China Sincalide Cck-8, CAS 25126-32-3 Snap-8 Ahk Melanotan II Ghk-Cu, Find details about China Sincalide Peptide, Cck-8 from Sincalide Cck-8, CAS 25126-32-3 Snap-8 Ahk Melanotan II Ghk-Cu - Xiamen Austronext Trading Co., Ltd.
TY - JOUR. T1 - Effects of 1-oleoyl-2-acetyl glycerol are distinct from those of phorbol ester in rat pancreatic acini. AU - Scott Brockenbrough, J.. AU - Korc, Murray. PY - 1987/4/20. Y1 - 1987/4/20. N2 - 1-oleoyl-2-acetyl glycerol (OAG), a potent activator of protein kinase C, inhibited the binding of 125I-labelled epidermal growth factor (EGF) in isolated rat pancreatic acini. Unlike cholecystokinin-octapeptide (CCK8) and the C-kinase activator 12-0-tetradecanoyl phorbol-13-acetate (TPA), two inhibitors of 125I-EGF endocytosis in the pancreas, OAG had no effect on the distribution of bound ligand between the cell surface and intracellular compartments. Unlike TPA, OAG failed to potentiate the inhibitory effects of the calcium ionophore A23187 on 125I-EGF cell-associated radioactivity and had no effect on either basal or carbachol-stimulated amylase release in acini. These data suggest that the actions of the synthetic diacylglycerol OAG are not fully equivalent with the action of other known ...
Y , StdInChIKey = , bioavailability = 100% , protein_bound = , metabolism = proteaze plazme , elimination_half-life = 13 minuta , excretion = N/A , pregnancy_AU = , pregnancy_US = , pregnancy_category= , legal_AU = , legal_CA = , legal_UK = , legal_US = , legal_status = , routes_of_administration = IV }} CCK-4 (holecistokininski tetrapeptid, Trp-Met-Asp-Phe-NH2; ili PTK7) je peptidni fragment izveden iz većeg peptidnog hormona holecistokinina. Za razliku od holecistokina koji ima niz uloga u gastrointestinalnom sistemu kao i u centralnom nervnom sistemu, CCK-4 deluje prvenstveno u mozgu kao stimulator anksioznosti. On pokazuje slabe GI efekte, za razliku od CCK-8 ili polipeptida pune dužine, CCK-58. CCK-4 proizvodi jake simptome anksioznosti u malim dozama, kao što je 50 μg,[1] i često se koristi u naučnim istraživanjima za indukovanje paničnih napada s ciljem testiranja novih anksiolitika.[2][3][4][5] Pošto je on peptid, CCK-4 mora biti administriran putem injekcije. U telu se brzo ...
ProSpecs Peptide Hormones include: ACTH, Antide, Argipressin, Atosiban, Buserelin, Cetrorelix, DDAVP, Deslorelin, Elcatonin, Exenatide, Exendin-4, Ganirelix, GHRL, GHRP-2, GHRP-6, Goserelin, Hexarelin, Histrelin, Lanreotide, Lypressin, MT-II, NAF, PMSG, Secretin, Sincalide, Pramlintide, Somatostatin, Terlipressin, Triptorelin Acetate, Thymopentin, Thymosin- α1, Thymosin β4, Vasopressin
The accompanying paper (Bignon et al., 1999) on SR146131 describes the compounds effects as a potent and selective agonist at both human and rodent CCK1 receptors in vitro. The present paper evaluated the drugs effects in vivo, and shows clearly that SR146131 can mimic, in a variety of test systems and in several species, a wide range of the effects of sulfated cholecystokinin octapeptide (CCK8S), which have previously been attributed to the stimulation of CCK1 receptors but not those related to the stimulation of CCK2 receptors.. SR146131 inhibited gastric emptying in mice, and also decreased gallbladder volume in this species after administration of low oral doses. SR146131 also reduced food intake in two rodent and one primate species. The compound reduced food intake in fasted rats, and in nonfasted rats in which food intake had been highly stimulated by the administration of NPY(1-36). Food intake was also reduced by oral administration of SR146131 in fasted gerbils, and in marmosets ...
As nouns the difference between octapeptide and octreotide is that octapeptide is an oligopeptide having eight amino acids while octreotide is...
