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24-methylenecholesterol + NADPH + H+
campesterol + NADP+
24-methylenecholesterol + NADPH + H+
dihydrobrassicasterol + NADP+
-
-
-
-
?
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-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+
5alpha-cholesta-7,24-dien-3beta-ol + NADPH
5alpha-cholesta-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+
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-5,7,24-trien-3beta-ol + NADPH + H+
cholesta-5,7-dien-3beta-ol + NADP+
-
-
-
-
?
cholesta-7,24-dien-3beta-ol + NADPH + H+
lathosterol + NADP+
-
-
-
-
?
cycloartenol + NADPH + H+
cycloartanol + NADP+
-
-
-
?
DELTA5,7-avenasterol + NADPH + H+
DELTA5,7-sitosterol + NADP+
DELTA7-avenasterol + NADPH + H+
DELTA7-sitosterol + NADP+
desmosterol + FADH2
cholesterol + FAD + H+
-
-
-
?
desmosterol + NADPH
cholesterol + NADP+
desmosterol + NADPH + H+
cholesterol + NADP+
ergosta-5,7,22,24(28)-tetraen-3beta-ol + NADPH + H+
ergosterol + NADP+
isofucosterol + NADPH + H+
sitosterol + NADP+
lanosterol + NADPH
24-dihydrolanosterol + NADP+
lanosterol + NADPH
4,4,14alpha-trimethyl-5alpha-cholesta-8-en-3beta-ol + NADP+
lanosterol + NADPH + H+
24-dihydrolanosterol + NADP+
-
-
-
?
lanosterol + NADPH + H+
4,4,14alpha-trimethyl-5alpha-cholesta-8-en-3beta-ol + NADP+
-
-
-
-
?
lanosterol + NADPH + H+
dihydrolanosterol + NADP+
-
-
-
-
?
zymosterol + NADPH
5alpha-cholesta-8-en-3beta-ol + NADP+
zymosterol + NADPH + H+
zymostenol + NADP+
-
-
-
-
?
additional information
?
-
24-methylenecholesterol + NADPH + H+
campesterol + NADP+
-
-
-
?
24-methylenecholesterol + NADPH + H+
campesterol + NADP+
GC-MS analysis suggests that the reaction proceeds with retention of the C-25 hydrogen. The 25-H retention is established by the incubation of the enzyme with (23,23,25-2H3,28-13C)-24-methylenecholesterol, followed by 13C NMR analysis of the resulting campesterol
-
-
?
24-methylenecholesterol + NADPH + H+
campesterol + NADP+
-
-
-
-
?
24-methylenecholesterol + NADPH + H+
campesterol + NADP+
-
-
-
-
?
4,4-dimethyl-5alpha-cholesta-8,24-dien-3beta-ol + NADPH
4,4-dimethyl-5alpha-cholesta-8-en-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-cholest-7-en-3beta-ol + NADP+
5alpha-cholesta-7,24-dien-3beta-ol + NADPH + H+
-
-
-
-
?
5alpha-cholest-7-en-3beta-ol + NADP+
5alpha-cholesta-7,24-dien-3beta-ol + NADPH + H+
-
-
-
-
r
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+
-
-
-
?
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
-
-
?
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+
-
-
i.e. lathosterol
-
?
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+
-
step in the biosynthesis of cholesterol from lanosterol
-
-
?
5alpha-cholesta-7,24-dien-3beta-ol + NADPH
5alpha-cholesta-7-en-3beta-ol + NADP+
-
-
lathosterol
?
5alpha-cholesta-7,24-dien-3beta-ol + NADPH
5alpha-cholesta-7-en-3beta-ol + NADP+
-
most reactive, best substrate, 17.8fold activity compared with lanosterol, 4,4',14alpha-trimethyl-5alpha-cholesta-8,24-dien-3beta-ol
lathosterol
?
5alpha-cholesta-7,24-dien-3beta-ol + NADPH
5alpha-cholesta-7-en-3beta-ol + NADP+
-
C-24 reduction of sterols probably takes place straight after sterol DELTA8-7 isomerization of zymosterol, which occurs several steps after C-32 demethylation of lanosterol in the 19-step pathway of cholesterol biosynthesis from lanosterol
-
-
?
5alpha-cholesta-7,24-dien-3beta-ol + NADPH
5alpha-cholesta-7-en-3beta-ol + NADP+
-
C-24 reduction of DELTA7,24-diene
-
-
?
