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Titolo:
Immunosuppressant FK506 does not exert beneficial effects in symptomatic G93A superoxide dismutase-1 transgenic mice
Autore:
Anneser, JMH; Gmerek, A; Gerkrath, J; Borasio, GD; Heumann, R;
Indirizzi:
Univ Munich, Klinikum Grosshadern, Dept Neurol, D-81366 Munich, Germany Univ Munich Munich Germany D-81366 Dept Neurol, D-81366 Munich, Germany Ruhr Univ Bochum, Dept Mol Neurobiochem, D-4630 Bochum, Germany Ruhr Univ Bochum Bochum Germany D-4630 robiochem, D-4630 Bochum, Germany
Titolo Testata:
NEUROREPORT
fascicolo: 12, volume: 12, anno: 2001,
pagine: 2663 - 2665
SICI:
0959-4965(20010828)12:12<2663:IFDNEB>2.0.ZU;2-1
Fonte:
ISI
Lingua:
ENG
Soggetto:
AMYOTROPHIC-LATERAL-SCLEROSIS; NERVE REGENERATION; CALCINEURIN; GLUTAMATE; BRAIN; DEPHOSPHORYLATION; APOPTOSIS; PROTECTS; RELEASE; FK-506;
Keywords:
calcineurin; familial amyotrophic lateral sclerosis; SODI; tacrolimus;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
19
Recensione:
Indirizzi per estratti:
Indirizzo: Borasio, GD Univ Munich, Klinikum Grosshadern, Dept Neurol, D-81366 Munich, Germany Univ Munich Munich Germany D-81366 , D-81366 Munich, Germany
Citazione:
J.M.H. Anneser et al., "Immunosuppressant FK506 does not exert beneficial effects in symptomatic G93A superoxide dismutase-1 transgenic mice", NEUROREPORT, 12(12), 2001, pp. 2663-2665

Abstract

The immunosuppressant drug FK506 has been shown to exert neuroprotective effects in various model systems via inhibition of the protein phosphatase calcineurin (CN). The enzyme Cu/ Zn-superoxide dismutase (SOD1), which is mutated in a familial form of amyotrophic lateral sclerosis (ALS), is an endogenous regulator of CN. Altered function of CN may therefore be involved inthe pathogenesis of ALS. We tested FK506 in a transgenic mouse model expressing mutated SOD1 for potential beneficial effects. This treatment, initiated after onset of symptoms, did not cause a reduction in the decline of motor function nor did it prolong survival. These results argue against a crucial role of CN in the process leading to motoneuronal degeneration in SOD1-mutated mice. NeuroReport 12:2663-2665 (C) 2001 Lippincott Williams & Wilkins.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 29/11/20 alle ore 10:25:57