ライフサイエンスコーパス: Williams

1 Williams 82 individuals exhibited variation in the numbe

2 Williams 82, the soybean cultivar used to produce the re

3 Williams developed in his 1966 book Adaptation and Natur

4 Williams et al claim that the data used in Sabo et al we

5 Williams has suggested that the Earth's obliquity may ha

6 Williams syndrome (WMS) is a rare sporadic disorder that

7 Williams syndrome (WS) and 7q11.23 duplication syndrome

8 Williams syndrome (WS) is a complex developmental disord

9 Williams syndrome (WS) is a developmental disorder cause

10 Williams syndrome (WS) is a developmental disorder cause

11 Williams syndrome (WS) is a developmental disorder with

12 Williams syndrome (WS) is a developmental disorder with

13 Williams syndrome (WS) is a genetic condition characteri

14 Williams syndrome (WS) is a genetic disorder caused by a

15 Williams Syndrome (WS) is a neurodevelopment disorder as

16 Williams syndrome (WS) is a neurodevelopmental disorder

17 Williams syndrome (WS) is a neurodevelopmental disorder

18 Williams syndrome (WS) is a neurogenetic-neurodevelopmen

19 Williams syndrome (WS) is a rare genetic disorder, cause

20 Williams syndrome (WS) offers an exciting model for soci

21 Williams syndrome (WS), a genetic disorder caused by hem

22 Williams syndrome (WS), a genetic disorder resulting fro

23 Williams syndrome (WS), a rare disorder caused by a hemi

24 Williams syndrome (WS), caused by a heterozygous microde

25 Williams syndrome (WS), caused by microdeletion of some

26 Williams syndrome is a complex developmental disorder th

27 Williams syndrome is a rare genetic disorder caused by h

28 Williams syndrome is also associated with specific neuro

29 Williams syndrome, caused by a hemizygous microdeletion

30 Williams' principle holds that, in order for an entity t

31 Williams-Beuren syndrome (also known as Williams syndrom

32 Williams-Beuren syndrome (WBS) is a developmental disord

33 Williams-Beuren syndrome (WBS) is a microdeletion disord

34 Williams-Beuren syndrome (WBS) is a neurodevelopmental d

35 Williams-Beuren syndrome (WBS), an autosomal dominant ge

36 Williams-Beuren syndrome (WBS), caused by a microdeletio

37 Williams-Beuren syndrome (WBS; OMIM 194050) is caused by

38 Williams-Beuren syndrome is a developmental multisystemi

39 Williams-Beuren syndrome is characterized by mild mental

40 n's syndrome (16%), Noonan's syndrome (15%), Williams' syndrome (12%), and 22q11.2 deletion syndrome

41 g module written by Goddard [1.], King [2.], Williams [3.], and Dean [4.] provides an overview of acc

42 .21 (48), 16p11.2 (autism, 34), and 7q11.23 (Williams-Beuren syndrome, 11).

43 used to perform in silico mapping on 80,700 Williams 82 BAC end sequences (BES).

44 sured with novel photoacoustic imaging and a Williams periodontal probe.

45 STSs) were anchored by PCR on a subset of a Williams 82 BstY I BAC library pooled into 208 pools in

46 uter-generated randomisation sequence with a Williams square design of size four to assign patients (

47 Gel-like dynamics with a Williams-Landel-Ferry temperature dependence then result

48 Application of activation, Williams-Landel-Ferry, and Rouse-Zimm models shows the m

49 dromes discussed include Angelman, Alagille, Williams, Langer-Giedeon, Prader-Willi, Smith-Magenis, M

50 Dodge LE, Ehrlich S, Meeker JD, Calafat AM, Williams PL, for the EARTH Study Team.

51 using the C4C risk factors with the 7PCL and Williams risk factors achieved the best performance, wit

52 on-deficit-hyperactivity disorder (ADHD) and Williams syndrome.

53 t issue of Molecular Cell, Pidoux et al. and Williams et al. identify S. pombe Scm3 as the proximate

54 ssues of Neuron and Cell (Herrera et al. and Williams et al.).

55 disorders such as schizophrenia, autism, and Williams syndrome.

56 viewpoints by Powers, Miller, and Cohen, and Williams and Dye, followed by a commentary by Fraser.

57 es relevant to autism spectrum disorders and Williams' syndrome.

