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1 nternal agonist (alpha-MSH) and antagonists (Agouti).
2 chromosome 13, close to the candidate locus Agouti.
4 s coat color in mouse offspring carrying the agouti A(vy) allele have received considerable attention
5 creased DNA methylation at the viable yellow agouti (A(vy)) locus in a sex-specific manner (P=0.004).
8 r by a high fat diet or by the lethal yellow agouti (A(y)) mutation, and this protective action was d
10 the somatosensory and visual cortices of the agouti, a diurnal rodent with a relatively big brain, us
12 if2s2, and induces the ectopic expression of agouti, all of which are potential TGCT-modifying mutati
13 we combined mutant alleles of Dnmt1 with an agouti allele (A(iapy)), which provided a coat color rea
14 thermore, our data suggest that this derived Agouti allele arose de novo after the formation of the S
15 ny of which were mosaic, transmitted altered Agouti alleles to F1 pups to yield an allelic series of
16 he negative regulator of adult pigmentation, Agouti, also plays a key developmental role in color pat
18 The coordinate and inverse regulation of Agouti and Corin renders pelage pigmentation sensitive t
20 s in the lymph nodes of EAE-susceptible Dark Agouti and EAE-resistant Piebald Virol Glaxo rats during
22 reated Lewis strain recipient rats from Dark Agouti and Lewis strain donors, respectively (unmodified
23 at have been studied to date, two key genes, Agouti and Melanocortin 1 receptor (Mc1r), encode a liga
25 strains (Sprague-Dawley, Brown Norway, Dark Agouti and PVG) were given access to running wheels (1 o
27 ectly associated with the promoter region of agouti, and genotypes at this locus obey simple Mendelia
28 putative candidate genes for melanism (ASIP [agouti] and MC1R) and identified three independent delet
30 the coat color distribution of viable yellow agouti (Avy) mouse offspring toward yellow by decreasing
32 no circulating leptin and infertile, obese, agouti (Ay/a) mice with high circulating leptin levels,
34 ocortin receptor 1 (Mc1r) and its antagonist Agouti, but the genetic and developmental mechanisms tha
35 Taken together, these results reveal that agouti can regulate adipogenesis at several levels and s
36 To simplify breeding schemes, the dominant agouti coat color gene was restored in JM8 cells by targ
37 ver, rather than eating the recovered seeds, agoutis continued to move and recache the seeds, up to 3
39 y, liver transplants from Lewis rats to dark agouti (DA) rats survive indefinitely without immunosupp
41 ozotocin (STZ)-induced diabetic Dilute Brown Agouti (DBA) and arginase-2-deficient mice (Arg2(-/-)).
42 tained from transgenic mice that overexpress agouti demonstrated that melanocortin receptor (MCR) sig
45 Agouti lethal yellow (A(y)) mice express agouti ectopically because of a genetic rearrangement at
46 hat ventral-specific embryonic expression of Agouti establishes a prepattern by delaying the terminal
47 beta-Catenin activity in the DP suppresses Agouti expression and activates Corin, a negative regula
48 individual hairs produced by an increase in Agouti expression caused by a cis-acting mutation (or mu
49 s in moderately obese mice, the link between agouti expression in human adipose tissue and obesity/ty
50 ease in both the level and spatial domain of Agouti expression prevents melanocyte maturation in a re
51 acting, tissue-specific changes in embryonic Agouti expression to produce large changes in adult colo
53 sts, a unique physiological function for the agouti family of proteins, and define a neuroendocrine a
54 rder of dominance, these are the unpatterned agouti form called "Abyssinian" or "ticked" (T(a)), foll
55 specifying coat color and acts downstream of agouti gene expression as a suppressor of the agouti pat
59 , which harbor a transposable element in the agouti gene, we tested the hypothesis that the metastabl
65 se tissue and that the ectopic expression of agouti in adipose tissue results in moderately obese mic
67 in gene-trap mice nor ectopic expression of agouti in transgenic or viable-yellow (A(vy)) mutants af
70 and excretion in bile of healthy Long-Evans agouti (LEA) rats versus LEC rats modeling Wilson diseas
75 We identified distinct regions within the Agouti locus associated with each color trait and found
76 tion revealed that TALEN pairs targeting the Agouti locus induced site-directed DNA breaks in zygotes
77 ain mutations elsewhere in the > or = 125-kb agouti locus that either reduce the level or alter the t
