ArticleBiophysical journal1999
Effects of channel cytoplasmic regions on the activation mechanisms of cardiac versus skeletal muscle Na(+) channels.
Article in Biophysical journal, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 23 citations in OpenAlex.
- Differential thermosensitivity in mixed syndrome cardiac sodium channel mutants.The Journal of physiology · 2015Article
- Sialic acids attached to N- and O-glycans within the Nav1.4 D1S5-S6 linker contribute to channel gating.Biochimica et biophysica acta · 2015Article
- Functional expression of "cardiac-type" Nav1.5 sodium channel in canine intracardiac ganglia.Heart rhythm · 2006Article
- Differential sialylation modulates voltage-gated Na+ channel gating throughout the developing myocardium.The Journal of general physiology · 2006Article
- Voltage-gated Na+ channels confer invasive properties on human prostate cancer cells.Pflugers Archiv : European journal of physiology · 2004Article
- Channel activation voltage alone is directly altered in an isoform-specific manner by Na(v1.4) and Na(v1.5) cytoplasmic linkers.The Journal of membrane biology · 2004Article
- Isoform-specific effects of sialic acid on voltage-dependent Na+ channel gating: functional sialic acids are localized to the S5-S6 loop of domain I.The Journal of physiology · 2002Article
- Channel cytoplasmic loops alter voltage-dependent sodium channel activation in an isoform-specific manner.The Journal of physiology · 2001Article
- Alternatively spliced alpha(1G) (Ca(V)3.1) intracellular loops promote specific T-type Ca(2+) channel gating properties.Biophysical journal · 2001Article
- Block of wild-type and inactivation-deficient cardiac sodium channels IFM/QQQ stably expressed in mammalian cells.Biophysical journal · 2000Article
- Residues in Na(+) channel D3-S6 segment modulate both batrachotoxin and local anesthetic affinities.Biophysical journal · 2000Article
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Functional comparison of skeletal muscle (rSkM1) and cardiac (hH1) voltage-gated sodium channel isoforms expressed in Chinese hamster ovary cells showed rSkM1 half-activation (V(a)) and inactivation (V(i)) voltages 7 and 10 mV more depolarized than hH1 V(a) and V(i), respectively. Internal papain perfusion removed fast inactivation from each isoform and caused a 20-mV hyperpolarizing shift in hH1 V(a), with an insignificant change in rSkM1 V(a). Activation voltage of the inactivation-deficient hH1 mutant, hH1Q3, was nearly identical to wild-type hH1 V(a), both before and after papain treatment, with hH1Q3 V(a) also shifted by nearly 20 mV after internal papain perfusion. These data indicate that while papain removes both hH1 and rSkM1 inactivation, it has a second effect only on hH1 that causes a shift in activation voltage. Internal treatment with an antibody directed against the III-IV linker essentially mimicked papain treatment by removing some inactivation from each isoform and causing a 12-mV shift in hH1 V(a), while rSkM1 V(a) remained constant. This suggests that some channel segment within, near, or interacting with the III-IV linker is involved in establishing hH1 activation voltage. Together the data show that rSkM1 and hH1 activation mechanisms are different and are the first to suggest a role for a cytoplasmic structure in the voltage-dependent activation of cardiac sodium channels.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.