TTC35 Activators encompass a selection of chemical compounds that are surmised to enhance the functional activity of TTC35 through distinct signaling pathways and biochemical mechanisms. Forskolin, Rolipram, and IBMX all work through increasing cAMP levels within the cell, which can subsequently activate protein kinase A (PKA). PKA phosphorylation is a post-translational modification that may affect proteins within the same signaling cascade as TTC35, thereby enhancing its activity. Similarly, PMA, by activating protein kinase C (PKC), and Ionomycin, through elevating intracellular calcium levels, can initiate signaling events that indirectly promote TTC35 function, possibly via calcium-dependent protein kinases and PKC-mediated pathways. Additionally, Dibutyryl-cAMP acts as a cAMP analog to activate PKA, while Epigallocatechin gallate (EGCG) serves to inhibit a variety of kinases, potentially decreasing competitive signaling and indirectly promoting pathways TTC35 is involved in.
LY294002 and PD98059, both inhibitors of PI3K and MEK respectively, along with U0126 and SB203580, which inhibit MEK and p38 MAPK, are all thought to modulate specific signaling pathways that can impact the functional activity of TTC35. By inhibiting these kinases, the cellular signaling landscape may shift in a manner that promotes the role of TTC35 within its respective pathways. A23187 aids in this process by increasing intracellular calcium, which can activate calcium-dependent kinases that may influence TTC35's activity. The collective action of these TTC35 Activators is to facilitate the enhancement of TTC35's role within its signaling networks by altering the phosphorylation states and signaling dynamics of the cell, without directly increasing the expression or requiring direct activation of TTC35 itself.
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