EC Number |
General Information |
Reference |
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3.3.2.11 | malfunction |
knockdown of D8D7I (3beta-hydroxysterol-DELTA8-DELTA7-isomerase) and DHCR7 (3beta-hydroxysterol-DELTA7-reductase) abolishes ChEH activity. D8D7I and DHCR7 cooperate in the ChEH activity |
706552 |
3.3.2.11 | malfunction |
patients suffering the lysosomal storage diseases Niemann-Pick types A, B, C1 and C2 (NPA, NPB, NPC) show elevated 5alpha-cholestane-3beta,5alpha,6beta-triol in plasma, presumably derived from free radical oxidation of cholesterol to 5,6-epoxycholesterol followed by hydrolysis to the triol by enzyme cholesterol epoxide hydrolase, ChEH |
753646 |
3.3.2.11 | metabolism |
cholesterol-5,6-epoxide pathway in normal breast and breast cancers, overview |
752861 |
3.3.2.11 | metabolism |
the enzymes ChEH, HSD11B1 and HSD11B2, and CYP27A1 sit at a fulcrum balancing the formation from 5alpha,6-epoxycholesterol of the tumour suppressor DDA and from 5,6-epoxycholesterol, through 5alpha-cholestane-3beta,5alpha,6beta-triol, the oncometabolite 3beta,5alpha-diHC-6O or the bile acid 3beta,5alpha,6beta-trihydroxycholanoic acid. 26-hydroxy-7-oxocholesterol activates the Hedgehog signalling pathway, constitutive activation of which is linked to tumorigenesis further connecting the HSD11B and CYP27A1 enzymes to oncology |
753646 |
3.3.2.11 | physiological function |
5,6-epoxycholesterol is hydrolysed by the enzyme cholesterol epoxide hydrolase (ChEH) to 3beta,5alpha,6beta-triol which itself is oxidised by hydroxysteroid dehydrogenase (HSD), steps leading to the acidic pathway of bile acid biosynthesis |
753646 |
3.3.2.11 | physiological function |
in breast tumors from patients, OCDO production as well as the expression of the enzymes involved in the pathway producing 6-oxo-cholestan-3beta,5alpha-diol (OCDO), namely ChEH subunits and 11beta-hydroxysteroid dehydrogenase of type 2 (HSD2), are higher compared to normal tissues, and overexpression of these enzymes correlates with a higher risk of patient death, indicating that this onco-metabolism is of major importance to breast cancer pathology. The ChEH product 5alpha-cholestane-3beta,5alpha,6beta-triol is metabolized into OCDO |
752861 |
3.3.2.11 | physiological function |
primary and secondary products of the enzyme's activity have tumor promoting and carcinogenic activity |
731385 |
3.3.2.11 | physiological function |
the enzyme plays a potential role in cancer progression and resistance |
731693 |
3.3.2.11 | physiological function |
the existence of ChEH activity in MCF-7 cells, and thus ChEH inhibition and accumulation are likely to play a role in the mechanism of induction of breast cancer cell differentiation and apoptosis by antiestrogen binding site (AEBS) ligands that require sterol autoxidation products |
706552 |