Chemical activators of IL-17C include a variety of compounds that can initiate a cascade of intracellular events, ultimately enhancing the activity of IL-17C. Compounds such as Phorbol 12-myristate 13-acetate (PMA) and 1,2-Dioctanoyl-sn-glycerol (DiC8) activate Protein Kinase C (PKC), which is known to phosphorylate a range of substrates, including transcription factors that can directly increase the activity of IL-17C. Similarly, ionophores like Ionomycin and A23187 increase intracellular calcium levels, which are critical for the activation of the NFAT pathway, a well-established modulator of IL-17C activity.
Additionally, compounds that modulate second messenger systems, such as Prostaglandin E2 (PGE2) and Forskolin, increase cyclic AMP (cAMP) levels. Elevated cAMP can activate CREB, a transcription factor that can enhance the activity of IL-17C. Bryostatin 1, although traditionally seen as a PKC modulator, can also lead to the activation of downstream pathways that feed into the regulation of IL-17C. Thapsigargin, by inhibiting the SERCA pump, leads to an increase in intracellular calcium, a driver of numerous signaling pathways, including those that could upregulate IL-17C activity. Anisomycin's role in activating MAPK pathways, including JNK and p38, can also contribute to the activation of transcription factors like AP-1, which are capable of enhancing IL-17C activity. Lastly, inhibitors like SB 203580 and U0126, while primarily known to block specific kinases, can induce a compensatory response in cells, leading to the activation of alternate pathways that may upregulate IL-17C activity. Each of these chemicals engages with specific cellular signaling pathways, which, through a network of intracellular interactions, can serve to enhance the functional activity of IL-17C.
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