Date published: 2025-10-11

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C4orf47 Activators

Chemical activators of C4orf47 can influence its activity through various biochemical pathways involving second messengers and protein phosphorylation. Calcium chloride and Ionomycin function by increasing intracellular calcium levels, which is a crucial secondary messenger in various signaling pathways. The elevated calcium levels can activate calcium-dependent protein kinases, such as calmodulin-dependent kinases, which can then phosphorylate C4orf47, leading to its activation. The ionophore A23187 also raises intracellular calcium levels, triggering a similar cascade of events that result in the activation of C4orf47. In parallel, Thapsigargin serves to disrupt calcium storage within the endoplasmic reticulum, causing an increase in cytosolic calcium that can further fuel the calcium-dependent activation of C4orf47.

In addition to calcium-mediated pathways, C4orf47 can also be activated through the modulation of cyclic AMP (cAMP) levels. Forskolin directly stimulates adenylyl cyclase, which increases intracellular cAMP levels, and this, in turn, activates protein kinase A (PKA). Once activated, PKA can phosphorylate C4orf47, thereby activating it. Dibutyryl cyclic AMP, a cell-permeable analog of cAMP, similarly activates PKA, which may result in the phosphorylation and subsequent activation of C4orf47. Phorbol 12-myristate 13-acetate (PMA) activates protein kinase C (PKC), which is known for its role in the phosphorylation of various proteins. Activated PKC can, therefore, phosphorylate and activate C4orf47. Chelerythrine, although primarily an inhibitor of PKC, can paradoxically lead to the activation of certain PKC isoforms, which then might contribute to the phosphorylation and activation of C4orf47. Lastly, Okadaic acid and Calyculin A inhibit protein phosphatases PP1 and PP2A, respectively, leading to a general increase in phosphorylation levels within the cell, which could include C4orf47, resulting in its activation. (-)-Blebbistatin and Epigallocatechin gallate (EGCG) affect the protein kinase networks indirectly; (-)-Blebbistatin by altering cytoskeletal dynamics which can influence signaling pathways leading to the activation of C4orf47, and EGCG by inhibiting certain kinases, potentially causing a compensatory activation of other kinases that then activate C4orf47.

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