Glucocerebrosidase deficiency accelerates the accumulation of proteinase K-resistant &#945;-synuclein and aggravates neurodegeneration in a Drosophila model of Parkinson's disease.

Suzuki, Mari; Fujikake, Nobuhiro; Takeuchi, Toshihide; Kohyama-Koganeya, Ayako; Nakajima, Kazuki; Hirabayashi, Yoshio; Wada, Keiji; Nagai, Yoshitaka

Glucocerebrosidase deficiency accelerates the accumulation of proteinase K-resistant α-synuclein and aggravates neurodegeneration in a Drosophila model of Parkinson's disease.

Suzuki, Mari; Fujikake, Nobuhiro; Takeuchi, Toshihide; Kohyama-Koganeya, Ayako; Nakajima, Kazuki; Hirabayashi, Yoshio; Wada, Keiji; Nagai, Yoshitaka.

Afiliação

Suzuki M; Department of Degenerative Neurological Diseases, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Kodaira, Tokyo 187-8502, Japan and.
Fujikake N; Department of Degenerative Neurological Diseases, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Kodaira, Tokyo 187-8502, Japan and.
Takeuchi T; Department of Degenerative Neurological Diseases, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Kodaira, Tokyo 187-8502, Japan and.
Kohyama-Koganeya A; Laboratory for Molecular Membrane Neuroscience, RIKEN Brain Science Institute, Wako, Saitama 351-0198, Japan.
Nakajima K; Laboratory for Molecular Membrane Neuroscience, RIKEN Brain Science Institute, Wako, Saitama 351-0198, Japan.
Hirabayashi Y; Laboratory for Molecular Membrane Neuroscience, RIKEN Brain Science Institute, Wako, Saitama 351-0198, Japan.
Wada K; Department of Degenerative Neurological Diseases, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Kodaira, Tokyo 187-8502, Japan and.
Nagai Y; Department of Degenerative Neurological Diseases, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Kodaira, Tokyo 187-8502, Japan and nagai@ncnp.go.jp.

Hum Mol Genet ; 24(23): 6675-86, 2015 Dec 01.

Article em En | MEDLINE | ID: mdl-26362253

Assuntos

Glucosilceramidase/genética; Transtornos Parkinsonianos/etiologia; alfa-Sinucleína/metabolismo; Animais; Modelos Animais de Doenças; Proteínas de Drosophila/genética; Drosophila melanogaster/metabolismo; Endopeptidase K/metabolismo; Técnicas de Silenciamento de Genes; Glucosilceramidase/deficiência; Glucosilceramidase/metabolismo; Glucosilceramidas/metabolismo; Humanos; Masculino; Transtornos Parkinsonianos/metabolismo; Transtornos Parkinsonianos/fisiopatologia; Agregação Patológica de Proteínas; Dobramento de Proteína; beta-Galactosidase/genética; beta-Galactosidase/metabolismo

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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Transtornos Parkinsonianos / Alfa-Sinucleína / Glucosilceramidase Tipo de estudo: Clinical_trials / Prognostic_studies / Risk_factors_studies Limite: Animals / Humans / Male Idioma: En Revista: Hum Mol Genet Ano de publicação: 2015 Tipo de documento: Article

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