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J. Biol. Chem., Vol. 278, Issue 2, 1029-1036, January 10, 2003
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From the We have previously shown that fibroblast growth
factor homologous factor 1B (FHF1B), a cytosolic member of the
fibroblast growth factor family, associates with the sensory
neuron-specific channel Nav1.9 but not with the other
sodium channels present in adult rat dorsal root ganglia neurons. We
show in this study that FHF1B binds to the C terminus of the cardiac
voltage-gated sodium channel Nav1.5 and modulates the
properties of the channel. The N-terminal 41 amino acid residues of
FHF1B are essential for binding to Nav1.5, and the
conserved acidic rich domain (amino acids 1773-1832) in the C
terminus of Nav1.5 is sufficient for association with this
factor. Binding of the growth factor to recombinant wild type human
Nav1.5 in human embryonic kidney 293 cells produces a
significant hyperpolarizing shift in the voltage dependence of channel
inactivation. An aspartic acid to glycine substitution at position 1790 of the channel, which underlies one of the LQT-3 phenotypes of cardiac
arrythmias, abolishes the interaction of the Nav1.5 channel
with FHF1B. This is the first report showing that interaction with a
growth factor can modulate properties of a voltage-gated sodium channel.
Modulation of the Cardiac Sodium Channel Nav1.5 by
Fibroblast Growth Factor Homologous Factor 1B*
§¶
,§¶**,§¶,§¶, and§¶
Department of Neurology and the
§ Paralyzed Veterans of America/Eastern Paralyzed
Veteran Association Neuroscience Research Center, Yale
University School of Medicine, New Haven, Connecticut 06510 and the
¶ Rehabilitation Research Center, Veterans Affairs Connecticut
Healthcare System, West Haven, Connecticut 06516
*
This work was supported in part by grants from the
Rehabilitation Research and Development Service and Medical Research
Services, by Department of Veterans Affairs, and the National Multiple
Sclerosis Society Grant RG-1912, and by gifts from the Paralyzed
Veterans of America and Eastern Paralyzed Veterans Association.The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
Supported by a Spinal Cord Research Fellowship from the
Eastern Paralyzed Veteran Association.
**
To whom correspondence should be addressed: Paralyzed Veterans of
America/Eastern Paralyzed Veteran Association Neuroscience Research
Center, Yale University School of Medicine, 127A, Bldg. 34, 950 Campbell Ave., West Haven, CT 06516. Tel.: 203-937-3802; Fax:
203-937-3801; E-mail: sulayman.dib-hajj@yale.edu.
Copyright © 2003 by The American Society for Biochemistry and Molecular Biology, Inc.
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