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End binding protein‐1 (EB1) complements microtubule‐associated protein‐1B during axonogenesis
Author(s) -
JiménezMateos Eva M.,
Paglini Gabriela,
GonzálezBillault Christian,
Cáceres Alfredo,
Avila Jesús
Publication year - 2005
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.20453
Subject(s) - microtubule , microbiology and biotechnology , binding protein , microtubule associated protein , plasma protein binding , chemistry , biology , biochemistry , gene
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. © 2005 Wiley‐Liss, Inc.