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Publication : End binding protein-1 (EB1) complements microtubule-associated protein-1B during axonogenesis.

First Author  Jiménez-Mateos EM Year  2005
Journal  J Neurosci Res Volume  80
Issue  3 Pages  350-9
PubMed ID  15789376 Mgi Jnum  J:105172
Mgi Id  MGI:3614250 Doi  10.1002/jnr.20453
Citation  Jimenez-Mateos EM, et al. (2005) End binding protein-1 (EB1) complements microtubule-associated protein-1B during axonogenesis. J Neurosci Res 80(3):350-9
abstractText  The different strains of microtubule-associated protein (MAP)-1B-deficient mice that have been generated appear to express different phenotypes. This variability could be the consequence of the distinct genetic backgrounds of the animals used to generate these lines. Certain proteins might be able to complement the deficit of MAP1B function in these mice. Therefore, we examined whether the concentrations of potential compensatory proteins varied among these mutant strains. In this way, we identified significant differences in the amounts of the microtubule-associated EB1 protein between two of these strains. Furthermore, in transfection studies, we demonstrated that the overexpression of end binding protein-1 (EB1) could facilitate axonogenesis in MAP1B-/- cells in which EB1 is normally weakly expressed. Thus, we suggest that EB1 could complement MAP1B function during neural development.
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