Adrenal medullary cells produce small amounts of CCK, although amidated and with a low degree of sulfation (98). The picture has varied (12) due to species differences and because the molecular pattern along the gut varies (59, 60). In man, CCK-33 predominates in plasma, but CCK-58, -22, and -8 are also present (11, 61). Moreover, cerebral CCK neurons are more abundant than neurons of other neuropeptides (42, 45, 46). While most peptidergic neurons occur in subcortical regions, CCK is expressed in the highest concentrations in neocortical neurons (39, 42, 47). The perikarya of the cortical CCK nerves are distributed in layers II–VI, with the highest frequency in layers II and III cck444 (42, 48).
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The assays have confirmed that protein- and fat-rich food is the most important stimulus (11, 54). Of the constituents, protein and l -amino acids as well as digested fat cause significant CCK release (54, 55). Carbohydrates only release small amounts of CCK (54), but hydrochloric acid also stimulates release (55). As described earlier (9), “the exomal unit of the CCK gene is seven kilobases interrupted by two introns (23). Whereas the function of the E-box and the GC-rich region is not fully clarified (26, 27), the combined CRE/TRE sequence plays an important role in the regulation of CCK transcription.
- CAMP accumulation was analyzed by a standard dose-response curve using GraphPad Prism 8.0 (GraphPad Software).
- Apart from ligand selectivity, huge differences in downstream G protein signaling are present between CCK1R and CCK2R.
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The cortical expression occurs in distal tubular cells and glomeruli, and the medullar CCK expression is confined to collecting ducts (102, 103). The discovery of renal CCK expression may have been stimulated by earlier findings of significant CCK1 and CCK2 receptor expression also in human kidney tissue (104, 105). It has led to suggestions of local regulatory functions of natriuresis and inflammation in the kidneys.
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Other constructs including the full-length and various site-directed mutated human CCK1R and CCK2R were cloned into the pcDNA3.1 vector for cAMP accumulation and NanoBiT–G protein dissociation assay. The intestinal hormone and neuromodulator cholecystokinin (CCK) receptors CCK1R and CCK2R act as a signaling hub in brain–gut axis, mediating digestion, emotion, and memory regulation. CCK receptors exhibit distinct preferences for ligands in different posttranslational modification (PTM) states. They exist in multiple molecular forms, sharing the same evolutionarily conserved pentapeptide motif, which comprises the minimal sequence required for biological activity and receptor activation (Fig. 1a).
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