Faculty Profiles - TAKAHASHI Kota

写真a

TAKAHASHI Kota

Organization

Academic Assembly Institute of Medicine and Dentistry - Assistant Professor

Homepage

https://www.med.niigata-u.ac.jp/bc2/en/

External link

Degree

PhD (Medical science) ( 2013.3 Tohoku University )

Research Interests

膜生物学
脂質生化学

Research Areas

Life Science / Medical biochemistry
Life Science / Cell biology
Life Science / Molecular biology

Research History (researchmap)

Department of Molecular Cell Biology, Graduate School of Medical and Dental Sciences, Niigata University Laboratory of Lipid Biochemistry Assistant Professor

2026.5

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Country：Japan

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University of Strasbourg Postdoctoral fellow

2022.4 - 2026.4

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Country：France

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Chiba University Assistant professor

2021.1 - 2022.3

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Country：Japan

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University of Helsinki Postdoctoral fellow

2017.3 - 2020.12

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Country：Finland

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Tohoku Medical and Pharmaceutical University

2013.4 - 2017.3

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Country：Japan

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Research History

Niigata University Institute of Medicine and Dentistry, Academic Assembly Assistant Professor

2026.5

Education

Tohoku University Graduate School of Medicine

2009.4 - 2013.3

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Professional Memberships

日本脂質生化学会

2017.4

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THE JAPANESE CANCER ASSOCIATION

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THE PHARMACEUTICAL SOCIETY OF JAPAN

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THE JAPANESE BIOCHEMICAL SOCIETY

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THE JAPANESE SOCIETY OF CARBOHYDRATE RESEARCH

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Papers

Sorting of lysosomal enzyme and autophagy are regulated by the GGA1-induced TGN lipid scrambling

Takefumi Uemura, Fabien Alpy, Nicolas Humbert, Ludovic Richert, Yasushi Sako, Kentaro Hanada, James Rae, Gašper Šolinc, Toshiyuki Yamaji, Thomas Wollert, Toshihide Kobayashi, Nario Tomishige, Yves Mély, Robert G Parton, Mitsuhiro Abe, Satoshi Waguri, Gregor Anderluh, Catherine Tomasetto, Frédéric Przybilla, Kohta Takahashi

Science Advances 2026.8

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Publishing type：Research paper (scientific journal)

DOI： 10.1126/sciadv.aec4519

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Using lipid binding proteins and advanced microscopy to study lipid domains. International journal

Nario Tomishige, Kohta Takahashi, Brigitte Pollet, Ludovic Richert, Yves Mély, Toshihide Kobayashi

Methods in enzymology 700 217 - 234 2024

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Language：English Publishing type：Research paper (scientific journal)

Sphingomyelin is postulated to form clusters with glycosphingolipids, cholesterol and other sphingomyelin molecules in biomembranes through hydrophobic interaction and hydrogen bonds. These clusters form submicron size lipid domains. Proteins that selectively binds sphingomyelin and/or cholesterol are useful to visualize the lipid domains. Due to their small size, visualization of lipid domains requires advanced microscopy techniques in addition to lipid binding proteins. This Chapter describes the method to characterize plasma membrane sphingomyelin-rich and cholesterol-rich lipid domains by quantitative microscopy. This Chapter also compares different permeabilization methods to visualize intracellular lipid domains.

DOI： 10.1016/bs.mie.2024.03.026

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N-acetylglucosamine-6-O sulfation on intestinal mucins prevents obesity and intestinal inflammation by regulating gut microbiota. International journal

Hirohito Abo, Aoi Muraki, Akihito Harusato, Tetsuya Imura, Maki Suzuki, Kohta Takahashi, Timothy L Denning, Hiroto Kawashima

JCI insight 8 ( 16 ) 2023.8

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Intestinal mucins play an essential role in the defense against bacterial invasion and the maintenance of gut microbiota, which is instrumental in the regulation of host immune systems; hence, its dysregulation is a hallmark of metabolic disease and intestinal inflammation. However, the mechanism by which intestinal mucins control the gut microbiota as well as disease phenotypes remains nebulous. Herein, we report that N-acetylglucosamine (GlcNAc)-6-O sulfation of O-glycans on intestinal mucins performs a protective role against obesity and intestinal inflammation. Chst4-/- mice, lacking GlcNAc-6-O sulfation of the mucin O-glycans, showed significant weight gain and increased susceptibility to dextran sodium sulfate-induced colitis as well as colitis-associated cancer accompanied by significantly reduced immunoglobulin A (IgA) production caused by an impaired T follicular helper cell-mediated IgA response. Interestingly, the protective effects of GlcNAc-6-O sulfation against obesity and intestinal inflammation depend on the gut microbiota, evidenced by the modulation of the gut microbiota by cohousing or microbiota transplantation reversing disease phenotypes and IgA production. Collectively, our findings provide insight into the significance of host glycosylation, more specifically GlcNAc-6-O sulfation on intestinal mucins, in protecting against obesity and intestinal inflammation via regulation of the gut microbiota.

