Several lines of evidenes have indicates that changes in te structure of neuronal cytoskeleton could be the source of the dramatic morphological changes that occur during neuronal diferentiation. It has been proposed that microtubule-associated proteins can contribute to the development of this phenomenon by controlling the dynamic properties of microtubules.
MAP1B is a neuron-specific microtubule associated protein implicated in the control of the dynamic stability of microtubules and in the cross-talk between microtubules and actin filaments.
Different MAPs can cotnribute to this maturation. MAP1B and MAP2 are implicated in the first steps of maturation, and MAP1B and Tau are implicated in the neuronal maturation.
The signalling cascades governing neuronal migration are believed to link extracellular signals to cytoskeletal components. We have observed that MAP1B could participate in the signalling of molecules, such as Netrin and Reelin, both implicated in the migration of neurons.
For neuronal migration to occur, the cell must undergo morphlogical changes that require modifications to the cytoskeleton. Several different microtubule-associated proteins (MAPs) or actin-binding proteins (ABPs) are thought to be involved in the migration of neurons. Therefore, we have specifically analyzed the interacion of two of the MAP family members, MAP1B and LIS1, and its implication in neuronal migration. This interaction regulates the cellular motor dynein function.
On the other hand, we have studied, why different strains of map1b-/- (NMR1 and C57/BL6) deficient mice develop different phenotypes .The resposible of these different phenotypes could be the existance of different genetic backgrounds.
Thus, we have tested in two of these strains the concentrations of proteins that could complement the microtubule associated proein MAP1B function.
In this study we have found a difference in the amount of microtubule associated EB1 proteín
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