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1 MC1R agonist- but not MC1R antagonist-conjugated nanopar
2 MC1R and MC3R mRNA and protein were both expressed in th
3 MC1R and TYR are associated with pigmentation, freckling
4 MC1R antagonists human beta-defensin 3 and agouti signal
5 MC1R encodes a cyclic AMP-stimulating G-protein-coupled
6 MC1R is a candidate gene involved in alternative male mo
7 MC1R nucleotide diversity, pi, was much higher (10.1 x 1
8 MC1R overexpression, treatment with the MC1R ligand, or
9 MC1R palmitoylation, primarily mediated by the protein-a
10 MC1R SNP R163Q was also significantly (P<0.001) associat
11 MC1R variants may influence orofacial pain perception an
12 MC1R was positively associated with BRAF V600E cases but
13 MC1R's associations with BRAF V600E cases limited to ind
14 MC1R, number of moles, skin reaction to first summer sun
15 MC1R- and VLA-4-targeting peptides and peptide-conjugate
16 MC1R-cAMP signaling promotes PKA-mediated phosphorylatio
17 ic loci: IRF4 (rs12203592, P=1.8 x 10(-27)), MC1R (compound heterozygosity score, P=2.3 x 10(-24)), a
18 mes 15q13.1 (HERC2/OCA2 region) and 16q24.3 (MC1R) regions that reached genome-wide significance with
19 y targeted expression of ZDHHC13 in C57BL/6J-MC1R(RHC) mice and subsequently inhibit melanomagenesis.
20 curve (AUC) for a model by Han et al. with 7 MC1R variants was 0.72 (95% confidence interval (CI): 0.
22 ude OCA2-HERC2 (combined P = 3.80 x 10(-8)), MC1R (P = 1.82 x 10(-13)), a region near TYR (P = 1.57 x
23 d in 94% of uveal melanoma metastases, and a MC1R-specific ligand (MC1RL) with high affinity and sele
25 sferase ZDHHC13, is essential for activating MC1R signalling, which triggers increased pigmentation,
27 exhibited excellent MC4R selectivity against MC1R whereas those with an amino acid had moderate MC4R/
28 ating cAMP signaling either by the agonistic MC1R ligand melanocyte stimulating hormone (MSH) or by p
29 less MC1R model containing Mc1r(-/-) albino, MC1R(+)Mc1r(-/-) albino, Mc1r(-/-) pigmented, and MC1R(+
31 a-melanocyte stimulating hormone (alphaMSH), MC1R function can be antagonized by a secreted factor, a
33 ecific interaction between MC1R antigens and MC1R-Abs when the target melanoma cells are present in t
36 n, inferring a steroidogenic-independent and MC1R-dispensable anti-proteinuric effect of melanocortin
37 stics (freckles, nevi, phenotypic index) and MC1R status with incident amelanotic melanomas were eval
38 r probe for small-animal PET of melanoma and MC1R expression in melanoma xenografted mouse models.
40 n to their functional relationship, OPN3 and MC1R colocalize at both the plasma membrane and in intra
42 ssociations between self-identified race and MC1R single-nucleotide polymorphisms (SNPs) with severit
49 with wild-type (WT), but not RHC-associated MC1R variants, which protects PTEN from WWP2-mediated de
54 sing due to the specific interaction between MC1R antigens and MC1R-Abs when the target melanoma cell
55 , fear of pain mediated the relation between MC1R variant status and dental fear (B = 1.60, 95% confi
58 sine monophosphate (cAMP) response evoked by MC1R via activation of the Galphai subunit of G proteins
61 and adolescents had higher odds of carrying MC1R r variants than did adult patients (OR 1.54, 95% CI
62 ans, the proportion of participants carrying MC1R variants imparting elevated skin cancer risk was co
63 s melanoma with an emphasis on CDKN2A, CDK4, MC1R, and MAPK pathway targets (e.g., RAS and BRAF), apo
65 VR susceptibility as a result of compromised MC1R function are unclear, but hypotheses include reduce
71 ese loci were replicated: 16q24 encompassing MC1R (combined P = 2.54 x 10(-27) for rs258322), 11q14-q
73 57BL/6J-Mc1r(e/e)J mice, in which endogenous MC1R is prematurely terminated, expressing Mc1r RHC vari
74 bearing uveal melanoma tumors or engineered MC1R-positive and -negative tumors were studied for biod
75 <15 min), renal and hepatobillary excretion, MC1R-specific tumor uptake, and minimal retention in oth
76 entally tested signal processing in the FGFR/MC1R/B-Raf/C-Raf/MAPK1,2 network in human melanoma cells
78 was tested in vitro for biostability and for MC1R-specific cytotoxicity in uveal melanoma cells, and
79 defensin 3 (HBD3) acted as an antagonist for MC1R, inhibiting the alpha-melanocortin (alpha-melanocyt
81 On the basis of our theoretical model for MC1R, using mutagenesis, we have examined 19 transmembra
86 The results highlight a central role for MC1R palmitoylation in pigmentation and protection again
89 anning, result in a shift in expression from MC1R in favour of chimeric MC1R-TUBB3 isoforms in cultur
91 strategy in mice to rescue loss-of-function MC1R in MC1R RHC variants for therapeutic benefit by act
92 The contribution of other loss-of-function MC1R variants (in particular rs1805005, rs2228479 and rs
