Formation of advanced glycation end-product-modified superoxide dismutase-1 (SOD1) is one of the mechanisms responsible for inclusions common to familial amyotrophic lateral sclerosis patients with SOD1 gene mutation, and transgenic mice expressing human SOD1 gene mutation.
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K. Nakashima | S. Sakoda | Masako Kato | S. Horiuchi | I. Nakano | D. Cleveland | E. Ohama | R. Nagai | A. Hirano | S. Kato | M. Kato | K. Asayama | Jian Liu | M. Takikawa | J. Liu | K. Nakashima