产品名称
Anthopleurin-A trifluoroacetate salt, >88% (HPLC)
assay
>88% (HPLC)
form
solid
storage temp.
−20°C
Application
Anthopleurin-A is a toxin used to study the gating mechanisms of sodium channels. Anthopleurin-A slows the repolarization phase of nerve and muscle action potentials by inactivating the sodium channel.
Biochem/physiol Actions
Anthopleurin-A slows the repolarization phase of nerve and muscle action potentials by inactivating the sodium channel. Anthopleurin-A shows a preference towards cardiac channels over the neuronal sodium channels. It is a toxin used to study the gating mechanisms of sodium channels.
Shown to have inotropic effects and not chronotropic effects on mammalian heart preparations.
General description
Synthetic peptide toxin that was originally isolated from the sea anemone, Anthopleura xanthogrammica.
Synthetic peptide toxin.
Other Notes
supplied as trifluoroacetate salt
存储类别
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
ppe
Eyeshields, Gloves, type N95 (US)
法规信息
新产品
此项目有
P K Pallaghy et al.
Biochemistry, 34(11), 3782-3794 (1995-03-21)
The three-dimensional structure in aqueous solution of the 49-residue polypeptide anthopleurin-A (AP-A), from the sea anemone Anthopleura xanthogrammica, has been determined from 1H NMR data. A restraint set consisting of 411 interproton distance restraints inferred from NOEs and 19 backbone
M J Scanlon et al.
Protein science : a publication of the Protein Society, 3(7), 1121-1124 (1994-07-01)
Anthopleurin-A (AP-A) is a member of a family of sea anemone-derived polypeptides that interact with sodium channels in a voltage-dependent manner, producing a positive inotropic effect on the mammalian heart. There has been considerable interest in this molecule as a
S G Priori et al.
Pacing and clinical electrophysiology : PACE, 20(8 Pt 2), 2052-2057 (1997-08-01)
The long QT syndrome (LQTS) is a familial disease characterized by prolonged ventricular repolarization and high incidence of malignant ventricular tachyarrhythmias often occurring in conditions of adrenergic activation. Recently, the genes for the LQTS inked to chromosomes 3 (LQT3), 7
N el-Sherif et al.
Circulation research, 79(3), 474-492 (1996-09-01)
We have previously developed a canine in vivo model of the long QT syndrome (LQTS) using the neurotoxin anthopleurin A (AP-A), which acts by slowing sodium channel inactivation. The recent discovery of a genetic mutation in the cardiac sodium channel
W Shimizu et al.
Circulation, 96(6), 2038-2047 (1997-10-10)
This study examines the contribution of transmural heterogeneity of transmembrane activity to phenotypic T-wave patterns and the effects of pacing and of sodium channel block under conditions mimicking HERG and SCN5A defects linked to the congenital long-QT syndrome (LQTS). A
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