ライフサイエンスコーパス: MAF

1 MAF amplification was assessed by fluorescence in-situ h

2 MAF is expressed in LECs but not in BECs.

3 MAF was also downregulated in human MPNST.

4 MAF, one of a family of large Maf bZIP transcription fac

5 MAF-box gene was overexpressed with controlled ventilati

6 MAF:MAFB regulated 393 genes altered in this setting.

7 MAFs ranged as high as 0.72, a level incompatible with p

8 roximately 0.97 to 5.37 km(3) (all +/-17%; 1 MAF approximately 1.233 km(3)), while total annual water

9 minor allele frequency (MAF)) and rare (<1% MAF) variants with large effect sizes may contribute to

10 io near DHX15 (rs7698250; P = 1.8 x 10(-10); MAF, 2.7%) and MGAT5B (rs7221059; P = 2.7 x 10(-8); MAF,

11 in European populations; however, allele 16 (MAF = 0.016 cases and 0.032 controls) was strongly assoc

12 jury molecule-1), rs7565788 (P=2.15x10(-16); MAF=0.22) in LRP2 (associated with trefoil factor 3 [TFF

13 11q13 (CCN D1), 3% 6p21 (CCN D3), 5% 16q23 (MAF), 2% 20q12 (MAFB), and 15% 4p16 (FGFR3 and MMSET).

14 the Latino sample (P=4.31 x 10(-6); OR=1.25; MAF=1.21%) and two genes harbouring functional variants

15 ele frequency (MAF) 0.11; blacks P = 10(-4), MAF 0.03] and gout (adjusted odds ratio 1.68 per risk al

16 gene, MAN1C1 (rs12130495; P = 9.9 x 10(-6); MAF, 13.3%) was associated with percent emphysema.

17 ication that includes eight groups: 11q; 6p; MAF; 4p; D1 (34%); D1+D2 (6%); D2 (17%); and none (2%).

18 an follow-up of 84.6 months (IQR 72.0-95.8), MAF status was not prognostic for invasive-disease-free

19 7%) and MGAT5B (rs7221059; P = 2.7 x 10(-8); MAF, 2.6%), which acts on alpha-linked mannose.

20 or 3 [TFF3]), and rs11048230 (P=4.77x10(-8); MAF=0.10) in an intergenic region near RASSF8 (associate

21 An HRP2 level of >0 U/mL had a MAF of 93% for cerebral malaria, with a MAF of 97% obser

22 ad a MAF of 93% for cerebral malaria, with a MAF of 97% observed for HRP2 levels of >/= 10 U/mL (the

23 ividuals, we reliably identified loci with a MAF of at least 12.5%.

24 We propose that paradoxically activated MAFs provide a "safe haven" for melanoma cells to tolera

25 s 45% of African Americans carry the allele (MAF 26%), which makes it a much more significant risk fa

26 14089985 is infrequent in African Americans (MAF = 3%), extremely rare in European Americans (MAF = 0

27 = 3%), extremely rare in European Americans (MAF = 0.03%), and monomorphic in Asian populations, sugg

28 two novel genes: HDGFL1 on chromosome 6 and MAF on chromosome 16.

29 n, c-Fos and c-Maf (also called JUN, FOS and MAF, respectively), were selective for their targets ove

30 AD001 blocked MAF-mediated tumor growth, and MAF regulated the mTOR pathway through DEPTOR.

31 ell help, including IL-21, CXCL13, ICOS, and MAF.

32 le proteins, myosin heavy chain isoform, and MAF-box mRNA were measured.

33 Both LD and MAF have a significant impact on the variable importance

34 storing genomic alignments, such as XMFA and MAF, are all indexed or ordered using a single reference

35 We also assessed interactions between MAF-positive status and menopausal status on efficacy of

36 e also found an inverse relationship between MAF and the proportion of nsSNPs predicted to be protein

37 RAD001 blocked MAF-mediated tumor growth, and MAF regulated the mTOR pa

38 the expression of muscle atrophy factor-box (MAF-box), the gene responsible for muscle atrophy, are u

39 nducing coordinate suppression of binding by MAF, lineage-determining transcription factors, and chro

40 ized, enriched for low-abundance proteins by MAF, digested endoproteolytically, randomized again, and

41 iated with sustained expression of GATA-3, c-MAF, and JunB in an IL-4-independent manner.

