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CUL9 antibody (C-Term)

CUL9 Reactivity: Human, Mouse, Rat WB, IHC, ELISA Host: Rabbit Polyclonal unconjugated
Catalog No. ABIN356104
  • Target See all CUL9 Antibodies
    CUL9 (Cullin 9 (CUL9))
    Binding Specificity
    • 7
    • 2
    • 2
    • 1
    • 1
    • 1
    • 1
    • 1
    C-Term
    Reactivity
    • 18
    • 7
    • 2
    • 1
    Human, Mouse, Rat
    Host
    • 15
    • 4
    Rabbit
    Clonality
    • 15
    • 4
    Polyclonal
    Conjugate
    • 19
    This CUL9 antibody is un-conjugated
    Application
    • 18
    • 9
    • 7
    • 6
    • 4
    • 4
    • 4
    • 1
    • 1
    • 1
    Western Blotting (WB), Immunohistochemistry (IHC), ELISA
    Cross-Reactivity
    Human, Mouse (Murine), Rat (Rattus)
    Purification
    affinity purified
    Immunogen
    17 amino acid synthetic peptide from near the carboxy terminus of human PARC.
    Isotype
    IgG
    Top Product
    Discover our top product CUL9 Primary Antibody
  • Application Notes
    Optimal working dilutions should be determined experimentally by the investigator.
    Restrictions
    For Research Use only
  • Format
    Liquid
    Storage
    -20 °C
  • Target
    CUL9 (Cullin 9 (CUL9))
    Alternative Name
    PARC/P53-associated Parkin-like Cytoplasmic Protein (CUL9 Products)
    Synonyms
    H7AP1 antibody, PARC antibody, RP3-330M21.2 antibody, parc antibody, 1810035I07Rik antibody, Cul-9 antibody, Parc antibody, mKIAA0708 antibody, RGD1562008 antibody, cullin-9 antibody, cullin 9 antibody, cullin-9 antibody, CUL9 antibody, LOC100083225 antibody, cul9 antibody, LOC100561099 antibody, Cul9 antibody
    Background
    PARC (p53 associated parkin like cytoplasmic protein) antibody directly interacted and formed an approximately 1MD complex with p53 in the cytoplasm of unstressed cells. In the absence of stress, inactivation of PARC induced nuclear localization of endogenous p53 and activated p53 dependent apoptosis. Overexpression of PARC promoted cytoplasmic sequestration of ectopic p53. Furthermore, abnormal cytoplasmic localization of p53 was observed in a number of neuroblastoma cell lines, RNA interference-mediated reduction of endogenous PARC significantly sensitized these neuroblastoma cells in the DNA damage response. These results revealed that PARC is a critical regulator in controlling p53 subcellular localization and subsequent function.
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