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1.3.1.72: DELTA24-sterol reductase

This is an abbreviated version!
For detailed information about DELTA24-sterol reductase, go to the full flat file.

Word Map on EC 1.3.1.72

Reaction

5alpha-Cholest-7-en-3beta-ol
+
NADP+
=
5alpha-cholesta-7,24-dien-3beta-ol
 +
NADPH
 +
H+

Synonyms

24,25-reductase, 24,25-sterol reductase, 24-dehydrocholesterol reductase, 24-reductase, 3 beta-hydroxysteroid-DELTA 24 reductase, 3-beta-hydroxysterol-DELTA24-reductase, 3beta -hydroxysterol DELTA24-reductase, 3beta-hydroxysteroid-DELTA24 reductase, 3beta-hydroxysterol DELTA24-reductase, 3beta-hydroxysterol-delta24 reductase, ArDWF1, C-24 reductase, dehydrocholesterol reductase, DELTA24 reductase, DELTA24-dehydrocholesterol reductase, DELTA24-reductase, DELTA24-sterol-DELTA24-reductase, desmosterol reductase, DHCR24, DHCR24-1, DHCR24-2, DIM, DIMINUTO/DWARF1, Dimunito/Dwarf1, DWARF1, DWF1, hydroxy steroid DELTA24-reductase, lanosterol 24-reductase, lanosterol DELTA24-reductase, lanosterol reductase, More, OsDWF1, reductase, hydroxy steroid DELTA24-, seladin-1, sterol 24,25-reductase, sterol 24-reductase, sterol 24DELTA-reductase, sterol C-24 reductase, sterol DELTA24 reductase, sterol DELTA24-reductase, sterol-DELTA24-reductase, ZmDWF1

ECTree

     1 Oxidoreductases
         1.3 Acting on the CH-CH group of donors
             1.3.1 With NAD+ or NADP+ as acceptor
                1.3.1.72 DELTA24-sterol reductase

Expression

Expression on EC 1.3.1.72 - DELTA24-sterol reductase

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EXPRESSION
ORGANISM
UNIPROT
LITERATURE
activation of constitutive androstane receptor (CAR) in cultured human hepatocytes increases mRNA levels of mouse Dhcr24 and human DHCR24. A CAR-responsive element is identified in the promoter of human DHCR24
-
activation of constitutive androstane receptor (CAR) in mouse livers increases mRNA levels of mouse Dhcr24 and human DHCR24
-
DHCR24 is overexpressed in hepatitis C virus-related hepatocellular carcinoma specifically induced by hepatitis C virus
DHCR24 is transcriptionally regulated by sterols via the sterol-regulatory element-binding protein-2 transcription factor
enzyme expression is down-regulated by application of castasterone and brassinolide
-
enzyme mRNA expression level is significantly increased in protein disulfide isomerase A3 siRNA-treated neurons
-
expression of DHCR24 is mediated by two sterol regulatory elements (SREs) in the promoter of the gene, assisted by two nearby NF-Y binding sites
-
hepatitis C virus induces the DHCR24 overexpression in human hepatocytes
-
histone acetylation also regulates DHCR24 expression, with a reduction in DHCR24 transcription correlating with recruitment of acetylated histones H3 and H4 to its promoter
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. Transcriptional regulation of DHCR24, detailed overview
the mRNA expression of the enzyme is significantly decreased in the cortical neurons treated with 0.00001 mM 1,25-dihydroxyvitamin D3
-
the sterol-regulated region is extremely GC rich and lies within a CpG island, a region of DNA with a high G and C content and a high frequency of CpG dinucleotides, which is conserved in mammals. In addition to containing a specificity protein 1 (Sp1) site required for augmentation of DHCR24 in HCV infection, this region is also important in epigenetic regulation of DHCR24. Methylation of this region decreases DHCR24 expression, with pronounced methylation occurring in cell types with low DHCR24 levels. Sex steroids, such as estrogens and androgens, are positive regulators of DHCR24, increasing gene expression via activation of their respective nuclear receptors, estrogen receptor and androgen receptor, overview. Adrenocorticotropic hormone (ACTH) stimulates the enzyme expression in adrenal gland
vascular endothelial cells have the capacity to instruct vascular smooth muscle cells to shut down the expression of the enzyme thereby limiting their cholesterol biosynthesis
-