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1 ium spiny neurons owing to activation of the melanocortin 4 receptor.
2 -acetyl alpha-MSH successfully activated the melanocortin 4 receptor.
3 in the search for novel ligands of the human melanocortin 4 receptor.
4 -alpha-MSH to cells overexpressing the human melanocortin-4 receptor.
5 for the melanocortin-3 receptor than for the melanocortin-4 receptor.
6 AGRP are functional antagonists of the human melanocortin-4 receptor.
7 tagonists of the melanocortin-3 receptor and melanocortin-4 receptor.
8 esting there is allosteric modulation of the melanocortin-4 receptor.
9 sequent activation of central nervous system melanocortin 4 receptors.
10 binding affinity for both melanocortin-3 and melanocortin-4 receptors.
11 A potent and selective antagonist of the melanocortin-4 receptor, 1-[2-[(1S)-(3-dimethylaminoprop
13 lanocyte-stimulating hormone (alphaMSH) is a melanocortin 4 receptor agonist, and its potency in redu
15 tion of body weight: PVN neurons express the melanocortin 4 receptor and appear to be physiological t
16 2) is an adaptor protein that contributes to melanocortin-4 receptor and prokineticin receptor 1 sign
18 The melanocortin pathway, specifically the melanocortin-4 receptor and the cognate endogenous agoni
20 tions in the coding region of the serpentine Melanocortin 4 receptor are the most common genetic caus
21 se can prevent the genetic predisposition of melanocortin-4 receptor-associated obesity and diabetes.
22 inity to the melanocortin 3 receptor and the melanocortin 4 receptor, but not to the melanocortin 1 r
23 e consider the structure and function of the melanocortin-4 receptor circuitry and its role in energy
25 not significantly altered in the ob, db, or melanocortin 4 receptor-deficient mouse model of obesity
26 hypothalamus; the MSH normally then binds to melanocortin-4 receptor expressing neurons and inhibits
30 tively low affinity for binding at the human melanocortin 4 receptor (hMC4R), were prepared by solid
35 or the interaction of ligands with the human melanocortin-4 receptor (hMC4R), agonist structure-activ
36 ossibly acting upstream or downstream of the melanocortin 4 receptor in the PVN, is responsible for s
37 egulation of signaling by melanocortin 3 and melanocortin 4 receptors in the CNS is controlled via ne
38 t a role for the melanocortin system and the melanocortin-4 receptor in the ring dove feeding behavio
41 derived peptides were optimized for in vitro melanocortin-4 receptor (MC-4R) binding affinity, agonis
43 the interaction between leptin, insulin, and melanocortin-4 receptors (MC-4Rs) in the control of rena
44 The centrally located melanocortin-3 and melanocortin-4 receptors (MC3R, MC4R) are involved in th
45 that intraventricular administration of the melanocortin 4 receptor (MC4-R) agonist MT II and antago
51 t genetic or pharmacological blockade of the melanocortin-4 receptor (MC4-R) attenuates uremia-associ
53 ays inverse agonism at constitutively active melanocortin-4 receptor (MC4-R) expressed on transfected
57 satiety and that activation of the neuronal melanocortin-4 receptor (MC4-R) is required for CCK-indu
58 fluorescent protein under the control of the melanocortin-4 receptor (MC4-R) promoter, we observed Y1
60 ceptors, melanocortin-3-receptor (MC3-R) and melanocortin-4-receptor (MC4-R), are expressed in many d
61 C) at the melanocortin 3 receptor (MC3R) and melanocortin 4 receptor (MC4R) and has been proposed to
63 ons in the coding sequence of the serpentine melanocortin 4 receptor (MC4R) are the most frequent gen
64 es between patients with SIM1 deficiency and melanocortin 4 receptor (MC4R) deficiency suggest that s
65 agouti peptide is a potent antagonist of the melanocortin 4 receptor (MC4R) expressed in neurons, and
66 oding mutations in conserved residues of the melanocortin 4 receptor (MC4R) gene, contributing to the
68 rosses the blood-brain barrier, binds to the melanocortin 4 receptor (MC4R) in the paraventricular an
79 ed genetic deletion of the gene encoding the melanocortin 4 receptor (MC4R), as well as pharmacologic
80 and anatomical approaches, we show that the melanocortin 4 receptor (MC4R), implicated in the contro
83 icosities in close apposition to a subset of melanocortin-4 receptor (MC4R(PVH)) cells, which are als
84 yte stimulating hormones (alpha-MSH) and the melanocortin-4 receptor (Mc4r) all lead to obesity in ma
87 ings suggest that the proximal region of the melanocortin-4 receptor (MC4R) C terminus is crucial not
93 ly significant heterozygous mutations in the Melanocortin-4 receptor (MC4R) have been implicated in 2
96 ological studies have defined a role for the melanocortin-4 receptor (Mc4r) in the regulation of ener
111 een the antagonist AGRP amino acids with the melanocortin-4 receptor (MC4R) may be important for the
113 e resulted in the discovery of over 70 human melanocortin-4 receptor (MC4R) polymorphisms observed as
117 in (AGRP) is an endogenous antagonist of the melanocortin-4 receptor (MC4R) that functions in the hyp
118 tribution of extracytoplasmic domains of the melanocortin-4 receptor (MC4R) to AGRP binding by making
119 actors that mediate their action through the melanocortin-4 receptor (MC4R) whereas AGRP is an opposi
122 ct of exogenous alpha-MSH is mediated by the melanocortin-4 receptor (MC4R), and what thermoeffector
123 f AgRP are not limited to its actions at the melanocortin-4 receptor (MC4R), because MC4R-deficient (
124 to play an important role downstream of the melanocortin-4 receptor (MC4R), but this hypothesis has
125 hypothalamus (PVN) were shown to contain the melanocortin-4 receptor (MC4R), concentrated in the vent
127 erge with GABAergic ARC(AgRP) projections on melanocortin-4 receptor (MC4R)-expressing satiety neuron
133 Both peptides bind with high affinity to the melanocortin-4 receptor (MC4R); existing data show that
135 ing and satiety are coordinated centrally by melanocortin-4 receptors (MC4R) in neurons of the hypoth
136 istic actions of these ligands at downstream melanocortin-4 receptors (MC4R) in the paraventricular n
146 n supraoptic oxytocin neurons, and alpha-MSH melanocortin-4 receptors (MC4Rs) are highly expressed in
150 ral despair, are prevented by blocking these melanocortin 4 receptor-mediated synaptic changes in viv
153 x 10(-6)) mapped 188 kb downstream of MC4R (melanocortin-4 receptor), mutations of which are the lea
154 does not suppress the obese phenotype of the melanocortin-4-receptor null allele or those of the mono
155 to moderately increased dietary fat content, melanocortin-4 receptor-null mutant (MC4R-/-) mice exhib
156 es not alter hypothalamic mRNA expression of melanocortin 4 receptor or adiponectin serum and mRNA ex
157 2) = 5.9) is also an antagonist at the brain melanocortin-4 receptor (pA(2) = 6.9), with no observabl
159 downstream of hypothalamic and/or brainstem melanocortin 4 receptors, that project via the autonomic
161 hingosine 1-phosphate receptor-3 (S1P3), the melanocortin-4 receptor, the Smoothened receptor, formyl
162 showed that potency of binding to the human melanocortin 4 receptor was not diminished for linker-li
163 POMC neurons and subsequent activation of melanocortin 4 receptors were critical for nicotinic-ind
164 of protease-activated receptors-1 and -2 and melanocortin-4 receptors yields agonists and/or antagoni
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