5alpha-cholesta-7,24-dien-3beta-ol + NADPH
5alpha-cholesta-7-en-3beta-ol + NADP+
-
most reactive, probably natural substrate
-
-
?
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+
-
-
-
?
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
-
-
?
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
-
-
?
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 lanosterol
-
-
?
DELTA5,7-avenasterol + NADPH + H+
DELTA5,7-sitosterol + NADP+
-
-
-
?
DELTA5,7-avenasterol + NADPH + H+
DELTA5,7-sitosterol + NADP+
-
-
-
?
DELTA7-avenasterol + NADPH + H+
DELTA7-sitosterol + NADP+
-
-
-
?
DELTA7-avenasterol + NADPH + H+
DELTA7-sitosterol + NADP+
-
-
-
?
desmosterol + NADPH
cholesterol + NADP+
-
5alpha-cholesta-5,24-dien-3beta-ol
-
-
?
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
-
-
?
desmosterol + NADPH
cholesterol + NADP+
-
preferred, best substrate
-
-
?
desmosterol + NADPH
cholesterol + NADP+
-
5alpha-cholesta-5,24-dien-3beta-ol
-
-
?
desmosterol + NADPH
cholesterol + NADP+
-
-
-
?
desmosterol + NADPH
cholesterol + NADP+
-
-
-
-
?
desmosterol + NADPH
cholesterol + NADP+
-
5.5fold activity compared with lanosterol, 4,4',14alpha-trimethyl-5alpha-cholesta-8,24-dien-3beta-ol
-
-
?
desmosterol + NADPH
cholesterol + NADP+
-
5alpha-cholesta-5,24-dien-3beta-ol
-
-
?
desmosterol + NADPH
cholesterol + NADP+
-
step in the biosynthesis of cholesterol from lanosterol
-
-
?
desmosterol + NADPH + H+
cholesterol + NADP+
-
-
-
-
?
desmosterol + NADPH + H+
cholesterol + NADP+
-
-
-
-
?
desmosterol + NADPH + H+
cholesterol + NADP+
-
-
-
-
?
desmosterol + NADPH + H+
cholesterol + NADP+
-
-
-
-
?
ergosta-5,7,22,24(28)-tetraen-3beta-ol + NADPH + H+
ergosterol + NADP+
-
-
-
?
ergosta-5,7,22,24(28)-tetraen-3beta-ol + NADPH + H+
ergosterol + NADP+
-
-
-
?
ergosta-5,7,22,24(28)-tetraen-3beta-ol + NADPH + H+
ergosterol + NADP+
-
-
-
?
ergosta-5,7,22,24(28)-tetraen-3beta-ol + NADPH + H+
ergosterol + NADP+
-
-
-
?
isofucosterol + NADPH + H+
sitosterol + NADP+
-
-
-
?
isofucosterol + NADPH + H+
sitosterol + NADP+
-
-
-
?
lanosterol + NADPH
24-dihydrolanosterol + NADP+
-
-
-
-
?
lanosterol + NADPH
24-dihydrolanosterol + 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
-
-
?
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
4,4,14alpha-trimethyl-5alpha-cholesta-8-en-3beta-ol + NADP+
-
4,4',14alpha-trimethyl-5alpha-cholesta-8,24-dien-3beta-ol
-
-
?
lanosterol + NADPH
4,4,14alpha-trimethyl-5alpha-cholesta-8-en-3beta-ol + NADP+
-
14alpha-methyl demethylase activity is dominant over 24-reductase activity, and blockade or removal of 14alpha-methyl demethylase activity is absolutely required for the detection of maximal 24-reductase activity when lanosterol substrate is present
-
-
?
lanosterol + NADPH
4,4,14alpha-trimethyl-5alpha-cholesta-8-en-3beta-ol + NADP+
-
4,4',14alpha-trimethyl-5alpha-cholesta-8,24-dien-3beta-ol
-
-
?
zymosterol + NADPH
5alpha-cholesta-8-en-3beta-ol + NADP+
-
-
-
-
?
zymosterol + NADPH
5alpha-cholesta-8-en-3beta-ol + NADP+
-
-
-
?
zymosterol + NADPH
5alpha-cholesta-8-en-3beta-ol + NADP+
-
-
-
-
?
zymosterol + NADPH
5alpha-cholesta-8-en-3beta-ol + NADP+
-
6.1fold activity compared with lanosterol, 4,4',14alpha-trimethyl-5alpha-cholesta-8,24-dien-3beta-ol
-
-
?
zymosterol + NADPH
5alpha-cholesta-8-en-3beta-ol + NADP+
-
5alpha-cholesta-8,24-dien-3beta-ol
-
-
?
additional information
?
