GAP-43 and BASP1 in Axon Regeneration: Implications for the Treatment of Neurodegenerative Diseases

• Main Authors: Daayun Chung, Andrew Shum, Gabriela Caraveo
• Format: Article
• Language: English
• Published: Frontiers Media S.A. 2020-09-01
• Series: Frontiers in Cell and Developmental Biology
• Subjects: GAP-43; BASP1; phosphorylation; neural injury response; axon regeneration; neurodegenerative diseases
• Online Access: https://www.frontiersin.org/article/10.3389/fcell.2020.567537/full

Growth-associated protein-43 (GAP-43) and brain acid-soluble protein 1 (BASP1) regulate actin dynamics and presynaptic vesicle cycling at axon terminals, thereby facilitating axonal growth, regeneration, and plasticity. These functions highly depend on changes in GAP-43 and BASP1 expression levels and post-translational modifications such as phosphorylation. Interestingly, examinations of GAP-43 and BASP1 in neurodegenerative diseases reveal alterations in their expression and phosphorylation profiles. This review provides an overview of the structural properties, regulations, and functions of GAP-43 and BASP1, highlighting their involvement in neural injury response and regeneration. By discussing GAP-43 and BASP1 in the context of neurodegenerative diseases, we also explore the therapeutic potential of modulating their activities to compensate for neuron loss in neurodegenerative diseases.