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Johansson G, Mahller YY, Collins MH, Kim MO, Nobukuni T, Perentesis J, et al

Korkut, A, Kanchi, RS, Li, X, Lorenzi, PL, Kwong, L, Roszik, J, Ling, S, Uppore Kukkillaya, AR, Liu, Y, Ju, Z, Hansel, DE, Li, S, Ajani, JA, Mani, S, Chen, J, Ma, W, Zhang, J, Broom, BM, Li, J, Liang, H, Liu, W, Lu, Y, Mills, GB, Weinstein, JN, Liu, X, Wang, L , Carvalho, AL, Fregnani, JG, Reis, RV, Scapulatempo, CN, Behrens, MC, Bondaruk, J, Broaddus, R, Czerniak, BA, Esmaeli, B, Fujimoto, J, Gershenwald, JE, Guo, CC, Lazar, A, Logothetis, CJ, Meric-Bernstam, F, Moran, C, Ramondetta, LM, Rice, DC, Sood, AK, Tamboli, P, Thompson, T, Troncoso, P, Tsao, A, Wistuba, II, von Deimling, A, Mishra, L, Akbani, R

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Furthermore, disease-related phenotypes were not observed in transgenic mice expressing human SOD1 that has multiple mutations including those at copper and zinc binding sites (H46R/H48Q/H63G/H71R/H80R/H120G) and two free Cys residues (C6G/C111S) with an ALS-linked mutation, H43R, and co-expression of wild-type human SOD1 did not cause the disease [35]