• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利：CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法，用中文像聊天一样搜索，搜遍4000万医学文献。AI智能推荐，让科研检索更轻松。

立即免费搜索

文件翻译

保留排版，准确专业，支持PDF/Word/PPT等文件格式，支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述，25分钟生成高质量综述，智能提取关键信息，辅助科研写作。

立即免费体验

相似文献

1
Slow Na+ channel inactivation must be disrupted to evoke prolonged depolarization-induced paralysis.必须破坏缓慢的钠离子通道失活，以诱发延长的去极化诱导麻痹。
Biophys J. 1994 Feb;66(2 Pt 1):542. doi: 10.1016/s0006-3495(94)80807-0.
2
Theoretical reconstruction of myotonia and paralysis caused by incomplete inactivation of sodium channels.钠通道不完全失活导致肌强直和麻痹的理论重构。
Biophys J. 1993 Jul;65(1):270-88. doi: 10.1016/S0006-3495(93)81045-2.
3
Loss of Na+ channel inactivation by anemone toxin (ATX II) mimics the myotonic state in hyperkalaemic periodic paralysis.海葵毒素（ATX II）导致的钠离子通道失活丧失可模拟高钾性周期性麻痹中的肌强直状态。
J Physiol. 1993 Jul;466:501-20.
4
Defective fast inactivation recovery and deactivation account for sodium channel myotonia in the I1160V mutant.I1160V突变体中钠通道肌强直的原因是快速失活恢复和去激活存在缺陷。
Biophys J. 1997 Oct;73(4):1896-903. doi: 10.1016/S0006-3495(97)78220-1.
5
Slow inactivation differs among mutant Na channels associated with myotonia and periodic paralysis.与肌强直和周期性麻痹相关的突变钠通道之间的缓慢失活存在差异。
Biophys J. 1997 Mar;72(3):1204-19. doi: 10.1016/S0006-3495(97)78768-X.
6
Inactivation defects caused by myotonia-associated mutations in the sodium channel III-IV linker.钠通道III-IV连接区中与肌强直相关的突变导致的失活缺陷。
J Gen Physiol. 1996 May;107(5):559-76. doi: 10.1085/jgp.107.5.559.
7
Slow inactivation of sodium channels: more than just a laboratory curiosity.钠通道的缓慢失活：不仅仅是实验室里的新奇现象。
Biophys J. 1996 Jul;71(1):5-7. doi: 10.1016/S0006-3495(96)79203-2.
8
Ultra-slow inactivation in mu1 Na+ channels is produced by a structural rearrangement of the outer vestibule.μ1钠通道中的超慢失活是由外前庭的结构重排产生的。
Biophys J. 1999 Mar;76(3):1335-45. doi: 10.1016/S0006-3495(99)77296-6.
9
Biophysical properties and slow voltage-dependent inactivation of a sustained sodium current in entorhinal cortex layer-II principal neurons: a whole-cell and single-channel study.内嗅皮层II层主要神经元中持续钠电流的生物物理特性及缓慢电压依赖性失活：全细胞和单通道研究
J Gen Physiol. 1999 Oct;114(4):491-509. doi: 10.1085/jgp.114.4.491.
10
Single-channel analysis of inactivation-defective rat skeletal muscle sodium channels containing the F1304Q mutation.对含有F1304Q突变的失活缺陷型大鼠骨骼肌钠通道进行单通道分析。
Biophys J. 1996 Sep;71(3):1285-94. doi: 10.1016/S0006-3495(96)79329-3.

