anti-Cholecystokinin (CCK) Antikörper

Cow (Bovine) Cholecystokinin (CCK) Interaktionspartner

1. This review explores the role of luminal cholecystokinin on the regulation of exocrine pancreatic secretion in author's studies of newborn calves.

Pig (Porcine) Cholecystokinin (CCK) Interaktionspartner

1. Haemodynamic changes seem to regulate regional proCCK expression in the mammalian heart.

2. We conclude that only a small fraction of neuronal CCK is nonsulfated. The intracellular distribution of nonsulfated CCK in neurons suggests that they contribute only modestly to the CCK transmitter activity.

3. Cardiac expression of pro-cholecystokinin is cell-specific, which differentiates the expression from that of intestinal endocrine cells and cerebral neurons.

4. This review explores the role of luminal cholecystokinin on the regulation of exocrine pancreatic secretion in author's studies of neonatal pigs.

Human Cholecystokinin (CCK) Interaktionspartner

1. Haemodynamic changes seem to regulate regional proCCK expression in the mammalian heart.

2. In patients with gastroesophageal reflux disease (GERD) an increase of cholecystokinin level is observed. The combination of GERD and type II diabetes is accompanied by a more prominent increase of cholecystokinin in blood serum.

3. We found the suicide-associated gene coexpression network. The reconstructed network consisted of 104 genes. Topological analysis showed that in total, CCK, INPP1, DDC, and NPY genes are the most fundamental hubs in the network

4. L-trp is a luminal regulator of CCK release with effects on gastric emptying, an effect that could be mediated by CCK. L-trp's effect on GLP-1 secretion is only minor. At the doses given, the two amino acids did not affect subjective appetite feelings.

5. The CCK polymorphism have reported significant association of -45C>T polymorphism with the presence of hallucinations.

6. CCK does not appear to play a unique independent role in satiety/satiation.

7. CCK release has been found to be halved in pregnant women with hyperemesis gravidarium, which supports the hypothesis that gastrointestinal motility is increased in pregnant women with hyperemesis gravidarium.

8. CCK in plasma is an independent marker of cardiovascular mortality in elderly female patients.

9. These data offer preliminary evidence supporting an association between the rs1799923 polymorphism in the CCK gene and PTSD

10. Data suggest that endocrine responses differ between jejunal and gastric enteral feeding, with higher peak plasma CCK (cholecystokinin), PYY (peptide YY), and GLP-1/2 (glucagon-like peptides 1/2) concentrations being attained after jejunal feeding.

11. active GLP-1 produced in the islet stimulates cholecystokinin production and secretion in a paracrine manner via cyclic AMP and CREB.

12. Cardiac expression of pro-cholecystokinin is cell-specific, which differentiates the expression from that of intestinal endocrine cells and cerebral neurons. Plasma Pro-CCK is a prognostic marker in patients with stable heart failure.

13. CCK binding modulates the contractile function of the lower esophageal sphincter through differential binding to the CCK-A receptor on the sling and clasp fibers

14. Data suggest that up-regulation of plasma CCK levels is 50% higher following breakfast of meal replacement beverage containing fat emulsion of rapeseed oil with droplet size of 0.1 um (versus 0.3 um); satiety response and food intake are unaffected.

15. These studies identify a key role for Cck in the development and treatment of mania.

16. Results suggest excessive local release of CCK in response to duodenal lipid in functional dyspepsia.

17. CCK enhances cholesterol absorption by activation of a pathway involving CCK1R/CCK2R, Gbetagamma, PI3K, Akt, Rab11a, and NPC1L.

18. This review will summarize what is known regarding CCK, its receptors, and pancreatic--{REVIEW}

19. We aimed to determine whether fasting or meal-stimulated ghrelin, PYY, CCK, and satiety responses are different between lean PCOS patients and healthy women.

20. hnRNP-K regulates extracellular matrix, cell motility, and angiogenesis pathways. Involvement of the selected genes (Cck, Mmp-3, Ptgs2, and Ctgf) and pathways was validated by gene-specific expression analysis

Mouse (Murine) Cholecystokinin (CCK) Interaktionspartner

1. Knockdown of CB1R in the CCK-D2 medium spiny neurons circuit elevated synaptic activity and promoted stress susceptibility.

2. Study shows that independent of the neurochemical content, cholecystokinin/type 1 cannabinoid receptor-expressing interneurons have similar physiological and morphological properties, providing an endocannabinoid-sensitive synaptic inhibition onto the amygdalar principal neurons.

3. In summary, our study is the first to indicate that CCK/CCK-AR pathway is critical and protective against liver I/R injury. The activation of this pathway not only prevents hepatocellular apoptosis, but also reduces inflammatory response by suppressing NF-kappaB.

4. CCK/GLP-1 play contributory roles in anorexia induction by trichothecenes T-2 toxin, HT-2 toxin, diacetoxyscirpenol and neosolaniol.

5. GPR120-induced incretin glucse-dependent insulinotropic polypeptide secretion is indirectly mediated by cholecystokinin.

6. Medullary interstitial cells respond to body fluid expansion by CCK release for feedback regulation of the late proximal tubular reabsorption.

7. results suggest that normal integration of CCK+ basket cells in cortical networks is key to support spatial coding in the hippocampus.

8. PC7 has a critical role in normal processing of cholecystokinin in mouse brain

9. These studies reemphasize the beneficial effects imparted by co-administration of obestatin and CCK8 and their potential use towards countering obesity.

10. new information on the cell specific localization of NUCB2/nesfatin-1 in the intestinal mucosa, and a novel function for nesfatin-1 in modulating intestinal CCK and PYY expression and secretion

11. Results showed that CCK is important for lipid transport and energy expenditure to control body weight in response to dietary lipid feeding

12. SP1 results in a CCK response deficiency that may contribute to the increased meal size and overall hyperphagia in synphillin-1 transgenic mice

13. active GLP-1 produced in the islet stimulates cholecystokinin production and secretion in a paracrine manner via cyclic AMP and CREB.

14. Data (including data from studies using transgenic mice) suggest that enhanced Cck expression in pancreatic beta-cells protects these cells from the cell-withering effects of aging, apoptotic stress, and (streptozotocin-induced) diabetes type 2.

15. Deoxynivalenol induced cholecystokinin and glucagon-like peptide 1 release by enteroendocrine cells in mediated by casR/TRPA1 signaling.

16. total Ca(2+) mobilization evoked by CCK-8 was attenuated by a 30% in the presence of 100 microM melatonin compared with the responses induced by CCK-8 alone.

17. Endogenous cholecystokinin is in part responsible for the development and progression of pancreatic cancer.

18. octapeptide exerts a direct effect on T cells, which is dependent on cholecystokinin-2 receptor

19. Data demonstrate that the ERK pathway is required for CCK-stimulated pancreatic adaptive growth.

20. I cells in duodenum are enriched in expression of CCK and ghrelin.