-
Dimunito/Dwarf1 (DWF1) is an oxidoreductase enzyme that is responsible for the conversion of C28- and C29-DELTA24(28)-olefinic sterols to 24-methyl- and 24-ethylcholesterols. ArDWF1 directly reduces 24-methylenecholesterol to produce campesterol without passing through a DELTA24(25) intermediate
-
-
?
additional information
?
-
-
the enzyme has enzyme activity not only for a sterol C-24 reductase, but also for a brassinosteroid C-24 reductase that catalyzes C-24 reduction of 6-deoxodolichosterone to 6-deoxocastasterone and of dolichosterone to castasterone in Arabidopsis thaliana
-
-
-
additional information
?
-
-
sterol 24,25-double bond reduction
-
-
?
additional information
?
-
-
the enzyme synthesizes cholesterol by transformation of dietary phytosterols through a dealkylation reaction
-
-
?
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
-
-
?
additional information
?
-
-
substrate specificity
-
-
?
additional information
?
-
-
sterol 24,25-double bond reduction
-
-
?
additional information
?
-
-
substrate specificity studies
-
-
?
additional information
?
-
-
enzyme of phytosterol metabolism to cholesterol
-
-
?
additional information
?
-
-
reduction of 24,25-double bond
-
-
?
additional information
?
-
-
insects are unable to synthesize sterols de novo and acquire sterols from their diet or from symbionts, sterol 24,25-reductase is an important enzyme of the pathway for the transformation of sitosterol, 24alpha-ethylcholesterol, together with stigmasterol, 24alpha-ethylcholesta-5,22-dien-3beta-ol, the predominant phytosterol in tobacco, to cholesterol
-
-
?
additional information
?
-
-
intracellular generation of reactive oxygen species in response to H2O2 is diminished in the presence of DHCR24, suggesting a reactive oxygen species-scavenging activity of DHCR24
-
-
?
additional information
?
-
-
Dimunito/Dwarf1 (DWF1) is an oxidoreductase enzyme that is responsible for the conversion of C28- and C29-DELTA24(28)-olefinic sterols to 24-methyl- and 24-ethylcholesterols. An in vivo assay of OsDWF1 supports the generally accepted two-step mechanism because the C-25 hydrogen of 24-methylenecholesterol is eliminated during its conversion to 24-methylcholesterol
-
-
?
additional information
?
-
-
substrate specificity
-
-
?
additional information
?
-
-
catalyzes reduction of DELTA24 double bond
-
-
?
additional information
?
-
-
anaerobic reduction of 24(25)-enes of lanosterol and other obligatory intermediates of cholesterol biosynthesis from lanosterol in mammals to produce 24(25)-dihydrosterols
-
-
?
additional information
?
-
-
C-24 reduction of sterols probably takes place straight after sterol DELTA8-7 isomerization of zymosterol, which occurs several steps after C-32 demethylation of lanosterol in the 19-step pathway of cholesterol biosynthesis from lanosterol
-
-
?
additional information
?
-
-
substrate specificity studies
-
-
?
additional information
?
-
-
reduction of DELTA24 double bond is one of the necessary reactions during cholesterol synthesis
-
-
?
additional information
?
-
-
cholesterogenic enzyme
-
-
?
additional information
?
-
-
cholesterogenic enzyme
-
-
?
additional information
?
-
-
important enzyme in the 19-step pathway of cholesterol biosynthesis from lanosterol
-
-
?
additional information
?
-
-
important enzyme in the 19-step pathway of cholesterol biosynthesis from lanosterol
-
-
?
Please wait a moment until the data is sorted. This message will disappear when the data is sorted.
