PMID: 9523581Apr 2, 1998Paper

Tetanus toxin enhances protein kinase C activity translocation and increases polyphosphoinositide hydrolysis in rat cerebral cortex preparations

Journal of Neurochemistry
C GilJ Aguilera

Abstract

Tetanus toxin (TeTx) has been recently demonstrated to be a Zn2+-dependent endopeptidase that cleaves synaptobrevin, a protein in part responsible for neurotransmitter release. Nevertheless, certain aspects of TeTx action, for example, the causal relationship between TeTx and protein kinase C (PKC; EC 2.7.1.37) activity cannot be explained by this cleavage alone. In the present study, primary neurons from fetal rat brain, synaptosomes, and whole slices have been used to examine this issue. Low doses of TeTx (< or = 10(-8) M) caused PKC activity translocation in a manner similar to that produced by 12-O-tetradecanoylphorbol 13-acetate (TPA). TPA (< or = 10(-7) M) caused sustained PKC activity translocation, whereas TeTx produced translocation followed by relocation, depending on the dose and time of exposure. Immunoidentification with a monoclonal antibody recognizing both alpha and beta isoforms revealed that TeTx induced moderate losses of PKC in the cytosolic fraction, without a comparable increase in the particulate fraction. Although moderate losses of activity were also noticed in the cytosolic fraction, the inconsistency with respect to activity translocation may be explained by translocation of additional PKC isoforms th...Continue Reading

Citations

Dec 13, 2000·FEBS Letters·A NajibJ Aguilera
Jul 28, 2012·International Journal of Molecular Sciences·Ana C CalvoRosario Osta
Feb 20, 2003·Neurochemistry International·Carles GilJosé Aguilera
Oct 7, 2004·Neuroscience·S E Bradford, J V Nadler
Mar 14, 2002·International Journal of Medical Microbiology : IJMM·Judit Herreros, Giampietro Schiavo

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