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153 results on '"Tadokoro, Yuko"'

1. Targeting cis-regulatory elements of FOXO family is a novel therapeutic strategy for induction of leukemia cell differentiation

Author

Kurayoshi, Kenta, Takase, Yusuke, Ueno, Masaya, Ohta, Kumiko, Fuse, Kyoko, Ikeda, Shuji, Watanabe, Takayoshi, Nishida, Yuki, Horike, Shin-ichi, Hosomichi, Kazuyoshi, Ishikawa, Yuichi, Tadokoro, Yuko, Kobayashi, Masahiko, Kasahara, Atsuko, Jing, Yongwei, Shoulkamy, Mahmoud I., Meguro-Horike, Makiko, Kojima, Kensuke, Kiyoi, Hitoshi, Sugiyama, Hiroshi, Nagase, Hiroki, Tajima, Atsushi, and Hirao, Atsushi

Published
2023
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3. A Supramolecular Biosensor for Rapid and High-Throughput Quantification of a Disease-Associated Niacin Metabolite

Author

Ueno, Masaya, Sugiyama, Hiroki, Li, Feng, Nishimura, Tatsuya, Arakawa, Hiroshi, Chen, Xi, Cheng, Xiaoxiao, Takeuchi, Shinji, Takeshita, Yumie, Takamura, Toshinari, Miyagi, Sakae, Toyama, Tadashi, Soga, Tomoyoshi, Masuo, Yusuke, Kato, Yukio, Nakamura, Hiroyuki, Tsujiguchi, Hiromasa, Hara, Akinori, Tajima, Atsushi, Noguchi-Shinohara, Moeko, Ono, Kenjiro, Kurayoshi, Kenta, Kobayashi, Masahiko, Tadokoro, Yuko, Kasahara, Atsuko, Shoulkamy, Mahmoud I., Maeda, Katsuhiro, Ogoshi, Tomoki, and Hirao, Atsushi

Abstract

Metabolic abnormalities play a pivotal role in various pathological conditions, necessitating the quantification of specific metabolites for diagnosis. While mass spectrometry remains the primary method for metabolite measurement, its limited throughput underscores the need for biosensors capable of rapid detection. Previously, we reported that pillar[6]arene with 12 carboxylate groups (P6AC) forms host–guest complexes with 1-methylnicotinamide (1-MNA), which is produced in vivo by nicotinamide N-methyltransferase (NNMT). P6AC acts as a biosensor by measuring the fluorescence quenching caused by photoinduced electron transfer upon 1-MNA binding. However, the low sensitivity of P6AC makes it impractical for detecting 1-MNA in unpurified biological samples. In this study, we found that P6A with 12 sulfonate groups (P6AS) is a specific and potent supramolecular host for 1-MNA interactions even in biological samples. The 1-MNA binding affinity of P6AS in water was found to be (5.68 ± 1.02) × 106M–1, which is approximately 700-fold higher than that of P6AC. Moreover, the 1-MNA detection limit of P6AS was determined to be 2.84 × 10–7M, which is substantially lower than that of P6AC. Direct addition of P6AS to culture medium was sufficient to quantify 1-MNA produced by cancer cells. Furthermore, this sensor was able to specifically detect 1-MNA even in unpurified human urine. P6AS therefore enables rapid and high-throughput quantification of 1-MNA, and further improvement of our strategy will contribute to the establishment of high-throughput screening of NNMT inhibitors, diagnosis of liver diseases, and imaging of human cancer cells in vivo.

Published
2024
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6. Data from NKX2.2 Suppresses Self-Renewal of Glioma-Initiating Cells

Author

Muraguchi, Teruyuki, primary, Tanaka, Shingo, primary, Yamada, Daisuke, primary, Tamase, Akira, primary, Nakada, Mitsutoshi, primary, Nakamura, Hideo, primary, Hoshii, Takayuki, primary, Ooshio, Takako, primary, Tadokoro, Yuko, primary, Naka, Kazuhito, primary, Ino, Yasushi, primary, Todo, Tomoki, primary, Kuratsu, Jun-ichi, primary, Saya, Hideyuki, primary, Hamada, Jun-ichiro, primary, and Hirao, Atsushi, primary

