Tomoshige Kino, MD, PhD

Principal Investigator – Associate Level
Laboratory of Molecular and Genomic Endocrinology

Email: tkino (@)
Phone: +974 4003 7566
Google Scholar

  • Biography

    Dr. Kino is a member of the US Endocrine Society and the Japan Endocrine Society. He is also a councilor of the Japan Endocrine Society. He previously worked and/or is currently working as a board member for prestigious scientific Journals, including Endocrinology, Molecular Endocrinology, Molecular and Cellular Endocrinology and Frontiers in Genomic Endocrinology. Prior to joining Sidra Dr. Kino is a head of the Unit of Molecular Hormone Action in the Program in Reproductive and Adult Endocrinology, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, USA. Dr. Kino received his bachelor degree in Medical Science in the Chiba University Medical School, and received the medical license from the Ministry of Health, Labor and Welfare of Japan. He subsequently completed residency in Internal Medicine in this University Hospital. He obtained board certification on General Internal Medicine from the Japanese Society of Internal Medicine and on Endocrinology and Metabolism from the Japan Endocrine Society. He received his doctor degree in Medical Science from the Chiba University Medical School, Chiba, Japan.
  • Our Research and Approach

    The research group investigates pathologic causes and subsequent development of rational treatment for target common diseases, such as abnormal pregnancy, problems in oocyte/embryonic development, childhood growth retardation, obesity, diabetes mellitus and adrenal cancer/begin adenomas. We hypothesize that abnormal regulation on relevant key genes through genome alteration in regulatory elements (e.g., promoters and enhancers) and/or regulatory non-coding (nc) RNA genes play major roles based on reported evidence. Using cutting-edge methodologies and bioinformatical analyses, we reveal comprehensive genome-wide changes in transcriptomes (both mRNAs and ncRNAs), epigenome and genome variants, and their cause-consequence relationship observed/functional in these pathologic conditions.
  • Lab Members

    Alexandra K. Marr, PhD
    Staff Scientist
    Email: akmarr (@)

    Zohreh T. Calderone, PhD
    Staff Scientist
    E-mail: zcalderone (@ )


  • Mackeh R., Marr A. K., Fadda A. and Kino T. C2H2-type zinc finger proteins: Evolutionally old and new interaction partners of the nuclear hormone receptors. Nucl Recept Signal (2018) 15: 1, 2018.
  • Kino T. GR-regulating serine/threonine kinases: new physiologic and pathologic implications. Trends Endocrinol Metab (2018) 29: 260.
  • Mackeh R., Marr A.K., Dargham S., Syed N., Fakhro K. and Kino T. ­­Single Nucleotide Variations of the Human Nuclear Hormone Receptor Genes in 60,000 Individuals. J Endocr Soc (2018) 2: 77-90.
  • Fadda A., Najeeb, S., Mackeh R., Papadopoulou A., Suzuki S., Jithesh P.V. and Kino T. Genome-wide regulatory roles of the C2H2-type zinc finger protein ZNF764 on the glucocorticoid receptor. Sci Rep (2017) 7: 41598.
  • Habib T., Sadoun A., Nader N., Suzuki S., Liu W., Jithesh P.V. and Kino T. AKT1 has dual actions on the glucocorticoid receptor by cooperating with 14-3-3. Mol Cell Endocrinol (2017) 439: 431-443.
  • Hurt D.E., Suzuki S., Mayama T., Charmandari E. and Kino T. Structural analysis on the pathologic mutant glucocorticoid receptor ligand-binding domains. Mol Endocrinol (2016) 30: 173.
  • Papadopoulou A., Siamatras T., Delgado-Morales R., Amin N.D., Shukla S., Zheng Y.L., Pant H.C., Almeida O.F.X. and Kino T. Acute and chronic stress differentially regulate cyclin-dependent kinase 5 activity in mouse brain: Implication to local glucocorticoid actions and major depression Trans Psychiatry (2015) 5, e578.
  • Kino T., Hurt D.E., Ichijo T., Nader N. and Chrousos G.P.Non-coding RNA repressor for the glucocorticoid receptor. Sci Signal (2010) 3: ra8.
  • Kino T., Takatori H., Manoli I., Wang Y-H., Tiulpakov A., Blackman M.R., Su Y.A., Chrousos G.P., DeCherney A.H. and Segars J.H. Brx mediates the response of lymphocytes to osmotic stress through activation of NFAT5.Sci Signal (2009) 2: ra5.
  • Kino T., Gragerov A., Kopp J.B., Stauber R.H., Pavlakis G.N., and Chrousos G.P. Human immunodeficiency virus type-1 Vpr is a glucocorticoid receptor coactivator. J Exp Med (1999) 189: 51-61.