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1 composite modified fluorine doped tin oxide (FTO).
2 1L1, TERT, 19p13.1, 20q11, MDM4, 2p24.1, and FTO).
3  by fat mass and obesity-associated protein (FTO).
4  known: ABH1 to ABH8 and the obesity-related FTO.
5 1 diabetes loci and FCRL3, GAD2, TCF7L2, and FTO.
6 either CRISPR/Cas9 or shRNA targeted against Fto.
7 levels in/near LEP, SLC32A1, GCKR, CCNL1 and FTO.
8   In fasted rats, myocardial uptake of (18)F-FTO (0.70 +/- 0.30% dose kg [body mass]/g [tissue mass])
9 ents were significantly associated with BMI (FTO: 0.43 [95% confidence interval, 0.32-0.54] kg/m(2) p
10 activator (TANK) (2p24.2), and rs10163409 in FTO (16q12.2) were among the top associations (P < 10(-5
11 yers coated Au, 2D material (black-P) coated FTO, (3-aminophenyl) triethoxysilane modified TiO2, were
12 adipocyte proliferation, and is increased in FTO-4 MEFs and reduced in FTO-KO MEFs.
13 predicted from these findings, fat pads from FTO-4 mice fed a high-fat diet show more numerous adipoc
14 asts (MEFs) derived from FTO overexpression (FTO-4) mice exhibit increased potential for adipogenic d
15                     Overall, carriers of the FTO A allele had an increased risk of CHD (odds ratio, 1
16 its fat mass and obesity-associated protein (FTO) activity, thereby increasing global N(6)-methyladen
17 HE, LRRC14, FUK, NPRL3, EVL, SLCO3A1, PSMA4, FTO, ADCK5, PP1R16A and TEP1.
18  study, we demonstrate that gene variants of FTO affect dopamine (D2)-dependent midbrain brain respon
19         Here we demonstrate that variants of FTO affect dopamine-dependent midbrain brain responses a
20 in the fat mass and obesity-associated gene (FTO) affect adiposity in an age-dependent fashion in chi
21                   Our data indicate that the FTO allele associated with obesity represses mitochondri
22 risk allele rs8050136 in the first intron of FTO alters a regulatory element recognized by the transc
23                    The recent discovery that FTO, an obesity risk gene, encodes an m(6)A demethylase
24 animal PET studies were performed with (18)F-FTO and (18)F-FTP in rats.
25 tion of two additional AlkB family proteins, FTO and ALKBH5, showed that they possess demethylase act
26        This is the first study investigating FTO and BMI within the context of MDD, and the results i
27 her regions (CDKN2A-CDKN2B (CAD) and CDKAL1, FTO and HHEX (T2D)), the 95% sets were small, thereby ex
28 blood clearance and avid extraction of (18)F-FTO and of (18)F-FTP into the heart and liver.
29 target of obesity-associated variants within FTO and represents a novel determinant of body mass and
30 , thereby leading to decreased expression of FTO and retinitis pigmentosa GTPase regulator-interactin
31 sis for this association, we discovered that FTO and RPGRIP1L (a ciliary gene located in close proxim
32 influence on adiposity via remote effects on Fto and Rpgrip1l expression.
33 P110, leading to the following: 1) decreased FTO and RPGRIP1L mRNA levels; 2) reduced LEPR traffickin
34 sk (A) allele shows reduced affinity for the FTO and RPGRIP1L transcriptional activator P110, leading
35 tin signaling that is, in part, regulated by FTO and RPGRIP1L.
36  lower DeltaWC and DeltaWCBMI, regardless of FTO and TCF7L2 risk alleles.
