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Fabrication and Characterization of Ultrathin-ring Electrodes for Pseudo-steady-state Amperometric Detection.

Analytical sciences : the international journal of the Japan Society for Analytical Chemistry

Kitazumi Y, Hamamoto K, Noda T, Shirai O, Kano K.
PMID: 26165281
Anal Sci. 2015;31(7):603-7. doi: 10.2116/analsci.31.603.

The fabrication of ultrathin-ring electrodes with a diameter of 2 mm and a thickness of 100 nm is established. The ultrathin-ring electrodes provide a large density of pseudo-steady-state currents, and realize pseudo-steady-state amperometry under quiescent conditions without a Faraday...

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Kitazumi Y, Hamamoto K, Noda T, et al. Fabrication and Characterization of Ultrathin-ring Electrodes for Pseudo-steady-state Amperometric Detection. Anal Sci. 2015;31(7):603-7doi: 10.2116/analsci.31.603.
Kitazumi, Y., Hamamoto, K., Noda, T., Shirai, O., & Kano, K. (2015). Fabrication and Characterization of Ultrathin-ring Electrodes for Pseudo-steady-state Amperometric Detection. Analytical sciences : the international journal of the Japan Society for Analytical Chemistry, 31(7), 603-7. https://doi.org/10.2116/analsci.31.603
Kitazumi, Yuki, et al. "Fabrication and Characterization of Ultrathin-ring Electrodes for Pseudo-steady-state Amperometric Detection." Analytical sciences : the international journal of the Japan Society for Analytical Chemistry vol. 31,7 (2015): 603-7. doi: https://doi.org/10.2116/analsci.31.603
Kitazumi Y, Hamamoto K, Noda T, Shirai O, Kano K. Fabrication and Characterization of Ultrathin-ring Electrodes for Pseudo-steady-state Amperometric Detection. Anal Sci. 2015;31(7):603-7. doi: 10.2116/analsci.31.603. PMID: 26165281.
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Assessment of Brown Adipocyte Thermogenic Function by High-throughput Respirometry.

Bio-protocol

Mahdaviani K, Benador I, Shirihai O.
PMID: 29770346
Bio Protoc. 2015 Nov 05;5(21). doi: 10.21769/BioProtoc.1641.

Brown adipose tissue (BAT) has the unique ability to dramatically increase mitochondrial uncoupled fuel oxidation for thermogenesis in response to adrenergic stimulation. A key parameter in assessing brown adipocyte thermogenic capacity is mitochondrial uncoupling as determined by respiration. Measuring...

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Mahdaviani K, Benador I, Shirihai O. Assessment of Brown Adipocyte Thermogenic Function by High-throughput Respirometry. Bio Protoc. 2015;5(21)doi: 10.21769/BioProtoc.1641.
Mahdaviani, K., Benador, I., & Shirihai, O. (2015). Assessment of Brown Adipocyte Thermogenic Function by High-throughput Respirometry. Bio-protocol, 5(21), . https://doi.org/10.21769/BioProtoc.1641
Mahdaviani, Kiana, et al. "Assessment of Brown Adipocyte Thermogenic Function by High-throughput Respirometry." Bio-protocol vol. 5,21 (2015). doi: https://doi.org/10.21769/BioProtoc.1641
Mahdaviani K, Benador I, Shirihai O. Assessment of Brown Adipocyte Thermogenic Function by High-throughput Respirometry. Bio Protoc. 2015 Nov 05;5(21). doi: 10.21769/BioProtoc.1641. PMID: 29770346; PMCID: PMC5951411.
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A precision therapeutic strategy for hexokinase 1-null, hexokinase 2-positive cancers.

Cancer & metabolism

Xu S, Catapang A, Braas D, Stiles L, Doh HM, Lee JT, Graeber TG, Damoiseaux R, Shirihai O, Herschman HR.
PMID: 29988332
Cancer Metab. 2018 Jun 28;6:7. doi: 10.1186/s40170-018-0181-8. eCollection 2018.

BACKGROUND: Precision medicine therapies require identification of unique molecular cancer characteristics. Hexokinase (HK) activity has been proposed as a therapeutic target; however, different hexokinase isoforms have not been well characterized as alternative targets. While HK2 is highly expressed in...