DOI： 10.1172/jci.insight.165944

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Identification of Crucial Amino Acid Residues for Antimicrobial Activity of Angiogenin 4 and Its Modulation of Gut Microbiota in Mice. International journal

Mst Farzana Sultana, Maki Suzuki, Fumiya Yamasaki, Wataru Kubota, Kohta Takahashi, Hirohito Abo, Hiroto Kawashima

Frontiers in microbiology 13 900948 - 900948 2022

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Angiogenin 4 bearing ribonuclease activity is an endogenous antimicrobial protein expressed in small and large intestine. However, the crucial amino acid residues responsible for the antibacterial activity of Ang4 and its impact on gut microbiota remain unknown. Here, we report the contribution of critical amino acid residues in the functional regions of Ang4 to its activity against Salmonella typhimurium LT2 and the effect of Ang4 on gut microbiota in mice. We found that Ang4 binds S. typhimurium LT2 through two consecutive basic amino acid residues, K58 and K59, in the cell-binding segment and disrupts the bacterial membrane integrity at the N-terminal α-helix containing residues K7 and K30, as evidenced by the specific mutations of cationic residues of Ang4. We also found that the RNase activity of Ang4 was not involved in its bactericidal activity, as shown by the H12 mutant, which lacks RNase activity. In vivo administration of Ang4 through the mouse rectum and subsequent bacterial 16S rRNA gene sequencing analyses demonstrated that administration of Ang4 not only increased beneficial bacteria such as Lactobacillus, Akkermansia, Dubosiella, Coriobacteriaceae UCG-002, and Adlercreutzia, but also decreased certain pathogenic bacteria, including Alistipes and Enterohabdus, indicating that Ang4 regulates the shape of gut microbiota composition. We conclude that Ang4 kills bacteria by disrupting bacterial membrane integrity through critical basic amino acid residues with different functionalities rather than overall electrostatic interactions and potentially maintains gut microflora in vivo under physiological and pathophysiological conditions.

DOI： 10.3389/fmicb.2022.900948

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ORP2 couples LDL-cholesterol transport to FAK activation by endosomal cholesterol/PI(4,5)P2 exchange. International journal

Kohta Takahashi, Kristiina Kanerva, Lauri Vanharanta, Leonardo Almeida-Souza, Daniel Lietha, Vesa M Olkkonen, Elina Ikonen

The EMBO journal 40 ( 14 ) e106871 2021.7

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Low-density lipoprotein (LDL)-cholesterol delivery from late endosomes to the plasma membrane regulates focal adhesion dynamics and cell migration, but the mechanisms controlling it are poorly characterized. Here, we employed auxin-inducible rapid degradation of oxysterol-binding protein-related protein 2 (ORP2/OSBPL2) to show that endogenous ORP2 mediates the transfer of LDL-derived cholesterol from late endosomes to focal adhesion kinase (FAK)-/integrin-positive recycling endosomes in human cells. In vitro, cholesterol enhances membrane association of FAK to PI(4,5)P2 -containing lipid bilayers. In cells, ORP2 stimulates FAK activation and PI(4,5)P2 generation in endomembranes, enhancing cell adhesion. Moreover, ORP2 increases PI(4,5)P2 in NPC1-containing late endosomes in a FAK-dependent manner, controlling their tubulovesicular trafficking. Together, these results provide evidence that ORP2 controls FAK activation and LDL-cholesterol plasma membrane delivery by promoting bidirectional cholesterol/PI(4,5)P2 exchange between late and recycling endosomes.

