Wild-type nonneuronal cells extend survival of SOD1 mutant motor neurons in ALS mice

Science

Volumn 302, Issue 5642, 2003, Pages 113-117

  Clement, A M ^a,b,c,h   Nguyen, M D ^d,i   Roberts, E A ^a,b   Garcia, M L ^a,b,c   Boillee S ^a,b,c   Rule, M ^e   McMahon, A P ^e   Doucette, W ^f   Siwek, D ^g   Ferrante, R J ^g   Brown Jr , R H ^f   Julien, J P ^d,j   Goldstein, L S B ^a,b   Cleveland, D W ^a,b,c  

^a UNIVERSITY OF CALIFORNIA   (United States)

^b UNIVERSITY OF CALIFORNIA   (United States)

^c UNIVERSITY OF CALIFORNIA   (United States)

^d MONTREAL GENERAL HOSPITAL   (Canada)

^e HARVARD UNIVERSITY   (United States)

^f MASSACHUSETTS GENERAL HOSPITAL   (United States)

^g BOSTON UNIVERSITY SCHOOL OF MEDICINE   (United States)

^h JOHANNES GUTENBERG UNIVERSITY   (Germany)

ⁱ HARVARD MEDICAL SCHOOL   (United States)

^j UNIVERSITÉ LAVAL   (Canada)

more..

Author keywords

[No Author keywords available]

Indexed keywords

COPPER; MUTAGENESIS; NEUROLOGY; TOXICITY; ZINC;

MOTOR NEURONS;

CELLS;

COPPER ZINC SUPEROXIDE DISMUTASE;

MUTATION; NEUROLOGY; TOXICITY;

AMYOTROPHIC LATERAL SCLEROSIS; ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ARTICLE; CELL SURVIVAL; CHIMERA; CONTROLLED STUDY; MOTONEURON; MOUSE; NERVE CELL; NERVE DEGENERATION; NEUROPATHOLOGY; NEUROTOXICITY; NONHUMAN; PRIORITY JOURNAL; PROTEIN EXPRESSION; WILD TYPE;

AMYOTROPHIC LATERAL SCLEROSIS; ANIMALS; AXONS; CELL SURVIVAL; CHIMERA; HUMANS; MICE; MICE, INBRED C57BL; MICE, INBRED STRAINS; MICE, TRANSGENIC; MOTOR NEURONS; MUTATION; NERVE DEGENERATION; NEUROFILAMENT PROTEINS; SPINAL CORD; SUPEROXIDE DISMUTASE; SURVIVAL RATE; UBIQUITIN;

ANIMALIA;

EID: 0141642203     PISSN: 00368075     EISSN: None     Source Type: Journal    
DOI: 10.1126/science.1086071     Document Type: Article

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36. We gratefully acknowledge A.-K. Hadjantonakis (Columbia University, New York, NY) and A. Nagy (Mount Sinai Hospital, Toronto) for providing the E-YFP-ES cells; P. Hince and D, Houle for their technical help; and J. Folmer (Johns Hopkins, Baltimore, MD). This work was supported by the grants from the NIH (NS 27036 to D.W.C, HD 30249 to A.P.M., AG 13846 to R.J.F., AG 12992 to R.H.B. and R.J.F, and NS 31248 and NS 37912 to R.H.B.); the Center for ALS Research at Johns Hopkins (to D.W.C and L.S.B.G.); the ALS Association (to A.P.M. and R.H.B.); the Canadian Institutes of Health Research (CIHR) (to J.-P.J.); the Angel Fund for ALS Research; and Project ALS (to R.H.B.); and the Veterans Administration (R.J.F.). A.M.C. was supported in part by a fellowship from the German Research Council (DFG, Cl-175). M.D.N. is a recipient of a K. M. Hunter/CIHR Scholarship. M.L.G. is the recipient of a postdoctorat fellowship from the NIH. S.B. is a recipient of a Fondation pour la Recherche Medicate fellowship. J.-P.J. is a recipient of a CIHR Senior Investigator Award. D.W.C. receives salary support from the Ludwig Institute for Cancer Research. L.S.B.G. is an Investigator of the Howard Hughes Medical Institute.