Being there: cellular targeting of voltage-gated sodium channels in the heart

被引：7

作者：

Bennett, Vann ^{[1
,2
,3
]}

Healy, Jane ^{[1
,2
,3
]}

机构：

[1] Duke Univ, Med Ctr, Howard Hughes Med Inst, Durham, NC 27710 USA

[2] Duke Univ, Med Ctr, Dept Cell Biol, Durham, NC 27710 USA

[3] Duke Univ, Med Ctr, Dept Biochem, Durham, NC 27710 USA

来源：

JOURNAL OF CELL BIOLOGY | 2008年 / 180卷 / 01期

关键词：

D O I：

10.1083/jcb.200712098

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Voltage-gated sodium (Na-v) channels in cardiomyocytes are localized in specialized membrane domains that optimize their functions in propagating action potentials across cell junctions and in stimulating voltage-gated calcium channels located in T tubules. Mutation of the ankyrin-binding site of Na(v)1.5, the principal Nav channel in the heart, was previously known to cause cardiac arrhythmia and the retention of Na(v)1.5 in an intracellular compartment in cardiomyocytes. Conclusive evidence is now provided that direct interaction between Na(v)1.5 and ankyrin-G is necessary for the expression of Na(v)1.5 at the cardiomyocyte cell surface.

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页码：13 / 15

页数：3

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