[Participation of proteinkinase CK2 in regulation of human erythrocytes plasma membrane redox system activity: relative contribution of ca(2+)-dependent and ca(2+)-independent mechanisms of its activation]

Ukr Biokhim Zh (1999). 2012 Sep-Oct;84(5):55-61.
[Article in Ukrainian]

Abstract

Involvement of protein kinase CK2 (2.7.11.1) in modulation of live cells trans-plasma membrane electron transport was first discovered. Using human erythrocytes a decrease of plasma membrane redox system (PMRS) activity is shown under the action of specific protein kinase CK2 inhibitors. Using inhibitory analysis the activity regulation of human erythrocytes PMRS by Ca(2+)-dependent and Ca(2+)-independent mechanisms were investigated. It was shown that functional Ca(2+)-antagonists (nitrendipine and calmidazolium) significantly increased, and functional Ca(2+)-agonists to some extent reduced or did not affect the trans-plasma membrane electron transport in these cells.

MeSH terms

  • 3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester / pharmacology
  • Calcimycin / pharmacology
  • Calcium / metabolism*
  • Calcium Channel Agonists / pharmacology
  • Calcium Channel Blockers / pharmacology
  • Calcium Signaling / physiology*
  • Casein Kinase II / antagonists & inhibitors
  • Casein Kinase II / metabolism*
  • Cells, Cultured
  • Electron Transport / drug effects
  • Erythrocyte Membrane / drug effects
  • Erythrocyte Membrane / enzymology*
  • Erythrocytes / drug effects
  • Erythrocytes / enzymology*
  • Humans
  • Imidazoles / pharmacology
  • Nitrendipine / pharmacology
  • Oxidation-Reduction
  • Protein Kinase Inhibitors / pharmacology

Substances

  • Calcium Channel Agonists
  • Calcium Channel Blockers
  • Imidazoles
  • Protein Kinase Inhibitors
  • Calcimycin
  • calmidazolium
  • 3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester
  • Nitrendipine
  • Casein Kinase II
  • Calcium