Naoto Hoshi

Associate Professor, Pharmacology
School of Medicine

Joint Appointment, Physiology and Biophysics
School of Medicine

M.D., Kanazawa University School of Medicine, Kanazawa, Japan., 1990


Ph.D., Kanazawa University Graduate School of Medicine, Kanazawa, Japan, 1999

Phone: (949) 824-0969 (ofc.), 824-0970 (lab)
Fax: (949) 824-4855
Email: nhoshi@uci.edu

University of California, Irvine
Department of Pharmacology
360 Med Surge 2
Mail Code: 4625
Irvine, CA 92697

picture of Naoto  Hoshi

Research
Interests
Physiological role and regulation of the M-channel, molecular biology, electrophysiology and live cell FRET imaging
   
URLs Pharmacology Home Page
   
Dr. Hoshi's lab
   
See below for selected publications or click here for additional piblication listings available via PubMed
   
Academic
Distinctions
2000, Juzen alumni award for young scientist
2004, Young scientist award from Uehara memorial foundation
2007, Juzen Medical award
   
Research
Abstract
The Hoshi laboratory studies physiological role and regulation of the M-channel, a sub-threshold ion channel that regulates neuronal excitability. We have demonstrated that the AKAP150 macromolecular complex integrates multiple signals to regulate this channel. Genetic removal of AKAP150 resulted in tolerance to seizure induction. One of our goals is to control pathological neuronal activity through the M-channel modulators. The laboratory is now focused on understanding the physiological and pathological role of M-current suppression in learning and memory as well as in seizures. The laboratory utilizes molecular biology, electrophysiology, live cell FRET imaging and behavioral neuroscience.
   
Publications Hoshi, N., Zhang, J. S., Omaki, M., Takeuchi, T., Yokoyama, S., Wanaverbecq, N., Langeberg, L. K., Yoneda, Y., Scott, J. D., Brown, D. A., and Higashida, H. (2003). AKAP150 signaling complex promotes suppression of the M-current by muscarinic agonists. Nat. Neurosci. 6, 564-571.

Hoshi, N., Langeberg, L. K., and Scott, J. D. (2005). Distinct enzyme combinations in AKAP signalling complexes permit functional diversity. Nat. Cell Biol. 7, 1066-1073.
Above article was selected as “News & Views” in Nat. Cell Biol. and “This week in signal transduction” at Science’s STKE.

Bauman, A. L., Soughayer, J., Nguyen, B. T., Willoughby, D., Carnegie, G., K., Wong, W., Hoshi, N., Langeberg, L. K., Cooper, D.M.F., Dessauer, C. W. and Scott, J. D. (2006). Dynamic regulation of cAMP synthesis through anchored PKA- adenylyl cyclase V/VI complexes. Mol. Cell 23, 925-931.

Gold, M., G., Lygren, B., Dolurno, P., Hoshi, N., McConnachie, G., Taskén, K., Carlson, C. R., Scott, J. D., and Barford D. (2006) Molecular Basis of AKAP Specificity for PKA Regulatory Subunits. Mol. Cell 24, 383-395.

Saneyoshi, T., Wayman, G., Fortin, D., Davare, M., Hoshi, N., Nozaki, N., Natsume, T., Soderling, T. R. (2008) Activity-Dependent Synaptogenesis: Regulation by a CaM-Kinase Kinase/CaM-Kinase I/betaPIX Signaling Complex. Neuron 57, 94-107.

Tunquist, B. J.*, Hoshi, N*, Guire, E. S., Zhang, F, Mullendorff, K, Langeberg, L. K., Raber, J & Scott, J. D. (2008) Loss of AKAP150 perturbs distinct neuronal processes in mice. Proc. Natl. Acad. Sci. U S A 105, 12557-11262
* co-first authors

Hoshi, N, Langeberg, L. K., Gould, C. M., Newton, A. C., and Scott, J. D. (2010) Interaction with AKAP79 modifies the cellular pharmacology of PKC. Mol. Cell 37, 541-550.
Above article was selected for “preview” in Mol. Cell and as an “exceptional” article by Faculty of 1000 Biology.

Smith, I. M., Hoshi, N. (2011) ATP competitive Protein kinase C inhibitors demonstrate distinct state-dependent inhibition. Plos One 6, e26338.

Kosenko, A., Kang, S., Smith, I. M., Greene, D. Langeberg, L. K., Scott, J. D., & Hoshi, N (2012) Coordinated signal integration at the M-type potassium channel upon muscarinic stimulation EMBO J. 31, 3147-3156.
Above article is selected as a “recommended” article by Faculty of 1000 Biology.

Greene, D., Kang, S., Kosenko, A and Hoshi, N. (2012) Adrenergic regulation of HCN4 channel requires protein association with beta 2 adrenergic receptor J. Biol. Chem. 287, 23690-23697.

Nguyen, H. M., Miyazaki, H., Hoshi, N., Smith, B. J., Nukina, N., Goldin, A. L., and Chandy, K. G. (2012) Modulation of voltage-gated K+ channels by the sodium channel ß1 subunit PNAS. 109, 18577-18582 .
Above article is selected as a “recommended” article by Faculty of 1000 Biology.

Kosenko, A. and Hoshi, N. (2013) A Change in Configuration of the Calmodulin-KCNQ Channel Complex Underlies Ca2+-Dependent Modulation of KCNQ Channel Activity Plos One 8, e82290.

Kang, S., Xu, M., Cooper, E. C. and Hoshi, N. (2014) Channel anchored protein kinase CK2 and protein phosphatase 1 reciprocally regulate KCNQ2-containing M-channels via phosphorylation of calmodulin J. BIol. Chem. 289, 11536-11544.

Kay, HY, Greene, DL, Kang, S, Kosenko, A, Hoshi, N. (2015) M-current preservation contributes to anticonvulsant effects of valproic acid. J. Clin. Invest. 125, 3904-3914.

Jiang, L, Kosenko, A, Yu, C, Huang, L, Li, X, Hoshi, N. (2015) Activation of m1 muscarinic acetylcholine receptor induces surface transport of KCNQ channel via CRMP-2 mediated pathway. J. Cell Sci. 128,4235-4245.
   
Grant National Institute of Neurological Disorders and Storke (NINDS) R01 NS067288, 01/15/10-11/30/15, $1,076,250 direct costs, Regulations and function of the M-channel (Role: P.I.).
   
Professional
Societies
Society for Neuroscience (USA)
Japanese Neurochemistry Society (council member, 2000-presen
Japanese Biochemistry Society
   
Graduate Programs Pharmacological Sciences

Interdepartmental Neuroscience Program

Medicinal Chemistry and Pharmacology

   
   
Link to this profile http://www.faculty.uci.edu/profile.cfm?faculty_id=5556
   
Last updated 12/05/2016