Tanaka Tsutomu

Faculty of Medicine Pathological Science Department of Microbiology and ImmunologyAssistant Professor
Institute for Integrated Innovations Institute for Vaccine Research and DevelopmentAssistant Professor
Last Updated :2025/06/07

■Researcher basic information

Degree

  • Doctor of Veterinary Science, Yamaguchi University, Sep. 2015

Researchmap personal page

Research Keyword

  • autoimmunity
  • cancer immunology

Research Field

  • Life sciences, Molecular biology
  • Life sciences, Immunology
  • Life sciences, Tumor biology

Educational Organization

■Career

Career

  • Oct. 2022 - Present
    Hokkaido University, 医学研究院 病理系部門 微生物学免疫学分野, 助教
  • Oct. 2021 - Sep. 2022
    National Institutes of Health, Research Fellow
  • Oct. 2016 - Sep. 2021
    National institutes of Health, Visiting Fellow
  • Mar. 2018 - Feb. 2020
    米国衛生研究所, JSPS-NIH Research Fellow
  • Oct. 2015 - Sep. 2016
    Hokkaido University, Institute for Genetic Medicine, 博士研究員

Educational Background

  • Apr. 2012 - Sep. 2015, Yamaguchi University, The United Graduate School of Veterinary Sciences
  • Apr. 2006 - Mar. 2012, Tottori University, Faculty of Agriculture, School of Veterinary Medicine

■Research activity information

Awards

  • 2020, NIH Fellows Award for Research Excellence (FARE)               
  • Nov. 2014, 日本臨床ストレス応答学会, 若手研究奨励賞               
    田中 努