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Xu S, Catapang A, Braas D, et al. A precision therapeutic strategy for hexokinase 1-null, hexokinase 2-positive cancers. Cancer Metab. 2018;6:7doi: 10.1186/s40170-018-0181-8.
Xu, S., Catapang, A., Braas, D., Stiles, L., Doh, H. M., Lee, J. T., Graeber, T. G., Damoiseaux, R., Shirihai, O., & Herschman, H. R. (2018). A precision therapeutic strategy for hexokinase 1-null, hexokinase 2-positive cancers. Cancer & metabolism, 67. https://doi.org/10.1186/s40170-018-0181-8
Xu, Shili, et al. "A precision therapeutic strategy for hexokinase 1-null, hexokinase 2-positive cancers." Cancer & metabolism vol. 6 (2018): 7. doi: https://doi.org/10.1186/s40170-018-0181-8
Xu S, Catapang A, Braas D, Stiles L, Doh HM, Lee JT, Graeber TG, Damoiseaux R, Shirihai O, Herschman HR. A precision therapeutic strategy for hexokinase 1-null, hexokinase 2-positive cancers. Cancer Metab. 2018 Jun 28;6:7. doi: 10.1186/s40170-018-0181-8. eCollection 2018. PMID: 29988332; PMCID: PMC6022704.
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Deletion of ABCB10 in beta-cells protects from high-fat diet induced insulin resistance.

Molecular metabolism

Shum M, Segawa M, Gharakhanian R, Viñuela A, Wortham M, Baghdasarian S, Wolf DM, Sereda SB, Nocito L, Stiles L, Zhou Z, Gutierrez V, Sander M, Shirihai OS, Liesa M.
PMID: 34823065
Mol Metab. 2021 Nov 22;101403. doi: 10.1016/j.molmet.2021.101403. Epub 2021 Nov 22.

AIMS: The contribution of beta-cell dysfunction to type 2 diabetes (T2D) is not restricted to insulinopenia in the late stages of the disease. Elevated fasting insulinemia in normoglycemic humans is a major factor predicting the onset of insulin resistance...

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Shum M, Segawa M, Gharakhanian R, et al. Deletion of ABCB10 in beta-cells protects from high-fat diet induced insulin resistance. Mol Metab. 2021;101403doi: 10.1016/j.molmet.2021.101403.
Shum, M., Segawa, M., Gharakhanian, R., Viñuela, A., Wortham, M., Baghdasarian, S., Wolf, D. M., Sereda, S. B., Nocito, L., Stiles, L., Zhou, Z., Gutierrez, V., Sander, M., Shirihai, O. S., & Liesa, M. (2021). Deletion of ABCB10 in beta-cells protects from high-fat diet induced insulin resistance. Molecular metabolism, 101403. https://doi.org/10.1016/j.molmet.2021.101403
Shum, Michael, et al. "Deletion of ABCB10 in beta-cells protects from high-fat diet induced insulin resistance." Molecular metabolism vol. (2021): 101403. doi: https://doi.org/10.1016/j.molmet.2021.101403
Shum M, Segawa M, Gharakhanian R, Viñuela A, Wortham M, Baghdasarian S, Wolf DM, Sereda SB, Nocito L, Stiles L, Zhou Z, Gutierrez V, Sander M, Shirihai OS, Liesa M. Deletion of ABCB10 in beta-cells protects from high-fat diet induced insulin resistance. Mol Metab. 2021 Nov 22;101403. doi: 10.1016/j.molmet.2021.101403. Epub 2021 Nov 22. PMID: 34823065.
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ATP-consuming futile cycles as energy dissipating mechanisms to counteract obesity.

Reviews in endocrine & metabolic disorders

Brownstein AJ, Veliova M, Acin-Perez R, Liesa M, Shirihai OS.
PMID: 34741717
Rev Endocr Metab Disord. 2021 Nov 06; doi: 10.1007/s11154-021-09690-w. Epub 2021 Nov 06.

Obesity results from an imbalance in energy homeostasis, whereby excessive energy intake exceeds caloric expenditure. Energy can be dissipated out of an organism by producing heat (thermogenesis), explaining the long-standing interest in exploiting thermogenic processes to counteract obesity. Mitochondrial...

