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XB-ART-7233
Nat Neurosci 2002 May 01;55:431-7. doi: 10.1038/nn840.
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A protein kinase A-dependent molecular switch in synapsins regulates neurite outgrowth.

Kao HT , Song HJ , Porton B , Ming GL , Hoh J , Abraham M , Czernik AJ , Pieribone VA , Poo MM , Greengard P .


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Cyclic AMP (cAMP) promotes neurite outgrowth in a variety of neuronal cell lines through the activation of protein kinase A (PKA). We show here, using both Xenopus laevis embryonic neuronal culture and intact X. laevis embryos, that the nerve growth-promoting action of cAMP/PKA is mediated in part by the phosphorylation of synapsins at a single amino acid residue. Expression of a mutated form of synapsin that prevents phosphorylation at this site, or introduction of phospho-specific antibodies directed against this site, decreased basal and dibutyryl cAMP-stimulated neurite outgrowth. Expression of a mutation mimicking constitutive phosphorylation at this site increased neurite outgrowth, both under basal conditions and in the presence of a PKA inhibitor. These results provide a potential molecular approach for stimulating neuron regeneration, after injury and in neurodegenerative diseases.

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Species referenced: Xenopus laevis
Genes referenced: camp syn1