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1 Citations
Facts about Cytochrome P450 7A1.
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Human | |
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Gene Name: | CYP7A1 |
Uniprot: | P22680 |
Entrez: | 1581 |
Belongs to: |
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cytochrome P450 family |
Cholesterol 7-alpha-hydroxylase; cholesterol 7-alpha-monooxygenase; CP7A; CYP7; CYP7A1; CYP7MGC126826; CYPVII; Cytochrome P450 7A1; cytochrome P450, family 7, subfamily A, polypeptide 1; cytochrome P450, subfamily VIIA (cholesterol 7 alpha-monooxygenase); cytochrome P450, subfamily VIIA polypeptide 1; EC 1.14.13; EC 1.14.13.17; MGC138389; polypeptide 1
Mass (kDA):
57.661 kDA
Human | |
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Location: | 8q12.1 |
Sequence: | 8; NC_000008.11 (58490178..58500163, complement) |
Detected in liver.
Endoplasmic reticulum membrane; Single-pass membrane protein. Microsome membrane; Single-pass membrane protein.
Research on cancer is one of the many purposes for monoclonal CYP7A1 antibodies. Scientists can spot changes in the abundance of the enzyme's mRNA and activity with this antibody as it is specific for it. Researchers can submit their findings for specific species or samples to earn credit for the product. This antibody is available to all scientists around the globe. These are the best uses and benefits of the CYP7A1 monoclonal anti-body.
We analyzed CYP7A1's mRNA as well as enzyme activity in wildtype mice as well as knockout mice. We found that mice lacking CYP7A1 have a smaller bile acid pool size, and less syntheses of bile acids. The bile acids pools of male mice are bigger than those of female mice. This indicates that CYP7A1 is involved in bile-acid synthesis.
Cyp7A1 is involved in the biosynthetic procedure of cholesterol into a multitude of secondary and primary bile acids. Cyp7a1 is a key player in the negative feedback regulation of these pathways. The absence of Cyp8b1 gene blocks cholate or bile acid formation. The bile acid concentration of Cyp8b1/ mice is large and a significant amount of cholate is present.
In addition, a null mutation in the gene is the cause of no detectable CYP7A mRNA or protein. Cyp7a1mice carry CYP7A1 mRNA inactive or lacking and CYP7A1 activation that is not detectable. These mice also have normal levels of BIP the immunoglobulin heavy-chain binding protein.
In addition to its function in RNA metabolism, Apobec-1 also has been shown to enhance RNA turnover. Apobec-1-mediated C to U editing of RNA requires stoichiometric proportions of trans-acting proteins. Apobec-1's mediated modulation of Cyp7A1 mRNA expression could result in the expression of micro-RNAs in a way that differs between HepG2 cell types and Apobec-1 mice.
Moreover, Cyp7A1 mRNA levels in wildtype mice are significantly lower than those in Cyp8b1/-mice. The mice are not able to process LDLC however their plasma LDLC levels are higher than those of their Cyp8b1-/ counterparts. Thus, CYP7 is a significant regulator of cholesterol homeostasis.
The mRNA of CYP8B1 in mice deficient in the PXR mutation is only detected in the liver. These mice were crossed with wild-type mice. Hence, these mice will have a mutant allele following homologous recombination within embryonic stem cells. When the heterozygous mice were genotyped, they showed a decrease in CYP8B1 mRNA levels, while the wild-type mice have an increase in CYP7A1's expression.
The composition of bile acids is affected by Cyp8b1. Wildtype mice experience a decrease in cholate levels as a result of the loss of Cyp8b1. The bile acids produced were 85% cholate and 4percent b-muricholate. The proportion of cholate and deoxycholate in wild type mice was compared to that of mutant mice.
Additionally, a decrease in Cyp7A1 mRNA in Apobec-1-mice resulted from increased cholesterol production and gallstone formation. Furthermore, Apobec-1 mice had accelerated gallstone formation, as well as an increased metabolism of biliary lipids. These changes were consistent with an increased bile acid hydrophobicity index.
To determine the levels of mRNA and enzyme activities in wildtype mice, total RNA from the livers of cyp7a1 knockout and chromosomal leukemia (CFP) was isolated. The RNA was isolated using DNA-free RNA isolation kits. Reverse transcription and PCR were conducted using a PRISM7900HT Sequence Detection system. The cDNA primer sequences for CYP7A1 and SHP were respectively TGCACCTCGAAT and CAAGACAACTGACATCAACTAAACAACTAAACTA.
The CYP7A1 marker performs many useful functions, ranging from checking cholesterol metabolism and preventing the development of HFD, a type of liver disease known as fatty. This marker was knocked out in mice who were intolerant to obesity, insulin resistance and fat liver. These mice had lower expression of a key enzyme in the conjugation of Bile Acids, bile Acid-CoA.
Each group was comprised of N = 6-7 mice. Samples were randomly chosen from each group for analysis of data. The analyzed data were processed using GraphPad Prism 9.1. A single wildtype mouse that had extremely high BA levels was not included in statistical analysis. Means were presented as boxplots , with S.E., and statistical significance was assessed using an t-test for two-tailed students at P 0.05.
The CYP7A1 marker may also be helpful in understanding the relationship between cholesterol metabolism and expression of Tff3. The CYP7A1 marker can help researchers understand the role played by Bile acids in cholestasis. A recent study revealed that both the rat and the human Cyp7A1 gene is involved in the biosynthesis of cholesterol, bile acids and bile acids. The CYP7A1 protein is crucial for the biosynthesis and regulation of lipid metabolism. It also regulates bile Acid synthesizing.
The CYP7A1 marker also proved helpful in studies that examined the role of theliver in a variety of diseases. In the HNF4a mouse model of gene-deficiency fatty liver was associated with increased triglycerides and free fatty acids. The HNF4a mice with KO had more lipid-metabolizing enzymes that their WT counterparts.
HNF4a, GR4a, and GR4a both are involved in regulating the expression of liver-specific fat catabolic genes as well as lipogenic genes. The inhibition of HNF4a or GR4a by HFHS reduces liver X receptor-mediated expression of lipogenic genes. Similar to GR, HNF4a also co-regulate PPARg. Together, these proteins protect against hyperlipidemia and fatty liver.
EGFR, STAT3, and STAT3 have been proven to be responsible for impaired liver regeneration. Inhibition of these genes could result in a fibrosis of the liver. GR has also been found to increase osteopontin production. Similarly, osteopontin is known to promote cholangiocarcinogenesis. It isn't yet certain if EGFR or GR are the most significant cause of this condition.
Boster Bio's Anti-CYP7A1 monoclonal antigen is highly sensitive and specific. These antibodies are validated for immunohistochemistry, Western Blotting, ELISA, and Flow Cytometry. A biotechnology company that in boster antibodies. The company offers several types of conjugates to anti-CYP7A1 antibody.
CYP7A1 belongs to the cytochrome P450 enzyme family. It is the main enzyme responsible for limiting the rate in cholesterol catabolism and biosynthesis of bile acids. CYP7A1 catalyzes the transformation of cholesterol + NADPH + O2 to 7-alpha-hydroxycholesterol. It is regulated by the bile acid receptor FXR. It is located in the mitochondria of both the liver as well as the kidney.
PMID: 8439551 by Nishimoto M., et al. Structure of the gene encoding human liver cholesterol 7 alpha- hydroxylase.
PMID: 2384150 by Noshiro M., et al. Molecular cloning and sequence analysis of cDNA encoding human cholesterol 7 alpha-hydroxylase.
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