Date published: 2025-9-14

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TCEANC Activators

TCEANC Activators are diverse in their mechanisms of action but converge on the common outcome of enhancing the functional activity of this transcription elongation factor. Some of these activators achieve this by manipulating levels of cellular second messengers such as cyclic AMP (cAMP). For instance, compounds that elevate intracellular cAMP act as upstream signals that activate protein kinase A (PKA), which in turn may phosphorylate TCEANC, leading to its activation. This can be accomplished through direct stimulation of adenylate cyclase or by preventing the degradation of cAMP via inhibition of phosphodiesterases. Similarly, an analog of cAMP that is cell-permeable can directly activate PKA, subsequently resulting in the activation of TCEANC. In addition to cAMP-related pathways, certain activators work by modulating intracellular calcium concentrations. These activators can either directly increase calcium levels or function as ionophores, facilitating the influx of calcium, which then activates calmodulin-dependent kinases capable of phosphorylating TCEANC.

Other activators influence TCEANC activity by targeting protein kinases directly. Some compounds activate protein kinase C (PKC), which may phosphorylate TCEANC as part of its broad spectrum of cellular targets. On the other hand, certain activators can inhibit protein phosphatases, leading to a net increase in protein phosphorylation within the cell, thereby potentially enhancing TCEANC activity. Additionally, polyamines and certain polyphenolic compounds are known to modulate multiple cellular signaling pathways, which might culminate in the phosphorylation and activation of TCEANC. Certain activators also increase cGMP levels, which can influence the activity of various kinases, indirectly leading to the activation of TCEANC.

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