DOI： 10.15252/embj.2020106871

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ORP2 interacts with phosphoinositides and controls the subcellular distribution of cholesterol. International journal

Annika Koponen, Amita Arora, Kohta Takahashi, Henriikka Kentala, Annukka M Kivelä, Eeva Jääskeläinen, Johan Peränen, Pentti Somerharju, Elina Ikonen, Tapani Viitala, Vesa M Olkkonen

Biochimie 158 90 - 101 2019.3

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ORP2 is a sterol-binding protein with documented functions in lipid and glucose metabolism, Akt signaling, steroidogenesis, cell adhesion, migration and proliferation. Here we investigate the interactions of ORP2 with phosphoinositides (PIPs) by surface plasmon resonance (SPR), its affinity for cholesterol with a pull-down assay, and its capacity to transfer sterol in vitro. Moreover, we determine the effects of wild-type (wt) ORP2 and a mutant with attenuated PIP binding, ORP2(mHHK), on the subcellular distribution of cholesterol, and analyze the interaction of ORP2 with the related cholesterol transporter ORP1L. ORP2 showed specific affinity for PI(4,5)P2, PI(3,4,5)P3 and PI(4)P, with suggestive Kd values in the μM range. Also binding of cholesterol by ORP2 was detectable, but a Kd could not be determined. Wt ORP2 was in HeLa cells mainly detected in the cytosol, ER, late endosomes, and occasionally on lipid droplets (LDs), while ORP2(mHHK) displayed an enhanced LD localization. Overexpression of wt ORP2 shifted the D4H cholesterol probe away from endosomes, while ORP2(mHHK) caused endosomal accumulation of the probe. Although ORP2 failed to transfer dehydroergosterol in an in vitro assay where OSBP is active, its knock-down resulted in the accumulation of cholesterol in late endocytic compartments, as detected by both D4H and filipin probes. Interestingly, ORP2 was shown to interact and partially co-localize on late endosomes with ORP1L, a cholesterol transporter/sensor at ER-late endosome junctions. Our data demonstrates that ORP2 binds several phosphoinositides, both PI(4)P and multiply phosphorylated species. ORP2 regulates the subcellular distribution of cholesterol dependent on its PIP-binding capacity. The interaction of ORP2 with ORP1L suggests a concerted action of the two ORPs.

DOI： 10.1016/j.biochi.2018.12.013

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Murine Sialidase Neu3 facilitates GM2 degradation and bypass in mouse model of Tay-Sachs disease Reviewed

Volkan Seyrantepe, Secil Akyildiz Demir, Zehra Kevser Timur, Johanna Von Gerichten, Christian Marsching, Esra Erdemli, Emin Oztas, Kohta Takahashi, Kazunori Yamaguchi, Nurselin Ates, Buket Dönmez Demir, Turgay Dalkara, Katrin Erich, Carsten Hopf, Roger Sandhoff, Taeko Miyagi

Experimental Neurology 299 ( Pt A ) 26 - 41 2018.1

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Language：English Publishing type：Research paper (scientific journal) Publisher：Academic Press Inc.

DOI： 10.1016/j.expneurol.2017.09.012

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Biological and Pathological Roles of Ganglioside Sialidases. Reviewed

Miyagi T, Takahashi K, Yamamoto K, Shiozaki K, Yamaguchi K

Progress in molecular biology and translational science 156 121 - 150 2018.1

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DOI： 10.1016/bs.pmbts.2017.12.005

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Sialidase NEU3 defines invasive potential of human glioblastoma cells by regulating calpain-mediated proteolysis of focal adhesion proteins Reviewed

Kohta Takahashi, Sergei Proshin, Kazunori Yamaguchi, Yoji Yamashita, Ryuichi Katakura, Koji Yamamoto, Hiroshi Shima, Masahiro Hosono, Taeko Miyagi

BIOCHIMICA ET BIOPHYSICA ACTA-GENERAL SUBJECTS 1861 ( 11 ) 2778 - 2788 2017.11

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DOI： 10.1016/j.bbagen.2017.07.023

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Neuraminidases 3 and 4 regulate neuronal function by catabolizing brain gangliosides Reviewed

Xuefang Pan, Camila De Britto Para De Aragao, Juan P. Velasco-Martin, David A. Priestman, Harry Y. Wu, Kohta Takahashi, Kazunori Yamaguchi, Luisella Sturiale, Domenico Garozzo, Frances M. Platt, Nathalie Lamarche-Vane, Carlos R. Morales, Taeko Miyagi, Alexey V. Pshezhetsky

FASEB JOURNAL 31 ( 8 ) 3467 - 3483 2017.8

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DOI： 10.1096/fj.201601299R

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Upregulation of sialidase NEU3 in head and neck squamous cell carcinoma associated with lymph node metastasis Reviewed

Kiyoto Shiga, Kohta Takahashi, Ikuro Sato, Kengo Kato, Shigeru Saijo, Setsuko Moriya, Masahiro Hosono, Taeko Miyagi