58 tic syndromes such as Down syndrome (DS) and Williams syndrome (WS), difficulties with executive func

59 ng of an individual with severe epilepsy and Williams-Beuren syndrome identified a frameshifting de n

60 (DS; N = 557; Mage = 16.52; 233 female) and Williams syndrome (WS, N = 247; Mage = 18.43; 113 female

61 h the genetic variations leading to FraX and Williams syndrome are different, important similarities

62 lopmental correlates, occur in both FraX and Williams syndrome including aberrant frontostriatal path

63 ular machinery and processes across FraX and Williams syndrome occur as well - microRNAs involved in

64 pmental morphologic feature between FraX and Williams syndrome.

65 al features of fragile X syndrome (FraX) and Williams syndrome and to review the putative neural and

66 Haroush and Williams trained pairs of monkeys to play in a prisoner'

67 characterized mainly by hyposociability, and Williams syndrome (WS), whose subjects exhibit hypersoci

68 lains the informative schemes by Rudolph and Williams.

69 Suwannee River humic acid (SRHA) and Williams Lake hydrophobic acid (WLHPoA) substantially en

70 e, Miller-Dieker lissencephaly syndrome, and Williams-Beuren syndrome--in which the deleted region en

71 eported SCIN reduction, such as Tourette and Williams syndromes.SIGNIFICANCE STATEMENT Selecting the

72 Dravet, Fragile X, Prader-Willi, Turner, and Williams syndromes.

73 sphere geometry was introduced by Vallee and Williams with the concept of entasis, which is frequentl

74 xample of Williams-Beuren syndrome (WBS) and Williams-Beuren region duplication syndrome to illustrat

75 y deleted regions of Prader-Willi, Angelman, Williams, Smith-Magenis, and DiGeorge/velocardiofacial s

76 SoyBase also contains the well-annotated 'Williams 82' genomic sequence and associated data mining

77 zygous mice (the same frizzled 9 genotype as Williams syndrome patients) were intermediate between wi

78 However, as Williams and Baum suggest in their Perspective, the disc

79 Williams-Beuren syndrome (also known as Williams syndrome) is caused by a deletion of a 1.55- to

80 condition or in syndromic conditions such as Williams-Beuren syndrome.

81 y exhibited gene content differences between Williams 82 individuals.

82 Genomic structural variation between Williams and Kingwa was maintained between the Williams

83 isite Langmuir model, augmented with a Bragg-Williams model for lateral interactions, to calculate ad

84 he microkinetic model (e.g., using the Bragg-Williams approximation) to describe the experimental dat

85 Combined with the Bragg-Williams/Langmuir model and taking into account the expe

86 537 See related article by Williams and colleagues, p.

87 , we modified the cascade of care defined by Williams et al. for use in Rhode Island using key nation

88 See also the editorial by Williams and Estes in this issue.

89 See also the editorial by Williams and Newby in this issue.

90 See also the editorial by Williams in this issue.

91 etic determinants of cognition is offered by Williams syndrome (WS), a well-characterized hemideletio

92 traditional extra-binomial model proposed by Williams and can analyse both rare and common variants w

93 As proposed by Williams, we overcome the problem of susceptibility to o

94 In 1957 G.C. Williams predicted that higher adult death rates select

95 As demonstrated earlier by Shilov, Cambie, Williams, Fahey, and others, alkenes can undergo a conce

96 opy number variation (CNV) at 7q11.23 causes Williams-Beuren syndrome (WBS) and 7q microduplication s

97 q11.23, where the reciprocal deletion causes Williams-Beuren syndrome, characterized by a highly soci

98 us deletion of the elastin gene (ELN) causes Williams-Beuren syndrome (WBS), while single nucleotide

99 y 25 genes on chromosome 7q11.23 that causes Williams syndrome (WS) includes genes that regulate cyto

100 7q11, the reciprocal of the deletion causing Williams-Beuren syndrome.

101 mygdala coupling, both of which characterize Williams' syndrome.

102 Charleese Williams is the winner of the 2021 Rising Black Scientis

103 is normalization do not follow the classical Williams-Landel-Ferry (WLF) equation developed for long-

104 phenotype of the usually sporadic condition Williams syndrome.

