Gap-43 (Phospho-Ser⁴¹) Polyclonal Antibody

Gap-43 is thought to have an important role in development and plasticity because it is expressed at high levels in neuronal growth cones during development and during axonal regeneration.¹ There is also evidence from knockout animals that Gap-43 serves to amplify path finding signals from the growth cone.² Gap-43 is thought to mediate at least some of these effects via interaction with actin. Importantly, phosphorylation at Ser⁴¹ by protein kinase C (Catalog No. 1609-PKC) modulates the interaction of Gap-43 with actin and may also affect neurotransmitter release during forms of plasticity like LTP.^3,4

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1. Benowitz, L.I., and Routtenberg, A. Gap-43: An intrinsic determinant of neuronal development and plasticity. Trends Neurosci. 20, 84-91 (1997).

2. Strittmatter, S.M., Fankhauser, C., Huang, P.L., et al. Neuronal pathfinding is abnormal in mice lacking the neuronal growth cone protein Gap-43. Cell 80, 445-452 (1995).

3. He, Q., Dent, E.W., and Meiri, K.F. Modulation of actin filament behavior by Gap-43 (neuromodulin) is dependent on the phosphorylation status of serine 41, the protein kinase C site. J. Neurosci. 17, 3515-3524 (1997).

4. Hulo, S., Alberi, S., Laux, T., et al. A point mutant of Gap-43 induces enhanced short-term and long-term hippocampal plasticity. Eur. J. Neurosci. 15, 1976-1982 (2002).