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1 nder the association of Galpha subunits with GPR54.
2 roperties, or protein interaction network of GPR54.
3 le of inducing an LH surge in the absence of GPR54.
4 pocampal neurons, which are known to express GPR54.
5                                 Mutations in GPR54, a G protein-coupled receptor gene, cause autosoma
6 s1 gene codes for kisspeptin, which binds to GPR54, a G-protein-coupled receptor.
7 cociously, and we describe the expression of GPR54 and KiSS-1 in the hypothalamus during the peripube
8 ree were homozygous for an L148S mutation in GPR54, and an unrelated proband with idiopathic hypogona
9                 The peptide and its receptor GPR54 are abundant in the hypothalamus and have been imp
10                               Kisspeptin and GPR54 are expressed in discrete regions of the forebrain
11         Kisspeptin and its cognate receptor, GPR54, are critical for reproductive development and for
12 lated by neuronal activity and activation of GPR54 by kisspeptin may in turn contribute to sustain ba
13  We showed previously that the activation of GPR54 by kisspeptin-10 suppressed CXCR4-mediated chemota
14  that the activation of its cognate receptor GPR54 by kisspeptin-10 suppressed the capacity of the pr
15 Activation of the G-protein-coupled receptor GPR54 by kisspeptins during normal puberty promotes the
16      Activation of KISS1 receptor (KISS1R or GPR54) by its ligands (Kisspeptins) regulates a diverse
17       We demonstrate here that activation of GPR54 can also abolish the activation of Akt by the tyro
18 RH) secretion, and mutations or deletions of GPR54 cause hypogonadotropic hypogonadism in humans and
19 S) in the second intracellular loop (IL2) of GPR54 causes idiopathic hypogonadotropic hypogonadism, a
20                                  Deletion of Gpr54 decreases Bmp7 expression and Smad1 phosphorylatio
21                                          The Gpr54-deficient mice had isolated hypogonadotropic hypog
22                               In parallel, a Gpr54-deficient mouse model was created and phenotyped.
23                          Here we report that Gpr54 deletion leads to kidney branching morphogenesis a
24 itative PCR data showing kisspeptin receptor GPR54 expression in the arcuate nucleus, and the attenua
25                         In contrast, diverse GPR54 functional responses are markedly inhibited by the
26 y, we used female mice with deletions in the GPR54 gene [GPR54 knock-outs (KOs)] to test the hypothes
27 ome (KS), whereas mutations in the GNRHR and GPR54 genes cause idiopathic hypogonadotropic hypogonadi
28 (e.g. Rgs2, Rgs4, Rgs5, Rgs16, Gpr23, Gpr30, Gpr54, Gpr64, and Gna13).
29 ptin fibers, express the kisspeptin receptor GPR54 in the preoptic region, but not in the tuberal reg
30                                              Gpr54 inactivation results in a high risk of low glomeru
31          We show here that the activation of GPR54 induced immediate and profound changes of cell mor
32      We also demonstrated that activation of GPR54 inhibited Akt phosphorylation after the activation
33                                              GPR54 is a G-protein-coupled receptor, which binds kissp
34                               Interestingly, GPR54 is also highly expressed in granule cells of the h
35        The G-protein-coupled receptor (GPCR) GPR54 is essential for the development and maintenance o
36                                              Gpr54 is expressed in condensed mesenchyme at E12.5 and
37                             However, whether Gpr54 is involved in embryonic kidney development and ho
38                                     However, GPR54 is necessary for proper male-like development of s
39 t study examined how expression of KiSS1 and GPR54 is regulated in rat hippocampus, using in vivo and
40 metastasis suppressor KiSS1 and its receptor GPR54 is still incompletely characterized.
41 the cognate ligand for the metastin receptor GPR54, is a peptide known to dramatically reduce metasta
42               G-protein-coupled receptor 54 (Gpr54, KISS1 receptor) plays critical roles in puberty r
43 heral or central administration in Kiss1- or Gpr54 (Kiss1r)-null mutant mice.
44  and its cognate G protein-coupled receptor, GPR54 (kisspeptin receptor, Kiss-R), are critical for th
45               Using adult wild-type (WT) and GPR54 knock-out (KO) mice, we first tested whether kissp
46 emale mice with deletions in the GPR54 gene [GPR54 knock-outs (KOs)] to test the hypothesis that kiss
47 e found that hormone-replaced gonadectomized GPR54 KO males and females displayed appropriate gender-
48    Interestingly, adult testosterone-treated GPR54 KO males displayed "female-like" numbers of tyrosi
49 es, whereas similarly treated WT females and GPR54 KO males showed no preference for either sex.
