Anti-Estrogen Receptor alpha(ER), clone YN00806m

Estrogen receptor (ER) is a steroid receptor of nuclear receptor superfamily, which consists of 553 aa. ER have three domains: the central domain of DNA binding, the hormone binding domain of C-terminal and the transcriptional activation domain of N-terminal. ER is involved in the regulation of female sex hormones, mainly mediating the growth, differentiation and other functions of 17 (E2) on several target tissues . ER alpha is expressed in the nucleus of epithelial cells of normal breast and endometrium, and also in breast cancer. Immunohistochemistry analysis showed that the overall survival rate of steroid positive prediction is good. RE alpha can also be used as a tumor marker combined with anti-progesterone receptor. Protein function: Nuclear hormone receptor. The steroid hormones and their receptors are involved in the regulation of eukaryotic gene expression and affect cellular proliferation and differentiation in target tissues. Ligand-dependent nuclear transactivation involves either direct homodimer binding to a palindromic estrogen response element (ERE) sequence or association with other DNA-binding transcription factors, such as AP-1/c-Jun, c-Fos, ATF-2, Sp1 and Sp3, to mediate ERE- independent signaling. Ligand binding induces a conformational change allowing subsequent or combinatorial association with multiprotein coactivator complexes through LXXLL motifs of their respective components. Mutual transrepression occurs between the estrogen receptor (ER) and NF-kappa-B in a cell-type specific manner. Decreases NF-kappa- B DNA-binding activity and inhibits NF-kappa-B-mediated transcription from the IL6 promoter and displace RELA/p65 and associated coregulators from the promoter. Recruited to the NF-kappa-B response element of the CCL2 and IL8 promoters and can displace CREBBP. Present with NF-kappa-B components RELA/p65 and NFKB1/p50 on ERE sequences. Can also act synergistically with NF-kappa-B to activate transcription involving respective recruitment adjacent response elements, the function involves CREBBP. Can activate the transcriptional activity of TFF1. Also mediates membrane-initiated estrogen signaling involving various kinase cascades. Essential for MTA1-mediated transcriptional regulation of BRCA1 and BCAS3 (PubMed:17922032). [The UniProt Consortium]