37                   In vivo, the expression of Fto and the m(6)A methyltransferase, Mettl3 correlated w
38                       In Stage 1, two known (FTO and TMEM18) and six novel (PEX2, MTFR2, SSFA2, IARS2
39 atio, 1.15 (1.04-1.26) per kg/m(2), P=0.005 (FTO) and 1.11 (1.05-1.17) per kg/m(2), P<0.001 (BMI gene
40 , CDK10, MYH7B, SLC45A2, MTAP, ATM, CLPTM1L, FTO, and CASP8) that have previously been published with
41 , -6), Fts, Ftm, and Fto, of which only Ftm, Fto, and Fts are expressed in primordial germ cells of t
42 CY5, JAZF1, CDKN2A/B, TCF7L2, KCNQ1, MTNR1B, FTO, and HNF1B) were nominally associated with PCa (P <
43 TTL3 and METTL14 and demethylases ALKBH5 and FTO, and knockdown of methyltransferases increases, whil
44 the SEC16B/RASAL, TMEM18, MSRA, SOX6, MTCH2, FTO, and MC4R genes.
45 (SEC16B, TMEM18, ETV5, GNPDA2, TFAP2B, BDNF, FTO, and MC4R) were found to be associated with BMI in A
46                In vivo manipulation of CUX1, Fto, and/or Rpgrip1l expression in mice affected adiposi
47  we demonstrate that the splicing effects of FTO are dependent on the catalytic activity in vivo and
48 besity-associated noncoding sequences within FTO are functionally connected, at megabase distances, w
49 etardation, and mice globally overexpressing FTO are obese.
50 in the fat mass and obesity-associated gene (FTO) are associated with human obesity and obesity-prone
51 oximity to the transcriptional start site of FTO) are regulated by isoforms P200 and P110 of the tran
52                            Given the role of FTO as a demethylase of N6-methyladenosine (m6A), we wen
53 de analysis of RNA demethylation and uncover FTO as a potent regulator of nuclear mRNA processing eve
54                             The discovery of FTO as the first m6A mRNA demethylase established the co
55  is suggested for developing next-generation FTO as well as other TCO films with better than ever con
56  increases transcriptional activity from the FTO as well as RPGRIP1L minimal promoters.
57                            Here we show that FTO, as an m(6)A demethylase, plays a critical oncogenic
58 s of this study indicate that the effects of FTO-associated SNPs on energy homeostasis are due in par
59 lored whether physical activity modifies the FTO association with coronary heart disease (CHD).
60                                 We show that FTO binds preferentially to pre-mRNAs in intronic region
61 ine mammalian AlkB homologs exist (ALKBH1-8, FTO), but only a subset functions as DNA/RNA repair enzy
62 he Fluorine doped tin oxide glass electrode (FTO) by drop-casting method for better immobilization of
63 eptin were inversely linked to the number of FTO C risk alleles (P = 0.001; relative serum leptin dif
64  positive relationship between the number of FTO C risk alleles and plasma ghrelin levels was found (
65 g glucose levels may amplify obesity-risk in FTO carriers and lead to an exaggerated weight gain over
66 l role in the design of active and selective FTO catalysts.
67  locus, fat mass obesity-associated protein (FTO), cohorts with Illumina MetaboChip genotype data (n
68               Thus, our results suggest that FTO could modulate obesity by regulating the activity of
69                                 We find that FTO deficiency could reduce the proliferation and neuron
70                    Our results indicate that Fto deficiency increases the expression of genes related
71 ovel finding of increased Irx3 expression in Fto-deficient mice after high-fat feeding indicating a c
72                                Wild type and Fto-deficient mice were exposed to standard or high-fat
73 interaction is functional; overexpression of FTO delays the dephosphorylation of cAMP response elemen
74                                              FTO demethylates N6-methyladenosine, a potential regulat
75                                              FTO did not modify observed associations.
76 nd offer insight into potential link between FTO, dietary protein intake and adiposity.
77 in the fat mass and obesity-associated gene (FTO) drive the development of obesity in humans are poor
78 gether, these results show the importance of FTO during memory formation and, furthermore, implicate
79 activity has been suggested to attenuate the FTO effect on obesity, but it is unknown whether this is
80      Vitamin D status significantly modified FTO effects (P for interaction = 0.02).
81             The ssDNA-nanocomposite modified FTO electrode exhibited optimum current within 5s, at pH
82   By fabricating Fe2O3NPs/rGO/PEDOT modified FTO electrode for determining ACh level in serum samples
83 surface of ZnO/Pt-Pd nanocomposites modified FTO electrode.
