Title : A fine balance between Prpf19 and Exoc7 in achieving degradation of aggregated protein and suppression of cell death in spinocerebellar ataxia type 3.

Pub. Date : 2021 Feb 2

PMID : 33542212






5 Functional Relationships(s)
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1 Polyglutamine (polyQ) diseases comprise Huntington"s disease and several subtypes of spinocerebellar ataxia, including spinocerebellar ataxia type 3 (SCA3). polyglutamine ataxin 3 Homo sapiens
2 Polyglutamine (polyQ) diseases comprise Huntington"s disease and several subtypes of spinocerebellar ataxia, including spinocerebellar ataxia type 3 (SCA3). polyglutamine ataxin 3 Homo sapiens
3 Polyglutamine (polyQ) diseases comprise Huntington"s disease and several subtypes of spinocerebellar ataxia, including spinocerebellar ataxia type 3 (SCA3). polyglutamine ataxin 3 Homo sapiens
4 Polyglutamine (polyQ) diseases comprise Huntington"s disease and several subtypes of spinocerebellar ataxia, including spinocerebellar ataxia type 3 (SCA3). polyglutamine ataxin 3 Homo sapiens
5 Our data suggest that Exoc7/exo70 exerts its ATXN3-polyQ-modifying effect through regulating the E3 ligase function of Prpf19/prp19. polyglutamine ataxin 3 Homo sapiens