ZNF543 can induce its activity through a variety of intracellular signaling pathways. Forskolin, by raising intracellular cyclic AMP (cAMP) levels, activates protein kinase A (PKA), which can phosphorylate and activate ZNF543. The mechanism is similar with Isoproterenol and Dibutyryl-cAMP, both of which increase cAMP levels, subsequently activating PKA and enhancing the phosphorylation state of ZNF543. Epidermal Growth Factor (EGF) operates through a different mechanism, binding to its receptor EGFR and initiating a cascade that activates the MAPK/ERK pathway, culminating in the phosphorylation and activation of ZNF543. Phorbol 12-myristate 13-acetate (PMA) stimulates protein kinase C (PKC), another kinase that can phosphorylate a range of substrates including ZNF543, altering its activity.
ZNF543 activation include those mediated by changes in intracellular calcium levels. Ionomycin elevates calcium concentrations inside cells, which can activate calcium-dependent kinases capable of modifying ZNF543. Bradykinin also raises intracellular calcium levels through its G protein-coupled receptors and the subsequent production of inositol trisphosphate (IP3), which may lead to the activation of ZNF543. Insulin triggers the PI3K/Akt pathway that can phosphorylate various proteins, possibly leading to modifications of ZNF543. Lithium chloride acts indirectly by inhibiting GSK-3β, affecting the Wnt signaling pathway and possibly leading to the activation of ZNF543. Sodium butyrate alters chromatin structure, potentially enhancing ZNF543's ability to bind DNA. Finally, Calyculin A helps maintain the phosphorylated state of proteins by inhibiting protein phosphatases known to dephosphorylate proteins like ZNF543.
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