Overview |
bs-70016r-100ul |
Androgen Receptor (Ser94) Antibody |
WB |
Specific for endogenous levels of the ~110k AR protein phosphorylated at Ser94. Immunolabeling is blocked by preadsorption of antibody with the phospho-peptide that was used to generate the antibody but not by the corresponding dephospho-peptide. |
Human |
Non-Human Primate |
Specifications |
Unconjugated |
Rabbit |
Synthetic phospho-peptide corresponding to amino acid residues surrounding Ser94 of human androgen receptor, conjugated to keyhole limpet hemocyanin (KLH). |
Ser94 |
Polyclonal |
IgG |
Lot Dependent |
Antigen Affinity purification from Pooled whole antiserum |
10 mM HEPES (pH 7.5), 150 mM NaCl, 100 µg per ml BSA and 50% glycerol. |
Storage at -20°C is recommended, as aliquots may be taken without freeze/thawing due to presence of 50% glycerol. Stable for at least 1 year at -20°C. |
Target |
367 |
P10275 |
AIS antibody, ANDR_HUMAN antibody, Androgen nuclear receptor variant 2 antibody, Androgen receptor (dihydrotestosterone receptor; testicular feminization; spinal and bulbar muscular atrophy; Kennedy disease) antibody, Androgen receptor antibody, androgen receptor splice variant 4b antibody, AR antibody, AR8 antibody, DHTR antibody, Dihydro testosterone receptor antibody, Dihydrotestosterone receptor (DHTR) antibody, Dihydrotestosterone receptor antibody, HUMARA antibody, HYSP1 antibody, KD antibody, Kennedy disease (KD) antibody, NR3C4 antibody, Nuclear receptor subfamily 3 group C member 4 (NR3C4) antibody, Nuclear receptor subfamily 3 group C member 4 antibody, SBMA antibody, SMAX1 antibody, Spinal and bulbar muscular atrophy (SBMA) antibody, Spinal and bulbar muscular atrophy antibody, Testicular Feminization (TFM) antibody, TFM antibody |
The androgen receptor (AR) is a DNA-binding transcription factor that regulates genes critical for the development and maintenance of the male sexual phenotype. Defects in androgen receptor have been shown to play a role in prostate cancer, and inhibition of AR activity through modulation of signal transduction pathways may delay prostate cancer progression (Heinlein and Chang 2004). Multiple phosphorylation sites have been identified on the androgen receptor that affect cross-talk between growth factor signaling and androgen in prostate development and cancer (Gioeli et al., 2002). One of these sites, at Ser94, appears constitutively phosphorylated and exhibits no response to treatments with stimulating hormone (Gioeli et al., 2002). The site at Ser94 is unique among the AR phosphorylation sites in that it does not achieve a maximal level of phosphorylation between translation and the initial round of nuclear import, having a strong bias for androgen-independent phosphorylation in the cytoplasm (Kesler et al., 2007). |
Application Dilution |
WB |
1:300-5000 |