Bombesin-like receptor 3
BRS3 | |||
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Identifiers | |||
Gene ontology | |||
Molecular function | |||
Cellular component | |||
Biological process | |||
Sources:Amigo / QuickGO |
Ensembl | |||||||||
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UniProt | |||||||||
RefSeq (mRNA) | |||||||||
RefSeq (protein) | |||||||||
Location (UCSC) | Chr X: 136.49 – 136.49 Mb | Chr X: 56.09 – 56.09 Mb | |||||||
PubMed search | [3] | [4] |
View/Edit Human | View/Edit Mouse |
The bombesin receptor subtype 3 also known as BRS-3 or BB3[5] is a protein which in humans is encoded by the BRS3 gene.[6][7]
Function
Mammalian bombesin-like peptides are widely distributed in the central nervous system as well as in the gastrointestinal tract, where they modulate smooth-muscle contraction, exocrine and endocrine processes, metabolism, and behavior. They bind to G protein-coupled receptors on the cell surface to elicit their effects. Bombesin-like peptide receptors include gastrin-releasing peptide receptor, neuromedin B receptor, and bombesin-like receptor-3 (BRS3; this article).[7][8]
BB3 is a G protein-coupled receptor.[6] BB3 only interacts with known naturally occurring bombesin-related peptides with low affinity and therefore, as it has no natural high-affinity ligand, is classified as an orphan receptor.[6][9][10]
References
- ^ a b c GRCh38: Ensembl release 89: ENSG00000102239 – Ensembl, May 2017
- ^ a b c GRCm38: Ensembl release 89: ENSMUSG00000031130 – Ensembl, May 2017
- ^ "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
- ^ "Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
- ^ "Bombesin Receptors: BB3". IUPHAR Database of Receptors and Ion Channels. International Union of Basic and Clinical Pharmacology. Archived from the original on 2016-03-03. Retrieved 2007-10-25.
- ^ PMID 8383682.
- ^ S2CID 1012779.
- ^ "Entrez Gene: BRS3 bombesin-like receptor 3".
- PMID 9325344.
- PMID 18055507.
Further reading
- Gorbulev V, Akhundova A, Grzeschik KH, Fahrenholz F (1994). "Organization and chromosomal localization of the gene for the human bombesin receptor subtype expressed in pregnant uterus" (PDF). FEBS Lett. 340 (3): 260–4. S2CID 99786.
- Fathi Z, Corjay MH, Shapira H, et al. (1993). "BRS-3: a novel bombesin receptor subtype selectively expressed in testis and lung carcinoma cells". J. Biol. Chem. 268 (8): 5979–84. PMID 8383682.
- Kane MA, Toi-Scott M, Johnson GL, et al. (1996). "Bombesin-like peptide receptors in human bronchial epithelial cells". Peptides. 17 (1): 111–8. S2CID 30893871.
- Ohki-Hamazaki H, Watase K, Yamamoto K, et al. (1997). "Mice lacking bombesin receptor subtype-3 develop metabolic defects and obesity". Nature. 390 (6656): 165–9. S2CID 4400418.
- Ryan RR, Weber HC, Hou W, et al. (1998). "Ability of various bombesin receptor agonists and antagonists to alter intracellular signaling of the human orphan receptor BRS-3". J. Biol. Chem. 273 (22): 13613–24. PMID 9593699.
- Liu J, Lao ZJ, Zhang J, et al. (2002). "Molecular basis of the pharmacological difference between rat and human bombesin receptor subtype-3 (BRS-3)". Biochemistry. 41 (28): 8954–60. PMID 12102638.
- Ross MT, Grafham DV, Coffey AJ, et al. (2005). "The DNA sequence of the human X chromosome". Nature. 434 (7031): 325–37. PMID 15772651.
- Hou X, Wei L, Harada A, Tatamoto K (2007). "Activation of bombesin receptor subtype-3 stimulates adhesion of lung cancer cells". Lung Cancer. 54 (2): 143–8. PMID 16979789.
- Tan YR, Qin XQ, Xiang Y, et al. (2007). "PPARalpha and AP-2alpha regulate bombesin receptor subtype 3 expression in ozone-stressed bronchial epithelial cells". Biochem. J. 405 (1): 131–7. PMID 17355223.
External links
- "Bombesin Receptors: BB3". IUPHAR Database of Receptors and Ion Channels. International Union of Basic and Clinical Pharmacology. Archived from the original on 2016-03-03. Retrieved 2007-10-25.
- bombesin+receptor+subtype+3 at the U.S. National Library of Medicine Medical Subject Headings (MeSH)
- Human BRS3 genome location and BRS3 gene details page in the UCSC Genome Browser.
This article incorporates text from the United States National Library of Medicine, which is in the public domain.