Zobrazeno 1 - 10
of 44
pro vyhledávání: '"Shuji, Matsuda"'
Autor:
Chenguang Li, Takao Senda, Kazuyoshi Sakai, Takanori Onouchi, Shuji Matsuda, Masaya Hirayama, Nami Yamada
Publikováno v:
Medical Molecular Morphology. 54:31-40
In the present study, we examined morphology and function of hippocampus in the APC1638T/1638T mouse. Expression levels of the APC mRNA and protein were both identical in the hippocampus of the APC+/+ and APC1638T/1638T mice. The dentate gyrus of the
Publikováno v:
Medical Molecular Morphology. 51:227-236
Adenomatous polyposis coli (APC) is a large protein with multiple binding partners, suggesting diverse functions besides its well-known role in the destruction of β-catenin. To elucidate these complex functions, it is crucial to evaluate the precise
Autor:
Shuji Matsuda, Takao Senda
Publikováno v:
Medical Molecular Morphology. 52:1-7
There are several theories regarding the etiologies of Alzheimer disease (AD). Considering that all genes responsible for familial AD are amyloid protein precursor (APP) or APP metabolizing enzymes, surely aberrant APP metabolism is crucial to pathog
Publikováno v:
PLoS ONE, Vol 4, Iss 11, p e7900 (2009)
BACKGROUND:Mutations in the integral membrane protein 2B, also known as BRI(2), a type II trans-membrane domain protein cause two autosomal dominant neurodegenerative diseases, Familial British and Danish Dementia. In these conditions, accumulation o
Externí odkaz:
https://doaj.org/article/857c122cc54d40c9abdce199daf87ba5
Publikováno v:
Medical Molecular Morphology. 50:94-102
The adenomatous polyposis coli (APC) is a multifunctional protein as well as a tumor suppressor. To determine the functions of the C-terminal domain of APC, we explored APC 1638T/1638T (APC1638T) mice that express a truncated APC lacking the C-termin
Autor:
Satoru, Enomoto, Shuji, Matsuda
Publikováno v:
国際学研究. 1:21-38
Autor:
Monica Vitale, Luciano D'Adamio, Shuji Matsuda, Andrea Scaloni, Giovanni Renzone, Nicola Zambrano
Publikováno v:
Journal of Biomedicine and Biotechnology
2012:728178 (2012). doi:10.1155/2012/728178
info:cnr-pdr/source/autori:Vitale M, Renzone G, Matsuda S, Scaloni A, D'Adamio L, Zambrano N./titolo:Proteomic characterization of a mouse model of familial Danish dementia./doi:10.1155%2F2012%2F728178/rivista:Journal of Biomedicine and Biotechnology (Print)/anno:2012/pagina_da:/pagina_a:/intervallo_pagine:/volume:2012:728178
Journal of Biomedicine and Biotechnology, Vol 2012 (2012)
2012:728178 (2012). doi:10.1155/2012/728178
info:cnr-pdr/source/autori:Vitale M, Renzone G, Matsuda S, Scaloni A, D'Adamio L, Zambrano N./titolo:Proteomic characterization of a mouse model of familial Danish dementia./doi:10.1155%2F2012%2F728178/rivista:Journal of Biomedicine and Biotechnology (Print)/anno:2012/pagina_da:/pagina_a:/intervallo_pagine:/volume:2012:728178
Journal of Biomedicine and Biotechnology, Vol 2012 (2012)
A dominant mutation in theITM2B/BRI2gene causes familial Danish dementia (FDD) in humans. To model FDD in animal systems, a knock-in approach was recently implemented in mice expressing a wild-type and mutant allele, which bears the FDD-associated mu
Publikováno v:
Journal of Alzheimer's Disease. 27:385-391
An autosomal dominant mutation in the BRI2/ITM2B gene causes Familial Danish Dementia (FDD). We have generated a mouse model of FDD, called FDDKI, genetically congruous to the human disease. These mice carry one mutant and one wild type Bri2/Itm2b al
Publikováno v:
The EMBO Journal. 30:2501-2509
An autosomal dominant mutation in the BRI2/ITM2B gene causes familial Danish dementia (FDD). Analysis of FDDKI mice, a mouse model of FDD genetically congruous to the human disease since they carry one mutant and one wild-type Bri2/Itm2b allele, has
Publikováno v:
Proceedings of the National Academy of Sciences. 107:20822-20827
According to the prevailing “amyloid cascade hypothesis,” genetic dementias such as Alzheimer’s disease and familial Danish dementia (FDD) are caused by amyloid deposits that trigger tauopathy, neurodegeneration, and behavioral/cognitive altera