Ready to be labeled using established conjugation methods. No BSA or other carrier proteins that could interfere with conjugation.
Measured by its ability to neutralize GM‑CSF-induced proliferation in the DA3 mouse myeloma cell line. Ihle, J. N. et al. (1984) Advances in Viral Oncology. In G. Klein (eds): Raven Press, New York, NY. 4:95. The Neutralization Dose (ND50) is typically 0.02-0.12 µg/mL in the presence of 0.1 ng/mL Recombinant Mouse GM‑CSF.
Please Note: Optimal dilutions should be determined by each laboratory for each application.
are available in the Technical Information section on our website.
Cell Proliferation Induced by GM‑CSF and Neutralization by Mouse GM‑CSF R alpha Antibody.
Recombinant Mouse GM‑CSF (Catalog # 415-ML) stimulates proliferation in the DA3 mouse myeloma cell line in a dose-dependent manner (orange line). Proliferation elicited by Recombinant Mouse GM‑CSF (0.1 ng/mL) is neutralized (green line) by increasing concentrations of Rat Anti-Mouse GM‑CSF R alpha Monoclonal Antibody (Catalog # MAB6130). The ND50 is typically 0.02-0.12 µg/mL.
Detection of GM-CSF R alpha in J774A.1 Mouse Cell Line by Flow Cytometry.
J774A.1 mouse reticulum cell sarcoma macrophage cell line was stained with Rat Anti-Mouse GM‑CSF R alpha Monoclonal Antibody (Catalog # MAB6130, filled histogram) or isotype control antibody (Catalog # MAB006, open histogram), followed by Allophycocyanin-conjugated Anti-Rat IgG Secondary Antibody (Catalog # F0113).
GM‑CSF R alpha in J774A.1 Mouse Cell Line.
GM‑CSF R alpha was detected in immersion fixed J774A.1 mouse reticulum cell sarcoma macrophage cell line using Rat Anti-Mouse GM‑CSF R alpha Monoclonal Antibody (Catalog # MAB6130) at 10 µg/mL for 3 hours at room temperature. Cells were stained using the NorthernLights™ 557-conjugated Anti-Rat IgG Secondary Antibody (red, upper panel; Catalog # NL013) and counterstained with DAPI (blue, lower panel). Specific staining was localized to cell surfaces and cytoplasm. View our protocol for Fluorescent ICC Staining of Cells on Coverslips.
Preparation and Storage
Sterile PBS to a final concentration of 0.5 mg/mL.
Reconstitution Buffer Available
The product is shipped at ambient temperature. Upon receipt, store it immediately at the temperature recommended below. *Small pack size (SP) is shipped with polar packs. Upon receipt, store it immediately at -20 to -70 °C
Stability & Storage
Use a manual defrost freezer and avoid repeated freeze-thaw cycles.
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.
Background: GM-CSF R alpha
Granulocyte macrophage colony stimulating factor receptor alpha (GM-CSF R alpha ), also known as CD116, is a component of the receptor complex that mediates cellular responses to GM-CSF. GM-CSF promotes the differentiation and mobilization of granulocyte-macrophage, erythroid, megakaryocyte, and eosinophil progenitors. It enhances the activation of myeloid cell effector functions and plays a role in the development of Th1 biased immune responses, allergic inflammation, and autoimmunity (1-4). Mature mouse GM-CSF R alpha is an 80 kDa type I transmembrane glycoprotein that consists of a 298 amino acid (aa) extracellular domain (ECD) with two fibronectin type III domains and a juxtamembrane WSXWS motif, a 21 aa transmembrane segment, and a 40 aa cytoplasmic domain (5). Within the ECD, mouse GM-CSF R alpha shares approximately 33% and 58% aa sequence identity with human and rat GM-CSF R alpha, respectively. Soluble forms of the human receptor retain the ability to bind GM-CSF (6, 7). GM-CSF R alpha is expressed on hematopoietic stem cells, progenitor and differentiated cells in the myeloid lineage, vascular endothelial cells, placenta, and non‑hematopoietic solid tumor cells (8). GM-CSF R alpha associates with the common beta chain/CD131 ( beta c), a 135 kDa transmembrane protein that is also the signal transducing component of the receptors for IL-3 and IL-5 (9, 10). Association with beta c converts GM-CSF R alpha from a low affinity to a high affinity receptor for GM-CSF (9-11). The shared usage of beta c underlies the synergism between GM-CSF, IL-3, and IL-5 in their effects on myeloid cell differentiation and activation (1, 2).
Martinez-Moczygemba, M. and D.P. Huston (2003) J. Allergy Clin. Immunol. 112:653.
Fleetwood, A.J. et al. (2005) Crit. Rev. Immunol. 25:405.
Eksioglu, E.A. et al. (2007) Exp. Hematol. 35:1163.
Cao, Y. (2007) J. Clin. Invest. 117:2362.
Park, L.S. et al. (1992) Proc. Natl. Acad. Sci. 89:4295.
Pelley, J.L. et al. (2007) Exp. Hematol. 35:1483.
Raines, M.A. et al. (1991) Proc. Natl. Acad. Sci. 88:8203.
Chiba, S. et al. (1990) Cell Regul. 1:327.
Kitamura, T. et al. (1991) Proc. Natl. Acad. Sci. 88:5082.
Hayashida, K. et al. (1990) Proc. Natl. Acad. Sci. 87:9655.
R&D Systems personnel manually curate a database that contains references using R&D Systems products.
The data collected includes not only links to publications in PubMed,
but also provides information about sample types, species, and experimental conditions.
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