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4. The neuronal Golgi apparatus is fragmented in transgenic mice expressing a mutant human SOD1, but not in mice expressing the human NF-H gene. Stieber A, Gonatas JO, Collard J, Meier J, Julien J, Schweitzer P, Gonatas NK. J Neurol Sci; 2000 Feb 01; 173(1):63-72. PubMed ID: 10675581 [Abstract] [Full Text] [Related]
5. Interaction between familial amyotrophic lateral sclerosis (ALS)-linked SOD1 mutants and the dynein complex. Zhang F, Ström AL, Fukada K, Lee S, Hayward LJ, Zhu H. J Biol Chem; 2007 Jun 01; 282(22):16691-9. PubMed ID: 17403682 [Abstract] [Full Text] [Related]
6. Human Cu/Zn superoxide dismutase (SOD1) overexpression in mice causes mitochondrial vacuolization, axonal degeneration, and premature motoneuron death and accelerates motoneuron disease in mice expressing a familial amyotrophic lateral sclerosis mutant SOD1. Jaarsma D, Haasdijk ED, Grashorn JA, Hawkins R, van Duijn W, Verspaget HW, London J, Holstege JC. Neurobiol Dis; 2000 Dec 01; 7(6 Pt B):623-43. PubMed ID: 11114261 [Abstract] [Full Text] [Related]
8. Slowing of axonal transport is a very early event in the toxicity of ALS-linked SOD1 mutants to motor neurons. Williamson TL, Cleveland DW. Nat Neurosci; 1999 Jan 01; 2(1):50-6. PubMed ID: 10195180 [Abstract] [Full Text] [Related]