TFG activators predominantly function by influencing the adrenergic receptors or the prostaglandin E2 receptors, which further stimulate the adenylate cyclase to elevate the intracellular cAMP levels. This increase in cAMP can activate protein kinase A (PKA), which then phosphorylates and activates the cAMP-response element-binding protein (CREB).
CREB, being a transcription factor, can act on the Nfkbia gene, which encodes IκBα. IκBα is an inhibitor of the NF-κB pathway, which TFG is known to interact with. Therefore, the activation of IκBα indirectly enhances the functional activity of TFG by controlling the activity of the NF-κB pathway. This indirect activation of TFG via modulation of the NF-κB pathway is a common mechanism shared among the identified TFG activators.
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