Molecular cloning and characterization of avian bombesin‐like peptide receptors: new tools for investigating molecular basis for ligand selectivity

Iwabuchi, Maiko; Ui-Tei, Kumiko; Yamada, Katsushi; Matsuda, Yoichi; Sakata, Yasushi; Tanaka, Kohichi; Ohki‐Hamazaki, Hiroko

doi:10.1038/sj.bjp.0705282

Cited by 27 publications

(13 citation statements)

References 44 publications

(46 reference statements)

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“…In consistent with this view, GRP-R gene is localized on chromosone X in human (Xp22) and mouse and on chick chromosome 1 (1q23-q24), in the region where chicken homologs of other human X-linked genes have also been mapped (Iwabuchi et al, 2003). Human BRS-3 gene is mapped to chromosome X (Xq26-q28) and mouse BRS-3 gene is also mapped to chromosome X. NMB-R gene is localized to human 6q21-qter and to mouse chromosome 10.…”

Section: Bombesin-like Peptide Receptors Are Phylogenetically Conservedmentioning

confidence: 53%

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Development and function of bombesin-like peptides and their receptors

Ohki‐Hamazaki

Iwabuchi

Maekawa³

2005

Int. J. Dev. Biol.

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Amphibian bombesin and its related peptides consist a family of neuropeptides in many vertebrate species. Bombesin and two major bombesin-like peptide in mammals, gastrinreleasing peptide (GRP) and neuromedin B (NMB), have been shown to elicit various physiological effects. These include inhibition of feeding, smooth muscle contraction, exocrine and endocrine secretions, thermoregulation, blood pressure and sucrose regulations and cell growth. Receptors for GRP and NMB (GRP-R and NMB-R), as well as third subtype of bombesin-like peptide receptor (BRS-3) have been cloned. These receptors are G-protein-coupled receptors and are expressed in various brain regions and in the digestive tract. In this paper, we will summarize studies on these peptides and their receptors, with special reference to research using gene-knockout mice. These studies clearly demonstrated the role of three receptors in vivo and in vitro. We will also discuss the phylogeny of these receptors. KEY WORDS: gastrin-releasing peptide, neuromedin B, bombesin-like peptide receptor subtype-3 (BRS-3)Int.

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Section: Bombesin-like Peptide Receptors Are Phylogenetically Conservedmentioning

confidence: 53%

“…Another subtype of bombesin-like peptide receptor was cloned from chick brain (Iwabuchi et al, 2003). This subtype, called BRS-3.5, has moderate affinity for bombesin but low affinity for both GRP and NMB.…”

Section: Cloning Of Bombesin-like Peptide Receptor Subtype-3 (Brs-3)mentioning

confidence: 99%

Development and function of bombesin-like peptides and their receptors

Ohki‐Hamazaki

Iwabuchi

Maekawa³

2005

Int. J. Dev. Biol.

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151

123

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“…The current terminology adopted by several receptor classification guides uses the names BB1, BB2, and BB3 for NMBRs, GRPRs, and BRS-3 receptor, respectively. More recently, novel bombesin receptors with no mammalian equivalents have been identified in amphibians (BB4; Nagalla et al, 1995) and chickens (chBRS-3.5; Iwabuchi et al, 2003). Figure 1 illustrates the mammalian bombesin receptors and their endogenous ligands in mammals described to date.…”

Section: Mammalian Bombesin Receptorsmentioning

confidence: 99%

Bombesin receptor regulation of emotional memory

Roesler

Kent²,

Schröder³

et al. 2012

Reviews in the Neurosciences

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Mammalian bombesin-like peptides neuromedin B (NMB) and gastrin-releasing peptide (GRP) act by activating NMB receptors (NMBR, BBl) and GRP receptors (GRPR,BB2), respectively. These two bombesin receptors are members of the G-protein-coupled receptor (GPCR) superfamily.In the brain, NMBR and GRPR are highly expressed in the brain areas involved in memory processing and emotional responses, such as the hippocampus and the amygdaloid nuclei. An increasing number of pharmacological and genetic studies in rodents indicate that NMBRs and GRPRs in brain regions including the dorsal hippocampus,the nucleus tractus solitarius, the basolateral amygdala,and cortical areas, regulate memory formation and expression, particularly for memories related to emotionally arousing tasks. GRPR signaling interacts with multiple protein kinase pathways as well as with other neurotransmitter,hormone, and growth factor systems in influencing memory formation. Together with evidence from human studies, the findings from rodent experiments suggest that bombesin receptors may be therapeutic targets in brain disorders involving memory dysfunction and anxiety.

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“…Both GRP and NMB regulate feeding, because treatment with these peptides, as well as BN, decreased the amount of metabolite consumed (4 -6). Meanwhile, five types of BN receptors have been cloned, namely the GRP receptor (GRP-R) (7,8), NMB receptor (NMB-R) (9), BN receptor subtype-3 (BRS-3) (10), BB4 (11), and BRS-3.5 (12). Endogenous ligands for BRS-3 and BRS-3.…”

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confidence: 99%

Leptin Resistance and Enhancement of Feeding Facilitation by Melanin-Concentrating Hormone in Mice Lacking Bombesin Receptor Subtype-3

2004

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Mice lacking either bombesin receptor subtype (BRS)-3 or gastrin-releasing peptide receptor (GRP-R) exhibit feeding abnormalities. However, it is unclear how these receptors are associated with feeding regulation. In BRS-3-deficient mice, we found hyperphagia, subsequent hyperleptinemia, and brain leptin resistance that occurred after the onset of obesity. To explore the cause of this phenomenon, we examined changes in feeding responses to appetite-related neuropeptides in BRS-3-deficient, GRP-R-deficient, and wild-type littermate mice. Among orexigenic neuropeptides, the hyperphagic response to melanin-concentrating hormone (MCH) was significantly enhanced in BRS-3-deficient mice but not in GRP-R-deficient mice. In addition, the levels of MCH-R and prepro-MCH mRNAs in the hypothalamus of BRS-3-deficient mice were significantly more elevated than those of wild-type littermates. There was no significant difference in feeding between BRS-3-deficient and wild-type littermate mice after treatment with bombesin (BN), although the hypophagic response to low-dose BN was significantly suppressed in the GRP-R-deficient mice. These results suggest that upregulation of MCH-R and MCH triggers hyperphagia in BRS-3-deficient mice. From these results, we assume that the BRS-3 gene deletion upsets the mechanism by which leptin decreases the expression of MCH-R and that this effect may be mediated through neural networks independent of BN-related peptides such as GRP-R. Diabetes 53: 570 -576, 2004

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Molecular cloning and characterization of avian bombesin‐like peptide receptors: new tools for investigating molecular basis for ligand selectivity

Cited by 27 publications

References 44 publications

Development and function of bombesin-like peptides and their receptors

Development and function of bombesin-like peptides and their receptors

Bombesin receptor regulation of emotional memory

Leptin Resistance and Enhancement of Feeding Facilitation by Melanin-Concentrating Hormone in Mice Lacking Bombesin Receptor Subtype-3

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