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NDRG Family Antibody Sampler Kit
Primary Antibodies
Antibody Sampler Kit

NDRG Family Antibody Sampler Kit #12795

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Product Description

The NDRG Family Antibody Sampler Kit provides an economical means of detecting members of the NDRG protein family. The kit includes enough antibody to perform four western blot experiments per primary antibody.

Specificity / Sensitivity

Each antibody in the NDRG Family Antibody Sampler Kit recognizes endogenous levels of its respective target protein and does not cross-react with other family members. Phospho-NDRG1 (Thr346) (D98G11) XP® Rabbit mAb may cross-react with other conserved phosphorylation sites on NDRG1 at positions Thr356 and Thr366.

Source / Purification

Modification state monoclonal antibodies are produced by immunizing animals with a synthetic phosphopeptide corresponding to residues surrounding Ser330 of human NDRG1 protein or to residues surrounding Thr346 of mouse NDRG1 protein. Total monoclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues near the carboxy terminus of human NDRG1 protein or to residues surrounding Gly217 of human NDRG4 protein. Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Lys25 of human NDRG2 protein or to residues near the carboxy terminus of human NDRG3 protein. Polyclonal antibodies are purified by protein A and peptide affinity chromatography.


The NDRG (N-Myc downstream-regulated gene) family consisting of NDRG1, NDRG2, NDRG3, and NDRG4 are structurally related proteins with roles in cell proliferation, differentiation, apoptosis, stress responses, and cell migration/metastasis (1-3). NDRG1 was originally identified as a protein that was upregulated in N-Myc knockout mice (1). Proteins in the NDRG family, particularly NDRG1 and NDRG2, have been reported to be down-regulated in various cancer tissues and have been suggested to function as a tumor suppressors (4,5).

Ubiquitously expressed N-Myc downstream-regulated gene 1 (NDRG1) is highly responsive to a variety of stress signals, including DNA damage, hypoxia, and elevated levels of nickel and calcium (6-9). Expression of NDRG1 is elevated in N-Myc defective mice and is negatively regulated by N- and c-Myc (1,10). Expression of NDRG1 and NDRG2 is upregulated by p53 and HIF-1 and contributes to apoptosis driven by those pathways (8,9,11-14).

Research studies show that NDRG1 may play a role in cancer progression by promoting differentiation, inhibiting growth, and modulating metastasis and angiogenesis (7,8,10,15,16). Nonsense mutation in the corresponding NDRG1 gene can 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 (17,18). NDRG1 is upregulated during mast cell maturation and its deletion leads to attenuated allergic responses (19). Elevated NDRG2 expression has been observed with Alzheimer's disease (20). Both NDGR1 and NDGR2 are phosphorylated at multiple sites by Akt and/or SGK1, although the precise physiological role of this phosphorylation is unclear (21,22). NDRG1 is phosphorylated by SGK1 at Thr328, Ser330, Thr346, Thr356, and Thr366. Phosphorylation by SGK1 primes NDRG1 for phosphorylation by GSK-3.

NDRG3 is most highly expressed in the testis, prostate, ovary, and brain and is upregulated by androgen in prostate cell lines, promoting cell growth in those cell lines (2,23-25). Unlike other widely expressed family members, several alternatively spliced NDRG4 (Bdm1) isoforms are expressed primarily in the heart and brain (2,3,26,27). Expression of NDRG4 is reduced in the brain of patients with Alzheimer's disease, but is elevated in glioblastoma where it contributes to cell cycle progression and survival (3,28). NDRG4 also may be inactivated by promoter methylation in colorectal cancer and function as a tumor suppressor gene (29).

  1. Shimono, A. et al. (1999) Mech Dev 83, 39-52.
  2. Qu, X. et al. (2002) Mol Cell Biochem 229, 35-44.
  3. Zhou, R.H. et al. (2001) Genomics 73, 86-97.
  4. Yao, L. et al. (2008) Acta Biochim Biophys Sin (Shanghai) 40, 625-35.
  5. Ellen, T.P. et al. (2008) Carcinogenesis 29, 2-8.
  6. Zhou, D. et al. (1998) Cancer Res 58, 2182-9.
  7. van Belzen, N. et al. (1997) Lab Invest 77, 85-92.
  8. Kurdistani, S.K. et al. (1998) Cancer Res 58, 4439-44.
  9. Park, H. et al. (2000) Biochem Biophys Res Commun 276, 321-8.
  10. Li, J. and Kretzner, L. (2003) Mol Cell Biochem 250, 91-105.
  11. Stein, S. et al. (2004) J Biol Chem 279, 48930-40.
  12. Cangul, H. (2004) BMC Genet 5, 27.
  13. Wang, L. et al. (2008) Cell Physiol Biochem 21, 239-50.
  14. Liu, N. et al. (2008) Nucleic Acids Res 36, 5335-49.
  15. Maruyama, Y. et al. (2006) Cancer Res 66, 6233-42.
  16. Nishio, S. et al. (2008) Cancer Lett 264, 36-43.
  17. Kalaydjieva, L. et al. (2000) Am J Hum Genet 67, 47-58.
  18. Okuda, T. et al. (2004) Mol Cell Biol 24, 3949-56.
  19. Taketomi, Y. et al. (2007) J Immunol 178, 7042-53.
  20. Mitchelmore, C. et al. (2004) Neurobiol Dis 16, 48-58.
  21. Murray, J.T. et al. (2004) Biochem J 384, 477-88.
  22. Burchfield, J.G. et al. (2004) J Biol Chem 279, 18623-32.
  23. Okuda, T. and Kondoh, H. (1999) Biochem Biophys Res Commun 266, 208-15.
  24. Zhao, W. et al. (2001) Biochim Biophys Acta 1519, 134-8.
  25. Wang, W. et al. (2009) Int J Cancer 124, 521-30.
  26. Yamauchi, Y. et al. (1999) Brain Res Mol Brain Res 68, 149-58.
  27. Nakada, N. et al. (2002) Brain Res Dev Brain Res 135, 45-53.
  28. Schilling, S.H. et al. (2009) J Biol Chem 284, 25160-9.
  29. Melotte, V. et al. (2009) J Natl Cancer Inst 101, 916-27.

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For Research Use Only. Not For Use In Diagnostic Procedures.
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