Structural Biophysics Laboratory, Center for Cancer Research National Cancer Institute, Frederick, MD, USA.
EMBO J. 2013 Jul 31;32(15):2087-9. doi: 10.1038/emboj.2013.158. Epub 2013 Jul 12.
Mutations in Parkin represent ~50% of disease-causing defects in autosomal recessive-juvenile onset Parkinson's disease (AR-JP). Recently, there have been four structural reports of autoinhibited forms of this RING-IBR-RING (RBR) ubiquitin ligase (E3) by the Gehring, Komander, Johnston and Shaw groups. The important advances from these studies set the stage for the next steps in understanding the molecular basis for Parkinson's disease (PD).
Parkin 中的突变代表常染色体隐性遗传少年型帕金森病（AR-JP）中约 50%的致病缺陷。最近，Gehring、Komander、Johnston 和 Shaw 小组已经有了关于这种 RING-IBR-RING（RBR）泛素连接酶（E3）的自动抑制形式的四项结构报告。这些研究的重要进展为理解帕金森病（PD）的分子基础的下一步奠定了基础。
