Disease relevance of LOC617510

• SW-1990 and MIA PaCa-2 pancreatic cancer cell lines were grown in serum-supplemented and serum-free medium in the presence of pancreastatin (10(-11)-10(-6) M), or cholecystokinin (CCK) (10(-11)-10(-8) M) or combinations thereof [1].
• This relationship has been investigated by clinical studies of symptoms associated with gallstones, by investigation of gallbladder emptying and cholecystokinin (CCK) release in patients with gallstones, and after cholecystectomy, or truncal vagotomy, and in the irritable bowel syndrome (IBS) [2].

High impact information on LOC617510

• Intraduodenal perfusion of phenylalanine and oleic acid increased plasma cholecystokinin (CCK) from a basal level of 0.9 +/- 0.06 to 5.3 +/- 0.9 pM and 7.2 +/- 1.3 pM, respectively [3].
• In contrast, intraduodenal perfusion of phenylalanine (10 mM) produced a significant increase in plasma CCK levels (6.7 +/- 0.8 pM) and a three- to fourfold increase in pancreatic enzyme outputs [4].
• Perfusion of the duodenum with bovine trypsin (1 g/L) reduced the plasma CCK levels to basal values and significantly attenuated the phenylalanine-stimulated enzyme secretion to 63% +/- 4% of control [4].
• The findings suggest that CCK-8 sulfate in dopamine/CCK coexistence regions is involved in regulating dopamine release [5].
• Only structurally related peptides inhibited CCK binding, and good correlation existed between relative potencies for binding inhibition and for stimulating gallbladder contraction [6].

Biological context of LOC617510

• The sequence for porcine CCK-58 predicted from CCK cDNA was identical with the amino acid sequence of the peptide purified from different lots of animals [7].
• The authors report that cholecystokinin (CCK), via its subtype 2 receptor (CCK2R) located presynaptically on cerebral arteries, mediates the release of nitric oxide (NO), which induces vasodilatation [8].
• These complex interactions between opioids and endogenous CCK receptor systems have suggested the need for a new paradigm in drug design for some states of chronic pain [9].
• Neither peptide produced a discernible change in mean heart rate or aortic blood pressure, or in the mean arterial plasma concentrations of enteroglucagon, gastric inhibitory peptide (GIP), gastrin or cholecystokinin (CCK) [10].
• The effects of glyceryl trinitrate (GTN), sodium nitroprusside and Kreb's solution upon CCK-stimulated muscle contraction were examined [11].

Anatomical context of LOC617510

• This degree of enrichment for plasma membranes was adequate for the initial biochemical characterization of this CCK receptor [6].
• The major labeled band of Mr = 70,000-85,000 has a lower apparent Mr than that of the analogous band in pancreas labeled with similar methods, supporting the molecular heterogeneity of CCK receptors on these two target tissues [6].
• To study proximal events in cholecystokinin (CCK) action on bovine gall bladder smooth muscle, we used the hormone analogue D-Tyr-Gly-[(N1e28,31)CCK-26-32]-phenethyl ester (OPE), which has unique biological properties [12].
• The influence of CCK on the upper gut microstructure in neonatal calves could be either direct via activation of CCK-A receptors located in the mucosa of the upper gut or indirect by modulation of the secretion of pancreatic juice [13].
• Caerulein (10(-10)-10(-7) M), a CCK receptor agonist, increased formation of inositol phosphates in primary cultured bovine adrenal medullary (BAM) chromaffin cells in a concentration-dependent manner [14].

Associations of LOC617510 with chemical compounds

• Thus, the gall bladder CCK receptor is a single molecule capable of assuming two interconvertible affinity states, regulated by a guanine nucleotide-binding protein [12].
• Pancreatic exocrine secretion and duodenal EMG were studied following intraduodenal CCK-A receptor antagonist (Tarazepide), intravenous atropine, and intravenous or intraduodenal CCK-8 administrations [15].
• Six kinds of endocrine cells - serotonin (5-HT)-, somatostatin-, gastrin-, motilin-, cholecystokinin (CCK)- and bovine pancreatic polypeptide (BPP)-immunoreactive cells - were identified in this study [16].
• Cat CCK-58 with a serine at position 40, the same residue found in pig, mouse, cow and rabbit CCK-58, can be used as a unique bioprobe for defining how amino terminal amino acids influence the structure and bioactivity of the carboxyl terminal region of CCK [17].
• CCK-induced pancreatic secretion was abolished by SR 27897 (15 nmol kg-1 min-1, 55 min) and reduced by PD 135158 (0.15 nmol kg-1 min-1, 55 min) [18].

Analytical, diagnostic and therapeutic context of LOC617510

• Molecular cloning of cholecystokinin (CCK) mRNA from porcine brain and gut has demonstrated that CCK is synthesized as an identical precursor in both tissues [7].
• We used our radioimmunoassay to investigate whether chymotrypsin, rather than trypsin, could be the major mediator of negative feedback control of CCK release [19].
• Plasma CCK increased significantly after intravenous infusion, but remained unchanged after intraduodenal infusion [20].
• In the in vivo experiments, pancreastatin (15 micrograms/kg) did not affect growth of SW-1990 xenografts to nude mice, but inhibited CCK-stimulated growth transiently [1].
• In order to know the effects of weaning and volatile fatty acid feeding on gastric leptin expression, we investigated the expression of leptin and CCK receptor mRNA in the bovine rumen, abomasum and duodenum using RT-PCR in 3-week-old pre-weaning, 13-week-old post-weaning and adult animals [21].

References