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Reactivity | Human Mouse Rat |
Tested applications | WB IHC IF |
Recommended Dilution | WB 1:500 - 1:2000 IHC 1:50 - 1:200 IF 1:50 - 1:200 |
Calculated MW | 43kDa |
Observed MW | Refer to Figures |
Immunogen | Recombinant protein of human NDRG1 |
Storage Buffer | Store at -20℃. Avoid freeze / thaw cycles. Buffer: PBS with 0.02% sodium azide, 50% glycerol, pH7.3. |
Synonym | CAP43; CMT4D; DRG1; GC4; HMSNL; NDR1; NMSL; PROXY1; RIT42; RTP; TARG1; TDD5; |
Western blot analysis of extracts of various cell lines, using NDRG1 antibody.
Immunohistochemistry of paraffin-embedded rat heart using NDRG1 antibody at dilution of 1:100 (x400 lens).
Immunohistochemistry of paraffin-embedded mouse kidney using NDRG1 antibody at dilution of 1:100 (x400 lens).
Immunofluorescence analysis of MCF7 cell using NDRG1 antibody. Blue: DAPI for nuclear staining.
Immunofluorescence analysis of U2OS cell using NDRG1 antibody. Blue: DAPI for nuclear staining.
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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