42 fluenced by known genetic lesions, such as c-MAF- and MAFB-, CCND1- and CCND3-, and MMSET-activating

43 abolished T-bet expression, and increased c-MAF and GATA-3 protein in vivo.

44 of distinct cell types in the gonad: MAFB, C-MAF, and VCAM1.

45 ultiple myelomas harboring cyclin D1/D3 or c-MAF/MAFB translocations.

46 ene signatures were observed in cases with c-MAF and MAFB activation and CCND1 and CCND3 activation,

47 is present in 88% of the 32 selected cases (MAF = 66%), so sequencing a subset of these cases can re

48 Paradoxically, chronic MAF overexpression enhanced MPNST cell tumor growth in v

49 ed and enzymatically converted to the cloned MAF, designated CdMAF.

50 diabetes in the general population (combined MAF 0.22%; OR 5.04; 95% CI 1.99-12.80; P = 0.0007).

51 c variance attributed to genome-wide common (MAF > 0.01) HapMap 3 SNPs (hg(2)) accounted for on avera

52 Based on sequence conservation, MAF, and location on a complete model of alphaIIbbeta3,

53 ative colitis patients and 295,446 controls, MAF=up to 0.78%) in RNF186, a single-exon ring finger E3

54 n at 10p13 with rs10904849 intronic to CUBN (MAF = 0.32, P = 7.01 x 10(-8); OR = 1.14).

55 tap water and concentrated with the new CUF-MAF concentration method by a volumetric factor of 10(4)

56 on the macrophage/osteoclast precursors, DBP-MAF, CSF-1, and the combination of these compounds were

57 MMSET knockdown decreased MAF transcription and cell viability.

58 ChIP-seq analysis demonstrated MAF:MAFB binding to known epidermal differentiation TF g

59 (e.g. different MSP thresholds for different MAFs).

60 se variant encoding p.Ala210Thr in HLA-DQA1 (MAF = 19.1%, rs9272785), associated with M. tuberculosis

61 Based on these data, we established MAF thresholds of 0.005 for autosomal-recessive variants

62 silencing the cellular transcription factor MAF (musculoaponeurotic fibrosarcoma oncogene homolog).

63 enriched for binding by transcription factor MAF.

64 um generated a macrophage-activating factor (MAF), whereas cultivation of lyso-Pc-treated B cells alo

65 e precursor of macrophage activating factor (MAF).

66 ation (NMF), maximum autocorrelation factor (MAF), and probabilistic latent semantic analysis (PLSA))

67 hod based on monolithic affinity filtration (MAF) for the concentration and purification of waterborn

68 n downregulation of other members of the FLC/MAF gene family, including the photoperiodic pathway reg

69 SZ (p = 0.021 for MAF < 0.5%, p = 0.003 for MAF < 0.1%).

70 ators, was associated with SZ (p = 0.021 for MAF < 0.5%, p = 0.003 for MAF < 0.1%).

71 e multisystem disorder, provide evidence for MAF governing a wider range of developmental programs th

72 s and eye defects as previously reported for MAF/Maf loss of function but includes sensorineural deaf

73 We identify a novel role for MAF as a transcriptional repressor, preventing expressio

74 ranscription factors are dimers of JUN, FOS, MAF and activating transcription factor (ATF) family pro

75 gulate the metabolically available fraction (MAF) of the total metal pool by increasing the net accum

76 s a process of multi-affinity fractionation (MAF) and quantitative label-free liquid chromatography t

77 to calculate malaria-attributable fractions (MAFs) and retinopathy-attributable fractions (RAFs).

78 P brain PET imaging: multiacquisition frame (MAF) and event-by-event (EBE).

79 dentified: 20 with minor allele frequencies (MAF) >0.05 and 12 with MAF >0.10.

80 ding variants with minor allele frequencies (MAF) >1% that were identified were presumed initially to

81 variants, 96% had minor allele frequencies (MAF) < 0.1%, indicating their rarity.

82 en those with high minor allele frequencies (MAF).

83 phisms (SNPs) with minor allele frequencies (MAFs) > 0.05 were found among the 512 tested accessions.

84 how that SNPs with minor allele frequencies (MAFs) of 0.1-1% explain a substantial fraction of prosta

85 ntrols, indicating a minor allele frequency (MAF) > 0.00006.

