Human Gastrin/Cholecystokinin Type B Receptor (CCKBR) ELISA Kit

Product specifications

ELISA Kits

Gastrin/Cholecystokinin Type B Receptor (CCKBR)

Human

Colorimetric

Quantitative

Sandwich

78.13 pg/ml - 5000 pg/ml

46.88 pg/ml

Optimal dilutions/concentrations should be determined by the end user.

96 tests

5 × 96 tests

10 × 96 tests

Lyophilized

ELISA

Serum, plasma and other biological fluids.

Shipped within 5-7 working days. The validity for this kit is at least 6 months. Up to 12 months validity can be provided on request.

Shipped at 4 °C. Upon receipt, store the kit according to the storage instruction in the kit's manual.

No

CCKBR,CCK2 receptor,CK-B receptor,cholecystokinin-2 receptor ,CHOLREC,gastrin/cholecystokinin type B receptor,CCK-B/gastrin receptor,CCK-2R,CCK-B,CCK2R,GASR

Elisa kits for CCKBR

RUO

Validity: The validity for this kit is at least 6 months. Up to 12 months validity can be provided on request.
This product is for research use only.   The range and sensitivity is subject to change. Please contact us for the latest product information. For accurate results, sample concentrations must be diluted to mid-range of the kit. If you require a specific range, please contact us in advance or write your request in your order comments.   Please note that our ELISA and CLIA kits are optimised for detection of native samples, rather than recombinant proteins. We are unable to guarantee detection of recombinant proteins, as they may have different sequences or tertiary structures to the native protein.

Descripción

CCKBR, also known as CCK2R, is a G protein-coupled receptor (GPCR) that binds both gastrin and cholecystokinin (CCK) peptides, playing critical roles in gastrointestinal function and brain signaling. It is expressed in the stomach, pancreas, brain, and certain tumors. In the gastrointestinal system, CCKBR regulates gastric acid secretion by stimulating parietal cells and promotes gastric mucosal growth, supporting digestive processes. In the central nervous system, CCKBR is involved in modulating anxiety, pain, and satiety through interactions with neurotransmitter systems. Its activation triggers pathways like phospholipase C (PLC), calcium mobilization, and MAPK signaling, leading to cellular proliferation, enzyme secretion, and neuronal modulation. CCKBR is highly implicated in gastric and pancreatic cancers, where gastrin-mediated activation enhances cell proliferation, survival, and tumor progression. Overexpression of CCKBR has been observed in gastric adenocarcinomas, making it a potential therapeutic target. Additionally, dysregulation of CCKBR signaling contributes to gastrointestinal disorders, including peptic ulcers and Zollinger-Ellison syndrome, characterized by excessive gastrin production. CCKBR is also being explored in neuropsychiatric research for its roles in anxiety and pain modulation. Overall, CCKBR regulates digestive and neuronal processes but contributes to disease progression when overexpressed or dysregulated.

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