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Brownstein AJ, Veliova M, Acin-Perez R, et al. ATP-consuming futile cycles as energy dissipating mechanisms to counteract obesity. Rev Endocr Metab Disord. 2021;doi: 10.1007/s11154-021-09690-w.
Brownstein, A. J., Veliova, M., Acin-Perez, R., Liesa, M., & Shirihai, O. S. (2021). ATP-consuming futile cycles as energy dissipating mechanisms to counteract obesity. Reviews in endocrine & metabolic disorders, . https://doi.org/10.1007/s11154-021-09690-w
Brownstein, Alexandra J, et al. "ATP-consuming futile cycles as energy dissipating mechanisms to counteract obesity." Reviews in endocrine & metabolic disorders vol. (2021). doi: https://doi.org/10.1007/s11154-021-09690-w
Brownstein AJ, Veliova M, Acin-Perez R, Liesa M, Shirihai OS. ATP-consuming futile cycles as energy dissipating mechanisms to counteract obesity. Rev Endocr Metab Disord. 2021 Nov 06; doi: 10.1007/s11154-021-09690-w. Epub 2021 Nov 06. PMID: 34741717.
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Mitochondrial oxidative function in NAFLD: Friend or foe?.

Molecular metabolism

Shum M, Ngo J, Shirihai OS, Liesa M.
PMID: 33276146
Mol Metab. 2021 Aug;50:101134. doi: 10.1016/j.molmet.2020.101134. Epub 2020 Dec 01.

BACKGROUND: Mitochondrial oxidative function plays a key role in the development of non-alcoholic fatty liver disease (NAFLD) and insulin resistance (IR). Recent studies reported that fatty liver might not be a result of decreased mitochondrial fat oxidation caused by...

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Shum M, Ngo J, Shirihai OS, et al. Mitochondrial oxidative function in NAFLD: Friend or foe?. Mol Metab. 2020;50:101134doi: 10.1016/j.molmet.2020.101134.
Shum, M., Ngo, J., Shirihai, O. S., & Liesa, M. (2021). Mitochondrial oxidative function in NAFLD: Friend or foe?. Molecular metabolism, 50101134. https://doi.org/10.1016/j.molmet.2020.101134
Shum, Michael, et al. "Mitochondrial oxidative function in NAFLD: Friend or foe?." Molecular metabolism vol. 50 (2021): 101134. doi: https://doi.org/10.1016/j.molmet.2020.101134
Shum M, Ngo J, Shirihai OS, Liesa M. Mitochondrial oxidative function in NAFLD: Friend or foe?. Mol Metab. 2021 Aug;50:101134. doi: 10.1016/j.molmet.2020.101134. Epub 2020 Dec 01. PMID: 33276146; PMCID: PMC8324685.
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Mitochondrial oxidative function in NAFLD: Friend or foe?.

Molecular metabolism

Shum M, Ngo J, Shirihai OS, Liesa M.
PMID: 33276146
Mol Metab. 2021 Aug;50:101134. doi: 10.1016/j.molmet.2020.101134. Epub 2020 Dec 01.

BACKGROUND: Mitochondrial oxidative function plays a key role in the development of non-alcoholic fatty liver disease (NAFLD) and insulin resistance (IR). Recent studies reported that fatty liver might not be a result of decreased mitochondrial fat oxidation caused by...

Cite
Shum M, Ngo J, Shirihai OS, et al. Mitochondrial oxidative function in NAFLD: Friend or foe?. Mol Metab. 2020;50:101134doi: 10.1016/j.molmet.2020.101134.
Shum, M., Ngo, J., Shirihai, O. S., & Liesa, M. (2021). Mitochondrial oxidative function in NAFLD: Friend or foe?. Molecular metabolism, 50101134. https://doi.org/10.1016/j.molmet.2020.101134
Shum, Michael, et al. "Mitochondrial oxidative function in NAFLD: Friend or foe?." Molecular metabolism vol. 50 (2021): 101134. doi: https://doi.org/10.1016/j.molmet.2020.101134
Shum M, Ngo J, Shirihai OS, Liesa M. Mitochondrial oxidative function in NAFLD: Friend or foe?. Mol Metab. 2021 Aug;50:101134. doi: 10.1016/j.molmet.2020.101134. Epub 2020 Dec 01. PMID: 33276146; PMCID: PMC8324685.
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Author Correction: LKB1 loss links serine metabolism to DNA methylation and tumorigenesis.

Nature

Kottakis F, Nicolay BN, Roumane A, Karnik R, Gu H, Nagle JM, Boukhali M, Hayward MC, Li YY, Chen T, Liesa M, Hammerman PS, Wong KK, Hayes DN, Shirihai OS, Dyson NJ, Haas W, Meissner A, Bardeesy N.
PMID: 31695192
Nature. 2019 Nov;575(7783):E5. doi: 10.1038/s41586-019-1696-z.

An Amendment to this paper has been published and can be accessed via a link at the top of the paper.