Papers

  • Amplified Type I Interferon Response in Sjögren's Disease via Ectopic Toll‐Like Receptor 7 Expression in Salivary Gland Epithelial Cells Induced by Lysosome‐Associated Membrane Protein 3
    Hiroyuki Nakamura, Tsutomu Tanaka, Changyu Zheng, Sandra A. Afione, Tatsuya Atsumi, Masayuki Noguchi, Fabiola Reis Oliveira, Ana Carolina F. Motta, Fernando Chahud, Eduardo M. Rocha, Blake M. Warner, John A. Chiorini
    Arthritis & Rheumatology, Jul. 2024
    Scientific journal
  • The balance between nuclear import and export of NLRC5 regulates MHC class I transactivation
    Baohui Zhu, Ryota Ouda, Ning An, Tsutomu Tanaka, Koichi S. Kobayashi
    Journal of Biological Chemistry, May 2024
    Scientific journal
  • LAMP3 induces lysosome‐dependent cell death by impairing autophagic caspase‐8 degradation in Sjögren's salivary glands
    Hiroyuki Nakamura, Tsutomu Tanaka, Changyu Zheng, Sandra A Afione, Blake M. Warner, Masayuki Noguchi, Tatsuya Atsumi, John A. Chiorini
    Arthritis & Rheumatology, 25 Apr. 2023, [Lead author]
    Scientific journal
  • Salivary gland LAMP3 mRNA expression is a possible predictive marker in the response to hydroxychloroquine in Sjögren’s disease
    Hiroyuki Nakamura, Tsutomu Tanaka, Youngmi Ji, Changyu Zheng, Sandra A. Afione, Blake M. Warner, Fabiola Reis Oliveira, Ana Carolina F. Motta, Eduardo M. Rocha, Masayuki Noguchi, Tatsuya Atsumi, John A. Chiorini
    PLOS ONE, 18, 2, Public Library of Science ({PLoS}), 23 Feb. 2023, [Lead author]
    English, Scientific journal, Hydroxychloroquine (HCQ) is a lysosomotropic agent that is commonly used for treating Sjögren’s disease (SjD). However, its efficacy is controversial because of the divergent response to the drug among patients. In a subgroup of SjD patients, lysosome-associated membrane protein 3 (LAMP3) is elevated in expression in the salivary glands and promotes lysosomal dysregulation and lysosome-dependent apoptotic cell death. In this study, chloroquine (CQ) and its derivative HCQ were tested for their ability to prevent LAMP3-induced apoptosis, in vitro and on a mouse model of SjD. In addition, efficacy of HCQ treatment was retrospectively compared between high LAMP3 mRNA expression in minor salivary glands and those with LAMP3 mRNA levels comparable with healthy controls. Study results show that CQ treatment stabilized the lysosomal membrane in LAMP3-overexpressing cells via deactivation of cathepsin B, resulting in decreased apoptotic cell death. In mice with established SjD-like phenotype, HCQ treatment also significantly decreased apoptotic cell death and ameliorated salivary gland hypofunction. Retrospective analysis of SjD patients found that HCQ tended to be more effective in improving disease activity index, symptom severity and hypergammaglobulinemia in patients with high LAMP3 expression compared those with normal LAMP3 expression. Taken together, these findings suggested that by determining salivary gland LAMP3 mRNA level, a patient’s response to HCQ treatment could be predicted. This finding may provide a novel strategy for guiding the development of more personalized medicine for SjD.
  • LAMP3 transfer via extracellular particles induces apoptosis in Sjögren’s disease
    Tsutomu Tanaka, Hiroyuki Nakamura, Duy T. Tran, Blake M. Warner, Yan Wang, Tatsuya Atsumi, Masayuki Noguchi, John A. Chiorini
    Scientific Reports, 13, 1, Springer Science and Business Media {LLC}, 14 Feb. 2023, [Lead author]
