The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)



Gene Review

Gast  -  gastrin

Mus musculus

Synonyms: GAS, Gas, Gastrin
Welcome! If you are familiar with the subject of this article, you can contribute to this open access knowledge base by deleting incorrect information, restructuring or completely rewriting any text. Read more.

Disease relevance of Gast


Psychiatry related information on Gast


High impact information on Gast

  • Excitation of the non-cholinergic nerves stimulates amylase secretion by a different intracellular coupling mechanism from that activated by cholinergic nerves or by peptides belonging to the cholecystokinin, gastrin or bombesin families [8].
  • In addition, there was a twofold increase in activated parietal cells resulting in a twofold increase in basal and stimulated gastric acid output and an undetectable serum gastrin level [9].
  • Previous studies have shown that the gene encoding the hormone gastrin is activated during colon cancer progression and the less-processed forms of gastrin are important colonic trophic factors [10].
  • APC(min-/+) mice overexpressing one of the alternatively processed forms of gastrin, glycine-extended gastrin, show a significant increase in polyp number [10].
  • Activation of gastrin by beta-catenin may therefore represent an early event in colorectal tumorigenesis and may contribute significantly toward neoplastic progression [10].

Chemical compound and disease context of Gast


Biological context of Gast

  • Both parietal cell number and level of H(+)/K(+)-ATPase messenger RNA (mRNA) were reduced in the mutant strains, but gastrin-CCK double-KO mice displayed more active parietal cells and larger acid output than the gastrin KO mice [15].
  • CONCLUSIONS: These findings show an essential physiologic role for gastrin in glucose homeostasis; however, the gastrin gene is not essential for murine islet development or the adaptive islet proliferative response to beta-cell injury [1].
  • Peroxisome proliferators-activated receptor gamma (PPARgamma) has been shown to suppress cell proliferation and tumorigenesis, whereas the gastrointestinal regulatory peptide gastrin stimulates the growth of neoplastic cells [2].
  • The results of these studies demonstrate that the trophic properties of gastrin in CRC may be mediated in part by transactivation of the EGFR and phosphorylation of ERK1/2, leading to degradation of PPARgamma protein and a decrease in PPARgamma activation [2].
  • Gross morphology and histology of 12-month-old wild-type (WT), gastrin-deficient (G-/-) and somatostatin-deficient (SOM-/-) mice were examined [5].

Anatomical context of Gast

  • Altered control of gastric acid secretion in gastrin-cholecystokinin double mutant mice [15].
  • Oxyntic D-cell density was the same in both mutant strains, but the D cells were more active in the gastrin KO than in the double-KO mice [15].
  • METHODS: Acid was measured after pylorus ligation, and biopsies from gastrin knockout (KO), gastrin-CCK double-KO, and wild-type (WT) mice were collected for biochemical, immunocytochemical, and electron-microscopic examination [15].
  • Initially, using growth assays, we determined that the human CRC cell line DLD-1 expressed both functional PPARgamma and gastrin receptors [2].
  • To clarify the roles of hypergastrinaemia in the gastric mucosa, a gastrin receptor antagonist (AG041R) was administered [4].

Associations of Gast with chemical compounds

  • The acid response to histamine in double-KO mice was unchanged whereas that to gastrin was diminished, but it could be restored by infusion of gastrin [15].
  • Furthermore, mutation of PPARgamma at serine 84 reduced the effects of G-17, as evident by inability of G-17 to attenuate PPARgamma promoter activity, degrade PPARgamma, or inhibit the growth suppressing effects of PPARgamma [2].
  • Gastrin 17 and pentagastrin did not affect glucose- or carbachol-induced insulin release, whereas they inhibited L-IPNA-induced insulin secretion [16].
  • However, co-stimulation with EGF and gastrin synergistically induced COX-2 protein and mRNA expression and PGE2 secretion [17].
  • Inhibition of de novo protein synthesis by cycloheximide did not block COX-2 mRNA induction by gastrin [17].