105 Cultivar Williams 82 has served as the reference genome for the s

106 troduction of PSS1 into the soybean cultivar Williams 82, the transgenic plants exhibited enhanced re

107 sciptome of seed development in the cultivar Williams, the reference cultivar for the first soybean g

108 BAC clones spanning this region in cultivar "Williams 82" [rps2, Rmd (adult onset), rj2].

109 rogen fixation with soybean (Glycine max cv. Williams 82).

110 Duplication (dup7q11.23) and deletion (Williams syndrome) of chromosomal region 7q11.23 cause n

111 ral, and gene content variation of different Williams 82 individuals.

112 iniscent of the human microdeletion disorder Williams-Beuren syndrome (WBS); craniofacial imaging rev

113 The neurodevelopmental disorder Williams-Beuren syndrome (WBS), is caused by a microdele

114 commonly deleted in the congenital disorder, Williams syndrome.

115 keletal dynamics and is a candidate gene for Williams' syndrome.

116 ngle genes have been identified, whereas for Williams and Langer-Giedion syndromes, more than one gen

117 ditional statistical filtering options (e.g. Williams' trend test), curve fitting models, Linux and M

118 e flavoenzyme described by S. Liao and H. G. Williams-Ashman, thus establishing their genetic identit

119 j4 genotypes, including the reference genome Williams 82.

120 tropy) in the somatic environment, as George Williams called for in 1957, and how they make the dispo

121 the oft-quoted evolutionary theorist George Williams, "It is remarkable that after a seemingly mirac

122 nd the least reduction in the placebo group (Williams test = 4.97, P < .01).

123 invariably deleted in the haploinsufficiency Williams-Beuren Syndrome.

124 tested reorientation in individuals who have Williams syndrome (WS), a genetic disorder that results

125 consisted of 5 learning tasks: detour, Hebb-Williams, radial maze, olfactory foraging, and fear cond

126 periments used 2 versions of a modified Hebb-Williams maze to test the role of the dorsal hippocampus

127 elf had significant positive effects on Hebb-Williams maze learning.

128 This study indicates that Hebb-Williams maze performance deficits after unilateral ento

129 adult, male Sprague-Dawley rats in the Hebb-Williams maze were examined at 6 months after unilateral

130 on the privileged Trost and Pfaltz-Helmchen-Williams PHOX ligands often require high loadings, speci

131 omposite ]) were compared by using Hotelling-Williams test.

132 t contains the Xenopus ortholog of the human Williams syndrome transcription factor (WSTF).

133 , we isolated a Xenopus homolog of the human Williams-Beuren syndrome critical region 11 (XWBSCR11),

134 on structure of the PHD motif from the human Williams-Beuren syndrome transcription factor (WSTF) pro

135 In Williams syndrome (WS), a deletion of approximately 1.5

136 cumscribed set of genes that are affected in Williams syndrome, along with the well-characterized neu

137 be structurally and functionally altered in Williams syndrome, providing a target for investigating

138 Thus, in contrast to the conclusions in Williams et al., this could indeed be a "Rosetta stone"

139 ed for effects of the LIMK1 gene, deleted in Williams syndrome and important for neuronal maturation

140 ly flanking the interval commonly deleted in Williams syndrome have facilitated the identification of

141 by one of multiple genes that is deleted in Williams syndrome individuals, is the only currently kno

142 factors (TFs) among the 28 genes deleted in Williams syndrome, and prior mouse models of each TF sho

143 s one of about 20 genes typically deleted in Williams syndrome.

144 t the 7q11.23 region hemizygously deleted in Williams-Beuren syndrome (WBS), a complex multisystemic

145 b region on chromosome 7 which is deleted in Williams-Beuren syndrome (WBS).

146 SCR11), one of the genes commonly deleted in Williams-Beuren syndrome patients.

147 ome 7q11.23 that is hemizgygously deleted in Williams-Beuren syndrome, a multisystemic developmental

148 We review the flaws in Williams' model, explore alternative explanations for co

149 nectivity patterns similar to those found in Williams syndrome were associated with sequence variatio

150 nce that the absence of one or more genes in Williams syndrome leads to highly circumscribed patholog

151 Silencing GmMYB29A2 in Williams 82, a soybean variety that encodes the resistan

152 and effects of specific genes hemideleted in Williams syndrome.

