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NME1 / NDKA Antibody (FITC), Mouse MAb

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NME1Antibody Product Information
Antigen:Recombinant Human NME1 / NDKA protein (Catalog#11615-H07E)
Clone ID:01
Ig Type:Mouse IgG1
Concentration:10 μl/Test, 0.1 mg/ml
Formulation:Aqueous solution containing 0.5% BSA and 0.09% sodium azide
Preparation:This antibody was produced from a hybridoma resulting from the fusion of a mouse myeloma with B cells obtained from a mouse immunized with purified, recombinant Human NME1 / NDKA (rh NME1 / NDKA; Catalog#11615-H07E; NP_000260.1; Ala 2-Glu 152) and conjugated with FITC under optimum conditions, the unreacted FITC was removed.
NME1Antibody Usage Guide
Specificity:Human NME1 / NDKA
Storage:This antibody is stable for 12 months from date of receipt when stored at 2℃-8℃. Protected from prolonged exposure to light. Do not freeze !
Sodium azide is toxic to cells and should be disposed of properly. Flush with large volumes of water during disposal.

Flow cytometric analysis of Human NME1 expression in HeLa cells. The cells were treated according to manufacturer’s manual (BD Pharmingen™ Cat. No. 554714), and then stained with FITC Mouse anti-NME1 (11615-MM01-F). The fluorescence histograms were derived from gated events with the forward and side light-scatter characteristics of intact cells.


NME1, also known as Nucleoside Diphosphate Kinase A (NDK-A), or NM23-H1, belongs to the NDK family. NM23-H1 is known to have a metastasis suppressive activity in many tumor cells. Recent studies have shown that the interacting proteins with NM23-H1 which mediate the cell proliferation, may act as modulators of the metastasis suppressor activity. The interacting proteins with NM23-H1 can be classified into 3 groups. The first group of proteins can be classified as upstream kinases of NM23-H1 such as CKI and Aurora-A/STK15. The second group of proteins acts as downstream effectors for the regulation of specific gene transcriptions, GTP-binding protein functions, and signal transduction in Erk signal cascade. The third group of proteins can be classified as bi-directionally influencing binding partners of NM23-H1. As a result, the interactions with NM23-H1 and binding partners have implications in the biochemical characterization involved in metastasis and tumorigenesis. NDKA is increased in human postmortem cerebrospinal fluid (CSF), a model of global brain insult, suggesting that measurement in CSF and, more importantly, in plasma may be useful as a biomarker of stroke. Additionally, NM23-H1 significantly reduces metastasis without effects on primary tumor size and was the first discovered metastasis suppressor gene.

  • Allard L, et al. (2005) PARK7 and nucleoside diphosphate kinase A as plasma markers for the early diagnosis of stroke. Clin Chem. 51(11): 2043-51.
  • Steeg PS, et al. (2008) Clinical-translational approaches to the Nm23-H1 metastasis suppressor. Clin Cancer Res. 14(16): 5006-12.
  • Kim HD, et al. (2009) Regulators affecting the metastasis suppressor activity of Nm23-H1. Mol Cell Biochem. 329(1-2): 167-73.
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