81 (Dcc) mutations, and identified mutations in Agouti (Met1Leu, Dcc4), Sox18 (Leu220ter, Dcc1), Keratin
83 otes, and a keratin-14 (K14) promoter-driven agouti minigene was introduced onto the inverted chromos
84 c coinjection of TALEN mRNAs directed to the Agouti, miR-205, and the Arf tumor suppressor loci yield
86 h there was no apparent relationship between agouti mRNA levels and BMI, agouti mRNA levels were sign
87 tionship between agouti mRNA levels and BMI, agouti mRNA levels were significantly elevated in subjec
88 cytes revealed that insulin did not regulate agouti mRNA, whereas dexamethasone treatment potently in
91 eveal that Mc1r is epistatic to variation at Agouti or K and that the epistatic relationship between
92 on (180 nmol) of either GSH adduct into Dark Agouti or Sprague-Dawley rats only 5-(glutathion-S-yl)-a
95 hat BMP signaling controls the expression of Agouti protein in the hair follicle and provide evidence
96 pic hormone, melanocyte stimulating hormone, agouti protein ligands (in rodents), c-Kit, and the endo
97 We transplanted cardiac allografts from Dark Agouti rat and Balb mouse donors to fully major histocom
99 ey transplantations were performed from dark agouti rat strain (DA) to Wistar furth rat strain rats a
101 grey matter demyelination was set up in Dark Agouti rats and analysed using quantitative immunohistoc
104 s were transplanted to Lewis or control dark agouti rats on subtherapeutic doses of cyclosporin.
105 a into the subarachnoid space of female Dark Agouti rats pre-immunized with a subclinical dose of mye
108 n structural/pathological correlates in Dark Agouti rats with experimental autoimmune encephalomyelit
109 utside the CNS and AZD8797 treatment in Dark Agouti rats with myelin oligodendrocyte glycoprotein-ind
114 ed expression of the orexigenic neuropeptide agouti related protein (AgRP) in the BMPR1A-deficient AR
116 hypothalamus (ARH) that contains orexigenic agouti-related peptide (AgRP) and anorexigenic pro-opiom
117 g-responsive hypothalamic neurons expressing agouti-related peptide (AgRP) and neuropeptide Y (Npy).
119 w leptin-sensing neuron population, multiple agouti-related peptide (AgRP) and pro-opiomelanocortin (
121 te time periods, and measured the density of Agouti-Related Peptide (AgRP) containing projections fro
122 ing view is that the orexigenic neuropeptide agouti-related peptide (AgRP) exerts the opposite action
123 ivate or inhibit ArcN NPY neurons expressing agouti-related peptide (AgRP) in mice, we have demonstra
126 M glucose concentrations, more inhibition of agouti-related peptide (AgRP) mRNA and AMP-activated pro
127 ine leptin inhibits neuropeptide Y (NPY) and agouti-related peptide (AgRP) neuronal activity, resulti
133 hysiologic regulation.SIGNIFICANCE STATEMENT Agouti-related peptide (AgRP) neurons play an important
136 ns, including proopiomelanocortin (POMC) and agouti-related peptide (AgRP) neurons, also release amin
137 ns, including proopiomelanocortin (POMC) and agouti-related peptide (AgRP) neurons, also release amin
138 ic proopiomelanocortin (POMC) and orexigenic agouti-related peptide (AgRP) neurons, electrophysiologi
140 eurons [e.g., proopiomelanocortin (POMC) and agouti-related peptide (AgRP) neurons], and as a result,
141 euron populations specified by expression of agouti-related peptide (AGRP) or pro-opiomelanocortin (P
144 conversely, administration of the antagonist Agouti-related peptide (Agrp) to wild-type mice enhanced
145 neurons expressing neuropeptide Y (NPY) and agouti-related peptide (AgRP) via GABA-dependent signali
146 gnaling from hypothalamic neurons expressing agouti-related peptide (AgRP) was genetically inactivate
147 of hypothalamic 'hunger neurons' (expressing agouti-related peptide (AgRP)) bypasses these signals to
149 iomelanocortin (POMC), neuropeptide Y (NPY), agouti-related peptide (AGRP), somatostatin, and dopamin
150 a-MSH) and to an antagonist/inverse agonist, agouti-related peptide (AgRP), which are released by ups
151 ific Cre-driver mice to reexpress RIIbeta in agouti-related peptide (AgRP)-, proopiomelanocortin (POM
152 es the activity of neuropeptide Y (NPY)- and agouti-related peptide (AgRP)-co-producing (NPY/AgRP) ne
155 expressing and hunger signaling (orexigenic) agouti-related peptide (AgRP)-expressing neurons are key
160 hibition of neural melanocortin receptors by agouti-related peptide also attenuated rhythmicity in th