CANCER SCIENCE 106 ( 11 ) 1544 - 1553 2015.11

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DOI： 10.1111/cas.12810

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Sialidase NEU3 contributes neoplastic potential on colon cancer cells as a key modulator of gangliosides by regulating Wnt signaling. Reviewed

Takahashi K, Hosono M, Sato I, Hata K, Wada T, Yamaguchi K, Nitta K, Shima H, Miyagi T

International journal of cancer 137 ( 7 ) 1560 - 1573 2015.4

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DOI： 10.1002/ijc.29527

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Potentiation of epidermal growth factor-mediated oncogenic transformation by sialidase NEU3 leading to Src activation. Reviewed

Yamamoto K, Takahashi K, Shiozaki K, Yamaguchi K, Moriya S, Hosono M, Shima H, Miyagi T

PloS one 10 ( 3 ) e0120578 2015.3

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DOI： 10.1371/journal.pone.0120578

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Phosphatidic acid-mediated activation and translocation to the cell surface of sialidase NEU3, promoting signaling for cell migration. Reviewed

Shiozaki K, Takahashi K, Hosono M, Yamaguchi K, Hata K, Shiozaki M, Bassi R, Prinetti A, Sonnino S, Nitta K, Miyagi T

FASEB journal : official publication of the Federation of American Societies for Experimental Biology 29 ( 5 ) 2099 - 2111 2015.2

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DOI： 10.1096/fj.14-262543

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Plasma membrane-associated sialidase confers cancer initiation, promotion and progression. Reviewed

Miyagi T, Takahashi K, Shiozaki K, Yamaguchi K, Hosono M

Advances in experimental medicine and biology 842 139 - 145 2015.1

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DOI： 10.1007/978-3-319-11280-0_9

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Sialidase significance for cancer progression Reviewed

Taeko Miyagi, Kohta Takahashi, Keiko Hata, Kazuhiro Shiozaki, Kazunori Yamaguchi

GLYCOCONJUGATE JOURNAL 29 ( 8-9 ) 567 - 577 2012.12

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DOI： 10.1007/s10719-012-9394-1

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Sialidase NEU4 Hydrolyzes Polysialic Acids of Neural Cell Adhesion Molecules and Negatively Regulates Neurite Formation by Hippocampal Neurons Reviewed

Kohta Takahashi, Junya Mitoma, Masahiro Hosono, Kazuhiro Shiozaki, Chihiro Sato, Kazunori Yamaguchi, Ken Kitajima, Hideyoshi Higashi, Kazuo Nitta, Hiroshi Shima, Taeko Miyagi

JOURNAL OF BIOLOGICAL CHEMISTRY 287 ( 18 ) 14816 - 14826 2012.4

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DOI： 10.1074/jbc.M111.324186

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Plasma membrane-associated sialidase (NEU3) regulates progression of prostate cancer to androgen-independent growth through modulation of androgen receptor signaling Reviewed

S. Kawamura, I. Sato, T. Wada, K. Yamaguchi, Y. Li, D. Li, X. Zhao, S. Ueno, H. Aoki, T. Tochigi, M. Kuwahara, T. Kitamura, K. Takahashi, S. Moriya, T. Miyagi

CELL DEATH AND DIFFERENTIATION 19 ( 1 ) 170 - 179 2012.1

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DOI： 10.1038/cdd.2011.83

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Regulation of Sialyl Lewis Antigen Expression in Colon Cancer Cells by Sialidase NEU4 Reviewed

Kazuhiro Shiozaki, Kazunori Yamaguchi, Kohta Takahashi, Setsuko Moriya, Taeko Miyagi

JOURNAL OF BIOLOGICAL CHEMISTRY 286 ( 24 ) 21052 - 21061 2011.6

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DOI： 10.1074/jbc.M111.231191

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Total Synthesis of the Proposed Structure for Aromin and Its Structural Revision. International journal

Shunya Takahashi, Daisuke Satoh, Misato Hayashi, Kohta Takahashi, Kazunori Yamaguchi, Takemichi Nakamura, Hiroyuki Koshino

The Journal of organic chemistry 81 ( 22 ) 11222 - 11234 2016.11

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This paper describes the first total synthesis of the proposed structure for aromin, an annonaceous acetogenin possessing an unusual bis-THF ring system, and its 4S,7R-isomer. The key steps involve an oxidative cyclization of a couple of terminal-diene alcohols and an intermolecular metathesis of an alkenyl tetrahydrofuran with an enone carrying a tetrahydrofuranyl lactone. The spectral data of both samples did not match those of aromin. Re-examination of the NMR data using the CAST/CNMR Structure Elucidator and chemical derivations suggested that the real structure of aromin should be revised to be a tetrahydropyran acetogenin, montanacin D. Cytotoxicities in human solid tumor cell lines for synthetic samples were also evaluated.