Physical interactions of Gast


Regulatory relationships of Gast


Other interactions of Gast

  • In the gastrin-CCK double-KO mice, acid secretion is only controlled by cholinergic vagal stimulation, which normalizes the acid output [15].
  • The results suggest that VIP, secretin and gastrin display their effects on insulin secretion through different mechanisms [16].
  • Recent studies suggest that COX-2 expression levels could mediate the growth effects of gastrin [17].
  • Effect of carboxypeptidase E deficiency on progastrin processing and gastrin messenger ribonucleic acid expression in mice with the fat mutation [23].
  • In wild-type mice, somatostatin-14, SMS 201-995, and the SSTR2-preferential agonist, DC 32-87, inhibited gastrin-stimulated acid secretion with an order of potency SMS 201-995>DC 32-87>somatostatin-14 [24].

Analytical, diagnostic and therapeutic context of Gast


  1. Hypoglycemia, defective islet glucagon secretion, but normal islet mass in mice with a disruption of the gastrin gene. Boushey, R.P., Abadir, A., Flamez, D., Baggio, L.L., Li, Y., Berger, V., Marshall, B.A., Finegood, D., Wang, T.C., Schuit, F., Drucker, D.J. Gastroenterology (2003) [Pubmed]
  2. Attenuation of peroxisome proliferator-activated receptor gamma (PPARgamma) mediates gastrin-stimulated colorectal cancer cell proliferation. Chang, A.J., Song, D.H., Wolfe, M.M. J. Biol. Chem. (2006) [Pubmed]
  3. The murine gastrin promoter is synergistically activated by transforming growth factor-beta/Smad and Wnt signaling pathways. Lei, S., Dubeykovskiy, A., Chakladar, A., Wojtukiewicz, L., Wang, T.C. J. Biol. Chem. (2004) [Pubmed]
  4. Gastric mucosal hyperplasia via upregulation of gastrin induced by persistent activation of gastric innate immunity in major histocompatibility complex class II deficient mice. Fukui, T., Nishio, A., Okazaki, K., Uza, N., Ueno, S., Kido, M., Inoue, S., Kitamura, H., Kiriya, K., Ohashi, S., Asada, M., Tamaki, H., Matsuura, M., Kawasaki, K., Suzuki, K., Uchida, K., Fukui, H., Nakase, H., Watanabe, N., Chiba, T. Gut (2006) [Pubmed]
  5. Chronic gastritis in the hypochlorhydric gastrin-deficient mouse progresses to adenocarcinoma. Zavros, Y., Eaton, K.A., Kang, W., Rathinavelu, S., Katukuri, V., Kao, J.Y., Samuelson, L.C., Merchant, J.L. Oncogene (2005) [Pubmed]
  6. Pancreatic gastrin stimulates islet differentiation of transforming growth factor alpha-induced ductular precursor cells. Wang, T.C., Bonner-Weir, S., Oates, P.S., Chulak, M., Simon, B., Merlino, G.T., Schmidt, E.V., Brand, S.J. J. Clin. Invest. (1993) [Pubmed]
  7. Differential involvement of CCK-A and CCK-B receptors in the regulation of locomotor activity in the mouse. Vasar, E., Harro, J., Lang, A., Pôld, A., Soosaar, A. Psychopharmacology (Berl.) (1991) [Pubmed]
  8. Control of enzyme secretion by non-cholinergic, non-adrenergic nerves in guinea pig pancreas. Pearson, G.T., Davison, J.S., Collins, R.C., Petersen, O.H. Nature (1981) [Pubmed]
  9. TFF2/SP-deficient mice show decreased gastric proliferation, increased acid secretion, and increased susceptibility to NSAID injury. Farrell, J.J., Taupin, D., Koh, T.J., Chen, D., Zhao, C.M., Podolsky, D.K., Wang, T.C. J. Clin. Invest. (2002) [Pubmed]
  10. Gastrin is a target of the beta-catenin/TCF-4 growth-signaling pathway in a model of intestinal polyposis. Koh, T.J., Bulitta, C.J., Fleming, J.V., Dockray, G.J., Varro, A., Wang, T.C. J. Clin. Invest. (2000) [Pubmed]
