Date published: 2025-9-16

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WBSCR28 Activators

WBSCR28 Activators encompass a selection of chemical compounds that indirectly boost the functional performance of WBSCR28 through diverse cellular signaling pathways. Forskolin, Rolipram, IBMX, Cilostazol, Sildenafil citrate, and Isoproterenol all function by increasing cyclic nucleotide levels (cAMP or cGMP), which in turn activate protein kinases such as PKA and PKG. Forskolin directly stimulates adenylate cyclase, while Rolipram and IBMX prevent cAMP degradation by inhibiting phosphodiesterase 4 and non-selectively inhibiting phosphodiesterases, respectively. EGCG, by inhibiting competitive kinase signaling, may also provide a more favorable context for WBSCR28 activity. Sildenafil and Zaprinast, which inhibit phosphodiesterase 5, and Cilostazol, a phosphodiesterase 3 inhibitor, elevate cGMP and cAMP levels, respectively. These elevated levels of cyclic nucleotides could potentially lead to the phosphorylation and enhancement of WBSCR28 activity through PKA or PKG signaling pathways.

In addition to the cyclic nucleotide pathway modulators, other compounds like Okadaic acid, PMA, Ionomycin, and Anisomycin are known to influence the phosphorylation status of proteins, which can indirectly affect the activity of WBSCR28. Okadaic acid, by inhibiting protein phosphatases, could maintain the phosphorylation state of proteins, potentially affecting WBSCR28 activity. PMA, as a PKC activator, may enhance WBSCR28 activity through PKC-mediated signaling events. Ionomycin, by increasing intracellular calcium levels,could activate calcium-dependent protein kinases, leading to phosphorylation events that may indirectly boost WBSCR28 function. Anisomycin's role in activating stress-activated protein kinases such as JNK suggests another potential route for the enhancement of WBSCR28, as JNK-mediated phosphorylation can modulate various protein functions. Collectively, these WBSCR28 Activators, by manipulating signaling pathways that govern phosphorylation states, contribute to the indirect enhancement of the functional activity of WBSCR28 without necessitating direct activation or upregulation of the protein's expression.

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