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

Daayun Chung, Andrew Shum, Gabriela Caraveo*

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

5 Scopus citations

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 languageEnglish (US)
Article number567537
JournalFrontiers in Cell and Developmental Biology
Volume8
DOIs
StatePublished - Sep 3 2020

Keywords

  • BASP1
  • GAP-43
  • axon regeneration
  • neural injury response
  • neurodegenerative diseases
  • phosphorylation

ASJC Scopus subject areas

  • Developmental Biology
  • Cell Biology

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