The review abstract describes BASP1 as regulating actin dynamics and presynaptic vesicle cycling at axon terminals, supporting axonal growth, regeneration, and plasticity.
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BASP1
Candidate: concept label1 source documents4 linked claims
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brain acid-soluble protein 1
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Studies in neurodegenerative diseases report altered expression and phosphorylation profiles of GAP-43 and BASP1.
Quoted textsource-backed
Interestingly, examinations of GAP-43 and BASP1 in neurodegenerative diseases reveal alterations in their expression and phosphorylation profiles.
GAP-43 and BASP1 regulate actin dynamics and presynaptic vesicle cycling at axon terminals and thereby facilitate axonal growth, regeneration, and plasticity.
Quoted textsource-backed
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.
The functions of GAP-43 and BASP1 in axonal growth-related processes depend strongly on expression levels and post-translational modifications such as phosphorylation.
Quoted textsource-backed
These functions highly depend on changes in GAP-43 and BASP1 expression levels and post-translational modifications such as phosphorylation.
The review explores the therapeutic potential of modulating GAP-43 and BASP1 activities to compensate for neuron loss in neurodegenerative diseases.
Quoted textsource-backed
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.