Structural determinants of L-type channel activation in segment IIS6 revealed by a retinal disorder. - Wikidata - awgldk - TriplyDB

Structural determinants of L-type channel activation in segment IIS6 revealed by a retinal disorder.

Structural determinants of L-type channel activation in segment IIS6 revealed by a retinal disorder.

http://www.wikidata.org/entity/Q38660530

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The role of distal S6 hydrophobic residues in the voltage-dependent gating of CaV2.3 channels.A genetic screen for dihydropyridine (DHP)-resistant worms reveals new residues required for DHP-blockage of mammalian calcium channels Cooperative activation of the T-type CaV3.2 channel: interaction between Domains II and III.Molecular endpoints of Ca2+/calmodulin- and voltage-dependent inactivation of Ca(v)1.3 channels Probing the architecture of an L-type calcium channel with a charged phenylalkylamine: evidence for a widely open pore and drug trapping Pore stability and gating in voltage-activated calcium channels Molecular dynamics and mutational analysis of a channelopathy mutation in the IIS6 helix of Ca V 1.2.An autism-associated mutation in CaV1.3 channels has opposing effects on voltage- and Ca(2+)-dependent regulation.Channelopathies in Cav1.1, Cav1.3, and Cav1.4 voltage-gated L-type Ca2+ channels.Timothy mutation disrupts the link between activation and inactivation in Ca(V)1.2 protein.Interaction of diltiazem with an intracellularly accessible binding site on Ca(V)1.2.Conformational changes induced in voltage-gated calcium channel Cav1.2 by BayK 8644 or FPL64176 modify the kinetics of secretion independently of Ca2+ influx.Different pathways for activation and deactivation in CaV1.2: a minimal gating model A molecular model of the inner pore of the Ca channel in its open state.Physicochemical properties of pore residues predict activation gating of Ca V1.2: a correlation mutation analysis.Methods for quantification of pore-voltage sensor interaction in Ca(V)1.2.Upward movement of IS4 and IIIS4 is a rate-limiting stage in Cav1.2 activation.Key role of segment IS4 in Cav1.2 inactivation: link between activation and inactivation.State-dependent inter-repeat contacts of exceptionally conserved asparagines in the inner helices of sodium and calcium channels.Neutralisation of a single voltage sensor affects gating determinants in all four pore-forming S6 segments of Ca(V)1.2: a cooperative gating model.Coupled and independent contributions of residues in IS6 and IIS6 to activation gating of CaV1.2.Pleiotropic effects of schizophrenia-associated genetic variants in neuron firing and cardiac pacemaking revealed by computational modeling.The role of the GX9GX3G motif in the gating of high voltage-activated Ca2+ channels.

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P2860

Structural determinants of L-type channel activation in segment IIS6 revealed by a retinal disorder.

http://www.wikidata.org/entity/Q38660530

description

2005 nî lūn-bûn

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2005年の論文

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2005年学术文章

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2005年学术文章

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2005年学术文章

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2005年学术文章

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2005年学术文章

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2005年學術文章

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2005年學術文章

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2005年學術文章

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name

Structural determinants of L-t ...... evealed by a retinal disorder.

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type

label

Structural determinants of L-t ...... evealed by a retinal disorder.

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Structural determinants of L-t ...... evealed by a retinal disorder.

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P1433

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P1433

Journal of Biological Chemistry

P1476

Structural determinants of L-t ...... evealed by a retinal disorder.

@en

P2093

Annette Hohaus

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Eugen N Timin

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Marion A Maw

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Michaela Kudrnac

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Rainer Marksteiner

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Stanislav Berjukow

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Stanislav Beyl

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Steffen Hering

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P2860

Improved patch-clamp techniques for high-resolution current recording from cells and cell-free membrane patches

A CACNA1F mutation identified in an X-linked retinal disorder shifts the voltage dependence of Cav1.4 channel activation.

A simple method for displaying the hydropathic character of a protein

Crystal structure and mechanism of a calcium-gated potassium channel

Structure and regulation of voltage-gated Ca2+ channels

Cloning and expression of a cardiac/brain beta subunit of the L-type calcium channel

Cav1.4alpha1 subunits can form slowly inactivating dihydropyridine-sensitive L-type Ca2+ channels lacking Ca2+-dependent inactivation

Engineering hybrid genes without the use of restriction enzymes: gene splicing by overlap extension

Tagging with green fluorescent protein reveals a distinct subcellular distribution of L-type and non-L-type Ca2+ channels expressed in dysgenic myotubes.

Reversed voltage-dependent gating of a bacterial sodium channel with proline substitutions in the S6 transmembrane segment.

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38471-38477

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scholarly article

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10.1074/JBC.M507013200

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P433

46

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280

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2005-09-12T00:00:00Z

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16157588

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3189691

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