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anti-Human CCKBR Antibodies:
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Human Polyclonal CCKBR Primary Antibody for IHC, ELISA - ABIN185407
Olszewska-Pazdrak, Townsend, Hellmich: Agonist-independent activation of Src tyrosine kinase by a cholecystokinin-2 (CCK2) receptor splice variant. in The Journal of biological chemistry 2004
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Human Polyclonal CCKBR Primary Antibody for IF (p), IHC (p) - ABIN734318
Mohammad, Ozaki, Takeuchi, Unno, Yamoto, Morioka, Takiguchi, Ikeda: Functional compensation between cholecystokinin-1 and -2 receptors in murine paraventricular nucleus neurons. in The Journal of biological chemistry 2012
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Human Polyclonal CCKBR Primary Antibody for ICC, IF - ABIN251249
Berna, Seiz, Nast, Benten, Bläker, Koch, Lohse, Pace: CCK1 and CCK2 receptors are expressed on pancreatic stellate cells and induce collagen production. in The Journal of biological chemistry 2010
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Cow (Bovine) Polyclonal CCKBR Primary Antibody for EIA, IHC (p) - ABIN372564
El-Kouhen, Morisset: Cholecystokinin and Somatostatin Negatively Affect Growth of the Somatostatin-RIN-14B Cells. in International journal of endocrinology 2009
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Cow (Bovine) Polyclonal CCKBR Primary Antibody for IHC (p), ELISA - ABIN547452
Kossatz, Béhé, Mansi, Saur, Czerney, Kaiser, Hilger: Multifactorial diagnostic NIR imaging of CCK2R expressing tumors. in Biomaterials 2013
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Human Polyclonal CCKBR Primary Antibody for WB - ABIN6713105
Xu, Chen, Shao, Li, Xu, Zhang, Zhu, Zhou, He, Sun: Gastrin acting on the cholecystokinin2 receptor induces cyclooxygenase-2 expression through JAK2/STAT3/PI3K/Akt pathway in human gastric cancer cells. in Cancer letters 2013
Human Polyclonal CCKBR Primary Antibody for FACS, ICC - ABIN5692993
Li, Huang, Liu: Changes in FABP1 and gastrin receptor expression in the testes of rats that have undergone electrical injury. in Experimental and therapeutic medicine 2015
we found that all eight neuroendocrine neoplasm expressed CCKBR and neuroendocrine markers in a majority of tumor cells. The same markers were also expressed in a proportion of adenocarcinomas supporting the view that gastrin is important in the development of gastric cancer
We concluded that low serum gastrin is related to increased risk of ER(+) BC development. The results also established that CCKBR/ERK/P65 signaling function is generally tumor suppressive in ER(+) BC, indicating therapies should focus on restoring, not inhibiting, CCKBR/ERK/P65 pathway activity.
High CCK2R expression is associated with cancer.
These results suggest that Z-360 exerts an anti-tumor effect through a reduction in anti-apoptosis factors by blocking CCK2R
High CCK-BR expression is associated with Gastric Cancer.
There is no identifiable link between nuclear CCK2R expression and all the clinicopathological characteristics examined in a cohort of Taiwanese colon cancer patients.
Our study showed significantly higher expression of CCKAR and down regulation of CCKBR in pancreatic cancer as compared to control while CCKBR/GR was detected in majority of stomach cancer samples. Thus, our study suggests that CCK and Gs receptors may have diagnostic and therapeutic implications.
Data indicate that variant c.811+32C>A in cholecystokinin-B receptor gene (CCKBR) does not have a significant impact on pancreatic cancer risk or survival in a Hungarian cohort.
The neurotransmitter cholecystokinin (CCK), along with its receptors, CCKAR and CCKBR, have been previously associated with psychiatric disorders, suggesting that variants near these genes may play a role in the pre-pulse/startle response in this cohort
This study showed that CCK2 receptors were highly expressed within the cytoplasmic area of cancerous cells, whereas the levels were very low in normal tissues.
There is functional synergy between cholecystokinin receptors CCKAR and CCKBR in mammalian brain development.
CCK-BR SNP predicts survival and should be studied as a candidate genetic biomarker for those at risk of pancreatic cancer.
treatment with gastrin, a CCK2R agonist, stimulated the secretion of GLP-1, and that this effect was likely due to increased expression of proglucagon and PCSK1 (also known as prohormone convertase 3 (PC3 gene)).