84 ene pyrrole onto a fluorine-doped tin oxide (FTO) electrode allowed the targeted orientation of the f
85 xidation occurs at fluoride-doped tin oxide (FTO) electrodes that have been surface-modified by addit
86                                              FTO enhances leukemic oncogene-mediated cell transformat
87 aste responsiveness, risk allele carriers of FTO exhibit dose-dependent increments in both impulsivit
88 subsequent studies in mice demonstrated that FTO expression levels influence body mass and compositio
89  between the obesity-associated variants and FTO expression or function has been made.
90                  SNPs in the first intron of FTO (fat mass and obesity associated) are strongly assoc
91 ociation between the rs993609 variant of the FTO (fat mass and obesity associated) gene and body mass
92                             Variation in the FTO (fat mass and obesity associated) gene has been show
93 ethyltransferase-like 3) and the demethylase FTO (fat mass and obesity-associated protein).
94 e of the best characterized RNA demethylase, FTO (fat mass and obesity-associated) in memory.
95  study, we prepare fluorine doped tin oxide (FTO) films by chemical vapor deposition with inclusions
96  in/near HSD17B11, VCAN, ADAMTSL3, IRS1, and FTO for total lean body mass and for three single-nucleo
97 d transcripts by limiting the m(6)A 'eraser' FTO from demethylation.
98 ration on other regions which highlights the FTO, GCKR and ABO regions.
99 commonly carried obesity-risk variant in the FTO gene (rs1421085 single-nucleotide polymorphism) infl
100 ction and obesity have focused mostly on the FTO gene and physical activity, whereas little attention
101                       Common variants in the FTO gene are associated with adiposity in children and y
102 ers (AA/AT) and nonrisk carriers (TT) of the FTO gene for analyses.
103          We analysed 88 polymorphisms in the FTO gene in a clinically ascertained sample of 2442 MDD
104                                          The FTO gene is one of the most consistently replicated loci
105                            Evidence that the FTO gene may influence weight partly through its effects
106 that obesity-related risk allele carriers of FTO gene show dose-dependent increments in body mass ind
107                                              FTO gene variants have been associated with obesity phen
108 tion between several SNPs in intron 8 of the FTO gene, including rs16953002, which replicated using 1
109 e to genome-wide significance was within the FTO gene, which is involved in regulation of bodyweight-
110 isk carriers than in nonrisk carriers of the FTO gene.
111 ions in the fat mass and obesity-associated (FTO) gene are associated with obesity.
112 ions in the fat mass and obesity-associated (FTO) gene are linked to obesity.
113 isms in the fat mass and obesity-associated (FTO) gene have been associated with obesity in humans.
114 tron of the fat mass and obesity-associated (FTO) gene have the largest effect.
115 fect of the fat mass and obesity-associated (FTO) gene on adiposity is well established, there is a l
116         The fat mass and obesity-associated (FTO) gene plays a pivotal role in regulating body weight
117 isms in the fat mass and obesity-associated (FTO) gene represent common alleles that are strongly ass
118 609 in the fat mass- and obesity-associated (FTO) gene was recently shown to affect appetite, and the
119                                              FTO genetic variation was evaluated by genotyping 262 ta
120   Two genetic instruments for BMI were used: FTO genotype (rs1558902) and a BMI gene score comprising
121 T genotype and high activity, the effects of FTO genotype and physical activity on CHD risk were appr
122          We examined the interaction between FTO genotype and protein intake on the long-term changes
123 d adiposity measures were found, none of the FTO genotype by PA interaction assessments revealed nomi
124               Protein intakes did not modify FTO genotype effects on other appetite measures.
125 l-weight AA and TT humans, we found that the FTO genotype modulates the neural responses to food imag
126 y that used fat mass and obesity-associated (FTO) genotype as an IV to estimate the effect of obesity
127 at the fat mass and obesity-associated gene (FTO) genotype may interact with dietary intakes in relat
128 ormation on fat-mass and obesity-associated (FTO) genotype risk had a greater effect on a reduction o
129  of BMI and fat mass and obesity-associated (FTO) genotype with asthma explained the different direct
130 h significant associations between the three FTO genotypes and adiposity measures were found, none of
131 oparticles (AuNPs)/fluorine doped tin oxide (FTO) glass electrode.