Published
2023
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7. Supplementary Figures 1-5, Table 1 from NKX2.2 Suppresses Self-Renewal of Glioma-Initiating Cells

Author

Muraguchi, Teruyuki, primary, Tanaka, Shingo, primary, Yamada, Daisuke, primary, Tamase, Akira, primary, Nakada, Mitsutoshi, primary, Nakamura, Hideo, primary, Hoshii, Takayuki, primary, Ooshio, Takako, primary, Tadokoro, Yuko, primary, Naka, Kazuhito, primary, Ino, Yasushi, primary, Todo, Tomoki, primary, Kuratsu, Jun-ichi, primary, Saya, Hideyuki, primary, Hamada, Jun-ichiro, primary, and Hirao, Atsushi, primary

Published
2023
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9. RHEB is a potential therapeutic target in T cell acute lymphoblastic leukemia

Author

Pham, Loc Thi, primary, Peng, Hui, additional, Ueno, Masaya, additional, Kohno, Susumu, additional, Kasada, Atuso, additional, Hosomichi, Kazuyoshi, additional, Sato, Takehiro, additional, Kurayoshi, Kenta, additional, Kobayashi, Masahiko, additional, Tadokoro, Yuko, additional, Kasahara, Atsuko, additional, Shoulkamy, Mahmoud I., additional, Xiao, Bo, additional, Worley, Paul F., additional, Takahashi, Chiaki, additional, Tajima, Atsushi, additional, and Hirao, Atsushi, additional

Published
2022
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15. mTORC1 is essential for leukemia propagation but not stem cell self-renewal

Author

Hoshii, Takayuki, Tadokoro, Yuko, Naka, Kazuhito, Ooshio, Takako, Muraguchi, Teruyuki, Sugiyama, Naoyuki, Soga, Tomoyoshi, Araki, Kimi, Yamamura, Ken-ichi, and Hirao, Atsushi

Subjects
Leukemia -- Development and progression -- Care and treatment, Stem cells -- Genetic aspects -- Growth, Phosphorylation -- Research, Company growth, Health care industry
Abstract

Although dysregulation of mTOR complex 1 (mTORC1) promotes leukemogenesis, how mTORC1 affects estab-lished leukemia is unclear. We investigated the role of mTORC1 in mouse hematopoiesis using a mouse model of conditional deletion of Raptor, an essential component of mTORC1. Raptor deficiency impaired granulocyte and B cell development but did not alter survival or proliferation of hematopoietic progenitor cells. In a mouse model of acute myeloid leukemia (AML), Raptor deficiency significantly suppressed leukemia progression by causing apoptosis of differentiated, but not undifferentiated, leukemia cells. mTORC1 did not control cell cycle or cell growth in undifferentiated AML cells in vivo. Transplantation of Raptor-deficient undifferentiated AML cells in a limiting dilution revealed that mTORC1 is essential for leukemia initiation. Strikingly, a subset of AML cells with undifferentiated phenotypes survived long-term in the absence of mTORC1 activity. We further demonstrated that the reactivation of mTORC1 in those cells restored their leukemia-initiating capacity. Thus, AML cells lacking mTORC1 activity can self-renew as AML stem cells. Our findings provide mechanistic insight into how residual tumor cells circumvent anticancer therapies and drive tumor recurrence., Introduction mTOR is an evolutionarily conserved kinase in eukaryotes that plays a critical role in sensing and responding to factors such as nutrient availability, energy sufficiency, stress, hormones, and mitogens. [...]

Published
2012
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16. TGF-β-FOXO signalling maintains lleukaemiainitiating cells in chronic myeloid lleukaemia

Author

Naka, Kazuhito, Hoshii, Takayuki, Muraguchi, Teruyuki, Tadokoro, Yuko, Ooshio, Takako, Kondo, Yukio, Nakao, Shinji, Motoyama, Noboru, and Hirao, Atsushi

Subjects
Tyrosine -- Research, Myeloproliferative disorders -- Research, Chronic myeloid leukemia -- Research, Transforming growth factors -- Analysis, DNA binding proteins -- Analysis, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

