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Details for receptor: CCK-2

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EndoNet ID: ENR00781

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Synonyms

  • CCK-B
  • CCK2
  • cholecystokinin receptor 2
  • gastrin/cholecystokinin type B receptor
  • CCK-2
  • gastrin-CCKB

General information

  • 95% of pancreatic islet cells expressing CCK-B/G receptor were glucagon-producing (alpha-) cells. In contrast, insulin-, somatostatin-, and pancreatic polypeptide–producing cells did not express any significant CCK-B/G receptor immunoreactivity. [1]
  • Activation of CCK-2 leads to an increase in intracellular Ca2+ and PKC. [2]
  • Belongs to the seven-transmembrane domain, G-coupled, receptor superfamily. [2]
  • Normally coupled to Galpha(q/11). [2]
  • RT-PCR demonstrated the expression of both CCK1-R and CCK2-R in the zona glomerulosa (ZG), but not zona fasciculata-reticularis cells of the human adrenal cortex. [3]

Links to other resources

UniProt P32239
Ensembl ENST00000334619

Binding hormones

  • gastrin-34
  • gastrin-17
  • cholecystokinin
    • Binding to CCK-B receptors stimulates gastric acid secretion.
  • gastrin
  • cholecystokinin 39
    • CCK peptides also share their carboxyl-terminal tetrapeptide-amide with all molecular forms of gastrin, with this region providing the pharmacophoric domain for the type 2 CCK receptor (CCK2 receptor). [4]

Anatomical structures with this receptor

  • cell_of_adrenal_gland_zona_glomerulosa

    Influences

    • positive aldosterone
      • CCK stimulates aldosterone secretion via specific receptors (CCK1-Rs and CCK2-Rs in rats, and CCK2-Rs in humans) located in zona glomerulosa cells and coupled to the adenylate cyclase-dependent signaling cascade. [5]
      • CCK and the CCK2-R agonist pentagastrin enhanced basal aldosterone secretion from zona glomerulosa (ZG) cells without affecting cortisol production from zona fasciculata-reticularis cells. [3]
      • The aldosterone response to CCK and pentagastrin was suppressed by a CCK2-R antagonist, but not by a CCK1-R antagonist. [3]
      • In contrast with rats, in humans the aldosterone secretagogue effect of CCK appears to be exclusively mediated by CCK2-R. [3]

  • oxyntic_cell_of_gastric_gland

    Induced phenotypes

    • positive regulation of gastric acid secretion
      • The CCK2 receptor stimulate the acid secretion from parietal cells in the digestive system. [6]
      • CCK-2R is necessary to respond to carbachol as well as to produce the maximal acid secretion. The role of CCK-1R in acid secretion is less important. [7]

  • alpha_cell_of_islet_of_Langerhans

    Influences

    • positive glucagon
      • The CCK-B/G receptor agonists gastrin and cholecystokinin stimulated the release of glucagon in a dose-dependent manner. [1]

  • enterochromaffin_like_cell

    Influences

    • positive histamine
      • CCK2 receptors mediate the release of histamine from enterchromaffin-like cells in the stomach. [8]

    Induced phenotypes

    • positive regulation of smooth muscle proliferation

  • intestinal_smooth_muscle_cell

    Induced phenotypes

    • induction of smooth muscle contraction
      • The CCK2 receptors mediate an inhibitory effect on human colonic smooth muscle and an inhihitory action of CCK on motor function of human distal colon. [9]
    • CCK2R protein has been demonstrated in the stomach muscularis. [10]

  • smooth_muscle

  • neuron

  • digestive_system

    Influences

    • somatostatin

  • D_cell_of_gastrointestinal_tract

    Influences

    • positive somatostatin
      • CCK and gastrin stimulate somatostatin secretion. [11]
    • negative gastrin
      • Gasrin secretion is inhibitted by gastric acid, probably via the paracrine mediator somatostatin [12]

  • hypothalamus

    Induced phenotypes

    • negative regulation of appetite
      • Cholecystokinin is released by the gastrointestinal system during meals and induces an anorexigenic response. [13]
      • This physiological pathway is believed to be an essential component of postprandial satiety. [14]
      • CCK activates POMC cells in the nucleus of the solitary tract (NTS), which is located in the brainstem. This effect of peripheral CCK is dependent upon melanocortin signaling, because in the absence of MC4R or by pharmacological inhibition of MC4R in the NTS, the anorexigenic effects of CCK are blocked. [15]

  • mucosa_of_small_intestine

    • CCK2R protein has been demonstrated in the stomach mucosa. [16]

  • colon

    Induced phenotypes

    • induction of smooth muscle contraction
      • The CCK2 receptors mediate an inhibitory effect on human colonic smooth muscle and an inhihitory action of CCK on motor function of human distal colon. [9]
Reference