TY - JOUR. T1 - Multiple kinases phosphorylate the pancreatic cholecystokinin receptor in an agonist-dependent manner. AU - Gates, L. K.. AU - Ulrich, C. D.. AU - Miller, L. J.. PY - 1993/1/1. Y1 - 1993/1/1. N2 - The cholecystokinin (CCK) receptor on the rat pancreatic acinar cell is a guanine nucleotide-binding protein (G protein)-coupled receptor, which was recently demonstrated to be phosphorylated in response to agonist stimulation (Klueppelberg et al., J. Biol. Chem. 266: 17744-17746, 1991). In this work, we establish that this receptor is phosphorylated in response to a variety of homologous and heterologous secretagogues and that these phosphorylation events represent action by more than one protein kinase. One subgroup of kinases includes one or more isotype of protein kinase C (PKC), and is capable of playing a role in homologous and heterologous desensitization. A second subgroup of kinases that acts on the CCK receptor was defined by its resistance to 10 μM staurosporine, which was ...
TY - JOUR. T1 - A role for cholecystokinin-stimulated protein tyrosine phosphorylation in regulated secretion by the pancreatic acinar cell. AU - Lutz, M. P.. AU - Sutor, S. L.. AU - Abraham, R. T.. AU - Miller, L. J.. PY - 1993/1/1. Y1 - 1993/1/1. N2 - Cholecystokinin (CCK) is a gastrointestinal hormone that acts through a G protein-coupled receptor to stimulate pancreatic enzyme secretion. In this work, we demonstrate that CCK stimulation of dispersed pancreatic acini results in increased tyrosine phosphorylation of several cellular proteins. This is mediated via a calcium-dependent pathway, also activated by a phenethyl ester analogue of CCK and calcium ionophores, and by a protein kinase C-dependent cascade, also activated by the phorbol ester 12-O- tetradecanoylphorbol-13-acetate. All demonstrable stimulated tyrosine phosphorylation events were inhibited by genistein, with different subsets of proteins affected by staurosporine and H-7. The importance of tyrosine phosphorylation events in ...
The cat caudate nucleus has been reported to possess a rich and fairly even distribution of nerve endings, containing both dopamine- and cholecystokinin-like peptides. In this study, the effect of cholecystokinin-octapeptide (CCK-8) on basal and electrically evoked tritium outflow from slices of cat caudate nucleus previously labeled with [3H]dopamine was examined. Evoked tritium outflow from slices of cat caudate nucleus was Ca2+ dependent and abolished by tetrodotoxin, suggesting that it reflects action potential-induced [3H]dopamine release. In the presence of bovine serum albumin and bacitracin, the sulfated but not the unsulfated form of CCK-8 inhibited both basal and electrically evoked tritium outflow from slices of cat caudate nucleus at very low concentrations. CCK-8 sulfate was efficient in causing this effect in concentrations down to 10(-14) M, and the maximum effect was obtained with 10(-11) M. In contrast, without bovine serum albumin and bacitracin, no inhibitory effect of CCK-8 ...
The IUPHAR/BPS Guide to Pharmacology. desulfated cholecystokinin-8 ligand page. Quantitative data and detailed annnotation of the targets of licensed and experimental drugs.
CCKAR山羊多克隆抗体(ab77269)可与大鼠, 人样本反应并经WB, ELISA, IHC, ICC/IF实验严格验证,Abcam CCKAR抗体被1篇文献引用。所有产品均提供质保服务,中国75%以上现货。
Creative Peptides offers Octapeptide 1 for your research. We also provide custom peptide synthesis, process development, GMP manufacturing.
We have previously demonstrated [M. Campos-Toimil, T. Bagrij, J.M. Edwardson, P. Thomas, Two modes of secretion in pancreatic acinar cells: involvement of phosphatidylinositol 3-kinase and regulation by capacitative Ca2+ entry, Curr. Biol. 12 (2002) 211-215] that in rat pancreatic acinar cells, Gd3+-sensitive Ca2+ entry is instrumental in governing which second messenger pathways control secretory activity. However, in those studies, we were unable to demonstrate a significant increase in cytoplasmic [Ca2+] during agonist application as a result of this entry pathway. In the present study, we combined pharmacology with ratiometric imaging of fura-2 fluorescence to resolve this issue. We found that 2 μM Gd3+ significantly inhibits store-mediated Ca2+ entry. Furthermore, both the protonophore, CCCP (5 μM) and the mitochondrial Ca2+-uptake blocker, RU360 (10 μM), led to an enhancement of the plateau phase of the biphasic Ca2+ response induced by acetylcholine (1 μM). This enhancement was ...
