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CRMP-2 binds to tubulin heterodimers to promote microtubule assembly.

Nature cell biology | Aug 31, 2002

http://www.ncbi.nlm.nih.gov/pubmed/12134159

Regulated increase in the formation of microtubule arrays is thought to be important for axonal growth. Collapsin response mediator protein-2 (CRMP-2) is a mammalian homologue of UNC-33, mutations in which result in abnormal axon termination. We recently demonstrated that CRMP-2 is critical for axonal differentiation. Here, we identify two activities of CRMP-2: tubulin-heterodimer binding and the promotion of microtubule assembly. CRMP-2 bound tubulin dimers with higher affinity than it bound microtubules. Association of CRMP-2 with microtubules was enhanced by tubulin polymerization in the presence of CRMP-2. The binding property of CRMP-2 with tubulin was apparently distinct from that of Tau, which preferentially bound microtubules. In neurons, overexpression of CRMP-2 promoted axonal growth and branching. A mutant of CRMP-2, lacking the region responsible for microtubule assembly, inhibited axonal growth and branching in a dominant-negative manner. Taken together, our results suggest that CRMP-2 regulates axonal growth and branching as a partner of the tubulin heterodimer, in a different fashion from traditional MAPs.

Pubmed ID: 12134159 RIS Download

Mesh terms: Animals | Axons | Cell Line | Cercopithecus aethiops | Dimerization | Fibroblasts | Green Fluorescent Proteins | Hippocampus | In Vitro Techniques | Intercellular Signaling Peptides and Proteins | Kinetics | Luminescent Proteins | Microtubules | Mutation | Nerve Tissue Proteins | Neurons | Protein Binding | Rats | Recombinant Fusion Proteins | Tubulin | Vero Cells

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