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Science 12 October 2001:
Vol. 294. no. 5541, pp. 333 - 339
DOI: 10.1126/science.1063395
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Research Articles

Signaling to the Nucleus by an L-type Calcium Channel-Calmodulin Complex Through the MAP Kinase Pathway

Ricardo E. Dolmetsch, Urvi Pajvani, Katherine Fife, James M. Spotts, Michael E. Greenberg*

Increases in the intracellular concentration of calcium ([Ca2+]i) activate various signaling pathways that lead to the expression of genes that are essential for dendritic development, neuronal survival, and synaptic plasticity. The mode of Ca2+ entry into a neuron plays a key role in determining which signaling pathways are activated and thus specifies the cellular response to Ca2+. Ca2+ influx through L-type voltage-activated channels (LTCs) is particularly effective at activating transcription factors such as CREB and MEF-2. We developed a functional knock-in technique to investigate the features of LTCs that specifically couple them to the signaling pathways that regulate gene expression. We found that an isoleucine-glutamine ("IQ") motif in the carboxyl terminus of the LTC that binds Ca2+-calmodulin (CaM) is critical for conveying the Ca2+ signal to the nucleus. Ca2+-CaM binding to the LTC was necessary for activation of the Ras/mitogen-activated protein kinase (MAPK) pathway, which conveys local Ca2+ signals from the mouth of the LTC to the nucleus. CaM functions as a local Ca2+ sensor at the mouth of the LTC that activates the MAPK pathway and leads to the stimulation of genes that are essential for neuronal survival and plasticity.

Division of Neuroscience, Children's Hospital and Department of Neurobiology, Harvard Medical School, Enders Pediatric Research Laboratories, Room 260, 300 Longwood Avenue, Boston, MA 02115, USA.
*   To whom correspondence should be addressed. E-mail: michael.greenberg{at}tch.harvard.edu

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   Abstract »    Full Text »    PDF »
Identification and analysis of plasticity-induced late-response genes.
S. J. Hong, H. Li, K. G. Becker, V. L. Dawson, and T. M. Dawson (2004)
PNAS 101, 2145-2150
   Abstract »    Full Text »    PDF »
Several Structural Domains Contribute to the Regulation of N-type Calcium Channel Inactivation by the {beta}3 Subunit.
S. C. Stotz, W. Barr, J. E. McRory, L. Chen, S. E. Jarvis, and G. W. Zamponi (2004)
J. Biol. Chem. 279, 3793-3800
   Abstract »    Full Text »    PDF »
Functional roles of cytoplasmic loops and pore lining transmembrane helices in the voltage-dependent inactivation of HVA calcium channels.
S. C. Stotz, S. E. Jarvis, and G. W. Zamponi (2004)
J. Physiol. 554, 263-273
   Abstract »    Full Text »    PDF »
Intracellular Ca2+ regulates responsiveness of cardiac L-type Ca2+ current to protein kinase A: role of calmodulin.
K. B. Walsh and Q. Cheng (2004)
Am J Physiol Heart Circ Physiol 286, H186-H194
   Abstract »    Full Text »    PDF »
A New Role for IQ Motif Proteins in Regulating Calmodulin Function.
J. A. Putkey, Q. Kleerekoper, T. R. Gaertner, and M. N. Waxham (2003)
J. Biol. Chem. 278, 49667-49670
   Abstract »    Full Text »    PDF »
Decoding of synaptic voltage waveforms by specific classes of recombinant high-threshold Ca2+ channels.
Z. Liu, J. Ren, and T. H Murphy (2003)
J. Physiol. 553, 473-488
   Abstract »    Full Text »    PDF »
Identification and Functional Characterization of Voltage-dependent Calcium Channels in T Lymphocytes.
M. F. Kotturi, D. A. Carlow, J. C. Lee, H. J. Ziltener, and W. A. Jefferies (2003)
J. Biol. Chem. 278, 46949-46960
   Abstract »    Full Text »    PDF »
The L-type calcium channel C-terminus: sparking interest beyond its role in calcium-dependent inactivation.
G. W Zamponi (2003)
J. Physiol. 552, 333
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Antiarrhythmic Drug Target Choices and Screening.
M. C. Sanguinetti and P. B. Bennett (2003)
Circ. Res. 93, 491-499
   Abstract »    Full Text »    PDF »
Transcriptional regulation by calcium, calcineurin, and NFAT.
P. G. Hogan, L. Chen, J. Nardone, and A. Rao (2003)
Genes & Dev. 17, 2205-2232
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Calmodulin Binds to the C Terminus of Sodium Channels Nav1.4 and Nav1.6 and Differentially Modulates Their Functional Properties.
R. I. Herzog, C. Liu, S. G. Waxman, and T. R. Cummins (2003)
J. Neurosci. 23, 8261-8270
   Abstract »    Full Text »    PDF »


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