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4,4-dimethyl-5alpha-cholesta-8,14,24-trien-3beta-ol + NADPH
4,4-dimethyl-5alpha-cholesta-8,14-dien-3beta-ol + NADP+
-
-
-
?
4,4-dimethyl-5alpha-cholesta-8,24-dien-3beta-ol + NADPH
4,4-dimethyl-5alpha-cholesta-8-en-3beta-ol + NADP+
-
-
-
?
5alpha-cholesta-7,24-dien-3beta-ol + NADPH
5alpha-cholest-7-en-3beta-ol + NADP+
-
-
-
?
7-dehydrodesmosterol + NADPH
7-dehydrocholesterol + NADP+
-
-
-
?
cholesta-5,24-dien-3beta-ol + NADPH + H+
cholest-5-en-3beta-ol + NADP+
desmosterol + FADH2
cholesterol + FAD + H+
-
-
-
?
lanosterol + NADPH + H+
24-dihydrolanosterol + NADP+
-
-
-
?
zymosterol + NADPH
5alpha-cholesta-8-en-3beta-ol + NADP+
-
-
-
?
5alpha-cholest-7-en-3beta-ol + NADP+
5alpha-cholesta-7,24-dien-3beta-ol + NADPH + H+
-
-
-
-
?
5alpha-cholesta-7,24-dien-3beta-ol + NADPH
5alpha-cholest-7-en-3beta-ol + NADP+
cholesta-5,7,24-trien-3beta-ol + NADPH
cholest-5,7-dien-3beta-ol + NADP+
cholesta-5,7,24-trien-3beta-ol + NADPH + H+
7-dehydrocholesterol + NADP+
-
-
-
-
?
cholesta-7,24-dien-3beta-ol + NADPH + H+
lathosterol + NADP+
-
-
-
-
?
desmosterol + NADPH
cholesterol + NADP+
desmosterol + NADPH + H+
cholesterol + NADP+
-
-
-
-
?
lanosterol + NADPH
24-dihydrolanosterol + NADP+
lanosterol + NADPH
4,4,14alpha-trimethyl-5alpha-cholesta-8-en-3beta-ol + NADP+
-
4,4',14alpha-trimethyl-5alpha-cholesta-8,24-dien-3beta-ol
-
-
?
lanosterol + NADPH + H+
4,4,14alpha-trimethyl-5alpha-cholesta-8-en-3beta-ol + NADP+
-
-
-
-
?
zymosterol + NADPH
5alpha-cholesta-8-en-3beta-ol + NADP+
-
-
-
-
?
zymosterol + NADPH + H+
zymostenol + NADP+
-
-
-
-
?
additional information
?
-
cholesta-5,24-dien-3beta-ol + NADPH + H+
cholest-5-en-3beta-ol + NADP+
-
-
-
?
cholesta-5,24-dien-3beta-ol + NADPH + H+
cholest-5-en-3beta-ol + NADP+
-
-
-
-
?
cholesta-5,24-dien-3beta-ol + NADPH + H+
cholest-5-en-3beta-ol + NADP+
-
-
-
?
cholesta-5,24-dien-3beta-ol + NADPH + H+
cholest-5-en-3beta-ol + NADP+
reduction of desmosterol to cholesterol is dependent on FAD
-
-
?
cholesta-5,24-dien-3beta-ol + NADPH + H+
cholest-5-en-3beta-ol + NADP+
-
reduction of desmosterol to cholesterol is dependent on FAD
-
-
?
5alpha-cholesta-7,24-dien-3beta-ol + NADPH
5alpha-cholest-7-en-3beta-ol + NADP+
-
-
-
-
?
5alpha-cholesta-7,24-dien-3beta-ol + NADPH
5alpha-cholest-7-en-3beta-ol + NADP+
-
best substrate
i.e.lathosterol
-
?
5alpha-cholesta-7,24-dien-3beta-ol + NADPH
5alpha-cholest-7-en-3beta-ol + NADP+
-
2 major alternate routes for cholesterol biosynthesis, step in the biosynthesis of cholesterol from lanosterol
-
-
?
5alpha-cholesta-7,24-dien-3beta-ol + NADPH
5alpha-cholest-7-en-3beta-ol + NADP+
-
step in the biosynthesis of cholesterol from lanosterol
-
-
?
cholesta-5,7,24-trien-3beta-ol + NADPH
cholest-5,7-dien-3beta-ol + NADP+
-
-
-
-
?
cholesta-5,7,24-trien-3beta-ol + NADPH
cholest-5,7-dien-3beta-ol + NADP+
-
step in the biosynthesis of cholesterol from desmosterol
-
-
?
cholesta-5,7,24-trien-3beta-ol + NADPH
cholest-5,7-dien-3beta-ol + NADP+
-
step in the biosynthesis of cholesterol from lanosterol
-
-
?
desmosterol + NADPH
cholesterol + NADP+
-
-
-
-
?
desmosterol + NADPH
cholesterol + NADP+
-
5alpha-cholesta-5,24-dien-3beta-ol
-
-
?
desmosterol + NADPH
cholesterol + NADP+
-
step in the biosynthesis of cholesterol from lanosterol
-
-
?
lanosterol + NADPH
24-dihydrolanosterol + NADP+
-
-
-
-
?
lanosterol + NADPH
24-dihydrolanosterol + NADP+
-
step in the biosynthesis of cholesterol from lanosterol
-
-
?
additional information
?
-
-
catalyzes reduction of DELTA24 double bond
-
-
?
additional information
?
-
-
reduction of DELTA24 double bond is one of the necessary reactions during cholesterol synthesis
-
-
?
additional information
?
-
-
cholesterogenic enzyme
-
-
?
additional information
?
-
-
important enzyme in the 19-step pathway of cholesterol biosynthesis from lanosterol
-
-
?
additional information
?
-
-
enzyme deficiency due to mutation cause desmosterolosis, an autosomal recessive disorder of cholesterol biosynthesis, patients show elevated levels of cholesterol precursor desmosterol in plasma and tissue
-
-
?
Please wait a moment until the data is sorted. This message will disappear when the data is sorted.
cholesta-5,24-dien-3beta-ol + NADPH + H+
cholest-5-en-3beta-ol + NADP+
5alpha-cholest-7-en-3beta-ol + NADP+
5alpha-cholesta-7,24-dien-3beta-ol + NADPH + H+
-
-
-
-
?
5alpha-cholesta-7,24-dien-3beta-ol + NADPH
5alpha-cholest-7-en-3beta-ol + NADP+
cholesta-5,7,24-trien-3beta-ol + NADPH
cholest-5,7-dien-3beta-ol + NADP+
cholesta-5,7,24-trien-3beta-ol + NADPH + H+
7-dehydrocholesterol + NADP+
-
-
-
-
?
cholesta-7,24-dien-3beta-ol + NADPH + H+
lathosterol + NADP+
-
-
-
-
?
desmosterol + NADPH
cholesterol + NADP+
desmosterol + NADPH + H+
cholesterol + NADP+
-
-
-
-
?
lanosterol + NADPH
24-dihydrolanosterol + NADP+
-
step in the biosynthesis of cholesterol from lanosterol
-
-
?
lanosterol + NADPH + H+
4,4,14alpha-trimethyl-5alpha-cholesta-8-en-3beta-ol + NADP+
-
-
-
-
?
zymosterol + NADPH + H+
zymostenol + NADP+
-
-
-
-
?
additional information
?
