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   1  GPCR subgroups (e.g., the ancestral gastrin/cholecystokinin receptor).                              
     2 ily A G protein-coupled receptor, the type 1 cholecystokinin receptor.                               
     3  new molecular model of the agonist-occupied cholecystokinin receptor.                               
     4 antagonist and agonist ligands of the type A cholecystokinin receptor.                               
     5 alpha13 downstream of gastrin and the type 2 cholecystokinin receptor.                               
     6 udied in solution and docked at type A and B cholecystokinin receptors.                              
     7 l sequencing of labeled wild-type and mutant cholecystokinin receptors.                              
     8 iod, inducible/reversible forebrain-specific cholecystokinin receptor-2 transgenic (IF-CCKR-2 tg) mic
     9 r 1 (NTSR1), neuropeptide S receptor (NPSR), cholecystokinin receptor A (CCKAR), and the kappa-opioid
    10     Similarly, peptides mimicking the TMs of cholecystokinin receptor A, were found to abolish ligand
  
  
    13 emonstrate that antagonist occupation of the cholecystokinin receptor also results in receptor intern
  
    15  mass and protein content was independent of cholecystokinin receptors, associated with a rapid incre
    16 e were built into two homology models of the cholecystokinin receptor, based on the recent crystal st
  
    18 red Ca2+ signaling with up-regulation of the cholecystokinin receptor but minimal effect upon express
    19 titative autoradiography was used to analyze cholecystokinin receptor (CCK-R) binding in the ventrome
  
    21 f a new antagonist radioligand of the type 1 cholecystokinin receptor (CCK1R), (2-fluorophenyl)-2,3-d
    22 rminants for this pocket within type 1 and 2 cholecystokinin receptors (CCK1R and CCK2R), we prepared
  
    24 ssessment of sites of phosphorylation of the cholecystokinin receptor (CCKR) in its native milieu in 
    25  within the second extracellular loop of the cholecystokinin receptor interacts with a specific acidi
    26 ndependent risk factor for gallstone disease.Cholecystokinin receptors may be responsible for the alt
    27 ative pain-facilitating neurons, or block of cholecystokinin receptors prevented or significantly att
    28 ype animals and mice lacking the other known cholecystokinin receptor subtype, cholecystokinin-B/gast
    29 surface and within the helical bundle of the cholecystokinin receptor to the amino terminus of a full
  
    31 , the position 33 probe docked at the type A cholecystokinin receptor was more easily quenched in the
    32  whereas the same probe docked at the type B cholecystokinin receptor was more easily quenched in the
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