Disease relevance of ATP4A

• Vacuolar H+-ATPase B1 Subunit Mutations that Cause Inherited Distal Renal Tubular Acidosis Affect Proton Pump Assembly and Trafficking in Inner Medullary Collecting Duct Cells [1].
• Proton pump inhibitor-therapy refractory gastro-oesophageal reflux disease patients, who are they [2]?
• Proton pump inhibitor or testing for Helicobacter pylori as the first step for patients presenting with dyspepsia? A cluster-randomized trial [3].
• Proton pump inhibitors (PPIs) are the mainstay of therapy in Barrett's esophagus, and have numerous beneficial effects including symptom control, reduction of inflammation, and promotion of the development of squamous islands [4].
• Methods Proton pump inhibitor use and the presence of fundic gland polyps were assessed in consecutive patients undergoing oesophagogastroduodenoscopy [5].

High impact information on ATP4A

• Proton pump inhibitors are used extensively for the treatment of gastric acid-related disorders because they produce a greater degree and longer duration of gastric acid suppression and, thus, better healing rates, than histamine H(2) receptor antagonists [6].
• Conclusions Proton pump inhibitors suppress cellular proliferation in Barrett's oesophagus with the gastric-predominant mucin phenotype but not in that with the intestinal-predominant mucin phenotype [7].
• Proton pump inhibitors inhibit the gastric H+/K+-ATPase via covalent binding to cysteine residues of the proton pump [8].
• Proton pump inhibitors can modify the intragastric release of other drugs from their dosage forms by elevating pH (e.g. reducing the antifungal activity of ketoconazole) [6].
• Proton pump inhibitors (PPIs) have been shown to be effective in preventing gastric and duodenal ulcers in high-risk patients taking nonsteroidal anti-inflammatory drugs (NSAIDs); by contrast, scarce information is available concerning the effects of PPIs on intestinal damage induced by NSAIDs in humans or in experimental animals [9].

Biological context of ATP4A

• Fluorescence in situ hybridization with gene-specific cosmid clones localized ATP4A to the q13.1 region, and proximal to ATP1A3, which maps to the q13.2 region, of Chr 19 [10].
• These results indicate that ATP4A and ATP1A3 are linked in both the mouse and human genomes [10].
• For these genes (LEAP-1 and ATP4A), there was no correlation between methylation and expression [11].

Anatomical context of ATP4A

• Proton pump inhibitors (PPIs) are targeted to the gastric acid pump, H+, K(+)-adenosine triphosphatase (ATPase) [12].
• Proton pump inhibitors reduce gallbladder function [13].

Analytical, diagnostic and therapeutic context of ATP4A

• Fundoplication is associated with a high recurrence rate, surgical failure and significant morbidity and mortality.Since Proton Pump Inhibitors (PPIs) were introduced in the 1990s they have come to play a larger part in the medical management of GOR in children with NI [14].

References