Abstract：
:Gastric acid secretion is mediated by the H/K-ATPase of parietal cells. Activation of acid secretion involves insertion of H/K-ATPase into the parietal cell plasmalemma, while its cessation is associated with reinternalization of the H/K-ATPase into an intracellular storage compartment. The cytoplasmic tail of the H/K-ATPase beta subunit includes a four residue sequence homologous to tyrosine-based endocytosis signals. We generated transgenic mice expressing H/K-ATPase beta subunit in which this motif's tyrosine residue is mutated to alanine. Gastric glands from animals expressing mutant beta subunit constitutively secrete acid and continuously express H/K-ATPase at their cell surfaces. Thus, the beta subunit's tyrosine-based signal is required for the internalization of H/K-ATPase and for the termination of acid secretion. As a consequence of chronic hyperacidity, the mice develop gastric ulcers and a hypertrophic gastropathy resembling Menetrier's disease.
journal_name
Celljournal_title
Cellauthors
Courtois-Coutry N,Roush D,Rajendran V,McCarthy JB,Geibel J,Kashgarian M,Caplan MJdoi
10.1016/s0092-8674(00)80510-3subject
Has Abstractpub_date
1997-08-08 00:00:00pages
501-10issue
3eissn
0092-8674issn
1097-4172pii
S0092-8674(00)80510-3journal_volume
90pub_type
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