SLC10A4, a member of the solute carrier family 10, is a transmembrane protein crucial for the cellular uptake of various compounds, including bile acids, steroids, and thyroid hormones. As a transporter located on the cell membrane, SLC10A4 plays a vital role in maintaining cellular homeostasis by regulating the intracellular concentration of its substrates. Its function is essential for multiple physiological processes, such as bile acid recycling, steroid hormone signaling, and thyroid hormone metabolism. Dysfunction of SLC10A4 has been implicated in various pathological conditions, underscoring the significance of its precise regulation in cellular function and health.
Inhibition of SLC10A4 involves a variety of molecular mechanisms aimed at reducing or abolishing its transport activity. One common mechanism of inhibition is the competitive binding of specific inhibitors to the substrate-binding site of SLC10A4, thereby preventing the binding and transport of endogenous substrates. Additionally, inhibitors may act by altering the conformation of SLC10A4 or disrupting its interaction with essential cofactors or regulatory proteins, ultimately impairing its transport function. Furthermore, inhibition of SLC10A4 can occur through the modulation of downstream signaling pathways involved in its regulation, leading to the suppression of transporter expression or activity. Overall, understanding the diverse mechanisms of SLC10A4 inhibition is crucial for elucidating its physiological role.
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