INSERM, UMR_S975 (Formerly UMR_S679), Hôpital de la Salpêtrière, Paris, France.
Neurobiol Aging. 2010 Jun;31(6):1069-71; discussion 1072-4. doi: 10.1016/j.neurobiolaging.2009.06.008. Epub 2009 Dec 8.
Meeus et al. (2009) reported no pathogenic mutations in a comprehensive genetic analysis of the entire GRB10-interacting GYF protein-2 gene (GIGYF2) in a Belgian series of both familial and sporadic patients with Parkinson's disease (PD). Although we initially proposed that GIGYF2 corresponds to the PARK11 locus, in familial PD, we found no causative variations in a follow-up study in which GIGYF2 was screened in an independent series of 185 patients with autosomal dominant PD, mostly of French origin. Together, these results do not support a major role of GIGYF2 in PD.
Meeus 等人(2009 年)在对来自比利时的家族性和散发性帕金森病(PD)患者的整个 GRB10 相互作用 GYF 蛋白-2 基因(GIGYF2)进行全面的遗传分析中,并未报告任何致病性突变。虽然我们最初提出 GIGYF2 对应于 PARK11 基因座,但在家族性 PD 的后续研究中,我们在一个独立的、由 185 名常染色体显性 PD 患者组成的系列中,对 GIGYF2 进行了筛查,这些患者大多来自法国,未发现致病变异。这些结果均不支持 GIGYF2 在 PD 中起主要作用。