132 nO/Pt-Pd) modified fluorine doped tin oxide (FTO) glass plate was fabricated for detection of consens
133 five established obesity risk variants (near FTO, GNPDA2, MTCH2, TMEM18, and NEGR1) with BMI across f
134                          Here we report that FTO has a role in white adipose tissue which modifies it
135  human fat mass- and obesity-associated gene Fto have been linked with higher body mass index, but th
136  per 1-U increase, P<0.001) and incident AF (FTO, hazard ratio, 1.07 [1.02-1.11] per A-allele, P=0.00
137  2HG in inhibiting proliferation/survival of FTO-high cancer cells via targeting FTO/m(6)A/MYC/CEBPA
138 ing glucose or triglycerides can amplify the FTO impact on BMI.
139                                  The role of FTO in neurodevelopment and neurogenesis, however, remai
140 es in animals suggest the potential roles of FTO in regulating food intake.
141 te the genetic influence of polymorphisms in FTO in relation to body mass index (BMI) in two independ
142                       We describe a role for FTO in the coupling of amino acid levels to mammalian ta
143 eracts with the promoters of IRX3 as well as FTO in the human, mouse and zebrafish genomes.
144           Furthermore, targeted knockdown of FTO in the mPFC led to enhanced consolidation of cued fe
145          Knocking down the m(6)A demethylase FTO in the mPFC, which increases total m(6)A level, resu
146  associated with expression of IRX3, but not FTO, in human brains.
147 , modulation of m(6)A by the RNA demethylase FTO influenced the degradation profiles of a subset of t
148                                              FTO influences adipogenesis by regulating events early i
149                 The mechanisms through which FTO influences growth and body composition are unknown.
150               However, it is unclear whether FTO influences longitudinal trajectories of adiposity an
151                                  To identify FTO inhibitors, we screened a set of 2OG analogues and r
152 the development of more potent and selective FTO inhibitors.
153 th cyclic and acyclic 2OG analogues that are FTO inhibitors.
154   Using multiple assays, we demonstrate that FTO interacts with three isoforms of calcium/calmodulin-
155 , alpha-ketoglutarate dependent dioxygenase (FTO), interleukin 6 (IL6), insulin receptor (INSR), neur
156 for GCKR, and for variants in four T2D loci (FTO, IRS1, KLF14 and PPARG) which exert their action via
157 at feeding indicating a complex link between FTO, IRX3 and fat metabolism.
158                                              FTO is a 2-oxoglutarate (2OG)-dependent N-methyl nucleic
159                                              FTO is a nuclear protein and its physiological function
160                            Here we show that FTO is expressed in adult neural stem cells and neurons
161                             We observed that FTO is expressed in the nuclei, dendrites and near dendr
162 FTO/sTiO2/mpTiO2/MAPI/Spiro-OMeTAD/Au, where FTO is fluorine-doped tin oxide, sTiO2 indicates solid-T
163                                              FTO is highly expressed in AMLs with t(11q23)/MLL rearra
164                   This finding suggests that FTO is involved in the mechanism underlying the associat
165                                 Variation in FTO is the most important common genetic determinant of
166                                              FTO is the strongest known genetic susceptibility locus
167        Fat mass and obesity-associated gene (FTO) is a member of the Fe (II)- and oxoglutarate-depend
168 The fat mass and obesity associated protein (FTO) is a potential target for anti-obesity medicines.
169  Fischer-Tropsch synthesis of lower olefins (FTO) is an alternative process for the production of key
170 the fat mass and obesity-associated protein (FTO) is an m(6)A demethylase indicates that this modific
171 nic differentiation, while MEFs derived from FTO knockout (FTO-KO) mice show reduced adipogenesis.
172                                              FTO knockout (KO) results in substantial changes in pre-
173          The alternative splicing effects of FTO KO anti-correlate with METTL3 knockdown suggesting t
174 6A-linked DRACH motifs partially rescues the FTO KO phenotype in a reporter system.
175 nd is increased in FTO-4 MEFs and reduced in FTO-KO MEFs.