Chronic myeloid lleukaemia (CML) is caused by a defined genetic abnormality that generates BCR-ABL, a constitutively active tyrosine kinase (1). It is widely believed that BCR-ABL activates Akt signalling that suppresses the forkhead O transcription factors (FOXO), supporting the proliferation or inhibiting the apoptosis of CML cells (2-4). Although the use of the tyrosine kinase inhibitor imatinib is a breakthrough for CML therapy, imatinib does not deplete the lleukaemia-initiating cells (LICs) that drive the recurrence of CML (5-8).Here, using a syngeneic transplantation system and a CML-like myeloproliferative disease mouse model, we show that Foxo3a has an essential role in the maintenance of CML LICs. We find that cells with nuclear localization of Foxo3a and decreased Akt phosphorylation are enriched in the LIC population. Serial transplantation of LICs generated from [Foxo3a.sup.+/+] and [Foxo3a.sup.-/-] mice shows that the ability of LICs to cause disease is significantly decreased by Foxo3a deficiency. Furthermore, we find that TGF-β is a critical regulator of Akt activation in LICs and controls Foxo3a localization. A combination of TGF-β inhibition, Foxo3a deficiency and imatinib treatment led to efficient depletion of CML in vivo. Furthermore, the treatment of human CML LICs with a TGF-β inhibitor impaired their colony-forming ability in vitro. Our results demonstrate a critical role for the TGF-β-FOXO pathway in the maintenance of LICs, and strengthen our understanding of the mechanisms that specifically maintain CML LICs in vivo., Although tyrosine kinase inhibitor (TKI) therapy of CML patients efficiently induces the death of lleukaemia cells (5-8), LICs in these patients can survive this therapy. To understand the molecular mechanisms [...]

Published
2010
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18. Pillar[6]arene acts as a biosensor for quantitative detection of a vitamin metabolite in crude biological samples

Author

00447682, Ueno, Masaya, Tomita, Takuya, Arakawa, Hiroshi, Kakuta, Takahiro, Yamagishi, Tada-aki, Terakawa, Jumpei, Daikoku, Takiko, Horike, Shin-ichi, Si, Sha, Kurayoshi, Kenta, Ito, Chiaki, Kasahara, Atsuko, Tadokoro, Yuko, Kobayashi, Masahiko, Fukuwatari, Tsutomu, Tamai, Ikumi, Hirao, Atsushi, Ogoshi, Tomoki, 00447682, Ueno, Masaya, Tomita, Takuya, Arakawa, Hiroshi, Kakuta, Takahiro, Yamagishi, Tada-aki, Terakawa, Jumpei, Daikoku, Takiko, Horike, Shin-ichi, Si, Sha, Kurayoshi, Kenta, Ito, Chiaki, Kasahara, Atsuko, Tadokoro, Yuko, Kobayashi, Masahiko, Fukuwatari, Tsutomu, Tamai, Ikumi, Hirao, Atsushi, and Ogoshi, Tomoki

Abstract

Metabolic syndrome is associated with obesity, hypertension, and dyslipidemia, and increased cardiovascular risk. Therefore, quick and accurate measurements of specific metabolites are critical for diagnosis; however, detection methods are limited. Here we describe the synthesis of pillar[n]arenes to target 1-methylnicotinamide (1-MNA), which is one metabolite of vitamin B3 (nicotinamide) produced by the cancer-associated nicotinamide N-methyltransferase (NNMT). We found that water-soluble pillar[5]arene (P5A) forms host–guest complexes with both 1-MNA and nicotinamide, and water-soluble pillar[6]arene (P6A) selectively binds to 1-MNA at the micromolar level. P6A can be used as a “turn-off sensor” by photoinduced electron transfer (detection limit is 4.38 × 10−6 M). In our cell-free reaction, P6A is used to quantitatively monitor the activity of NNMT. Moreover, studies using NNMT-deficient mice reveal that P6A exclusively binds to 1-MNA in crude urinary samples. Our findings demonstrate that P6A can be used as a biosensor to quantify 1-MNA in crude biological samples.

