Altered frequency-dependent inactivation and steady-state inactivation of polyglutamine-expanded alpha1A in SCA6.
about
Molecular mechanism of Spinocerebellar Ataxia type 6: glutamine repeat disorder, channelopathy and transcriptional dysregulation. The multifaceted aspects of a single mutation.Arrhythmogenesis in Timothy Syndrome is associated with defects in Ca(2+)-dependent inactivationMutational consequences of aberrant ion channels in neurological disorders.T-type current modulation by the actin-binding protein Kelch-like 1.C-terminal splice variants of P/Q-type Ca2+ channel CaV2.1 α1 subunits are differentially regulated by Rab3-interacting molecule proteins.
P2860
Altered frequency-dependent inactivation and steady-state inactivation of polyglutamine-expanded alpha1A in SCA6.
description
2006 nî lūn-bûn
@nan
2006年の論文
@ja
2006年論文
@yue
2006年論文
@zh-hant
2006年論文
@zh-hk
2006年論文
@zh-mo
2006年論文
@zh-tw
2006年论文
@wuu
2006年论文
@zh
2006年论文
@zh-cn
name
Altered frequency-dependent in ...... mine-expanded alpha1A in SCA6.
@en
type
label
Altered frequency-dependent in ...... mine-expanded alpha1A in SCA6.
@en
prefLabel
Altered frequency-dependent in ...... mine-expanded alpha1A in SCA6.
@en
P2860
P1476
Altered frequency-dependent in ...... mine-expanded alpha1A in SCA6.
@en
P2093
Haiyan Chen
P2860
P304
P356
10.1152/AJPCELL.00353.2006
P577
2006-10-04T00:00:00Z