Hiroaki Kaku

555 total citations
21 papers, 443 citations indexed

About

Hiroaki Kaku is a scholar working on Immunology, Molecular Biology and Epidemiology. According to data from OpenAlex, Hiroaki Kaku has authored 21 papers receiving a total of 443 indexed citations (citations by other indexed papers that have themselves been cited), including 12 papers in Immunology, 7 papers in Molecular Biology and 5 papers in Epidemiology. Recurrent topics in Hiroaki Kaku's work include Immune Cell Function and Interaction (8 papers), Immunotherapy and Immune Responses (6 papers) and T-cell and B-cell Immunology (6 papers). Hiroaki Kaku is often cited by papers focused on Immune Cell Function and Interaction (8 papers), Immunotherapy and Immune Responses (6 papers) and T-cell and B-cell Immunology (6 papers). Hiroaki Kaku collaborates with scholars based in United States, Japan and New Zealand. Hiroaki Kaku's co-authors include Thomas L. Rothstein, Nichol E. Holodick, Kai Cheng, Yousef Al‐Abed, Daniel O. Griffin, Tâm D. Quách, Joseph R. Tumang, Rubén Francés, Kiyoshi Takatsu and Keisuke Horikawa and has published in prestigious journals such as SHILAP Revista de lepidopterología, The Journal of Immunology and International Journal of Molecular Sciences.

In The Last Decade

Hiroaki Kaku

21 papers receiving 440 citations

Peers

Hiroaki Kaku

IMMUN

PHYSI

ONCOL

EPIDE

Timo Lischke Germany

Esther Zumaquero United States

Eleni Adamopoulou Germany

Flavia Bottarel Italy

Donatella Buonfiglio Italy

Atsunobu Takeda Japan

Luc‐Marie Gerland France

Wim van Schooten United States

Alexander J. Finn United States

Akie Maehara Japan

Timo Lischke Germany

Hiroaki Kaku

324 ×1.2

IMMUN

89 ×0.9

70 ×1.3

PHYSI

121 ×2.5

ONCOL

40 ×1.0

EPIDE

Citations per year, relative to Hiroaki Kaku Hiroaki Kaku (= 1×) peers Timo Lischke

Countries citing papers authored by Hiroaki Kaku

Since Specialization

Citations

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

Fields of papers citing papers by Hiroaki Kaku

Since Specialization

Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by Hiroaki Kaku. 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 Hiroaki Kaku. The network helps show where Hiroaki Kaku may publish in the future.

Co-authorship network of co-authors of Hiroaki Kaku

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

All Works

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20 of 20 papers shown

Kaku, Hiroaki, et al.. (2024). A novel approach to Parkinson’s disease treatment with a potentially dual-acting therapeutic agent that targets α-synuclein aggregation and neuron death. Neural Regeneration Research. 19(12). 2577–2578. 4 indexed citations

Kaku, Hiroaki, et al.. (2023). Newfound physiological function of FAIM protein offers hope of novel disease-modifying therapy for Alzheimer’s disease. Neural Regeneration Research. 18(12). 2677–2679. 1 indexed citations

Kaku, Hiroaki, et al.. (2022). Microparticle immunocapture assay for quantitation of protein multimer amount and size. Cell Reports Methods. 2(5). 100214–100214. 4 indexed citations

Kaku, Hiroaki, et al.. (2022). Small Heat Shock Proteins Collaborate with FAIM to Prevent Accumulation of Misfolded Protein Aggregates. International Journal of Molecular Sciences. 23(19). 11841–11841. 4 indexed citations

Kaku, Hiroaki, et al.. (2021). Fas Apoptosis Inhibitory Molecule Blocks and Dissolves Pathological Amyloid-β Species. Frontiers in Molecular Neuroscience. 14. 750578–750578. 3 indexed citations

