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Gene transfer demonstrates that muscle is not a primary target for non-cell-autonomous toxicity in familial amyotrophic lateral sclerosis.
Miller TM, Kim SH, Yamanaka K, Hester M, Umapathi P, Arnson H, Rizo L, Mendell JR, Gage FH, Cleveland DW, Kaspar BK. Miller TM, et al. Among authors: cleveland dw. Proc Natl Acad Sci U S A. 2006 Dec 19;103(51):19546-51. doi: 10.1073/pnas.0609411103. Epub 2006 Dec 12. Proc Natl Acad Sci U S A. 2006. PMID: 17164329 Free PMC article.
Elevated free nitrotyrosine levels, but not protein-bound nitrotyrosine or hydroxyl radicals, throughout amyotrophic lateral sclerosis (ALS)-like disease implicate tyrosine nitration as an aberrant in vivo property of one familial ALS-linked superoxide dismutase 1 mutant.
Bruijn LI, Beal MF, Becher MW, Schulz JB, Wong PC, Price DL, Cleveland DW. Bruijn LI, et al. Among authors: cleveland dw. Proc Natl Acad Sci U S A. 1997 Jul 8;94(14):7606-11. doi: 10.1073/pnas.94.14.7606. Proc Natl Acad Sci U S A. 1997. PMID: 9207139 Free PMC article.
Absence of neurofilaments reduces the selective vulnerability of motor neurons and slows disease caused by a familial amyotrophic lateral sclerosis-linked superoxide dismutase 1 mutant.
Williamson TL, Bruijn LI, Zhu Q, Anderson KL, Anderson SD, Julien JP, Cleveland DW. Williamson TL, et al. Among authors: cleveland dw. Proc Natl Acad Sci U S A. 1998 Aug 4;95(16):9631-6. doi: 10.1073/pnas.95.16.9631. Proc Natl Acad Sci U S A. 1998. PMID: 9689132 Free PMC article.
425 results