Premium
Activation of signal transduction pathways involving trkA, PLCγ‐1, PKC isoforms and ERK‐1/2 by tetanus toxin
Author(s) -
Gil Carles,
Chaı̈b-Oukadour Imane,
Pelliccioni Patricia,
Aguilera José
Publication year - 2000
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(00)02002-0
Subject(s) - protein kinase c , mapk/erk pathway , tropomyosin receptor kinase a , signal transduction , microbiology and biotechnology , kinase , phosphorylation , gene isoform , biology , phospholipase c , chemistry , receptor , biochemistry , nerve growth factor , gene
Previous reports have demonstrated that tetanus toxin (TeTx) induces activation and down‐regulation of protein kinase C (PKC). In the present work the differential activation of PKC isoforms and of signal transduction pathways, including nerve growth factor receptor trkA, phospholipase Cγ‐1 (PLCγ‐1), and extracellular regulated kinases 1 and 2 (ERK‐1/2) by TeTx in a synaptosome‐enriched P 2 fraction from rat brain is reported. TeTx induces clear translocation from the soluble (cytosolic) compartment to the particulate (membranous) compartment of PKC‐β, ‐γ and ‐δ isoforms, whereas PKC‐ϵ showed a slight decrease of its soluble fraction immunoreactivity. On the contrary, the PKC‐ζ isoform shows no consistent response, whereas down‐regulation of total PKC‐α immunoreactivity is shown. Immunoprecipitation assays against phosphotyrosine show an increase of trkA and PLCγ‐1 phosphorylation. Moreover, trkA activation is corroborated using phospho‐specific antibodies against phosphorylated trkA. On the other hand, TeTx‐induced stimulation of mitogen‐activated protein (MAP) kinase activity is observed, this event also being detected by Western analysis using phospho‐specific antibodies against ERK‐1/2.