Transferrinm Solution Activators
Transferrin Activators encompass a range of chemical compounds that indirectly enhance the functional activity of Transferrin, primarily through their interactions with iron metabolism and related cellular processes. Deferoxamine, by chelating iron, decreases its cellular availability, which in turn stimulates the expression of Transferrin receptors, thereby indirectly enhancing Transferrin's role in iron transport. Similarly, Iron(III) citrate and Ferric ammonium citrate, both providing sources of ferric iron, bind to Transferrin and increase its iron carriage capacity, thereby facilitating more efficient iron transport. Copper(II) sulfate indirectly influences Transferrin's activity by affecting iron export mechanisms, which in turn impacts Transferrin-mediated iron transport. The impact of ethanol, which alters iron metabolism, leading to potential iron overload, consequently results in increased Transferrin saturation and activity as the body attempts to regulate iron levels.
Furthermore, hormonal and nutrient influences, such as Estrogen and Vitamin A, modulate iron homeostasis, indirectly enhancing Transferrin's transport function. Estrogens affect hepcidin levels, a key iron regulator, thus modifying intestinal iron absorption and release from macrophages, in turn influencing Transferrin activity. Vitamin A plays a role in the mobilization of iron, enhancing the utilization of Transferrin in iron transport. Additionally, Curcumin, through its iron-chelating properties, and Zinc sulfate, by competing for iron absorption, indirectly modulate Transferrin's activity in maintaining iron homeostasis. Lead(II) acetate, by disrupting iron metabolism and potentially leading to anemia, inadvertently increases the demand for Transferrin-mediated iron transport. Lastly, Cobalt chloride, a hypoxia-mimicking agent, enhances Transferrin expression by stabilizing hypoxia-inducible factors, thereby indirectly augmenting Transferrin's functional role in iron transportation under normoxic conditions. Collectively, these activators, through their diverse but interconnected mechanisms, significantly influence Transferrin's capacity and efficiency in iron transport within the body.
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| Product Name | CAS # | Catalog # | QUANTITY | Price | Citations | RATING |
|---|---|---|---|---|---|---|
Deferoxamine | 70-51-9 | sc-507390 | 5 mg | $250.00 | ||
Deferoxamine chelates iron, reducing its availability. This reduction in iron triggers an increased expression of Transferrin receptors on the cell surface to enhance iron uptake, indirectly increasing the functional activity of Transferrin in iron transport. | ||||||
Iron(III) citrate | 3522-50-7 | sc-286019 sc-286019A | 100 g 250 g | $45.00 $85.00 | ||
Iron(III) citrate provides a source of ferric iron, which binds to Transferrin, enhancing its role in iron transport. The binding of iron to Transferrin stabilizes the protein and increases its affinity for Transferrin receptors, thus enhancing Transferrin-mediated iron uptake in cells. | ||||||
Purmorphamine | 483367-10-8 | sc-202785 sc-202785A | 1 mg 5 mg | $56.00 $180.00 | 18 | |
Hypoxia-inducible factor stabilizers like Roxadustat stabilize HIF under normoxic conditions. Stabilized HIF increases the expression of genes involved in iron metabolism, including Transferrin and its receptor, thereby indirectly enhancing Transferrin’s iron-binding and transport functions. | ||||||
Ammonium iron(III) citrate | 1185-57-5 | sc-227256 sc-227256A sc-227256B sc-227256C | 100 g 1 kg 5 kg 10 kg | $49.00 $82.00 $367.00 $683.00 | 2 | |
Ferric ammonium citrate is a source of iron that binds to Transferrin, enhancing its iron transport capacity. The binding of iron to Transferrin promotes its interaction with Transferrin receptors, thereby facilitating iron uptake and distribution in the body. | ||||||
Copper(II) sulfate | 7758-98-7 | sc-211133 sc-211133A sc-211133B | 100 g 500 g 1 kg | $45.00 $120.00 $185.00 | 3 | |
Copper(II) sulfate indirectly affects Transferrin activity by influencing iron metabolism. Copper is essential for the function of hephaestin, a protein involved in iron export. Alterations in iron export can modulate cellular iron levels, indirectly impacting Transferrin-mediated iron transport. | ||||||
β-Estradiol | 50-28-2 | sc-204431 sc-204431A | 500 mg 5 g | $62.00 $178.00 | 8 | |
Estrogens can influence iron metabolism by affecting hepcidin levels, a key regulator of iron homeostasis. Lowered hepcidin levels can increase intestinal iron absorption and release from macrophages, indirectly enhancing Transferrin's role in iron transport and distribution. | ||||||
Vitamin A | 68-26-8 | sc-280187 sc-280187A | 1 g 10 g | $377.00 $2602.00 | ||
Vitamin A affects iron metabolism by modulating the expression of proteins involved in iron transport, including Transferrin. It can enhance the mobilization and utilization of iron, indirectly increasing the functional activity of Transferrin in iron transport. | ||||||
Curcumin | 458-37-7 | sc-200509 sc-200509A sc-200509B sc-200509C sc-200509D sc-200509F sc-200509E | 1 g 5 g 25 g 100 g 250 g 1 kg 2.5 kg | $36.00 $68.00 $107.00 $214.00 $234.00 $862.00 $1968.00 | 47 | |
Curcumin can modulate iron metabolism by chelating iron and affecting its availability. This modulation can influence the expression and activity of Transferrin, as the body adjusts to changes in iron homeostasis, potentially enhancing Transferrin-mediated iron transport. | ||||||
Zinc | 7440-66-6 | sc-213177 | 100 g | $47.00 | ||
Zinc sulfate influences iron metabolism by competing for absorption in the intestine. This competition can indirectly affect Transferrin activity, as alterations in iron absorption may lead to adjustments in Transferrin-mediated iron transport to maintain iron homeostasis. | ||||||
Lead(II) Acetate | 301-04-2 | sc-507473 | 5 g | $83.00 | ||
Lead(II) acetate exposure disrupts various aspects of iron metabolism, potentially leading to anemia. This disruption can indirectly increase the demand for iron transport, potentially enhancing the functional activity of Transferrin as the body attempts to compensate for impaired erythropoiesis. | ||||||