Corrigendum: Parkinson-causing α-synuclein missense mutations shift native tetramers to monomers as a mechanism for disease initiation

Similar Items

• Parkinson-causing α-synuclein missense mutations shift native tetramers to monomers as a mechanism for disease initiation
  od: Dettmer, Ulf, i dr.
  Izdano: (2015)
• KTKEGV repeat motifs are key mediators of normal α-synuclein tetramerization: Their mutation causes excess monomers and neurotoxicity
  od: Dettmer, Ulf, i dr.
  Izdano: (2015)
• In Vivo Cross-linking Reveals Principally Oligomeric Forms of α-Synuclein and β-Synuclein in Neurons and Non-neural Cells
  od: Dettmer, Ulf, i dr.
  Izdano: (2013)
• Purification of α-Synuclein from Human Brain Reveals an Instability of Endogenous Multimers as the Protein Approaches Purity
  od: Luth, Eric S., i dr.
  Izdano: (2014)
• Abrogating native α-synuclein tetramers in mice causes a L-DOPA responsive motor syndrome closely resembling Parkinson’s disease
  od: Nuber, Silke, i dr.
  Izdano: (2018)