176 ation, while MEFs derived from FTO knockout (FTO-KO) mice show reduced adipogenesis.
177                                  The loss of FTO leads to decreased brain size and body weight.
178 mechanistic insight into how upregulation of FTO leads to obesity.
179                                  The loss of FTO led to the altered expression of several key compone
180 e polymorphisms among 9 genes (ADRB3, ENPP1, FTO, LEP, PPARG, PPARGC1A, SLC2A2, TCF7L2, and UCP2) ass
181 irectly test this, we artificially decreased FTO levels in dorsal hippocampus of otherwise normal (wi
182 r conditioning transiently (0.5 h) decreased Fto levels in these neurons, with the largest decrease i
183                           Association of the FTO locus with adiposity in humans may reflect functiona
184 vival of FTO-high cancer cells via targeting FTO/m(6)A/MYC/CEBPA signaling.
185            The present findings suggest that FTO may facilitate weight gain in humans by shifting the
186                  These findings suggest that FTO may influence body composition through playing a rol
187 riants in (or near) the NEGR1, TMEM18, BDNF, FTO, MC4R, and KCTD15 genes and macronutrient intake (ca
188       Maternal risk allele score and SNPs in FTO, MC4R, and TMEM18 were positively associated with pr
189  robustly associated with adult BMI (in/near FTO, MC4R, TMEM18, GNPDA2, KCTD15, NEGR1, BDNF, ETV5, SE
190 tworks for 4 known m6A (de)methylases, i.e., FTO, METTL3, METTL14 and WTAP.
191 s from AA human subjects exhibited increased FTO mRNA, reduced ghrelin mRNA N6-methyladenosine methyl
192 r contextual fear conditioning suggests that FTO normally constrains memory formation.
193 fy and replicate an association with SNPs in FTO not related to body mass index (BMI).
194              Although the association of the FTO obesity locus with leptin levels is abolished by adj
195 gestive behavior, and offer insight into how FTO obesity-risk alleles predispose to increased energy
196 , we showed that subjects homozygous for the FTO "obesity-risk" rs9939609 A allele have dysregulated
197  these neurons, with the largest decrease in FTO observed near synapses.
198                              The decrease in FTO observed shortly after contextual fear conditioning
199                              O2 reduction at FTO occurs at -0.33 V vs NHE, allowing for in situ detec
200 e IrxB cluster (Irx3, -5, -6), Fts, Ftm, and Fto, of which only Ftm, Fto, and Fts are expressed in pr
201                                The effect of FTO on adipogenesis appears to be mediated via enhanced
202 se and triglyceride levels with rs9939609 in FTO on BMI.
203 istory of depression moderates the effect of FTO on BMI.
204 rotein itself, loss of function mutations in FTO or its murine homologue Fto result in severe growth
205                        Reduced expression of Fto or Rpgrip1l affects leptin receptor isoform b traffi
206 se embryonic fibroblasts (MEFs) derived from FTO overexpression (FTO-4) mice exhibit increased potent
207                              In cell models, FTO overexpression reduced ghrelin mRNA N6-methyladenosi
208  a previously established adiposity locus in FTO (P = 3 x 10(-26)) and identified two new loci associ
209 n independent loci (P < 5.0 x 10(-)(8)) near FTO (P = 3.72 x 10(-)(2)(3)), TMEM18 (P = 3.24 x 10(-)(1
210 -8)), 2p24.1 (P = 4.6 x 10(-8)) and 16q12.2 (FTO, P = 4.0 x 10(-8)), were associated with ER-negative
211               These results together suggest FTO plays important roles in neurogenesis, as well as in
212 NA modification, but the mechanisms by which FTO predisposes humans to obesity remain unclear.
213 n the fat mass- and obesity-associated gene (FTO) predisposing to obesity and diabetes mellitus have
214                                              FTO preferentially demethylates m(6)Am rather than N(6)-
215 dration of ethanol and by CO2 conversion via FTO process, (ii) the catalytic synthesis of butadiene f
216 ffect is mediated through the actions of the FTO protein itself, loss of function mutations in FTO or
217 n(s) that could directly interact with human FTO protein.
