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1.14.99.38: cholesterol 25-monooxygenase

This is an abbreviated version!
For detailed information about cholesterol 25-monooxygenase, go to the full flat file.

Word Map on EC 1.14.99.38

Reaction

cholesterol
+
reduced acceptor
+
O2
=
25-hydroxycholesterol
+
acceptor
+
H2O

Synonyms

CH25A, CH25H, cholesterol 25-hydroxylase, cholesterol 25-monooxygenase, cholesterol-25-hydroxylase, CYP1A2, CYP27A1, CYP2C9, CYP2D6, CYP3A, Cyp3a11, CYP3A4

ECTree

     1 Oxidoreductases
         1.14 Acting on paired donors, with incorporation or reduction of molecular oxygen
             1.14.99 Miscellaneous
                1.14.99.38 cholesterol 25-monooxygenase

Expression

Expression on EC 1.14.99.38 - cholesterol 25-monooxygenase

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EXPRESSION
ORGANISM
UNIPROT
LITERATURE
activation of the innate immune system by TLR ligands induces 25-hydroxycholesterol production which results in suppression of IgA class switching in B cells
both IFN-alpha- and IFN-gamma induce the enzyme in bone marrow-derived macrophages
enzyme expression is not induced by interferons in human cells and knockdown of STAT-1 has no effect on the induction of the enzyme
-
exposure to DNA methyltransferase inhibitors and decitabine enhances enzyme mRNA expression in myelodysplasia/leukemia cell lines
induction of Ch25h is JAK- and STAT1-dependent, overview
induction of CYP3A by pregnenolone-16 alpha-carbonitrile causes accumulation of 25-hydroxycholesterol in cell line AML12 derived from mouse liver, the induction is not suppressed by the addition of desmosterol. Although the transcription of Ch25h is also upregulated by addition of pregnenolone-16 alpha-carbonitrile, the protein level of CH25H is not elevated. Desmosterol does not affect the expression of cellular CYP3A protein, but CH25H protein level is obviously decreased by desmosterol treatment
porcine reproductive and respiratory syndrome virus infection significantly downregulates the expression of the enzyme in cells
-
pseudorabies virus infection of porcine alveolar macrophages is attenuated by enzyme overexpression (24 h post infection)
-
the enzyme expression in primary human hepatocytes is primarily and transiently induced by type I interferon. Infection with hepatitis C virus causes up-regulation of the enzyme in vivo
the enzyme expression is induced by feeding a Western diet
-
the enzyme is upregulated upon poly(I:C) treatment or hepatitis C virus infection in hepatocytes
-
the enzyme mRNA expression level is originally low in myelodysplasia/leukemia cell lines. Enzyme knockdown partially protects the cells from decitabine-induced cell death
vasoprotective stimuli such as pulsatile shear stress and statins increase the expression of the enzyme via Krueppel-like factor 4