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Published on: October 30, 2018
GAP-43 regulates NCAM-180-mediated neurite outgrowth
Irina Korshunova1, Vera Novitskaya, Darya Kiryushko
1Protein Laboratory, Institute of Molecular Pathology, University of Copenhagen, DK-2200 Copenhagen, Denmark. irina@plab.ku.dk
Journal of Neurochemistry
|January 11, 2007
Summary
Growth-associated protein (GAP-43) enhances neurite extension by modulating neural cell adhesion molecule (NCAM) signaling pathways. GAP-43 acts as a switch, influencing whether NCAM signaling involves spectrin or Fyn kinase.
Area of Science:
- Neuroscience
- Cell Biology
- Molecular Biology
Background:
- Neural cell adhesion molecule (NCAM) and growth-associated protein (GAP-43) are crucial for neuronal development and plasticity.
- Their interdependent functions are vital, but the underlying mechanisms remain unclear.
Purpose of the Study:
- To elucidate the mechanisms governing the functional association between GAP-43 and NCAM.
- To investigate how GAP-43 influences NCAM-mediated neurite outgrowth.
Main Methods:
- Overexpression of GAP-43 in PC12E2 cells and hippocampal neurons.
- Analysis of neurite extension in the presence and absence of homophilic NCAM binding.
- Investigation of GAP-43 phosphorylation by protein kinase C (PKC) and casein kinase II (CKII).
Main Results:
- GAP-43 overexpression potentiates neurite extension, dependent on its membrane association.
- Phosphorylation of GAP-43 by PKC and CKII is critical for NCAM-induced neurite outgrowth.
- GAP-43 presence shifts NCAM signaling from a Fyn-dependent pathway to an NCAM-180/spectrin/GAP-43 pathway.
Conclusions:
- GAP-43 acts as a functional switch for NCAM-180 signaling.
- Cellular localization of GAP-43 and NCAM determines the predominant signaling pathway activated by NCAM binding.
- This provides insight into the regulation of neuronal development and plasticity.
