PI31 Is an Adaptor Protein for Proteasome Transport in Axons and Required for Synaptic Development
作者: Kai LiuSandra JonesAdi MinisJose RodriguezHenrik MolinaHermann Steller
作者单位: 1Strang Laboratory of Apoptosis and Cancer Biology, The Rockefeller University, 1230 York Avenue, New York, NY 10065, USA
2Proteomics Resource Center, The Rockefeller University, New York, NY 10065, USA
刊名: Developmental Cell, 2019, Vol.50 (4), pp.509-524.e10
来源数据库: Elsevier Journal
DOI: 10.1016/j.devcel.2019.06.009
关键词: ProteasomeUbiquitin-proteasome systemProtein degradationMicrotubule-dependent transportDyneinAxonSynapseNeurodegenerative diseaseParkinson's diseaseDrosophila
原始语种摘要: Summary(#br)Protein degradation by the ubiquitin-proteasome system is critical for neuronal function. Neurons utilize microtubule-dependent molecular motors to allocate proteasomes to synapses, but how proteasomes are coupled to motors and how this is regulated to meet changing demand for protein breakdown remain largely unknown. We show that the conserved proteasome-binding protein PI31 serves as an adaptor to couple proteasomes with dynein light chain proteins (DYNLL1/2). The inactivation of PI31 inhibited proteasome motility in axons and disrupted synaptic proteostasis, structure, and function. Moreover, phosphorylation of PI31 by p38 MAPK enhanced binding to DYNLL1/2 and promoted the directional movement of proteasomes in axons, suggesting a mechanism to regulate loading of...
全文获取路径: Elsevier  (合作)
影响因子:12.861 (2012)

  • contribute 贡献
  • regulated 规定
  • protein 蛋白质
  • disrupted 断线状
  • inactivation 失活
  • coupled 耦合
  • impairment 减损
  • breakdown 故障
  • adaptor 注料口衬套
  • ubiquitin 泛激素