Kiyama, H.; Shiosaka, S.; Kubota, Y.; Cho, H.J.; Takagi, H.; Tateishi, K.; Hashimura, E.; Hamaoka, T.; Tohyama, M., 1983: Ontogeny of cholecystokinin-8 containing neuron system of the rat: an immunohistochemical analysis--II. Lower brain stem
Gentaur molecular products has all kinds of products like :search , Meridian Life Science \ Rabbit anti Cholecystokinin Receptor A \ D24010R for more molecular products just contact us
TY - JOUR. T1 - Isolated pancreatic acini from suckling and weanling rats. T2 - Changes in amino acid incorporation and carbachol-stimulated amylase secretion with age. AU - Pollack, Paul F.. AU - Verbridge, Jill. AU - Thornburg, William. AU - Koldovsky, Otakar. AU - Korc, Murray. PY - 1986/1/1. Y1 - 1986/1/1. N2 - To characterize the changes in pancreatic function during postnatal development, isolated pancreatic acini were prepared from rats aged 8-9, 12-14 and 20 days and from adult rats. Isolated acini maintained a normal microscopic appearance and viability as judged by exclusion of trypan blue and linear incorporation of tritiated leucine into total protein. The rate of incorporation in 8-day-old acini was 20% of that observed in adult rats. Significant dose-dependent increases in amylase release in response to carbachol were observed in all age groups; stimulated amylase secretion was significantly less in the 8- to 9- and 12- to 14-day-old animals than in the 20-day-old and adult rats. ...
The gastric enterochromaffin-like (ECL) cell se cretes histamine in response to secretagogues (gastrin, acetylcholine) by calcium signaling-dependent exocytosis of intracellular vacuoles containing the hormone. ECL cells were isolated from rat fundic gastric mucosa by elutriation and density-gradient centrifugation. Currents across the plasma membrane were measured using whole cell patch-clamp methods. These cells had a low conductance of 0.5 nS and resting potential of -50 mV Depolarization activated a K+ current that was blocked by Ba2+. Steady-state current in absence of K+ was due to Cl- because of the magnitude of the reversal potential and the effects of Cl- removal. Stimulation of secretion by gastrin, cholecystokinin octapeptide (CCK-8), and the phorbol ester 12-O-tetradecanoylphorbol 13-acetate activated the Cl- conductance with a time course similar to that of histamine release. Therefore the ECL cell maintains a high resting potential, largely due to K+ currents, and stimulation of ...
In the present study, we characterized the metabolic profile of the recently described lean Cck1r−/− rat on a Fischer 344 background. With our unique animal model, we hypothesized that the lean Cck1r−/− rats would show increased meal size and energy expenditure relative to their Fischer 344 wild-type counterparts. Cck1r−/− rats consumed larger meals during the dark cycle and smaller meals during the light cycle. These effects were accompanied by increased total spontaneous activity and energy expenditure during the dark cycle, as well as an apparent shift toward increased fat utilization as demonstrated by the reduction in RQ during the light cycle. On the basis of the findings in the OLETF rats (3), we predicted that both Cck1r+/+ and Cck1r−/− rats would show increased weight gain during chronic exposure to a highly palatable, HFD. Indeed, both Cck1r+/+ and Cck1r−/− rats were prone to DIO when maintained on a HFD, which was associated with increased serum leptin levels. We ...
Cholecystokinin tetrapeptide (CCK-4, also PTK7) is a peptide fragment derived from the larger peptide hormone cholecystokinin. CCK-4 acts primarily in the brain as an anxiogenic, although it does retain some GI effects, but not as much as CCK-8 or the full length polypeptide CCK-58.
L-365260 is a selective cholecystokinin receptor 2 (CCK2) antagonist (IC50 values are 2 and 280 nM at CCK2 and CCK1 receptors respectively).