-
cholesta-5,24-dien-3beta-ol + NADPH + H+
cholest-5-en-3beta-ol + NADP+
-
-
-
?
cholesta-5,24-dien-3beta-ol + NADPH + H+
cholest-5-en-3beta-ol + NADP+
-
-
-
-
?
cholesta-5,24-dien-3beta-ol + NADPH + H+
cholest-5-en-3beta-ol + NADP+
-
-
-
?
cholesta-5,24-dien-3beta-ol + NADPH + H+
cholest-5-en-3beta-ol + NADP+
reduction of desmosterol to cholesterol is dependent on FAD
-
-
?
cholesta-5,24-dien-3beta-ol + NADPH + H+
cholest-5-en-3beta-ol + NADP+
-
reduction of desmosterol to cholesterol is dependent on FAD
-
-
?
5alpha-cholesta-7,24-dien-3beta-ol + NADPH
5alpha-cholest-7-en-3beta-ol + NADP+
-
2 major alternate routes for cholesterol biosynthesis, step in the biosynthesis of cholesterol from lanosterol
-
-
?
5alpha-cholesta-7,24-dien-3beta-ol + NADPH
5alpha-cholest-7-en-3beta-ol + NADP+
-
step in the biosynthesis of cholesterol from lanosterol
-
-
?
cholesta-5,7,24-trien-3beta-ol + NADPH
cholest-5,7-dien-3beta-ol + NADP+
-
step in the biosynthesis of cholesterol from desmosterol
-
-
?
cholesta-5,7,24-trien-3beta-ol + NADPH
cholest-5,7-dien-3beta-ol + NADP+
-
step in the biosynthesis of cholesterol from lanosterol
-
-
?
desmosterol + NADPH
cholesterol + NADP+
-
5alpha-cholesta-5,24-dien-3beta-ol
-
-
?
desmosterol + NADPH
cholesterol + NADP+
-
step in the biosynthesis of cholesterol from lanosterol
-
-
?
additional information
?
-
-
reduction of DELTA24 double bond is one of the necessary reactions during cholesterol synthesis
-
-
?
additional information
?
-
-
cholesterogenic enzyme
-
-
?
additional information
?
-
-
important enzyme in the 19-step pathway of cholesterol biosynthesis from lanosterol
-
-
?
additional information
?
-
-
enzyme deficiency due to mutation cause desmosterolosis, an autosomal recessive disorder of cholesterol biosynthesis, patients show elevated levels of cholesterol precursor desmosterol in plasma and tissue
-
-
?
Please wait a moment until the data is sorted. This message will disappear when the data is sorted.
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brassicasterol
competitive
U18666A
an inhibitor of DHCR24 activity, prevents ACTH-induced translocation of the enzyme to the nucleus in adrenal cells but not in prostate cancer cells
(1R,3aR,5aS,7S,9aS,9bR,11aR)-9a,11a-dimethyl-1-[(2R,3E)-4-phenylbut-3-en-2-yl]-2,3,3a,5,5a,6,7,8,9,9a,9b,10,11,11a-tetradecahydro-1H-cyclopenta[a]phenanthren-7-ol
-
-
-
(1R,3aR,5aS,7S,9aS,9bR,11aR)-9a,11a-dimethyl-1-[(2S)-1-oxopropan-2-yl]-2,3,3a,5,5a,6,7,8,9,9a,9b,10,11,11a-tetradecahydro-1H-cyclopenta[a]phenanthren-7-yl acetate
-
-
-
(20S)-pregn-5-ene-3,20-diol
-
-
-
(2S)-2-((3S,5S,10S,13R,17R)-3-hydroxy-10,13-dimethyl-2,3,4,5,6,9,10,11,12,13,14,15,16,17-tetradecahydro-1H-cyclopenta[a]phenanthren-17-yl)-N-methylpropanamide
-
1 microM, 58% inhibition of total cholesterol production. Acts both on sterol reductoase and lathosterol oxidase
(2S)-2-((3S,5S,10S,13R,17R)-3-hydroxy-10,13-dimethyl-2,3,4,5,6,9,10,11,12,13,14,15,16,17-tetradecahydro-1H-cyclopenta[a]phenanthren-17-yl)-N-propylpropanamide
-
1 microM, 45% inhibition of total cholesterol production. Acts both on sterol reductoase and lathosterol oxidase
(2S)-2-((3S,5S,10S,13R,17R)-3-hydroxy-10,13-dimethyl-2,3,4,5,6,9,10,11,12,13,14,15,16,17-tetradecahydro-1H-cyclopenta[a]phenanthren-17-yl)propanamide
-
1 microM, 75% inhibition of total cholesterol production
(2S)-2-[(1R,3aR,5aS,7S,9aS,9bR,11aR)-7-(acetyloxy)-9a,11a-dimethyl-2,3,3a,5,5a,6,7,8,9,9a,9b,10,11,11a-tetradecahydro-1H-cyclopenta[a]phenanthren-1-yl]propanoic acid
-
-
-
(2S)-2-[(1R,3aR,5aS,7S,9aS,9bR,11aR)-7-hydroxy-9a,11a-dimethyl-2,3,3a,5,5a,6,7,8,9,9a,9b,10,11,11a-tetradecahydro-1H-cyclopenta[a]phenanthren-1-yl]-N-methylpropanamide
-
-
-
(2S)-N-ethyl-2-((3S,5S,10S,13R,17R)-3-hydroxy-10,13-dimethyl-2,3,4,5,6,9,10,11,12,13,14,15,16,17-tetradecahydro-1H-cyclopenta[a]phenanthren-17-yl)propanamide
-
1 microM, 61% inhibition of total cholesterol production
(3S,20S)-20-(aminomethyl)-pregn-7-en-3-yl acetate
-
-
-
(3S,20S)-20-(ethoxyaminocarbonyl)-pregn-7-en-3-yl acetate
-
-
-
(3S,20S)-20-(hydroxycarbamoyl)-pregn-7-en-3-yl acetate
-
-
-
(3S,20S)-20-(hydroxymethyl)-pregn-7-en-3-ol
-
-
-
(3S,20S)-20-(methoxyaminocarbonyl)-pregn-7-en-3-ylacetate
-
-
-
(3S,20S)-20-(methyl-carbamoyl)-pregn-7-en-3beta-ol
-
i.e. MGI-21
-
(3S,20S)-20-(N,N-dimethylaminocarbonyl)-pregn-7-en-3-yl acetate
-
-
-
(3S,20S)-20-[((E)-2-methylbut-2-enoyloxy)methyl]-pregn-7-en-3-yl acetate
-
-
-
(3S,20S)-20-[((E)-but-2-enoyloxy)methyl]-pregn-7-en-3-yl acetate
-
-
-
(3S,20S)-20-[(butanoylamino)methyl]-pregn-7-en-3-ylacetate
-
-
-
(3S,20S)-20-[(dimethylamino)acetoxymethyl]-pregn-7-en-3-yl acetate
-
-
-
(3S,20S)-20-[(formyloxy)methyl]-pregn-7-en-3-yl acetate
-
-
-
(3S,20S)-20-[(N-methyl-N-butanoylamino)methyl]-pregn-7-en-3-yl acetate
-
-
-
(3S,20S)-20-[(N-methyl-N-propanoylamino)methyl]-pregn-7-en-3-yl acetate
-
-
-
(3S,20S)-20-[(propanylamino)methyl]-pregn-7-en-3-yl acetate
-
-
-
(3S,20S)-20-[N-methyl-N-(2-methylpropyl)-aminocarbonyl]-pregn-7-en-3-yl acetate
-
-
-
(3S,5S,10S,13R,17R)-10,13-dimethyl-17-((S)-1-(methylamino)-1-oxopropan-2-yl)-2,3,4,5,6,9,10,11,12,13,14,15,16,17-tetradecahydro-1H-cyclopenta[a]phenanthren-3-yl acetate
-
1 microM, 84% inhibition of total cholesterol production. Acts both on sterol reductoase and lathosterol oxidase
(3S,5S,10S,13R,17R)-10,13-dimethyl-17-((S)-1-oxo-1-(propylamino)propan-2-yl)-2,3,4,5,6,9,10,11,12,13,14,15,16,17-tetradecahydro-1H-cyclopenta[a]phenanthren-3-yl acetate
