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CUL9 anticorps (C-Term)

CUL9 Reactivité: Humain, Souris, Rat WB, IHC, ELISA Hôte: Lapin Polyclonal unconjugated
N° du produit ABIN356104
  • Antigène Voir toutes CUL9 Anticorps
    CUL9 (Cullin 9 (CUL9))
    Épitope
    • 7
    • 2
    • 2
    • 1
    • 1
    • 1
    • 1
    • 1
    C-Term
    Reactivité
    • 18
    • 7
    • 2
    • 1
    Humain, Souris, Rat
    Hôte
    • 15
    • 4
    Lapin
    Clonalité
    • 15
    • 4
    Polyclonal
    Conjugué
    • 19
    Cet anticorp CUL9 est non-conjugé
    Application
    • 18
    • 9
    • 7
    • 6
    • 4
    • 4
    • 4
    • 1
    • 1
    • 1
    Western Blotting (WB), Immunohistochemistry (IHC), ELISA
     Réactivité croisée
    Humain, Souris, Rat (Rattus)
    Purification
    affinity purified
    Immunogène
    17 amino acid synthetic peptide from near the carboxy terminus of human PARC.
    Isotype
    IgG
    Top Product
    Discover our top product CUL9 Anticorps primaire
  • Indications d'application
    Optimal working dilutions should be determined experimentally by the investigator.
    Restrictions
    For Research Use only
  • Format
    Liquid
    Stock
    -20 °C
  • Antigène
    CUL9 (Cullin 9 (CUL9))
    Autre désignation
    PARC/P53-associated Parkin-like Cytoplasmic Protein (CUL9 Produits)
    Synonymes
    anticorps H7AP1, anticorps PARC, anticorps RP3-330M21.2, anticorps parc, anticorps 1810035I07Rik, anticorps Cul-9, anticorps Parc, anticorps mKIAA0708, anticorps RGD1562008, anticorps cullin-9, anticorps cullin 9, anticorps cullin-9, anticorps CUL9, anticorps LOC100083225, anticorps cul9, anticorps LOC100561099, anticorps Cul9
    Sujet
    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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