help button home button Biophys. J.
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS

Biophysical Journal 73: 1885-1895 (1997)
© 1997 the Biophysical Society

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Smith, M R
Right arrow Articles by Goldin, A L
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Smith, M R
Right arrow Articles by Goldin, A L

Interaction between the sodium channel inactivation linker and domain III S4-S5.

M R Smith and A L Goldin

Department of Microbiology and Molecular Genetics, University of California, Irvine 92697-4025, USA.

ABSTRACT

The III-IV linker (L(III-IV)) of the rat brain sodium channel is critical for fast inactivation, possibly forming a fast inactivation particle. Inactivation can be disrupted by mutation of a conserved alanine at position 1329 in the S4-S5 loop of domain III. Combination of a charged mutation at 1329 with a compensatory (opposite) charge mutation at position 1489 in L(III-IV) partially restores inactivation of the channel. The compensatory charge mutant channel has a single-channel mean open time that is similar to that of the wild-type channel and is approximately 50 times shorter than that of the L(III-IV) mutant channel. The results of thermodynamic cycle analysis indicate that the mutations in domain III S4-S5 and L(III-IV) have a coupling energy of 2.8 kcal/mol, indicating that the two mutations act interdependently. These data suggest that L(III-IV) interacts directly with A1329, which may form part of the docking site if L(III-IV) is a fast inactivation particle.




This article has been cited by other articles:


Home page
 Cardiovasc ResHome page
S. Casini, H. L. Tan, Z. A. Bhuiyan, C. R. Bezzina, P. Barnett, E. Cerbai, A. Mugelli, A. A.M. Wilde, and M. W. Veldkamp
Characterization of a novel SCN5A mutation associated with Brugada syndrome reveals involvement of DIIIS4-S5 linker in slow inactivation
Cardiovasc Res, December 1, 2007; 76(3): 418 - 429.
[Abstract] [Full Text] [PDF]

Home page
 Biophys. JHome page
J. R. Groome, M. C. Dice, E. Fujimoto, and P. C. Ruben
Charge Immobilization of Skeletal Muscle Na+ Channels: Role of Residues in the Inactivation Linker
Biophys. J., September 1, 2007; 93(5): 1519 - 1533.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
A. Lampert, S. D. Dib-Hajj, L. Tyrrell, and S. G. Waxman
Size Matters: Erythromelalgia Mutation S241T in Nav1.7 Alters Channel Gating
J. Biol. Chem., November 24, 2006; 281(47): 36029 - 36035.
[Abstract] [Full Text] [PDF]

Home page
 Proc. Natl. Acad. Sci. USAHome page
H. H. Zakon, Y. Lu, D. J. Zwickl, and D. M. Hillis
Sodium channel genes and the evolution of diversity in communication signals of electric fishes: Convergent molecular evolution
PNAS, March 7, 2006; 103(10): 3675 - 3680.
[Abstract] [Full Text] [PDF]

Home page
 Cardiovasc ResHome page
J. P.P. Smits, M. W. Veldkamp, C. R. Bezzina, Z. A. Bhuiyan, H. Wedekind, E. Schulze-Bahr, and A. A.M. Wilde
Substitution of a conserved alanine in the domain IIIS4-S5 linker of the cardiac sodium channel causes long QT syndrome
Cardiovasc Res, August 15, 2005; 67(3): 459 - 466.
[Abstract] [Full Text] [PDF]

Home page
 J. Physiol.Home page
M. Bouhours, S. Luce, D. Sternberg, J. C. Willer, B. Fontaine, and N. Tabti
A1152D mutation of the Na+ channel causes paramyotonia congenita and emphasizes the role of DIII/S4-S5 linker in fast inactivation
J. Physiol., June 1, 2005; 565(2): 415 - 427.
[Abstract] [Full Text] [PDF]

Home page
 J. Physiol.Home page
M. O. Popa, A. K Alekov, S. Bail, F. Lehmann-Horn, and H. Lerche
Cooperative effect of S4-S5 loops in domains D3 and D4 on fast inactivation of the Na+ channel
J. Physiol., November 15, 2004; 561(1): 39 - 51.
[Abstract] [Full Text] [PDF]

