Ken‐Ichi Takemaru

7.8k total citations
58 papers, 3.3k citations indexed

About

Ken‐Ichi Takemaru is a scholar working on Molecular Biology, Genetics and Cell Biology. According to data from OpenAlex, Ken‐Ichi Takemaru has authored 58 papers receiving a total of 3.3k indexed citations (citations by other indexed papers that have themselves been cited), including 42 papers in Molecular Biology, 24 papers in Genetics and 14 papers in Cell Biology. Recurrent topics in Ken‐Ichi Takemaru's work include Genetic and Kidney Cyst Diseases (19 papers), Wnt/β-catenin signaling in development and cancer (18 papers) and Cancer-related gene regulation (16 papers). Ken‐Ichi Takemaru is often cited by papers focused on Genetic and Kidney Cyst Diseases (19 papers), Wnt/β-catenin signaling in development and cancer (18 papers) and Cancer-related gene regulation (16 papers). Ken‐Ichi Takemaru collaborates with scholars based in United States, Japan and France. Ken‐Ichi Takemaru's co-authors include Randall T. Moon, Feng‐Qian Li, Hitoshi Ueda, Susumu Hirose, Feng-Qian Li, Joel M. Levine, Richard W. Carthew, Shinji Yamaguchi, Young Sik Lee and Yang Zhang and has published in prestigious journals such as Nature, Proceedings of the National Academy of Sciences and Journal of Biological Chemistry.

In The Last Decade

Ken‐Ichi Takemaru

55 papers receiving 3.2k citations

Peers

Ken‐Ichi Takemaru
John J. Schwarz United States
Miguel Manzanares Spain
Ritsuko Takada Japan
Ralph A.W. Rupp Germany
Yoshiko Takahashi Japan
Joan Galcerán Spain
Stéphane D. Vincent France
Lauro Sumoy Spain
Tadahiro Iimura Japan
Luc Leyns Belgium
John J. Schwarz United States
Ken‐Ichi Takemaru
Citations per year, relative to Ken‐Ichi Takemaru Ken‐Ichi Takemaru (= 1×) peers John J. Schwarz

Countries citing papers authored by Ken‐Ichi Takemaru

Since Specialization
Citations

This map shows the geographic impact of Ken‐Ichi Takemaru'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 Ken‐Ichi Takemaru with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Ken‐Ichi Takemaru more than expected).

Fields of papers citing papers by Ken‐Ichi Takemaru

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by Ken‐Ichi Takemaru. 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 Ken‐Ichi Takemaru. The network helps show where Ken‐Ichi Takemaru may publish in the future.

Co-authorship network of co-authors of Ken‐Ichi Takemaru

This figure shows the co-authorship network connecting the top 25 collaborators of Ken‐Ichi Takemaru. A scholar is included among the top collaborators of Ken‐Ichi Takemaru 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 Ken‐Ichi Takemaru. Ken‐Ichi Takemaru is excluded from the visualization to improve readability, since they are connected to all nodes in the network.