    English, Scientific journal, AbstractSjögren’s disease (SjD) is an autoimmune disease that affects exocrine tissues and is characterized by increased apoptosis in salivary and lacrimal glands. Although the pathogenic mechanism triggering SjD is not well understood, overexpression of lysosome-associated membrane protein 3 (LAMP3) is associated with the disease in a subset of SjD patients and the development of SjD-like phenotype in mice. In this study, histological analysis of minor salivary glands of SjD patients suggested that LAMP3-containing material is being ejected from cells. Follow-on in vitro experiments with cells exposed to extracellular particles (EPs) derived from LAMP3-overexpressing cells showed increased apoptosis. Proteomics identified LAMP3 as a major component of EPs derived from LAMP3-overexpressing cells. Live-cell imaging visualized release and uptake of LAMP3-containing EPs from LAMP3-overexpressing cells to naïve cells. Furthermore, experiments with recombinant LAMP3 protein alone or complexed with Xfect protein transfection reagent demonstrated that internalization of LAMP3 was required for apoptosis in a caspase-dependent pathway. Taken together, we identified a new role for extracellular LAMP3 in cell-to-cell communication via EPs, which provides further support for targeting LAMP3 as a therapeutic approach in SjD.
  • Association of G protein‐coupled receptor 78 with salivary dysfunction in male Sjögren's patients
    Tsutomu Tanaka, Maria Cambraia Guimaro Diniz, Hiroyuki Nakamura, Paola Perez, Youngmi Ji, Drew G. Michael, Sandra A. Afione, Changyu Zheng, Corinne Goldsmith, William D. Swaim, Anne Marie Lynge Pedersen, John A. Chiorini
    Oral Diseases, Wiley, 18 Jan. 2023, [Lead author]
    English, Scientific journal
  • Correction of LAMP3-associated salivary gland hypofunction by aquaporin gene therapy
    Hiroyuki Nakamura, Tsutomu Tanaka, Changyu Zheng, Sandra A. Afione, Blake M. Warner, Masayuki Noguchi, Tatsuya Atsumi, John A. Chiorini
    Scientific Reports, 12, 1, 18570, Springer Science and Business Media {LLC}, 03 Nov. 2022, [Lead author]
    English, Scientific journal, AbstractSjögren’s disease (SjD) is a chronic autoimmune sialadenitis resulting in salivary gland hypofunction with dry mouth symptom. Previous studies showed that lysosome-associated membrane protein 3 (LAMP3) overexpression is involved in the development of salivary gland hypofunction associated with SjD. However, the molecular mechanisms are still unclear, and no effective treatment exists to reverse gland function in SjD. Analysis on salivary gland samples from SjD patients showed that salivary gland hypofunction was associated with decreased expression of sodium–potassium-chloride cotransporter-1 (NKCC1) and aquaporin 5 (AQP5), which are membrane proteins involved in salivation. Further studies revealed that LAMP3 overexpression decreased their expression levels by promoting endolysosomal degradation. Additionally, we found that LAMP3 overexpression enhanced gene transfer by increasing internalization of adeno-associated virus serotype 2 (AAV2) via the promoted endolysosomal pathway. Retrograde cannulation of AAV2 vectors encoding AQP1 gene (AAV2-AQP1) into salivary glands induced glandular AQP1 expression sufficient to restore salivary flow in LAMP3-overexpressing mice. LAMP3 could play a critical role in the development of salivary gland hypofunction in SjD by promoting endolysosomal degradation of NKCC1 and AQP5. But it also could enhance AAV2-mediated gene transfer to restore fluid movement through induction of AQP1 expression. These findings suggested that AAV2-AQP1 gene therapy is useful in reversing salivary gland function in SjD patients.
  • Indocyanine green conjugated phototheranostic nanoparticle for photodiagnosis and photodynamic therapy
    Kenta Shinoda, Akiko Suganami, Yasumitsu Moriya, Masamichi Yamashita, Tsutomu Tanaka, Akane S. Suzuki, Hiroshi Suito, Yasunori Akutsu, Kengo Saito, Yoko Shinozaki, Kazuoki Isojima, Naohito Nakamura, Yasushi Miyauchi, Hiroshi Shirasawa, Hisahiro Matsubara, Yoshiharu Okamoto, Toshinori Nakayama, Yutaka Tamura
    Photodiagnosis and Photodynamic Therapy, 39, 103041, 103041, Elsevier BV, Sep. 2022
    Scientific journal
  • Enteric viruses replicate in salivary glands and infect through saliva