95 Furthermore, in the absence of functional MC1R, fewer p53 clones were observed in pigmented than i
97 onstructed from four pre-selected functional MC1R SNPs (p = 2.69 x 10(-12)), which was replicated in
98 d gene expression of IL-7, IL-7R, IFN-gamma, MC1R, NF-kappaB, phosphorylated NF-kappaB (p-NF-kappaB),
99 Consistent with this hypothesis, the gene MC1R exhibits reduced diversity in African populations f
101 ariants in the melanocortin 1 receptor gene (MC1R) might increase the risk of childhood and adolescen
107 how MC1R photoprotects, an in vivo hairless MC1R model containing Mc1r(-/-) albino, MC1R(+)Mc1r(-/-)
108 uptake in the B16F10 murine model, with high MC1R expression, but much lower uptake in the A375M huma
111 r (FGFR) and melanocyte stimulating hormone (MC1R) receptors stimulates B-Raf and C-Raf isoforms that
117 gnalling protein, blocks activation of human MC1R, its action is unlike that on the mouse receptor in
119 y in mice to rescue loss-of-function MC1R in MC1R RHC variants for therapeutic benefit by activating
122 ed podocytopathy was completely preserved in MC1R-null mice, marked by reduced albuminuria and dimini
123 Brief treatment with alpha-MSH resulted in MC1R desensitization, whereas continuous treatment up to
124 in IRF4 (Phet = 3.94 x 10(-4)), rs1805007 in MC1R (Phet = 7.71 x 10(-3)), and two SNPs in DEF8 (rs426
126 we investigated whether genetic variants in MC1R modulate the risk of PD by sequencing the entire ge
129 nset BCC risk prediction model incorporating MC1R and indoor tanning extends the work of other skin c
130 ibitor ML349 treatment efficiently increases MC1R signaling and represses UVB-induced melanomagenesis
131 llow pheomelanin pigment, whereas increasing MC1R activity stimulates the production of black/brown e
132 protein-acyl transferase, whether increasing MC1R palmitoylation represents a viable therapeutic targ
133 irm that ASIP diminishes agonist-independent MC1R basal signaling whereas HBD3 is a neutral MC1R anta
135 We conclude that genetic variations in IRF4, MC1R, RALY/ASIP, and BNC2 contribute to the acquired amo
137 ism promoting trafficking of MC4R and likely MC1R away from the lysosome toward the cell surface.
138 Along with two known pigmentation loci, MC1R and OCA2, the IRF4 rs12203592 T allele was associat
146 ling pathway interacts with the p53-POMC/MSH-MC1R signaling pathway, and both are crucial in melanoge
149 1R basal signaling whereas HBD3 is a neutral MC1R antagonist that blocks activation by melanocortins.
150 yellow (e/e) mouse, bearing a nonfunctional MC1R, thereby incrementing our knowledge on this topic.
152 coefficient 1.32; 95% CI: 0.23-2.40) but not MC1R SNP genotype was associated with increased itch sco
153 s study identifies and characterizes a novel MC1R isoform (MC1R350) generated by alternative splicing
159 mber of red hair/low pigmentation alleles of MC1R; we found that together these MC1R alleles explaine
160 he sensor performance, such as the amount of MC1R-Abs loaded, incubation time with the target melanom
167 ther phenotypic characteristics, carriage of MC1R variants, and history of amelanotic melanoma are as
168 ompared with wild-type carriers, carriers of MC1R variants were at higher melanoma risk after statist
171 ts into the pleiotropic molecular effects of MC1R signaling that may function during development and
173 he biological consequences of the failure of MC1R variants to suppress PI3K/AKT signaling are highly
177 contact with the first extracellular loop of MC1R through a series of key hydrophobic interactions.
182 in a large study comparing the prevalence of MC1R variants in child or adolescent patients with melan
183 addition to the MC1R genotype, regulation of MC1R expression and activity is expected to affect human
184 teristics may not modify the relationship of MC1R variants and melanoma risk, and suggest that associ
186 ally derived characterization of the role of MC1R variants in red hair colour and offer a powerful, e
188 facilitated by a distinguishing structure of MC1R, in which loss-of-function variants are never found
189 /F10 melanoma tumors with high expression of MC1Rs and Fox Chase Scid mice bearing human A375M melano
190 rt a model of strong selective constraint on MC1R in Northern Island Melanesia This absence of strong
191 typed for single-nucleotide polymorphisms on MC1R and completed self-report measures of fear of pain
194 were 2387 patients with data for phenotypes, MC1R genotype, and primary melanomas scored for histopat
195 agouti signaling protein, the physiological MC1R antagonist, and were absent in melanocytes expressi
199 iant and one r variant (defined as any non-R MC1R variant; OR, 1.6; 95% CI, 1.3-2.2) and among those
203 oding region of the melanocortin-1 receptor (MC1R) gene is associated with constitutive pigmentation
204 hat variants of the melanocortin 1 receptor (MC1R) gene may predict greater levels of dental fear.
