International Journal of Biological Engineering

International Journal of Biological Engineering is an international peer-reviewed multidisciplinary journal publishing original scientific research in all fields of biological pharmacy. Original research work that contributes significantly to further the scientific knowledge in biological pharmacy will be appreciated.

Robert Raike

Editorial Board Member of International Journal of Biological Engineering

Post-doctoral Fellow, Emory University School of Medicine Departments of Pharmacology and Neurology, USA

Research Areas

Neuroscience - Studying The Neurogenetic Mechanisms of Movement Disorders In Mice.


1998-2004Ph.DUniversity of Minnesota, Mpls, MN, A potential Mouse Model of Episodic Ataxia Type 2, Adviser: Christopher M. Gomez, MD, PhD
1994-1998BARutgers University, New Brunswick, NJ, Adviser: George C. Wagner, PhD


2008-presentPostdoctoral Research Fellow, Pharmacology and Neurology Departments, Emory University, Atlanta, GA
2004-2008Postdoctoral Research Fellow, Neurology Department, Johns Hopkins University, Baltimore, MD
1998-2004Graduate Research Assistant, Neurology Department, University of Minnesota, Minneapolis, MN
1996-1998Undergraduate Research Assistant, Psychology Department, Rutgers University, New Brunswick, NJ
1997-1998Junior Laboratory Technician, QualTech Labs, Inc., Ocean, NJ

Publications: Conferences/Workshops/Symposiums/Journals/Books

[1]  Restituito, S, Thompson, RM, Eliet, J, Raike, RS, Riedl, M, Charnet, P and Gomez, CM. (2000), The polyglutamine expansion in spinocerebellar ataxia type 6 causes a beta subunit-specific, enhanced activation of P/Q-type calcium channels in Xenopus oocytes. Journal of Neuroscience.20(17): 6394-403.
[2]  Subramony, SH, Schott, K, Raike, R, Callahan, J, Langford, L, Christova, P, Anderson, JH and Gomez, CM. (2003) Novel CACNA1A mutation causes febrile episodic ataxia with interictal ocular motor and posture abnormalities. Annals of Neurology. 4(6): 725-31.
[3]  Weisz, CJC, Raike, RS, Soria-Jasso, LE and Hess, EJ. (2005) Potassium channel blockers inhibit the triggers of attacks in the calcium channel mouse mutant tottering. Journal of Neuroscience.24(16): 4141-45.
[4]  Raike, RS, Jinnah, HA and Hess, EJ. (2005) Animal Models of Generalized Dystonia. NeuroRx.2(3): 504-12.
[5]  Raike, RS, Kordasiewicz, HB, Thompson, RM and Gomez, CM. (2007) Dominant-negative suppression of Cav2.1 currents by alpha1 2.1 truncations requires the conserved interaction domain for beta subunits. Molecular and Cellular Neuroscience. 34(2): 168-177.
[6]  Raike, RS, Jinnah, HA and Hess, EJ. Kainic Acid Model of Dystonia. (2010) In: Kompoliti K, and Verhagen Metman L (eds.) Encyclopedia of Movement Disorders, vol. 2, pp. 101-102 Oxford: Academic Press.
[7]  Todorov, B, Hoebeek, FE, Haasdijk ED, Frants, RR, Raike, RS, Hess, EJ, de Zeeuw, CI and van den Maagdenberg, AMJM. (In Press) Purkinje cell-specific ablation of CaV2.1 channels is sufficient to cause cerebellar ataxia in mice. Cerebellum.
[8]  Raike, RS, Pizoli, CE, Weisz, CJC, van den Maagdenberg, AMJM, Jinnah, HA and Hess, EJ. (In Revision) A small region of cerebellar dysfunction can drive focal dystonia.
[9]  Raike, RS, Weisz, CJ, Terzi, MC, van den Maagdenberg, AMJM, Jinnah, HA and Hess, EJ. (In Review) Mechanisms underlying the triggers of episodic neurological dysfunction in mouse models of CaV2.1 channelopathy.