-
1 microM, 71% inhibition of total cholesterol production. Acts both on sterol reductoase and lathosterol oxidase
(3S,5S,10S,13R,17R)-17-((S)-1-(ethylamino)-1-oxopropan-2-yl)-10,13-dimethyl-2,3,4,5,6,9,10,11,12,13,14,15,16,17-tetradecahydro-1H-cyclopenta[a]phenanthren-3-yl acetate
-
1 microM, 97% inhibition of total cholesterol production
(3S,5S,10S,13R,17R)-17-((S)-1-amino-1-oxopropan-2-yl)-10,13-dimethyl-2,3,4,5,6,9,10,11,12,13,14,15,16,17-tetradecahydro-1H-cyclopenta[a]phenanthren-3-yl acetate
-
1 microM, 94% inhibition of total cholesterol production
(7S,9aR,11aS)-1-[(2S)-1-hydroxypropan-2-yl]-9a,11a-dimethyl-2,3,3a,3b,4,6,7,8,9,9a,9b,10,11,11a-tetradecahydro-1H-cyclopenta[a]phenanthren-7-ol
-
-
-
(7S,9aS,11aR)-1-[(2S)-1-hydroxypropan-2-yl]-9a,11a-dimethyl-2,3,3a,5,5a,6,7,8,9,9a,9b,10,11,11a-tetradecahydro-1H-cyclopenta[a]phenanthren-7-yl acetate
-
-
-
24(S),25-epoxycholesterol
-
incubation with 24(S),25-epoxycholesterol results in accumulation of desmosterol at the expense of cholesterol, consistent with inhibition of DHCR24 activity
3-beta-(2-(diethylamino)ethoxy)androst-5-en-17-one
-
-
3beta-[2-(diethylamino)ethoxy]androst-5-en-17-one
-
i.e. U18666A
4-[(E)-2-((3S,20R)-3-hydroxypregn-7-en-20-yl)-ethenyl]-1-methylpyridinium iodide
-
i.e. DR 258
-
5,22-cholestedien-3beta-ol
-
desmosterol isomer, competitive inhibition
6-(6-aminohexyl)-5-chloronaphthalene-1-sulfonamide
-
brassicasterol
-
DELTA22-unsaturated phytosterol, competitive inhibition
ergosterol
-
DELTA22-unsaturated phytosterol, competitive inhibition
N,N-dimethyl-3beta-hydroxy-cholenamide
-
-
-
N,N-dimethyl-3beta-hydroxycholenamide
-
-
-
N-(6-aminohexyl)-5-chloro-1-naphthalene sulfonamide
-
W-7, specific, dose-dependent inhibition
stigmasterol
-
DELTA22-unsaturated phytosterol, competitive inhibition
Trifluoperazine
-
specific, dose-dependent inhibition
6-(6-aminohexyl)-5-chloronaphthalene-1-sulfonamide
-
-
-
6-(6-aminohexyl)-5-chloronaphthalene-1-sulfonamide
-
i.e. W-7
-
Calmodulin antagonists
-
specific, dose-dependent inhibition
-
Calmodulin antagonists
-
calmodulin antagonists inhibit reduction of DELTA24 double bond
-
Triparanol
-
-
Triparanol
-
1-[p-(beta-diethylaminoethoxy)-phenyl]-1-(p-tolyl)-2-(p-chlorophenyl)-ethanol, MER 29
additional information
inhibitors of protein kinase C ablate DHCR24 activity, although not through a known phosphorylation site T110. PKC inhibitors, BIM and Ro-318220, reduce cholesterol levels and accumulate desmosterol within 4 h, indicating decreased DHCR24 activity
-
additional information
-
inhibitors of protein kinase C ablate DHCR24 activity, although not through a known phosphorylation site T110. PKC inhibitors, BIM and Ro-318220, reduce cholesterol levels and accumulate desmosterol within 4 h, indicating decreased DHCR24 activity
-
additional information
no feedback inhibition by cholesterol. C-22 unsaturated sterols (phytosterols stigmasterol, brassicasterol, and the yeast sterol ergosterol) competitively inhibit DHCR24 enzyme activity, with no inhibition observed by phytosterols with a saturated side chain (beta-sitosterol and campesterol)
-
additional information
-
no feedback inhibition by cholesterol. C-22 unsaturated sterols (phytosterols stigmasterol, brassicasterol, and the yeast sterol ergosterol) competitively inhibit DHCR24 enzyme activity, with no inhibition observed by phytosterols with a saturated side chain (beta-sitosterol and campesterol)
-
additional information
-
inhibition mechanism of DELTA22-unsaturated phytosterols
-
Please wait a moment until the data is sorted. This message will disappear when the data is sorted.
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Adenoma
Expression of the antiapoptotic gene seladin-1 and octreotide-induced apoptosis in growth hormone-secreting and nonfunctioning pituitary adenomas.
Adrenal Gland Neoplasms
Seladin-1 expression is regulated by promoter methylation in adrenal cancer.
Adrenocortical Adenoma
Seladin-1/DHCR24 expression in normal ovary, ovarian epithelial and granulosa tumours.
Adrenocortical Adenoma
The human homolog of Diminuto/Dwarf1 gene (hDiminuto): a novel ACTH-responsive gene overexpressed in benign cortisol-producing adrenocortical adenomas.
Alzheimer Disease
Alzheimer's disease: brain desmosterol levels.
Alzheimer Disease
Androgen receptor regulation of the seladin-1/DHCR24 gene: altered expression in prostate cancer.
Alzheimer Disease
Aromatase/Seladin-1 Interactions in Human Neuronal Cell Culture, the Hippocampus of Healthy Rats and Transgenic Alzheimer's Disease Mice.
Alzheimer Disease
DHCR24 exerts neuroprotection upon inflammation-induced neuronal death.
Alzheimer Disease
DHCR24 overexpression modulates microglia polarization and inflammatory response via Akt/GSK3? signaling in A?25-35 treated BV-2 cells.
Alzheimer Disease
Down-regulation of seladin-1 increases bace1 levels and activity through enhanced GGA3 depletion during apoptosis.
Alzheimer Disease
Effect of hesperetin against oxidative stress via ER- and TrkA-mediated actions in PC12 cells.
Alzheimer Disease
Estrogen receptor-mediated neuroprotection: The role of the Alzheimer's disease-related gene seladin-1.
Alzheimer Disease
Expression of the antiapoptotic gene seladin-1 and octreotide-induced apoptosis in growth hormone-secreting and nonfunctioning pituitary adenomas.
Alzheimer Disease
Gender dependent effect of DHCR24 polymorphism on the risk for Alzheimer's disease.