218 e-dependent fat mass and obesity-associated (FTO) protein oxidize N(6)-methyladenosine to generate N(
219 anistic basis of the association between the FTO region and obesity.
220                       The obesity-associated FTO region directly interacts with the promoters of IRX3
221                                          The FTO region harbors the strongest genetic association wit
222                                   Given that Fto regulates D2/3R signaling in mice, we tested in huma
223                       Our findings show that FTO regulates ghrelin, a key mediator of ingestive behav
224 ion mutations in FTO or its murine homologue Fto result in severe growth retardation, and mice global
225 ants who were informed that they carried the FTO risk allele (level 3 AT/AA carriers) than in the non
226 e genotype-phenotype correlation between the FTO risk allele and BMI, with an observed inflection poi
227 in weight and WC at month 6 were greater for FTO risk carriers than for noncarriers in the level 3 gr
228 he first time the dynamic connection between FTO RNA binding and demethylation activity that influenc
229          There were allele-dosage effects on FTO, RPGRIP1L, and AKT-interacting protein (AKTIP) expre
230  of these genetic variations on hypothalamic FTO, RPGRIP1L, and possibly other genes.
231                                    Decreased Fto/Rpgrip1l expression in the arcuate hypothalamus coin
232 een rs1432679 (EBF1), rs17817449 (MIR1972-2: FTO), rs12710696 (2p24.1), and rs3757318 (ESR1) and adju
233                      Obesity risk alleles at FTO rs1421085 significantly predicted more eating episod
234 xamine the evidence for interactions between FTO (rs1421085) and various lifestyle and environmental
235                                              FTO rs1558902 was genotyped in 742 obese adults who were
236     In addition, subjects were genotyped for FTO rs17817449 (AA, n = 345 [35%]; AC/CA, n = 481 [48.8%
237 -effects meta-analysis model showed that the FTO rs8050136 A allele (n = 36,973) was positively assoc
238  ADAMT59 rs4607103, CDKN2A/2B rs1801282, and FTO rs8050136), two in non-Hispanic blacks (with ADAMT59
239 on-Hispanic whites (with CDKAL1 rs471253 and FTO rs8050136), two in non-Hispanic blacks (with IGFBP2
240 ound heterogeneity in the association of the FTO (rs8050136) variant with BMI across the four adultho
241 4), p=0.05]; [CAPN10 (rs2975760), p=0.031]; [FTO (rs8050136), p=0.023]; [FTO (rs9939609), p=0.018] an
242                                              FTO rs9939609 (T>A) polymorphism was genotyped in 2 Swed
243   Our data suggest that individuals with the FTO rs9939609 A allele might obtain more benefits in a r
244                                              FTO rs9939609 A-allele carriers have an increased CHD ri
245                        Our data suggest that FTO rs9939609 affects child weight gain, and genotype ef
246                      We investigated whether FTO rs9939609 and TCF7L2 rs7903146 modified the associat
247                    We assessed the effect of FTO rs9939609 on BMI and BMI-for-age Z score changes dur
248                                          The FTO rs9939609 SNP showed nominal evidence for associatio
249 tes, DNA was collected and genotyped for the FTO rs9939609 variant using real-time PCR.
250 sing a well-known obesity risk polymorphism (FTO rs9939609) in a sample of 78 children (ages 9-12 y),
251 760), p=0.031]; [FTO (rs8050136), p=0.023]; [FTO (rs9939609), p=0.018] and [SLC30A8 (rs13266634), p=0
252 common variants known to associate with BMI: FTO(rs9939609); MC4R(rs17782313); and TMEM18(rs6548238).
253  to examine: (i) the association between the FTO-rs9939609 variant (or a proxy single-nucleotide poly
254           The minor allele (A-allele) of the FTO-rs9939609 variant was associated with higher BMI in
255                                This suggests FTO's function may be broader than the existing paradigm
256 he BAT2 and MC4R genes and 3 SNPs within the FTO, SEC16B, and SH2B1 genes were significantly associat
257  including seven previously identified loci (FTO, SEC16B, MC4R, GIPR-QPCTL, ADCY3-DNAJC27, BDNF and M
258                               High levels of FTO sensitize leukemic cells to R-2HG, whereas hyperacti
259 This PDNA modified electrode (PDNA/ZnO/Pt-Pd/FTO) served as a signal amplification platform for the d
260             The less common alleles at the 4 FTO single nucleotide polymorphisms showed a reduction o
261                                              FTO (single nucleotide polymorphism rs9939609) was genot
262 onvert light into electricity by fabricating FTO/SnO(2)/polyad electrodes.
