AH receptor: Difference between revisions
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AH receptor (AHR, dioxin receptor, aryl hydrocarbon receptor) | AH receptor (AHR, dioxin receptor, aryl hydrocarbon receptor): a cell protein that initiates many of the effects of dioxin-like chemicals. Its primary function in the body is uncertain, and it is structurally related to many other important cell proteins involved for instance in rhythmic functions (clock proteins) and organ development. | ||
''Mechanism'': When TCDD or other dioxins enter the cell, they bind to AHR, this moves from cellular cytoplasm to nucleus, forms a pair with another protein [[ARNT]], and this heterodimer (complex of two separate proteins) binds to [[DNA]]. This binding initiates the activation of a number of genes depending on the binding site of the dimer. Because it initiates the reading of a gene (transcription), it is called a [[Transcription factor]] (see this). After | |||
a high dose of dioxin, AH receptor may activate or inhibit hundreds of genes in rats (see ''Tijet et al., Molec. Pharmacol. 2006:69:140–153'').One of the best studied of such genes is the gene of CYP1A1 enzyme, which is a xenobiotic metabolising enzyme. CYP1A1 oxidises many foreign chemicals and makes them more water-soluble usually aided by a second enzyme conjugating it to a water-soluble carrier molecule (see [[Metabolism]]). Activation of CYP1A1 gene increases the enzymatic activity even by a factor of several hundred. It is not known which gene is (genes are) responsible for the toxic effects of dioxins (for more information on AHR, see ''Lindén et al., Front. Neuroendocrinol. 2010:31:452–478'', [http://pubmed.gov/20624415]). | |||
[[category:Dioxin synopsis]] | [[category:Dioxin synopsis]] | ||
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AH receptor (AHR, dioxin receptor, aryl hydrocarbon receptor): a cell protein that initiates many of the effects of dioxin-like chemicals. Its primary function in the body is uncertain, and it is structurally related to many other important cell proteins involved for instance in rhythmic functions (clock proteins) and organ development.
Mechanism: When TCDD or other dioxins enter the cell, they bind to AHR, this moves from cellular cytoplasm to nucleus, forms a pair with another protein ARNT, and this heterodimer (complex of two separate proteins) binds to DNA. This binding initiates the activation of a number of genes depending on the binding site of the dimer. Because it initiates the reading of a gene (transcription), it is called a Transcription factor (see this). After a high dose of dioxin, AH receptor may activate or inhibit hundreds of genes in rats (see Tijet et al., Molec. Pharmacol. 2006:69:140–153).One of the best studied of such genes is the gene of CYP1A1 enzyme, which is a xenobiotic metabolising enzyme. CYP1A1 oxidises many foreign chemicals and makes them more water-soluble usually aided by a second enzyme conjugating it to a water-soluble carrier molecule (see Metabolism). Activation of CYP1A1 gene increases the enzymatic activity even by a factor of several hundred. It is not known which gene is (genes are) responsible for the toxic effects of dioxins (for more information on AHR, see Lindén et al., Front. Neuroendocrinol. 2010:31:452–478, [1]).