Complete information for CCKBR gene (Protein Coding), Cholecystokinin B Receptor, including: function, proteins, disorders, pathways, orthologs, and expression. GeneCards - The Human Gene Compendium
Thank you for your interest in spreading the word about Biochemical Society Transactions.. NOTE: We only request your email address so that the person you are recommending the page to knows that you wanted them to see it, and that it is not junk mail. We do not capture any email address.. ...
tuftsinyltuftsin: octapeptide consisting of 2 moles of tufsin; better than tuftsin in prolonging life of syngeneic mice injected with L1210 leukemia cells
TY - JOUR. T1 - Cholecystokinin secretagogue-induced gastroprotection. T2 - Role of nitric oxide and blood flow. AU - West, Sonlee D.. AU - Helmer, Kenneth S.. AU - Chang, Lily K.. AU - Cui, Yan. AU - Greeley, George H.. AU - Mercer, David W.. PY - 2003/3/1. Y1 - 2003/3/1. N2 - This study was done to examine the role of CCK in gastric mucosal defense and to assess the gastroprotective roles of nitric oxide and blood flow. In rats, the CCK secretagogues oleate and soybean trypsin inhibitor augmented gastric mucosal blood flow and prevented gastric injury from luminal irritants. Type A CCK receptor blockade negated CCK secretagogue-induced gastroprotection and exacerbated gastric injury from bile and ethanol but did not block adaptive cytoprotection. CCK secretagogue-induced gastroprotection and hyperemia were negated by nonselective nitric oxide synthase (NOS) inhibition (nG-nitro-L-arginine methyl ester) but not by selective inducible NOS inhibition (aminoguanidine). Gastric mucosal ...
The mechanisms regulating the proliferation and differentiation processes that give rise to and maintain the gastric epithelium have not yet been completely elucidated.. In the present studies, in vitro models were established and the influence of growth factors and extracellular matrix proteins on these processes were investigated. Pentagastrin and hydrocortisone were found to accelerate the development of H,KTPase-positive parietal cells and other epithelial cells from undifferentiated gastric epithelial cells of foetal rats. These undifferentiated cells and also presumably immature epithelial cells in the progenitor zone of adult gastric glands were shown to express cholecystokinin-2 (CCK2) receptors and are therefore targets for the trophic action of gastrin.. H,K-ATPase-positive parietal cells in the progenitor zone of adult glands were also found to express CCK2 receptors, indicating that gastrin may stimulate maturation of the parietal cell lineage even during adult life. Parietal cells ...
To identify the molecular components of the vasoactive intestinal peptide (VIP) binding sites in the liver, 125I-labelled VIP was covalently linked to liver membranes by using the cleavable cross-linker dithiobis(succinimidylpropionate). Purified rat liver plasma membranes were incubated with 125I-VIP, washed and treated with 1 mM-cross-linker. Polyacrylamide-gel electrophoresis of membrane proteins followed by autoradiography revealed a major 125I-VIP-protein complex of Mr 51 000. A minor Mr 89 000 complex was also observed. An identical pattern of protein labelling was obtained using crude membranes from rat liver. Labelling of the Mr 51 000 and 89 000 species was specific in that it could be abolished by native VIP, but was unaffected by 1 microM-glucagon and cholecystokinin octapeptide. Densitometric scanning of autoradiographs indicated that the labelling of the two species was abolished by similar low VIP concentrations (0.1-100 nM). It was also reduced by two VIP agonists, peptide ...
Receptor ligands, identified as antagonists, based on the absence of stimulation of signaling, can rarely stimulate receptor internalization. d-Tyr-Gly-[(Nle(28,31),d-Trp(30))CCK-26-32]-2-phenylethyl ester (d-Trp-OPE) is such a ligand that binds to the cholecystokinin (CCK) receptor and stimulates internalization. Here, the molecular basis of this trafficking event is explored, with the assumption that ligand binding initiates conformational change, exposing an epitope to direct endocytosis. Ligand-stimulated internalization was studied morphologically using fluorescent CCK and d-Trp-OPE. d-Trp-OPE occupation of Chinese hamster ovary cell receptors stimulated internalization into the same region as CCK. Arrestin-biased action was ruled out using morphological translocation of fluorescent arrestin 2 and arrestin 3, moving to the membrane in response to CCK, but not d-Trp-OPE. Possible roles of the carboxyl terminus were studied using truncated receptor constructs, eliminating the proline-rich distal tail
Definition of cholecystokinin in the Financial Dictionary - by Free online English dictionary and encyclopedia. What is cholecystokinin? Meaning of cholecystokinin as a finance term. What does cholecystokinin mean in finance?
