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1 -acetyl alpha-MSH successfully activated the melanocortin 4 receptor.
2 in the search for novel ligands of the human melanocortin 4 receptor.
3 highly mutated and well-established target, melanocortin 4 receptor.
4 independently of leptin, GLP-1 receptor and melanocortin 4 receptor.
5 than for the well-established obesity target melanocortin 4 receptor.
6 ium spiny neurons owing to activation of the melanocortin 4 receptor.
7 esting there is allosteric modulation of the melanocortin-4 receptor.
8 -alpha-MSH to cells overexpressing the human melanocortin-4 receptor.
9 for the melanocortin-3 receptor than for the melanocortin-4 receptor.
10 AGRP are functional antagonists of the human melanocortin-4 receptor.
11 tagonists of the melanocortin-3 receptor and melanocortin-4 receptor.
12 nist or micromolar agonist activities at the melanocortin-4 receptor.
13 cy of TCMCB07, a synthetic antagonist of the melanocortin-4 receptor.
14 sequent activation of central nervous system melanocortin 4 receptors.
15 binding affinity for both melanocortin-3 and melanocortin-4 receptors.
17 A potent and selective antagonist of the melanocortin-4 receptor, 1-[2-[(1S)-(3-dimethylaminoprop
18 e in regulating signaling and trafficking of melanocortin 4 receptor, a critical controller of energy
20 lanocyte-stimulating hormone (alphaMSH) is a melanocortin 4 receptor agonist, and its potency in redu
22 tion of body weight: PVN neurons express the melanocortin 4 receptor and appear to be physiological t
23 2) is an adaptor protein that contributes to melanocortin-4 receptor and prokineticin receptor 1 sign
25 The melanocortin pathway, specifically the melanocortin-4 receptor and the cognate endogenous agoni
27 tions in the coding region of the serpentine Melanocortin 4 receptor are the most common genetic caus
29 se can prevent the genetic predisposition of melanocortin-4 receptor-associated obesity and diabetes.
30 inity to the melanocortin 3 receptor and the melanocortin 4 receptor, but not to the melanocortin 1 r
31 leads to an increased number of monomers of melanocortin-4 receptor by disrupting receptor oligomers
32 e consider the structure and function of the melanocortin-4 receptor circuitry and its role in energy
33 s and duplications) and a Mendelian disease (melanocortin 4 receptor deficiency (MC4R)) that affect B
35 characterized by excessive hunger, including melanocortin-4 receptor deficiency, that present with lo
36 not significantly altered in the ob, db, or melanocortin 4 receptor-deficient mouse model of obesity
38 hypothalamus; the MSH normally then binds to melanocortin-4 receptor expressing neurons and inhibits
45 harmacological blockade and knockdown of the melanocortin-4 receptor gene in the DMV abolish this sti
46 tively low affinity for binding at the human melanocortin 4 receptor (hMC4R), were prepared by solid
52 or the interaction of ligands with the human melanocortin-4 receptor (hMC4R), agonist structure-activ
53 ossibly acting upstream or downstream of the melanocortin 4 receptor in the PVN, is responsible for s
54 egulation of signaling by melanocortin 3 and melanocortin 4 receptors in the CNS is controlled via ne
55 t a role for the melanocortin system and the melanocortin-4 receptor in the ring dove feeding behavio
56 cy of TCMCB07, a synthetic antagonist of the melanocortin-4 receptor, in mitigating anorexia and weig
62 essory protein 2 has multiple effects on the melanocortin-4 receptor: it enhances G protein-mediated
65 derived peptides were optimized for in vitro melanocortin-4 receptor (MC-4R) binding affinity, agonis
67 the interaction between leptin, insulin, and melanocortin-4 receptors (MC-4Rs) in the control of rena
68 The centrally expressed melanocortin-3 and melanocortin-4 receptors (MC3R and MC4R, respectively) a
69 The centrally located melanocortin-3 and melanocortin-4 receptors (MC3R, MC4R) are involved in th
71 that intraventricular administration of the melanocortin 4 receptor (MC4-R) agonist MT II and antago
78 t genetic or pharmacological blockade of the melanocortin-4 receptor (MC4-R) attenuates uremia-associ
80 ays inverse agonism at constitutively active melanocortin-4 receptor (MC4-R) expressed on transfected
84 satiety and that activation of the neuronal melanocortin-4 receptor (MC4-R) is required for CCK-indu
85 fluorescent protein under the control of the melanocortin-4 receptor (MC4-R) promoter, we observed Y1
87 ceptors, melanocortin-3-receptor (MC3-R) and melanocortin-4-receptor (MC4-R), are expressed in many d
89 C) at the melanocortin 3 receptor (MC3R) and melanocortin 4 receptor (MC4R) and has been proposed to
91 ons in the coding sequence of the serpentine melanocortin 4 receptor (MC4R) are the most frequent gen
92 Accordingly, exogenous stimulation of the melanocortin 4 receptor (Mc4r) by cotreating mice with F
93 oylglycerol (2-AG) regulates the activity of melanocortin 4 receptor (MC4R) cells in the paraventricu
94 es between patients with SIM1 deficiency and melanocortin 4 receptor (MC4R) deficiency suggest that s
96 agouti peptide is a potent antagonist of the melanocortin 4 receptor (MC4R) expressed in neurons, and
98 oding mutations in conserved residues of the melanocortin 4 receptor (MC4R) gene, contributing to the
100 rial who carried pathogenic mutations in the melanocortin 4 receptor (MC4R) gene, the most common gen
101 We show that Opn3 is coexpressed with the melanocortin 4 receptor (Mc4r) in a population of PVN ne
102 rosses the blood-brain barrier, binds to the melanocortin 4 receptor (MC4R) in the paraventricular an
117 ated whether the effect of GNAS mutations on melanocortin 4 receptor (MC4R) signaling explains the ob
119 n suggests brain origin, whether the central melanocortin 4 receptor (Mc4r) system directly modulates
120 The central melanocortin system acts through melanocortin 4 receptor (MC4R) to control appetite, food
122 ed genetic deletion of the gene encoding the melanocortin 4 receptor (MC4R), as well as pharmacologic
123 and anatomical approaches, we show that the melanocortin 4 receptor (MC4R), implicated in the contro
124 dorsal raphe nucleus (dlDRN) expressing the melanocortin 4 receptor (MC4R), which in turn innervate
126 sity (DIO), leptin receptor (LepR)-null, and melanocortin 4 receptor (MC4R)-null mice-in this study,
