Estrogen receptor-dependent transcriptional

Norris J, Fan D, Aleman C et al. Identification of a new subclass of Alu DNA repeats which can function as estrogen receptor-dependent transcriptional enhancers. J Biol Chem 1995 270[39] 22777-22782. 

The glycosides forms of the isoflavones have a weaker estrogenic action compared with their aglycone counterparts. In fact, they bind weakly to both ERot and ERP and the receptor-dependent transcriptional expression is poor. Once the glucose molecule is removed, the isoflavones bind more strongly to the estrogen receptor (Morito et al., 2001). 

A methanol extract of cola showed a time-, dose-, and estrogen receptor-dependent stimulation of the pS2 gene in estrogen receptor-positive human breast cancer cells (MCF-7), while an acetone extract showed no transcription stimulation of pS2 (Fontenot et al. 2007). 

As expected, in vitro transcription assays involving PARP-1, NAD, and PARC illustrate these predicted outcomes (Kim et al, 2004). Even when driven by a transcriptional activator, such as estradiol-bound estrogen receptor, transcription is repressed when PARP-1 is added to chromatin templates. The repression is reversed by NAD+, and the NAD+-dependent effects are reversed by PARC (Kim et al, 2004). This system for transcriptional control shifts new importance onto the enzymes responsible for synthesis of NAD+ in the nucleus, such as nicotinamide mononucleotide adenylyltransferase-1 (Magni et al, 2004). Because NAD+ facilitates the decompaction of chromatin and the derepression of transcription, nuclear NAD+ biosynthetic enzymes may play critical roles as cofactors. 

Reporter gene assays that measure ER binding-dependant transcriptional and translational activity. The yeast-based assays fall within this group. The vast majority of yeast-based assays are based on S. cerevisiae containing a stably transfected human estrogen, receptor (hER), although there are several variations in strain and detection method (NICEATM, 2002)... 

Schreurs, R.H., M.E. Quaedackers, W. Seinen and B. Van der Burg. Transcriptional activation of estrogen receptor ERalpha and ERbeta by polycyclic musks is cell type dependent. Toxicol. Appl. Pharmacol. 183 ... 

The anti-estrogen, tamoxifen, is the most commonly used hormonal therapy for breast cancer and has demonstrated positive effects on the cardiovascular and skeletal systems of postmenopausal women but is associated with an increased risk of uterine cancer. Tamoxifen is described as a SERM, a selective estrogen receptor modulator with a tissue selective profile that is caused by the different distribution of the a- and /3-subtypes of the estrogen receptor (ERa and ER/3) that activate and inhibit transcription respectively (77). These selective effects have been ascribed to differential interactions with gene promotor elements and coregulatory proteins depending on whether the ERa interacts directly, or in a tethered manner with DNA (78). In uterine tissue, tamoxifen interacts with a specific coactivator, SRCl, that is abundant in uterine tissue. 

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