Conclusion
The regulation of taurine biosynthesis can be summarized as following: (i) When neurons are stimulated, the arrival of action potential will open the voltage-dependent Ca2+-channel, resulting in an increase of intracellular free Ca2+, [Ca2+]i, (ii) Elevation of [Ca2+]i will trigger release of taurine as well as activation of PKC, which in turn activates CSAD through protein phosphorylation; (iii) The activated CSAD then synthesizes more taurine to replenish that lost due to stimulation-mediated release; (iv) When intracellular taurine reach a certain level, it then inhibits the activation of PKC directly or indirectly (possibly through regulating Ca2+ availability), thus shutting down activation of CSAD through inhibition of CSAD phosphorylation by PKC; and (v) CSAD soon returns to its inactive state through the action of a protein phosphatase, most likely PrP-2C. The mode of action of taurine inlowering the level of [Ca2+]i, is at least partially due to its inhibition on the reverse mode of Na+-Ca2+ exchanger activity
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Wu, JY. et al. (2002). Mode of Action of Taurine and Regulation Dynamics of Its Synthesis in the CNS. In: Della Corte, L., Huxtable, R.J., Sgaragli, G., Tipton, K.F. (eds) Taurine 4. Advances in Experimental Medicine and Biology, vol 483. Springer, Boston, MA. https://doi.org/10.1007/0-306-46838-7_4
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