1.14.14.23: cholesterol 7alpha-monooxygenase
This is an abbreviated version!
For detailed information about cholesterol 7alpha-monooxygenase, go to the full flat file.
Word Map on EC 1.14.14.23
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1.14.14.23
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lipoprotein
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hepatocytes
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triglyceride
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biliary
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hmg-coa
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farnesoid
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fecal
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low-density
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hypercholesterolemia
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cholic
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high-fat
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chenodeoxycholic
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3-hydroxy-3-methylglutaryl
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ba
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cyp8b1
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cholestyramine
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enterohepatic
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cholestasis
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hdl
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gallstone
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hypocholesterolemic
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27-hydroxylase
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oxysterols
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cholesteryl
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hmgcr
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cyp27a1
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taurocholate
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cholesterol-lowering
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hypolipidemic
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ldl-cholesterol
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acyl-coa:cholesterol
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27-hydroxycholesterol
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alpha-hydroxylation
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lithogenic
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ursodeoxycholic
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lxralpha
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hnf4alpha
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cyp3a11
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sult2a1
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4alpha
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cholesterogenesis
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gut-liver
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npc1l1
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cholesterol-free
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srebp2
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ldl-receptor
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c1-like
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medicine
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analysis
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obeticholic
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cholestanol
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guggulsterone
- 1.14.14.23
- lipoprotein
- hepatocytes
- triglyceride
- biliary
- hmg-coa
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farnesoid
-
fecal
-
low-density
- hypercholesterolemia
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cholic
-
high-fat
-
chenodeoxycholic
-
3-hydroxy-3-methylglutaryl
- ba
- cyp8b1
- cholestyramine
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enterohepatic
- cholestasis
- hdl
- gallstone
-
hypocholesterolemic
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27-hydroxylase
- oxysterols
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cholesteryl
- hmgcr
- cyp27a1
- taurocholate
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cholesterol-lowering
-
hypolipidemic
-
ldl-cholesterol
-
acyl-coa:cholesterol
- 27-hydroxycholesterol
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alpha-hydroxylation
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lithogenic
-
ursodeoxycholic
-
lxralpha
-
hnf4alpha
- cyp3a11
- sult2a1
- 4alpha
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cholesterogenesis
-
gut-liver
-
npc1l1
-
cholesterol-free
-
srebp2
-
ldl-receptor
-
c1-like
- medicine
- analysis
-
obeticholic
- cholestanol
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guggulsterone
Reaction
Synonyms
7alpha-hydroxylase, bile acid-synthetic enzyme, C7alphaOH, cholesterol 7 alpha-hydroxylase, cholesterol 7-alpha hydroxylase, Cholesterol 7-alpha-hydroxylase, Cholesterol 7-alpha-monooxygenase, cholesterol 7a-hydroxylase, cholesterol 7alpha hydroxylase, cholesterol 7alpha-hydroxylase, cholesterol-NADPH oxidoreductase, 7alpha-hydroxylating, CYP125A4, CYP7A, CYP7A1, Cyp7alpha1, CYPVII, cytochrome P450 125A4, EC 1.14.13.17, hepatic cholesterol 7alpha-hydroxylase, More, oxygenase, cholesterol 7alpha-mono-
ECTree
1.14.14.23 cholesterol 7alpha-monooxygenaseAdvanced search results
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results (General Information
General Information on EC 1.14.14.23 - cholesterol 7alpha-monooxygenase
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GENERAL INFORMATION 
ORGANISM
UNIPROT
COMMENTARY 
LITERATURE
malfunction
heat shock factor-1 ablation not only eliminates heat shock response, but it also transcriptionally upregulates CYP7A1 and MDR1/P-gp axis in atherogenic western diet-diet fed HSF-1 and low density lipoproteins receptor double knock out mice to reduce atherosclerosis
metabolism
physiological function
additional information
metabolism
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cholesterol 7alpha-hydroxylase, Cyp7a1, catalyzes the rate-limiting step of the classical pathway of bile acid synthesis and is the major mechanism for cholesterol catabolism and removal from the body. Cyp7a1 regulation, detailed overview
