The protein-protein interaction (PPI) between Ataxin-1 (ATXN1) have been implicated in spinocerebellar ataxia type 1 (SCA1), a neurodegenerative disease primarily caused by polyglutamine expansion in the ATXN1 protein [1].
Function
Disease
Relevance
Structural highlights
Mutation studies of the complex showed that highly conserved residues of CIC, W37, L40, and V41 display hydrophobic contacts with highly conserved residues of the AXH domain, V591, S602, and L686. These residues were found to be required for the PPI interaction as any combination mutation of these residues lead to the disruption of the PPI formation.
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