161 A expression of the orexigenic neuropeptides Agouti-related peptide and melanin-concentrating hormone
162 kinase kinase beta or AMPK greatly increases Agouti-related peptide and melanin-concentrating hormone
163 e excited orexigenic neurons that synthesize agouti-related peptide and neuropeptide Y but inhibited
164 coadministration of the alpha-MSH antagonist agouti-related peptide blocked the anorexigenic effects
165 2-null mice, while the density of orexigenic agouti-related peptide fibers in the mutant mice appeare
170 etrogradely labeled neurons contained either agouti-related peptide or cocaine/amphetamine-regulated
171 wise, treatment of WT mice with intracranial agouti-related peptide reversed the cachexic effects of
172 ter (that controlling the Agrp gene encoding agouti-related peptide) responsive to BDNF-induced physi
175 subsets (proopiomelanocortin, neuropeptide Y/agouti-related peptide, and steroidogenic factor 1), tho
176 ding those producing pro-opiolemelanocortin, agouti-related peptide, hypocretin/orexin, melanin-conce
177 increase in the appetite-regulating proteins agouti-related peptide, neuropeptide Y, and uncoupling p
178 knockdown of Sirtuin 1 Sirt1 in hypothalamic Agouti-related peptide-expressing neurons, which renders
180 vity, and expression of pro-opiomelanocortin/agouti-related peptide/neuropeptide Y in the hypothalamu
182 ssing the endogenous melanocortin antagonist agouti-related protein (AgRP) also exhibit obesity, incr
185 w that changes in hypothalamic expression of agouti-related protein (Agrp) and neuropeptide Y (Npy) c
186 e expression of the orexigenic neuropeptides agouti-related protein (AgRP) and neuropeptide Y (NPY).
187 ) whether food deprivation (FD) co-increases agouti-related protein (AgRP) and PPARgamma mRNA express
188 we examined the role of insulin signaling in agouti-related protein (AgRP) and pro-opiomelanocortin (
190 eurons that express neuropeptide Y (NPY) and agouti-related protein (AgRP) are thought to be critical
192 imulating hormone (alpha-MSH) and orexigenic Agouti-related protein (AgRP) from discrete hypothalamic
193 the ability of proopiomelanocortin (POMC) or agouti-related protein (Agrp) hypothalamic neurons to se
194 ablation of hypothalamic neurons expressing agouti-related protein (AgRP) in adult mice leads to ano
205 olves targeting the human DT receptor to the agouti-related protein (Agrp) locus so that systemic adm
206 examine the importance of GABA release from agouti-related protein (AgRP) neurons (which also releas
207 examine the importance of GABA release from agouti-related protein (AgRP) neurons (which also releas
209 crease but their size increase in orexigenic agouti-related protein (Agrp) neurons during the transit
212 used targeted knock-ins to express InsRs in agouti-related protein (AgRP) or proopiomelanocortin (PO
213 ther, CTRP13 and the orexigenic neuropeptide agouti-related protein (AgRP) reciprocally regulate each
214 ithin the hypothalamus, neurons that express agouti-related protein (AgRP) sense orexigenic factors a
217 re, the endogenous MC3R and MC4R antagonist, agouti-related protein (AgRP), hyperpolarizes POMC and R
219 e (alpha-MSH) and its endogenous antagonist, agouti-related protein (AgRP), is fundamental for the ce
222 A expression levels of neuropeptide Y (NPY), agouti-related protein (AGRP), proopiomelanocortin (POMC
223 luding those producing neuropeptide Y (NPY), Agouti-related protein (AGRP), proopiomelanocortin (POMC
224 othalamic GHS-R1a, neuropeptide Y (NPY), and agouti-related protein (AgRP), suggesting that prolonged
225 are absent in mice lacking the gene encoding agouti-related protein (Agrp), suggesting that this func
227 gonists, agouti signaling protein (ASIP) and agouti-related protein (AGRP), were assessed by studying
228 neurons containing neuropeptide Y (NPY) and agouti-related protein (AgRP), which are conditional pac
237 ture-activity relationship study of chimeric agouti-related protein (AGRP)/[Nle4,DPhe7]alpha-melanocy
238 enic neuropeptides [neuropeptide Y (NPY) and agouti-related protein (AgRP)] and activates expression
239 lpha-MSH(4-10)-NH(2) (SHU9119)] and natural [agouti-related protein (AGRP)] MC3R antagonists but not
241 ing hormone, oxytocin, arginine vasopressin, agouti-related protein and alpha-melanocyte stimulating
242 orexigenic neuropeptides neuropeptide Y and agouti-related protein and down-regulation of expression
243 be mediated by leptin action on arcuate NPY/agouti-related protein and proopiomelanocortin neurons.