86 6.7 million common (minor allele frequency (MAF) > 0.05) and 2.7 million low-frequency (0.005 < MAF

87 orphisms (SNPs) with minor allele frequency (MAF) >0.01 using linear regression of VSS height score o

88 t the nine SNPs with minor allele frequency (MAF) >1% within ECRs.

89 were common, with a minor allele frequency (MAF) >5%, one had low frequency (MAF 1%-5%), and 11 were

90 s to capture common [minor allele frequency (MAF) >or= 5%] variation among Caucasians.

91 43571823-T947M) with minor allele frequency (MAF) < 1% and 1 common variant (rs2298813-A528T) with MA

92 s, including 6 rare (minor allele frequency (MAF) < 1%) or low-frequency (1% < MAF < 5%) variants wit

93 nsider variants with minor allele frequency (MAF) < 1%.

94 e and low-frequency (minor allele frequency (MAF) < 5%) coding variants associated with BMI.

95 3 rare variants with minor allele frequency (MAF) <0.5%.

96 whites: P = 10(-30), minor allele frequency (MAF) 0.11; blacks P = 10(-4), MAF 0.03] and gout (adjust

97 amine low-frequency (minor allele frequency (MAF) 0.5-5%) and rare (MAF < 0.5%) nonsynonymous variant

98 an uncommon variant [minor allele frequency (MAF) = 0.025] located ~800 kb from ADIPOQ that showed st

99 omosome 6 (rs314276, minor allele frequency (MAF) = 0.33, P = 1.5 x 10(-8)).

100 (HLAs): rs557011[T] (minor allele frequency (MAF) = 40.2%), associated with M. tuberculosis infection

101 mprinted KCNQ1 gene (minor allele frequency (MAF) = 7.7% in Sardinia versus <1% elsewhere) reduces he

102 atically affected by minor allele frequency (MAF) and linkage disequilibrium (LD).

103 ned here as having a minor allele frequency (MAF) between 0.5 and 5%] and rare (MAF below 0.5%) varia

104 which low-frequency (minor allele frequency (MAF) between 1-5%) and rare (MAF </= 1%) variants contri

105 orphisms (SNPs) with minor allele frequency (MAF) of >5% are preferentially used in case-control asso

106 one infant only with minor allele frequency (MAF) of 0.0023.

107 ion of variants to a minor allele frequency (MAF) of 0.1%.

108 causal variant has a minor allele frequency (MAF) of 1.3% in the general population and 8.2% in 329 c

109 tified using minimum minor allele frequency (MAF) of 5%.

110 Using a minor allele frequency (MAF) threshold of 2%, we identified 189 heteroplasmies i

111 tion of the observed minor allele frequency (MAF) to that predicted from the sequence data was 0.58.

112 The minor allele frequency (MAF) was greater for MUC5B rs35705950 in patients with c

113 by analyzing common [minor allele frequency (MAF)>0.05] variants in increasingly large sample sizes f

114 low frequency (1-5% minor allele frequency (MAF)) and rare (<1% MAF) variants with large effect size

115 tability varies with minor allele frequency (MAF), linkage disequilibrium (LD) and genotype certainty

116 to markers with low minor allele frequency (MAF).

117 ual common variants (minor allele frequency (MAF)0.05), aggregate low frequency variants (0.05>MAF0.0

118 e identified a rare (minor allele frequency (MAF)=1%) missense c.1114C>T mutation (rs115482041) in th

119 proportion (MSP) and minor allele frequency (MAF)] to remove SNPs with insufficient genotyping qualit

120 s ratio (OR) = 0.68, minor allele frequency (MAF)cases = 0.0059, MAFcontrols = 0.0093), a risk varian

121 Two intermediate frequency (MAF 0.01-0.05) nonsynonymous changes also showed no stat

122 when the causal variant is of low frequency (MAF < 0.01).

123 eotide polymorphisms are with low frequency (MAF < 5%) in Europeans.

124 frequency (MAF) >5%, one had low frequency (MAF 1%-5%), and 11 were rare (MAF <1%).