Kaku, Hiroaki & Thomas L. Rothstein. (2020). FAIM Is a Non-redundant Defender of Cellular Viability in the Face of Heat and Oxidative Stress and Interferes With Accumulation of Stress-Induced Protein Aggregates. Frontiers in Molecular Biosciences. 7. 32–32. 13 indexed citations

Kaku, Hiroaki, et al.. (2020). FAIM Opposes Aggregation of Mutant SOD1 That Typifies Some Forms of Familial Amyotrophic Lateral Sclerosis. Frontiers in Neuroscience. 14. 110–110. 10 indexed citations

Kaku, Hiroaki, Nichol E. Holodick, Joseph R. Tumang, & Thomas L. Rothstein. (2017). CD25+ B-1a Cells Express Aicda. Frontiers in Immunology. 8. 672–672. 6 indexed citations

Rothstein, Thomas L., Daniel O. Griffin, Nichol E. Holodick, Tâm D. Quách, & Hiroaki Kaku. (2013). Human B‐1 cells take the stage. Annals of the New York Academy of Sciences. 1285(1). 97–114. 129 indexed citations

10.

Kaku, Hiroaki, et al.. (2013). A novel mechanism of B-cell mediated immune suppression through adenosine production (P1084). The Journal of Immunology. 190(Supplement_1). 185.16–185.16. 1 indexed citations

11.

Tumang, Joseph R., et al.. (2011). A CD25− Positive Population of Activated B1 Cells Expresses LIFR and Responds to LIF. SHILAP Revista de lepidopterología. 2. 6–6. 14 indexed citations

12.

Kaku, Hiroaki & Thomas L. Rothstein. (2010). Correction: Fas Apoptosis Inhibitory Molecule Enhances CD40 Signaling in B Cells and Augments the Plasma Cell Compartment. The Journal of Immunology. 185(1). 771–771. 2 indexed citations

13.

Kaku, Hiroaki, et al.. (2010). Cation Nonstoichiometry in Y123 Sintered Bulks and Thin Films. IEEE Transactions on Applied Superconductivity. 21(3). 2745–2748. 3 indexed citations

14.

Kaku, Hiroaki & Thomas L. Rothstein. (2009). Fas Apoptosis Inhibitory Molecule Expression in B Cells Is Regulated through IRF4 in a Feed-Forward Mechanism. The Journal of Immunology. 183(9). 5575–5581. 17 indexed citations

15.

Kaku, Hiroaki & Thomas L. Rothstein. (2009). Octamer binding protein 2 (Oct2) regulates PD-L2 gene expression in B-1 cells through lineage-specific activity of a unique, intronic promoter. Genes and Immunity. 11(1). 55–66. 17 indexed citations

16.

Kaku, Hiroaki & Thomas L. Rothstein. (2009). Fas Apoptosis Inhibitory Molecule Enhances CD40 Signaling in B Cells and Augments the Plasma Cell Compartment. The Journal of Immunology. 183(3). 1667–1674. 16 indexed citations

17.

Hara‐Yokoyama, Miki, Tomoko Kimura, Hiroaki Kaku, et al.. (2007). Alteration of enzymatic properties of cell-surface antigen CD38 by agonistic anti-CD38 antibodies that prolong B cell survival and induce activation. International Immunopharmacology. 8(1). 59–70. 4 indexed citations

18.

Francés, Rubén, et al.. (2006). B-1 cells express transgelin 2: Unexpected lymphocyte expression of a smooth muscle protein identified by proteomic analysis of peritoneal B-1 cells. Molecular Immunology. 43(13). 2124–2129. 19 indexed citations

19.

Kaku, Hiroaki. (2002). NF-kappaB is required for CD38-mediated induction of Cgamma1 germline transcripts in murine B lymphocytes. International Immunology. 14(9). 1055–1064. 37 indexed citations

20.

Horikawa, Keisuke, Hiroaki Kaku, Hiroshi Nakajima, et al.. (2001). Essential Role of Stat5 for IL-5-Dependent IgH Switch Recombination in Mouse B Cells. The Journal of Immunology. 167(9). 5018–5026. 30 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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