The aryl hydrocarbon receptor (AHR) is a ligand activated transcription factor that controls the expression of a diverse set of genes. In the absence of ligand, AHR is retained in the cytoplasm. Upon ligand binding AHR translocates to the nucleus where it forms a heterodimer with aryl hydrocarbon receptor nuclear translocator (ARNT) (1). This receptor complex then recognizes AHR-response elements in target genes to regulate their transcription. AHR is well known for its ability to bind to the toxic chemical 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). TCDD is a highly toxic and carcinogenic compound that is produced as a side product during the industrial manufacturing of certain chemicals (1). The toxic effects of TCDD are mediated exclusively through binding to AHR. In addition to this role in TCDD toxicity, AHR functions during tumorigenesis and is found at elevated levels in aggressive tumors and tumor cell lines (2). Immunohistochemistry with AHR antibodies has shown elevated levels in primary breast cancer samples (3). AHR has also been shown to be important in the adaptive immune response and T-cell differentiation (4). In a study by Vogel et al. identified an interaction between AHR signaling and NF-κB (4). The researchers monitored AHR induction by LPS through western blots with an AHR antibody. They demonstrated AHR induction depends on NF-κB and identified NF-κB-binding elements upstream of the AHR gene (4). In an attempt to identify genes that mediate the toxic effects of TCDD, Fisher et al. analyzed genes that were upregulated in response to TCDD exposure (5). The authors performed chromatin immunoprecipitation with an AHR antibody to confirm direct transcriptional regulation of these candidate genes (5). Thombospondin-1 was identified by Dabir et al. as one of the many targets of AHR (6). The researchers performed immunostaining with an AHR antibody and showed AHR is induced in endothelial cells by high glucose levels (6). They then performed chromatin immunoprecipitation with the AHR antibody and showed AHR directly associates with the promoter of the thrombospondin-1 gene to activate its transcription (6). These results demonstrate a link between AHR activation and the observed pathological effects of hyperglycemia (6).
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