125 ntify low-frequency (minor allele frequency [MAF] >/=0.01 and <0.05) and rare (MAF <0.01) variants th

126 rare variants (e.g., minor allele frequency [MAF] <0.01) is the difficulty that automated clustering

127 requency of 82 rare (minor allele frequency [MAF] <0.01) nonsynonymous variants between type 2 diabet

128 betes risk (combined minor allele frequency [MAF] 0.22%; odds ratio [OR] 2.02; 95% CI 0.73-5.60; P =

129 European Americans (minor-allele frequency [MAF] 0.6%), whereas 45% of African Americans carry the a

130 arked by rs72647484 (minor allele frequency [MAF] = 0.09) near CDC42 and WNT4 (P = 1.21 x 10(-8), odd

131 n MAP1A (rs55707100, minor allele frequency [MAF] = 3.3%, p = 2 x 10(-10) for hemoglobin [HGB]) and H

132 y genetic variation (minor allele frequency [MAF]) approximately 0.1%-5% on MI/coronary artery diseas

133 9; P = 1.1 x 10(-9); minor allele frequency [MAF], 4.4%).

134 5820 (P=6.7x10(-49); minor allele frequency [MAF]=0.49) in HAVCR1 (associated with kidney injury mole

135 ommonly distributed (minor allele frequency, MAF > 5%) in Europeans, with comparable frequencies with

136 n height and common (minor allele frequency, MAF >/=5%) or infrequent (0.5% < MAF < 5%) variants acro

137 1.25, P = 5.8 x 10(-12)), and rs9271378[G] (MAF = 32.5%), associated with PTB (OR = 0.78, P = 2.5 x

138 -disease-free survival in the control group (MAF-positive vs MAF-negative: hazard ratio [HR] 0.92, 95

139 entinel variant and not in close LD (six had MAF <5%).

140 r database inspections revealed variants had MAF of </=1% in the general population.

141 % CI 0.56-0.98), but not in patients who had MAF-positive tumours.

142 Using 4 MM cell lines harboring MAF-, FGFR3/MMSET-, or CCND1-activating translocations,

143 is the major determinant of the heteroplasmy MAF in the offspring.

144 twin pairs, suggesting that the heteroplasmy MAF in the oocyte is the major determinant of the hetero

145 with greater confidence and relatively high MAF that should be suitable for genotyping in a wide var

146 identified a subset of high-confidence, high-MAF polymorphisms.

147 iable methods for the identification of high-MAF SNP loci in rhesus macaques.

148 loaponeurotic fibrosarcoma oncogene homolog (MAF), a leucine zipper-containing transcription factor o

149 loaponeurotic fibrosarcoma oncogene homolog (MAF), a transcriptional activator of key target genes, i

150 the present study, we have investigated how MAF overexpression impacts resistance to proteasome inhi

151 ataracts seen in Ofl heterozygotes and human MAF mutations are similar to one another, implying that

152 Module mapping of 1,046 TFs identified MAF and MAFB as necessary and sufficient for progenitor

153 Using transcriptome analysis we identified MAF as an NF1- regulated transcription factor and verifi

154 Our findings further implicate MAF/Maf in mammalian lens development and highlight the

155 inhibition selectively induced apoptosis in MAF-expressing myelomas, and FOS inactivation was simila

156 sociation with decreased ITGB7 expression in MAF-translocated MM cell lines.

157 for clinical evaluation of MEK inhibitors in MAF-expressing myeloma.

158 genital cataract we identified a mutation in MAF in a three-generation family with cataract, microcor

159 without CD20 myeloma, resembling outcomes in MAF/MAFB and proliferation entities.

160 Z twin pairs exhibited greater similarity in MAF at heteroplasmic sites than DZ twin pairs, suggestin

161 rces of technical variability: i) incomplete MAF and keratins; ii) globally- or segmentally-decreased

162 ation of MAF protein, resulting in increased MAF protein stability and PI resistance.

163 study describes a common mechanism inducing MAF transcription in both instances.

164 INTERPRETATION: MAF status can predict likelihood of benefit from adjuva

165 g both common variants and variants with low MAF) and statistical power, particularly for the analysi

166 0.05) and 2.7 million low-frequency (0.005 < MAF < 0.05) variants.

167 cemic traits based on low-frequency (0.005 < MAF </= 0.05) variants, and additional low-frequency, po

168 es, imputation of rare variants with 0.01% < MAF </= 0.5% with the combined reference panel increased

169 For rare variants with 0.01% < MAF </= 0.5%, imputation in the Framingham Heart Study w

170 frequency (MAF) < 1%) or low-frequency (1% < MAF < 5%) variants with platelet count (PLT), red blood

171 frequency, MAF >/=5%) or infrequent (0.5% < MAF < 5%) variants across the exome in African Americans

172 induced by complete inactivity and maintains MAF-box gene expression in control.