    S. Ghosh, M. Kumar, M. Santiana, A. Mishra, M. Zhang, H. Labayo, A. M. Chibly, H. Nakamura, T. Tanaka, W. Henderson, E. Lewis, O. Voss, Y. Su, Y. Belkaid, J. A. Chiorini, M. P. Hoffman, N. Altan-Bonnet
    Nature, 14 Jul. 2022
    Scientific journal
  • LAMP3 inhibits autophagy and contributes to cell death by lysosomal membrane permeabilization
    Tsutomu Tanaka, Blake M. Warner, Drew G. Michael, Hiroyuki Nakamura, Toshio Odani, Hongen Yin, Tatsuya Atsumi, Masayuki Noguchi, John A. Chiorini
    Autophagy, 03 Jul. 2022, [Lead author]
    Scientific journal
  • Lysosomal exocytosis of HSP70 stimulates monocytic BMP6 expression in Sjögren’s syndrome
    Ying-Qian Mo, Hiroyuki Nakamura, Tsutomu Tanaka, Toshio Odani, Paola Perez, Youngmi Ji, Benjamin N. French, Thomas J.F. Pranzatelli, Drew G. Michael, Hongen Yin, Susan S. Chow, Maryam Khalaj, Sandra A. Afione, Changyu Zheng, Fabiola Reis Oliveira, Ana Carolina F. Motta, Alfredo Ribeiro-Silva, Eduardo M. Rocha, Cuong Q. Nguyen, Masayuki Noguchi, Tatsuya Atsumi, Blake M. Warner, John A. Chiorini
    Journal of Clinical Investigation, American Society for Clinical Investigation, 15 Mar. 2022, [Lead author]
    Scientific journal
  • Lysosome-associated membrane protein 3 misexpression in salivary glands induces a Sjögren’s syndrome-like phenotype in mice
    Hiroyuki Nakamura, Tsutomu Tanaka, Thomas Pranzatelli, Youngmi Ji, Hongen Yin, Paola Perez, S, ra A Afione, Shyh-Ing Jang, Corrine Goldsmith, Chang Yu Zheng, William D Swaim, Blake M Warner, Noriyuki Hirata, Masayuki Noguchi, Tatsuya Atsumi, John A Chiorini
    Annals of the Rheumatic Diseases, 80, 8, 1031, 1039, {BMJ}, 03 Mar. 2021, [Lead author]
    English, Scientific journal, ObjectivesSjögren’s syndrome (SS) is an autoimmune sialadenitis with unknown aetiology. Although extensive research implicated an abnormal immune response associated with lymphocytes, an initiating event mediated by salivary gland epithelial cell (SGEC) abnormalities causing activation is poorly characterised. Transcriptome studies have suggested alternations in lysosomal function are associated with SS, but a cause and effect linkage has not been established. In this study, we demonstrated that altered lysosome activity in SGECs by expression of lysosome-associated membrane protein 3 (LAMP3) can initiate an autoimmune response with autoantibody production and salivary dysfunction similar to SS.MethodsRetroductal cannulation of the submandibular salivary glands with an adeno-associated virus serotype 2 vector encoding LAMP3 was used to establish a model system. Pilocarpine-stimulated salivary flow and the presence of autoantibodies were assessed at several time points post-cannulation. Salivary glands from the mice were evaluated using RNAseq and histologically.ResultsFollowing LAMP3 expression, saliva flow was significantly decreased and serum anti-Ro/SSA and La/SSB antibodies could be detected in the treated mice. Mechanistically, LAMP3 expression increased apoptosis in SGECs and decreased protein expression related to saliva secretion. Analysis of RNAseq data suggested altered lysosomal function in the transduced SGECs, and that the cellular changes can chemoattract immune cells into the salivary glands. Immune cells were activated via toll-like receptors by damage-associated molecular patterns released from LAMP3-expressing SGECs.ConclusionsThese results show a critical role for lysosomal trafficking in the development of SS and establish a causal relationship between LAMP3 misexpression and the development of SS.
  • Rescue of Adeno-Associated Virus Production by shRNA Cotransfection
    Tsutomu Tanaka, Maria C. Guimaro, Sandra A. Afione, Tsutomu Tanaka, John A. Chiorini
    Human Gene Therapy, 31, 19-20, 1068, 1073, Mary Ann Liebert Inc, 01 Oct. 2020
    English, Scientific journal
  • LAMP3 induces apoptosis and autoantigen release in Sjögren’s syndrome patients