50                  As predicted, we found that GPR54 KO mice do not exhibit a postovariectomy rise in L
51 onic GnRH/LH secretion would be disrupted in GPR54 KOs and that such animals would be incapable of sh
52 ns and produced a GnRH-dependent LH surge in GPR54 KOs.
53  on the antimetastatic function of KiSS1 and GPR54 largely focused on the autocrine inhibition of cel
54                            Among others, the GPR54-ligand KISS1 was identified as a direct transcript
55   The activation of ROCK also contributed to GPR54-mediated apoptosis in 293 cells, and its effect wa
56 n histochemistry indicated robust KiSS-1 and GPR54 mRNA expression in the region of the arcuate nucle
57 n intact females, but not in agonadal males, GPR54 mRNA levels in the hypothalamus increased approxim
58                                              GPR54 mRNA, on the other hand, was reduced by 20-30% at
59 increased plasma LH levels in both Kiss1 and Gpr54 mutant male mice similar to the responses in wild-
60 pathic hypogonadotropic hypogonadism without GPR54 mutations.
61 kisspeptin receptor (KISS1R, formerly called GPR54), neurokinin B (TAC3), and the neurokinin B recept
62                           Using a transgenic Gpr54-null IRES-LacZ knock-in mouse model, we demonstrat
63 ates a receptor coupled to Galphaq subunits (GPR54 or KiSS-1R).
64 us ligand for the G-protein-coupled receptor GPR54 (or AXOR12, or OT7T175).
65 e interaction of kisspeptin and its receptor GPR54 plays a crucial role in governing the onset of pub
66 ne metastasis suppression effect of KiSS1 on GPR54-positive tumor cells.
67 ns and mice, a loss of function mutations of GPR54 prevents the onset of puberty and leads to hypogon
68            Together, these data suggest that Gpr54 regulates Bmp7 expression through NFAT2 and Sp1 an
69 n and luciferase assays, we demonstrate that Gpr54 regulates NFAT2- and Sp1-mediated Bmp7 transcripti
70                                Activation of GPR54 resulted in the ERK-dependent expression of tumor
71 ings are consistent with the hypothesis that GPR54 signaling by its cognate ligand in the primate hyp
72                                   Kisspeptin-GPR54 signaling has been implicated in the regulation of
73  discusses the latest ideas about kisspeptin-GPR54 signaling in the neuroendocrine regulation of repr
74                 To further study the role of GPR54 signaling in the onset of primate puberty, we used
75 nts; however, the precise role of kisspeptin-GPR54 signaling in the regulation of gonadotropin secret
76           We also postulated that kisspeptin-GPR54 signaling is critical for the generation of the es
77 evelopment by androgens, we assessed whether GPR54 signaling is essential for sexual differentiation
78 KO) mice, we first tested whether kisspeptin-GPR54 signaling is necessary for male and female sexual
79        Our findings indicate that kisspeptin-GPR54 signaling is not required for male or female copul
80                    Next, we examined whether GPR54 signaling is required for proper display of olfact
81                    Thus, in mice, kisspeptin-GPR54 signaling is required for the tonic stimulation of
82 nduced by SDF-1 indicates that activation of GPR54 signaling may negatively regulate the role of CXCR
83 KOs)] to test the hypothesis that kisspeptin-GPR54 signaling provides the drive necessary for tonic G
84      Other reproductive roles for kisspeptin-GPR54 signaling, including the regulation of development
85 on is disrupted in the absence of kisspeptin-GPR54 signaling.
86 also been shown in cells that do not express GPR54, suggesting a paracrine mechanism in which kisspep
87 ecapitulates the effects observed with L148S GPR54, suggesting the critical importance of this hydrop
88 GnRH neurons express the kisspeptin receptor GPR54 upon circuit formation, suggesting that the signal
89                                Activation of GPR54 was shown to inhibit cell motility and invasion of
90                             The signaling of GPR54 was sufficient to trigger apoptosis in epithelial
91 nal differences between wild-type and mutant GPR54 were examined in vitro.
92  examined for mutations in a candidate gene, GPR54, which encodes a G protein-coupled receptor.
93 the kisspeptins, and their cognate receptor, GPR54, which have been implicated in the regulation of G

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