Forskolin, a diterpene, serves as a catalyst to the adenylate cyclase system, boosting cAMP concentrations with a ripple effect that activates protein kinase A, an enzyme with the potential to modulate a suite of proteins, including TBC1D3H. The cAMP analog Dibutyryl-cAMP mirrors this activity, reinforcing the pathway and bolstering the probability of phosphorylation events that can impact TBC1D3H's behavior. Ionomycin, a calcium ionophore, sails through cellular membranes to elevate intracellular calcium levels, orchestrating a symphony of calmodulin-dependent kinases that may sway TBC1D3H's activity amidst their broad-spectrum tuning. In parallel, the compound W7 counters this by binding to calmodulin and disrupting calcium signals, proposing an alternative route to influence TBC1D3H's state. LY294002, an inhibitor that selectively targets PI3K, presenting an indirect yet potential avenue for the modulation of TBC1D3H through the perturbation of this axis.
Mitogen-activated protein kinase pathways, guardians of cellular response to a myriad of stimuli, are targeted by PD 98059, SB 203580, SP600125, and U0126. These agents selectively inhibit ERK, p38 MAPK, JNK, and MEK, respectively, each maneuvering the signaling pathways in a manner that can recalibrate the activity of proteins, possibly including TBC1D3H. Rapamycin, an inhibitor of the mTOR pathway, intercedes in a central regulatory node, with the capacity to adjust the functional dynamics of TBC1D3H. Epigallocatechin Gallate (EGCG) stands out as a multifaceted agent, capable of modulating diverse biological pathways, which in turn may cast an indirect influence on TBC1D3H.
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