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Increased sialidase activity in serum of cancer patients: Identification of sialidase and inhibitor activities in human serum. Reviewed

Hata K, Tochigi T, Sato I, Kawamura S, Shiozaki K, Wada T, Takahashi K, Moriya S, Yamaguchi K, Hosono M, Miyagi T

Cancer science 106 ( 4 ) 383 - 389 2015.3

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DOI： 10.1111/cas.12627

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Mammalian Sialidase Assays Reviewed

Taeko Miyagi, Kohta Takahashi, Kazuhiro Shiozaki, Kazunori Yamaguchi

Glycoscience: Biology and Medicine 1395 - 1402 2015.1

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Language：English Publishing type：Part of collection (book) Publisher：Springer Japan

DOI： 10.1007/978-4-431-54841-6_189

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Loss of Cellular Sialidases Does Not Affect the Sialylation Status of the Prion Protein but Increases the Amounts of Its Proteolytic Fragment C1. International journal

Elizaveta Katorcha, Nina Klimova, Natallia Makarava, Regina Savtchenko, Xuefang Pan, Ida Annunziata, Kohta Takahashi, Taeko Miyagi, Alexey V Pshezhetsky, Alessandra d'Azzo, Ilia V Baskakov

PloS one 10 ( 11 ) e0143218 2015

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The central molecular event underlying prion diseases involves conformational change of the cellular form of the prion protein (PrPC), which is a sialoglycoprotein, into the disease-associated, transmissible form denoted PrPSc. Recent studies revealed a correlation between the sialylation status of PrPSc and incubation time to disease and introduced a new hypothesis that progression of prion diseases could be controlled or reversed by altering the sialylation level of PrPC. Of the four known mammalian sialidases, the enzymes that cleave off sialic acid residues, only NEU1, NEU3 and NEU4 are expressed in the brain. To test whether cellular sialidases control the steady-state sialylation level of PrPC and to identify the putative sialidase responsible for desialylating PrPC, we analyzed brain-derived PrPC from knockout mice deficient in Neu1, Neu3, Neu4, or from Neu3/Neu4 double knockouts. Surprisingly, no differences in the sialylation of PrPC or its proteolytic product C1 were noticed in any of the knockout mice tested as compared to the age-matched controls. However, significantly higher amounts of the C1 fragment relative to full-length PrPC were detected in the brains of Neu1 knockout mice as compared to WT mice or to the other knockout mice. Additional experiments revealed that in neuroblastoma cell line the sialylation pattern of C1 could be changed by an inhibitor of sialylatransferases. In summary, this study suggests that targeting cellular sialidases is apparently not the correct strategy for altering the sialylation levels of PrPC, whereas modulating the activity of sialylatransferases might offer a more promising approach. Our findings also suggest that catabolism of PrPC involves its α-cleavage followed by desialylation of the resulting C1 fragments by NEU1 and consequent fast degradation of the desialylated products.

DOI： 10.1371/journal.pone.0143218

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Sialic acid-binding lectin (leczyme) induces apoptosis to malignant mesothelioma and exerts synergistic antitumor effects with TRAIL. Reviewed International journal

Takeo Tatsuta, Masahiro Hosono, Kohta Takahashi, Takashi Omoto, Yukiko Kariya, Shigeki Sugawara, Senitiroh Hakomori, Kazuo Nitta

International journal of oncology 44 ( 2 ) 377 - 84 2014.2

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Malignant mesothelioma is a highly aggressive tumor with poor prognosis. An effective drug for treatment of malignant mesothelioma is greatly needed. Sialic acid-binding lectin (SBL) isolated from oocytes of Rana catesbeiana is a multifunctional protein which has lectin activity, ribonuclease activity and antitumor activity, so it could be developed as a new type of anticancer drug. The validity of SBL for treatment of malignant mesothelioma was assessed using three malignant mesotheliomas and a non-malignant mesothlial cell line. Effectiveness of combinatorial treatment of SBL and tumor necrosis factor-related apoptosis inducing ligand (TRAIL) was also elucidated and characterized. SBL induced tumor-selective cytotoxicity that was attributed to induction of apoptosis. Combinatorial treatment of SBL and TRAIL showed synergistic apoptosis-inducing effect. Additional experiments revealed that Bid was the mediating molecule for the synergistic effect in SBL and TRAIL. These results suggested that SBL could be a promising candidate for the therapeutics for malignant mesothelioma. Furthermore, the combinatorial treatment of SBL and TRAIL could be an effective regimen against malignant mesothelioma.