173 ase 3beta (GSK3beta)-mediated degradation of MAF protein, resulting in increased MAF protein stabilit

174 o the translocation-mediated deregulation of MAF and MAFB, a known poor prognostic factor.

175 it transected the genomic-control domain of MAF, a basic region leucine zipper (bZIP) transcription

176 he basic region of the DNA-binding domain of MAF.

177 MAFB loss, indicating they act downstream of MAF:MAFB.

178 ate a potential correction for the effect of MAF using pseudocovariates.

179 Acute re-expression of MAF promoted expression of glial differentiation markers

180 High expression of MAF protein in t(14;16) was associated with significantl

181 High levels of MAF protein were found in t(14;16) cell lines; cell line

182 Loss of MAF or MAFB expression results in decreased APOBEC3B and

183 The second mode of MAF transcription occurred in myelomas with multiple mye

184 In contrast, overexpression of MAF resulted in increased resistance to PIs and reduced

185 ragmatic force and prevent overexpression of MAF-box.

186 The gene segments on mature peptide part of MAF-1 were cloned, based on the primers designed accordi

187 Reexpression of MAF rescued cells from death induced by MMSET depletion,

188 These results define the role of MAF and GSK3 in the resistance of t(14;16) MM to PIs and

189 s designed according to the cDNA sequence of MAF-1.

190 F:MAFB target gene subsets in the setting of MAF:MAFB loss, indicating they act downstream of MAF:MAF

191 lays the foundation for the further study of MAF-1 biological activity, the relationship between stru

192 blishes the recombinant expression system of MAF-1 (Musca domestica antifungal peptide-1) and demonst

193 We compared the distribution of MAFs of synonymous SNPs with that of nonsynonymous SNPs

194 ysregulate CCND1 (11q13) or CCND3 (6p21), or MAF (16q23) or MAFB (20q11) transcription factors that t

195 uced MAF mRNA in cells representing MMSET or MAF subgroups.

196 -9)) and a new independent variant in PDE8B (MAF=10.4%, P=5.94 x 10(-14)).

197 articularly for low-frequency polymorphisms (MAF < 5%), when low coverage sequence reads are added to

198 and sialidase generated a remarkably potent MAF, termed DBPMAF or GcMAF, respectively.

199 mutations were demonstrated to impair proper MAF phosphorylation, ubiquitination and proteasomal degr

200 The proposed MAF thresholds will facilitate clinical interpretation o

201 ADIPOQ-coding region detected variant R221S (MAF = 0.015, P = 2.9 x 10(-69)), which explained 17.1% o

202 lele Frequency = 0.27) and rs2293925 (R525W, MAF = 0.45), which tend to be mutually exclusive across

203 nor allele frequency (MAF) 0.5-5%) and rare (MAF < 0.5%) nonsynonymous variants, we analyzed exome ar

204 lele frequency (MAF) between 1-5%) and rare (MAF </= 1%) variants contribute to complex traits and di

205 frequency [MAF] >/=0.01 and <0.05) and rare (MAF <0.01) variants that influence plasma concentrations

206 requency (MAF) between 0.5 and 5%] and rare (MAF below 0.5%) variants.

207 n coding sequences and all but one are rare (MAF <2%) with SCr effects between 0.085 and 0.129 standa

208 Despite being twice as rare (MAF<0.5%), c.1114C>T showed similar effect and significa

209 and SEC24C (SEC24 family member C) had rare (MAF < 0.001) predicted deleterious single-nucleotide var

210 significant increase in the burden of rare (MAF </=1%) 1-30 kb CNV, 1-30 kb deletions, and 1-10 kb d

211 Four of the coding polymorphisms were rare (MAF < 1%) and three of those were novel.

212 low frequency (MAF 1%-5%), and 11 were rare (MAF <1%).

213 F3 levels identified 197 variants (152 rare; MAF<0.05), 31 of which (27 rare) were nonsynonymous.

214 petent cell of BL21(DE3) to gain recombinant MAF-1 fusion protein with His tag sequence through purif

215 nduct the Western Blotting test, recombinant MAF-1 fusion protein was used to produce the polyclonal

216 -regulated kinase (ERK)-MAP kinases, reduced MAF mRNA in cells representing MMSET or MAF subgroups.

217 monstrate that the MEK-ERK pathway regulates MAF transcription, providing molecular rationale for cli

218 controlled by the transcriptional regulators MAF:MAFB.

