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Titolo:
The channel hypothesis of Huntington's disease
Autore:
Kagan, BL; Hirakura, Y; Azimov, R; Azimova, R;
Indirizzi:
Univ Calif Los Angeles, Sch Med, Inst Neuropsychiat, Dept Psychiat, Los Angeles, CA 90024 USA Univ Calif Los Angeles Los Angeles CA USA 90024 Los Angeles, CA 90024 USA Univ Calif Los Angeles, Sch Med, Brain Res Inst, Los Angeles, CA 90024 USAUniv Calif Los Angeles Los Angeles CA USA 90024 Los Angeles, CA 90024 USA Waseda Univ, Adv Res Ctr Human Sci, Dept Mol Neurobiol, Waseda, Japan Waseda Univ Waseda Japan r Human Sci, Dept Mol Neurobiol, Waseda, Japan Uzbek Acad Sci, Inst Physiol & Biophys, Tashkent 700135, Uzbekistan Uzbek Acad Sci Tashkent Uzbekistan 700135 s, Tashkent 700135, Uzbekistan
Titolo Testata:
BRAIN RESEARCH BULLETIN
fascicolo: 3-4, volume: 56, anno: 2001,
pagine: 281 - 284
SICI:
0361-9230(200110/11)56:3-4<281:TCHOHD>2.0.ZU;2-B
Fonte:
ISI
Lingua:
ENG
Soggetto:
AMYLOID-BETA-PROTEIN; NEURONAL INTRANUCLEAR INCLUSIONS; CATION-SELECTIVE CHANNELS; BILAYER-MEMBRANES; CALCIUM CHANNELS; ION CHANNELS; FRAGMENT; REPEAT; NEURODEGENERATION; ACTIVATION;
Keywords:
Huntingtin; membranes; amyloid; bilayers; apoptosis; triplet repeat diseases;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
35
Recensione:
Indirizzi per estratti:
Indirizzo: Kagan, BL Univ Calif Los Angeles, Sch Med, Inst Neuropsychiat, Dept Psychiat, 760 Westwood Plaza, Los Angeles, CA 90024 USA Univ Calif Los Angeles 760 Westwood Plaza Los Angeles CA USA 90024
Citazione:
B.L. Kagan et al., "The channel hypothesis of Huntington's disease", BRAIN RES B, 56(3-4), 2001, pp. 281-284

Abstract

Extended tracts of polyglutamine (PG) have been implicated in the pathogenicity of the mutant protein huntingtin and have been shown to form ion channels in planar lipid bilayers. These lines of evidence suggest that huntingtin and other PG mutant proteins may damage cells via a channel mechanism. This mechanism could cause damage to the plasma membrane by running down ionic gradients, discharging membrane potential; or allowing influx of toxic ions such as Ca2+. PG damage to intracellular membranes such as the lysosomal membrane or the mitochondrial membrane could also injure cells via leakage of toxic enzymes or triggering of apoptosis. The channel mechanism is well-established for microbial toxins, and the existence of at least six other "amyloid" channels relevant to diseases such as Alzheimer's and Creutzfeld-Jakob, suggests that this may be a widespread pathogenic mechanism. (C) 2001 Elsevier Science Inc.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 04/04/20 alle ore 12:08:14