Date published: 2025-10-12

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CCDC128 Activators

Chemical activators of CCDC128 include a variety of compounds that can initiate intracellular signaling cascades resulting in the activation of the protein. Forskolin, a well-known adenylate cyclase activator, increases the levels of cAMP within the cell. Elevated cAMP directly activates protein kinase A (PKA), which can phosphorylate CCDC128, leading to its activation. Similarly, Dibutyryl-cAMP (db-cAMP), a membrane-permeable cAMP analog, diffuses into cells and mimics the action of cAMP, also activating PKA, which in turn can phosphorylate and activate CCDC128. Phorbol 12-myristate 13-acetate (PMA) is another activator that functions by directly stimulating protein kinase C (PKC), which has a broad range of substrates and can phosphorylate CCDC128 if it is among them.

Additional chemical activators influence the intracellular concentration of key ions and secondary messengers. For instance, Ionomycin acts by increasing intracellular calcium levels, which activates calmodulin-dependent kinase (CaMK), capable of phosphorylating CCDC128. Ouabain, by inhibiting the Na+/K+ ATPase, indirectly leads to a rise in intracellular calcium, again activating CaMK with similar potential effects on CCDC128. Calyculin A and Okadaic Acid both function by inhibiting protein phosphatases, such as PP1 and PP2A, which normally dephosphorylate proteins; their inhibition results in prolonged phosphorylation and thereby sustained activation of CCDC128. Anisomycin, which activates stress-activated protein kinases like JNK and p38 MAP kinase, could result in the activation of CCDC128 through phosphorylation events associated with these kinases. Epidermal Growth Factor (EGF) engages its receptor, triggering the MAPK/ERK signaling cascade, which is known to regulate a wide array of cellular proteins, potentially including the phosphorylation and activation of CCDC128. Insulin triggers the PI3K/AKT signaling pathway, leading to a series of phosphorylation events that can culminate in the activation of CCDC128. Lastly, S-Nitroso-N-acetylpenicillamine (SNAP) releases nitric oxide that activates guanylate cyclase, increasing cGMP levels, and BAY 11-7082 inhibits the NF-κB activation pathway; both these actions can lead to a cascade of downstream effects resulting in the activation of CCDC128.

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