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| Product Name | Recombinant Mouse RBP4 (carrier-free) |
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| Description | RBP4 belongs to the lipocalin family, and it is the retinol (vitamin A alcohol) specific transport protein present in plasma. It has a β barrel structure with a well defined cavity, which accommodates retinol. The stability of the retinol-RBP (holo-RBP) complex is further enhanced when the complex is bound to transthyretin (TTR). RBP4 delivers retinol from the liver stores to the peripheral tissues. The interaction of RBP-retinol complex with TTR prevents its loss by filtration through the kidney glomeruli. Apo-RBP4 (without retinol) is reabsorbed in the proximal tubular cells. A deficiency of vitamin A blocks secretion of the binding protein post-translationally and results in defective delivery and supply to the epidermal cells. Defects in RBP4 cause retinol-binding protein deficiency and may cause night vision problems. RBP4 has been described as an adipokine and is found to be expressed in adipose tissue and correlated with obesity, insulin resistance, and type 2 diabetes. It has been postulated that RBP4 acts as the mechanistic link by which decreased adipocyte GLUT4 expression contributes to insulin resistance. Circulating RBP4 concentrations are increased in insulin-resistant mice. Moreover, transgenic overexpression of human RBP4 and injection of recombinant RBP4 decreased insulin sensitivity are shown in normal mice, whereas genetic deletion of the RBP4 gene or normalization of RBP4 concentrations in obese mice improved insulin sensitivity. RBP4 concentrations are also increased in obese humans, and higher concentrations have been correlated with lower insulin sensitivity and other components of the metabolic syndrome. |
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| Size | 100 µg |
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| Concentration | n/a |
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| Applications | BA |
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| Other Names | Retinol-binding protein 4 (RBP), plasma retinol-binding protein (PRBP) |
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| Gene, Accession, CAS # | Gene ID: 19662 |
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| Catalog # | 760706 |
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| Order / More Info | Recombinant Mouse RBP4 (carrier-free) from BIOLEGEND |
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| Product Specific References | n/a |
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