Haruko Miyazaki, Ph.D.

Affiliations: 
Laboratory for Structural Neuropathology RIKEN Brain Science Institute, Wakō-shi, Saitama-ken, Japan 
Area:
polyglutamine disorders
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"Haruko Miyazaki"
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Publications

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Miyazaki H, Yamanaka T, Oyama F, et al. (2020) FACS array-based cell purification yields a specific transcriptome of striatal medium spiny neurons in a murine Huntington disease model. The Journal of Biological Chemistry
Yoshinaga S, Yamanaka T, Miyazaki H, et al. (2019) Preserved proteinase K-resistant core after amplification of alpha-synuclein aggregates: Implication to disease-related structural study. Biochemical and Biophysical Research Communications
Park H, Miyazaki H, Yamanaka T, et al. (2018) Non-coding RNA Neat1 and Abhd11os expressions are dysregulated in medium spiny neurons of Huntington disease model mice. Neuroscience Research
Okuzumi A, Kurosawa M, Hatano T, et al. (2018) Rapid dissemination of alpha-synuclein seeds through neural circuits in an in-vivo prion-like seeding experiment. Acta Neuropathologica Communications. 6: 96
Shimizu H, Tosaki A, Ohsawa N, et al. (2017) Parallel homodimer structures of the extracellular domains of the voltage-gated sodium channel β4 subunit explain its role in cell-cell adhesion. The Journal of Biological Chemistry
Ohno M, Kimura M, Miyazaki H, et al. (2016) Acidic mammalian chitinase is a proteases-resistant glycosidase in mouse digestive system. Scientific Reports. 6: 37756
Yamanaka T, Tosaki A, Miyazaki H, et al. (2016) Differential roles of NF-Y transcription factor in ER chaperone expression and neuronal maintenance in the CNS. Scientific Reports. 6: 34575
Shimizu H, Miyazaki H, Ohsawa N, et al. (2016) Structure-based site-directed photo-crosslinking analyses of multimeric cell-adhesive interactions of voltage-gated sodium channel β subunits. Scientific Reports. 6: 26618
Bosch MK, Nerbonne JM, Townsend RR, et al. (2016) Proteomic Analysis of Native Cerebellar iFGF14 Complexes. Channels (Austin, Tex.). 0
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
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