DOI： 10.3892/ijo.2013.2192

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Leczyme: a new candidate drug for cancer therapy. Reviewed International journal

Takeo Tatsuta, Shigeki Sugawara, Kohta Takahashi, Yukiko Ogawa, Masahiro Hosono, Kazuo Nitta

BioMed research international 2014 421415 - 421415 2014

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Sialic acid-binding lectin (SBL), isolated from oocytes of Rana catesbeiana, is leczyme and has both lectin and ribonuclease (RNase) activities. A remarkable antitumor effect of SBL has also been reported. SBL agglutinates various kinds of tumor cells but not normal cells. SBL agglutination activity is not affected by mono- or oligosaccharides. However, SBL-induced agglutination and antitumor effects are inhibited by sialomucin but not asialomucin. In addition, SBL has very little effect on sialidase-treated cells. SBL causes cancer-selective induction of apoptosis by multiple signaling pathways, which target RNA. Synergistic antitumor effects with other molecules, such as tumor necrosis factor-related apoptosis ligand (TRAIL) and interferon- γ (IFN-γ), have been reported. Thus, SBL may be a novel candidate molecule for anticancer drug development. Sialoglycoconjugates on the tumor cell surface may be associated with lectin activity and antitumor effects of SBL. We review the properties of SBL, particularly its lectin, RNase, and antitumor activities, and comprehensively examine the potential application of SBL for clinical purposes.

DOI： 10.1155/2014/421415

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A leczyme which has both lectin and ribonuclease activity causes a cancer-selective induction of apoptosis Reviewed

Takeo Tatsuta, Shigeki Sugawara, Kohta Takahashi, Masahiro Hosono

INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE 34 S57 - S57 2014

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Cancer-selective induction of apoptosis by leczyme. Reviewed International journal

Takeo Tatsuta, Shigeki Sugawara, Kohta Takahashi, Yukiko Ogawa, Masahiro Hosono, Kazuo Nitta

Frontiers in oncology 4 139 - 139 2014

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Sialic acid-binding lectin (SBL) is a multi-functional protein that is isolated from oocytes of Rana catesbeiana. It has both lectin and ribonuclease (enzyme) properties, and therefore is called leczyme. We examined the anti-tumor effects of SBL and discovered that SBL has potential as a new type of anti-cancer drug. SBL causes a cancer-selective induction of apoptosis by multiple signaling pathways whereby RNA is its target. It is suggested that the mitochondrial pathway and endoplasmic reticulum stress-mediated pathway participate in SBL-induced signaling. The synergistic anti-tumor effects with other molecules, such as tumor necrosis factor-related apoptosis ligand and interferon γ, have been reported. In this study, we summarize the effects of SBL and focus on its cancer-selective apoptotic properties. In addition, we present a possible explanation for its cancer specificity.

DOI： 10.3389/fonc.2014.00139

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MRP1 Expressed on Burkitt's Lymphoma Cells was Depleted by Catfish Egg Lectin Through Gb3-Glycosphingolipid and Enhanced Cytotoxic Effect of Drugs Reviewed

Yuki Fujii, Shigeki Sugawara, Daisuke Araki, Tasuku Kawano, Takeo Tatsuta, Kohta Takahashi, Sarkar M. A. Kawsar, Ryo Matsumoto, Robert A. Kanaly, Hidetaro Yasumitsu, Yasuhiro Ozeki, Masahiro Hosono, Taeko Miyagi, Sen-itiroh Hakomori, Motoaki Takayanagi, Kazuo Nitta

PROTEIN JOURNAL 31 ( 1 ) 15 - 26 2012.1

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DOI： 10.1007/s10930-011-9369-2

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Altered Expression of Sialidases in Human Cancer Reviewed

Taeko Miyagi, K. Takahashi, S. Moriya, K. Hata, K. Yamamoto, T. Wada, K. Yamaguchi, K. Shiozaki

BIOCHEMICAL ROLES OF EUKARYOTIC CELL SURFACE MACROMOLECULES 749 257 - 267 2012

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DOI： 10.1007/978-1-4614-3381-1_17

