Regulation of CA II and H⁺, K⁺‐ATPase Gene Expression in Canine Gastric Parietal Cells

Abstract

Acid secretagogue-specific receptor activation in parietal cells triggers rapid and coordinate gene expression of gastric H+,K(+)-ATPase and of CA II. The rapid rise in steady-state levels of CA II mRNA is due to new transcription of the CA II gene in stimulated cells. Although the presumed function of CA II in activated parietal cells is to catalyze the generation of HCO3- from OH-, regulation of CA II gene expression appears to be independent of the generation of H+ (and OH-) through the action of H+,K(+)-ATPase.

Altered expression of aquaporin 4 and H+/K+‐ATPase in the stomachs of peptide YY (PYY) transgenic mice

“…Conversely, pretreatment with famotidine, a potent histamine H 2 receptor antagonist, inhibited the increase of rat gastric H + /K + ‐ATPase mRNA expression subsequent to histamine infusion (Yamamoto et al, 1995). Similar results were obtained in isolated canine gastric parietal cells, in which histamine treatment induced rapid and co‐ordinate increases in the steady‐state levels of mRNAs encoding carbonic anhydrase II and H + /K + ‐ATPase (Campbell and Yamada, 1989), indicating that acid secretagogue‐specific receptor activation in parietal cells triggers co‐ordinate gene expression of the same proteins.…”

Cryo-EM structure of the RADAR supramolecular anti-phage defense complex

“…Profiling of polar metabolites was done as previously described (Campbell and Yamada, 1989) with minor modifications as described below. In brief, the analysis was performed using an Acquity I class UPLC System combined with a mass spectrometer (Thermo Exactive Plus Orbitrap), which was operated in a positive ionization mode using a mass range of 200–800 m/z.…”