Date published: 2025-9-14

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EG435927 Activators

Slco1a7, a member of the solute carrier organic anion transporter family, plays a crucial role in bile acid and bile salt transport. Predicted to enable bile acid transmembrane transporter activity and sodium-independent organic anion transmembrane transporter activity, Slco1a7 is integral to the plasma membrane. Its ortholog, SLCO1A2, in humans is implicated in bile acid homeostasis. Activation of Slco1a7 involves a sophisticated interplay of various chemicals that either directly up-regulate the transporter or indirectly influence pathways related to bile acid and organic anion transport. Rifampicin, a well-known inducer of nuclear receptors like PXR, may enhance Slco1a7 expression by inducing pathways involved in bile acid metabolism. Ursodeoxycholic acid, acting as a substrate for Slco1a7, stimulates the transporter, promoting bile acid transport.

Phenobarbital, through its activation of nuclear receptors, can up-regulate Slco1a7 and enhance bile acid and organic anion transport. Rosuvastatin, influencing cholesterol biosynthesis, indirectly activates Slco1a7 and may impact bile acid metabolism. Glycyrrhizin, a natural compound, stimulates Slco1a7 by interacting with nuclear receptors involved in bile acid regulation. Fexofenadine, acting as a substrate for Slco1a7, may up-regulate the transporter and influence organic anion transport. Cholic acid, Emodin, Efavirenz, Bezafibrate, Tauroursodeoxycholic acid, and Sulforaphane contribute to Slco1a7 activation through various mechanisms, including substrate activity, modulation of nuclear receptors, and influence on bile acid metabolism pathways. In summary, Slco1a7 activation is orchestrated by a diverse array of chemicals that intricately modulate its role in bile acid and organic anion transport. The complex interplay of these chemicals highlights the sophisticated regulation of Slco1a7 and provides potential avenues for further exploration in understanding and manipulating bile acid homeostasis.

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