Kenichi Otani

1.0k total citations
9 papers, 846 citations indexed

About

Kenichi Otani is a scholar working on Molecular Biology, Cell Biology and Surgery. According to data from OpenAlex, Kenichi Otani has authored 9 papers receiving a total of 846 indexed citations (citations by other indexed papers that have themselves been cited), including 7 papers in Molecular Biology, 5 papers in Cell Biology and 3 papers in Surgery. Recurrent topics in Kenichi Otani's work include Calpain Protease Function and Regulation (5 papers), Metabolism, Diabetes, and Cancer (5 papers) and Pancreatic function and diabetes (3 papers). Kenichi Otani is often cited by papers focused on Calpain Protease Function and Regulation (5 papers), Metabolism, Diabetes, and Cancer (5 papers) and Pancreatic function and diabetes (3 papers). Kenichi Otani collaborates with scholars based in United States, Japan and Canada. Kenichi Otani's co-authors include Kenneth S. Polonsky, James D. Johnson, Zhiqiang Han, Mitsuru Ohsugi, M. Alan Permutt, Szabolcs Fátrai, Ernesto Bernal‐Mizrachi, Graeme I. Bell, Yukio Horikawa and Aaron C. Baldwin and has published in prestigious journals such as Journal of Biological Chemistry, Journal of Clinical Investigation and Diabetes.

In The Last Decade

Kenichi Otani

9 papers receiving 828 citations

Peers

Kenichi Otani

MB

SURGE

CB

EDM

GENET

Yurika Nishiki United States

Françoise Van Eylen Belgium

Jean Lainé Canada

Salman Azhar United States

Scot R. Kimball United States

R Kiekens Belgium

T. Shirotani Japan

Peixiang Zhang United States

Yin He United States

Denise L. Roush United States

Yurika Nishiki United States

Kenichi Otani

212 ×0.4

MB

359 ×0.7

SURGE

178 ×0.6

CB

133 ×0.7

EDM

224 ×1.3

GENET

Citations per year, relative to Kenichi Otani Kenichi Otani (= 1×) peers Yurika Nishiki

Countries citing papers authored by Kenichi Otani

Since Specialization

Citations

This map shows the geographic impact of Kenichi Otani's research. It shows the number of citations coming from papers published by authors working in each country. You can also color the map by specialization and compare the number of citations received by Kenichi Otani with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Kenichi Otani more than expected).

Fields of papers citing papers by Kenichi Otani

Since Specialization

Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by Kenichi Otani. Nodes represent research fields, and links connect fields that are likely to share authors. Colored nodes show fields that tend to cite the papers produced by Kenichi Otani. The network helps show where Kenichi Otani may publish in the future.

Co-authorship network of co-authors of Kenichi Otani

This figure shows the co-authorship network connecting the top 25 collaborators of Kenichi Otani. A scholar is included among the top collaborators of Kenichi Otani based on the total number of citations received by their joint publications. Widths of edges represent the number of papers authors have co-authored together. Node borders signify the number of papers an author published with Kenichi Otani. Kenichi Otani is excluded from the visualization to improve readability, since they are connected to all nodes in the network.

All Works

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9 of 9 papers shown

1.

Johnson, James D., Kenichi Otani, Graeme I. Bell, & Kenneth S. Polonsky. (2009). Impaired insulin secretion in transgenic mice over-expressing calpastatin in pancreatic β-cells. Islets. 1(3). 242–248. 5 indexed citations

2.

Otani, Kenichi, Kenneth S. Polonsky, John O. Holloszy, & Dong‐Ho Han. (2006). Inhibition of calpain results in impaired contraction-stimulated GLUT4 translocation in skeletal muscle. American Journal of Physiology-Endocrinology and Metabolism. 291(3). E544–E548. 10 indexed citations

3.

García-Rovés, Pablo M., Terry E. Jones, Kenichi Otani, Dong‐Ho Han, & John O. Holloszy. (2005). Calcineurin Does Not Mediate Exercise-Induced Increase in Muscle GLUT4. Diabetes. 54(3). 624–628. 25 indexed citations

4.

Johnson, James D., Zhiqiang Han, Kenichi Otani, et al.. (2004). RyR2 and Calpain-10 Delineate a Novel Apoptosis Pathway in Pancreatic Islets. Journal of Biological Chemistry. 279(23). 24794–24802. 112 indexed citations

5.

Bernal‐Mizrachi, Ernesto, Szabolcs Fátrai, James D. Johnson, et al.. (2004). Defective insulin secretion and increased susceptibility to experimental diabetes are induced by reduced Akt activity in pancreatic islet β cells. Journal of Clinical Investigation. 114(7). 928–936. 185 indexed citations

6.

Otani, Kenichi, Rohit Kulkarni, Aaron C. Baldwin, et al.. (2004). Reduced β-cell mass and altered glucose sensing impair insulin-secretory function in βIRKO mice. American Journal of Physiology-Endocrinology and Metabolism. 286(1). E41–E49. 149 indexed citations

7.

Otani, Kenichi, Dong‐Ho Han, Eric L. Ford, et al.. (2004). Calpain System Regulates Muscle Mass and Glucose Transporter GLUT4 Turnover. Journal of Biological Chemistry. 279(20). 20915–20920. 52 indexed citations

8.

Bernal‐Mizrachi, Ernesto, Szabolcs Fátrai, James D. Johnson, et al.. (2004). Defective insulin secretion and increased susceptibility to experimental diabetes are induced by reduced Akt activity in pancreatic islet β cells. Journal of Clinical Investigation. 114(7). 928–936. 170 indexed citations

9.

Sreenan, Séamus, Kenichi Otani, Polly A. Hansen, et al.. (2001). Calpains Play a Role in Insulin Secretion and Action. Diabetes. 50(9). 2013–2020. 138 indexed citations

Rankless uses publication and citation data sourced from OpenAlex, an open and comprehensive bibliographic database. While OpenAlex provides broad and valuable coverage of the global research landscape, it—like all bibliographic datasets—has inherent limitations. These include incomplete records, variations in author disambiguation, differences in journal indexing, and delays in data updates. As a result, some metrics and network relationships displayed in Rankless may not fully capture the entirety of a scholar's output or impact.

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