206 show that the human melanocortin 1 receptor (MC1R) gene, a critical component of the facultative skin
207 1 that includes the Melanocortin-1 receptor (MC1R) gene, which regulates colour polymorphisms in nume
212 enetic variation in melanocortin-1 receptor (MC1R) is a known contributor to disease-free red hair in
214 Variation at the melanocortin 1 receptor (MC1R) is very common in most non-African world populatio
215 tion alleles of the melanocortin 1 receptor (MC1R) lead to red hair, freckling, and sun sensitivity.
216 S) are unknown, and melanocortin 1 receptor (MC1R) loss-of-function leads to fibrogenesis in experime
218 design of specific melanocortin-1 receptor (MC1R) targeted imaging probes, we report on the effect o
220 nformation based on melanocortin-1 receptor (MC1R) variants could inform prevention and screening rec
222 ndividuals carrying melanocortin-1 receptor (MC1R) variants, especially those associated with red hai
225 Loss-of-function in melanocortin 1 receptor (MC1R), a GS protein-coupled receptor that regulates sign
228 is regulated by the melanocortin 1 receptor (MC1R), is an effective protection against melanoma.
229 lls expressing melanocortin type-1 receptor (MC1R), that the nature of targeting ligands, i.e., wheth
230 tor, but not to the melanocortin 1 receptor (MC1R), whereas ASIP binds with high affinity to all thre
231 ific ligand for the melanocortin 1 receptor (MC1R), which has been evaluated as a cell-surface marker
235 ne, melanocyte stimulating hormone receptor (MC1R), is strongly associated with distinct differences
236 MSH) receptor (melanocortin type 1 receptor [MC1R]) is overexpressed in most murine and human melanom
238 fects on the melanocortin 1 and 4 receptors (MC1R and MC4R) in the skin and the brain, respectively,
241 in Hispanics and that carriage of high risk MC1R alleles occurs even among Hispanics with stronger A
244 that these Gd-Tx micelles are able to target MC1R-expressing xenograft tumors in vitro and in vivo mo
245 times more selective over this receptor than MC1R or MC5R, respectively, and had no detectable bindin
249 is study aimed to replicate the finding that MC1R variant status predicts dental fear and to determin
252 viduals with darker phenotypes indicate that MC1R genotypes specifically provide information about BR
255 ependent Caucasian populations, we show that MC1R variants are strongly associated with BRAF mutation
256 of young patients with melanoma showed that MC1R r variants were more prevalent in childhood and ado
258 tion and demonstrate for the first time that MC1R isoform-specific expression is closely related to s
271 ns unclear whether pigmentary effects of the MC1R can account for all of the increase in cancer risk.
272 ined in Melanesians the coding region of the MC1R gene was sequenced in 188 individuals from Northern
276 of mouse transgenics to demonstrate that the MC1R signaling pathway influences cancer risk via mechan
278 ategies in ruffs and other species, thus the MC1R gene is a strong candidate to play a role in altern
281 MC1R overexpression, treatment with the MC1R ligand, or treatment with small-molecule activators
282 lleles of MC1R; we found that together these MC1R alleles explained 4.1% of variance in skin pattern
284 has shown high in vitro binding affinity to MC1R and excellent in vivo melanoma-targeting profiles w
285 dividuals with red hair and fair skin due to MC1R gene variants are at higher risk of cutaneous neopl
286 We validate the importance of ZDHHC13 to MC1R signaling in vivo by targeted expression of ZDHHC13
287 that trout MRAP interacts with the two trout MC1R variants and MC2R, but failed to detect regulation
289 senescence; in the presence of BRAF(V600E), MC1R deficiency-induced elevated PI3K/AKT signaling driv
291 non-pigmentary effects in vivo and that when MC1R function is compromised the melanin type in skin is
292 alized upon ligand-receptor binding, whereas MC1R antagonist-conjugated HAuNS remain attached on the
293 nvironment, and Melanoma (GEM) study whether MC1R and phenotypes were associated with melanoma BRAF/N
295 0.66, 0.78), while that by Smith et al. with MC1R and indoor tanning had an AUC of 0.69 (95% CI: 0.63
296 btype, the risk for melanoma associated with MC1R is due to an increase in risk of developing melanom
297 hood and adolescent melanoma associated with MC1R variants by multivariable logistic regression.
298 ospheres (HAuNS, diameter=40 nm) coated with MC1R agonist are internalized upon ligand-receptor bindi