Early-phase drug discovery of β-III-spectrin actin-binding modulators for treatment of spinocerebellar ataxia type 5
Author:
Funder
National Institutes of Health
Publisher
Elsevier BV
Subject
Cell Biology,Molecular Biology,Biochemistry
Reference41 articles.
1. Characterization of a new beta-spectrin gene which is predominantly expressed in brain;Ohara;Brain Res. Mol. Brain Res.,1998
2. Targeted deletion of betaIII spectrin impairs synaptogenesis and generates ataxic and seizure phenotypes;Stankewich;Proc. Natl. Acad. Sci. U. S. A.,2010
3. Beta-III spectrin mutation L253P associated with spinocerebellar ataxia type 5 interferes with binding to Arp1 and protein trafficking from the Golgi;Clarkson;Hum. Mol. Genet.,2010
4. Spectrin mutations cause spinocerebellar ataxia type 5;Ikeda;Nat. Genet.,2006
5. A human beta-III-spectrin spinocerebellar ataxia type 5 mutation causes high-affinity F-actin binding;Avery;Sci. Rep.,2016
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1. Increased Actin Binding Is a Shared Molecular Consequence of Numerous SCA5 Mutations in β-III-Spectrin;Cells;2023-08-19
2. Cardiomyopathy-associated variants alter the structure and function of the α-actinin-2 actin-binding domain;Biochemical and Biophysical Research Communications;2023-08
3. Cardiomyopathy-Associated Variants Alter the Structure and Function of the α-Actinin-2 Actin-Binding Domain;2023-05-09
4. Drug discovery for heart failure targeting myosin-binding protein C;2023-04-05
5. Increased actin binding is a shared molecular consequence of numerous spinocerebellar ataxia mutations in β-III-spectrin;2023-02-21
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