ライフサイエンスコーパス: BRS-3

1 or (NMB-R), and bombesin receptor subtype 3 (BRS-3).

2 or (NMB-R), and bombesin receptor subtype 3 (BRS-3).

3 E3) that behaved almost identically to human BRS-3.

4 aBRS-3) for bombesin compared with wild-type BRS-3.

5 sin and GRP affinities relative to wild-type BRS-3.

6 RP-R with the homologous amino acid in human BRS-3.

7 ade in Balb 3T3 cells, which lack endogenous BRS-3.

8 s would not be conserved among homologues of BRS-3.

9 ayed an EC50 level of 5 nM for activation of BRS-3.

10 NMB-R increased the affinity of the mutated BRS-3 (4DeltaBRS-3) for bombesin compared with wild-type

11 which is roughly 1000-fold more potent than BRS-3 agonists described previously.

12 (13),Nle(14)]Bn-(6-14) has high affinity for BRS-3 and using this ligand showed BRS-3 has a unique ph

13 nd cDNA for rat bombesin receptor subtype-3 (BRS-3) and characterized its mRNA expression pattern and

14 ceptor (NMB-R), bombesin receptor subtype 3 (BRS-3), and bombesin receptor subtype 4 (bb4).

15 the species difference between rat and human BRS-3, and multiple residues in the E3 loop are involved

16 ly discovered peptide with high affinity for BRS-3, and various Bn receptor agonists and antagonists

17 sin-like peptides required for activation of BRS-3 are similar to those necessary for activation of t

18 rovides important information for evaluating BRS-3 as a potential therapeutic target for the treatmen

19 1993 was called bombesin receptor subtype 3 (BRS-3) because of 47-51% amino acid identity with bombes

20 in the nanomolar range; by comparison, human BRS-3 binds bombesin at much lower affinity (Kd >> 1 mic

21 ch are Balb/3T3 fibroblasts transfected with BRS-3 cDNA.

22 idization was performed to determine whether BRS-3 colocalizes with other neurotransmitters or neurop

23 BRS-3-containing neurons do not express some of the well

24 a recent targeted disruption study, in which BRS-3-deficient mice were generated, the mice developed

25 Mice deficient in BRS-3 develop late-onset mild obesity with metabolic def

26 Like GRP-R and NMB-R, BRS-3 did not catalyze GTPgammaS binding to Galphai/o or

27 rast, these four amino acid substitutions in BRS-3 did not result in the formation of a high affinity

28 ce similarity (80% identical), rat and human BRS-3 differ markedly in their pharmacological propertie

29 dY-bombesin had a very poor potency for rat BRS-3 (EC(50) = 2 microM).

30 ombesin-like peptides were shown to activate BRS-3 expressed in Xenopus laevis oocytes, but only at r

31 Many, but not all, of the BRS-3-expressing neurons were found to be glutamatergic,

32 ate the neurochemical characteristics of the BRS-3-expressing neurons, double in situ hybridization w

33 tituting these four divergent amino acids in BRS-3 for the conserved amino acids in either GRP-R or N

34 Nothing is known about mechanisms regulating BRS-3 gene expression and possible association with dise

35 The structural data of the BRS-3 genes derived from this study will permit future i

36 The loci of the BRS-3 genes were mapped to a syntenic region of the huma

37 tructure and chromosomal localization of the BRS-3 genes, bacteriophage P1 genomic clones, harboring

38 inity for BRS-3 and using this ligand showed BRS-3 has a unique pharmacology with high affinity for n

39 e two cell lines stably expressing the human BRS-3 (hBRS-3).

40 antagonists of the GRP receptor can activate BRS-3 in BR2 cells.

41 To study the pharmacology of BRS-3 in the context of a mammalian cell, we used BR2 ce

42 ] receptor, and bombesin receptor subtype 3 [BRS-3]) in human non-small cell lung carcinoma (NSCLC) c

43 ely high concentrations, which suggests that BRS-3 is an orphan receptor.

44 s, GRP-R and NMB-R, and a natural ligand for BRS-3 is currently unknown.

45 d thus provide pharmacological evidence that BRS-3 is in the BN receptor family.

46 The tissue distribution of BRS-3 is quite dissimilar compared to the other two BN r

47 Although the natural ligand for BRS-3 is still unknown, a synthetic peptide, dY-Q-W-A-V-

48 Bombesin receptor subtype-3 (BRS-3) is an orphan G-protein-coupled receptor (GPCR) in

49 Bombesin (Bn) receptor subtype 3 (BRS-3) is an orphan receptor that is a predicted member

50 ate identification of the natural ligand for BRS-3, its pharmacology, and cell biology.

51 ar modeling demonstrated these two selective BRS-3 ligands had a unique conformation of the position

52 log, D-Phe6-BN(6-13) propyl amide, activated BRS-3-mediated calcium mobilization with an EC50 level o

53 We report here a comprehensive mapping of BRS-3 mRNA in the rat and mouse brain through in situ hy

54 Interestingly, BRS-3 mRNA was found to partially colocalize with cortic

55 urthermore, we have identified an agonist of BRS-3, namely D-Phe6-Phe13-BN(6-13) propyl amide, which

56 r bb1), and the bombesin receptor subtype 3 (BRS-3, or bb3).

57 ar bombesin receptor subtypes, in particular BRS-3, possess distinct coupling preferences among membe

58 ich demonstrates 48% identity with the mouse BRS-3 protein and 53% identity with the mouse NMB-R prot

59 ines found that express sufficient levels of BRS-3 protein for study.

60 The analogous mutations in BRS-3 (R127Q, H294R, S205P, and S315A) together resulted

61 the affinity of NMB is increased in a mutant BRS-3 receptor (4DeltaBRS-3) that contains these four su

62 s demonstrated high affinity binding for the BRS-3 receptor.

63 harboring the genes for the human and mouse BRS-3, respectively, were isolated and their structure a

64 the third extracellular loop (E3) in the rat BRS-3 resulted in a chimeric receptor (RB3-E3) that beha

65 To date, BRS-3's natural ligand remains unknown, its pharmacology

66 present study we have attempted to identify BRS-3 selective ligands using a strategy of rational pep

67 this approach we have identified a number of BRS-3 selective ligands.

68 receptor, bombesin (Bn) receptor subtype 3 (BRS-3), shares high homology with bombesin receptors (ne

69 defects, while synthetic agonists activating BRS-3 show antiobesity profiles by inhibiting food intak

70 However, BRS-3 showed little, if any, coupling with squid Galphaq

71 with high affinity, but they are diverged in BRS-3, the bombesin receptor subtype that binds bombesin

72 Human bombesin receptor subtype 3 (BRS-3) was cloned based on its homology to the human gas

73 ne the intracellular signaling properties of BRS-3, we examined the ability of [D-Phe6,beta-Ala11,Phe

74 which individual extracellular loops of rat BRS-3 were replaced with the corresponding human sequenc

75 H-F-Nle-amide (dY-bombesin), activates human BRS-3 with an EC(50) of 1.2 nM.

76 one (GHRH), suggesting novel interactions of BRS-3 with stress- and growth-related endocrine systems.