Hiroki Ueda

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Doctor of Philosophy
Hiroki Ueda
Fukuoka, Japan
Alma materUniversity of Tokyo
Scientific career
InstitutionsUniversity of Tokyo
RIKEN Quantitative Biology Center
Kyoto University
Osaka University
Tohoku University

Hiroki R. Ueda (上田 泰己, Ueda Hiroki) is a Japanese Professor of biology at the University of Tokyo and the RIKEN Quantitative Biology Center. He is known for his studies on the circadian clock.


Dr. Hiroki R. Ueda was born in Fukuoka, Japan in 1975. He graduated from the Faculty of Medicine, the University of Tokyo in 2000, and obtained his Ph.D in 2004 from the same university.[1] He was appointed as a team leader in RIKEN Center for Developmental Biology (CDB) from 2003 and promoted to be a project leader at RIKEN CDB in 2009,[2] and to be a group director at RIKEN Quantitative Biology Center (QBiC) in 2011. He became a professor of Graduate School of Medicine, the University of Tokyo in 2013.[3] He is currently appointed as a team leader in RIKEN Center for Biosystems Dynamics Research (BDR), an affiliate professor in Graduate School of Information Science and Technology and an principle investigator in IRCN (International Research Center for Neurointelligence) in the University of Tokyo, an invited professor in Osaka University, and a visiting professor in Tokushima universities.


He has an expertise in systems biology and focus on chronobiology by investigating mammalian circadian clocks and sleep/wake cycles. He determined a basic structure of a transcriptional circuit of mammalian circadian clocks and identified multiple delayed negative feedback motifs.[4][5][6][7] He also focused on long-standing and unsolved questions in chronobiology and found that a singularity behavior (i.e. temporal stopping of circadian clocks) is caused by desynchronization of multiple cellular circadian oscillators,[8] and that temperature-insensitive biochemical reactions underlie temperature compensation of mammalian circadian clocks.[9][10] He also invented molecular-timetable methods to detect the circadian time of the body by measuring a snapshot information of circadian clocks.[11][12][13][14] For sleep/wake cycles, he found that Ca2+ and CaMKII-dependent hyperpolarization pathways underlie sleep homeostasis,[15][16][17][18][19] and that muscarinic receptors, M1 and M3, as essential genes for REM sleep.[20] To accelerate these studies, he also invented whole-brain and whole-body clearing and imaging methods called CUBIC,[21][22][23][24][25][26][27][28][29] as well as the next-generation mammalian genetics[30] such as Triple-CRISPR,[16] ES-mice[31][32] and SSS methods[16] for one-step production and analysis of KO and KI mice without crossing.[24][26]


He received awards, including Tokyo Techno Forum 21, Gold Medal (Tokyo Techno Forum 21, 2005), Young Investigator Awards (MEXT, 2006) and IBM Science Award (IBM, 2009), a Young Investigator Promotion Awards (Japanese Society for Chronobiology, 2007). He also received Tsukahara Award (Brain Science Foundation, 2012), Japan Innovator Awards (Nikkei Business Publications Inc. 2004), Teiichi Yamazaki Award (Foundation for Promotion of Material Science and Technology of Japan, 2015), Innovator of the Year (2017) and The Ichimura Prize in Science for Excellent Achievement (Ichimura Foundation for New Technology, 2018).