    Tsutomu Tanaka, Blake M. Warner, Toshio Odani, Youngmi Ji, Ying-Qian Mo, Hiroyuki Nakamura, Shyh-Ing Jang, Hongen Yin, Drew G. Michael, Noriyuki Hirata, Futoshi Suizu, Satoko Ishigaki, Fabiola Reis Oliveira, Ana Carolina F. Motta, Alfredo Ribeiro-Silva, Eduardo M. Rocha, Tatsuya Atsumi, Masayuki Noguchi, John A. Chiorini
    Scientific Reports, 10, 1, 15169, 15169, Springer Science and Business Media {LLC}, 16 Sep. 2020, [Lead author], [International Magazine]
    English, Scientific journal, AbstractPrimary Sjögren’s syndrome (pSS) is a complex autoimmune disease characterized by dysfunction of secretory epithelia with only palliative therapy. Patients present with a constellation of symptoms, and the diversity of symptomatic presentation has made it difficult to understand the underlying disease mechanisms. In this study, aggregation of unbiased transcriptome profiling data sets of minor salivary gland biopsies from controls and Sjögren’s syndrome patients identified increased expression of lysosome-associated membrane protein 3 (LAMP3/CD208/DC-LAMP) in a subset of Sjögren’s syndrome cases. Stratification of patients based on their clinical characteristics suggested an association between increased LAMP3 expression and the presence of serum autoantibodies including anti-Ro/SSA, anti-La/SSB, anti-nuclear antibodies. In vitro studies demonstrated that LAMP3 expression induces epithelial cell dysfunction leading to apoptosis. Interestingly, LAMP3 expression resulted in the accumulation and release of intracellular TRIM21 (one component of SSA), La (SSB), and α-fodrin protein, common autoantigens in Sjögren’s syndrome, via extracellular vesicles in an apoptosis-independent mechanism. This study defines a clear role for LAMP3 in the initiation of apoptosis and an independent pathway for the extracellular release of known autoantigens leading to the formation of autoantibodies associated with this disease.ClinicalTrials.gov Identifier: NCT00001196, NCT00001390, NCT02327884.
  • Autophagy as a modulator of cell death machinery
    Masayuki Noguchi, Noriyuki Hirata, Tsutomu Tanaka, Futoshi Suizu, Hiroshi Nakajima, John A. Chiorini
    Cell Death & Disease, 11, 7, Springer Science and Business Media {LLC}, 08 Jul. 2020
    English, Scientific journal, AbstractThe balance between cell death and survival is a critical parameter in the regulation of cells and the maintenance of homeostasis in vivo. Three major mechanisms for cell death have been identified in mammalian cells: apoptosis (type I), autophagic cell death (type II), and necrosis (type III). These three mechanisms have been suggested to engage in cross talk with each other. Among them, autophagy was originally characterized as a cell survival mechanism for amino acid recycling during starvation. Whether autophagy functions primarily in cell survival or cell death is a critical question yet to be answered. Here, we present a comprehensive review of the cell death-related events that take place during autophagy and their underlying mechanisms in cancer and autoimmune disease development.
  • Identification of RNA aptamer which specifically interacts with PtdIns(3)P
    Thoria Donia, Bala Jyoti, Futoshi Suizu, Noriyuki Hirata, Tsutomu Tanaka, Satoko Ishigaki, Pranzatelli Thomas J. F, Junko Nio-Kobayashi, Toshihiko Iwanaga, John A. Chiorini, Masayuki Noguchi
    Biochemical and Biophysical Research Communications, 517, 1, 146, 154, Elsevier {BV}, 24 Jul. 2019, [International Magazine]