219 nsynonymous SNV in GLP1R (A316T; rs10305492; MAF=1.4%) with lower FG (beta=-0.09+/-0.01 mmol l(-1), P

220 common missense variant in CPS1 (rs1047891, MAF = 0.33, discovery + replication p = 6.38 x 10(-10))

221 region flanking the FOXB1 gene (rs10519031, MAF 0.04, OR 3.0, 95% CI 2.02-4.49, p-value 6.68 x 10(-8

222 multiple domains 1 (CSMD1) gene (rs11136645; MAF = 0.49), was significantly associated with decreased

223 m, P = 8.3E-08), 13q14.2/SPRYD7/rs114089985 (MAF = 0.03, beta = 1.46 cm, P = 4.8E-10) and 17q23.3/GH2

224 ants near PLB1 with risk of RA (rs116018341 [MAF = 0.042] and rs116541814 [MAF = 0.021], combined P =

225 (rs116018341 [MAF = 0.042] and rs116541814 [MAF = 0.021], combined P = 3.2 x 10(-6)).

226 re synonymous variant in GFI1B (rs150813342, MAF = 0.009, discovery + replication p = 1.79 x 10(-27))

227 1.21 ) and at 16q24.1 marked by rs16941835 (MAF = 0.21, P = 5.06 x 10(-8); OR = 1.15) within the lon

228 for association: 5p13.3/C5orf22/rs17410035 (MAF = 0.10, beta = 0.64 cm, P = 8.3E-08), 13q14.2/SPRYD7

229 for hemoglobin [HGB]) and HNF4A (rs1800961, MAF = 2.4%, p < 3 x 10(-8) for hematocrit [HCT] and HGB)

230 lanking the DAD1 and OXA1L genes (rs1999071, MAF 0.32, OR 1.78, 95% CI 1.45-2.18, p-value 2.83 x 10(-

231 cm, P = 4.8E-10) and 17q23.3/GH2/rs2006123 (MAF = 0.30; beta = 0.47 cm; P = 4.7E-09).

232 as a less common variant E168G (rs200673353, MAF = 0.001), and studied their biochemical properties b

233 rare missense variant in ALAS2 (rs201062903, MAF = 0.2%) associated with lower mean corpuscular volum

234 drives the association signal (rs201622589, MAF 0.1%, odds ratio = 10.13, p-value = 0.042) and resul

235 th higher RBC distribution width (rs3211938, MAF = 8.7%, p = 7 x 10(-11)) and showed that it is assoc

236 We identify rs651007 (MAF=20%) in the first intron of ABO at the putative prom

237 2-4.49, p-value 6.68 x 10(-8) and rs8029377, MAF 0.03, OR 2.49, 95% CI 1.76-3.53, p-value 2.45 x 10(-

238 ultidimensional Assessment of Fatigue scale (MAF).

239 ain-of-function models showed that silencing MAF led to increased sensitivity to PIs, enhanced apopto

240 low-frequency variant near B4GALT6/SLC25A52 (MAF=3.2%, P=1.27 x 10(-9)) tagging a rare TTR variant (M

241 ent ways, as has been observed for the small MAF family of bZIP proteins in vertebrates.

242 All three are uncommon SNPs (MAF <or= 10%) that lie >70 kb 5' of IGF1.

243 of these TFs rescued expression of specific MAF:MAFB target gene subsets in the setting of MAF:MAFB

244 or TSH, we identify a novel variant in SYN2 (MAF=23.5%, P=6.15 x 10(-9)) and a new independent varian

245 ariants for lumbar spine BMD (rs11692564(T), MAF = 1.6%, replication effect size = +0.20 s.d., Pmeta

246 e effects on BMD near WNT16 (rs148771817(T), MAF = 1.2%, replication effect size = +0.41 s.d., Pmeta

247 mma-mediated gene repression and reveal that MAF regulates the macrophage enhancer landscape and is s

248 Our prior work showed that MAF is up-regulated in an additional 30% of multiple mye

249 The MAF column consists of a hydrolyzed macroporous epoxy-ba

250 The MAF method divides scan data into short subframes, recon

251 The MAF-1 recombinant fusion protein was purified to exhibit

252 A, the VAS requires standardization, and the MAF would benefit from further sensitivity data.

253 chromatin immunoprecipitation, FOS bound the MAF promoter, and MEK inhibition decreased this interact

254 mented medium was sufficient to generate the MAF.

