Английская Википедия:Cholecystokinin B receptor

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Версия от 04:49, 18 февраля 2024; EducationBot (обсуждение | вклад) (Новая страница: «{{Английская Википедия/Панель перехода}} {{Short description|Protein-coding gene in the species Homo sapiens}} {{Infobox_gene}} The '''cholecystokinin B receptor''' also known as '''CCKBR''' or '''CCK<sub>2</sub>''' is a protein<ref name="pmid10368033">{{cite journal | vauthors = Noble F, Roques BP | title = CCK-B receptor: chemistry, molecular biology, biochemistry and pharmacology | journal = Progress in Neurobiology |...»)
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Шаблон:Short description Шаблон:Infobox gene The cholecystokinin B receptor also known as CCKBR or CCK2 is a protein[1] that in humans is encoded by the CCKBR gene.[2]

This gene encodes a G protein-coupled receptor for gastrin and cholecystokinin (CCK),[3][4][5] 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.[6]

CNS effects

CCK receptors significantly influence neurotransmission in the brain, regulating anxiety, feeding, and locomotion. CCK-B expression may correlate parallel to anxiety and depression phenotypes in humans. CCK-B receptors possess a complex regulation of dopamine activity in the brain. CCK-B activation appears to possess a general inhibitory action on dopamine activity in the brain, opposing the dopamine-enhancing effects of CCK-A. However, the effects of CCK-B on dopamine activity vary depending on location.[7] CCK-B antagonism enhances dopamine release in rat striatum.[8] Activation enhances GABA release in rat anterior nucleus accumbens.[9] CCK-B receptors modulate dopamine release, and influence the development of tolerance to opioids.[10] CCK-B activation decreases amphetamine-induced DA release, and contributes to individual variability in response to amphetamine.[11]

In rats, CCK-B antagonism prevents the stress-induced reactivation of cocaine-induced conditioned place preference, and prevents the long-term maintenance and reinstatement of morphine-induced CPP.[12] Blockade of CCK-B potentiates cocaine-induced dopamine overflow in rat striatum.[8] CCK-B may pose a modulatory role in parkinson's disease. Blockade of CCK-B in dopamine-depleted squirrel monkeys induces significant enhancement of locomotor response to L-DOPA.[13] One study shows that visual hallucinations in Parkinson's disease are associated with cholecystokinin −45C>T polymorphism, and this association is still observed in the presence of the cholecystokinin-A receptor TC/CC genotype, indicating a possible interaction of these two genes in the visual hallucinogenesis in Parkinson's disease.[14]

Gastrointestinal Tract

The cholecystokinin B receptor is stimulated by CCK and gastrin in the stomach during digestion.

Selective Ligands

The cholecystokinin B receptor responds to a number of ligands.

Agonists

Antagonists

  • Proglumide
  • CI-988
  • CI-1015
  • L-365,260
  • L-369,293
  • YF476
  • YM-022
  • RP-69758
  • LY-225,910
  • LY-288,513
  • PD-135,158
  • PD-145,942

Inverse agonists

  • L-740,093

See also

References

Шаблон:Reflist

Further reading

Шаблон:Refbegin

Шаблон:Refend

External links

Шаблон:NLM content Шаблон:PDB Gallery Шаблон:G protein-coupled receptors Шаблон:Neuropeptide receptors

Партнерские ресурсы
Криптовалюты
Магазины
Хостинг
Разное

  1. ↑ Шаблон:Cite journal
  2. ↑ Шаблон:Cite journal
  3. ↑ Шаблон:Cite journal
  4. ↑ Шаблон:Cite journal
  5. ↑ Шаблон:Cite journal
  6. ↑ Шаблон:Cite web
  7. ↑ Шаблон:Cite journal
  8. ↑ 8,0 8,1 Шаблон:Cite journal
  9. ↑ Шаблон:Cite journal
  10. ↑ Шаблон:Cite journal
  11. ↑ Шаблон:Cite journal
  12. ↑ Шаблон:Cite journal
  13. ↑ Шаблон:Cite journal
  14. ↑ Шаблон:Cite journal
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