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Midkine is a member of a unique family of heparin-binding growth factors that are structurally different from other fibroblast growth factors (Muramatsu; Takada et al.). Midkine is a proinflammatory cytokine, promoting the migration of leukocytes, fibrinolysis, and acting as a chemotactic agent towards neutrophils (Muramatsu; Said et al.; Takada et al.). It also regulates growth, differentiation, and development during the midgestion stage of embryogenesis, and promotes angiogenesis (Muramatsu; Said et al.; Takada et al.). The protein structure consists of three antiparallel β-sheets and is highly conserved between species (Muramatsu; Takada et al.). While the exact signal pathway is not known, proposed pathways include promoting LRP, inhibiting Src kinase, activating paxillin and STAT1α, activating PI2 and MAP kinases, suppressing caspases, binding to α6β1-integrin and tetraspanin, activating FAK, phosphorylating STAT3, suppressing STAT5 phosphorylation, activating ALK, activating PI3 kinase and transcription of NFkB, binding to neuroglycan C or nucleolin, and binding to eIF3 (Muramatsu). In cultured cells, midkine influences growth and survival of neural precursor cells, synthesis of cytokines from endothelial and renal epithelial cells, and promotes synthesis of extracellular matrices from fibroblasts (Muramatsu; Takada et al.).
Alternative Names
Amphiregulin-associated protein, ARAP, MDK, MEK, Midgestation and kidney protein, MK1, MKARAP, NEGF2, NEGF2FLJ27379, Neurite outgrowth-promoting factor 2, Neurite outgrowth-promoting protein
(A) The binding activity of Human Recombinant Midkine was tested by functional ELISA with immobilized Human Recombinant Midkine at 10,000 ng/mL. Immobilized Human Recombinant Midkine can bind mouse SDC4-Fc with a linear range of 160 - 1250 ng/mL.
(B) Human Recombinant Midkine was resolved with SDS-PAGE under reducing (+) conditions and visualized by Coomassie Blue staining. Human Recombinant Midkine has a predicted molecular mass of 13.4 kDa and an aparent molecular mass of 18 kDa (Kaneda et al.).