TY - JOUR
T1 - GAP-43 and BASP1 in Axon Regeneration
T2 - Implications for the Treatment of Neurodegenerative Diseases
AU - Chung, Daayun
AU - Shum, Andrew
AU - Caraveo, Gabriela
N1 - Funding Information:
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.
Publisher Copyright:
© Copyright © 2020 Chung, Shum and Caraveo.
PY - 2020/9/3
Y1 - 2020/9/3
N2 - 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.
AB - 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.
KW - BASP1
KW - GAP-43
KW - axon regeneration
KW - neural injury response
KW - neurodegenerative diseases
KW - phosphorylation
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U2 - 10.3389/fcell.2020.567537
DO - 10.3389/fcell.2020.567537
M3 - Review article
C2 - 33015061
AN - SCOPUS:85090999906
SN - 2296-634X
VL - 8
JO - Frontiers in Cell and Developmental Biology
JF - Frontiers in Cell and Developmental Biology
M1 - 567537
ER -