anti-Cholecystokinin 8, Octapeptide (CCK8) Antibodies

Cholecystokinin is a brain/gut peptide. Additionally we are shipping Cholecystokinin 8, Octapeptide Kits (36) and and many more products for this protein.

list all antibodies Gene Name GeneID UniProt
CCK8 885 P06307
Anti-Mouse CCK8 CCK8 12424 P09240
Anti-Rat CCK8 CCK8 25298 P01355
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Top anti-Cholecystokinin 8, Octapeptide Antibodies at antibodies-online.com

Showing 10 out of 11 products:

Catalog No. Reactivity Host Conjugate Application Images Quantity Delivery Price Details
Human Rabbit Un-conjugated ELISA   100 μg 11 to 16 Days
$361.43
Details
Human Rabbit Un-conjugated ICC, IHC, WB   100 μg 15 to 18 Days
$332.00
Details
Human Rabbit Un-conjugated IHC   100 μL 11 to 16 Days
$683.57
Details
Human Rabbit Biotin IHC, ELISA, WB   100 μg 15 to 18 Days
$366.00
Details
Human Rabbit Un-conjugated IC, IHC, ELISA, WB   100 μg 11 to 16 Days
$512.29
Details
Hormone Rabbit Un-conjugated IF, IHC   100 μL 11 to 16 Days
$818.71
Details
Human Mouse Un-conjugated IF/ICC, IHC, IP, WB IHC-P analysis of Human Stomach Tissue, with DAB staining. IHC-P analysis of Human Liver Tissue, with DAB staining. 100 μg 11 to 18 Days
$341.12
Details
Hormone Rabbit Un-conjugated IHC   100 μL 11 to 16 Days
$710.29
Details
Human Rabbit Un-conjugated IF/ICC, IHC, IP, WB   100 μg 11 to 18 Days
$426.40
Details
Human Mouse Un-conjugated IHC DAB staining on IHC-P; Samples: Human Liver Tissue. DAB staining on IHC-P; Samples: Human Stomach Tissue. 100 μg 15 to 18 Days
$246.00
Details

Top referenced anti-Cholecystokinin 8, Octapeptide Antibodies

  1. Buffalo (Bubalus) Polyclonal CCK8 Primary Antibody for IEM, ICC - ABIN617891 : Miller: Migration of peptide-immunoreactive local circuit neurons to rat cingulate cortex. in Cerebral cortex (New York, N.Y. : 1991) 1993 (PubMed)
    Show all 132 Pubmed References

More Antibodies against Cholecystokinin 8, Octapeptide Interaction Partners

Human Cholecystokinin 8, Octapeptide (CCK8) interaction partners

  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 8, Octapeptide (CCK8) interaction partners

  1. Study found that CCK via CCK-B receptors enhances the GABAA receptor-mediated spontaneous inhibitory postsynaptic currents in mitral/tufted cells.

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

  3. 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.

  4. 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.

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

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

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

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

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

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

  11. 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

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

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

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

  15. 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.

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

  17. 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.

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

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

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

Cholecystokinin 8, Octapeptide (CCK8) Antigen Profile

Protein Summary

Cholecystokinin is a brain/gut peptide. In the gut, it induces the release of pancreatic enzymes and the contraction of the gallbladder. In the brain, its physiologic role is unclear. The cholecystokinin pro-hormone is processed by endo- and exo-proteolytic cleavages. Two transcript variants encoding the same protein have been found for this gene.

Gene names and symbols associated with CCK8

  • cholecystokinin (CCK) antibody
  • cholecystokinin-L (cck-l) antibody
  • cholecystokinin (Cck) antibody
  • CCK antibody
  • cck-l antibody
  • CCKN antibody

Protein level used designations for CCK8

cholecystokinin , cholecystokinin-L , Cholecystokinins , cholecystokinin triacontatriapeptide , prepro-cholecystokinin

GENE ID SPECIES
460290 Pan troglodytes
100271847 Felis catus
100194429 Salmo salar
885 Homo sapiens
12424 Mus musculus
25298 Rattus norvegicus
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