153 findings show that genetic heterogeneity in Williams 82 primarily originated from the differential s

154 localized failure of cortical maturation in Williams syndrome (WS), a genetic condition associated w

155 f primary visual cortex is grossly normal in Williams syndrome, consistent with the notion that neura

156 c valvular disease, such as that observed in Williams syndrome, and, as such, animal models involving

157 on of peripheral pulmonary stenosis (PPS) in Williams syndrome (WS) is limited.

158 Genetic/syndromic diagnoses included Williams syndrome (n=23), non-Williams familial arteriop

159 Selective, anti-Irving-Williams Zn(II) binding by B(2) is achieved through the

160 cells, favouring the binding of lower-Irving-Williams transition metals over Cu(2+), the most dominan

161 that thermodynamically overcomes the Irving-Williams restrictions in vitro and in cells, favouring t

162 ed complex stability according to the Irving-Williams series (Mn(II) < Fe(II) < Ni(II) < Co(II) < Cu(

163 II) in vitro, thus diverging from the Irving-Williams series without requiring auxiliary factors such

164 operties of metal ions and follow the Irving-Williams series(5) (Mn(2+) < Fe(2+) < Co(2+) < Ni(2+) <

165 nt metals at the opposite ends of the Irving-Williams series, a universal order of relative stabiliti

166 For instance, as described in the Irving-Williams series, Cu(2+) and Zn(2+) typically form more s

167 l ion affinity trend suggested by the Irving-Williams series, demonstrating that this trend operates

168 Consistent with the Irving-Williams series, MncA only binds Mn(2+) after folding in

169 mical convention by contradicting the Irving-Williams series, while the scope of reactivity remains u

170 inity to ligands, as described by the Irving-Williams series-is particularly difficult.

171 Cu(2+), the most dominant ion in the Irving-Williams series.

172 Co > Fe > Mg > Mn > Zn, following the Irving-Williams stability order.

173 ination geometry, thus countering the Irving-Williams trend.

174 In this issue, Williams et al. reveal a two-step plasma membrane repair

175 isconsin, Madison, with Bob Alberty and Jack Williams, then at Oxford University with A.G. ("Sandy")

176 epsilon(omega, T), and a general Kohlrausch-Williams-Watts (KWW) form for time-domain relaxation.

177 onential functions as well as the Kohlrausch-Williams-Watts (KWW) stretched exponential model.

178 ng spectrum are analyzed with the Kohlrausch-Williams-Watts formalism, the exponent beta decreases wi

179 arameter was calculated using the Kohlrausch-Williams-Watts function and found to be 0.39.

180 al but were well described by the Kohlrausch-Williams-Watts model, from which a characteristic rate c

181 mbination was quantified with the Kohlrausch-Williams-Watts model.

182 widely used US cultivars: the northern line Williams 82 (Wm82) and the southern line Lee.

183 ancing Translational Science, the Loughridge Williams Foundation, and the Betsy and Jonathan Blattmac

184 dina, Victoria Pastor, Sabine Ravnskov, Mary Williams and Arjen Biere)Plants constantly interact with

185 dissected seedlings of soybean (Glycine max 'Williams 82'), we show that genes involved in photosynth

186 Using G. max ([Williams 82/PI 518671]) as a reference, a G --> T(2,822)

187 al, but differ from the susceptible G. max ([Williams 82/PI 518671]) by the presence of several singl

188 548402]) allele in the susceptible G. max ([Williams 82/PI 518671]) genotype suppressed H. glycines

189 8402]) allele, but differs from the G. max ([Williams 82/PI 518671]) ortholog.

190 Overexpression of Gm-SYP38 rescues G. max [Williams 82/PI 518671], genetically rhg1 (-/-), by suppr

191 copy of a duplicated gene flanking the 2-Mb Williams-Beuren syndrome (WBS) common deletion at 7q11.2

192 With this in mind, Williams and co-workers developed a model that quantifie

193 ly 3.3 Mb of genomic sequence from the mouse Williams syndrome region, of which just over 1.4 Mb is f

194 In this issue of Neuron, Williams et al.

195 noses included Williams syndrome (n=23), non-Williams familial arteriopathy (n=12), and Alagille synd

196 m82.a6 with other near-gapless assemblies of Williams 82 reveal large regions of genomic heterogeneit

197 may help identify molecular determinants of Williams-Beuren syndrome.

198 tu hybridization, useful in the diagnosis of Williams syndrome.

