Gupta Amit, Anjomani-Virmouni Sara, Koundouros Nikos, Poulogiannis George
Signalling and Cancer Metabolism Team, Division of Cancer Biology, The Institute of Cancer Research, London, UK.
Division of Computational and Systems Medicine, Department of Surgery and Cancer, Imperial College, London, UK.
Mol Cell Oncol. 2017 May 19;4(6):e1329692. doi: 10.1080/23723556.2017.1329692. eCollection 2017.
Cancer and Parkinson disease (PD) derive from distinct alterations in cellular processes, yet there are pathogenic mutations that are unequivocally linked to both diseases. Here we expand on our recent findings that loss of parkin RBR E3 ubiquitin protein ligase (, best known as )-which is genetically linked to PD-promotes cancer progression via redox-mediated inactivation of phosphatase and tensin homolog (PTEN) by S-nitrosylation.
癌症和帕金森病（PD）源于细胞过程中的不同改变，但存在一些明确与这两种疾病都相关的致病突变。在此，我们进一步阐述我们最近的研究发现：与帕金森病存在遗传关联的帕金RBR E3泛素蛋白连接酶（最广为人知的是 ）的缺失，通过S-亚硝基化介导的氧化还原反应使磷酸酶和张力蛋白同源物（PTEN）失活，从而促进癌症进展。