    English, Scientific journal, The phosphinositide PtdIns(3)P plays an important role in autophagy; however, the detailed mechanism of its activity remains unclear. Here, we used a Systematic Evolution of Ligands by EXponential enrichment (SELEX) screening approach to identify an RNA aptamer of 40 nucleotides that specifically recognizes and binds to intracellular lysosomal PtdIns(3)P. Binding occurs in a magnesium concentration- and pH-dependent manner, and consequently inhibits autophagy as determined by LC3II/I conversion, p62 degradation, formation of LC3 puncta, and lysosomal accumulation of Phafin2. These effects in turn inhibited lysosomal acidification, and the subsequent hydrolytic activity of cathepsin D following induction of autophagy. Given the essential role of PtdIns(3)P as a key targeting molecule for autophagy induction, identification of this novel PtdIns(3)P RNA aptamer provides new opportunities for investigating the biological functions and mechanisms of phosphoinositides.
  • Functional characterization of lysosomal interaction of Akt with VRK2
    Noriyuki Hirata, Futoshi Suizu, Mami Matsuda-Lennikov, Tsutomu Tanaka, Tatsuma Edamura, Satoko Ishigaki, Thoria Donia, Pathrapol Lithanatudom, Chikashi Obuse, Toshihiko Iwanaga, Masayuki Noguchi
    Oncogene, 37, 40, 5367, 5386, Springer Science and Business Media {LLC}, Oct. 2018
    English, Scientific journal
  • Cancer-associated oxidoreductase ERO1-α promotes immune escape through up-regulation of PD-L1 in human breast cancer
    Tsutomu Tanaka, Goro Kutomi, Toshimitsu Kajiwara, Kazuharu Kukita, Vitaly Kochin, Takayuki Kanaseki, Tomohide Tsukahara, Yoshihiko Hirohashi, Toshihiko Torigoe, Yoshiharu Okamoto, Koichi Hirata, Noriyuki Sato, Yasuaki Tamura
    Oncotarget, 8, 15, 24706, 24718, Impact Journals, {LLC}, 11 Apr. 2017, [Lead author]
    English, Scientific journal
  • Hypoxia augments MHC class I antigen presentation via facilitation of ERO1-α-mediated oxidative folding in murine tumor cells
    Toshimitsu Kajiwara, Tsutomu Tanaka, Kazuharu Kukita, Goro Kutomi, Keita Saito, Koichi Okuya, Akari Takaya, Vitaly Kochin, Takayuki Kanaseki, Tomohide Tsukahara, Yoshihiko Hirohashi, Toshihiko Torigoe, Koichi Hirata, Noriyuki Sato, Yasuaki Tamura
    European Journal of Immunology, 46, 12, 2842, 2851, Wiley, Dec. 2016
    English, Scientific journal
  • Plasticity of lung cancer stem-like cells is regulated by the transcription factor HOXA5 that is induced by oxidative stress
    Hiroshi Saijo, Yoshihiko Hirohashi, Toshihiko Torigoe, Ryota Horibe, Akari Takaya, Aiko Murai, Terufumi Kubo, Toshimitsu Kajiwara, Tsutomu Tanaka, Yosuke Shionoya, Eri Yamamoto, Reo Maruyama, Munehide Nakatsugawa, Takayuki Kanaseki, Tomohide Tsukahara, Yasuaki Tamura, Yasushi Sasaki, Takashi Tokino, Hiromu Suzuki, Toru Kondo, Hiroki Takahashi, Noriyuki Sato
    Oncotarget, 7, 31, 50043, 50056, Impact Journals, {LLC}, 02 Aug. 2016
    English, Scientific journal
  • Phosphorylation‐dependent Akt–Inversin interaction at the basal body of primary cilia
    Futoshi Suizu, Noriyuki Hirata, Kohki Kimura, Tatsuma Edamura, Tsutomu Tanaka, Satoko Ishigaki, Thoria Donia, Hiroko Noguchi, Toshihiko Iwanaga, Masayuki Noguchi
    The EMBO Journal, 35, 12, 1346, 1363, {EMBO}, 15 Jun. 2016, [International Magazine]
    English, Scientific journal, A primary cilium is a microtubule-based sensory organelle that plays an important role in human development and disease. However, regulation of Akt in cilia and its role in ciliary development has not been demonstrated. Using yeast two-hybrid screening, we demonstrate that Inversin (INVS) interacts with Akt. Mutation in the INVS gene causes nephronophthisis type II (NPHP2), an autosomal recessive chronic tubulointerstitial nephropathy. Co-immunoprecipitation assays show that Akt interacts with INVS via the C-terminus. In vitro kinase assays demonstrate that Akt phosphorylates INVS at amino acids 864-866 that are required not only for Akt interaction, but also for INVS dimerization. Co-localization of INVS and phosphorylated form of Akt at the basal body is augmented by PDGF-AA Akt-null MEF cells as well as siRNA-mediated inhibition of Akt attenuated ciliary growth, which was reversed by Akt reintroduction. Mutant phosphodead- or NPHP2-related truncated INVS, which lack Akt phosphorylation sites, suppress cell growth and exhibit distorted lumen formation and misalignment of spindle axis during cell division. Further studies will be required for elucidating functional interactions of Akt-INVS at the primary cilia for identifying the molecular mechanisms underlying NPHP2.