Cholecystokinin A Receptor: A subtype of cholecystokinin receptor found primarily in the PANCREAS; STOMACH; INTESTINE; and GALLBLADDER. It plays a role in regulating digestive functions such as gallbladder contraction, pancreatic enzyme secretion and absorption in the GASTROINTESTINAL TRACT.
Bombesin pseudo-peptide analogues containing a hydroxamide function on the C-terminal part of the molecule, e.g. H-D-Phe-Gln-Trp-Ala-Val-Gly-His-Leu-NHOBzl 1 and H-D-Phe-Gln-Trp-Ala-Val-Gly-His-Leu-NHOH 2 were synthesized. These compounds were tested for their ability to recognize the bombesin receptor on rat pancreatic acini and on 3T3 cells, to stimulate (i) amylase secretion from rat pancreatic ...
Creative Biolabs provides Human anti-vesicular stomatitis virus octapeptide (VSV8) (aa 52-59) T cell receptor, pCDTCR1 product for Biopharmaceutical research,preclinical and clinical trials.
Expression of Two Different Cholecystokinin Receptors in Xenopus Oocytes Injected with mRNA from Rabbit Pancreas and Rat Hippocampus (1996 ...
Caffeine inhibits a low affinity but not a high affinity mechanism for cholecystokinin-evoked Ca2+ signalling and amylase release from guinea pig pancreatic acini.Naunyn ...
Gastrin is a peptide hormone that stimulates secretion of gastric acid by the parietal cells of the stomach. Gastrin binds to a G-protein coupled receptor encoded by the CCKBR gene that also binds cholecystokinin (CCK), a brain regulatory peptide. The receptor is therefore known as the gastrin/cholecystokinin type B receptor. It is also known as cholecystokinin B receptor, cholecystokinin-2 receptor, CCK-B, CCKB-R, CCKRB, CCK2R, and GASR. The gastrin/cholecystokinin receptor is expressed mostly in central nervous system and the gastrointestinal tract. A misspliced transcript variant of the CCKBR gene that includes an intron has been associated with colorectal and pancreatic tumors.. ...
CCK receptors significantly influence neurotransmission in the brain, regulating anxiety, feeding, and locomotion. CCK-B expression may correlate parallel to anxiety and depression phenotypes in humans. CCK-B receptors possess a complex regulation of dopamine activity in the brain. CCK-B activation appears to possess a general inhibitory action on dopamine activity in the brain, opposing the dopamine-enhancing effects of CCK-A. However, the effects of CCK-B on dopamine activity vary depending on location.[11] CCK-B antagonism enhances dopamine release in rat striatum.[12] Activation enhances GABA release in rat anterior nucleus accumbens.[13] CCK-B receptors modulate dopamine release, and influence the development of tolerance to opioids.[14] CCK-B activation decreases amphetamine-induced DA release, and contributes to individual variability in response to amphetamine.[15] In rats, CCK-B antagonism prevents the stress-induced reactivation of cocaine-induced conditioned place preference, and ...
1. A scheme of synthesis was developped for cholecystokinin (CCK 26-33, using solid-phase methodology and successfully applied to the synthesis of its C- and N-terminal fragments. 2. Using CCK 30-33 as model, it was found that deprotection of the ?-phenacyl ester, with a 1 M solution of sodium thiophenoxide in DMF, leads to the formation of an aminosuccylnyl peptide, prior to ammonolysis. 3. Selenophenol reagent successfully removes the ?-phenacyl ester on protected CCK 32-33 and on protected CCK 30-33 polymer prior to ammonolytic cleavage of peptides from the resin. 4. Treatment of Boc-Asp(?-OPac)-Tyr(0-2,4-Dnp)-Met-Gly-Trp(Nin-For)-Met-Asp(?-OPac)-Phe-polymer with a 1 M solution of selenophenol in DMF, leads to irreversible rearrangement of the 0-2,4-dinitrophenyl ether. 5. Undesirable side-reactions can be avoided by sequential deprotections and cleavage. The 0-2,4-dinitrophenyl ether is removed by thiolysis following by selenolysis of the ?-phenacyl esters. Cleavage of the peptide from the ...