metabolism
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the phosphorylation status of CYP7A1 chromatin is important in CYP7A1 regulation, overview
metabolism
bile acids such as chenodeoxycholic acid (CDCA) activate farnesoid X receptor FXR to increase transcription of small heterodimer partner SHP, an atypical nuclear receptor that lacks a DNA binding domain and represses CYP7A1 activation by suppression of transcription factors, liver receptor homolog-1 (NR5A2) and hepatocyte nuclear factor 4a (NR2A1), which are essential for CYP7A1 expression. A second negative feedback mechanism on CYP7A1 is found in the intestine, where activation of FXR induces fibroblast growth factor 15/19, a hormonal signaling molecule that represses CYP7A1 through interaction with the liver fibroblast growth factor receptor 4 via the c-Jun signaling pathway. Role for the vitamin D receptor on CYP7A1 regulation, overview
metabolism
bile acids such as chenodeoxycholic acid (CDCA) activate farnesoid X receptor FXR to increase transcription of small heterodimer partner SHP, an atypical nuclear receptor that lacks a DNA binding domain and represses CYP7A1 activation by suppression of transcription factors, liver receptor homolog-1 (NR5A2) and hepatocyte nuclear factor 4a (NR2A1), which are essential for CYP7A1 expression. A second negative feedback mechanism on CYP7A1 is found in the intestine, where activation of FXR induces fibroblast growth factor 15/19, a hormonal signaling molecule that represses CYP7A1 through interaction with the liver fibroblast growth factor receptor 4 via the c-Jun signaling pathway. Role for the vitamin D receptor on CYP7A1 regulation, overview
metabolism
Cyp7a1 is a bile acid-synthetic enzyme suppressed by FXR signaling in both liver and intestine in mice, bile acid profiling in untreated and bile acid-treated liver and intestine, overview
metabolism
hepatic conversion to bile acids is a major elimination route for cholesterol in mammals. CYP7A1 catalyzes the first and rate-limiting step in classic bile acid biosynthesis, converting cholesterol to 7alpha-hydroxycholesterol. Hydroxylation of the ring system of cholesterol in a regio- and stereospecific manner with further oxidation and shortening of the side chain produces water-soluble bile acids with powerful detergent properties to emulsify dietary lipids. Bile acids also serve as signaling molecules that bind to G-protein-coupled receptors and nuclear hormone receptors that regulate lipid, glucose, and energy metabolism
metabolism
HSF-1 deletion reduces atherosclerosis and enhances dietary cholesterol metabolism, by not only inducing hepatic MDR1/Pgp but also by enhancing CYP7A1 gene expression in the liver. HSF-1 is a metabolic regulator of dietary cholesterol
metabolism
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Cyp7a1 is a bile acid-synthetic enzyme suppressed by FXR signaling in both liver and intestine in mice, bile acid profiling in untreated and bile acid-treated liver and intestine, overview
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metabolism
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bile acids such as chenodeoxycholic acid (CDCA) activate farnesoid X receptor FXR to increase transcription of small heterodimer partner SHP, an atypical nuclear receptor that lacks a DNA binding domain and represses CYP7A1 activation by suppression of transcription factors, liver receptor homolog-1 (NR5A2) and hepatocyte nuclear factor 4a (NR2A1), which are essential for CYP7A1 expression. A second negative feedback mechanism on CYP7A1 is found in the intestine, where activation of FXR induces fibroblast growth factor 15/19, a hormonal signaling molecule that represses CYP7A1 through interaction with the liver fibroblast growth factor receptor 4 via the c-Jun signaling pathway. Role for the vitamin D receptor on CYP7A1 regulation, overview
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physiological function
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cholesterol 7 alpha-hydroxylase plays a critical role in regulation of bile acid synthesis in the liver
physiological function
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cholesterol 7alpha-hydroxylase is the rate-limiting enzyme in the bile acid biosynthetic pathway that converts cholesterol into bile acids in the liver. Bile acids play an important role in maintaining lipid, glucose, and energy homeostasis
physiological function
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regulation of Cyp7a1 expression is critical for maintenance of cholesterol and bile acid homeostasis
physiological function
CYP7A1 overexpression in transgenic mice leads to marked activation of the steroid response element-binding protein 2-regulated cholesterol metabolic network and absence of bile acid repression of lipogenic gene expression in livers. Cyp7a1-tg mice show significantly elevated hepatic cholesterol synthesis rates, but reduced hepatic fatty acid synthesis rates, which is accompanied by increased 14C-glucose-derived acetyl-coenzyme A incorporation into sterols for fecal excret
physiological function
transgenic mice overexpressing rat enzyme have 2fold higher isoform Cyp7a1 activity and bile acid pool than wild type mice. Gallbladder bile acid composition changes from predominantly cholic acid in wild type to chenodeoxycholic acid in trangenic mice. Transgenic mice have higher biliary and fecal cholesterol and bile acid secretion rates than wild type mice. Hepatic de novo cholesterol synthesis is markedly induced in trangenic mice but intestine fractional cholesterol absorption remains the same as wild type mice despite increased intestine bile acids. Hepatic but not intestinal expression of cholesterol transporters such as ABCG5/G8, SRB1 and bile acid transporters such as ABCB11 are significantly induced in transgenic mice
physiological function
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CYP7A1 overexpression leads to marked activation of the steroid response elementbinding protein 2-regulated cholesterol metabolic network and absence of bile acid repression of lipogenic gene expression in livers
physiological function