Alzheimer Disease
Genetic regulatory subnetworks and key regulating genes in rat hippocampus perturbed by prenatal malnutrition: implications for major brain disorders.
Alzheimer Disease
Heme oxygenase effect on mesenchymal stem cells action on experimental Alzheimer's disease.
Alzheimer Disease
Hippocampal DHCR24 down regulation in a rat model of streptozotocin-induced cognitive decline.
Alzheimer Disease
Identification and analysis of the promoter region of the human DHCR24 gene: involvement of DNA methylation and histone acetylation.
Alzheimer Disease
Interactions of Aromatase and Seladin-1: A Neurosteroidogenic and Gender Perspective.
Alzheimer Disease
Intermittent high glucose concentrations reduce neuronal precursor survival by altering the IGF system: the involvement of the neuroprotective factor DHCR24 (Seladin-1).
Alzheimer Disease
Is Seladin-1 Really a Selective Alzheimer's Disease Indicator?
Alzheimer Disease
Membrane cholesterol as a mediator of the neuroprotective effects of estrogens.
Alzheimer Disease
Neuronal differentiation of human mesenchymal stem cells: changes in the expression of the Alzheimer's disease-related gene seladin-1.
Alzheimer Disease
Neuronal differentiation of rat hair follicle stem cells: the involvement of the neuroprotective factor Seladin-1 (DHCR24).
Alzheimer Disease
Neuroprotective effects of estrogens: the role of cholesterol.
Alzheimer Disease
New insights on the neuroprotective role of sterols and sex steroids: The seladin-1/DHCR24 paradigm.
Alzheimer Disease
Prescription of lipophilic statins to Alzheimer's disease patients: some controversies to consider.
Alzheimer Disease
Recombinant adenovirus-mediated overexpression of 3?-hydroxysteroid-?24 reductase.
Alzheimer Disease
Regulation of cellular response to oncogenic and oxidative stress by Seladin-1.
Alzheimer Disease
Seladin-1 transcription is linked to neuronal degeneration in Alzheimer's disease.
Alzheimer Disease
Serum seladin-1 levels in diabetes mellitus and Alzheimer's disease patients.
Alzheimer Disease
Simvastatin modulates the Alzheimer's disease-related gene seladin-1.
Alzheimer Disease
Statin-like drugs for the treatment of brain cholesterol loss in Alzheimer's disease.
Alzheimer Disease
The association study between DHCR24 polymorphisms and Alzheimer's disease.
Alzheimer Disease
The selective Alzheimer's disease indicator-1 gene (Seladin-1/DHCR24) is a liver X receptor target gene.
Alzheimer Disease
Upregulation of seladin-1 and nestin expression in bone marrow mesenchymal stem cell transplantation via the ERK1/2 and PI3K/Akt signaling pathways in an Alzheimer's disease model.
Alzheimer Disease
[Seladin-1/DHCR24: a key protein of cell homeostasis and cholesterol biosynthesis]
Breast Neoplasms
24-Dehydrocholesterol reductase promotes the growth of breast cancer stem-like cells through the Hedgehog pathway.
Carcinogenesis
Androgen receptor signaling intensity is a key factor in determining the sensitivity of prostate cancer cells to selenium inhibition of growth and cancer-specific biomarkers.
Carcinoma
DHCR24 is an Independent Predictor of Progression in Patients with Non-Muscle-Invasive Urothelial Carcinoma, and Its Functional Role is Involved in the Aggressive Properties of Urothelial Carcinoma Cells.
Carcinoma
Seladin-1 expression is regulated by promoter methylation in adrenal cancer.
Carcinoma, Hepatocellular
Development of Serum DHCR24 Antibody as a Marker for Hepatocellular Carcinoma: The End of the Beginning.
Carcinoma, Hepatocellular
Genomic polymorphisms in 3?-hydroxysterol ?24-reductase promoter sequences.
Cardiomyopathy, Dilated
Dhcr24 activates the PI3K/Akt/HKII pathway and protects against dilated cardiomyopathy in mice.
Cataract
Cholesterol synthesis in the vertebrate retina: effects of U18666A on rat retinal structure, photoreceptor membrane assembly, and sterol metabolism and composition.
Cataract
E2012-induced cataract and its predictive biomarkers.
Chondrodysplasia Punctata
Genetic disorders of cholesterol biosynthesis in mice and humans.
Confusion
The Twisted Dwarf's ABC: How Immunophilins Regulate Auxin Transport.
Cystadenocarcinoma, Mucinous
Seladin-1/DHCR24 expression in normal ovary, ovarian epithelial and granulosa tumours.
Cystadenocarcinoma, Serous
Seladin-1/DHCR24 expression in normal ovary, ovarian epithelial and granulosa tumours.
delta24-sterol reductase deficiency
Desmosterolosis presenting with multiple congenital anomalies and profound developmental delay.
delta24-sterol reductase deficiency
DHCR24 Knock-Down Induced Tau Hyperphosphorylation at Thr181, Ser199, Thr231, Ser262, Ser396 Epitopes and Inhibition of Autophagy by Overactivation of GSK3?/mTOR Signaling.
delta24-sterol reductase deficiency
Phenotypic spectrum of fetal Smith-Lemli-Opitz syndrome.
Diabetes Mellitus
Serum seladin-1 levels in diabetes mellitus and Alzheimer's disease patients.
Diabetes Mellitus, Type 2
3?-Hydroxysteroid-?24 Reductase (DHCR24) Protects Pancreatic ? Cells from Endoplasmic Reticulum Stress-Induced Apoptosis by Scavenging Excessive Intracellular Reactive Oxygen Species.
Diabetic Neuropathies
Intermittent high glucose concentrations reduce neuronal precursor survival by altering the IGF system: the involvement of the neuroprotective factor DHCR24 (Seladin-1).
Dwarfism
Dominant and pleiotropic effects of a GAI gene in wheat results from a lack of interaction between DELLA and GID1.
Dwarfism
Molecular characterization of Rht-1 dwarfing genes in hexaploid wheat.
Dwarfism
The maize DWARF1 encodes a gibberellin 3-oxidase and is dual localized to the nucleus and cytosol.
Endometrial Neoplasms
Cholesterol Synthetase DHCR24 Induced by Insulin Aggravates Cancer Invasion and Progesterone Resistance in Endometrial Carcinoma.
Epilepsy
Interactions of Aromatase and Seladin-1: A Neurosteroidogenic and Gender Perspective.
Hepatitis B
Serum DHCR24 Auto-antibody as a new Biomarker for Progression of Hepatitis C.
Hepatitis C
Augmentation of DHCR24 expression by hepatitis C virus infection facilitates viral replication in hepatocytes.
Hepatitis C
Hepatitis C virus NS3-4A protease regulates the lipid environment for RNA replication by cleaving host enzyme 24-dehydrocholesterol reductase.
Hepatitis C
Serum DHCR24 Auto-antibody as a new Biomarker for Progression of Hepatitis C.
Hepatitis, Chronic
Serum DHCR24 Auto-antibody as a new Biomarker for Progression of Hepatitis C.
Herpes Zoster
24-dehydrocholesterol reductase/seladin-1: a key protein differentially involved in adrenocorticotropin effects observed in human and rat adrenal cortex.
Herpes Zoster
Seladin-1 expression in rat adrenal gland: effect of adrenocorticotropic hormone treatment.
Hypercholesterolemia
Desmosterol in brain is elevated because DHCR24 needs REST for Robust Expression but REST is poorly expressed.