Looking for online definition of CCKAR or what CCKAR stands for? CCKAR is listed in the Worlds largest and most authoritative dictionary database of abbreviations and acronyms
1. Niederau C, Lüthen R. The influence of CCK receptor antagonists on pancreatic feedback regulation. Internationales Symposium, Irsee, Bayern, Juni 1989. 2. Lüthen R, Niederau C, Niederau M, Borchard F, Strohmeyer G. Intrazelluläre Kompatimentierungsstörung bei experimenteller biliärer akuter Pankreatits. 44. Tagung der Dtsch. Ges. für Verdauungs- und Stoffwechselkrankheiten, Main, September 1989. Z Gastroentrol 1989, 27:536. 3. Niederau C, Lüthen R, Niederau M, Strohmeyer G. Langzeitwirkung von CCK-Stimulation und -Blockade auf Wachstum und Funktion des exokrinen Pankreas der Maus. 44. Tagung der Dtsch. Ges. für Verdauungs- und Stoffwechselkrankheiten, Mainz, September 1989. Z Gastroentrol 1989, 27:521. 4. Niederau M, Niederau C, Strohmeyer G, Lüthen R. Epidemiologie des Pankreaskarzinoms. 44. Tagung der Dt. Ges. f. Verdauungs- und Stoffwechselkrankheiten. September 89, Mainz. Z Gastroenterol 1989, 27:466. 5. Niederau C, Lüthen R, Niederau M, Strohmeyer G, Ferrell LD, Grendell JH. ...
GSK-7975A inhibits CRAC entry (Fura-2 340:380 normalized at 700 s). (A) Changes in mouse pancreatic acinar [Ca2+]C induced by CCK (1 nmol/L) with external physi
1KZW: Solution structure of human intestinal fatty acid binding protein with a naturally-occurring single amino acid substitution (A54T) that is associated with altered lipid metabolism
The effects of aspirin and ibuprofen on pepsinogen secretion were studied in isolated human peptic cells prepared from endoscopically obtained biopsy specimens after collagenase digestion, mechanical disruption, and percoll gradient centrifugation. Pharmacological concentrations of aspirin and ibuprofen (10(-8)-10(-4) M), potentiated histamine (10(-6)-10(-4)M) and forskolin (10(-5)M) stimulated pepsinogen secretion without affecting basal secretion, acetylcholine (10(-6)M) stimulated pepsinogen secretion or cell vitality. Augmentation of secretagogue stimulated pepsinogen secretion was dependent on extracellular calcium because potentiation was abolished by calcium depletion of the medium. Cimetidine inhibited the potentiation effect on histamine but not on forskolin stimulated pepsinogen secretion, thus suggesting that this augmentation was independent of histamine H2 receptors. Of interest, potentiation was also independent of endogenous prostaglandin inhibition because exogenous addition of ...
Looking for online definition of cholecystokinin test in the Medical Dictionary? cholecystokinin test explanation free. What is cholecystokinin test? Meaning of cholecystokinin test medical term. What does cholecystokinin test mean?
Shiratori K, Takeuchi T, Satake K, Matsuno S; Study Group of Loxiglumide in Japan. Clinical evaluation of oral administration of a cholecystokinin-A receptor antagonist (loxiglumide) to patients with acute, painful attacks of chronic pancreatitis: a multicenter dose-response study in Japan. Pancreas 2002; 25: e1-5. PMID: 12131781 ...
Cholecystokinin tetrapeptide (CCK-4, Trp-Met-Asp-Phe-NH2) is a peptide fragment derived from the larger peptide hormone cholecystokinin. Unlike cholecystokin which has a variety of roles in the gastrointestinal system as well as central nervous system effects, CCK-4 acts primarily in the brain as an anxiogenic, although it does retain some GI effects, but not as much as CCK-8 or the full length polypeptide CCK-58. CCK-4 reliably causes severe anxiety symptoms when administered to humans in a dose of as little as 50μg,[1] and is commonly used in scientific research to induce panic attacks for the purpose of testing new anxiolytic drugs.[2][3][4][5] Since it is a peptide, CCK-4 must be administered by injection, and is rapidly broken down once inside the body so has only a short duration of action,[6] although numerous synthetic analogues with modified properties are known.[7][8][9][10][11][12][13][14][15][16][17] ...
