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Gastrin I rat

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Gastrin I can be used to determine the expression of histidine decarboxylase and histamine metabolism.

Category

Others

Catalog number

BAT-010728

CAS number

81123-06-0

Molecular Formula

C94H128N22O31S2

Molecular Weight

2126.28

Specification
Reference Reading

IUPAC Name

(4S)-5-[[(2S)-1-[[(2S)-1-[[2-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-amino-1-oxo-3-phenylpropan-2-yl]amino]-3-carboxy-1-oxopropan-2-yl]amino]-4-methylsulfanyl-1-oxobutan-2-yl]amino]-3-(1H-indol-3-yl)-1-oxopropan-2-yl]amino]-2-oxoethyl]amino]-3-(4-hydroxyphenyl)-1-oxopropan-2-yl]amino]-1-oxopropan-2-yl]amino]-4-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-1-[(2S)-1-[(2S)-5-carbamimidamido-2-[[(2S)-5-oxopyrrolidine-2-carbonyl]amino]pentanoyl]pyrrolidine-2-carbonyl]pyrrolidine-2-carbonyl]amino]-4-methylsulfanylbutanoyl]amino]-4-carboxybutanoyl]amino]-4-carboxybutanoyl]amino]-4-carboxybutanoyl]amino]-4-carboxybutanoyl]amino]-5-oxopentanoic acid

Sequence

XRPPMEEEEEAYGWMDF (Modifications: X-1 = Pyr)

Storage

Store at -20°C

InChI

InChI=1S/C94H128N22O31S2/c1-48(79(133)113-65(43-50-19-21-52(117)22-20-50)80(134)100-47-71(119)103-66(44-51-46-99-54-15-8-7-14-53(51)54)89(143)109-61(35-40-148-2)88(142)114-67(45-77(130)131)90(144)112-64(78(95)132)42-49-12-5-4-6-13-49)101-81(135)56(24-30-72(120)121)104-83(137)57(25-31-73(122)123)105-84(138)58(26-32-74(124)125)106-85(139)59(27-33-75(126)127)107-86(140)60(28-34-76(128)129)108-87(141)62(36-41-149-3)110-91(145)68-17-10-38-115(68)93(147)69-18-11-39-116(69)92(146)63(16-9-37-98-94(96)97)111-82(136)55-23-29-70(118)102-55/h4-8,12-15,19-22,46,48,55-69,99,117H,9-11,16-18,23-45,47H2,1-3H3,(H2,95,132)(H,100,134)(H,101,135)(H,102,118)(H,103,119)(H,104,137)(H,105,138)(H,106,139)(H,107,140)(H,108,141)(H,109,143)(H,110,145)(H,111,136)(H,112,144)(H,113,133)(H,114,142)(H,120,121)(H,122,123)(H,124,125)(H,126,127)(H,128,129)(H,130,131)(H4,96,97,98)/t48-,55-,56-,57-,58-,59-,60-,61-,62-,63-,64-,65-,66-,67-,68-,69-/m0/s1

InChI Key

FUTWNIPXZKAJHO-FKZYTOAASA-N

Canonical SMILES

CC(C(=O)NC(CC1=CC=C(C=C1)O)C(=O)NCC(=O)NC(CC2=CNC3=CC=CC=C32)C(=O)NC(CCSC)C(=O)NC(CC(=O)O)C(=O)NC(CC4=CC=CC=C4)C(=O)N)NC(=O)C(CCC(=O)O)NC(=O)C(CCC(=O)O)NC(=O)C(CCC(=O)O)NC(=O)C(CCC(=O)O)NC(=O)C(CCC(=O)O)NC(=O)C(CCSC)NC(=O)C5CCCN5C(=O)C6CCCN6C(=O)C(CCCNC(=N)N)NC(=O)C7CCC(=O)N7

1. Novel expression of gastrin (cholecystokinin-B) receptors in azaserine-induced rat pancreatic carcinoma: receptor determination and characterization

W Zhou, S P Povoski, D S Longnecker, R H Bell Jr Cancer Res. 1992 Dec 15;52(24):6905-11.

