Kei Maruyama - Concepedia

Author

Kei Maruyama

Saitama Medical University

Also Known As

K Maruyama, K. MARUYAMA, K. Maruyama, K., Maruyama, KEI MARUYAMA, Kei MARUYAMA, Kei Maruyama, Keiko MARUYAMA

196

Publications

8.4K

Citations

H-Index

117

Concepts

All Affiliations

Saitama Medical University The University of Tokyo National Institute for Physiological Sciences RIKEN Center for Brain Science Tokyo Institute of Psychiatry

About

Kei Maruyama is an author at Saitama Medical University specializing in medicine, molecular biology, and natural sciences.

Top Concepts

#	Concept	H-Index	Publications	Citations
1	Medicine	32	54	4K
2	Natural Sciences	19	22	1.6K
3	Social Sciences	10	10	1.5K
4	Engineering	6	6	419
5	Health Sciences	1	1	26

Kei Maruyama

Publications

8.2K

Citations

H-Index

Page 1

	Year	Citations
Detection of Calcium Binding Proteins by 45Ca Autoradiography on Nitrocellulose Membrane after Sodium Dodecyl Sulfate Gel Electrophoresis1 Kei Maruyama, Takashi Mikawa, Setsuro EBASHl The Journal of Biochemistry	1984	768
Modeling Alzheimer’s Disease with iPSCs Reveals Stress Phenotypes Associated with Intracellular Aβ and Differential Drug Responsiveness Takayuki Kondo, Masashi Asai, Kayoko Tsukita, Cell stem cell Neurodegenerative DiseasesIntracellular AβAlzheimer's DiseaseStressMedicine	2013	741
Cleft palate and decreased brain γ-aminobutyric acid in mice lacking the 67-kDa isoform of glutamic acid decarboxylase Hideo Asada, Yuuki Kawamura, Kei Maruyama, Proceedings of the National Academy of Sciences	1997	550
The presenilin 2 mutation (N141I) linked to familial Alzheimer disease (Volga German families) increases the secretion of amyloid β protein ending at the 42nd (or 43rd) residue Taisuke Tomita, Kei Maruyama, Takaomi C. Saido, Proceedings of the National Academy of Sciences	1997	372
Mice Lacking the 65 kDa Isoform of Glutamic Acid Decarboxylase (GAD65) Maintain Normal Levels of GAD67 and GABA in Their Brains but Are Susceptible to Seizures Hideo Asada, Yuuki Kawamura, Kei Maruyama, Biochemical and Biophysical Research Communications Molecular NeuroscienceNeurophysiologyNeurotransmitterKda IsoformNeurology	1996	320
Neprilysin Degrades Both Amyloid β Peptides 1–40 and 1–42 Most Rapidly and Efficiently among Thiorphan- and Phosphoramidon-sensitive Endopeptidases Keiro Shirotani, Satoshi Tsubuki, Nobuhisa Iwata, Journal of Biological Chemistry	2001	307
Mutation of aspartic acid-351, lysine-352, and lysine-515 alters the Ca2+ transport activity of the Ca2+-ATPase expressed in COS-1 cells. Kei Maruyama, D H MacLennan Proceedings of the National Academy of Sciences Muscle FunctionLysine-515 AltersMolecular BiologyCellular PhysiologyCa2+ Transport Activity	1988	300
Putative function of ADAM9, ADAM10, and ADAM17 as APP -secretase Masashi Asai, Chinatsu Hattori, Beáta Szabó, Biochemical and Biophysical Research Communications BiologyEngineeringGeneticsComputational BiologyMolecular Genetics	2003	294
Membrane-anchored metalloprotease MDC9 has an α-secretase activity responsible for processing the amyloid precursor protein Hisashi Koike, Shigeo Tomioka, Hiroyuki Sorimachi, Biochemical Journal Mdc9-expressing CellsProtein SecretionProtein FunctionProtein AssemblyBiochemistry	1999	263
Berberine alters the processing of Alzheimer’s amyloid precursor protein to decrease Aβ secretion Masashi Asai, Nobuhisa Iwata, Ayumu Yoshikawa, Biochemical and Biophysical Research Communications Neurodegenerative DiseasesMolecular NeuroscienceAlzheimer's DiseaseDegenerative PathologyProtein Misfolding	2006	183

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