Protein Catagory: Transport/other Proteins
Typ: Human
CAS Number: 68476-36-8
Molecular Weight: 56,000 Da
Immunogen: No
Compound Purity: ≥95% by SDS-PAGE
Applications: Glycobiology, Vitamin D Metabolism, Inflammation, Liver Damage/Disease, Itai-Itai Disease, Autoimmune Disease, Diabetes, In Vitro Diagnostic
References: - Chapron, B. D., et al., (2018), 'Reevaluating the Role of Megalin in Renal Vitamin D Homeostasis Using a Human Cell-Derived Microphysiological System', ALTEX 35(4): pp 504-515. Available at: doi:10.14573/altex.1803161 - Lidberg, K. A., et al., (2024), 'Modeling cellular responses to serum and vitamin D in microgravity using a human kidney microphysiological system', npj Microgravity 10: 75. Available at: https://doi.org/10.1038/s41526-024-00415-2 - Gliozzi, M. L., et al., (2019), 'Hemoglobin alters vitamin carrier uptake and vitamin D metabolism in proximal tubule cells: implications for sickle cell disease', Am J Physiol Cell Physiol 317: pp C993–C1000. Available at: doi:10.1152/ajpcell.00287.2019 - Kanie, Y., et al., (2023), 'Investigation of the Protective Effect for GcMAF by a Glycosidase Inhibitor and the Glycan Structure of Gc Protein', Molecules, 28: pp 1570. Available at: https://doi.org/10.3390/molecules28041570 - Borges, C. R., et al., (2016), 'Glycan structure of Gc Protein-derived Macrophage Activating Factor as revealed by mass spectrometry', Archives of Biochemistry and Biophysics 606: pp 1e13. Available at: http://dx.doi.org/10.1016/j.abb.2016.08.006
Product Description: Vitamin D-binding protein (DBP/GC-globulin) serves as the primary transporter of vitamin D metabolites (25OHD, 1,25(OH)2D) in plasma, maintaining their solubility and bioavailability. Structurally, DBP comprises three domains, with domain I harboring a high-affinity binding site for vitamin D metabolites. Beyond sterol transport, DBP binds monomeric actin with nanomolar affinity, preventing pathological actin polymerization in circulation-a critical function during tissue injury. It also interacts with immune cells, binding to surface receptors on B and T lymphocytes to modulate chemotaxis and inflammatory responses. Reduced DBP levels correlate with severe liver diseases such as cirrhosis and acute-on-chronic liver failure, where impaired synthesis exacerbates vitamin D deficiency and actin scavenging dysfunction. In Itai-Itai disease, DBP loss in urine disrupts vitamin D transport, contributing to cadmium-induced osteomalacia7. Genetic polymorphisms (e.g., Gc1F, Gc1S, Gc2) influence DBP’s binding affinity, linking specific alleles to viral infection susceptibility and autoimmune disorders like lupus. Low DBP levels also associate with non-alcoholic fatty liver disease (NAFLD) progression and type 2 diabetes, where pancreatic α-cell dysfunction arises from disrupted actin cytoskeleton regulation.
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