Date published: 2025-9-14

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FAXC Activators

Chemical activators of FAXC play pivotal roles in its functional activation through various biochemical pathways and mechanisms. Phorbol 12-myristate 13-acetate (PMA) is one such activator that exerts its effect by directly targeting protein kinase C (PKC). Upon binding, PMA activates PKC, which then phosphorylates FAXC, leading to its activation. Similarly, Forskolin induces an increase in intracellular cAMP levels, which in turn triggers the activation of protein kinase A (PKA). PKA can phosphorylate FAXC, thereby activating it. Ionomycin, by increasing intracellular calcium levels, can also activate FAXC through the stimulation of calcium-dependent kinases that act upon this protein. Another activator, Okadaic Acid, inhibits protein phosphatases PP1 and PP2A, culminating in the sustained phosphorylation and subsequent activation of FAXC by preventing dephosphorylation.

In addition to these, Zinc Chloride and Magnesium Sulfate serve as essential cofactors for various kinases, which can phosphorylate FAXC, leading to its activation. Sodium Fluoride, by inhibiting serine/threonine phosphatases, indirectly contributes to the phosphorylation and activation of FAXC. The cAMP analog, Dibutyryl-cAMP, activates PKA, which then targets FAXC for phosphorylation and activation. Calyculin A, like Okadaic Acid, inhibits protein phosphatases and thus maintains FAXC in an activated state due to continued phosphorylation. 4-Phorbol, akin to PMA, activates PKC which phosphorylates and activates FAXC. Activation pathways also include stress responses where Anisomycin activates stress-activated protein kinases that phosphorylate FAXC. Lastly, Calcium Chloride provides a source of calcium ions, which are critical for the activation of calcium-dependent kinases that target and activate FAXC through phosphorylation. These diverse chemical activators, through their specific actions on kinases and phosphatases, ensure the phosphorylation and consequent activation of FAXC, delineating a complex network of regulatory mechanisms that control its function within the cell.

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