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Gene Review:

Atp4a - ATPase, H+/K+ exchanging, gastric, alpha...

Mus musculus

Synonyms: Gastric H(+)/K(+) ATPase subunit alpha, H+/K+-ATPase alpha, H+K+-transporting alpha 1, Potassium-transporting ATPase alpha chain 1, Proton pump

Malo, D. et al., Judd, L.M. et al., Spicer, Z. et al., Stiefel, U. et al.

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Disease relevance of Atp4a

CONCLUSIONS: Chronic achlorhydria and hypergastrinemia in aged Atp4a(-/-) mice produced progressive hyperplasia, mucocystic and incomplete intestinal metaplasia, and the upregulation of growth factors without histological evidence of neoplasia [1].
Gastric achlorhydria in H/K-ATPase-deficient (Atp4a(-/-)) mice causes severe hyperplasia, mucocystic metaplasia and upregulation of growth factors [1].
Proton pump inhibitor treatment of clindamycin-treated mice elevated the gastric pH and facilitated the establishment of colonization of the large intestine by vancomycin-resistant Enterococcus spp [2].
Suppression of Gastric Acid Production by Proton Pump Inhibitor Treatment Facilitates Colonization of the Large Intestine by Vancomycin-Resistant Enterococcus spp. and Klebsiella pneumoniae in Clindamycin-Treated Mice [2].

High impact information on Atp4a

Stomachs of adult Atp4a(-/-) mice exhibited metaplasia, which included the presence of ciliated cells [3].
However, Atp4a(-/-) parietal cells had dilated canaliculi and lacked typical canalicular microvilli and tubulovesicles, and subsets of these cells contained abnormal mitochondria and/or massive glycogen stores [3].
Segregation of restriction fragment length polymorphisms in backcross progeny of Mus musculus x Mus spretus mating confirmed this assignment and indicates that Atp4a and Atp1a3 (gene encoding the murine Na,K-ATPase alpha 3 subunit) are linked and separated by a distance of approximately 2 cM [4].
Linkage analysis in recombinant inbred (BXD) strains of mice localized Atp4a to mouse Chromosome (Chr) 7 [4].
To study this, mice lacking the gastric H/K-ATPase (Atp4a(-/-) mice) were used to determine whether chronic loss of acid secretion, with attendant hypergastrinemia, predisposes to cancer phenotype [1].

Anatomical context of Atp4a

Immunocytochemical, histological, and ultrastructural analyses of Atp4a(-/-) stomachs revealed the presence of chief cells, demonstrating that the lack of acid secretion does not interfere with their differentiation [3].

Analytical, diagnostic and therapeutic context of Atp4a

We have used linkage analysis and fluorescence in situ hybridization to determine the chromosomal organization and location of the mouse (Atp4a) and human (ATP4A) genes encoding the H,K-ATPase alpha subunit [4].

References

Gastric achlorhydria in H/K-ATPase-deficient (Atp4a(-/-)) mice causes severe hyperplasia, mucocystic metaplasia and upregulation of growth factors. Judd, L.M., Andringa, A., Rubio, C.A., Spicer, Z., Shull, G.E., Miller, M.L. J. Gastroenterol. Hepatol. (2005) [Pubmed]
Suppression of Gastric Acid Production by Proton Pump Inhibitor Treatment Facilitates Colonization of the Large Intestine by Vancomycin-Resistant Enterococcus spp. and Klebsiella pneumoniae in Clindamycin-Treated Mice. Stiefel, U., Rao, A., Pultz, M.J., Jump, R.L., Aron, D.C., Donskey, C.J. Antimicrob. Agents Chemother. (2006) [Pubmed]
Stomachs of mice lacking the gastric H,K-ATPase alpha -subunit have achlorhydria, abnormal parietal cells, and ciliated metaplasia. Spicer, Z., Miller, M.L., Andringa, A., Riddle, T.M., Duffy, J.J., Doetschman, T., Shull, G.E. J. Biol. Chem. (2000) [Pubmed]
Genes encoding the H,K-ATPase alpha and Na,K-ATPase alpha 3 subunits are linked on mouse chromosome 7 and human chromosome 19. Malo, D., Gros, P., Bergmann, A., Trask, B., Mohrenweiser, H.W., Canfield, V.A., Levenson, R. Mamm. Genome (1993) [Pubmed]

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