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  3. Androgen Receptor (AR-V7 Specific) (E3O8L) Rabbit Monoclonal Antibody (BSA and Azide Free)
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Androgen Receptor (AR-V7 Specific) (E3O8L) Rabbit Monoclonal Antibody (BSA and Azide Free) #23164

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  • WB
  • ELISA+

    Product Specifications

    REACTIVITY H
    SENSITIVITY Endogenous
    MW (kDa) 80
    Source/Isotype Rabbit IgG
    Application Key:
    • WB-Western Blotting 
    • ELISA+-ELISA and/or ELISA-like Assays 
    Species Cross-Reactivity Key:
    • H-Human 

    Product Information

    Product Usage Information

    This product is the carrier free version of product #19672. All data were generated using the same antibody clone in the standard formulation which contains BSA and glycerol.

    This formulation is ideal for use with technologies requiring specialized or custom antibody labeling, including fluorophores, metals, lanthanides, and oligonucleotides. It is not recommended for ChIP, ChIP-seq, CUT&RUN or CUT&Tag assays. If you require a carrier free formulation for chromatin profiling, please contact us. Optimal dilutions/concentrations should be determined by the end user.

    BSA and Azide Free antibodies are quality control tested by size exclusion chromatography (SEC) to determine antibody integrity.

    Formulation

    Supplied in 1X PBS (10 mM Na2HPO4, 3 mM KCl, 2 mM KH2PO4, and 140 mM NaCl (pH 7.8)). BSA and Azide Free.

    For standard formulation of this product see product #19672

    Storage

    Store at -20°C. This product will freeze at -20°C so it is recommended to aliquot into single-use vials to avoid multiple freeze/thaw cycles. A slight precipitate may be present and can be dissolved by gently vortexing. This will not interfere with antibody performance.

    Specificity / Sensitivity

    Androgen Receptor (AR-V7 Specific) (E3O8L) Rabbit Monoclonal Antibody (BSA and Azide Free) recognizes endogenous levels of total AR-V7 protein. This antibody does not cross-react with full-length AR protein, but immunoprecipitates a 120 kDa protein of unknown identity.

    Species Reactivity:

    Human

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Leu639 of human androgen receptor (V7 isoform) protein.

    Background

    Angiogenesis is defined as the physiological process by which new blood vessels are formed from pre-existing blood vessels. It is a critical process that enables specific physiological conditions in healthy adults, including development, skeletal muscle hypertrophy, and wound healing (1,2). Angiogenesis can be aberrantly activated to generate new blood vessels during pathological conditions such as cancer, neovascular disorders, and chronic inflammation. Angiogenesis is a complicated process regulated by multiple mechanisms and pathways (3). VEGFR2 is a member of the family of receptor tyrosine kinases (RTKs) mainly located in endothelial cells and is a major player in angiogenesis. VEGF-VEGFR2 ligand-receptor activation is the key signaling pathway for angiogenesis activation (4,5). Multiple non-VEGF RTK activations can replace VEGFR to promote angiogenesis (6,7), including PDGFR (9), FGFR (8), and Tie2 (10). These RTKs are targets for an antiangiogenic based disease treatment (11,12).

    The AR3 or AR-V7 isoform, which lacks the typical ligand binding domain, is created through the alternative splicing of cryptic exons (4-5). AR-V7 is frequently expressed in castration-resistant prostate cancer (CRPC) and while dependent on the activity of the full-length androgen receptor (AR-FL), AR-V7 can activate a completely distinct transcriptional program (6-8). While enzalutamide and abiraterone have been beneficial in treating CRPC through the ligand binding domain of AR-FL, resistance in patients has been shown to be associated with AR-V7 detection in circulating tumor cells (9-12). Studies probing into mechanisms of overcoming this resistance are currently being explored and may help in stratifying patient populations for more personalized therapies (13-15).
    1. Li, J. and Al-Azzawi, F. (2009) Maturitas 63, 142-8.
    2. Avila, D.M. et al. (2001) J. Steroid. Biochem. Mol. Biol. 76, 135-142.
    3. Montgomery, J.S. et al. (2001) J. Pathol. 195, 138-146.
    4. Leung, D.W. et al. (1989) Science 246, 1306-9.
    5. Jeltsch, M. et al. (2013) Cold Spring Harb Perspect Biol 5, a009183. doi: 10.1101/cshperspect.a009183.
    6. Zhao, Y. and Adjei, A.A. (2015) Oncologist 20, 660-73.
    7. Vimalraj, S. (2022) Int J Biol Macromol 221, 1428-1438.
    8. Lieu, C. et al. (2011) Clin Cancer Res 17, 6130-9.
    9. Hellberg, C. et al. (2010) Recent Results Cancer Res 180, 103-14.
    10. Duran, C.L. et al. (2021) Cancers (Basel) 13, 5730. doi: 10.3390/cancers13225730.
    11. Ramjiawan, R.R. et al. (2017) Angiogenesis 20, 185-204.
    12. Socinski, M.A. (2011) Cancer Treat Rev 37, 611-7.
    13. Hu, R. et al. (2009) Cancer Res 69, 16-22.
    14. Guo, Z. et al. (2009) Cancer Res 69, 2305-13.
    15. Watson, P.A. et al. (2010) Proc Natl Acad Sci U S A 107, 16759-65.
    16. Sun, S. et al. (2010) J Clin Invest 120, 2715-30.
    17. Hu, R. et al. (2012) Cancer Res 72, 3457-62.
    18. Scher, H.I. et al. (2012) N Engl J Med 367, 1187-97.
    19. de Bono, J.S. et al. (2011) N Engl J Med 364, 1995-2005.
    20. Ryan, C.J. et al. (2013) N Engl J Med 368, 138-48.
    21. Antonarakis, E.S. et al. (2014) N Engl J Med 371, 1028-38.
    22. Liu, C. et al. (2014) Clin Cancer Res 20, 3198-3210.
    23. Sarwar, M. et al. (2016) Oncotarget 7, 63065-63081.
    24. Ku, S.Y. et al. (2017) Science 355, 78-83.

    Alternate Names

    AIS; ANDR; Androgen receptor; Androgen receptor splice variant 3; AR; AR iso3; AR-V7; AR8; DHTR; Dihydrotestosterone receptor; HUMARA; HYSP1; KD; NR3C4; Nuclear receptor subfamily 3 group C member 4; SBMA; SMAX1; TFM

    Database Links

    UniProt ID: P10275-3


    Entrez-Gene Id: 367


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