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PMID:8876222
| Citation |
Nagata, A, Ito, M, Iwata, N, Kuno, J, Takano, H, Minowa, O, Chihara, K, Matsui, T and Noda, T (1996) G protein-coupled cholecystokinin-B/gastrin receptors are responsible for physiological cell growth of the stomach mucosa in vivo. Proc. Natl. Acad. Sci. U.S.A. 93:11825-30 |
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| Abstract |
Many peptide hormone and neurotransmitter receptors belonging to the seven membrane-spanning G protein-coupled receptor family have been shown to transmit ligand-dependent mitogenic signals in vitro. However, the physiological roles of the mitogenic activity through G protein-coupled receptors in vivo remain to be elucidated. Here we have generated G protein-coupled cholecystokinin (CCK)-B/gastrin receptor deficient-mice by gene targeting. The homozygous mice showed a remarkable atrophy of the gastric mucosa macroscopically, even in the presence of severe hypergastrinemia. The atrophy was due to a decrease in parietal cells and chromogranin A-positive enterochromaffin-like cells expressing the H+,K(+)-ATPase and histidine decarboxylase genes, respectively. Oral administration of a proton pump inhibitor, omeprazole, which induced hypertrophy of the gastric mucosa with hypergastrinemia in wild-type littermates, did not eliminate the gastric atrophy of the homozygotes. These results clearly demonstrated that the G protein-coupled CCK-B/gastrin receptor is essential for the physiological as well as pathological proliferation of gastric mucosal cells in vivo. |
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| Keywords |
Animals; Atrophy; Chromaffin Cells/physiology; Chromogranin A; Chromogranins/analysis; Chromogranins/physiology; DNA Probes; Gastric Mucosa/cytology; Gastric Mucosa/drug effects; Gastric Mucosa/pathology; Gastric Mucosa/physiology; Gastrins/secretion; Gene Expression; Genomic Library; H(+)-K(+)-Exchanging ATPase/biosynthesis; Histidine Decarboxylase/biosynthesis; Homozygote; Humans; Hypertrophy; Mice; Mice, Knockout; Omeprazole/pharmacology; Parietal Cells, Gastric/pathology; Parietal Cells, Gastric/physiology; Receptor, Cholecystokinin B; Receptors, Cholecystokinin/biosynthesis; Receptors, Cholecystokinin/genetics; Receptors, Cholecystokinin/physiology; Signal Transduction; Sincalide/metabolism |
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