| 摘要 |
Disclosed is a mutant human alpha-synuclein with decreased ability of forming aggregation. The mutant human alpha-synuclein of the invention is able to inhibit aggregation of the wild type human alpha-synuclein, Ala53Thr mutant human alpha-synuclein or Ala50Pro mutant human alpha-synuclein, thus is useful for investigation of pathology and treatment of Parkinson's disease and for research and development of gene therapy. Also disclosed is a partial structure peptide of human alpha-synuclein comprising amino acid substitutions as taught by the invention.
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