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R659S mutation of gammaPKC is susceptible to cell death: implication of this mutation/polymorphism in the pathogenesis of retinitis pigmentosa.

Abstract：

:It has been reported that mutations of gammaPKC cause hereditary spinocerebellar atrophy type 14 (SCA14). Our recent study has revealed that the SCA14 mutant gammaPKC is susceptible to aggregation and causes cell death. Among mutations/polymorphisms of gammaPKC, the R659S mutation was firstly segregated from families with hereditary retinitis pigmentosa type 11 (RP11). Although more reliable etiological mutations of RP11 were subsequently discovered in a human homologue of yeast pre-mRNA splicing gene (PRP31), the role of this R659S missense change in the pathogenicity of RP11 is still controversial. In this study, we overexpressed R659S gammaPKC in CHO cells and characterized the properties of this mutant protein. We found that R659S gammaPKC more prominently induced cell death than did wild-type. This mutant gammaPKC had higher basal activity than wild-type, however, no difference was found in the extent of aggregation and insolubility to detergent between R659S mutant and wild-type. These results suggest that the R659S mutation is susceptible to neuronal death and is involved in the pathogenesis of neurodegenerative diseases, including RP11.

journal_name

Neurochem Int

journal_title

Neurochemistry international

authors

Mochizuki H,Seki T,Adachi N,Saito N,Mishima HK,Sakai N

doi

10.1016/j.neuint.2006.05.005

subject

Has Abstract

pub_date

2006-12-01 00:00:00

pages

669-75

issue

7

eissn

0197-0186

issn

1872-9754

pii

S0197-0186(06)00196-3

journal_volume

49

pub_type

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