GM-CSF R alpha Protein, Mouse (HEK293, His)

GM-CSF R alpha is expressed on myeloid cells and on some non-hemopoietic cells, such as endothelial cells, not on T cells^[2].
The amino acid sequence of human GM-CSF R alpha protein has low homology for mouse GM-CSF R alpha protein.
GM-CSF receptor (GM-CSFR) consists of two subunits, an α-subunit, which binds the cytokine with low affinity, and a larger β-subunit (beta common; βc), responsible for signaling, forming a ternary receptor complex. Signal transduction in response to the cytokines interleukin (IL)-3 and IL-5 is also mediated by βc; therefore, receptor specificity is due to GM-CSFRα^[1]. After binding GM-CSF to its receptor, Janus-kinase-2 (JAK-2) is recruited to the cytoplasmic domain of the β chain, and activation of JAK-2 occurs, which subsequently induces STAT-5 phosphorylation. This signaling pathway induces migration of STAT-5 dimers to the nucleus and promotes the transcription of various genes such as pim-1 and CIS to induce cell differentiation^{[2] GM-CSFR α-subunit significantly increases positive synovial macrophages in the RA synovium. GM-CSFR α monoclonal antibody suppresses disease activity in the murine collagen-induced arthritis model[3].}