Published
2020

23. Poster Session

Author

Adachi, Eri, Ali, Mohamed A.E., Baba, Tomohisa, Domoto, Takahiro, Endo, Yoshio, Enkhtuya, Radnaa, Gunarta, I Ketut, Han, Tae-Su, Hayashi, Naoyuki, Hirose, Mayumi, Ishimura, Akihiko, Ju, Xiaoli, Kasada, Atsuo, Kitajima, Shunsuke, Kohno, Susumu, Kushiyama, Hiroko, Li, Zichen, Nishimura, Tatsunori, Ohta, Kumiko, Sakai, Katsuya, Sasaki, Nobunari, Sato, Tokiharu, Song, Yao, Tadokoro, Yuko, Yamada, Daisuke, Yoshida, Akiyo, Yoshimoto, Taisuke, and Zhao, Lu

Abstract

International Symposium on Tumor Biology in Kanazawa & Symposium on Drug Discoverry in Academics 2014 [DATE]: January 23(Thu)-24(Fri),2014, [Place]:Kanazawa Excel Hotel Tpkyu, Kanazawa, Japan, [Organizers]:Kanazawa Association of Tumor Biologists / Cancer Research Institute, Kanazawa University

Published
2014

24. Autophagy inhibition synergizes with calcium mobilization to achieve efficient therapy of malignant gliomas

Author

Vu, Ha Thi, primary, Kobayashi, Masahiko, additional, Hegazy, Ahmed M., additional, Tadokoro, Yuko, additional, Ueno, Masaya, additional, Kasahara, Atsuko, additional, Takase, Yusuke, additional, Nomura, Naho, additional, Peng, Hui, additional, Ito, Chiaki, additional, Ino, Yasushi, additional, Todo, Tomoki, additional, Nakada, Mitsutoshi, additional, and Hirao, Atsushi, additional

Published
2018
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25. Spred1 Safeguards Hematopoietic Homeostasis against Diet-Induced Systemic Stress

Author

Tadokoro, Yuko, primary, Hoshii, Takayuki, additional, Yamazaki, Satoshi, additional, Eto, Koji, additional, Ema, Hideo, additional, Kobayashi, Masahiko, additional, Ueno, Masaya, additional, Ohta, Kumiko, additional, Arai, Yuriko, additional, Hara, Eiji, additional, Harada, Kenichi, additional, Oshima, Masanobu, additional, Oshima, Hiroko, additional, Arai, Fumio, additional, Yoshimura, Akihiko, additional, Nakauchi, Hiromitsu, additional, and Hirao, Atsushi, additional

Published
2018
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26. Distinct roles of Rheb and Raptor in activating mTOR complex 1 for the self-renewal of hematopoietic stem cells

Author

Peng, Hui, primary, Kasada, Atsuo, additional, Ueno, Masaya, additional, Hoshii, Takayuki, additional, Tadokoro, Yuko, additional, Nomura, Naho, additional, Ito, Chiaki, additional, Takase, Yusuke, additional, Vu, Ha Thi, additional, Kobayashi, Masahiko, additional, Xiao, Bo, additional, Worley, Paul F., additional, and Hirao, Atsushi, additional

Published
2018
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27. Poster Session

Author

Adachi, Eri, Ali, Mohamed A.E., Baba, Tomohisa, Domoto, Takahiro, Endo, Yoshio, Enkhtuya, Radnaa, Gunarta, I Ketut, Han, Tae-Su, Hayashi, Naoyuki, Hirose, Mayumi, Ishimura, Akihiko, Ju, Xiaoli, Kasada, Atsuo, Kitajima, Shunsuke, Kohno, Susumu, Kushiyama, Hiroko, Li, Zichen, Nishimura, Tatsunori, Ohta, Kumiko, Sakai, Katsuya, Sasaki, Nobunari, Sato, Tokiharu, Song, Yao, Tadokoro, Yuko, Yamada, Daisuke, Yoshida, Akiyo, Yoshimoto, Taisuke, Zhao, Lu, Adachi, Eri, Ali, Mohamed A.E., Baba, Tomohisa, Domoto, Takahiro, Endo, Yoshio, Enkhtuya, Radnaa, Gunarta, I Ketut, Han, Tae-Su, Hayashi, Naoyuki, Hirose, Mayumi, Ishimura, Akihiko, Ju, Xiaoli, Kasada, Atsuo, Kitajima, Shunsuke, Kohno, Susumu, Kushiyama, Hiroko, Li, Zichen, Nishimura, Tatsunori, Ohta, Kumiko, Sakai, Katsuya, Sasaki, Nobunari, Sato, Tokiharu, Song, Yao, Tadokoro, Yuko, Yamada, Daisuke, Yoshida, Akiyo, Yoshimoto, Taisuke, and Zhao, Lu

