Zobrazeno 1 - 9
of 9
pro vyhledávání: '"Yuriy Y. Vilin"'
Publikováno v:
Epilepsia. 53:494-505
PURPOSE: A mutation in the β(1) subunit of the voltage-gated sodium (Na(V)) channel, β(1) (C121W), causes genetic epilepsy with febrile seizures plus (GEFS+), a pediatric syndrome in which febrile seizures are the predominant phenotype. Previous st
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::dd7e2303c513c8bd2384645d58c74b9d
https://doi.org/10.1111/j.1528-1167.2011.03389.x
https://doi.org/10.1111/j.1528-1167.2011.03389.x
Publikováno v:
Pfl�gers Archiv European Journal of Physiology. 442:204-211
Two mutations associated with idiopathic ventricular fibrillation (IVF) are localized within extracellular loops between segments DIIIS1-S2 (R1232W) and DIVS3-S4 (T1620M) of the human cardiac sodium channel (hNav1.5) alpha-subunit. We studied wild-ty
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::80bd9ca93980b41cbe02dcf26e4c480c
https://doi.org/10.1007/s004240100529
https://doi.org/10.1007/s004240100529
Publikováno v:
Biophysical Journal. 80:2221-2230
Slow inactivation determines the availability of voltage-gated sodium channels during prolonged depolarization. Slow inactivation in hNa V 1.4 channels occurs with a higher probability than hNa V 1.5 sodium channels; however, the precise molecular me
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::904011d02a796725e64aa482a49884d3
https://doi.org/10.1016/s0006-3495(01)76195-4
https://doi.org/10.1016/s0006-3495(01)76195-4
Autor:
Yuriy Y. Vilin, Peter C. Ruben
Publikováno v:
Cell Biochemistry and Biophysics. 35:171-190
Slow inactivation in voltage-gated sodium channels is a biophysical process that governs the availability of sodium channels over extended periods of time. Slow inactivation, therefore, plays an important role in controlling membrane excitability, fi
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::a88c0f8f1cac24dff61ec0111ae4977a
https://doi.org/10.1385/cbb:35:2:171
https://doi.org/10.1385/cbb:35:2:171
Publikováno v:
Biophysical Journal. 77(3):1384-1393
Skeletal and heart muscle excitability is based upon the pool of available sodium channels as determined by both fast and slow inactivation. Slow inactivation in hH1 sodium channels significantly differs from slow inactivation in hSkM1. The beta(1)-s
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::6c1ea6befdf29e6906585dfe82e874d3
Publikováno v:
Epilepsia. 53(3)
A mutation in the β(1) subunit of the voltage-gated sodium (Na(V)) channel, β(1) (C121W), causes genetic epilepsy with febrile seizures plus (GEFS+), a pediatric syndrome in which febrile seizures are the predominant phenotype. Previous studies of
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=pmid________::2b409c35a2dff7f17ae585071ceaff72
https://pubmed.ncbi.nlm.nih.gov/22292491
https://pubmed.ncbi.nlm.nih.gov/22292491
Publikováno v:
Biophysical Journal. 100:423a
Genetic epilepsy with febrile seizures plus (GEFS+) is a multifaceted pediatric epilepsy syndrome of which febrile seizures (FS) are one of the most common symptoms. A cysteine to tryptophan substitution at position 121 (C121W) in β1 subunit of NaV
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::69e47ed186b346bb59060ada86a1c851
https://doi.org/10.1016/j.bpj.2010.12.2506
https://doi.org/10.1016/j.bpj.2010.12.2506
Publikováno v:
FEBS Letters. (2-3):163-169
The effects on slow inactivation (SI) of charge substitutions, neutralizations, and reversals were studied for the negatively charged residues D1309 and EE1314,15 surrounding the IFM motif in the DIII–DIV cytoplasmic linker – the putative fast in
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::0b75b74663a3cfd1cb78126eef12e56d
Autor:
Yuriy Y. Vilin, Peter C. Ruben
Publikováno v:
Biophysical Journal. (3):251a
Brain sodium channels play a crucial role in neuronal excitability. Ischemia leads to decreased sodium influx that, as suggested by previous studies, may be caused by channel protonation. Using whole-cell recordings we studied effects of low extracel
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::5eae72e76dc88120d048799347863727