Date published: 2025-9-13

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ZNF529 Activators

ZNF529 include a variety of compounds that initiate intracellular signaling pathways, culminating in the modulation of this protein's activity. Forskolin, by elevating cAMP levels, indirectly stimulates protein kinase A (PKA), which can then phosphorylate ZNF529, leading to its activation. Similarly, dibutyryl-cAMP, a cAMP analog, also activates PKA, which targets proteins associated with ZNF529 for phosphorylation. PMA, a known activator of protein kinase C (PKC), can directly or indirectly lead to the phosphorylation and subsequent activation of ZNF529 by modulating PKC or its downstream effectors. Bryostatin 1, which binds to and modulates PKC, also plays a role in the phosphorylation cascade that can activate ZNF529.

Ionomycin increases intracellular calcium levels, which can activate calcineurin. The activated calcineurin can then dephosphorylate regulatory proteins, triggering signaling cascades that can lead to ZNF529 activation. Insulin, through its activation of the PI3K/Akt pathway, can phosphorylate various substrates that either interact directly with ZNF529 or modify its regulation. Equally, the Epidermal Growth Factor (EGF) initiates a signaling cascade via the EGFR that includes the MAPK/ERK pathway, potentially leading to phosphorylation events that activate ZNF529. Anisomycin, which activates MAPKs such as JNK and p38, engages in signaling pathways that can result in the activation of ZNF529. The phosphatase inhibitors okadaic acid and calyculin A prevent dephosphorylation, thereby ensuring a higher level of protein phosphorylation that can activate ZNF529. Lastly, sphingosine-1-phosphate (S1P) and FTY720 (after in vivo conversion to FTY720-P) bind to their respective receptors, initiating signaling cascades that can include the activation of ZNF529 as part of their downstream effects.

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