Product Pathways - Development
NDRG1 (D8G9) XP® Rabbit mAb #9485
|9485S||100 µl (10 western blots)||---||In Stock||---|
|9485P||40 µl (4 western blots)||---||In Stock||---|
|9485||carrier free and custom formulation / quantity||email request|
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|W||1:1000||Human, Monkey||Endogenous||46, 48||Rabbit IgG|
Species cross-reactivity is determined by western blot.
Applications Key: W=Western Blotting, IP=Immunoprecipitation, IHC-P=Immunohistochemistry (Paraffin), IF-IC=Immunofluorescence (Immunocytochemistry)
Specificity / Sensitivity
NDRG1 (D8G9) XP® Rabbit mAb recognizes endogenous levels of total NDRG1 protein.
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues near the carboxy terminus of human NDRG1 protein.
Western blot analysis of extracts from various cell lines using NDRG1 (D8G9) XP® Rabbit mAb (upper) and β-Actin (D6A8) Rabbit mAb #8457 (lower).
Immunohistochemical analysis of paraffin-embedded human colon carcinoma using NDRG1 (D8G9) XP® Rabbit mAb.
Immunohistochemical analysis of paraffin-embedded human lung carcinoma using NDRG1 (D8G9) XP® Rabbit mAb.
Immunohistochemical analysis of paraffin-embedded human lymphoma using NDRG1 (D8G9) XP® Rabbit mAb in the presence of control peptide (left) or antigen-specific peptide (right).
N-myc downstream-regulated gene 1 (NDRG1), also termed Cap43, Drg1, RTP/rit42, and Proxy-1, is a member of the NDRG family, which is composed of four members (NDRG1-4) that function in growth, differentiation, and cell survival (1-5). NDRG1 is ubiquitously expressed and highly responsive to a variety of stress signals including DNA damage (4), hypoxia (5), and elevated levels of nickel and calcium (2). Expression of NDRG1 is elevated in N-myc defective mice and is negatively regulated by N- and c-myc (1,6). During DNA damage, NDRG1 is induced in a p53-dependent fashion and is necessary for p53-mediated apoptosis (4,7). Research studies have shown that NDRG1 may also play a role in cancer progression by promoting differentiation, inhibiting growth, and modulating metastasis and angiogenesis (3,4,6,8,9). Nonsense mutation of the NDRG1 gene has been shown to cause hereditary motor and sensory neuropathy-Lom (HMSNL), which is supported by studies demonstrating the role of NDRG1 in maintaining myelin sheaths and axonal survival (10,11). NDRG1 is up-regulated during mast cell maturation and its deletion leads to attenuated allergic responses (12). Both NDRG1 and NDRG2 are substrates of SGK1, although the precise physiological role of SGK1-mediated phosphorylation is not known (13). NDRG1 is phosphorylated by SGK1 at Thr328, Ser330, Thr346, Thr356, and Thr366. Phosphorylation by SGK1 primes NDRG1 for phosphorylation by GSK-3.
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- Nishio, S. et al. (2008) Cancer Lett 264, 36-43.
- Kalaydjieva, L. et al. (2000) Am J Hum Genet 67, 47-58.
- Okuda, T. et al. (2004) Mol Cell Biol 24, 3949-56.
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- Murray, J.T. et al. (2004) Biochem J 384, 477-88.
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For Research Use Only. Not For Use In Diagnostic Procedures.
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Cell Signaling Technology® is a trademark of Cell Signaling Technology, Inc.