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Titlebook: Clostridial Neurotoxins; The Molecular Pathog Cesare Montecucco Book 1995 The Editor(s) (if applicable) and The Author(s), under exclusive

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Neuroexocytosis,transfer is achieved by exocytotic release of chemical messengers, the neurotransmitters, into the extracellular space upon stimulation. Two major classes of chemical messengers exist: small molecules such as amino acids or amines (the so-called classical neurotransmitters) and neuropeptides. The tw
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Neurospecific Binding, Internalization, and Retrograde Axonal Transport, exert their effects on a cytosolic substrate (. and . 1978). Although many of the details remain to be determined, generally it is accepted that the clostridial neurotoxins (CNTs) interact with membrane receptors and are translocated into the cytosol where they act to block release of neurotransmit
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Immunodiagnosis and Immunotherapy of Tetanus and Botulinum Neurotoxins,apter reviews the past and current literature on vaccines and various antibody-based products for treatment or prevention of poisonings by both botulinum and tetanus neurotoxins. We also review the techniques employed for their detection and identification.
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Clinical Use of Botulinum Neurotoxins,ence with this toxin to correct strabismus in humans (. 1981). Since then BoNT injections have been demonstrated to be a safe and efficient therapy for a large number of neurologic and nonneurologic diseases (. and . 1991). In December 1989 the United States Food and Drug Administration approved BoN
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Neurospecific Binding, Internalization, and Retrograde Axonal Transport,ne domain, and the L chain is the catalytic domain (reviewed by . 1991; . 1992). This chapter summarizes current data on the binding of CNTs to sensitive cells and the mechanism whereby the toxins are thought to gain access to their cytoplasmic targets.
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Intracellular Targets and Metalloprotease Activity of Tetanus and Botulism Neurotoxins,t was not unexpected that clostridial neurotoxins are enzymes, acting in the neuron cytosol (. et al. 1993a). In fact, an enzyme can modify one after another all the target molecules present in the system and hence one single molecule of an enzymic toxin is able to intoxicate a synapse. TeNT and the
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