@article{YadavSelvarajBenderetal.2016,
  author    = {Yadav, Preeti and Selvaraj, Bhuvaneish T. and Bender, Florian L. P. and Behringer, Marcus and Moradi, Mehri and Sivadasan, Rajeeve and Dombert, Benjamin and Blum, Robert and Asan, Esther and Sauer, Markus and Julien, Jean-Pierre and Sendtner, Michael},
  title     = {Neurofilament depletion improves microtubule dynamics via modulation of Stat3/stathmin signaling},
  series = {Acta Neuropathologica},
  volume    = {132},
  journal   = {Acta Neuropathologica},
  number    = {1},
  doi       = {10.1007/s00401-016-1564-y},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-188234},
  pages     = {93-110},
  year      = {2016},
  abstract  = {In neurons, microtubules form a dense array within axons, and the stability and function of this microtubule network is modulated by neurofilaments. Accumulation of neurofilaments has been observed in several forms of neurodegenerative diseases, but the mechanisms how elevated neurofilament levels destabilize axons are unknown so far. Here, we show that increased neurofilament expression in motor nerves of pmn mutant mice, a model of motoneuron disease, causes disturbed microtubule dynamics. The disease is caused by a point mutation in the tubulin-specific chaperone E (Tbce) gene, leading to an exchange of the most C-terminal amino acid tryptophan to glycine. As a consequence, the TBCE protein becomes instable which then results in destabilization of axonal microtubules and defects in axonal transport, in particular in motoneurons. Depletion of neurofilament increases the number and regrowth of microtubules in pmn mutant motoneurons and restores axon elongation. This effect is mediated by interaction of neurofilament with the stathmin complex. Accumulating neurofilaments associate with stathmin in axons of pmn mutant motoneurons. Depletion of neurofilament by Nefl knockout increases Stat3-stathmin interaction and stabilizes the microtubules in pmn mutant motoneurons. Consequently, counteracting enhanced neurofilament expression improves axonal maintenance and prolongs survival of pmn mutant mice. We propose that this mechanism could also be relevant for other neurodegenerative diseases in which neurofilament accumulation and loss of microtubules are prominent features.},
  language  = {en}
}
@article{WeberOsbornFrankeetal.1977,
  author    = {Weber, Klaus and Osborn, Mary and Franke, Werner W. and Seib, Erinita and Scheer, Ulrich and Herth, Werner},
  title     = {Identification of microtubular structures in diverse plant and animal cells by immunological cross-reaction revealed in immunofluorescence microscopy using antibodies against tubulin from porcine brain},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-41383},
  year      = {1977},
  abstract  = {Antibody against tubulin from porcine brain was used to evaluate the immunological cross reactivity of tubulin from a variety of animal and plant cells. Indirect immunofluorescence microscopy revealed microtubule-containing structures including cytoplasmic microtubules, spindle microtubules, cilia and fIagella. Thus tubulin from diverse species of both mammals and plants show immunological cross-reactivity with tubulin from porcine brain. Results obtained by immunofluorescence microscopy are whenever possible compared with previously known ultrastructural results obtained by electron microscopy.},
  subject      = {Cytologie},
  language  = {en}
}