2012 Ph.D. Medical Science,
Kyushu University, Fukuoka, Japan
2007 M.D. Medicine
Akita University, Akita, Japan
Department of Microbiology and Immunology
The Kanie lab is interested in elucidating the molecular mechanisms of the formation of the primary cilium.
The primary cilium is an organelle that extends from the cell surface whose central function is to serve as a signaling hub, sensing numerous extracellular signals via receptors (e.g. GPCRs) that are specifically accumulated on the ciliary portion of the cell membrane (Fig.1A). This organelle is fundamentally important for vertebrate development. It modulates survival and patterning of embryos via critical signaling pathways, such as Hedgehog signal transduction (Fig.1B). Structural and/or functional defects in primary cilia result in developmental disorders and syndromes ranging from neural tube, brain and skeletal malformations, to obesity, intellectual disability, retinal degeneration, and polycystic kidney disease, which all together are called ciliopathies (Fig.1B).
The Kanie lab strives to understand how this tiny organelle forms, using various state-of-the art techniques, including super resolution microscopies (STORM, 3D-SIM, and advanced live cell imaging), mass spectrometry, and sophisticated biochemistry.
The Kanie lab also strives to generate excellent next generation scientists. The lab is committed to provide sufficient education to perform accurate and reproducible research, conduct well-planned experiments with optimal controls, develop a broad range of knowledge, and discuss a wide scope of biological topics with joy.
The lab is currently accepting scientists from all career stages (e.g., undergraduate, graduate student, and postdoctoral fellows) as well as all disciplines. If you are interested in the lab, please contact directly to Dr. Tomoharu Kanie (Tomoharu-Kanie@ouhsc.edu)
University of Oklahoma Health Sciences Center
Department of Cell Biology
940 Stanton L. Young Blvd, BMSB111
Oklahoma City, OK 73104
Kanie T and Jackson PK. Connecting autoimmune disease to Bardet-Biedl syndrome and primary cilia. EMBO rep., 2021 Feb 3; 22(2):e52180.
Lee IT, Nakayama T, Wu CT, Goltsev Y, Jiang S, Gall PA, Liao CK, Shih LC, Schurch CM, McIlwain DR, Chu P, Borchard NA, Zarabanda D, Dholakia SS, Yang A, Kim D, Kanie T, Lin CD, Tsai MH, Phillips KM, Kim R, Overdevest JB, Tyler MA, Yan CH, Lin CF, Lin YT, Bau DT, Tsay GJ, Patel ZM, Tsou YA, Tai CJ, Yeh TH, Hwang PH, Nolan GP, Nayak JV, Jackson PK. Robust ACE2 protein expression localizes to the motile cilia of the respiratory tract epithelia and is not increased by ACE inhibitors or angiotensin receptor blockers, Nature communication. 2020; 11: 5453.
Kanie T and Jackson PK. Guanine Nucleotide Exchange Assay Using Fluorescent MANT-GDP. Bio Protoc., 2018 Apr 5; 8(7): e2795.
Kanie T, Abbott KL, Mooney NA, Plowed ED, Demeter J, and Jackson PK The CEP19-RABL2 GTPase complex binds IFT-B to initiate intraflagellar transport at the ciliary base. Developmental Cell, 2017 Jul 10; 42(1), 22-36.e12
Tateishi Y, Matsumoto A, Kanie T, Hara E, Nakayama K, Nakayama KI (2012). Development of mice without Cip/Kip CDK inhibitors. Biochem. Biophys. Res. Commun., 2012 Oct 19; 427, 285-292
Kanie T, Onoyama I, Matsumoto A, Yamada M, Nakatsumi H, Tateishi Y, Yamamura S, Tsunematsu R, Matsumoto M, Nakayama KI Genetic reevaluation of the role of F-box proteins in cyclin D1 degradation. Molecular and Cellular Biology, 2012 Feb; 32: 590-605
Matsumoto A, Takeishi S, Kanie T, Susaki E, Onoyama I, Tateishi Y, Nakayama K, Nakayama KI (2011) p57 is required for quiescence and maintenance of adult hematopoietic stem cells. Cell Stem Cell, 2011 Sep 2; 9: 262-71
Last modified 01/19/2022