Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01350 (gastrin)
 9,683 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Regulatory relationship and gain control between cytosolic free Ca2+ concentration (Cai) and cytosolic pH (pHi) were evaluated by two different cell types, gastric parietal cells, and blood platelets. Studies were carried out in both single cells and populations of cells, using Ca2(+)-indicative probe fura-2 (1-(2-(5'-carboxyoxazol-2'-yl)-6-aminobenzofuran-5-oxy)-2-(2 '-amino-5'- methylphenoxy)ethane-N,N,N',N'-tetraacetic acid) and pH-indicative probe BCECF (2',7'-bis(carboxyethyl)carboxyfluorescein). Stimulation of single and populational parietal cells and platelets with gastrin and thrombin, respectively, resulted in an increase in Cai. In both populational cell types, an initial change in pHi during agonist stimulation occurred almost simultaneously with the mobilization of Ca2+; an initial transient decrease in pHi was followed by a slower increase in pHi above the prestimulation level. When populational platelets were preloaded with the Ca2+ chelator BAPTA (1,2-bis(o-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid), the thrombin-induced initial large increase in Cai was apparently inhibited, whereas the pHi decrease induced by thrombin was not altered. This suggests that the initial Cai change is not a prerequisite for the pHi change. The effect of pHi on Cai was examined next. In both single and populational cell types, application of the K(+)-H+ ionophore nigericin, which induced a transient decrease in pHi, led to the release of Ca2+ from intracellular stores. In single parietal cells double-labeled with fura-2 and BCECF, a temporal decrease in pHi preceded the rise in Cai after stimulation with nigericin. A decrease in pHi and an increase in Cai occurred at 1.5 and 4 s, respectively. In single parietal cells, replacement of medium Na+ with N-methyl-D-glucamine (NMG+), which also induced a decrease in pHi, resulted in repetitive Ca2+ spike oscillations. The source of Ca2+ utilized for the Ca2+ oscillation that was induced by NMG+ originated from the agonist-sensitive pool. Thus, several maneuvers, which were capable of decreasing pHi, led to an increase in Cai. Cytosolic acidification may be a part of the trigger for Ca2+ mobilization from intracellular stores in both parietal cells and platelets.
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PMID:Cytosolic acidification leads to Ca2+ mobilization from intracellular stores in single and populational parietal cells and platelets. 190 Jul 92

Evidence is accumulating that gastrin precursors may act as growth factors for the colonic mucosa in vivo. The aims of this study were to prepare recombinant human progastrin(6-80) and to investigate its structure and biological activities in vitro. Human progastrin(6-80) was expressed in Escherichia coli as a glutathione S-transferase fusion protein. After thrombin cleavage progastrin(6-80) was purified by reverse phase high pressure liquid chromatography and characterized by radioimmunoassay, amino acid sequencing, and mass spectrometry. Assays for metal ions by atomic emission spectroscopy revealed the presence of a single tightly bound calcium ion. Progastrin(6-80) at concentrations in the pm to nm range stimulated proliferation of the conditionally transformed mouse colon cell line YAMC. The observations that progastrin(6-80) did not bind to either the cholecystokinin (CCK)-A or the gastrin/CCK-B receptor expressed in COS cells and that antagonists selective for either receptor did not reverse the proliferative effects of progastrin(6-80) suggested that progastrin(6-80) stimulated proliferation independently of either the CCK-A or the gastrin/CCK-B receptor. We conclude that recombinant human progastrin(6-80) is biologically active and contains a single calcium ion. With the exception of the well known zinc-dependent polymerization of insulin and proinsulin, this is the first report of selective, high affinity binding of metal ions to a prohormone.
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PMID:Biologically active recombinant human progastrin(6-80) contains a tightly bound calcium ion. 1111 48

(-)-Epigallocatechin gallate, (-)-Gossypol; Ad.hIFN-beta, AF-37702, Agatolimod sodium, Agomelatine, Alvocidib hydrochloride, ARC-1779; Belimumab, BIBW-2992, Binodenoson, Bortezomib, Bosutinib, Brivaracetam; Cediranib, Clevidipine, CNTO-328, CP-751871, Curcumin; Darapladib, Deforolimus, Denosumab, Desvenlafaxine succinate, Dipyridamole/prednisolone, Dronedarone hydrochloride, DTPw-HBV/Hib 2.5; Ecogramostim, Elacytarabine, Eltrombopag, Eprodisate sodium; Farnesylthiosalicylic acid, Febuxostat, Fenretinide, Ferumoxytol, FMP2.1/AS02A, Forodesine hydrochloride, FP-0011; HuLuc-63, Human Fibroblast Growth Factor 1; Idraparinux sodium, Indium 111 (111In) ibritumomab tiuxetan, Interleukin-21, Ipilimumab, ISS-1018, ITF-2357; Lapaquistat acetate, Laropiprant, Liposomal vincristine, LY-518674; Masitinib mesylate, MAXY-G34, MGCD-0103, Midostaurin, Mitumprotimut-T, MK-0343, MLN-1202, MM-093, Motexafin gadolinium; NB-001, NB-002, Niacin/laropiprant; Oblimersen sodium, Ocrelizumab, Omacetaxine mepesuccinate; Panobinostat, Patupilone, PBI-1402, Perifosine, PHA-739358, Plerixafor hydrochloride, Prasugrel; Regadenoson, RHAMM R3 peptide, Rilonacept, Rivaroxaban, Romiplostim; Safinamide mesilate, Salinosporamide A, Selenite sodium, Sotrastaurin; Thrombin alfa, Tipifarnib, TRO-19622; Vatalanib succinate, Vernakalant hydrochloride, VRC-WNVDNA017-00-VP; YM-155, Yttrium 90 (90Y) ibritumomab tiuxetan; Zosuquidar trihydrochloride.
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PMID:Gateways to clinical trials. 1859 9