24-methylenecholesterol + NADPH + H+
campesterol + 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+
5alpha-cholesta-7,24-dien-3beta-ol + NADPH
5alpha-cholesta-7-en-3beta-ol + NADP+
cholesta-5,24-dien-3beta-ol + NADPH + H+
cholest-5-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+
ergosta-5,7,22,24(28)-tetraen-3beta-ol + NADPH + H+
ergosterol + NADP+
lanosterol + NADPH
24-dihydrolanosterol + NADP+
lanosterol + NADPH + H+
4,4,14alpha-trimethyl-5alpha-cholesta-8-en-3beta-ol + NADP+
-
-
-
-
?
lanosterol + NADPH + H+
dihydrolanosterol + NADP+
-
-
-
-
?
zymosterol + NADPH + H+
zymostenol + NADP+
-
-
-
-
?
additional information
?
-
24-methylenecholesterol + NADPH + H+
campesterol + NADP+
-
-
-
?
24-methylenecholesterol + NADPH + H+
campesterol + NADP+
-
-
-
-
?
5alpha-cholest-7-en-3beta-ol + NADP+
5alpha-cholesta-7,24-dien-3beta-ol + NADPH + H+
-
-
-
-
?
5alpha-cholest-7-en-3beta-ol + NADP+
5alpha-cholesta-7,24-dien-3beta-ol + NADPH + H+
-
-
-
-
r
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
-
-
?
5alpha-cholesta-7,24-dien-3beta-ol + NADPH
5alpha-cholest-7-en-3beta-ol + NADP+
-
step in the biosynthesis of cholesterol from lanosterol
-
-
?
5alpha-cholesta-7,24-dien-3beta-ol + NADPH
5alpha-cholesta-7-en-3beta-ol + NADP+
-
C-24 reduction of sterols probably takes place straight after sterol DELTA8-7 isomerization of zymosterol, which occurs several steps after C-32 demethylation of lanosterol in the 19-step pathway of cholesterol biosynthesis from lanosterol
-
-
?
5alpha-cholesta-7,24-dien-3beta-ol + NADPH
5alpha-cholesta-7-en-3beta-ol + NADP+
-
C-24 reduction of DELTA7,24-diene
-
-
?
5alpha-cholesta-7,24-dien-3beta-ol + NADPH
5alpha-cholesta-7-en-3beta-ol + NADP+
-
most reactive, probably natural substrate
-
-
?
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+
-
-
-
?
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
-
-
?
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
-
-
?
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
-
-
?
desmosterol + NADPH
cholesterol + NADP+
-
5alpha-cholesta-5,24-dien-3beta-ol
-
-
?
desmosterol + NADPH
cholesterol + NADP+
-
5alpha-cholesta-5,24-dien-3beta-ol
-
-
?
desmosterol + NADPH
cholesterol + NADP+
-
step in the biosynthesis of cholesterol from lanosterol
-
-
?
desmosterol + NADPH + H+
cholesterol + NADP+
-
-
-
-
?
desmosterol + NADPH + H+
cholesterol + NADP+
-
-
-
-
?
desmosterol + NADPH + H+
cholesterol + NADP+
-
-
-
-
?
desmosterol + NADPH + H+
cholesterol + NADP+
-
-
-
-
?
ergosta-5,7,22,24(28)-tetraen-3beta-ol + NADPH + H+
ergosterol + NADP+
-
-
-
?
ergosta-5,7,22,24(28)-tetraen-3beta-ol + NADPH + H+
ergosterol + NADP+
-
-
-
?
lanosterol + NADPH
24-dihydrolanosterol + NADP+
-
step in the biosynthesis of cholesterol from lanosterol
-
-
?
lanosterol + NADPH
24-dihydrolanosterol + NADP+
-
step in the biosynthesis of cholesterol from lanosterol
-
-
?
additional information
?
-
-
the enzyme synthesizes cholesterol by transformation of dietary phytosterols through a dealkylation reaction
-
-
?
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
-
-
?
additional information
?
-
-
enzyme of phytosterol metabolism to cholesterol
-
-
?
additional information
?
-
-
reduction of 24,25-double bond
-
-
?
additional information
?
-
-
insects are unable to synthesize sterols de novo and acquire sterols from their diet or from symbionts, sterol 24,25-reductase is an important enzyme of the pathway for the transformation of sitosterol, 24alpha-ethylcholesterol, together with stigmasterol, 24alpha-ethylcholesta-5,22-dien-3beta-ol, the predominant phytosterol in tobacco, to cholesterol
-
-
?
additional information
?
-
-
anaerobic reduction of 24(25)-enes of lanosterol and other obligatory intermediates of cholesterol biosynthesis from lanosterol in mammals to produce 24(25)-dihydrosterols
-
-
?
additional information
?
