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CCK — CCKBR

Pathways - manually collected, often from reviews:

• Reactome Reaction: CCK → CCKBR (direct_complex) Pisegna et al., Biochem Biophys Res Commun 1992*, Takahashi et al., Proc Natl Acad Sci U S A 1985*, Ulrich et al., Biochem Biophys Res Commun 1993*
• Reactome Reaction: CCK → CCKBR (reaction) Rubio et al., Genomics 1999, Pisegna et al., Biochem Biophys Res Commun 1992*, Dowal et al., J Biol Chem 2006, Lambert et al., Science signaling 2008, Amatruda et al., Proc Natl Acad Sci U S A 1991, Ferguson et al., J Biol Chem 1986, Takahashi et al., Proc Natl Acad Sci U S A 1985*, Ulrich et al., Biochem Biophys Res Commun 1993*, Chen et al., Biochim Biophys Acta 1996
• WikiPathways Cell-type Dependent Selectivity of CCK2R Signaling: CCK → Complex of GNAI1-CCKBR (activation)
• WikiPathways Cell-type Dependent Selectivity of CCK2R Signaling: CCK → Complex of GNAQ-CCKBR (activation)

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

• IRef Biogrid Interaction: CCK — CCKBR (direct interaction, pull down) Harikumar et al., J Biol Chem 2005*
• IRef Biogrid Interaction: CCK — CCKBR (direct interaction, pull down) Aloj et al., J Nucl Med 2004*
• IRef Biogrid Interaction: CCK — CCKBR (direct interaction, pull down) Galés et al., Mol Pharmacol 2003*
• IRef Hprd Interaction: CCK — CCKBR (in vivo) Silvente-Poirot et al., J Biol Chem 1999*, Galés et al., Mol Pharmacol 2003*, Aloj et al., J Nucl Med 2004*, Aloj et al., Cancer Biother Radiopharm 2004*, Harikumar et al., J Biol Chem 2005*
• IRef Hprd Interaction: CCK — CCKBR (in vitro) Silvente-Poirot et al., J Biol Chem 1999*, Galés et al., Mol Pharmacol 2003*, Aloj et al., J Nucl Med 2004*, Aloj et al., Cancer Biother Radiopharm 2004*, Harikumar et al., J Biol Chem 2005*
• IRef Intact Interaction: Complex of CCK-CCK-CCKBR (physical association, scintillation proximity assay) Bono et al., Cancer Cell 2013
• IRef Intact Interaction: CCK — CCKBR (physical association, scintillation proximity assay) Bono et al., Cancer Cell 2013

Text-mined interactions from Literome

Reeve et al., Am J Physiol Gastrointest Liver Physiol 2004 : The presence of CCK ( 58 ) ( ns ) and its ability to selectively stimulate the CCK(B) receptor without stimulation of the CCK(A) receptor suggest that CCK ( 58 ) ( ns ) may have unique physiological properties, especially tissues where the nonsulfated peptide can act as a paracrine or neurocrine agent
Zhou et al., Neuropeptides 1993 : The results suggest that an increased release of CCK-8 following EA may limit the effect of opioid peptides, and that the CCK-B receptor mediates the anti-opioid effect of CCK-8 in rat spinal cord
Heim et al., J Physiol Pharmacol 1995 : The CCKB receptor preferring agonists gastrin-17-I, desulfated CCK-8 and CCK-4 had only small stimulatory effects ( < 12 % of maximal CCK-8 effect, EC50 's in the low nanomolar range ) and did not inhibit the CCK-8 response, suggesting that they were acting at CCKB but not, as partial agonists, at CCKA receptors. A71378 had its main stimulatory effect in low and a slight additional effect in high concentrations ( EC50 80 pmol/l and > 1 mumol/l ), respectively, while A72962 had its main stimulatory effect in high concentrations ( EC50 > 1 mumol/l )
Ma et al., Peptides 1996 : The effects of S-CCK-8 and NS-CCK-8 were mediated by the CCKB receptor
Xu et al., Neuroendocrinology 1996 (Pituitary Neoplasms) : Paracrine stimulation of cell growth by cholecystokinin/gastrin through cholecystokinin-B receptor on GH3 cells in vitro ... These findings provided the first evidence for an autocrine/paracrine role of CCK and gastrin on stimulation of GH3 cell growth through the CCK-B receptor
Schutte et al., J Auton Nerv Syst 1997 : The results demonstrate that the excitatory effects of CCK-8 are mediated by both CCKA and CCKB receptor subtypes