Many reports have emphasized the role of gastrin as a growth factor for normal gastrointestinal mucosa and gastrointestinal cancers. Recent studies have pointed out that this peptide acts also as a growth factor for the pancreatic cancer cell line AR42J. This effect is mediated by gastrin [cholecystokinin (CCK)-B] receptors. In the present study, we investigated gastrin (CCK-B) receptor expression in the azaserine-induced rat pancreatic carcinoma DSL-6, comparing it to normal rat pancreas, and we also characterized CCK receptor subtypes in this tumor. The results showed that there is extensive gastrin binding to the DSL-6 pancreatic carcinoma. No evidence of specific gastrin binding to normal pancreas was found. Analysis of the ability of gastrin-17-I to inhibit 125I-gastrin-I binding demonstrated that gastrin bound to a single class of receptors with a Kd of 0.21 +/- 0.04 nM and a binding capacity of 184 +/- 29 fmol/mg protein. 125I-Gastrin-I binding was inhibited by the specific CCK-B receptor antagonist L365,260 approximately 40 times more effectively than by the specific CCK-A receptor antagonist L364,718. Analysis of the ability of cholecystokinin octapeptide (CCK-8) to inhibit 125I-Bolton-Hunter-CCK-8 binding revealed two CCK binding sites, i.e., a high affinity site and a low affinity site. The observed binding affinities of CCK-8 were then introduced into the computer analysis of the dose-inhibition curve of the ability of gastrin-17-I to inhibit binding of 125I-Bolton-Hunter-CCK-8, which was significantly better fit by a three-site model than by a two-site model. The three sites meet the criteria for CCK-B, high affinity CCK-A, and low affinity CCK-A receptors. The binding capacity of CCK-B receptors constitutes 34% of the total high affinity CCK binding sites. This study demonstrated that DSL-6 pancreatic carcinoma expresses three subtypes of CCK receptors. Gastrin (CCK-B) receptors, which were not detected in normal rat pancreas, constitute about one third of the total high affinity CCK receptors. We suggest that novel expression of gastrin (CCK-B) receptors may be generated by gene mutation or amplification during carcinogenesis and may play an important role in promoting tumor growth.

2. Mitogenic effect of gastrin and expression of gastrin receptors in duct-like cells of rat pancreas

I Rooman, J Lardon, D Flamez, F Schuit, L Bouwens Gastroenterology. 2001 Oct;121(4):940-9. doi: 10.1053/gast.2001.27998.

Background & aims: Ductular metaplastic cells are observed during pancreas injury. Growth control by gastrin and expression of gastrin/cholecystokinin (CCK) B receptors were evaluated in these cells. Methods: Acinoductal transdifferentiation was induced in vitro by culturing of acinar cells, and ductular metaplasia was obtained in vivo by ligation of the pancreatic ducts. Mitogenic effects of gastrin I on ductal complexes in vivo and of tetragastrin, pentagastrin, and gastrin I and II, with or without the CCK-B receptor antagonist L-365,260, on duct-like cells in vitro were analyzed by 5-bromo-2'-deoxyuridine labeling. Immunocytochemistry, Western blotting, and reverse-transcription polymerase chain reaction were applied for detection of the CCK-B receptor. Results: Gastrin analogues induced a mitogenic stimulus in the duct-like cells in vitro and in ductal complexes in duct-ligated rat pancreas. Immunocytochemistry showed expression of CCK-B receptors in these models and in fetal but not normal adult exocrine pancreas. Additionally, up-regulation of CCK-B receptors during ductular metaplasia was shown by Western blotting and reverse-transcription polymerase chain reaction. Conclusions: Duct-like pancreatic epithelial cells in vitro and ductal complexes in vivo express gastrin/CCK-B receptors and proliferate in response to gastrin.

3. Distribution and metabolism of gastrin. An experimental study of the fate of 123 I-gastrin in the rat as studied by external detection with a gamma camera

H Lundqvist, S Gustavsson, G Lundqvist Eur Surg Res. 1978;10(2):109-20. doi: 10.1159/000127998.

In anesthetized rats, the activity distribution of intravenously administered synthetic human gastrin I, labelled with 123 I, was recorded externally by a gamma camera. In intact rats activity was found to accumulate in the kidneys and later in the stomach. After bilateral nephrectomy, the gastric apperance of activity was delayed. In both cases, the gastric activity is considered to emanate not from intact 123 I-gastrin but from free iodide, split off during gastrin degradation. The renal accumulation of gastrin in intact animals as well as the delayed gastric uptade of iodide in nephrectomized animals support the hypothesis that the kidneys are important organs for gastrin metabolism.