Abstract

International Symposium on Tumor Biology in Kanazawa & Symposium on Drug Discoverry in Academics 2014 [DATE]: January 23(Thu)-24(Fri),2014, [Place]:Kanazawa Excel Hotel Tpkyu, Kanazawa, Japan, [Organizers]:Kanazawa Association of Tumor Biologists / Cancer Research Institute, Kanazawa University

Published
2017

28. Functional dissection of hematopoietic stem cell populations with a stemness-monitoring system based on NS-GFP transgene expression

Author

Ali, Mohamed A. E., primary, Fuse, Kyoko, additional, Tadokoro, Yuko, additional, Hoshii, Takayuki, additional, Ueno, Masaya, additional, Kobayashi, Masahiko, additional, Nomura, Naho, additional, Vu, Ha Thi, additional, Peng, Hui, additional, Hegazy, Ahmed M., additional, Masuko, Masayoshi, additional, Sone, Hirohito, additional, Arai, Fumio, additional, Tajima, Atsushi, additional, and Hirao, Atsushi, additional

Published
2017
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29. Therapeutic Strategy for Targeting Aggressive Malignant Gliomas by Disrupting Their Energy Balance

Author

Hegazy, Ahmed M., primary, Yamada, Daisuke, additional, Kobayashi, Masahiko, additional, Kohno, Susumu, additional, Ueno, Masaya, additional, Ali, Mohamed A.E., additional, Ohta, Kumiko, additional, Tadokoro, Yuko, additional, Ino, Yasushi, additional, Todo, Tomoki, additional, Soga, Tomoyoshi, additional, Takahashi, Chiaki, additional, and Hirao, Atsushi, additional

Published
2016
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32. Strong therapeutic potential of γ-secretase inhibitor MRK003 for CD44-high and CD133-low glioblastoma initiating cells

Author

Tanaka, Shingo, primary, Nakada, Mitsutoshi, additional, Yamada, Daisuke, additional, Nakano, Ichiro, additional, Todo, Tomoki, additional, Ino, Yasushi, additional, Hoshii, Takayuki, additional, Tadokoro, Yuko, additional, Ohta, Kumiko, additional, Ali, Mohamed A. E., additional, Hayashi, Yutaka, additional, Hamada, Jun-ichiro, additional, and Hirao, Atsushi, additional

Published
2014
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34. Association of a murine leukaemia stem cell gene signature based on nucleostemin promoter activity with prognosis of acute myeloid leukaemia in patients

Author

Ali, Mohamed A.E., primary, Naka, Kazuhito, additional, Yoshida, Akiyo, additional, Fuse, Kyoko, additional, Kasada, Atsuo, additional, Hoshii, Takayuki, additional, Tadokoro, Yuko, additional, Ueno, Masaya, additional, Ohta, Kumiko, additional, Kobayashi, Masahiko, additional, Takahashi, Chiaki, additional, and Hirao, Atsushi, additional

Published
2014
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35. Structural and functional changes of sulfated glycosaminoglycans in Xenopus laevis during embryogenesis

Author

1000070240017, Yamada, Shuhei, Onishi, Masako, Fujinawa, Reiko, Tadokoro, Yuko, Okabayashi, Koji, Asashima, Makoto, 1000060154449, Sugahara, Kazuyuki, 1000070240017, Yamada, Shuhei, Onishi, Masako, Fujinawa, Reiko, Tadokoro, Yuko, Okabayashi, Koji, Asashima, Makoto, 1000060154449, and Sugahara, Kazuyuki