Our results indicate a promoting role of CCK2R on GIST tumourigenesis, particularly in tumours of gastric origin.
The gastrin receptor is a promising tumor cell surface target for future prostate-cancer-specific imaging applications.
DeltaFosB induction in prelimbic area occurred selectively in susceptible mice after chronic social defeat stress and produced these effects partly through induction of the cholecystokinin (CCK)-B receptor.
some CCKBR polymorphisms may contribute to an underlying predisposition towards suicidal behaviour in bipolar disorder.
CCKBR and Bcl-2 were identified as targets of miR-148a.
Gastric mucosal injury with H. pylori infection destroys the pH barrier on the foveolar epithelium and may induce gastrin receptor expression through pH changes.
Suggest that CCK2R-mediated COX-2 up-regulation via JAK2/STAT3/PI3K/Akt pathway is involved in the proliferative effect of gastrin on human gastric cancer cells.
Our data suggest a progression model for BE to EAC in which CCK2R+ progenitor cells, stimulated by hypergastrinemia, proliferate to give rise to metaplasia and dysplasia.
CCKBR and D5R synergistically interact in the kidney, which may contribute to the maintenance of normal sodium balance following an increase in sodium intake
findings provide novel evidence that Cnr1 contributes to cued fear expression via an interaction with the CCKB receptor.
mice lacking CCK receptors exhibited a functional shift from the gastrin-CCK pathways to the neuronal pathway in control of the ECL cells and eventually the acid secretion
CCK2R labels +4 antral stem cells that can be activated and expanded by progastrin, thus identifying one hormonal trigger for gastric stem cell interconversion and a potential target for gastric cancer chemoprevention and therapy.
CCK-1 and -2 receptors may function synergistically in single PaPo neurons and deletion of CCK-1 receptors may facilitate CCK-2 receptor signaling.
cholecystokinin receptor-2 has a role in stress-triggered fear memory and anxiety in the mouse
shift of breakpoint on Arrhenius plot established in CCK(2) receptor-deficiency confirms that such kind of alteration in Na(+),K(+)-ATPase temperature dependence is likely related to the homeostatic adjustment of altered function of the sodium pump.
Environmental enrichment has beneficial effects in neuropathic conditions and reinforce the causal link between CCK(2) receptors, mechanical sensitivity and the development of CCI-induced hypersensitivity.
The gastrin receptor promotes pancreatic growth in transgenic mice.
Anxiety-related behaviors in cholecystokinin-A, B, and AB receptor gene knockout mice in the plus-maze.
the targeted genetic suppression of cholecystokinin B receptor increased the sensitivity of pre- and post-synaptic dopamine D(2) receptors
Na-pump kinetic properties are differently altered in the brain regions of mice deficient in this receptor
These results suggest that mice lacking the CCK2 receptor gene are less anxious than normal mice.
possibility that the C-terminal tyrosine 438 of the CCK2 receptor associates with the SH2 domains of phospholipase C gamma1 was examined
The targeted mutation of CCK(2) receptors selectively antagonised the behavioural changes induced by the individual housing in females, but not in male mice.
This study suggests that not only pain sensitivity, but also mechanical sensitivity and the development of neuropathic pain are regulated by antagonistic interactions between CCK and opioid systems.
CCK2R expression in pancreas of Elas-CCK2 mice leads to the activation of JAK2 and STAT3
CCK2 receptors have roles in carcinogen-induced preneoplastic lesions formation in murine pancreatic acinar cells
This gene encodes a G-protein coupled receptor for gastrin and cholecystokinin (CCK), regulatory peptides of the brain and gastrointestinal tract. This protein is a type B gastrin receptor, which has a high affinity for both sulfated and nonsulfated CCK analogs and is found principally in the central nervous system and the gastrointestinal tract. A misspliced transcript variant including an intron has been observed in cells from colorectal and pancreatic tumors.
cholecystokinin B receptor
, gastrin/cholecystokinin type B receptor
, CCK-B receptor
, CCK2 receptor
, cholecystokinin-2 receptor
, gastrin receptor
, CCK(B) receptor
, CCK-B/gastrin receptor
, CCK2/gastrin receptor
, Cholecystokinin-2 receptor
, gastrin/CCK-B receptor
, cholecystokinin receptor