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Androgen Receptor (AR-V7 specific) Antibody [F19P24]

Cat.No.: F1669

    Application: Reactivity:

    Usage Information

    Dilution
    1:1000
    1:250
    Application
    WB, IHC
    Reactivity
    Human
    Source
    Rabbit Monoclonal Antibody
    Storage Buffer
    PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3
    Storage (from the date of receipt)
    -20°C (avoid freeze-thaw cycles), 2 years
    Predicted MW Observed MW
    68 kDa 80 kDa
    *Why do the predicted and actual molecular weights differ?
    The following reasons may explain differences between the predicted and actual protein molecular weight.
    Positive Control 22Rv1 (1% SDS Hot lysis)
    Negative Control Human prostate cancer tissue; Human liver tissue; Human hepatocellular carcinoma tissue; Human fetal liver; T-47D cells; PC-3 cells; LNCaP cells; 22Rv1 (RIPA lysis method)

    Datasheet & SDS

    Biological Description

    Specificity
    Androgen Receptor (AR-V7 specific) Antibody [F19P24] detects endogenous levels of total Androgen Receptor (AR-V7 specific) protein.
    Clone
    F19P24
    Synonym(s)
    AR; NR3C4; Androgen receptor; Dihydrotestosterone receptor; Nuclear receptor subfamily 3 group C member 4
    Background
    Androgen Receptor variant 7 (AR-V7) is a constitutively active splice variant of the full-length androgen receptor, generated by alternative splicing that retains the N-terminal transactivation domain, the DNA-binding domain with two zinc fingers, and the hinge region, but lacks the ligand-binding domain, which is replaced by a unique 16-amino-acid cryptic exon at the C-terminus. This structural alteration allows AR-V7 to enter the nucleus independently of androgen binding and importin-α/β pathways, exhibit high intranuclear mobility, form homodimers through the DNA-binding domain, and bind DNA to activate a distinct set of target genes. In castration-resistant prostate cancer, AR-V7 drives androgen receptor signaling even in low-androgen conditions by activating genes involved in proliferation and survival, such as EDN2, TMPRSS2, and KLK3, while also regulating isoform-specific alternative splicing events and contributing to therapy resistance against anti-androgens. AR-V7 promotes tumor progression and poor clinical outcomes, and its detection in circulating tumor cells serves as a biomarker for stratifying patients.
    References
    • https://pubmed.ncbi.nlm.nih.gov/32989253/
    • https://pubmed.ncbi.nlm.nih.gov/20823238/

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