  • Cancer-associated oxidoreductase ERO1-α drives the production of VEGF via oxidative protein folding and regulating the mRNA level
    Tsutomu Tanaka, Goro Kutomi, Toshimitsu Kajiwara, Kazuharu Kukita, Vitaly Kochin, Takayuki Kanaseki, Tomohide Tsukahara, Yoshihiko Hirohashi, Toshihiko Torigoe, Yoshiharu Okamoto, Koichi Hirata, Noriyuki Sato, Yasuaki Tamura
    British Journal of Cancer, 114, 11, 1227, 1234, Springer Science and Business Media {LLC}, 24 May 2016, [Lead author, Corresponding author]
    English, Scientific journal
  • Primary Cilium-Mediated Crosstalk of Signaling Cascades in Ciliogenesis: Implications for Tumorigenesis and Senescence
    Futoshi Suizu, Noriyuki Hirata, Satoko Ishigaki, Tatsuma Edamura, Kohki Kimura, Tsutomu Tanaka, Masayuki Noguchi
    Cell Communication Insights, 8, 13, 24, Portico, 19 May 2016
    Scientific journal
  • Liposomally formulated phospholipid-conjugated indocyanine green for intra-operative brain tumor detection and resection
    Akiko Suganami, Yasuo Iwadate, Sayaka Shibata, Masamichi Yamashita, Tsutomu Tanaka, Natsuki Shinozaki, Ichio Aoki, Naokatsu Saeki, Hiroshi Shirasawa, Yoshiharu Okamoto, Yutaka Tamura
    International Journal of Pharmaceutics, 496, 2, 401, 406, Elsevier {BV}, 30 Dec. 2015
    English, Scientific journal
  • CpG-A stimulates Hsp72 secretion from plasmacytoid dendritic cells, facilitating cross-presentation
    Tsutomu Tanaka, Toshimitsu Kajiwara, Goro Kutomi, Takehiro Kurotaki, Keita Saito, Takayuki Kanaseki, Tomohide Tsukahara, Yoshihiko Hirohashi, Toshihiko Torigoe, Koichi Hirata, Yoshiharu Okamoto, Noriyuki Sato, Yasuaki Tamura
    Immunology Letters, 167, 1, 34, 40, Elsevier {BV}, Sep. 2015, [Lead author]
    English, Scientific journal
  • Cancer-Associated Oxidase ERO1-α Regulates the Expression of MHC Class I Molecule via Oxidative Folding
    Kazuharu Kukita, Yasuaki Tamura, Tsutomu Tanaka, Toshimitsu Kajiwara, Goro Kutomi, Keita Saito, Koichi Okuya, Akari Takaya, Takayuki Kanaseki, Tomohide Tsukahara, Yoshihiko Hirohashi, Toshihiko Torigoe, Tomohisa Furuhata, Koichi Hirata, Noriyuki Sato
    The Journal of Immunology, 194, 10, 4988, 4996, The American Association of Immunologists, 15 May 2015
    English, Scientific journal
  • Cancer-Associated Oxidoreductase ERO1-α Drives the Production of Tumor-Promoting Myeloid-Derived Suppressor Cells via Oxidative Protein Folding
    Tsutomu Tanaka, Toshimitsu Kajiwara, Toshihiko Torigoe, Yoshiharu Okamoto, Noriyuki Sato, Yasuaki Tamura
    The Journal of Immunology, 194, 4, 2004, 2010, The American Association of Immunologists, 15 Feb. 2015, [Lead author]
    English, Scientific journal
  • Heat shock protein 90 targets a chaperoned peptide to the static early endosome for efficient cross‐presentation by human dendritic cells
    Tsutomu Tanaka, Koichi Okuya, Goro Kutomi, Akari Takaya, Toshimitsu Kajiwara, Takayuki Kanaseki, Tomohide Tsukahara, Yoshihiko Hirohashi, Toshihiko Torigoe, Koichi Hirata, Yoshiharu Okamoto, Noriyuki Sato, Yasuaki Tamura
    Cancer Science, 106, 1, 18, 24, Wiley, Jan. 2015, [Lead author]
    English, Scientific journal
  • Human endoplasmic reticulum oxidoreductin 1-α is a novel predictor for poor prognosis of breast cancer
    Goro Kutomi, Yasuaki Tamura, Tsutomu Tanaka, Toshimitsu Kajiwara, Kazuharu Kukita, Tousei Ohmura, Hiroaki Shima, Tomoko Takamaru, Fukino Satomi, Yasuyo Suzuki, Toshihiko Torigoe, Noriyuki Sato, Koichi Hirata
    Cancer Science, 104, 8, 1091, 1096, Wiley, Aug. 2013
    English, Scientific journal