-
-
C-24 reduction of sterols probably takes place straight after sterol DELTA8-7 isomerization of zymosterol, which occurs several steps after C-32 demethylation of lanosterol in the 19-step pathway of cholesterol biosynthesis from lanosterol
-
-
?
additional information
?
-
-
reduction of DELTA24 double bond is one of the necessary reactions during cholesterol synthesis
-
-
?
additional information
?
-
-
cholesterogenic enzyme
-
-
?
additional information
?
-
-
cholesterogenic enzyme
-
-
?
additional information
?
-
-
important enzyme in the 19-step pathway of cholesterol biosynthesis from lanosterol
-
-
?
additional information
?
-
-
important enzyme in the 19-step pathway of cholesterol biosynthesis from lanosterol
-
-
?
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(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(R,S),25-epimino-lanosterol
-
iminiolanosterol, IL, potent inhibitor, IC50: 0.002 mM
24(S),25-epoxycholesterol
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
6-(6-aminohexyl)-5-chloronaphthalene-1-sulfonamide
-
i.e. W-7
-
azasteroids
-
mechanism of inhibition
-
N,N-dimethyl-3beta-hydroxy-cholenamide
-
-
-
N,N-dimethyl-3beta-hydroxycholenamide
-
-
-
N-(6-aminohexyl)-5-chloro-1-naphthalene sulfonamide
SH42
-
potent inhibitor
-
tamoxifen
-
inhibition mechanism and pattern, uncompetitive, 50% inhibition at 0.004 mM, cytotoxic in vivo, inhibitory effect on th whole cholesterol biosynthetic pathway, overview
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
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
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
-
-
3-beta-(2-(diethylamino)ethoxy)androst-5-en-17-one
-
U18666A, non-competitive inhibition, Ki: 0.000157 mM, IC50 about 0.00015 mM, 690fold higher affinity for the enzyme than substrate lanosterol
3-beta-(2-(diethylamino)ethoxy)androst-5-en-17-one
-
-
5,22-cholestedien-3beta-ol
-
desmosterol isomer, competitive inhibition
5,22-cholestedien-3beta-ol
-
desmosterol isomer, competitive inhibition
brassicasterol
-
DELTA22-unsaturated phytosterol, competitive inhibition
brassicasterol
competitive
brassicasterol
-
DELTA22-unsaturated phytosterol, competitive inhibition
Calmodulin antagonists
-
calmodulin antagonists inhibit reduction of DELTA24 double bond; specific, dose-dependent inhibition
-
Calmodulin antagonists
-
calmodulin antagonists inhibit reduction of DELTA24 double bond; specific, dose-dependent inhibition
-
ergosterol
-
DELTA22-unsaturated phytosterol, competitive inhibition
ergosterol
-
DELTA22-unsaturated phytosterol, competitive inhibition
N-(6-aminohexyl)-5-chloro-1-naphthalene sulfonamide
-
W-7, specific, dose-dependent inhibition
N-(6-aminohexyl)-5-chloro-1-naphthalene sulfonamide
-
70% inhibition; W-7, specific, dose-dependent inhibition
stigmasterol
-
DELTA22-unsaturated phytosterol, competitive inhibition
stigmasterol
-
DELTA22-unsaturated phytosterol, competitive inhibition
Trifluoperazine
-
specific, dose-dependent inhibition
Trifluoperazine
-
73% inhibition; specific, dose-dependent inhibition
Triparanol
-
-
Triparanol
-
1-[p-(beta-diethylaminoethoxy)-phenyl]-1-(p-tolyl)-2-(p-chlorophenyl)-ethanol, MER 29
Triparanol
-
4-chloro-alpha-[4-[2-diethylaminoethoxy]phenyl]-alpha-(4-methylphenyl)benze-methanol; non-competitive inhibition, specific inhibitor, Ki: 0.000523 mM, IC50 about 0.0008 mM, 208fold higher affinity for the enzyme than substrate lanosterol
Triparanol
-
1-[p-(beta-diethylaminoethoxy)-phenyl]-1-(p-tolyl)-2-(p-chlorophenyl)-ethanol, MER 29
additional information
-
inhibition mechanism of DELTA22-unsaturated phytosterols
-
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
-
no inhibition by lovastatin, mevalonolactone, Squalestatin 1, (E)-N-ethyl-N-(6,6-dimethyl-2-hepten-4-ynyl)-3-((3,3'-bithiophen-5-yl)methoxy)benzenemethanamine, NB-598, trans-1,4-bis(2-chlorobenzylaminomethyl)cyclohexane dihydrochloride, AY-9944 and CN- ion
-
additional information
-
inhibition mechanism of DELTA22-unsaturated phytosterols
-
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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
-
0.002
24(R,S),25-epimino-lanosterol
Manduca sexta
-
iminiolanosterol, IL, potent inhibitor, IC50: 0.002 mM
0.00015
3-beta-(2-(diethylamino)ethoxy)androst-5-en-17-one
Rattus norvegicus
-
U18666A, non-competitive inhibition, Ki: 0.000157 mM, IC50 about 0.00015 mM, 690fold higher affinity for the enzyme than substrate lanosterol
1.019
hesperidin
Leishmania donovani
pH and temperature not specified in the publication
0.000005
SH42
Mus musculus
-
pH and temperature not specified in the publication
-
0.0008
Triparanol
Rattus norvegicus
-