Hypothyroidism
Crosstalk between thyroid hormone receptor and liver X receptor in the regulation of selective Alzheimer's disease indicator-1 gene expression.
Infections
3?-Hydroxysteroid-?24 Reductase (DHCR24) Protects Pancreatic ? Cells from Endoplasmic Reticulum Stress-Induced Apoptosis by Scavenging Excessive Intracellular Reactive Oxygen Species.
Infections
Augmentation of DHCR24 expression by hepatitis C virus infection facilitates viral replication in hepatocytes.
Infections
Blood-based gene expression profile of oxidative stress and antioxidant genes for identifying surrogate markers of liver tissue injury in chronic hepatitis C patients.
Infections
Genomic polymorphisms in 3?-hydroxysterol ?24-reductase promoter sequences.
Infections
Hepatitis C virus impairs P53 via persistent over-expression of 3{beta}-hydroxysterol {delta}24-reductase.
Infections
Oxidative Stress and Immune Responses During Hepatitis C Virus Infection in Tupaia belangeri.
Infections
Role of oxidative stress in hepatocarcinogenesis induced by hepatitis C virus.
Infections
The heterotrimeric G protein alpha subunit acts upstream of the small GTPase Rac in disease resistance of rice.
Leishmaniasis
Hesperidin Targets Leishmania donovani Sterol C-24 Reductase to Fight against Leishmaniasis.
Liver Cirrhosis
Serum DHCR24 Auto-antibody as a new Biomarker for Progression of Hepatitis C.
Liver Diseases
Serum DHCR24 Auto-antibody as a new Biomarker for Progression of Hepatitis C.
Lymphatic Metastasis
Cholesterol Synthetase DHCR24 Induced by Insulin Aggravates Cancer Invasion and Progesterone Resistance in Endometrial Carcinoma.
Malnutrition
Genetic regulatory subnetworks and key regulating genes in rat hippocampus perturbed by prenatal malnutrition: implications for major brain disorders.
Melanoma
DHCR24 gene expression is upregulated in melanoma metastases and associated to resistance to oxidative stress-induced apoptosis.
Metabolism, Inborn Errors
Genetic disorders of cholesterol biosynthesis in mice and humans.
Mevalonate Kinase Deficiency
Genetic disorders of cholesterol biosynthesis in mice and humans.
Myocardial Infarction
MicroRNA-124 regulates cardiomyocyte apoptosis and myocardial infarction through targeting Dhcr24.
Neoplasm Metastasis
DHCR24 gene expression is upregulated in melanoma metastases and associated to resistance to oxidative stress-induced apoptosis.
Neoplasm Metastasis
Evolution of the androgen receptor pathway during progression of prostate cancer.
Neoplasm Metastasis
MicroRNA Profiling and Target Genes Related to Metastasis of Salivary Adenoid Cystic Carcinoma.
Neoplasms
24-Dehydrocholesterol reductase promotes the growth of breast cancer stem-like cells through the Hedgehog pathway.
Neoplasms
An Integrative In Silico Mathematical Modelling Study of The Anti-Cancer Effect of Clove Extract ( Syzygium aromaticum ) Combined with In Vitro Metabolomics Study Using 1HNMR Spectroscopy.
Neoplasms
Cholesterol Synthetase DHCR24 Induced by Insulin Aggravates Cancer Invasion and Progesterone Resistance in Endometrial Carcinoma.
Neoplasms
DHCR24 gene expression is upregulated in melanoma metastases and associated to resistance to oxidative stress-induced apoptosis.
Neoplasms
DHCR24 predicts poor clinicopathological features of patients with bladder cancer: A STROBE-compliant study.
Neoplasms
Editorial: Is the diminuto/dwarf1 gene involved in physiologic adrenocortical size regulation and tumor formation?
Neoplasms
Evolution of the androgen receptor pathway during progression of prostate cancer.
Neoplasms
Gene expression in normal urothelium depends on location within the bladder: a possible link to bladder carcinogenesis.
Neoplasms
Polybrominated diphenyl ethers cause oxidative stress in human umbilical vein endothelial cells.
Neoplasms
Seladin-1 and testicular germ cell tumours: new insights into cisplatin responsiveness.
Neoplasms
Seladin-1 is a novel lipopolysaccharide (LPS)-responsive gene and inhibits the tumour necrosis factor-alpha production and osteoclast formation in response to LPS.
Neoplasms, Germ Cell and Embryonal
Seladin-1 and testicular germ cell tumours: new insights into cisplatin responsiveness.
Neuroblastoma
3 ?-hydroxysteroid-? 24 reductase (DHCR24) protects neuronal cells from apoptotic cell death induced by endoplasmic reticulum (ER) stress.
Neuroblastoma
Aromatase/Seladin-1 Interactions in Human Neuronal Cell Culture, the Hippocampus of Healthy Rats and Transgenic Alzheimer's Disease Mice.
Neuroblastoma
Down-regulation of seladin-1 increases bace1 levels and activity through enhanced GGA3 depletion during apoptosis.
Neuroblastoma
Membrane cholesterol as a mediator of the neuroprotective effects of estrogens.
Neuroblastoma
Prevention of prion propagation by dehydrocholesterol reductase inhibitors in cultured cells and a therapeutic trial in mice.
Neuroblastoma
Seladin-1/DHCR24 protects neuroblastoma cells against Abeta toxicity by increasing membrane cholesterol content.
Neuroblastoma
The membrane topological analysis of 3?-hydroxysteroid-Delta24 reductase (DHCR24) on endoplasmic reticulum.
Neurodegenerative Diseases
Estrogen and selective estrogen receptor modulators exert neuroprotective effects and stimulate the expression of selective Alzheimer's disease indicator-1, a recently discovered antiapoptotic gene, in human neuroblast long-term cell cultures.
Neurodegenerative Diseases
Identification and analysis of the promoter region of the human DHCR24 gene: involvement of DNA methylation and histone acetylation.
Neuroinflammatory Diseases
DHCR24 exerts neuroprotection upon inflammation-induced neuronal death.
Ototoxicity
Inhibition of DHCR24 increases the cisplatin-induced damage to cochlear hair cells in vitro.
Ovarian Neoplasms
The plasma peptides of ovarian cancer.
Peritonitis
Inhibition of ?24-dehydrocholesterol reductase activates pro-resolving lipid mediator biosynthesis and inflammation resolution.
Pheochromocytoma
3beta-Hydroxysteroid-delta24 reductase is a hydrogen peroxide scavenger, protecting cells from oxidative stress-induced apoptosis.
Pituitary Neoplasms
Expression of the antiapoptotic gene seladin-1 and octreotide-induced apoptosis in growth hormone-secreting and nonfunctioning pituitary adenomas.
Prostatic Neoplasms
Inhibition of DHCR24/Seladin-1 impairs cellular homeostasis in prostate cancer.
Prostatic Neoplasms
Modulation of long noncoding RNAs by risk SNPs underlying genetic predispositions to prostate cancer.
Prostatic Neoplasms
Novel biomarkers for prostate cancer including noncoding transcripts.
Smith-Lemli-Opitz Syndrome
Defects in cholesterol synthesis genes in mouse and in humans: lessons for drug development and safer treatments.
Smith-Lemli-Opitz Syndrome
Phenotypic spectrum of fetal Smith-Lemli-Opitz syndrome.
Smith-Lemli-Opitz Syndrome
Subcellular localization of sterol biosynthesis enzymes.