255 However, the MAF precursor activity of patient plasma Gc protein was

256 blurring due to the intraframe motion in the MAF motion-correction method.

257 ed viruses to the macroporous surface of the MAF column at pH 3, concentrated matrix components by CU

258 Members of the MAF family of basic region/leucine zipper transcription

259 and reproduction are expressed based on the MAF of copper, the sensitivity of the two species appear

260 better recovers the fine structures than the MAF method, as compared with anesthetized studies.

261 We found that the MAF distribution of possibly and probably damaging SNPs

262 s shifted toward rare SNPs compared with the MAF distribution of benign and synonymous SNPs that are

263 cells alone modified mouse DBP to yield the MAF.

264 The MAFs were similar to those for IPF (UCSF 33.3%, p=0.09;

265 found that the V256I variant was enriched to MAF = 0.64 in NCI-60 lung carcinoma cell lines, whereas

266 es, whereas the TOP1MT R525W was enriched to MAF = 0.65 in the NCI-60 melanoma cell lines.

267 tation introducing a stop codon (p.Tyr35Ter, MAF = 0.01%), who weighed 7 kg more than non-carriers.

268 ANCR and TINCR lncRNAs as essential upstream MAF:MAFB regulators.

269 d pathogenic deafness variants using variant MAFs from multiple distinct ethnicities and sequenced by

270 P=1.27 x 10(-9)) tagging a rare TTR variant (MAF=0.4%, P=2.14 x 10(-11)).

271 single variant analysis for common variants (MAF > 0.01) and rare variant analysis for low frequency

272 en after adjusting for more common variants (MAF > 1%).

273 t meta-analysis results for common variants (MAF>/=1%) associated with TSH and FT4 (N=16,335).

274 e combined effect of low frequency variants (MAF </= 5%) provided strong evidence of association with

275 lustering pattern of rare missense variants (MAF < 0.01) in a protein is associated with mode of inhe

276 not identify any protein-modifying variants (MAF > 0.01) with moderate or large effect sizes in endom

277 unidentified, nonsynonymous PPARG variants (MAF < 0.5%).

278 nalysis for low frequency and rare variants (MAF < 0.05).

279 (0.05>MAF0.005) and aggregate rare variants (MAF<0.005).

280 Analysis of rare variants (MAF<1%) using sequence kernel association testing reveal

281 regulated transcription factor and verified MAF regulation through RAS/MAPK/AP-1 signaling in malign

282 cy due to reactivation of mTOR signaling via MAF.

283 rvival in the control group (MAF-positive vs MAF-negative: hazard ratio [HR] 0.92, 95% CI 0.59-1.41),

284 c acid group) and the remaining tumours were MAF negative.

285 184 (21%) tumours were MAF positive (85 in the control groups and 99 in the zol

286 ts showed that six of these 11 (WWOX, WFDC1, MAF, FOXF1, MVD and the predicted novel transcript Q9H0B

287 n 3%) similarly to the static study, whereas MAF motion correction using the standard algorithm setti

288 We investigated whether MAF amplification (a biomarker for bone metastasis) in p

289 Is and identifies a novel mechanism by which MAF protein levels are regulated by PIs, which in turn c

290 r allele frequencies (MAF) >0.05 and 12 with MAF >0.10.

291 and 1 common variant (rs2298813-A528T) with MAF = 14.9% segregated within families and were deemed d

292 Genes associated with MAF-binding enhancers were suppressed in macrophages iso

293 00C > A and -181A > C were more common (with MAF of 0.46 and 0.49, respectively) and showed string ev

294 nation assays for 12 SNPs from 11 genes with MAF>0.05 and genotyped these SNPs in Caucasian subjects

295 In patients with MAF-negative tumours, zoledronic acid was associated wit

296 nts not postmenopausal at randomisation with MAF-positive tumours, zoledronic acid was associated wit

297 (SNVs) were observed and 80% were rare with MAF <1%.

298 n increasing imputation accuracy of SNP with MAF below 0.1 and for SNP located in the chromosomal ext

299 quate statistical power to analyze SNPs with MAF <5%.

300 42% of the variance contributed by SNPs with MAF of 0.1-50%).

301 novel) and captured 85% of the variants with MAF>/=1% found by the 1000 Genomes Project in Europe-anc