CYP26A1
CYP26A1 is a member of the cytochrome P450 superfamily of enzymes. These enzymes are monooxygenases which catalyze many reactions involved in drug metabolism and synthesis of cholesterol, steroids, and other lipids. The CYP26A1 enzyme is specifically involved in the metabolism of retinoic acid, a derivative of vitamin A that plays a crucial role in cell differentiation, growth, and embryonic development.
Function[edit | edit source]
CYP26A1 is responsible for the hydroxylation of retinoic acid, converting it into more polar metabolites that are more easily excreted from the body. This process is essential for maintaining the appropriate levels of retinoic acid, as both deficiency and excess of retinoic acid can lead to severe developmental abnormalities and diseases.
Gene[edit | edit source]
The CYP26A1 gene is located on chromosome 10 in humans. It is one of three known genes in the CYP26 family, the others being CYP26B1 and CYP26C1. These genes share a high degree of sequence similarity and functional overlap, but they are expressed in different tissues and at different stages of development.
Clinical Significance[edit | edit source]
Mutations in the CYP26A1 gene can lead to disorders related to retinoic acid metabolism. Abnormal levels of retinoic acid have been implicated in various conditions, including congenital malformations, cancer, and skin disorders. Understanding the function and regulation of CYP26A1 is therefore important for developing therapeutic strategies for these conditions.
Expression[edit | edit source]
CYP26A1 is expressed in various tissues, including the liver, kidney, and brain. Its expression is tightly regulated by retinoic acid levels, ensuring a feedback mechanism that maintains homeostasis.
Related Enzymes[edit | edit source]
Other enzymes involved in retinoic acid metabolism include CYP26B1, CYP26C1, and CYP2C8. These enzymes work together to regulate the concentration of retinoic acid in different tissues and at different developmental stages.
See Also[edit | edit source]
References[edit | edit source]
External Links[edit | edit source]
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