Post by Max on Jun 12, 2005 18:56:01 GMT -5
(Ro)accutane induced significant interaction with the dopamine beta hydroxylase
Shared location between the dopamine beta hydroxylase and the retinoid x receptor alpha
Targets of retinoid regulation include dopamine D2 receptor and tyrosine hydroxylase and dopamine â-hydroxylase [6]. The dopamine beta-hydroxylase (DBH), is an enzyme that produces noradrenalin from dopamine [2]. The retinoid X receptor alpha is one of a number of retinoic acid receptors which are members of the steroid/thyroid hormone superfamily. Localization of RXRA was achieved using the polymerase chain reaction on a panel of somatic cell hybrids. A cosmid clone was isolated using the RXRA PCR product, and this was used to further localize the gene by fluorescence in situ hybridization to chromosome 9q34 distal to the dopamine beta hydroxylase gene (DBH) [1]. Since retinoid signalling is required for normal expression of D2 receptors, it is possible that 13-cis-RA has an effect on D2 receptors but this has not been tested [6].
Transcription through AP-2
In adult mammals, AP-2 is expressed in both neural and non-neural tissues. However, the function of AP-2 in different neuronal phenotypes is poorly understood. In this study, transcriptional regulation of tyrosine hydroxylase (TH) and dopamine beta-hydroxylase (DBH) genes by AP-2 was investigated. AP-2 binding sites were identified in the upstream regions of both genes. Exogenous expression of AP-2 robustly transactivated TH and DBH promoter activities in non-catecholaminergic cell lines. While AP-2 regulates the DBH promoter activity via a single site, transactivation of the TH promoter by AP-2 appears to require multiple sites. In support of this, mutation of multiple AP-2 binding sites but not that of single site diminished the basal promoter activity of the TH gene in cell lines that express TH and abolished transactivation by exogenous AP-2 expression in cell lines that do not express TH. In contrast, mutation of a single AP-2 binding site of the DBH gene completely abolished transactivation by AP-2. [3].
Transcription through angiotensin receptors
Long-term AT(1) receptor blockade decreased adrenomedullary AT(1) receptor binding, AT(2) receptor binding and AT(2) receptor protein, rat tyrosine hydroxylase (TH) mRNA, norepinephrine (NE) content, Fos-related antigen 2 (Fra-2) protein, phosphorylated cAMP response element binding protein (pCREB), and ERK2 [4].
The dopamine D(2) receptor (D(2)R) is involved in the regulation of acethylcholin (ACh) release in the hippocampus [5].
Location Dopamine receptor D4: 11p15.5 (genatlas)
Shared location between the dopamine beta hydroxylase and the retinoid x receptor alpha
Targets of retinoid regulation include dopamine D2 receptor and tyrosine hydroxylase and dopamine â-hydroxylase [6]. The dopamine beta-hydroxylase (DBH), is an enzyme that produces noradrenalin from dopamine [2]. The retinoid X receptor alpha is one of a number of retinoic acid receptors which are members of the steroid/thyroid hormone superfamily. Localization of RXRA was achieved using the polymerase chain reaction on a panel of somatic cell hybrids. A cosmid clone was isolated using the RXRA PCR product, and this was used to further localize the gene by fluorescence in situ hybridization to chromosome 9q34 distal to the dopamine beta hydroxylase gene (DBH) [1]. Since retinoid signalling is required for normal expression of D2 receptors, it is possible that 13-cis-RA has an effect on D2 receptors but this has not been tested [6].
Transcription through AP-2
In adult mammals, AP-2 is expressed in both neural and non-neural tissues. However, the function of AP-2 in different neuronal phenotypes is poorly understood. In this study, transcriptional regulation of tyrosine hydroxylase (TH) and dopamine beta-hydroxylase (DBH) genes by AP-2 was investigated. AP-2 binding sites were identified in the upstream regions of both genes. Exogenous expression of AP-2 robustly transactivated TH and DBH promoter activities in non-catecholaminergic cell lines. While AP-2 regulates the DBH promoter activity via a single site, transactivation of the TH promoter by AP-2 appears to require multiple sites. In support of this, mutation of multiple AP-2 binding sites but not that of single site diminished the basal promoter activity of the TH gene in cell lines that express TH and abolished transactivation by exogenous AP-2 expression in cell lines that do not express TH. In contrast, mutation of a single AP-2 binding site of the DBH gene completely abolished transactivation by AP-2. [3].
Transcription through angiotensin receptors
Long-term AT(1) receptor blockade decreased adrenomedullary AT(1) receptor binding, AT(2) receptor binding and AT(2) receptor protein, rat tyrosine hydroxylase (TH) mRNA, norepinephrine (NE) content, Fos-related antigen 2 (Fra-2) protein, phosphorylated cAMP response element binding protein (pCREB), and ERK2 [4].
The dopamine D(2) receptor (D(2)R) is involved in the regulation of acethylcholin (ACh) release in the hippocampus [5].
Location Dopamine receptor D4: 11p15.5 (genatlas)