  1. ^ "Hiroki Ueda". Neuroinformatics. Retrieved 2017-10-28.
  2. ^ "Hiroki Ueda". The Node. The Company of Biologists. Retrieved 2017-10-28.
  3. ^ "CSCB Seminar Series: "Towards Organisms-level Systems and Synthetic Biology." by Dr. Hiroki Ueda". Retrieved 2017-10-28.
  4. ^ Ueda; et al. (2002-08-01). "A transcription factor response element for gene expression during circadian night". Nature. 418 (6897): 534–539. doi:10.1038/nature00906. ISSN 0028-0836. PMID 12152080.
  5. ^ Ueda; et al. (February 2005). "System-level identification of transcriptional circuits underlying mammalian circadian clocks". Nature Genetics. 37 (2): 187–192. doi:10.1038/ng1504. ISSN 1061-4036. PMID 15665827.
  6. ^ Ukai-Tadenuma; et al. (October 2008). "Proof-by-synthesis of the transcriptional logic of mammalian circadian clocks". Nature Cell Biology. 10 (10): 1154–1163. doi:10.1038/ncb1775. ISSN 1476-4679. PMID 18806789.
  7. ^ Ukai-Tadenuma; et al. (2011-01-21). "Delay in feedback repression by cryptochrome 1 is required for circadian clock function". Cell. 144 (2): 268–281. doi:10.1016/j.cell.2010.12.019. ISSN 1097-4172. PMID 21236481.
  8. ^ Ukai; et al. (November 2007). "Melanopsin-dependent photo-perturbation reveals desynchronization underlying the singularity of mammalian circadian clocks". Nature Cell Biology. 9 (11): 1327–1334. doi:10.1038/ncb1653. ISSN 1465-7392. PMID 17952058.
  9. ^ Isojima; et al. (2009-09-15). "CKIepsilon/delta-dependent phosphorylation is a temperature-insensitive, period-determining process in the mammalian circadian clock". Proceedings of the National Academy of Sciences of the United States of America. 106 (37): 15744–15749. doi:10.1073/pnas.0908733106. ISSN 1091-6490. PMC 2736905. PMID 19805222.
  10. ^ Shinohara; et al. (2017-09-07). "Temperature-Sensitive Substrate and Product Binding Underlie Temperature-Compensated Phosphorylation in the Clock". Molecular Cell. 67 (5): 783–798.e20. doi:10.1016/j.molcel.2017.08.009. ISSN 1097-4164. PMID 28886336.
  11. ^ Ueda; et al. (2004-08-03). "Molecular-timetable methods for detection of body time and rhythm disorders from single-time-point genome-wide expression profiles". Proceedings of the National Academy of Sciences of the United States of America. 101 (31): 11227–11232. doi:10.1073/pnas.0401882101. ISSN 0027-8424. PMC 509173. PMID 15273285.
  12. ^ Minami; et al. (2009-06-16). "Measurement of internal body time by blood metabolomics". Proceedings of the National Academy of Sciences of the United States of America. 106 (24): 9890–9895. doi:10.1073/pnas.0900617106. ISSN 1091-6490. PMC 2689311. PMID 19487679.
  13. ^ Kasukawa; et al. (2012-09-11). "Human blood metabolite timetable indicates internal body time". Proceedings of the National Academy of Sciences of the United States of America. 109 (37): 15036–15041. doi:10.1073/pnas.1207768109. ISSN 1091-6490. PMC 3443163. PMID 22927403.
  14. ^ Narumi; et al. (2016-06-14). "Mass spectrometry-based absolute quantification reveals rhythmic variation of mouse circadian clock proteins". Proceedings of the National Academy of Sciences of the United States of America. 113 (24): E3461–3467. doi:10.1073/pnas.1603799113. ISSN 1091-6490. PMC 4914154. PMID 27247408.
  15. ^ Tatsuki; et al. (2016-04-06). "Involvement of Ca(2+)-Dependent Hyperpolarization in Sleep Duration in Mammals". Neuron. 90 (1): 70–85. doi:10.1016/j.neuron.2016.02.032. ISSN 1097-4199. PMID 26996081.
  16. ^ a b c Sunagawa; et al. (2016-01-26). "Mammalian Reverse Genetics without Crossing Reveals Nr3a as a Short-Sleeper Gene". Cell Reports. 14 (3): 662–677. doi:10.1016/j.celrep.2015.12.052. ISSN 2211-1247. PMID 26774482.