引用本文的文献

1
Novel compound heterozygous mutations in as a potential genetic cause contributing to myopathic manifestations: A case report and literature review.作为导致肌病表现的潜在遗传原因的新型复合杂合突变：一例报告及文献综述。
Heliyon. 2024 Mar 22;10(7):e28684. doi: 10.1016/j.heliyon.2024.e28684. eCollection 2024 Apr 15.
2
A Novel Therapeutic Formulation for the Improved Treatment of Indian Red Scorpion () Venom-Induced Toxicity-Tested in and Rodent Models.一种新型治疗制剂，可改善印度红蝎（）毒液诱导的毒性-在和啮齿动物模型中进行了测试。
Toxins (Basel). 2023 Aug 14;15(8):504. doi: 10.3390/toxins15080504.
3
Substitutions of the S4DIV R2 residue (R1451) in Na1.4 lead to complex forms of paramyotonia congenita and periodic paralyses.S4DIV R2 残基（R1451）的取代导致先天性副肌强直和周期性瘫痪的复杂形式。
Sci Rep. 2018 Feb 1;8(1):2041. doi: 10.1038/s41598-018-20468-0.
4
Sodium Channelopathies of Skeletal Muscle.骨骼肌钠通道病
Handb Exp Pharmacol. 2018;246:309-330. doi: 10.1007/164_2017_52.
5
A recessive Nav1.4 mutation underlies congenital myasthenic syndrome with periodic paralysis.一种隐性Nav1.4突变是导致伴有周期性麻痹的先天性肌无力综合征的根本原因。
Neurology. 2016 Jan 12;86(2):161-9. doi: 10.1212/WNL.0000000000002264. Epub 2015 Dec 11.
6
Channelopathies of skeletal muscle excitability.骨骼肌兴奋性通道病
Compr Physiol. 2015 Apr;5(2):761-90. doi: 10.1002/cphy.c140062.
7
Enhanced slow inactivation of the human skeletal muscle sodium channel causing normokalemic periodic paralysis.人类骨骼肌钠通道增强的缓慢失活导致正常血钾型周期性麻痹。
Cell Mol Neurobiol. 2014 Jul;34(5):707-14. doi: 10.1007/s10571-014-0052-y. Epub 2014 Mar 29.
8
Keeping hyperactive voltage-gated sodium channels in silent mode.使过度活跃的电压门控钠通道保持沉默状态。
J Physiol. 2012 Jun 1;590(11):2543-4. doi: 10.1113/jphysiol.2012.229310.
9
Cold-induced disruption of Na+ channel slow inactivation underlies paralysis in highly thermosensitive paramyotonia.寒冷诱导的钠离子通道缓慢失活破坏是高度热敏性周期性瘫痪中麻痹的基础。
J Physiol. 2009 Apr 15;587(Pt 8):1705-14. doi: 10.1113/jphysiol.2008.165787. Epub 2009 Feb 16.
10
Genotype-phenotype correlation and therapeutic rationale in hyperkalemic periodic paralysis.高钾性周期性麻痹的基因型-表型相关性及治疗原理
Neurotherapeutics. 2007 Apr;4(2):216-24. doi: 10.1016/j.nurt.2007.02.001.

本文引用的文献

1
Theoretical reconstruction of myotonia and paralysis caused by incomplete inactivation of sodium channels.钠通道不完全失活导致肌强直和麻痹的理论重构。
Biophys J. 1993 Jul;65(1):270-88. doi: 10.1016/S0006-3495(93)81045-2.
2
Na+ currents near and away from endplates on human fast and slow twitch muscle fibers.人类快肌和慢肌纤维终板附近及远离终板处的钠离子电流。
Muscle Nerve. 1993 Sep;16(9):922-9. doi: 10.1002/mus.880160906.
3
Adynamia episodica hereditaria with myotonia: a non-inactivating sodium current and the effect of extracellular pH.遗传性发作性肌无力伴肌强直：一种非失活钠电流及细胞外pH值的影响
Muscle Nerve. 1987 May;10(4):363-74. doi: 10.1002/mus.880100414.
4
Comparison between slow sodium channel inactivation in rat slow- and fast-twitch muscle.大鼠慢肌和快肌中慢钠通道失活的比较。
J Physiol. 1987 Feb;383:339-48. doi: 10.1113/jphysiol.1987.sp016412.
5
Slow sodium channel inactivation in rat fast-twitch muscle.大鼠快肌中慢钠通道失活
J Physiol. 1987 Feb;383:327-37. doi: 10.1113/jphysiol.1987.sp016411.
6
Na+ current densities and voltage dependence in human intercostal muscle fibres.人类肋间肌纤维中的钠离子电流密度与电压依赖性
J Physiol. 1992 Dec;458:85-97. doi: 10.1113/jphysiol.1992.sp019407.
7
Steady-state availability of sodium channels. Interactions between activation and slow inactivation.钠通道的稳态可用性。激活与缓慢失活之间的相互作用。
Biophys J. 1992 Apr;61(4):941-55. doi: 10.1016/S0006-3495(92)81901-X.

Slow Na+ channel inactivation must be disrupted to evoke prolonged depolarization-induced paralysis.

作者信息

Ruff R L

出版信息

Biophys J. 1994 Feb;66(2 Pt 1):542. doi: 10.1016/s0006-3495(94)80807-0.

DOI:10.1016/s0006-3495(94)80807-0
PMID:8161707
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1275721/
Abstract
摘要