Abstract

Xenopus laevis is an excellent animal for analyzing early vertebrate development. Various effects of glycosaminoglycans (GAGs) on growth factor-related cellular events during embryogenesis have been demonstrated in Xenopus. To elucidate the relationship between alterations in fine structure and changes in the specificity of growth factor-binding during Xenopus development, heparan sulfate (HS) and chondroitin/dermatan sulfate (CS/DS) chains were isolated at four different embryonic stages and their structure and growth factor-binding capacities were compared. The total amounts of both HS and CS/DS chains decreased from the pre-midblastula transition to the gastrula stage, but increased exponentially during the following developmental stages. The length of HS chains was not significantly affected by development, whereas that of CS/DS chains increased with development. The disaccharide composition of GAGs in embryos also changed during development. The degree of sulfation of the HS chains gradually decreased with development. The predominant sulfation position in the CS/DS chains shifted from C4 to C6 of GalNAc during embryogenesis. Growth factor-binding experiments using a BIAcore system demonstrated that GAGs bound growth factors including fibroblast growth factors-1, and -2, midkine, and pleiotrophin, with comparable affinities. These affinities significantly varied during development, although the correlation between the structural alterations of GAGs and the change in the ability to bind growth factors remains to be clarified. Expression of saccharide sequences, which specifically interact with a growth factor, might be regulated during development.

Published
2009

37. mTORC1 Inactivation Prevents and Eradicates Acute Lymphoblastic T-Cell Leukemia

Author

Hoshii, Takayuki, primary, Kasada, Atsuo, additional, Hatakeyama, Tomoki, additional, Ohtani, Masashi, additional, Tadokoro, Yuko, additional, Naka, Kazuhito, additional, Ikenoue, Tsuneo, additional, Ikawa, Tomokatsu, additional, Kawamoto, Hiroshi, additional, Araki, Kimi, additional, Yamamura, Ken-ichi, additional, Iwama, Atsushi, additional, Matsuda, Satoshi, additional, and Hirao, Atsushi, additional

Published
2013
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39. Nucleostemin in Injury-Induced Liver Regeneration

Author

Shugo, Haruhiko, primary, Ooshio, Takako, additional, Naito, Masako, additional, Naka, Kazuhito, additional, Hoshii, Takayuki, additional, Tadokoro, Yuko, additional, Muraguchi, Teruyuki, additional, Tamase, Akira, additional, Uema, Noriyuki, additional, Yamashita, Taro, additional, Nakamoto, Yasunari, additional, Suda, Toshio, additional, Kaneko, Shuichi, additional, and Hirao, Atsushi, additional

Published
2012
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41. Hair Follicle Stem Cells Provide a Functional Niche for Melanocyte Stem Cells

Author

Tanimura, Shintaro, primary, Tadokoro, Yuko, additional, Inomata, Ken, additional, Binh, Nguyen Thanh, additional, Nishie, Wataru, additional, Yamazaki, Satoshi, additional, Nakauchi, Hiromitsu, additional, Tanaka, Yoshio, additional, McMillan, James R., additional, Sawamura, Daisuke, additional, Yancey, Kim, additional, Shimizu, Hiroshi, additional, and Nishimura, Emi K., additional

Published
2011
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42. NKX2.2 Suppresses Self-Renewal of Glioma-Initiating Cells

Author

Muraguchi, Teruyuki, primary, Tanaka, Shingo, additional, Yamada, Daisuke, additional, Tamase, Akira, additional, Nakada, Mitsutoshi, additional, Nakamura, Hideo, additional, Hoshii, Takayuki, additional, Ooshio, Takako, additional, Tadokoro, Yuko, additional, Naka, Kazuhito, additional, Ino, Yasushi, additional, Todo, Tomoki, additional, Kuratsu, Jun-ichi, additional, Saya, Hideyuki, additional, Hamada, Jun-ichiro, additional, and Hirao, Atsushi, additional

Published
2011
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50. Two mouse piwi-related genes: miwi and mili

Author

Kuramochi-Miyagawa, Satomi, primary, Kimura, Tohru, additional, Yomogida, Kentaro, additional, Kuroiwa, Asato, additional, Tadokoro, Yuko, additional, Fujita, Yukiko, additional, Sato, Masatake, additional, Matsuda, Yoichi, additional, and Nakano, Toru, additional

Published
2001
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