  11. Hypergastrinemia in response to gastric inflammation suppresses somatostatin. Zavros, Y., Rieder, G., Ferguson, A., Samuelson, L.C., Merchant, J.L. Am. J. Physiol. Gastrointest. Liver Physiol. (2002) [Pubmed]
  12. Helicobacter pylori can induce heparin-binding epidermal growth factor expression via gastrin and its receptor. Dickson, J.H., Grabowska, A., El-Zaatari, M., Atherton, J., Watson, S.A. Cancer Res. (2006) [Pubmed]
  13. Potential role of endocrine gastrin in the colonic adenoma carcinoma sequence. Watson, S.A., Morris, T.M., McWilliams, D.F., Harris, J., Evans, S., Smith, A., Clarke, P.A. Br. J. Cancer (2002) [Pubmed]
  14. Effects of gastrin, proglumide, and somatostatin on growth of human colon cancer. Smith, J.P., Solomon, T.E. Gastroenterology (1988) [Pubmed]
  15. Altered control of gastric acid secretion in gastrin-cholecystokinin double mutant mice. Chen, D., Zhao, C.M., Håkanson, R., Samuelson, L.C., Rehfeld, J.F., Friis-Hansen, L. Gastroenterology (2004) [Pubmed]
  16. Effects of vasoactive intestinal polypeptide (VIP), secretin and gastrin on insulin secretion in the mouse. Ahrén, B., Lundquist, I. Diabetologia (1981) [Pubmed]
  17. Gastrin and EGF synergistically induce cyclooxygenase-2 expression in Swiss 3T3 fibroblasts that express the CCK2 receptor. Slice, L.W., Hodikian, R., Zhukova, E. J. Cell. Physiol. (2003) [Pubmed]
  18. Gastrin stabilises beta-catenin protein in mouse colorectal cancer cells. Song, D.H., Kaufman, J.C., Borodyansky, L., Albanese, C., Pestell, R.G., Wolfe, M.M. Br. J. Cancer (2005) [Pubmed]
  19. Novel expression of gastrin (CCK-B) receptors in pancreatic carcinomas and dysplastic pancreas from transgenic mice. Povoski, S.P., Zhou, W., Longnecker, D.S., Bell, R.H. Am. J. Surg. (1994) [Pubmed]
  20. Unique roles of G protein-coupled histamine H2 and gastrin receptors in growth and differentiation of gastric mucosa. Fukushima, Y., Matsui, T., Saitoh, T., Ichinose, M., Tateishi, K., Shindo, T., Fujishiro, M., Sakoda, H., Shojima, N., Kushiyama, A., Fukuda, S., Anai, M., Ono, H., Oka, M., Shimizu, Y., Kurihara, H., Nagai, R., Ishikawa, T., Asano, T., Omata, M. Eur. J. Pharmacol. (2004) [Pubmed]
  21. Gastrin mediates the gastric mucosal proliferative response to feeding. Ohning, G.V., Wong, H.C., Lloyd, K.C., Walsh, J.H. Am. J. Physiol. (1996) [Pubmed]
  22. Gastrin stimulates the growth of gastric pit cell precursors by inducing its own receptors. Nakajima, T., Konda, Y., Izumi, Y., Kanai, M., Hayashi, N., Chiba, T., Takeuchi, T. Am. J. Physiol. Gastrointest. Liver Physiol. (2002) [Pubmed]
  23. Effect of carboxypeptidase E deficiency on progastrin processing and gastrin messenger ribonucleic acid expression in mice with the fat mutation. Udupi, V., Gomez, P., Song, L., Varlamov, O., Reed, J.T., Leiter, E.H., Fricker, L.D., Greeley, G.H. Endocrinology (1997) [Pubmed]
  24. Role of somatostatin receptors on gastric acid secretion in wild-type and somatostatin receptor type 2 knockout mice. Piqueras, L., Martínez, V. Naunyn Schmiedebergs Arch. Pharmacol. (2004) [Pubmed]
  25. Establishment of a human gastrinoma in nude mice. Upp, J.R., Trudel, J.L., Townsend, C.M., Alexander, R.W., Rajaraman, S., Nealon, W.H., Greeley, G.H., Thompson, J.C. Surgery (1988) [Pubmed]
  26. Antral G-cell in gastrin and gastrin-cholecystokinin knockout animals. Friis-Hansen, L., Wierup, N., Rehfeld, J.F., Sundler, F. Cell Tissue Res. (2005) [Pubmed]
  27. Release of transgenic human insulin from gastric g cells: a novel approach for the amelioration of diabetes. Lu, Y.C., Sternini, C., Rozengurt, E., Zhukova, E. Endocrinology (2005) [Pubmed]
WikiGenes - Universities