non-competitive inhibition, specific inhibitor, Ki: 0.000523 mM, IC50 about 0.0008 mM, 208fold higher affinity for the enzyme than substrate lanosterol
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malfunction
-
DHCR24 knockout mice die within a few hours after birth. Cultured metatarsal bones from newborn knockout mice show a significant retarded growth. Absence of proliferating chondrocytes in the growth plate and abnormal hypertrophy of prehypertrophic chondrocytes are observed in the bones from knockout mice
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
-
insulin-induced reactive oxygen species production is enhanced by siRNA for DHCR24
malfunction
-
overexpression of DHCR24 protects ATDC5 cells from H2O2-induces hypertrophy. Insulin-induced hypertrophic differentiation of ATDC5 cells is associated with production of reactive oxygen species and pretreatment of the cells with siRNA for DHCR24 mRNA accelerates the hypertrophic differentiation
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
-
loss of DWF1 results in severe developmental and growth defects
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%
malfunction
the enzyme dim mutant plants, similarly to the dwarf5-2, show a dwarf phenotype due to the deficiency in brassinosteroids, caused by a block in the D24-sterol-D24-reductase activity. Compared to the wild-type, the dim plants show reduced levels of campesterol and sitosterol associated to an increase of 24-methylene cholesterol and isofucosterol, their respective metabolic precursors and substrates of DIM. Mutant dim seedlings have short hypocotyls, petioles, and roots. Leaves of dim are round, curly, and dark green in color. In adult flowering plants, dim shows extremely short inflorescences with small flowers and severely reduced fertility. Phenotype, overview
malfunction
-
enzyme inhibition leads to increased inflammation resolution and selectively decreases proinflammatory cell influx
malfunction
-
the blockade of the enzyme activity impairs adhesion, migration and proliferation of vascular smooth muscle cells
malfunction
-
the enzyme dim mutant plants, similarly to the dwarf5-2, show a dwarf phenotype due to the deficiency in brassinosteroids, caused by a block in the D24-sterol-D24-reductase activity. Compared to the wild-type, the dim plants show reduced levels of campesterol and sitosterol associated to an increase of 24-methylene cholesterol and isofucosterol, their respective metabolic precursors and substrates of DIM. Mutant dim seedlings have short hypocotyls, petioles, and roots. Leaves of dim are round, curly, and dark green in color. In adult flowering plants, dim shows extremely short inflorescences with small flowers and severely reduced fertility. Phenotype, overview
-
metabolism
-
desmosterol suffice as a cholesterol replacement. Although a wide range of sterols and cholesterol analogues such as beta-sitosterol, ergosterol and 5beta-cholestan-3beta-ol are unable to support cell proliferation, 5alpha-cholestan-3beta-ol, i.e. dihydrocholesterol, and desmosterol can
metabolism
-
desmosterol suffice as a cholesterol replacement. Although a wide range of sterols and cholesterol analogues such as beta-sitosterol, ergosterol and 5beta-cholestan-3beta-ol are unable to support cell proliferation, while 5alpha-cholestan-3beta-ol, i.e. dihydrocholesterol, can do so, pathway regulation, detailed overview
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
metabolism
-
the enzyme catalyzes the final step in cholesterol biosynthesis
metabolism
the enzyme is involved in the sterol biosynthetic pathway in Arabidopsis thaliana, overview
metabolism
-
biosynthesis of 24-methylene brassinosteroid is an alternative route for generating castasterone, which is mediated and regulated by the enzyme in Arabidopsis thaliana
metabolism
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isoform DHCR24-1 but not DHCR24-2 contributes to conversion of phytosterols to cholesterol mainly in the midgut of Bombyx mori larvae
metabolism
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the enzyme is involved in the sterol biosynthetic pathway in Arabidopsis thaliana, overview
-
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
ArDWF1 functions as the sole enzyme responsible for biosynthesis of 24-methylcholesterol in the Ajuga plant
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
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invertebrates such as Bombyx mori (silkworm), which cannot perform de novo cholesterol synthesis, also possess a DHCR24 homologue. This protein provides the organism with cholesterol by transformation of dietary phytosterols through a dealkylation reaction, similar to the DWF1 catalyzed reaction from Arabidopsis thaliana. Furthermore, this reaction is FAD and NADPH dependent