Tauopathies
DHCR24 Knock-Down Induced Tau Hyperphosphorylation at Thr181, Ser199, Thr231, Ser262, Ser396 Epitopes and Inhibition of Autophagy by Overactivation of GSK3?/mTOR Signaling.
Tauopathies
DHCR24 Knockdown Lead to Hyperphosphorylation of Tau at Thr181, Thr231, Ser262, Ser396, and Ser422 Sites by Membrane Lipid-Raft Dependent PP2A Signaling in SH-SY5Y Cells.
Urinary Bladder Neoplasms
DHCR24 predicts poor clinicopathological features of patients with bladder cancer: A STROBE-compliant study.
Urinary Bladder Neoplasms
Involvement of Seladin-1 in goniothalamin-induced apoptosis in urinary bladder cancer cells.
Virus Diseases
Augmentation of DHCR24 expression by hepatitis C virus infection facilitates viral replication in hepatocytes.
Wilms Tumor
Gene expression during ovarian differentiation in parasitic and non-parasitic lampreys: implications for fecundity and life history types.
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0.0000029
(1R,3aR,5aS,7S,9aS,9bR,11aR)-9a,11a-dimethyl-1-[(2R,3E)-4-phenylbut-3-en-2-yl]-2,3,3a,5,5a,6,7,8,9,9a,9b,10,11,11a-tetradecahydro-1H-cyclopenta[a]phenanthren-7-ol
Homo sapiens
-
at 37°C, pH not specified in the publication
-
0.000823
(2S)-2-[(1R,3aR,5aS,7S,9aS,9bR,11aR)-7-hydroxy-9a,11a-dimethyl-2,3,3a,5,5a,6,7,8,9,9a,9b,10,11,11a-tetradecahydro-1H-cyclopenta[a]phenanthren-1-yl]-N-methylpropanamide
Homo sapiens
-
at 37°C, pH not specified in the publication
-
0.000198
(3S,20S)-20-(aminomethyl)-pregn-7-en-3-yl acetate
Homo sapiens
-
at 37°C, pH not specified in the publication
-
0.0000001
(3S,20S)-20-(hydroxymethyl)-pregn-7-en-3-ol
Homo sapiens
-
at 37°C, pH not specified in the publication
-
0.000805
(3S,20S)-20-(methoxyaminocarbonyl)-pregn-7-en-3-ylacetate
Homo sapiens
-
at 37°C, pH not specified in the publication
-
0.000203
(3S,20S)-20-[((E)-2-methylbut-2-enoyloxy)methyl]-pregn-7-en-3-yl acetate
Homo sapiens
-
at 37°C, pH not specified in the publication
-
0.0000063
(3S,20S)-20-[((E)-but-2-enoyloxy)methyl]-pregn-7-en-3-yl acetate
Homo sapiens
-
at 37°C, pH not specified in the publication
-
0.0169
(3S,20S)-20-[(butanoylamino)methyl]-pregn-7-en-3-ylacetate
Homo sapiens
-
at 37°C, pH not specified in the publication
-
0.0000055
(3S,20S)-20-[(dimethylamino)acetoxymethyl]-pregn-7-en-3-yl acetate
Homo sapiens
-
at 37°C, pH not specified in the publication
-
0.0000042
(3S,20S)-20-[(formyloxy)methyl]-pregn-7-en-3-yl acetate
Homo sapiens
-
at 37°C, pH not specified in the publication
-
0.0000025
(7S,9aR,11aS)-1-[(2S)-1-hydroxypropan-2-yl]-9a,11a-dimethyl-2,3,3a,3b,4,6,7,8,9,9a,9b,10,11,11a-tetradecahydro-1H-cyclopenta[a]phenanthren-7-ol
Homo sapiens
-
at 37°C, pH not specified in the publication
-
0.0000033
(7S,9aS,11aR)-1-[(2S)-1-hydroxypropan-2-yl]-9a,11a-dimethyl-2,3,3a,5,5a,6,7,8,9,9a,9b,10,11,11a-tetradecahydro-1H-cyclopenta[a]phenanthren-7-yl acetate
Homo sapiens
-
at 37°C, pH not specified in the publication
-
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additional information
-
the hepatitis C virus-expressing hepatoblastoma-derived cell line, RzM6-LC, shows augmented tumorigenicity. DHCR24 expression reflects tumorigenicity, overview. Ectopic or HCV-induced DHCR24 overexpression results in resistance to oxidative stress-induced apoptosis and suppressed p53 activity. DHCR24 overexpression in these cells paralleles the increased interaction between p53 and MDM2, a p53-specific E3 ubiquitin ligase, in the cytoplasm. Persistent DHCR24 overexpression does not alter the phosphorylation status of p53 but results in decreased acetylation of p53 at Lys residues 373 and 382 in the nucleus after treatment with H2O2. DHCR24 overexpression inhibits polyubiquitination in RzM6-LC cells and H358, p53 null, cells. Ectopic expression of DHCR24 does not inhibit apoptotic response to H2O2 in WI38 cells
malfunction
(A-I)rHDL-mediated induction of HO-1 is reduced in human coronary artery endothelial cells transfected with DHCR24 siRNA. The activation of phosphatidylinositol 3-kinase/Akt by (A-I)rHDL is decreased in human coronary artery endothelial cells that are transfected with DHCR24 siRNA
malfunction
2-152a MAb-mediated binding of a cytotoxic agent (a saponin-conjugated secondary antibody) to surface DHCR24 leads to significant cytotoxicity. HCV replication can be suppressed by inhibiting DHCR24 with an enzymatic inhibitor
malfunction
loss of DHCR24 results in severe developmental and growth defects. Missense mutations in DHCR24, which result in diminished protein activity, can lead to a rare autosomal recessive disorder, desmosterolosis. The single nucleotide polymorphism, rs600491 (T allele) is significantly correlating with Alzheimer's disease risk in men. Four single nucleotide polymorphisms in the DHCR24 promoter correlate with hepatitis C virus (HCV) induced hepatocellular carcinoma and cirrhosis. The enzyme can be involved in Alzheimer's disease and is downregulated in affected regions of Alzheimer's disease (AD) brains, Overexpressing DHCR24 in cell culture protects cells from apoptosis, through inhibiting caspase-3 and amyloid beta toxicity. DHCR24 is implicated in the anti-inflammatory effects of HDL and resulting cardiovascular disease. Altered expression of a subset of androgen receptor-related genes, such as DHCR24, is observed in prostate cancer, overexpression of DHCR24 is a hallmark of prostate cancer, with high levels observed in low-grade prostate cancer, which diminish as the cancer progresses to a higher grade
malfunction
mutating residues T110, Y299, and Y507 of known phosphorylation sites inhibits DHCR24 activity. Seven missense mutations in DHCR24 have been described in desmosterolosis: R94H, R103C, E191K, N294T, K306N, Y471S, E480K. PKC inhibition results in desmosterol accumulation
malfunction
overexpression of DHCR24 enhances 7-dehydrocholesterol reductase, DHCR7, activity, but only when a functional form of DHCR24 is used. When the DHCR24 gene is knocked down by siRNA, DHCR7 activity is also ablated. Knockdown of DHCR7 has no effect on DHCR24 activity, while knockdown of DHCR24 decreases DHCR7 activity by about 60%
metabolism
DHCR24 catalyzes the ultimate step in the Bloch pathway of cholesterol synthesis
metabolism
DHCR24 is the final enzyme in cholesterol synthesis, role of signaling in regulating cholesterol homeostasis
metabolism
substrate channeling in the cholesterol metabolon of choleterol biosynthesis, cholesterol synthesis proteins identified by LC-MS/MS after DHCR24 immunoprecipitation
physiological function
3beta-hydroxysteroid-DELTA24 reductase (DHCR24) is an endoplasmic reticulum-localized multifunctional enzyme that possesses anti-apoptotic and cholesterol-synthesizing activities. Overexpression of DHCR24 protects neuronal cells from tunicamycin-induced apoptosis. DHCR24 may function as a neuroprotective protein under endoplasmic reticulum stress. Overexpression of DHCR24 inhibits apoptotic cell signaling and reduces or delays activation of endoplasnic reticlum stress-related cell signaling during unfolded protein response in mouse embryonic fibroblast N2A cells, overview. Elevated cholesterol levels may contribute to the neuroprotective function of DHCR24
physiological function
as well as playing an essential role in the regulation of cholesterol synthesis, DHCR24 is important in other cellular processes, such as signaling, the formation of lipid rafts, mediating cell stress responses, and regulating steroidogenesis, in steroidogenesis and bile acid synthesis, cell survival, and chlolesterol homeostasis and membranes. DHCR24 is modulating oxidative stress. DHCR24 or seladin-1 plays an important role in stress signaling and apoptosis: up-regulated in response to cell stress (oxidative- and amyloid b-toxicity) promoting cell survival by inhibiting caspase-3 activation, and deactivated by caspase cleavage during apoptosis. The enzyme is regulated by the following transcription factors/proteins: sterol regulatory element binding protein 2, nuclear factor Y (via methylation), specificity protein 1, estrogen receptor, androgen receptor, thyroid hormone receptor, constitutive androstane receptor, and pregnane X receptor