263 n of the resulting fluorine-doped tin oxide (FTO)|SnO2/TiO2|-[Ru(a) (II)-Ru(b) (II)-OH2](4+)(Al2O3 or
264 onium lead iodide (MAPI) cells of the design FTO/sTiO2/mpTiO2/MAPI/Spiro-OMeTAD/Au, where FTO is fluo
265           The combination of gold NIs on the FTO substrate, causing NIs size and pattern irregularity
266 ensional arrays of these nanotubes formed on FTO substrates are applied as photoanode in a dye-sensit
267 t in young compared with older adulthood for FTO, suggesting changes by age, generation, or secular t
268     Its electron relays were directed to the FTO surface, thus promoting DET.
269 ose to ADCY3, GNPDA2, TMEM18, SEC16B, FAIM2, FTO, TFAP2B, TNNI3K, MC4R, GPR61, LMX1B and OLFM4 associ
270 L1, IGF2BP2, ARHGEF11, JAZF1, CDC123/CAMK1D, FTO, TSPAN8/LGR5, KCNQ1, THADA, ADAMTS9, NOTCH2, NXPH1,
271                                   Decreasing FTO using either method specifically enhanced contextual
272 dy mass index (BMI)-increasing allele of the FTO variant (rs1421085) was associated with higher prote
273 ot find significant interactions between the FTO variant and dietary intake of total energy, protein,
274  intake and (ii) the interaction between the FTO variant and dietary intake on BMI.
275           We report interactions between the FTO variant and each of: frequency of alcohol consumptio
276 ciation between the BMI-increasing allele of FTO variant and higher dietary protein intake and offer
277                      We tested the effect of FTO variant on weight loss in response to 2-year diet in
278 etely; however, additional IV analyses using FTO variant rs1558902 and the other BMI-related SNPs sep
279 n in individuals with the risk allele of the FTO variant rs1558902.
280             The BMI-increasing allele of the FTO variant showed a significant association with higher
281            Linear regression analyses of the FTO variants and BMI yielded 10 SNPs significantly assoc
282 A influences and interactive effects between FTO variants and PA on measures of adiposity in Latinos.
283  determine whether individuals with specific FTO variants exhibit differential responses to PA interv
284 diposity measures are associated with PA and FTO variants in Latinos, but the impact of their interac
285 y be broader than the existing paradigm that FTO variants influence multiple traits only through thei
286                                 Furthermore, FTO variants modulate the connectivity in a basic reward
287 more, dynamic causal modeling confirmed that FTO variants modulate the connectivity in a basic reward
288 hysical activity (PA) modifies the effect of FTO variants on obesity in Latino populations.
289               The interactive relation among FTO variants, dietary intake and body mass index (BMI) i
290               A practical synthesis of (18)F-FTO was developed, providing a radiotracer of high radio
291                                        (18)F-FTO was synthesized from a corresponding bromoester.
292 analog, 18-(18)F-fluoro-4-thia-oleate ((18)F-FTO), was evaluated in relationship to the previously de
293     To understand the molecular functions of FTO, we performed a yeast two-hybrid screen to identify
294  that binding of P200 to this site represses FTO, whereas binding of P110 increases transcriptional a
295 slide covered with fluorine-doped tin oxide (FTO), which acts as a biosensor.
296 ous thin film material, designated as CoPIZA/FTO, which is equipped with large cavities and access to
297 ucibly associated variants within introns of FTO with increased risk for obesity and type 2 diabetes
298  additional evidence that the association of FTO with obesity is partially mediated by dietary intake
299 ed polyoxotitanate nanocrystals deposited on FTO working electrodes.
300 ice, we tested in humans whether variants in FTO would interact with a variant in the ANKK1 gene, whi

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