heat shock factor-1 knockout enhances cholesterol 7alpha hydroxylase (CYP7A1) and multidrug transporter (MDR1) gene expressions to attenuate atherosclerosis
physiological function
hepatic conversion to bile acids is a major elimination route for cholesterol in mammals. CYP7A1 catalyzes the first and rate-limiting step in classic bile acid biosynthesis, converting cholesterol to 7alpha-hydroxycholesterol
physiological function
thyroid hormone modulates serum cholesterol by acting on thyroid hormone receptor beta1 in liver to regulate metabolic gene sets. One important thyroid hormone regulated step involves induction of Cyp7a1, an enzyme in the cytochrome P450 family, which enhances cholesterol to bile acid conversion and plays a crucial role in regulation of serum cholesterol levels
physiological function
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utilization of cholesterol is initiated by three cholesterol hydroxylases, CYP125A3, CYP142A2, and CYP125A4. A CYP125A3/CYP142A2 double knockout mutant of Mycobacterium smegmatis is still able to grow on cholesterol as sole carbom source, albeit at a slower rate than the wild-type
physiological function
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cholesterol 7alpha-hydroxylase is the rate-limiting enzyme in the bile acid biosynthetic pathway that converts cholesterol into bile acids in the liver. Bile acids play an important role in maintaining lipid, glucose, and energy homeostasis
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additional information
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high glucose stimulates bile acid synthesis and induces mRNA expression of cholesterol 7 alpha-hydroxylase, the key regulatory gene in bile acid synthesis. Glucose decreases H3K9 methylation in CYP7A1 chromatin. Knockdown of ATP-citrate lyase, which converts citrate to acetyl-CoA, decreases histone acetylation, and attenuates glucose induction of CYP7A1 mRNA expression
additional information
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lipid responses of 67 subjects of different promoter variants -204A > C, 31 AA and 36 AC+ CC, to plant sterols, overview. Compared to AA-subjects, C-carriers show significantly higher adjusted mean reductions in total cholesterol and increases in lathosterol-to-cholesterol ratios
additional information
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transgenic mice overexpressing Cyp7a1 in the liver are resistant to high-fat diet-induced obesity, fatty liver, and insulin resistance. Cyp7a1-tg mice show increased hepatic cholesterol catabolism and an increased bile acid pool, they have increased secretion of hepatic very low density lipoprotein but maintained plasma triglyceride homeostasis, phenotype, overview
additional information
activation of the vitamin D receptor represses hepatic SHP to increase levels of human CYP7A1 and reduce cholesterol
additional information
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activation of the vitamin D receptor represses hepatic SHP to increase levels of human CYP7A1 and reduce cholesterol
additional information
identification of a motif of residues that promote cholest-4-en-3-one binding parallel to the heme, thus positioning the C7 atom for hydroxylation. Orientation of cholesterol in the different leaflets of the lipid bilayer can be recognized for further binding by CYP7A1 alone or in complex with protein partners
additional information
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identification of a motif of residues that promote cholest-4-en-3-one binding parallel to the heme, thus positioning the C7 atom for hydroxylation. Orientation of cholesterol in the different leaflets of the lipid bilayer can be recognized for further binding by CYP7A1 alone or in complex with protein partners
additional information
in farnesoid X receptor-deficient and wild-type mice with hypercholesterolemia, injection of 1alpha,25-dihydroxyvitamin D3 consistently reduces levels of plasma and liver cholesterol and farnesoid X receptor small heterodimer partner Shp mRNA, and increases hepatic Cyp7a1 mRNA and protein. Activation of the vitamin D receptor represses hepatic SHP to increase levels of mouse CYP7A1 and reduce cholesterol
additional information
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in farnesoid X receptor-deficient and wild-type mice with hypercholesterolemia, injection of 1alpha,25-dihydroxyvitamin D3 consistently reduces levels of plasma and liver cholesterol and farnesoid X receptor small heterodimer partner Shp mRNA, and increases hepatic Cyp7a1 mRNA and protein. Activation of the vitamin D receptor represses hepatic SHP to increase levels of mouse CYP7A1 and reduce cholesterol
additional information
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the ability of CYP125A4 to oxidize 7alpha-hydroxycholesterol is due, at least in part, to the presence of a smaller amino acid side chain facing C-7 of the sterol substrate than in CYP125A3
additional information
thyroid hormones regulate cholesterol to bile acid conversion in similar ways in humans and rodent experimental models
additional information
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thyroid hormones regulate cholesterol to bile acid conversion in similar ways in humans and rodent experimental models
additional information
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transgenic mice overexpressing Cyp7a1 in the liver are resistant to high-fat diet-induced obesity, fatty liver, and insulin resistance. Cyp7a1-tg mice show increased hepatic cholesterol catabolism and an increased bile acid pool, they have increased secretion of hepatic very low density lipoprotein but maintained plasma triglyceride homeostasis, phenotype, overview
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additional information
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in farnesoid X receptor-deficient and wild-type mice with hypercholesterolemia, injection of 1alpha,25-dihydroxyvitamin D3 consistently reduces levels of plasma and liver cholesterol and farnesoid X receptor small heterodimer partner Shp mRNA, and increases hepatic Cyp7a1 mRNA and protein. Activation of the vitamin D receptor represses hepatic SHP to increase levels of mouse CYP7A1 and reduce cholesterol
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