Mizuki Yamada
Affiliations: | Laboratory for Structural Neuropathology | RIKEN Brain Science Institute, Wakō-shi, Saitama-ken, Japan |
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"Mizuki Yamada"Mean distance: 106866 (cluster 31) | S | N | B | C | P |
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Publications
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Kino Y, Washizu C, Kurosawa M, et al. (2016) FUS/TLS acts as an aggregation-dependent modifier of polyglutamine disease model mice. Scientific Reports. 6: 35236 |
Kino Y, Washizu C, Kurosawa M, et al. (2015) FUS/TLS deficiency causes behavioral and pathological abnormalities distinct from amyotrophic lateral sclerosis. Acta Neuropathologica Communications. 3: 24 |
Kino Y, Washizu C, Aquilanti E, et al. (2011) Intracellular localization and splicing regulation of FUS/TLS are variably affected by amyotrophic lateral sclerosis-linked mutations. Nucleic Acids Research. 39: 2781-98 |
Bauer PO, Goswami A, Wong HK, et al. (2010) Harnessing chaperone-mediated autophagy for the selective degradation of mutant huntingtin protein. Nature Biotechnology. 28: 256-63 |
Yamanaka T, Tosaki A, Miyazaki H, et al. (2010) Mutant huntingtin fragment selectively suppresses Brn-2 POU domain transcription factor to mediate hypothalamic cell dysfunction. Human Molecular Genetics. 19: 2099-112 |
Miyazaki H, Oyama F, Kurosawa M, et al. (2009) Correlation between nuclear accumulation and dysregulation of sodium channel β4 subunit in HD transgenic mice Neuroscience Research. 65: S247 |
Wong HK, Bauer PO, Kurosawa M, et al. (2008) Blocking acid-sensing ion channel 1 alleviates Huntington's disease pathology via an ubiquitin-proteasome system-dependent mechanism. Human Molecular Genetics. 17: 3223-35 |
Nucifora FC, Sasaki M, Peters MF, et al. (2001) Interference by huntingtin and atrophin-1 with cbp-mediated transcription leading to cellular toxicity. Science (New York, N.Y.). 291: 2423-8 |