Home page
 CirculationHome page
M. Tateyama, J. Kurokawa, C. Terrenoire, I. Rivolta, and R.S. Kass
Stimulation of Protein Kinase C Inhibits Bursting in Disease-Linked Mutant Human Cardiac Sodium Channels
Circulation, July 1, 2003; 107(25): 3216 - 3222.
[Abstract] [Full Text] [PDF]

Home page
 Mol. Pharmacol.Home page
C. Nau, S.-Y. Wang, and G. K. Wang
Point Mutations at L1280 in Nav1.4 Channel D3-S6 Modulate Binding Affinity and Stereoselectivity of Bupivacaine Enantiomers
Mol. Pharmacol., June 1, 2003; 63(6): 1398 - 1406.
[Abstract] [Full Text] [PDF]

Home page
 Cardiovasc ResHome page
H. L Tan, C. R Bezzina, J. P.P Smits, A. O Verkerk, and A. A.M Wilde
Genetic control of sodium channel function
Cardiovasc Res, March 15, 2003; 57(4): 961 - 973.
[Abstract] [Full Text] [PDF]

Home page
 Biophys. JHome page
S. Ding and R. Horn
Effect of S6 Tail Mutations on Charge Movement in Shaker Potassium Channels
Biophys. J., January 1, 2003; 84(1): 295 - 305.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
V. Yarov-Yarovoy, J. C. McPhee, D. Idsvoog, C. Pate, T. Scheuer, and W. A. Catterall
Role of Amino Acid Residues in Transmembrane Segments IS6 and IIS6 of the Na+ Channel alpha Subunit in Voltage-dependent Gating and Drug Block
J. Biol. Chem., September 13, 2002; 277(38): 35393 - 35401.
[Abstract] [Full Text] [PDF]

Home page
 NeurologyHome page
S. Bendahhou, T. R. Cummins, R. W. Kula, Y.-H. Fu, and L. J. Ptacek
Impairment of slow inactivation as a common mechanism for periodic paralysis in DIIS4-S5
Neurology, April 23, 2002; 58(8): 1266 - 1272.
[Abstract] [Full Text] [PDF]

Home page
 Proc. Natl. Acad. Sci. USAHome page
M. Mantegazza, F. H. Yu, W. A. Catterall, and T. Scheuer
Role of the C-terminal domain in inactivation of brain and cardiac sodium channels
PNAS, December 6, 2001; (2001) 211563298.
[Abstract] [Full Text] [PDF]

Home page
 Cardiovasc ResHome page
C. R Bezzina, M. B Rook, and A. A.M Wilde
Cardiac sodium channel and inherited arrhythmia syndromes
Cardiovasc Res, February 1, 2001; 49(2): 257 - 271.
[Full Text] [PDF]

Home page
 Cardiovasc ResHome page
J. R. Balser
Structure and function of the cardiac sodium channels
Cardiovasc Res, May 1, 1999; 42(2): 327 - 328.
[Abstract] [Full Text] [PDF]

Home page
 J. Neurosci.Home page
T. R. Cummins, J. R. Howe, and S. G. Waxman
Slow Closed-State Inactivation: A Novel Mechanism Underlying Ramp Currents in Cells Expressing the hNE/PN1 Sodium Channel
J. Neurosci., December 1, 1998; 18(23): 9607 - 9619.
[Abstract] [Full Text] [PDF]

Home page
 CirculationHome page
N. G. Kambouris, H. B. Nuss, D. C. Johns, G. F. Tomaselli, E. Marban, and J. R. Balser
Phenotypic Characterization of a Novel Long-QT Syndrome Mutation (R1623Q) in the Cardiac Sodium Channel
Circulation, February 24, 1998; 97(7): 640 - 644.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
S. C. Stotz and G. W. Zamponi
Identification of Inactivation Determinants in the Domain IIS6 Region of High Voltage-activated Calcium Channels
J. Biol. Chem., August 24, 2001; 276(35): 33001 - 33010.
[Abstract] [Full Text] [PDF]

Home page
 Proc. Natl. Acad. Sci. USAHome page
M. Mantegazza, F. H. Yu, W. A. Catterall, and T. Scheuer
Role of the C-terminal domain in inactivation of brain and cardiac sodium channels
PNAS, December 18, 2001; 98(26): 15348 - 15353.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1997 by the Biophysical Society.