Abstract
Original studies suggested that tetanus toxin (TT) in vivo exerts its paralytic effect on cholinergic nerve terminals in rabbit iris by interfering with cyclic GMP pathway (Fedinec, et al. 1976 and King, et al. 1978). One possible target site of TT for this effect is guanylate cyclase, the enzyme that catalyzes the formation of cyclic GMP. There are two forms of guanylate cyclases—soluble and membrane bound. Thus, if TT exerts its paralytic activity through the interference with guanylate cyclase activity, then the toxin could cause such interference by acting on soluble or membrane bound guanylate cyclase. In this study we have considered the latter possibility. Specifically, using the combined tools of immunology and genetically-tailored mutants, we have studied the effect of TT directly on the basal activity of plasma membrane guanylate cyclase, GCα (Duda et al., 1991), and on the ANF-dependent cyclase activity of the genetically-constructed ANF receptor guanylate cyclases, GCα-DmutGln338Leu364 and GCα-SmutLeu364.
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Fedinec, A.A., Duda, T., Bizzini, B., Cooper, N.G.F., Sharma, R.K. (1993). Tetanus Toxin Inhibits a Membrane Guanylate Cyclase Transduction System. In: DasGupta, B.R. (eds) Botulinum and Tetanus Neurotoxins. Springer, Boston, MA. https://doi.org/10.1007/978-1-4757-9542-4_28
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DOI: https://doi.org/10.1007/978-1-4757-9542-4_28
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