDHL). A defect in sterol-4 alpha-carboxylate 3-dehydrogenase, which normally catalyzes the reaction 3-beta-hydroxy-4-beta-methyl-5-alpha-cholest-7-ene-4-alpha-carboxylate + NAD+ = 4-alpha-methyl-5-alpha-cholest-7-en-3-one + CO2 + NADH, causes accumulation of 8(9)cholestenol and 8-dehydrocholesterol in plasma. Symptoms of CHILD syndrome include hearing defects, hemidysplasia, unilateral hypomelia, ichthyosiform nevi, limb abnormalities, lung hypoplasia, and punctate calcifications.
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Creator: Ana Marcu Created On: September 10, 2018 at 15:51 Last Updated: September 10, 2018 at 15:51 |
PW000096View Pathway |
disease
CHILD SyndromeHomo sapiens
CHILD Syndrome, (Congenital Hemidysplasia with Icthyosiform Erythroderma and Limb Defects; Ichthyosiform Eruthroderma, Unilateral, with Epsilateral Malformations, Especially Absence Deformity of Limbs) is caused by a mutation in the gene encoding NADH steroid dehydrogenase-like protein (NSDHL). A defect in sterol-4 alpha-carboxylate 3-dehydrogenase, which normally catalyzes the reaction 3-beta-hydroxy-4-beta-methyl-5-alpha-cholest-7-ene-4-alpha-carboxylate + NAD+ = 4-alpha-methyl-5-alpha-cholest-7-en-3-one + CO2 + NADH, causes accumulation of 8(9)cholestenol and 8-dehydrocholesterol in plasma. Symptoms of CHILD syndrome include hearing defects, hemidysplasia, unilateral hypomelia, ichthyosiform nevi, limb abnormalities, lung hypoplasia, and punctate calcifications.
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Creator: WishartLab Created On: August 01, 2013 at 15:52 Last Updated: August 01, 2013 at 15:52 |
PW095688View Pathway |
Chitin BiosynthesisDrosophila melanogaster
Chitin is a linear homopolymer of N-acetyl-β-D-glucosamine residues linked by β-1,4 glycosidic bonds to form microfibrils. These become the structural component to cell walls and many extracellular matrices such as cuticles and exoskeleton of insects. This process is highly conserved and occurs in many different organisms including insects and fungi. Chitin exist in several crystaline forms termed α, β and γ chitin, the most abundant being α chitin (reviewed in [Merzendorfer11]). Chitin and lipids are secreted by epidermal cells and form the basis for the cuticle material and layered structure.
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Creator: Chelsea Hong Created On: August 18, 2018 at 13:23 Last Updated: August 18, 2018 at 13:23 |
PW122516View Pathway |
Chitin DigestionClostridium taeniosporum
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Creator: Sizhe Qiu Created On: May 26, 2019 at 16:49 Last Updated: May 26, 2019 at 16:49 |
PW002042View Pathway |
Chitobiose DegradationEscherichia coli
Diacetylchitobiose (also known as N,N'-diacetylchitobiose and chitobiose) is a sole source of carbon for E.coli. PTS system mannitol-specific EIICBA component facilitates the imports of diacetylchitobiose as well as the phosphorylation to diacetylchitobiose 6'-phosphate. Later on, diacetylchitobiose 6'-phosphate is hydrolyzed to N-monoacetylchitobiose 6'-phosphate, which also produce acetic acid. N-monoacetylchitobiose 6'-phosphate undergoes further hydrolyzation to form N-Acetyl-D-Glucosamine 6-Phosphate and glucosamine by monoacetylchitobiose-6-phosphate hydrolase.
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Creator: Ana Marcu Created On: October 07, 2015 at 15:17 Last Updated: October 07, 2015 at 15:17 |
PW147038View Pathway |
Chlophedianol Drug Metabolism PathwayHomo sapiens
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Creator: Ray Kruger Created On: October 10, 2023 at 13:42 Last Updated: October 10, 2023 at 13:42 |