Anti-Nardilysin (NRDC), clone 2E6

Anti-Nardilysin (NRDC), clone 2E6, Cat. No. MABS2058, is a mouse monoclonal antibody tht detects Nardilysin (NRDC) and has been tested for use in Chromatin Immunoprecipitation (ChIP) and Western Blotting.

Chromatin Immunoprecipitation Analysis (ChIP): A representative lot detected Nardilysin (NRDC) in Chromatin Immunoprecititation applications (Morita, Y., et. al. (2017). Sci Rep. 7(1):14801; Nishi, K., et. al. (2016). Diabetes. 65(10):3015-27).

Western Blotting Chromatin Immunoprecipitation (ChIP)

Clone 2E6 is a mouse monoclonal antibody that was generated in Nardilysin-deficient mice. It detects human and murine Nardilysin.

A recombinant fragment corresponding to 814 amino acids from murine Nardilysin.

Stable for 1 year at 2-8°C from date of receipt.

Purified mouse monoclonal antibody IgG1 in buffer containing 0.1 M Tris-Glycine (pH 7.4), 150 mM NaCl with 0.05% sodium azide.

Evaluated by Western Blotting in mouse brain tissue lysate.

Western Blotting Analysis: 1 µg/mL of this antibody detected Nardilysin (NRDC) in mouse brain tissue lysate.

Nardilysin (UniProt: Q8BHG1; also known as EC: 3.4.24.61, N-arginine dibasic convertase, NRD convertase, NRD-C, Nardilysin convertase) is encoded by the Nrdc (also known as Nrd1) gene (Gene ID: 230598) in murine species. NRD-C is a metalloendopeptidase of the M16 family that cleaves peptides on the N-terminus of arginine residues in dibasic pairs. It is synthesized with a signal peptide (aa 1-18), which is subsequently cleaved off in the mature form. It promotes ecto-domain shedding of the precursor forms of various growth factors and cytokines by enhancing the protease activities of ADAM proteins. NRD-C is reported to bind to the extracellular domain of ADAM17 and directly enhance its catalytic activity. Its levels are shown to be elevated in serum and epithelium of gastric cancer and NRDC knockdown attenuates gastric cancer cell growth in vitro and in xenograft models. In mitochondria, it serves as a co-chaperone for proper folding of alpha-ketoglutarate dehydrogenase (alpha-KGDH) and absence of NRDC can lead to a severe reduction of alpha-KGDH. NRD-C is shown to inhibit pancreatitis and suppresses pancreatic ductal adenocarcinoma in mice. Its deletion in pancreatic tissue is reported to leads to spontaneous chronic pancreatitis concomitant with acinar-to-ductal conversion, increased apoptosis, and pancreatic atrophy in mice. (Ref.: Kanda, K., et al. (2012). EMBO Mol. Med. 4(5); 396-411; Yoon WH., et al. (2017). Neuron 93(1); 115-131; Ikuda, K., et al (2018). Gut (In Press; 10.1136/gutjnl-2017-315425).

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