Chemical activators of cysteine rich tail 1 can influence the activity of this protein through various biochemical pathways. Phorbol 12-myristate 13-acetate (PMA) is one such chemical, which activates protein kinase C (PKC) directly. The activated PKC then phosphorylates cysteine rich tail 1, leading to its activation. Forskolin is another activator that works by increasing the levels of cAMP within the cell, thereby activating protein kinase A (PKA). PKA then targets cysteine rich tail 1 for phosphorylation, resulting in its activation. Okadaic acid and Calyculin A function by inhibiting protein phosphatases 1 and 2A, enzymes that normally dephosphorylate proteins. This inhibition results in the sustained phosphorylation and consequent activation of cysteine rich tail 1. Similarly, Thapsigargin raises intracellular calcium levels by inhibiting the SERCA pump, which triggers the activation of calcium-dependent kinases that can phosphorylate and activate cysteine rich tail 1.
Continuing with the theme of calcium signaling, Ionomycin increases intracellular calcium concentrations by acting as a calcium ionophore, leading to the activation of calcium-dependent kinases that target cysteine rich tail 1. 4-Phorbol and (-)-Indolactam V specifically activate PKC isozymes, which then phosphorylate cysteine rich tail 1, thus activating it. Dibutyryl-cAMP, a cAMP analog, activates PKA, which in turn can phosphorylate and activate cysteine rich tail 1. Bryostatin 1, an activator of PKC, also contributes to the phosphorylation and activation of cysteine rich tail 1. Hyperforin activates TRPC6 channels that facilitate calcium influx, subsequently activating downstream calcium-responsive pathways that include cysteine rich tail 1. Lastly, Anisomycin, despite being a protein synthesis inhibitor, activates stress-activated protein kinases, which then lead to the phosphorylation and activation of cysteine rich tail 1, highlighting the complex interplay between synthesis inhibition and kinase activation pathways.
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