Palytoxin and the sodium/potassium pump-phosphorylation and potassium interaction

被引:11
|
作者
Rodrigues, Antonio M. [1 ,2 ]
Infantosi, Antonio F. C. [2 ]
de Almeida, Antonio-Carlos G. [1 ]
机构
[1] Univ Fed Sao Joao del Rei, Dept Biomed Engn, Lab Expt & Computat Neurosci, Sao Joao Del Rei, MG, Brazil
[2] Univ Fed Rio de Janeiro, COPPE, Biomed Engn Program, BR-21941 Rio De Janeiro, Brazil
关键词
NA+-ATPASE ACTIVITY; SODIUM-PUMP; NA; K-ATPASE; CHANNELS; NA+; K+-ATPASE; STATE; DEPHOSPHORYLATION; SIMULATION; MECHANISM; OCCLUSION;
D O I
10.1088/1478-3975/6/3/036010
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
We proposed a reaction model for investigating interactions between K+ and the palytoxin-sodium-potassium (PTX-Na+/K+) pump complex under conditions where enzyme phosphorylation may occur. The model is composed of (i) the Albers-Post model for Na+/K+-ATPase, describing Na+ and K+ pumping; (ii) the reaction model proposed for Na+/K+-ATPase interactions with its ligands (Na+, K+, ATP, ADP and P) and with PTX. A mathematical model derived for representing the reactions was used to simulate experimental studies of the PTX-induced current, in different concentrations for the pump ligands. The simulations allow interpretation of the simultaneous action of Na+/K+-ATPase phosphorylation and K+ on the PTX-induced channels. The results suggest that (i) phosphorylation increases the PTX toxic effect, increasing its affinity and reducing the K+ occlusion rate, and (ii) K+ causes channel blockage, increases the toxin dissociation rate and impedes the induced channel phosphorylation, implying reduction of the PTX toxic effect.
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页数:13
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