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J-GLOBAL ID:200902192896304044   Reference number:01A0535685

Formation of advanced glycation end-product-modified superoxide dismutase-1(SOD1) is one of the mechanisms responsible for inclusions common to familial amyotrophic lateral sclerosis patients with SOD1 gene mutation, and transgenic mice expressing human SOD1 gene mutation.

高度にグリコシル化を受けた終末産物で修飾されたスーパーオキシドジスムターゼ-1(SOD1)の形成が,SOD1遺伝子変異を伴う家族性筋萎縮性側索硬化症患者およびヒトSOD1変異遺伝子を発現するトランスジェニックマウスに共通した封入体の形成機序の一要因である
Author (9):
Material:
Volume: 21  Issue:Page: 67-81  Publication year: Mar. 2001 
JST Material Number: W0751A  ISSN: 0919-6544  Document type: Article
Article type: 解説  Country of issue: Australia (AUS)  Language: ENGLISH (EN)
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Neurologic diagnosis  ,  Basic neurology 
Reference (38):
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  • KATO, S. Recent advances in research on neuropathological aspects of familial amyotrophic lateral sclerosis with superoxide dismutase 1 gene mutations: Neuronal Lewy body-like hyaline inclusions and astrocytic hyaline inclusions. Histol Histopathol. 1999, 14, 973-989
  • KATO, S. New consensus research on neuropathological aspects of familial amyotrophic lateral sclerosis with superoxide dismutase 1 (SOD1) gene mutations: Inclusions containing SOD1 in neurons and astrocytes. ALS Other Motor Neuron Disorders. 2000, 1, 163-184
  • ENGEL, WK. An inherited disease similar to amyotrophic lateral sclerosis with a pattern of posterior column involvement: An intermediate form?. Brain. 1959, 82, 203-220
  • CHARCOT, JM. Deux cas d'atrophie musculaire progressive avec lesions de la substance grise et des faisceaux antero-lateraux de la moelle epiniere. Arch Physiol (Paris). 1869, 2, 744-760
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