1991 B. S. (with Honors), State University of New York
at Binghamton.
(Biochemistry, Psychology).
1996 Ph. D., Pharmacology & Toxicology, Medical College of Virginia,
Virginia Commonwealth University, Richmond, VA.
1996-1998 Postdoctoral Fellow, Vollum Institute, Oregon Health Sciences
University, Portland, OR. (Laboratory of Dr. Neil V. Marrion).
1998-2001 Postdoctoral Fellow, HHMI, Vollum Institute, Oregon Health
Sciences University, Portland, OR. (Laboratory of Dr. John D. Scott).
Research Interest:
Neuronal electrical activity, which underlies brain
function, is generated from the movement of ions across the plasma membrane
through specialized proteins called ion channels. Channels are characterized
by the stimuli that elicit their opening and/or closing (gating) as
well as by their biophysical, pharmacological, and molecular properties
in addition to their anatomical distribution at both the system and
subcellular level. Moreover, ion channel activity is subject to regulation
by a variety of biochemical signals. This combination of properties
provides a rich repertoire of electrical activity endowing neurons with
the ability to receive, store, process, and transfer information thereby
allowing organisms to respond appropriately to both fixed and changing
stimuli as well as to adapt their behavior in response to experience.
My research ultimately seeks to address how the functional properties
of neurons arise from their complement of channels, receptors, and signaling
systems? To address this question my research employs a combination
of electrophysiological, biochemical and molecular techniques.
Ongoing research in my lab is focused on understanding the mechanisms
whereby kinases and phosphatases are directed towards receptors for
the excitatory neurotransmitter glutamate and voltage-gated calcium
channels to allow modulation of channel activity. Modulation of the
phosphorylation state and function of glutamate receptor channels and
calcium channels by co-localized signaling complexes are likely to play
important roles in controlling excitatory synaptic transmission and
neuronal excitability. Understanding basic mechanisms that serve as
control elements for synaptic transmission and neuronal excitability
may provide novel therapeutic targets for treating neurological disorders.
Selected Publications:
Liang, Y. and Tavalin, S. J. (2007) Auxiliary β subunits differentially
determine PKA utilization of distinct regulatory sites on CaV1.3 L-type
Ca2+ channels. Channels 1:102-112. (click here for pdf version)
Gardner, L. A., Tavalin, S. J., Goehring, A. S., Scott, J. D., and
Bahouth, S. W. (2006) AKAP79-mediated targeting of the cyclic AMP-dependent
protein kinase to the β1-adrenergic receptor promotes recycling
and function resensitization of the receptor. J. Biol. Chem. 281:
33537-33553. (click here for pdf version)
Pérez-Otaño, I., Lujan, R., Tavalin, S. J., Plomann,
M., Modregger, J. Liu, X.-B., Jones, E. G., Heinemann, S. F., Lo, D.
C., and Ehlers, M. D. (2006) Synaptic Removal of NR3A-Containing NMDA
Receptors by PACSIN1/Syndapin1. Nat. Neurosci. 9:611-621.
(click here for pdf version)
Tavalin, S. J., Shepherd, D., Cloues, R. C, Bowden, S. E. H.,
and Marrion, N. V. (2004) Modulation of single channels underlying
hippocampal L-type current enhancement by agonists depends on the permeant
ion. J. Neurophysiol. 92: 824-837. (click here for pdf
version)
Dell”Acqua, M. L.*, Dodge, K. L.*, Tavalin, S. J., and Scott,
J. D. (2002). Mapping the PP-2B anchoring site on AKAP79: direct binding
and phosphatase inhibition mediated through residues 315-360. J.
Biol. Chem. 277: 48796-48802. (click here for pdf version)
Tavalin, S. J., Colledge, M., Hell, J. W., Langeberg,
L. K., Huganir, R. L., and Scott, J. D. (2002). Regulation of GluR1
by the A-Kinase Anchoring Protein 79 (AKAP79) signaling complex shares
properties with long-term depression. J. Neurosci. 22: 3044-3051. (click
here for pdf version)
Westphal, R. S.*, Tavalin, S. J.*, Lin, J. W., Alto, N. M., Fraser,
I. D. C., Langeberg, L. K. Sheng, M., and Scott, J. D. (1999). Regulation
of NMDA receptors by an associated phosphatase-kinase signaling complex.
Science, 285: 93-96. (click
here for pdf version)
Marrion, N. V. and Tavalin S. J. (1998). Selective activation of Ca2+-activated
K+ channels by co-localized Ca2+ channels in hippocampal neurons. Nature,
395: 900-905. (click
here for pdf version)
Fraser, I. D. C., Tavalin, S. J., Lester, L. B., Langeberg, L. K., Westphal,
A. M., Dean, R. A., Marrion, N. V., and Scott, J. D. (1998). A novel
lipid-anchored A-kinase anchoring protein facilitates cAMP-responsive
membrane events. EMBO J., 17: 2261-2272. (click
here for pdf version)
Cloues, R. K., Tavalin, S. J., and Marrion, N. V. (1997). _-Adrenergic
stimulation selectively inhibits long-lasting L-type calcium channel
facilitation in hippocampal pyramidal neurons. J. Neurosci. 17: 5493-6503.
(click
here for pdf version)
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