Date published: 2025-9-14

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FTSJD1 Activators

Forskolin directly stimulates adenylate cyclase to increase intracellular cAMP, which activates protein kinase A (PKA). PKA then has the capacity to phosphorylate diverse proteins and may target FTSJD1. Ionomycin, a known calcium ionophore, raises intracellular calcium levels and can activate calcium-dependent kinases that engage with FTSJD1's regulation. Phorbol 12-myristate 13-acetate, known as PMA, activates protein kinase C (PKC), which phosphorylates a variety of substrates and can influence the function of FTSJD1. Lithium chloride takes a different route by inhibiting glycogen synthase kinase-3 (GSK-3), potentially impacting FTSJD1 through altered phosphorylation pathways. Dibutyryl-cAMP, a synthetic cAMP analog, permeates cells to activate PKA, offering another phosphorylation avenue to affect FTSJD1.

Sodium butyrate, acting as a histone deacetylase inhibitor, can shift gene expression patterns, potentially leading to an increase in FTSJD1 expression. Resveratrol activates sirtuins and AMPK, key players in cellular stress and metabolic regulation, which may have implications for FTSJD1 activity. Rapamycin, an antifungal agent, inhibits mTOR signaling and can indirectly modulate FTSJD1 activity through this intricate pathway. Isoproterenol, a beta-adrenergic agonist, increases cAMP much like forskolin, suggesting PKA activation and possible effects on FTSJD1. Dexamethasone, a glucocorticoid, binds to its receptor to modulate gene transcription, potentially altering FTSJD1 expression. Retinoic acid interacts with its nuclear receptors affecting gene expression, which can lead to alterations in proteins associated with FTSJD1's function. The epidermal growth factor (EGF) binds to its receptor, initiating a signaling cascade that can result in the modulation of proteins, including FTSJD1.

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