physiological function
lipid-free apoA-I and (A-I)rHDL inhibit inflammation by increasing DHCR24 expression, which, in turn, activates phosphatidylinositol 3-kinase/Akt and induces HO-1
physiological function
surface DHCR24 on hepatocellular carcinoma cells can function as a carrier for internalization, e.g. of hepatitis C virus, HCV. DHCR24-mediated cholesterol biosynthesis plays a crucial role in the HCV life cycle. Antibody 2-152a MAb-mediated binding of 2ndAb-Sap to surface DHCR24 on hepatocellular carcinoma cells predicted to lead to internalization of 2ndAb-Sap and subsequent cell death
physiological function
the enzyme activity is regulated by signaling through kinases and reversible phosphorylation
physiological function
the enzyme DELTA24-sterol reductase DHCR24 is involved in the cholesterol biosynthesis catalyzing the reduction of desmosterol to cholesterol. DHCR24 controls the activity of 7-dehydrocholesterol , DHCR7, which is important for both cholesterol and vitamin D synthesis. DHCR24 is involved in a remarkable diversity of cellular functions (e.g., oxidative stress, neuroprotection, cell survival), and is implicated in many diseases including cardiovascular disease, hepatitis C, certain cancers, and neurodegenerative diseases
physiological function
the enzyme has neuroprotective and cholesterol-synthesizing activities. DHCR24 overexpression confers neuroprotection against apoptosis caused by amyloid beta deposition
malfunction
-
DHCR24 overexpressed in CHO cells show that untreated CHO-DHCR24 cells have a higher cholesterol to desmosterol ratio. In the CHO-DHCR24 cells, more 24(S),25-epoxycholesterol is required to attain the same cholesterol to desmosterol ratio as in CHO cells expressing an empty vector. Thus, with DHCR24 overexpression, the effect of 24(S),25-epoxycholesterol on the cholesterol to desmosterol ratio is blunted
malfunction
-
the blockade of the enzyme activity impairs adhesion, migration and proliferation of vascular smooth muscle cells
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E480K
site-directed mutagenesis, mutation of a C-terminal domain residue, about 50% of wild-type activity remain
R103C
site-directed mutagenesis, mutation of a FAD binding domain residue
R94H
site-directed mutagenesis, mutation of a FAD binding domain residue, about 20% of wild-type activity remain
T110A
site-directed mutagenesis, mutation and inactivation of the phosphorylation site results in 60% loss of activity compared to wild-type
T110E
site-directed mutagenesis, DHCR24 activity of the phosphomimetic T110E mutant is similar to wild-type activity
Y299F
site-directed mutagenesis, compared with wild-type DHCR24, the mutant Y299F stable cells contain reduced DHCR24 mRNA expression while having comparable DHCR24 protein levels, the mutant enzyme activity is reduced by 40% compared to the wild-type
Y300F
site-directed mutagenesis, compared with wild-type DHCR24, the mutant Y299F stable cells contain comparable DHCR24 mRNA expression while having reduced DHCR24 protein levels, the mutant enzyme activity is similar to the wild-type
Y321F
site-directed mutagenesis, the mutant enzyme activity is similar to the wild-type
Y507F
site-directed mutagenesis, the mutant enzyme activity is reduced by 60% compared to the wild-type
E191K
-
natural mutant, 20% residual enzyme activity
K306N
-
natural mutant, 50% residual enzyme activity
N294T
-
natural mutant, 14.4% residual enzyme activity
E191K
decreased activity
E191K
site-directed mutagenesis, mutation of a FAD binding domain residue, 19.9% of wild-type activity remain
K306N
decreased activity
K306N
site-directed mutagenesis, mutation of a C-terminal domain residue, 49.8% of wild-type activity remain
N294T
decreased activity
N294T
site-directed mutagenesis, mutation of a C-terminal domain residue, 14.4% of wild-type activity remain
Y471S
decreased activity
Y471S
a desmosterolosis mutant of DHCR24 that results in a complete loss of DHCR24 activity
Y471S
site-directed mutagenesis, mutation of a C-terminal domain residue, inactive mutant
N294T/K306N
-
natural mutant, 0.8% residual enzyme activity
N294T/K306N
-
mutant shows diminished activity
additional information
construction of a specific chimeric antibody 2-152a MAb
additional information
construction of a truncated DHCR24, DELTA23 DHCR24, lacking the secretory signal peptide
additional information
neuroblastoma N2A cells are infected with adenovirus expressing myc-tagged DHCR24 (Ad-DHCR24) or lacZ (Ad-lacZ, serving as a control) and subjected to endoplasmic reticulum-stress, induced with tunicamycin. Cells infected with Ad-DHCR24-myc are resistant to TM-induced apoptosis, and show weaker level of caspase-12 activity. The cells also exhibit lower levels of Bip and CHOP proteins than Ad-LacZ-infected cells. A stronger and rapid activation of PERK, and a prolonged activation of JNK and p38 are observed in Ad-LacZinfected cells. The generation of intracellular reactive oxygen species from endoplasmic reticulum stress is also diminished by the overexpression of DHCR24 and intracellular cholesterol level is elevated, accompanied by a well-organized formation of caveolae (cholesterol-rich microdomain) on the plasma membrane, and improved colocalization of caveolin-1 and insulin-like growth factor 1 receptor. DHCR24 can protect neuronal cells from apoptosis induced by endoplasmic reticulum stress
additional information
the DHCR24 gene is knocked down by siRNA, DHCR24 knockdown decreases DHCR24 activity almost completely in CHO-EV and CHO-DHCR24 Y471S compared with CHODHCR24 cells
additional information
-
the DHCR24 gene is knocked down by siRNA, DHCR24 knockdown decreases DHCR24 activity almost completely in CHO-EV and CHO-DHCR24 Y471S compared with CHODHCR24 cells
additional information
vascular HO-1 and DHCR24 are knocked down by loading HO-1 and DHCR24 siRNA into the space between the collar and carotid artery at the time of collar implantation. Preincubation of human coronary artery endothelial cells with (A-I)rHDL before activation with tumor necrosis factor-alpha increases DHCR24 and HO-1 mRNA levels and inhibits cytokine-induced vascular cell adhesion molecule-1 and intercellular adhesion molecule-1 expression. (A-I)rHDL-mediated induction of HO-1 is reduced in human coronary artery endothelial cells transfected with DHCR24 siRNA. Transfection of human coronary artery endothelial cells with HO-1 siRNA and tin-protoporphyrin-IX treatment does not inhibit the (A-I)rHDL-mediated increase in DHCR24 expression. Inhibition of phosphatidylinositol 3-kinase/Akt reduces the (A-I)rHDL-mediated increase in HO-1, but not DHCR24 expression. The activation of phosphatidylinositol 3-kinase/Akt by (A-I)rHDL is decreased in human coronary artery endothelial cells that are transfected with DHCR24 siRNA
additional information
-
DNA and amino acid sequence determination and analysis of natural desmosterolysis mutant gene containing mutations e.g. Y471S, N294T, K306N, and E191K on either 2 alleles, differing between different patients, phenotypes, overview
additional information
-
silencing of DHCR24 and HCV by siRNA
additional information
-
mutant is constructed bearing a deleted transmembrane (TM) domain. This mutant is localized to the cytoplasm
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Filipovic, I.; Buddecke, E.
