Product Pathways - Cytoskeletal Signaling
LLGL1 (D2B5A) Rabbit mAb #12159
|12159S||100 µl (10 western blots)||---||In Stock||---|
|12159||carrier free and custom formulation / quantity||email request|
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|W||1:1000||Human, Monkey||Endogenous||130||Rabbit IgG|
Species cross-reactivity is determined by western blot.
Applications Key: W=Western Blotting, IF-IC=Immunofluorescence (Immunocytochemistry)
Specificity / Sensitivity
LLGL1 (D2B5A) Rabbit mAb recognizes endogenous levels of total LLGL1 protein. This antibody does not cross-react with LLGL2.
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Leu757 of human LLGL1 protein.
Western blot analysis of extracts from various cell lines using LLGL1 (D2B5A) Rabbit mAb (upper) or GAPDH (D16H11) XP® Rabbit mAb #5174 (lower).
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).
- Agrawal, N. et al. (1995) Dev Biol 172, 218-29.
- Massimi, P. et al. (2008) Exp Cell Res 314, 3306-17.
- Strand, D. et al. (1995) Oncogene 11, 291-301.
- Schimanski, C.C. et al. (2005) Oncogene 24, 3100-9.
- Kuphal, S. et al. (2006) Oncogene 25, 103-10.
- Lu, X. et al. (2009) Clin Cancer Res 15, 3287-96.
- Müsch, A. et al. (2002) Mol Biol Cell 13, 158-68.
- Yamanaka, T. et al. (2003) Curr Biol 13, 734-43.
- Mechler, B.M. et al. (1985) EMBO J 4, 1551-7.
- Sripathy, S. et al. (2011) Mol Cell Biol 31, 2920-33.
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