Pérez de la Mora, M., Hernández-Gómez, A. M., Arizmendi-García, Y., Jacobsen, K. X., Lara-García, D., Flores-Gracia, C., Crespo-Ramírez, M., Gallegos-Cari, A., Nuche-Bricaire, A. and Fuxe, K. (2007), Role of the amygdaloid cholecystokinin (CCK)/gastrin-2 receptors and terminal networks in the modulation of anxiety in the rat. Effects of CCK-4 and CCK-8S on anxiety-like behaviour and [3H]GABA release. European Journal of Neuroscience, 26: 3614-3630. doi: 10.1111/j.1460-9568.2007.05963.x ...
AequoScreen® Double Transfected Cell Lines: Cholecystokinin, CCKA subtype. Human Recombinant, in 1321N1 host cell. Two vials of cryopreserved cells are shipped per order. A detailed technical dossier includes sequence, culture conditions and pharmacological properties of the recombinant receptor. All cell lines are tested for the absence of mycoplasma. Terms and conditions apply. Some products are not available in some countries. Please inquire at your local sales office for more information.. Features:. ...
3H]-(+/-)-L-364,718 a new, potent and selective nonpeptide peripheral cholecystokinin (CCK) antagonist bound saturably and reversibly to rat pancreatic membranes. The radioligand recognized a single class of binding sites with a high affinity (Kd = 0.23 nM). The binding of [3H]-(+/-)-L-364,718 was stereospecific in that the more biologically active (-)-enantiomer demonstrated greater potency than the (+)-enantiomer. The rank order of potency of various CCK agonists and antagonists in displacing [3H]-(+/-)-L-364,718 correlated with their ability to displace [125I]CCK-8 and their known pharmacological activities in peripheral tissues. However, the absolute potencies of agonists were greater in displacing [125I]CCK-8 than [3H]-(+/-)-L-364,718. As described for other physiologically relevant receptor systems, the potency for displacement of [3H]-(+/-)-L-364,718 binding by CCK agonists, but not antagonists, was reduced by guanosine 5-(beta, gamma-imido)triphosphate and NaCl and enhanced by MgCl2. ...
Monoklonale und polyklonale Cholecystokinin Antikörper für viele Methoden. Ausgesuchte Qualitäts-Hersteller für Cholecystokinin Antikörper. Hier bestellen.
The present study demonstrates, using a strain of rats deficient in CCK-A receptors, that the c-Fos protein expression in the NTS induced by exogenous peripheral administration of CCK is mediated by CCK-A receptors. In addition, the significant reduction in the number of activated neurons in the NTS in OLETF rats after feeding suggests that CCK-A receptors are involved in the activation of NTS neurons in response to a meal. Consistent with this finding in CCK-A-deficient rats, activation of NTS neurons in response to feeding was also markedly reduced by pretreatment with MK329, a potent CCK-A receptor antagonist. In addition, exogenous CCK decreased cumulative food intake in Sprague-Dawley and in LETO rats but had no effect on food intake in CCK-A receptor-deficient OLETF rats. Thus, in the absence of CCK-A receptors and neuronal activation of NTS neurons, CCK had no effect on food intake, suggesting that activation of NTS neurons is required to initiate the satiety response to CCK. We have ...
Cytosolic free calcium concentrations ([Ca2+]i) and amylase secretion were measured in isolated rat pancreatic acini loaded with the intracellularly trapped fluorescent indicator quin2. Both caerulein and carbamoylcholine caused a rapid increase in [Ca2+]i, with a maximal 3-fold increase at 10(-9) M-caerulein and 10(-4) M-carbamoylcholine. However, caerulein (10(-12) M and 10(-11) M) as well as carbamoylcholine (10(-7) M) caused a significant stimulation of amylase release, while not inducing any detectable rise in [Ca2+]i. Changes in [Ca2+]i after addition of either secretagogue were transient and did not last more than 2-3 min. By contrast, when amylase secretion was monitored as a function of time, two distinct secretory phases could be observed upon addition of either carbamoylcholine (10(-5) M) or caerulein (10(-10) M). An initial, rapid phase (0-5 min) which caused a 6-7-fold increase above basal, followed by a sustained (5-30 min), but less marked, secretory rate (2-3-fold above basal). ...