244 ons but has limited effect on neuropeptide Y/agouti-related protein and proopiomelanocortin neurons.
245 howed that in the DMH abundant alpha-MSH and agouti-related protein fibers are in close apposition to
246 adrenocorticotropin (ACTH)], the antagonist agouti-related protein hAGRP(87-132), and synthetic agon
251 1, which caused increased neuropeptide Y and agouti-related protein mRNAs in the hypothalamus, stimul
252 sm in proopiomelanocortin and neuropeptide Y/agouti-related protein neurons and links hypothalamic AM
253 ate nucleus, specifically the neuropeptide Y/agouti-related protein neurons and the dorsal medial nuc
254 CK1 in either pro-opiomelanocortin (POMC) or agouti-related protein neurons, mediators of leptin acti
256 ession of key orexigenic (neuropeptide Y and agouti-related protein) and anorexigenic (pro-opiomelano
257 e appetite-stimulating (neuropeptide Y, NPY; agouti-related protein, AGRP) and appetite-inhibiting (c
258 gen, decreases AMPK activity in PVH, whereas agouti-related protein, an orexigen, increases AMPK acti
259 rons were stained for a second neuropeptide, agouti-related protein, immunoreactivity was found in th
262 ivation of ARC glia enhances the activity of agouti-related protein/neuropeptide Y (AgRP/NPY)-express
263 RNAs in the hypothalamus, stimulation of the agouti-related protein/neuropeptide Y neurons, and activ
264 dullin (hazard ratio per log increase 2.53), agouti-related protein; (1.48), chitinase-3-like protein
267 ed that the stepwise dispersal was caused by agoutis repeatedly stealing and recaching each other's b
271 ion can be antagonized by a secreted factor, agouti signal protein (ASP), which is responsible for th
272 is accompanied by strongly reduced levels of Agouti signal protein and enhanced expression of microph
274 and hMC4R) and their endogenous antagonists, agouti signaling protein (ASIP) and agouti-related prote
277 cortisol implants increase the expression of agouti signaling protein (ASIP) mRNA in skin, likely exp
279 lved in feather development or pigmentation: agouti signaling protein (ASIP), follistatin (FST), ecod
280 MC1R antagonists human beta-defensin 3 and agouti signaling protein blocked MSH- but not forskolin-
282 their effects were abrogated by an analog of agouti signaling protein, the physiological MC1R antagon
283 cortin gene transcript, and two antagonists, agouti-signaling protein (ASP) and agouti-related protei
285 melanocortin 1 receptor with the antagonist agouti-signaling protein decreased the proportion of mat
286 shown by blockade with a peptide analogue of agouti-signaling protein) and imitated by adrenocorticot
288 although the endogenous receptor antagonist, agouti signalling protein, blocks activation of human MC
295 regnancy induces CpG hypermethylation at the agouti viable yellow (A(vy)) allele in A(vy)/a offspring
298 putedly megafaunal seeds by Central American agoutis, which scatter-hoard seeds in shallow caches in
299 AT in the presence of obesity, obesity-prone agouti yellow mice (A(y)/a) on a hyperlipidemia-prone LD
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