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
physiological function
the enzyme has neuroprotective and cholesterol-synthesizing activities. DHCR24 overexpression confers neuroprotection against apoptosis caused by amyloid beta deposition
physiological function
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the enzyme is an important protein in plant sterol (phytosterol) and steroid (brassinosteroid) synthesis, by catalyzing the isomerisation of the DELTA24(28) bond, and the subsequent reduction of the DELTA24(25) bond in various sterol precursors
physiological function
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the enzyme functions in biosynthesis of active brassinosteroids in Arabidopsis thaliana. Enzyme overexpression enhances growth and development in Arabidopsis
additional information
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J774 cells, that lack a full-length transcript for DHCR24, consequently accumulate desmosterol
additional information
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J774 cells, that lack a full-length transcript for DHCR24, consequently accumulate desmosterol
additional information
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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
additional information
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while cholesterol itself may not be unique in its ability to sustain mammalian life, sterols very much like cholesterol, such as desmosterol, appear to be absolutely required
additional information
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while cholesterol itself may not be unique in its ability to sustain mammalian life, sterols very much like cholesterol, such as desmosterol, appear to be absolutely required
additional information
ArDWF1 has another unique property in that only campesterol is formed by the direct reduction catalyzed by the enzyme. Ajuga plants have unique sterol profiles in which clerosterol and dehydroclerosterol are the major sterols
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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
decreased activity
E191K
-
natural mutant, 20% residual enzyme activity
E191K
site-directed mutagenesis, mutation of a FAD binding domain residue, 19.9% of wild-type activity remain
K306N
decreased activity
K306N
-
natural mutant, 50% residual enzyme activity
K306N
site-directed mutagenesis, mutation of a C-terminal domain residue, 49.8% of wild-type activity remain
N294T
decreased activity
N294T
-
natural mutant, 14.4% residual enzyme activity
N294T
site-directed mutagenesis, mutation of a C-terminal domain residue, 14.4% of wild-type activity remain
N294T/K306N
-
natural mutant, 0.8% residual enzyme activity
N294T/K306N
-
mutant shows diminished activity
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
additional information
construction of a diminuto/dwarf1 (dim) T-DNA insertion mutant. The dim mutant plants, similarly to the dwarf5-2, show a dwarf phenotype due to the deficiency in brassinosteroids, caused by a block in the D24-sterol-D24-reductase activity. Compared to the wild-type, the dim plants show reduced levels of campesterol and sitosterol associated to an increase of 24-methylene cholesterol and isofucosterol, their respective metabolic precursors and substrates of DIM, complementation experiments with dwarf5-2, dim, and ste1-1
additional information
-
construction of a diminuto/dwarf1 (dim) T-DNA insertion mutant. The dim mutant plants, similarly to the dwarf5-2, show a dwarf phenotype due to the deficiency in brassinosteroids, caused by a block in the D24-sterol-D24-reductase activity. Compared to the wild-type, the dim plants show reduced levels of campesterol and sitosterol associated to an increase of 24-methylene cholesterol and isofucosterol, their respective metabolic precursors and substrates of DIM, complementation experiments with dwarf5-2, dim, and ste1-1
-
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
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
DHCR24 knockout mice, development of the epidermis, especially keratinization, is impaired, altered expression of filaggrin, loricrin, and involcrin, transepidermal water loss is markedly increased, impaired skin barrier function
additional information
construction of transgenic maize plants generated with double-stranded ZmDWF1 RNA, some mutants show a dwarfed phenotype varying in severity
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