Mimicking of K+ activation by double mutation of glutamate 795 and glutamate 820 of gastric H+,K+-ATPase

Biochemistry. 2001 May 29;40(21):6527-33. doi: 10.1021/bi002456z.

Abstract

Six double mutants of Glu(795) and Glu(820) present in transmembrane domains 5 and 6 of the alpha-subunit of rat gastric H(+),K(+)-ATPase were generated and expressed with the baculovirus expression system. Five of the six mutants exhibited an SCH 28080-sensitive ATPase activity in the absence of K(+). The activity levels decreased in the following order: E795Q/E820A > E795Q/E820Q > E795Q/E820D congruent with E795A/E820A > E795L/E820Q. The E795L/E820D mutant possessed no constitutive activity. The relative low ATPase activity of the E795L/E820Q mutant is due to its low phosphorylation rate so that the dephosphorylation step was no longer rate-limiting. The constitutively active mutants showed a much lower vanadate sensitivity than the wild-type enzyme and K(+)-sensitive mutants, indicating that these mutants have a preference for the E(1) conformation. In contrast to the constitutively active single mutants generated previously, the double mutants exhibited a high spontaneous dephosphorylation rate at 0 degrees C compared to that of the wild-type enzyme. In addition, the H(+),K(+)-ATPase inhibitor SCH 28080 increased the steady-state phosphorylation level of the constitutively active mutants, due to the formation of a stable complex with the E(2)-P form. These studies further substantiate the idea that the empty ion binding pockets of some mutants apparently mimic the K(+)-filled binding pocket of the native enzyme.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenosine Triphosphatases / antagonists & inhibitors
  • Adenosine Triphosphatases / genetics
  • Adenosine Triphosphatases / metabolism
  • Amino Acid Substitution / genetics*
  • Animals
  • Baculoviridae / genetics
  • Enzyme Activation / drug effects
  • Enzyme Activation / genetics
  • Enzyme Inhibitors / pharmacology
  • Glutamic Acid / genetics*
  • H(+)-K(+)-Exchanging ATPase / genetics*
  • H(+)-K(+)-Exchanging ATPase / metabolism*
  • Hydroxylamine / pharmacology
  • Imidazoles / pharmacology
  • Mutagenesis, Site-Directed*
  • Phosphorylation / drug effects
  • Potassium / metabolism*
  • Proton Pump Inhibitors
  • Rats
  • Spodoptera / enzymology
  • Spodoptera / genetics
  • Stomach / enzymology*

Substances

  • Enzyme Inhibitors
  • Imidazoles
  • Proton Pump Inhibitors
  • Sch 28080
  • Hydroxylamine
  • Glutamic Acid
  • Adenosine Triphosphatases
  • H(+)-K(+)-Exchanging ATPase
  • Potassium