Several members of nuclear receptor family are directly associated with human malignancies including breast cancer, prostate cancer and leukemia. The pathogenesis of each of these diseases is underpinned by the activities of a member of the superfamily; estrogen receptor-alpha (ER alpha) in breast cancer, androgen receptor (AR) in prostate cancer, and retinoic acid receptor alpha (RAR alpha) in acute promyelocytic leukemia (1). Retinoic acid receptors are important in the regulation of growth and differentiation of epithelial tissues, embryonic and central nervous system development and hematopoiesis (2). Retinoids mediate their effect by two classes of nuclear receptor proteins, the retinoic acid receptors (RARs) and the retinoid X receptors (RXRs), that each consists of three isotypes (α, β, and γ) encoded in separate genes (3). Upon dimerization with RXR, RARs can bind to specific enhancer sequences in the DNA, so-called retinoic acid response elements (RAREs), resulting in transcriptional activation of target genes in the presence of ligand (4). The retinoic acid receptor alpha gene is the target of chromosomal rearrangements in all cases of acute promyelocytic leukemia (APL). RAR alpha is a negative regulator of promyelocyte differentiation when not complexed with RA, and stimulates this differentiation when bound to RA (5).
Synonym: HAP; NR1B2; RRB2 and RARB.
Recombinant RAR beta Ligand Binding Domain was expressed in a bacterial system and purified by an affinity column in combination with FPLC chromatography Research Use Only. RARβ can be applied in in vitro transcription assays, DNA-protein and protein-protein interaction assays. The purified recombinant protein is greater than 95% homogeneous and contains no detectable protease, DNase and RNase activity. 1 unit equals 1 nanogram (ng) 0.5 mg/ml (in 1 x dilution buffer A) 1 X RAR dilution buffer (A)
References: 1. Hart S.M. (2002) Biol. Res. 35, 295-3003 2. Kastner et al. (1995) Cell, 83, 859-869 3. Leid et al., (1992) Trends Biochem. Sci. 17, 427-433 4. Linney et al., (1992) Curr. Top. Dev. Biol. 27, 309-350 5. Piazza et al. (2002) Oncogene 20, 7216-7222
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