  17. ^ Tatsuki; et al. (May 2017). "Ca2+-dependent hyperpolarization hypothesis for mammalian sleep". Neuroscience Research. 118: 48–55. doi:10.1016/j.neures.2017.03.012. ISSN 1872-8111. PMID 28433628.
  18. ^ Ode; et al. (June 2017). "Fast and slow Ca2+-dependent hyperpolarization mechanisms connect membrane potential and sleep homeostasis". Current Opinion in Neurobiology. 44: 212–221. doi:10.1016/j.conb.2017.05.007. ISSN 1873-6882. PMID 28575719.
  19. ^ Shi; et al. (January 2018). "Ca2+ -Dependent Hyperpolarization Pathways in Sleep Homeostasis and Mental Disorders". BioEssays: News and Reviews in Molecular, Cellular and Developmental Biology. 40 (1): 1700105. doi:10.1002/bies.201700105. ISSN 1521-1878. PMID 29205420.
  20. ^ Niwa; et al. (2018-08-28). "Muscarinic Acetylcholine Receptors Chrm1 and Chrm3 Are Essential for REM Sleep". Cell Reports. 24 (9): 2231–2247.e7. doi:10.1016/j.celrep.2018.07.082. ISSN 2211-1247. PMID 30157420.
  21. ^ Susaki; et al. (2014-04-24). "Whole-brain imaging with single-cell resolution using chemical cocktails and computational analysis". Cell. 157 (3): 726–739. doi:10.1016/j.cell.2014.03.042. ISSN 1097-4172. PMID 24746791.
  22. ^ Tainaka; et al. (2014-11-06). "Whole-body imaging with single-cell resolution by tissue decolorization". Cell. 159 (4): 911–924. doi:10.1016/j.cell.2014.10.034. ISSN 1097-4172. PMID 25417165.
  23. ^ Susaki; et al. (November 2015). "Advanced CUBIC protocols for whole-brain and whole-body clearing and imaging". Nature Protocols. 10 (11): 1709–1727. doi:10.1038/nprot.2015.085. ISSN 1750-2799. PMID 26448360.
  24. ^ a b Susaki; et al. (2016-01-21). "Whole-body and Whole-Organ Clearing and Imaging Techniques with Single-Cell Resolution: Toward Organism-Level Systems Biology in Mammals". Cell Chemical Biology. 23 (1): 137–157. doi:10.1016/j.chembiol.2015.11.009. ISSN 2451-9448. PMID 26933741.
  25. ^ Tainaka; et al. (2016-10-06). "Chemical Principles in Tissue Clearing and Staining Protocols for Whole-Body Cell Profiling". Annual Review of Cell and Developmental Biology. 32: 713–741. doi:10.1146/annurev-cellbio-111315-125001. ISSN 1530-8995. PMID 27298088.
  26. ^ a b Kubota; et al. (2017-07-05). "Whole-Body Profiling of Cancer Metastasis with Single-Cell Resolution". Cell Reports. 20 (1): 236–250. doi:10.1016/j.celrep.2017.06.010. ISSN 2211-1247. PMID 28683317.
  27. ^ Nojima; et al. (2017-08-24). "CUBIC pathology: three-dimensional imaging for pathological diagnosis". Scientific Reports. 7 (1): 9269. doi:10.1038/s41598-017-09117-0. ISSN 2045-2322. PMC 5571108. PMID 28839164.
  28. ^ Murakami; et al. (April 2018). "A three-dimensional single-cell-resolution whole-brain atlas using CUBIC-X expansion microscopy and tissue clearing". Nature Neuroscience. 21 (4): 625–637. doi:10.1038/s41593-018-0109-1. ISSN 1546-1726. PMID 29507408.
  29. ^ Tainaka; et al. (2018-08-21). "Chemical Landscape for Tissue Clearing Based on Hydrophilic Reagents". Cell Reports. 24 (8): 2196–2210.e9. doi:10.1016/j.celrep.2018.07.056. ISSN 2211-1247. PMID 30134179.
  30. ^ Susaki; et al. (2017). "Next-generation mammalian genetics toward organism-level systems biology". NPJ Systems Biology and Applications. 3: 15. doi:10.1038/s41540-017-0015-2. ISSN 2056-7189. PMC 5459797. PMID 28649442.
  31. ^ Ode; et al. (2017-01-05). "Knockout-Rescue Embryonic Stem Cell-Derived Mouse Reveals Circadian-Period Control by Quality and Quantity of CRY1". Molecular Cell. 65 (1): 176–190. doi:10.1016/j.molcel.2016.11.022. ISSN 1097-4164. PMID 28017587.
  32. ^ Ukai; et al. (December 2017). "Production of knock-in mice in a single generation from embryonic stem cells". Nature Protocols. 12 (12): 2513–2530. doi:10.1038/nprot.2017.110. ISSN 1750-2799. PMID 29189772.

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