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Kottakis F, Nicolay BN, Roumane A, et al. Author Correction: LKB1 loss links serine metabolism to DNA methylation and tumorigenesis. Nature. 2019;575(7783):E5doi: 10.1038/s41586-019-1696-z.
Kottakis, F., Nicolay, B. N., Roumane, A., Karnik, R., Gu, H., Nagle, J. M., Boukhali, M., Hayward, M. C., Li, Y. Y., Chen, T., Liesa, M., Hammerman, P. S., Wong, K. K., Hayes, D. N., Shirihai, O. S., Dyson, N. J., Haas, W., Meissner, A., & Bardeesy, N. (2019). Author Correction: LKB1 loss links serine metabolism to DNA methylation and tumorigenesis. Nature, 575(7783), E5. https://doi.org/10.1038/s41586-019-1696-z
Kottakis, Filippos, et al. "Author Correction: LKB1 loss links serine metabolism to DNA methylation and tumorigenesis." Nature vol. 575,7783 (2019): E5. doi: https://doi.org/10.1038/s41586-019-1696-z
Kottakis F, Nicolay BN, Roumane A, Karnik R, Gu H, Nagle JM, Boukhali M, Hayward MC, Li YY, Chen T, Liesa M, Hammerman PS, Wong KK, Hayes DN, Shirihai OS, Dyson NJ, Haas W, Meissner A, Bardeesy N. Author Correction: LKB1 loss links serine metabolism to DNA methylation and tumorigenesis. Nature. 2019 Nov;575(7783):E5. doi: 10.1038/s41586-019-1696-z. PMID: 31695192.
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Publisher Correction: IAPP toxicity activates HIF1α/PFKFB3 signaling delaying β-cell loss at the expense of β-cell function.

Nature communications

Montemurro C, Nomoto H, Pei L, Parekh VS, Vongbunyong KE, Vadrevu S, Gurlo T, Butler AE, Subramaniam R, Ritou E, Shirihai OS, Satin LS, Butler PC, Tudzarova S.
PMID: 31366929
Nat Commun. 2019 Jul 31;10(1):3507. doi: 10.1038/s41467-019-11516-y.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

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Montemurro C, Nomoto H, Pei L, et al. Publisher Correction: IAPP toxicity activates HIF1α/PFKFB3 signaling delaying β-cell loss at the expense of β-cell function. Nat Commun. 2019;10(1):3507doi: 10.1038/s41467-019-11516-y.
Montemurro, C., Nomoto, H., Pei, L., Parekh, V. S., Vongbunyong, K. E., Vadrevu, S., Gurlo, T., Butler, A. E., Subramaniam, R., Ritou, E., Shirihai, O. S., Satin, L. S., Butler, P. C., & Tudzarova, S. (2019). Publisher Correction: IAPP toxicity activates HIF1α/PFKFB3 signaling delaying β-cell loss at the expense of β-cell function. Nature communications, 10(1), 3507. https://doi.org/10.1038/s41467-019-11516-y
Montemurro, Chiara, et al. "Publisher Correction: IAPP toxicity activates HIF1α/PFKFB3 signaling delaying β-cell loss at the expense of β-cell function." Nature communications vol. 10,1 (2019): 3507. doi: https://doi.org/10.1038/s41467-019-11516-y
Montemurro C, Nomoto H, Pei L, Parekh VS, Vongbunyong KE, Vadrevu S, Gurlo T, Butler AE, Subramaniam R, Ritou E, Shirihai OS, Satin LS, Butler PC, Tudzarova S. Publisher Correction: IAPP toxicity activates HIF1α/PFKFB3 signaling delaying β-cell loss at the expense of β-cell function. Nat Commun. 2019 Jul 31;10(1):3507. doi: 10.1038/s41467-019-11516-y. PMID: 31366929; PMCID: PMC6668385.
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Cellular Star Trek: A laser-based shuttle transfers mitochondria into cells.

Molecular metabolism

Las G, Shirihai O.
PMID: 27688994
Mol Metab. 2016 Jun 09;5(10):805-806. doi: 10.1016/j.molmet.2016.06.001. eCollection 2016 Oct.

No abstract available.