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MISC

Regulation of cell adhesion by sialidase

64 ( 3 ) 273 - 278 2013.5

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Language：Japanese

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Other Link： http://search.jamas.or.jp/link/ui/2013227021

Presentations

The transport of lysosomal enzymes and the fusion of autophagosomes and lysosomes are accompanied by lipid scrambling in the trans-Golgi network

Kohta Takahashi, Nario Tomishige, Mitsuhiro Abe, Gašper Šolinc, James Rae, Toshiyuki Yamaji, Takefumi Uemura, Satoshi Waguri, Kentaro Hanada, Yasushi Sako, Gregor Anderluh, Robert G. Parton, Yves Mély, Catherine Tomasetto, Fabien Alpy, Toshihide Kobayashi

20th GERLI International Lipid Meeting 2025.11

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LDL-induced changes in focal adhesion dynamics promote cell migration

Kohta Takahashi, Lappalainen P., Ikonen E.

International Conference of the Bioscience of Lipids 2018.9

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ホスファチジルセリンとEvt-2および形質膜シアリダーゼNEU3の相互作用とその意義

高橋耕太, 山口壹範, 宮城妙子, 細野雅祐

第58回日本脂質生化学会 2016.6

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リサイクリングエンドソームに局在するEvt-2と形質膜シアリダーゼNEU3の相互作用とその意義

高橋耕太, 山口壹範, 細野雅祐, 宮城妙子

第88回日本生化学大会合同大会 2015.12

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Sialidase NEU3 defines invasive potential of human glioblastoma cells by regulating calpain-mediated proteolysis of focal adhesion proteins

Kohta Takahashis, Kazunori Yamaguchi, Setsuko Moriya, Yoji Yamashita, Ryuichi Katakura, Masahiro Hosono, Taeko Miyagi

7th Asian Community of Glycoscience and Glycotechnology Conference 2015.11

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頭頸部がんにおけるシアリダーゼNEU3の発現上昇とそのリンパ節転移への関与

高橋耕太, 志賀清人, 加藤健吾, 西条茂, 森谷節子, 細野雅祐, 宮城妙子

第34回日本糖質学会年会 2015.7

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形質膜シアリダーゼによるグリオーマ細胞接着・運動の制御

高橋耕太, 森谷節子, 細野雅祐, 宮城妙子

第8回東北糖鎖研究会 2014.10

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ガングリオシドシアリダーゼNEU3によるグリオーマ細胞の接着・運動能制御

高橋耕太, 森谷節子, 細野雅祐, 宮城妙子

第87回日本生化学回大会 2014.10

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シアリダーゼNEU3によるWntシグナルを介した大腸がん細胞の造腫瘍能制御機構

高橋耕太, 和田正, 細野雅祐, 山口壹範, 仁田一雄, 宮城妙子

第72回日本癌学会学術総会 2013.10

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形質膜シアリダーゼNEU3はEGFRシグナリング活性化を介してがん化能を更新する

山本晃司, 高橋耕太, 細野雅祐, 森谷節子, 和田正, 秦敬子, 仁田一雄, 宮城妙子

第86回日本生化学会大会 2013.9

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Plasma membrane-associated sialidase NEU3 confers neoplasmtic potentiall on colon cancer cells by regulating Wnt/b-catnin signaling

Kohta Takahashi, Masahiro Hosono, Keiko Hata, Tadashi Wada, Kazunori Yamaguchi, Kazuo Nitta, Taeko Miyagi

Glyco 22 2013.6

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シアリダーゼNEU3によるWntシグナルを介した大腸がん細胞の造腫瘍能制御

高橋耕太, 細野雅祐, 秦敬子, 和田正, 山口壹範, 仁田一雄, 宮城妙子

2013.5

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シアリダーゼNEU3は大腸がん細胞のWnt/beta-cateninシグナリングを制御する

高橋耕太, 細野雅祐, 秦敬子, 和田正, 山口壹範, 仁田一雄, 宮城妙子

第85回日本生化学会大会 2012.12

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シアリダーゼNEU3はWnt/beta-cateninシグナリングの調節を介してがん幹細胞性の維持に関与する

高橋耕太, 和田正, 細野雅祐, 山口壹範, 仁田一雄, 宮城妙子

第71回癌学会学術総会 2012.9

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ポリシアル酸を分解する哺乳類シアリダーゼの同定とその機能解析