Calmodulin antagonists suppress cholesterol synthesis by inhibiting sterol DELTA24 reductase
Lipids
22
261-265
1987
Homo sapiens, Rattus norvegicus
brenda
Waterham, H.R.; Koster, J.; Romeijn, G.J.; Hennekam, R.C.M.; Vreken, P.; Andersson, H.C.; FitzPatrick, D.R.; Kelley, R.I.; Wanders, R.J.A.
Mutations in the 3beta-hydroxysterol DELTA24-reductase gene cause desmosterolosis, an autosomal recessive disorder of cholesterol biosynthesis
Am. J. Hum. Genet.
69
685-694
2001
Homo sapiens
brenda
Fernandez, C.; Suarez, Y.; Ferruelo, A.J.; Gomez-Coronado, D.; Lasuncion, M.A.
Inhibition of cholesterol biosynthesis by DELTA22-unsaturated phytosterols via competitive inhibition of sterol DELTA24-reductase in mammalian cells
Biochem. J.
366
109-119
2002
Homo sapiens, Rattus norvegicus
brenda
Giera, M.; Renard, D.; Ploessl, F.; Bracher, F.
Lathosterol side chain amidesa new class of human lathosterol oxidase inhibitors
Steroids
73
299-308
2008
Homo sapiens
brenda
Kuehnle, K.; Crameri, A.; Kaelin, R.E.; Luciani, P.; Benvenuti, S.; Peri, A.; Ratti, F.; Rodolfo, M.; Kulic, L.; Heppner, F.L.; Nitsch, R.M.; Mohajeri, M.H.
Prosurvival effect of DHCR24/seladin-1 in acute and chronic responses to oxidative stress
Mol. Cell. Biol.
28
539-550
2008
Homo sapiens
brenda
Pedretti, A.; Bocci, E.; Maggi, R.; Vistoli, G.
Homology modelling of human DHCR24 (seladin-1) and analysis of its binding properties through molecular docking and dynamics simulations
Steroids
73
708-719
2008
Homo sapiens (Q15392), Homo sapiens
brenda
Nishimura, T.; Kohara, M.; Izumi, K.; Kasama, Y.; Hirata, Y.; Huang, Y.; Shuda, M.; Mukaidani, C.; Takano, T.; Tokunaga, Y.; Nuriya, H.; Satoh, M.; Saito, M.; Kai, C.; Tsukiyama-Kohara, K.
Hepatitis C virus impairs p53 via persistent overexpression of 3beta-hydroxysterol DELTA24-reductase
J. Biol. Chem.
284
36442-36452
2009
Homo sapiens
brenda
Zerenturk, E.J.; Kristiana, I.; Gill, S.; Brown, A.J.
The endogenous regulator 24(S),25-epoxycholesterol inhibits cholesterol synthesis at DHCR24 (Seladin-1)
Biochim. Biophys. Acta
1821
1269-1277
2012
Cricetulus griseus, Homo sapiens
brenda
Zerenturk, E.J.; Sharpe, L.J.; Brown, A.J.
Sterols regulate 3beta-hydroxysterol DELTA24-reductase (DHCR24) via dual sterol regulatory elements: cooperative induction of key enzymes in lipid synthesis by Sterol Regulatory Element Binding Proteins
Biochim. Biophys. Acta
1821
1350-1360
2012
Homo sapiens
brenda
Lu, X.; Li, Y.; Liu, J.; Cao, X.; Wang, X.; Wang, D.; Seo, H.; Gao, B.
The membrane topological analysis of 3beta-hydroxysteroid-DELTA24 reductase (DHCR24) on endoplasmic reticulum
J. Mol. Endocrinol.
48
1-9
2012
Homo sapiens
brenda
Yoshinari, K.; Ohno, H.; Benoki, S.; Yamazoe, Y.
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Homo sapiens, Mus musculus
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Zerenturk, E.J.; Sharpe, L.J.; Brown, A.J.
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Homo sapiens (Q15392)
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Wu, B.; Chen, K.; Shrestha, S.; Ong, K.; Barter, P.; Rye, K.
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Homo sapiens (Q15392)
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Homo sapiens (Q15392), Homo sapiens
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Luu, W.; Hart-Smith, G.; Sharpe, L.J.; Brown, A.J.
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Homo sapiens (Q15392), Homo sapiens
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Lu, X.; Jia, D.; Zhao, C.; Wang, W.; Liu, T.; Chen, S.; Quan, X.; Sun, D.; Gao, B.
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Homo sapiens (Q15392), Homo sapiens, Rattus norvegicus (Q5BQE6)
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Saito, M.; Takano, T.; Nishimura, T.; Kohara, M.; Tsukiyama-Kohara, K.
3beta-hydroxysterol DELTA24-reductase on the surface of hepatitis C virus-related hepatocellular carcinoma cells can be a target for molecular targeting therapy
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Homo sapiens (Q15392)
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Lu, X.; Li, Y.; Wang, W.; Chen, S.; Liu, T.; Jia, D.; Quan, X.; Sun, D.; Chang, A.K.; Gao, B.
3 beta-hydroxysteroid-DELTA 24 reductase (DHCR24) protects neuronal cells from apoptotic cell death induced by endoplasmic reticulum (ER) stress
PLoS ONE
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Homo sapiens (Q15392)
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Zerenturk, E.J.; Sharpe, L.J.; Ikonen, E.; Brown, A.J.
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Arabidopsis thaliana, Bombyx mori, Homo sapiens (Q15392), Homo sapiens
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Kohlhaas, J.; Jaeger, M.; Lust, L.; De La Torre, C.; Hecker, M.; Korff, T.
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Homo sapiens
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Mueller, C.; Hemmers, S.; Bartl, N.; Plodek, A.; Koerner, A.; Mirakaj, V.; Giera, M.; Bracher, F.
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Homo sapiens
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