All Works

20 of 20 papers shown
1.
Takemaru, Ken‐Ichi, et al.. (2024). ciBAR1 loss in mice causes laterality defects, pancreatic degeneration, and altered glucose tolerance. Life Science Alliance. 8(2). e202402916–e202402916.
2.
Yamaguchi, Hiroyuki, Megumi Kitami, Margaret Li, et al.. (2024). Disruption of distal appendage protein CEP164 causes skeletal malformation in mice. Biochemical and Biophysical Research Communications. 741. 151063–151063.
3.
Hall, Jason C., Jennifer M. Bailey, Gregory J. Pazour, et al.. (2021). Loss of the ciliary protein Chibby1 in mice leads to exocrine pancreatic degeneration and pancreatitis. Scientific Reports. 11(1). 17220–17220. 6 indexed citations
4.
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6.
McClain, Steve A., Jonathan Li, David Pei‐Cheng Lin, et al.. (2017). Enhanced Mortality to Metastatic Bladder Cancer Cell Line MB49 in Vasoactive Intestinal Peptide Gene Knockout Mice. Frontiers in Endocrinology. 8. 162–162. 1 indexed citations
7.
Mancini, Manuela, Ken‐Ichi Takemaru, Fausto Castagnetti, et al.. (2015). 14-3-3 Binding and Sumoylation Concur to the Down-Modulation of β-catenin Antagonist chibby 1 in Chronic Myeloid Leukemia. PLoS ONE. 10(7). e0131074–e0131074. 14 indexed citations
8.
Lee, Yin Loon, Colin J. Comerci, Luís F. Menezes, et al.. (2014). Cby1 promotes Ahi1 recruitment to a ring-shaped domain at the centriole–cilium interface and facilitates proper cilium formation and function. Molecular Biology of the Cell. 25(19). 2919–2933. 49 indexed citations
9.
Chen, Jiang, Christine Laclef, Li Li, et al.. (2014). The Ciliopathy Gene Rpgrip1l Is Essential for Hair Follicle Development. Journal of Investigative Dermatology. 135(3). 701–709. 18 indexed citations
10.
Mancini, Manuela, Ken‐Ichi Takemaru, Enrica Borsi, et al.. (2013). Chibby drives β catenin cytoplasmic accumulation leading to activation of the unfolded protein response in BCR-ABL1+ cells. Cellular Signalling. 25(9). 1820–1827. 16 indexed citations
11.
Fischer, Victoria, et al.. (2011). Generation and Characterization of Monoclonal Antibodies Against Human Chibby Protein. Hybridoma. 30(2). 163–168. 6 indexed citations
12.
Li, Feng‐Qian, et al.. (2008). Chibby cooperates with 14-3-3 to regulate β-catenin subcellular distribution and signaling activity. The Journal of Cell Biology. 181(7). 1141–1154. 111 indexed citations
13.
Mak, Baldwin, Ken‐Ichi Takemaru, Heidi L. Kenerson, Randall T. Moon, & Raymond S. Yeung. (2003). The Tuberin-Hamartin Complex Negatively Regulates β-Catenin Signaling Activity. Journal of Biological Chemistry. 278(8). 5947–5951. 88 indexed citations
14.
Cheyette, Benjamin, Joshua S. Waxman, Jeffrey R. Miller, et al.. (2002). Dapper, a Dishevelled-Associated Antagonist of β-Catenin and JNK Signaling, Is Required for Notochord Formation. Developmental Cell. 2(4). 449–461. 217 indexed citations
15.
McGrew, L. Lynn, Ken‐Ichi Takemaru, Rebecca L. Bates, & Randall T. Moon. (1999). Direct regulation of the Xenopus engrailed-2 promoter by the Wnt signaling pathway, and a molecular screen for Wnt-responsive genes, confirm a role for Wnt signaling during neural patterning in Xenopus. Mechanisms of Development. 87(1-2). 21–32. 102 indexed citations
16.
Takemaru, Ken‐Ichi, Takahisa Ikegami, Hitoshi Ueda, et al.. (1999). Identification of the core domain and the secondary structure of the transcriptional coactivator MBF1. Genes to Cells. 4(7). 415–424. 17 indexed citations
17.
Takemaru, Ken‐Ichi, Satoshi Harashima, Hitoshi Ueda, & Susumu Hirose. (1998). Yeast Coactivator MBF1 Mediates GCN4-Dependent Transcriptional Activation. Molecular and Cellular Biology. 18(9). 4971–4976. 98 indexed citations
18.
Li, Feng‐Qian, Ken‐Ichi Takemaru, Masahide Goto, et al.. (1997). Transcriptional activation through interaction of MBF2 with TFIIA. Genes to Cells. 2(2). 143–153. 25 indexed citations
19.
Mizuno, Mamoru, Shoko Masuda, Ken‐Ichi Takemaru, et al.. (1996). Systematic sequencing of the 283 kb 210 -232  region of the Bacillus subtilis genome containing the skin element and many sporulation genes. Microbiology. 142(11). 3103–3111. 40 indexed citations
20.
Takemaru, Ken‐Ichi, Mamoru Mizuno, Tsutomu Sato, Michio Takeuchi, & Yasuo Kobayashi. (1995). Complete nucleotide sequence of a skin element excised by DNA rearrangement during sporulation in Bacillus subtilis. Microbiology. 141(2). 323–327. 90 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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