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Las G, Shirihai O. Cellular Star Trek: A laser-based shuttle transfers mitochondria into cells. Mol Metab. 2016;5(10):805-806doi: 10.1016/j.molmet.2016.06.001.
Las, G., & Shirihai, O. (2016). Cellular Star Trek: A laser-based shuttle transfers mitochondria into cells. Molecular metabolism, 5(10), 805-806. https://doi.org/10.1016/j.molmet.2016.06.001
Las, Guy, and Shirihai, Orian. "Cellular Star Trek: A laser-based shuttle transfers mitochondria into cells." Molecular metabolism vol. 5,10 (2016): 805-806. doi: https://doi.org/10.1016/j.molmet.2016.06.001
Las G, Shirihai O. Cellular Star Trek: A laser-based shuttle transfers mitochondria into cells. Mol Metab. 2016 Jun 09;5(10):805-806. doi: 10.1016/j.molmet.2016.06.001. eCollection 2016 Oct. PMID: 27688994; PMCID: PMC5034483.
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Fabrication of a Phosphate Ion Selective Electrode Based on Modified Molybdenum Metal.

Analytical sciences : the international journal of the Japan Society for Analytical Chemistry

Xu K, Kitazumi Y, Kano K, Sasaki T, Shirai O.
PMID: 31527318
Anal Sci. 2020 Feb 10;36(2):201-206. doi: 10.2116/analsci.19P296. Epub 2019 Sep 13.

A phosphate ion-selective electrode using molybdenum metal was constructed. The modified molybdenum electrode responded to HPO

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Xu K, Kitazumi Y, Kano K, et al. Fabrication of a Phosphate Ion Selective Electrode Based on Modified Molybdenum Metal. Anal Sci. 2019;36(2):201-206doi: 10.2116/analsci.19P296.
Xu, K., Kitazumi, Y., Kano, K., Sasaki, T., & Shirai, O. (2020). Fabrication of a Phosphate Ion Selective Electrode Based on Modified Molybdenum Metal. Analytical sciences : the international journal of the Japan Society for Analytical Chemistry, 36(2), 201-206. https://doi.org/10.2116/analsci.19P296
Xu, Kebin, et al. "Fabrication of a Phosphate Ion Selective Electrode Based on Modified Molybdenum Metal." Analytical sciences : the international journal of the Japan Society for Analytical Chemistry vol. 36,2 (2020): 201-206. doi: https://doi.org/10.2116/analsci.19P296
Xu K, Kitazumi Y, Kano K, Sasaki T, Shirai O. Fabrication of a Phosphate Ion Selective Electrode Based on Modified Molybdenum Metal. Anal Sci. 2020 Feb 10;36(2):201-206. doi: 10.2116/analsci.19P296. Epub 2019 Sep 13. PMID: 31527318.
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Comprehensive understanding of multiple actions of anticancer drug tamoxifen in isolated mitochondria.

Biochimica et biophysica acta. Bioenergetics

Unten Y, Murai M, Koshitaka T, Kitao K, Shirai O, Masuya T, Miyoshi H.
PMID: 34896079
Biochim Biophys Acta Bioenerg. 2021 Dec 08;1863(2):148520. doi: 10.1016/j.bbabio.2021.148520. Epub 2021 Dec 08.

Tamoxifen has been widely used in the treatment of estrogen receptor (ER)-positive breast cancer, whereas it also exhibits ER-independent anticancer effects in various cancer cell types. As one of the convincing mechanisms underlying the ER-independent effects, induction of apoptosis...

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Unten Y, Murai M, Koshitaka T, et al. Comprehensive understanding of multiple actions of anticancer drug tamoxifen in isolated mitochondria. Biochim Biophys Acta Bioenerg. 2021;1863(2):148520doi: 10.1016/j.bbabio.2021.148520.
Unten, Y., Murai, M., Koshitaka, T., Kitao, K., Shirai, O., Masuya, T., & Miyoshi, H. (2021). Comprehensive understanding of multiple actions of anticancer drug tamoxifen in isolated mitochondria. Biochimica et biophysica acta. Bioenergetics, 1863(2), 148520. https://doi.org/10.1016/j.bbabio.2021.148520
Unten, Yufu, et al. "Comprehensive understanding of multiple actions of anticancer drug tamoxifen in isolated mitochondria." Biochimica et biophysica acta. Bioenergetics vol. 1863,2 (2021): 148520. doi: https://doi.org/10.1016/j.bbabio.2021.148520
Unten Y, Murai M, Koshitaka T, Kitao K, Shirai O, Masuya T, Miyoshi H. Comprehensive understanding of multiple actions of anticancer drug tamoxifen in isolated mitochondria. Biochim Biophys Acta Bioenerg. 2021 Dec 08;1863(2):148520. doi: 10.1016/j.bbabio.2021.148520. Epub 2021 Dec 08. PMID: 34896079.
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Showing 1 to 12 of 49 entries