Human RGM-C/Hemojuvelin Antibody Summary
Accession # Q8ZVN8
This antibody functions as an ELISA capture antibody when paired with Mouse Anti-Human RGM‑C/Hemojuvelin Monoclonal Antibody (Catalog # MAB37201).
This product is intended for assay development on various assay platforms requiring antibody pairs. We recommend the Human RGM-C/Hemojuvelin DuoSet ELISA Kit (Catalog # DY3720-05) for convenient development of a sandwich ELISA.
Please Note: Optimal dilutions should be determined by each laboratory for each application. General Protocols are available in the Technical Information section on our website.
Human RGM‑C/Hemojuvelin ELISA Standard Curve. Recombinant Human RGM‑C/Hemojuvelin protein was serially diluted 2-fold and captured by Mouse Anti-Human RGM‑C/Hemojuvelin Monoclonal Antibody (Catalog # MAB3720) coated on a Clear Polystyrene Microplate (Catalog # DY990). Mouse Anti-Human RGM‑C/Hemojuvelin Monoclonal Antibody (Catalog # MAB37201) was biotinylated and incubated with the protein captured on the plate. Detection of the standard curve was achieved by incubating Streptavidin-HRP (Catalog # DY998) followed by Substrate Solution (Catalog # DY999) and stopping the enzymatic reaction with Stop Solution (Catalog # DY994).
Preparation and Storage
- 12 months from date of receipt, -20 to -70 °C as supplied.
- 1 month, 2 to 8 °C under sterile conditions after reconstitution.
- 6 months, -20 to -70 °C under sterile conditions after reconstitution.
RGM-C, also known as hemojuvelin, is a member of the repulsive guidance molecule (RGM) family of GPI-linked neuronal and muscle membrane glycoproteins (1, 2). RGM-C is expressed in striated muscle and periportal hepatocytes (3 - 5). The protein undergoes partial cleavage intracellularly, resulting in a disulfide-linked dimer of the 14 kDa N-terminal and 33 kDa C-terminal portions (4, 6, 7). The N-terminal fragment contains an RGD motif, while the C-terminal fragment carries the GPI attachment site (4, 7). Two alternatively spliced isoforms lack either approximately half or the entire N-terminal fragment. Full length RGM-C can also be released from the cell and circulates in the blood (6, 8). RGM-C is disrupted in type 2A juvenile hemochromatosis, a hereditary iron homeostasis disorder characterized by excessive iron accumulation (5). In mouse, loss of RGM-C function results in decreased expression of the iron regulatory hormone hepicidin and increased iron deposition in liver, pancreas, and heart (5, 9). Membrane associated RGM-C upregulates hepicidin while soluble RGM-C downregulates hepicidin expression (8). This appears to be an iron-responsive regulatory system, as high blood iron levels reduce the amount of soluble RGM-C produced (8). RGM-C, similar to RGM-A, associates with neogenin (7). Disease-related point mutations can prevent internal RGM-C cleavage or its ability to interact with neogenin (6, 7). Experimental inflammatory conditions result in decreased RGM-C expression and increased hepicidin expression, although the two effects occur independently (5, 10). RGM-C also functions as a BMP coreceptor and enhances BMP-2 and BMP-4 signaling (11). In this context, RGM-C enhances the BMP-2 upregulation of hepatic hepicidin (11). Mature human RGM-C shares 89% amino acid (aa) sequence identity with mouse and rat RGM-C. It shares 49% and 44% aa sequence identity with human RGM-A and RGM-B, respectively.
- Papanikolaou, G. et al. (2004) Nat. Genet. 36:77.
- Schmidtmer, J. and D. Engelkamp (2004) Gene Exp. Patterns 4:105.
- Oldekamp, J. et al. (2004) Gene Exp. Patterns 4:283.
- Niederkofler, V. et al. (2004) J. Neurosci. 24:808.
- Niederkofler, V. et al. (2005) J. Clin. Invest. 115:2180.
- Kuninger, D. et al. (2006) J. Cell Sci. 119:3273.
- Zhang, A.S. et al. (2005) J. Biol. Chem. 280:33885.
- Lin, L. et al. (2005) Blood 106:2884.
- Huang, F.W. et al. (2005) J. Clin. Invest. 115:2187.
- Krijt, J. et al. (2004) Blood 104:4308.
- Babitt, J.L. et al. (2006) Nat. Genet. 38:531.
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