129 T), neuronal nitric oxide synthase 1 (NOS1), melanocortin 4-receptor (MC4R), prodynorphin (PDYN)).
130 icosities in close apposition to a subset of melanocortin-4 receptor (MC4R(PVH)) cells, which are als
131 yte stimulating hormones (alpha-MSH) and the melanocortin-4 receptor (Mc4r) all lead to obesity in ma
132 rgy homeostasis, with key components such as melanocortin-4 receptor (MC4R) and adenylyl cyclase 3 (A
134 Loss-of-function mutations in the human melanocortin-4 receptor (MC4R) are associated with obesi
135 ings suggest that the proximal region of the melanocortin-4 receptor (MC4R) C terminus is crucial not
139 increased linear growth, mirroring Sim1 and Melanocortin-4 receptor (MC4R) haplo-insufficiency in mi
143 ly significant heterozygous mutations in the Melanocortin-4 receptor (MC4R) have been implicated in 2
146 ological studies have defined a role for the melanocortin-4 receptor (Mc4r) in the regulation of ener
164 een the antagonist AGRP amino acids with the melanocortin-4 receptor (MC4R) may be important for the
167 e resulted in the discovery of over 70 human melanocortin-4 receptor (MC4R) polymorphisms observed as
173 in (AGRP) is an endogenous antagonist of the melanocortin-4 receptor (MC4R) that functions in the hyp
174 tribution of extracytoplasmic domains of the melanocortin-4 receptor (MC4R) to AGRP binding by making
175 actors that mediate their action through the melanocortin-4 receptor (MC4R) whereas AGRP is an opposi
177 ing these methods, we performed a DMS of the melanocortin-4 receptor (MC4R), a G-protein-coupled rece
180 ct of exogenous alpha-MSH is mediated by the melanocortin-4 receptor (MC4R), and what thermoeffector
181 f AgRP are not limited to its actions at the melanocortin-4 receptor (MC4R), because MC4R-deficient (
182 to play an important role downstream of the melanocortin-4 receptor (MC4R), but this hypothesis has
183 hypothalamus (PVN) were shown to contain the melanocortin-4 receptor (MC4R), concentrated in the vent
185 erge with GABAergic ARC(AgRP) projections on melanocortin-4 receptor (MC4R)-expressing satiety neuron
192 Both peptides bind with high affinity to the melanocortin-4 receptor (MC4R); existing data show that
194 ing and satiety are coordinated centrally by melanocortin-4 receptors (MC4R) in neurons of the hypoth
195 istic actions of these ligands at downstream melanocortin-4 receptors (MC4R) in the paraventricular n
207 n supraoptic oxytocin neurons, and alpha-MSH melanocortin-4 receptors (MC4Rs) are highly expressed in
211 ral despair, are prevented by blocking these melanocortin 4 receptor-mediated synaptic changes in viv
212 tructural homology model of the active state melanocortin-4 receptor - melanocortin-receptor accessor
215 x 10(-6)) mapped 188 kb downstream of MC4R (melanocortin-4 receptor), mutations of which are the lea
216 does not suppress the obese phenotype of the melanocortin-4-receptor null allele or those of the mono
217 to moderately increased dietary fat content, melanocortin-4 receptor-null mutant (MC4R-/-) mice exhib
218 es not alter hypothalamic mRNA expression of melanocortin 4 receptor or adiponectin serum and mRNA ex
219 2) = 5.9) is also an antagonist at the brain melanocortin-4 receptor (pA(2) = 6.9), with no observabl
220 e central nervous system proopiomelanocortin-melanocortin 4 receptor pathway, and kidney compression
223 y protein that interacts with and influences melanocortin-4 receptor structure, biasing its signaling
224 downstream of hypothalamic and/or brainstem melanocortin 4 receptors, that project via the autonomic
226 hingosine 1-phosphate receptor-3 (S1P3), the melanocortin-4 receptor, the Smoothened receptor, formyl
227 showed that potency of binding to the human melanocortin 4 receptor was not diminished for linker-li
228 POMC neurons and subsequent activation of melanocortin 4 receptors were critical for nicotinic-ind
229 of protease-activated receptors-1 and -2 and melanocortin-4 receptors yields agonists and/or antagoni