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R Recombinant
Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.

LLGL1 (D2B5A) Rabbit mAb #12159

Filter:
  • WB
  • IF

    Supporting Data

    REACTIVITY H Mk
    SENSITIVITY Endogenous
    MW (kDa) 130
    Source/Isotype Rabbit IgG
    Application Key:
    • WB-Western Blotting 
    • IF-Immunofluorescence 
    Species Cross-Reactivity Key:
    • H-Human 
    • Mk-Monkey 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000
    Immunofluorescence (Immunocytochemistry) 1:50

    Storage

    Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA, 50% glycerol and less than 0.02% sodium azide. Store at –20°C. Do not aliquot the antibody.

    Protocol

    Specificity / Sensitivity

    LLGL1 (D2B5A) Rabbit mAb recognizes endogenous levels of total LLGL1 protein. This antibody does not cross-react with LLGL2.

    Species Reactivity:

    Human, Monkey

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Leu757 of human LLGL1 protein.

    Background

    In Drosophila, lethal giant larvae (lgl), discs large (dlg), and scribble (scrib) act as tumor suppressor genes. Their loss of function in flies causes neoplastic overgrowth of larval brain tissue and imaginal epithelial cells hallmarked by disruption of the cytoskeletal network and cellular polarity (1,2). The human homolog of the Drosophila lgl protein, lethal giant larvae protein homolog 1
    (LLGL1), is a cytoskeletal protein implicated in regulating cellular organization, migration, and cell polarity (3). As in Drosophila, decreased expression of LLGL1 correlates with an increased incidence of cellular overgrowth and malignant transformation (4-6). In mammalian epithelial cells, LLGL1 redistributes from the cytoplasm to regions of cell-cell contact, allowing the establishment and maintainence of a polarized morphology (7). LLGL1 also plays a role in the formation of epithelial junctions via its direct interactions with PAR6 and aPKC, the latter of which has been shown to phosphorylate LLGL1 at Ser663, thus restricting its localization to the basolateral region of the cell (8). LLGL1 may also play an additional, unrealized role in cellular development and differentiation as indicated by the fact that Drosophila lgl has been implicated in controlling self-renewal and differentiation of progenitor cells (9). Recent studies in mice have suggested that a mammalian LLGL1 homolog that does not have tumor suppressor-like acitvity, LLGL2, is required for proper polarized invasion of trophoblasts and efficient branching morphogenesis during placental development (10).
    For Research Use Only. Not For Use In Diagnostic Procedures.
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