|Reactivity||Human, Mouse, Rat|
|Calculated MW||99188 Da|
|Other Names||Androgen receptor, Dihydrotestosterone receptor, Nuclear receptor subfamily 3 group C member 4, AR, DHTR, NR3C4|
|Target/Specificity||A synthetic peptide corresponding to residues on the C-terminus of human Androgen Receptor was used as an immunogen.|
|Format||50 mM Tris-Glycine (pH 7.4), 0.15 M NaCl, 40% Glycerol, 0.01% sodium azide and 0.05% BSA.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.|
|Precautions||Androgen Antibody is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||Steroid hormone receptors are ligand-activated transcription factors that regulate eukaryotic gene expression and affect cellular proliferation and differentiation in target tissues. Transcription factor activity is modulated by bound coactivator and corepressor proteins. Transcription activation is down-regulated by NR0B2. Activated, but not phosphorylated, by HIPK3 and ZIPK/DAPK3.|
|Cellular Location||Nucleus. Cytoplasm. Note=Detected at the promoter of target genes (PubMed:25091737). Predominantly cytoplasmic in unligated form but translocates to the nucleus upon ligand- binding. Can also translocate to the nucleus in unligated form in the presence of RACK1.|
|Tissue Location||Isoform 2 is mainly expressed in heart and skeletal muscle (PubMed:15634333). Isoform 3 is expressed by basal and stromal cells of prostate (at protein level) (PubMed:19244107).|
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Provided below are standard protocols that you may find useful for product applications.
Androgen receptor (AR) is a member of the steroid receptor superfamily that may require coactivators for proper or maximal transactivation. (1). The androgen receptor (AR) is essential for the growth of prostate cancer cells. It has been reported that tyrosine phosphorylation of AR is induced by growth factors and elevated in hormone-refractory prostate tumors. Data suggest that growth factors and their downstream tyrosine kinases, which are elevated during hormone-ablation therapy, can induce tyrosine phosphorylation of AR and such modification may be important for prostate tumor growth under androgen-depleted conditions (2). Cellular signaling occurs following androgen binding to the AR and translocation to the nucleus. This activated complex associates with androgen-responsive elements contained in the DNA sequence of target genes, affecting the transcriptional activity of these genes. Mutations may result in changes in the function or expression of AR protein, or of growth factors and their receptors under the influence of AR coactivators, and AR amplification could lead to activation of the receptor by reduced levels of androgens (3).
1. Callewaert L, et al. Biochem Biophys Res Commun 306(1) 46-52, 2003.
2. Qiu Y, et al. Cancer Cell Vol 10:309-319, 2006.
3. Hamdy F, et al. Nature Clinical Practice Urology 2:368-399 2005.
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