Lectures, oral presentations, etc.

  • Increased expression of lysosomal associated membrane protein (LAMP) 3 in the salivary glands of Sjögren’s syndrome patients can stimulate stalled autophagy and apoptosis.               
    Tsutomu Tanaka, Blake M. Warner, Toshio Odani, Hongen Yin, Tatsuya Atsumi, Masayuki Noguchi, John A. Chiorini
    The 14th International Sjögren’s Syndrome Symposium, Apr. 2018, Poster presentation
    Apr. 2018
  • 腫瘍高発現性酸化酵素ERO1-αはEMTを調節し肺転移を制御する               
    田中 努, 田村 保明, 梶原 敏充, 鳥越 俊彦, 岡本 芳晴, 佐藤 昇志
    第10回日本臨床ストレス応答学会大会, Nov. 2015, Oral presentation
    Nov. 2015
  • Cancer specific oxidase ERO1-α promotes the immune escape via up-regulation of PD-L1.               
    田中 努, 田村 保明, 梶原 敏充, 九冨 五郎, 鳥越 俊彦, 岡本 芳晴, 平田 公一, 佐藤 昇志
    第74回日本癌学会総会, Oct. 2015, Oral presentation
    Oct. 2015
  • Enhanced expression of ERO1-α within tumors regulates the condition for tumor growth in vivo.               
    田中 努, 田村 保明, 梶原 敏充, 鳥越 俊彦, 岡本 芳晴, 佐藤 昇志
    第104回日本病理学会総会, Apr. 2015, Oral presentation
    Apr. 2015
  • 腫瘍に高発現する酸化酵素ERO1-αは、腫瘍増殖環境を整える               
    田中 努, 田村 保明, 梶原 敏充, 鳥越 俊彦, 岡本 芳晴, 佐藤 昇志
    第9回日本臨床ストレス応答学会大会, Nov. 2014, Oral presentation
    Nov. 2014
  • Enhanced expression of endoplasmic reticulum oxidoreductin 1-α (ERO1-α) promotes tumor growth and pulmonary metastasis.               
    田中 努, 田村 保明, 梶原 敏充, 鳥越 俊彦, 岡本 芳晴, 佐藤 昇志
    第73回日本癌学会総会, Sep. 2014, Poster presentation
    Sep. 2014
  • 腫瘍に高発現する酸化酵素ERO1-αは癌幹細胞形質の維持に関与する               
    田中 努, 田村 保明, 久木田 和晴, 梶原 敏充, 鳥越 俊彦, 岡本 芳晴, 佐藤 昇志
    第103回日本病理学会総会, Apr. 2014, Oral presentation
    Apr. 2014
  • Enhanced expression of endoplasmic reticulum disulfide oxidase 1-α (ERO1-α) inhibits anti-tumor immune response.               
    田中 努, 田村 保明, 久木田 和晴, 梶原 敏充, 鳥越 俊彦, 岡本 芳晴, 佐藤 昇志
    第72回日本癌学会総会, Oct. 2013, Oral presentation
    Oct. 2013
  • 腫瘍に高発現する酸化酵素ERO1-αは、抗腫瘍免疫応答を抑制する               
    田中 努, 田村 保明, 久木田 和晴, 梶原 敏充, 鳥越 俊彦, 岡本 芳晴, 佐藤 昇志
    第102回日本病理学会総会, Jun. 2013, Oral presentation
    Jun. 2013

Affiliated academic society

  • 2015 - Present
    日本免疫学会               
  • 2013 - Present
    日本病理学会               
  • 2012 - Present
    日本癌学会               

Research Themes

  • 選択的MHC発現誘導機構の解明と癌免疫への応用
    科学研究費助成事業
    31 Aug. 2023 - 31 Mar. 2025
    田中 努
    日本学術振興会, 研究活動スタート支援, 北海道大学, 23K19476
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