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Granulocyte-macrophage colony-stimulating factor receptor (GM-CSFR) and interleukin-3 receptor (IL-3R) are closely related type I cytokine receptors that regulate hematopoiesis and immune responses[7][3][9][6]. Both receptors are multimeric complexes composed of a ligand-specific alpha subunit (CSF2RA for GM-CSF; IL3RA for IL-3), and a shared common beta subunit (CSF2RB, also called βc or CD131), which is essential for high-affinity binding and signal transduction[5][7][4][2]. Upon ligand binding, the receptors oligomerize, resulting in the activation of downstream signaling cascades such as JAK2/STAT5, ERK, and PI3K, which control cell survival, proliferation, and differentiation[6][3][9]. These receptors play key roles in the proliferation and differentiation of hematopoietic progenitors, the function of mature myeloid cells, and the pathogenesis of inflammatory, allergic, and malignant diseases. Because of their roles in disease, especially in cancer and autoimmune disorders, both are considered important therapeutic targets, with monoclonal antibodies and other inhibitors in various stages of development and clinical use[6][7]. Note on correctness: There is a problem with the query as stated: “GM-CSF and IL-3 receptors” is not a single target but refers to two closely related, though distinct, receptors. Often, the term "βc family" or "common beta subunit (CSF2RB) receptor complex" is used to describe the shared subunit system for GM-CSF, IL-3, and IL-5, but therapeutically and structurally, GM-CSF receptor and IL-3 receptor are considered separate targets that share a key signaling component[7][5][4]. Thus, the entry as “GM-CSF and IL-3 receptors” is overly broad and conflates two closely related, yet distinct, targets. If specificity is needed, these should be captured as two targets: "Granulocyte-macrophage colony-stimulating factor receptor" and "Interleukin-3 receptor", each with their respective details.
Antagonism or inhibition of ligand (GM-CSF or IL-3) binding to its receptor Antagonism or inhibition of βc dimerization and signal transduction Downregulation of JAK2/STAT5 or other downstream signaling
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