@article{Muller2006mixed-7149,
  year={2006},
  title={A role for mixed lineage kinases in granule cell apoptosis induced by cytoskeletal disruption},
  number={5},
  volume={96},
  issn={0022-3042},
  journal={Journal of Neurochemistry},
  pages={1242--1252},
  author={Müller, Georg Johannes and Geist, Marie Aavang and Veng, Lone Merete and Willesen, Mette Georgi and Johansen, Flemming Fryd and Leist, Marcel and Vaudano, Elisabetta}
}

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    <dc:creator>Veng, Lone Merete</dc:creator>
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    <dc:contributor>Geist, Marie Aavang</dc:contributor>
    <dc:contributor>Müller, Georg Johannes</dc:contributor>
    <dc:contributor>Vaudano, Elisabetta</dc:contributor>
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    <dc:creator>Müller, Georg Johannes</dc:creator>
    <dc:contributor>Leist, Marcel</dc:contributor>
    <dcterms:bibliographicCitation>First publ. in: Journal of Neurochemistry 96 (2006), 5, pp. 1242-1252</dcterms:bibliographicCitation>
    <dc:creator>Johansen, Flemming Fryd</dc:creator>
    <dc:creator>Geist, Marie Aavang</dc:creator>
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    <dc:creator>Willesen, Mette Georgi</dc:creator>
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    <dcterms:title>A role for mixed lineage kinases in granule cell apoptosis induced by cytoskeletal disruption</dcterms:title>
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    <dc:contributor>Johansen, Flemming Fryd</dc:contributor>
    <dc:contributor>Veng, Lone Merete</dc:contributor>
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    <dcterms:issued>2006</dcterms:issued>
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    <dc:creator>Leist, Marcel</dc:creator>
    <dc:creator>Vaudano, Elisabetta</dc:creator>
    <dcterms:abstract xml:lang="eng">Microtubule disruption by colchicine induces apoptosis in selected neuronal populations. However, little is known about the upstream death signalling events mediating the neurotoxicity. We investigated first whether colchicine-induced granule cell apoptosis activates the c-Jun N-terminal kinase (JNK) pathway. Cultured murine cerebellar granule cells were exposed to 1 lM colchicine for 24 h. Activation of the JNK pathway was detected by western blotting as well as immunocytochemistry using antibodies against phosphoc- Jun (p-c-Jun). Next, adult male rats were injected intracerebroventricularly with colchicine (10 lg), and JNK pathway activation in dentate granule cells (DGCs) was detected by antibodies against p-c-Jun. The second part of the study tested the involvement of mixed lineage kinases (MLK) as upstream activators of the JNK pathway in colchicine toxicity, using CEP-1347, a potent MLK inhibitor. In vitro, significant inhibition of the JNK pathway, activated by colchicine, was achieved by 100 300 nM CEP-1347, which blocked both activation of cell death proteases and apoptosis. Moreover, CEP-1347 markedly delayed neurite fragmentation and cell degeneration. In vivo, CEP-1347 (1 mg/kg) significantly prevented p-c-jun increase following injection of colchicine, and enhanced survival of DGCs. We conclude that colchicineinduced neuronal apoptosis involves the JNK/MLK pathway, and that protection of granule cells can be achieved by MLK inhibition.</dcterms:abstract>
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