高橋耕太, 三苫純也, 塩崎一弘, 山口壹範, 細野雅祐, 佐藤ちひろ, 北島健, 東秀好, 仁田一雄, 宮城妙子

包括脳ネットワーク夏のワークショップ 2012.7

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ポリシアル酸を分解する哺乳類シアリダーゼの同定と海馬神経における役割

高橋耕太, 三苫純也, 塩崎一弘, 山口壹範, 細野雅祐, 佐藤ちひろ, 北島健, 東秀好, 仁田一雄, 宮城妙子

第5回東北糖鎖研究会 2011.12

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Language：Japanese Presentation type：Poster presentation

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Plasma membrane-associated sialidase NEU3 regulates cancer stem cell properties

Kohta Takahashi, Tadashi Wada, Kazunori Yamaguchi, Masahiro Hosono, Kazuo Nitta, Taeko Miyagi

2011.11

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Language：Japanese Presentation type：Oral presentation (general)

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Sialidase NEU4 hydrolyzes polysialic acid of neural cell adhesion molecule and negatively regulates neurite formation of hippocampal neuron International conference

Kohta Takahashi, Junya Mitoma, Kazuhiro Shiozaki, Kazunori Yamaguchi, Chihiro Sato, Ken Kitajima, Hideyoshi Higashi, Taeko Miyagi

2011.9

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Sialidase NEU4 catalyzes degradation of polysialic acid and negatively regulates outgrowth of hippocampal neuron

Kohta Takahashi, Junya Mitoma, Kazuhiro Shiozaki, Kazunori Yamaguchi, Masahiro Hosono, Chihiro Sato, Ken Kitajima, Hideyoshi Higashi, Kazuo Nitta, Taeko Miyagi

2011.9

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Plasma membrane-associated sialidase NEU3 contributes to maintenance of cancer stem cell properties Invited International conference

Kohta Takahashi, Setsuko Moriya, Keiko Hata, Tadashi Wada, Koji Yamamoto, Taeko Miyagi

U.S.-JAPAN CONFERENCE: INFLAMMATION,DIABETES AND CANCER 2011.8

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がん幹細胞と形質膜シアリダーゼNEU3

高橋耕太, 山口壹範, 和田正, 秦敬子, 森谷節子, 山本晃司, 宮城妙子

第77回日本生化学会東北支部例会 2011.7

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Language：Japanese Presentation type：Oral presentation (general)

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シアリダーゼNeu4による神経接着分子NCAMポリシアル酸分解の制御

高橋耕太

第83回生化学会大会 2010

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A role of plasma membrane-associated sialidase(NEU3) in maintenance of cancer stem cell phenotype

Kohta Takahashi

2010

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シアリダーゼNEU4による神経接着分子NCAMポリシアル酸の制御

高橋耕太

第76回日本生化学会東北支部大会例会 2010

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シアリダーゼによるCD44の機能制御

高橋耕太

2009

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Awards

若手優秀発表賞第38回日本分子生物学会年会• 第88回日本生化学会大会合同大会

2015.12

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鈴木紘一メモリアル賞第85回日本生化学会大会

2012.12

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包括型脳科学研究推進支援ネットワーク夏のワークショップ若手優秀発表賞

2012.7

高橋耕太

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みちのく糖鎖ポスター賞

2011.12 東北糖鎖研究会

高橋耕太, 三苫純也, 塩崎一弘, 山口壹範, 細野雅祐, 佐藤ちひろ, 北島健, 東秀好, 仁田一雄, 宮城妙子

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Research Projects

生体膜スフィンゴミエリンの分布と動態の分子解析

2022

System name：早石修記念海外留学助成 500万円

Awarding organization：小野薬品工業

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細胞内コレステロール輸送と細胞接着・遊走の共役的制御機構の解明

Grant number：21K20623

2021.8 - 2023.3

System name：科学研究費助成事業

Research category：研究活動スタート支援

Awarding organization：日本学術振興会

高橋耕太

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Grant amount：\3120000 （ Direct Cost: \2400000 、 Indirect Cost：\720000 ）

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膜コレステロールを介したT細胞免疫の制御機構

2021

System name：研究助成 300 万円

Awarding organization：持田記念医学薬学振興財団

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膜コレステロールを介したT細胞免疫の制御機構

2021

System name：千葉大学学内研究推進事業２０２１年度研究費獲得促進プログラム 100 万円

Awarding organization：千葉大学

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Regulation of LDL-cholesterol recycling to the plasma membrane

2020

Awarding organization：The Magnus Ehrnrooth Foundation, Post-Doc Grant 14, 500 euro

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