Date published: 2025-10-13

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FAM188A Activators

FAM188A Activators are a diverse array of chemical compounds that indirectly promote the functional activity of FAM188A through modulation of various signaling pathways and cellular processes. Forskolin and Rolipram both act by inhibiting the degradation of cAMP, with the former directly stimulating adenylate cyclase and the latter inhibiting phosphodiesterase-4. Elevated cAMP levels result in the activation of PKA, which could potentially phosphorylate FAM188A, thereby enhancing its functional activity. Similarly, Dibutyryl-cAMP, a synthetic analog of cAMP, directly activates PKA leading to the same outcome for FAM188A. Ionomycin and Phorbol 12-myristate 13-acetate (PMA) exert their effects through the modulation of intracellular calcium and activation of PKC, respectively, both of which may lead to the phosphorylation and subsequent activation of FAM188A. Sphingosine-1-phosphate (S1P) and Anisomycin engage with specific receptor-mediated pathways and stress-activated protein kinases, such as JNK, that could also facilitate the phosphorylation and enhancement of FAM188A's activity.

Further influencing the activity of FAM188A, compounds like Epigallocatechin Gallate (EGCG) and Zaprinast function by inhibiting various kinases and phosphodiesterases, thereby potentially relieving FAM188A from negative regulatory constraints and enhancing its activity. LY294002, U0126, and SB203580 indirectly contribute to FAM188A activation by modulating PI3K, MEK1/2, and p38 MAPK signaling pathways, respectively, which might reduce inhibitory signals thereby favoring pathways that lead to FAM188A activation. Collectively, these chemical activators, through their targeted effects on cellular signaling, facilitate the enhancement of FAM188A mediated functions. They do so by either promoting the activation of kinases that can directly phosphorylate FAM188A or by altering signaling pathways that reduce inhibitory influences on FAM188A, thus allowing for its enhanced activity without the need for upregulating its expression or direct activation.

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