Abstract
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.
| Original language | English (US) |
|---|---|
| Article number | 567537 |
| Journal | Frontiers in Cell and Developmental Biology |
| Volume | 8 |
| DOIs | |
| State | Published - Sep 3 2020 |
Funding
We would like to thank the members of the laboratory for constructive feedback. Funding. This review manuscript was supported by the Parkinson’s Foundation grant PF-JFA-1949 and the National Institute of Mental Health grant 2T32MH067564.
Keywords
- BASP1
- GAP-43
- axon regeneration
- neural injury response
- neurodegenerative diseases
- phosphorylation
ASJC Scopus subject areas
- Cell Biology
- Developmental Biology