199 A diagnosis of Williams-Beuren syndrome was made based on the microdele

200 e variation and key neural endophenotypes of Williams' syndrome and perhaps corticoamygdala regulatio

201 A new study uses the example of Williams-Beuren syndrome (WBS) and Williams-Beuren regio

202 VAS), and SVAS is also a frequent feature of Williams syndrome, where patients are hemizygous for ELN

203 s 82 genome sequence consists of a mosaic of Williams and Kingwa haplotypes.

204 not match the haplotype of either parent of Williams 82.

205 ation of a girl with a clinical phenotype of Williams-Beuren syndrome, associated with unilateral ant

206 d faster than that for the infrared probe of Williams et al., which measures the average helix conten

207 1.23 near the telomeric duplicated region of Williams-Beuren syndrome, a developmental disorder affec

208 of SVAS is quite variable, both in series of Williams syndrome patients and within SVAS kindreds, sug

209 ween these variants and neural signatures of Williams' syndrome in a normal population, using functio

210 man deletions make the positive sociality of Williams syndrome (WS) ideal for determining transcripti

211 e that should catalyze additional studies of Williams syndrome, including those that aim to character

212 tested), a prevalence comparable to that of Williams, Angelman and Prader-Willi syndromes.

213 olice) as measured using adapted versions of Williams' Everyday Discrimination Scale and Major Experi

214 RECENT FINDINGS: Research on Williams syndrome is taken as a model, used to demonstra

215 onor parent Kingwa into the recurrent parent Williams.

216 ns identical to those of C. diphtheriae Park-Williams No. 8 (tox type 1).

217 emizygous deletion in a patient with partial Williams syndrome suggests that loss of the LIM-Kinase1

218 Here, we reanalyze the data rescaled per Williams et al and following the methods in Sabo et al O

219 hared and symmetrically opposite phenotypes--Williams-Beuren syndrome and 7q-microduplication syndrom

220 lysed using one-stage mixed-effects Prentice-Williams-Peterson total-time models to obtain hazard rat

221 e hazard ratios with the use of the Prentice-Williams-Peterson total-time approach.

222 Previously, Williams et al. showed that the binding of this antibody

223 Disorder (ASD), Prader-Willi Syndrome (PWS), Williams Syndrome (WS) and Fragile X syndrome (FXS).

224 yrin framework (UNLPF-10) consisting of rare Williams beta-tetrakaidecahedral cages was constructed u

225 For example, the recent Williams et al.

226 ions of genomic heterogeneity, the reference Williams 82 genome sequence consists of a mosaic of Will

227 in', 'Eilon', 'Gruesa', 'Silver', 'Ricasa', 'Williams' and 'Zelig') was studied by gas chromatography

228 Rickey Williams provides a report on office economics that incl

229 wo prominent celebrity suicide events: Robin Williams during 2014 and Kate Spade and Anthony Bourdain

230 rtinez-Medina, A., Pastor, V., Ravnskov, S., Williams, M., and Biere, A.

231 DT-laced coating marketed in 1946 by Sherwin-Williams Research Laboratories.

232 Since Williams syndrome is associated with severe visuospatial

233 for human cognitive development, we studied Williams syndrome (WS), a developmental disorder that in

234 In a recent study, Williams and colleagues report that plant Guard receptor

235 xpressing GmMYB29A2 rendered the susceptible Williams variety incompatible.

236 e menopause, Down syndrome, Turner syndrome, Williams syndrome, chronic fatigue syndrome, IgA nephrop

237 article ends with a quotation from Tennessee Williams that reflects the theater, which has given me s

238 The Williams Syndrome Transcription Factor (WSTF), the produ

239 The Williams' nonbonded parameters combined with partial cha

240 .10% , specificity 61.07 +/- 0.90% ) and the Williams risk factors (sensitivity 66.32 +/- 1.90% , spe

241 .10% , specificity 49.49 +/- 0.50% ) and the Williams risk score (sensitivity 60.68 +/- 1.30% , speci

242 lliams and Kingwa was maintained between the Williams 82 individuals within the regions of heterogene

243 commonly deleted in patients affected by the Williams-Beuren syndrome, which is a complex neurodevelo

244 are associated with a cognitive defect, the Williams-Beuren cognitive profile.

245 ts, some of which may be responsible for the Williams syndrome phenotype.

246 actor family and are prime candidates in the Williams syndrome, a complex neurodevelopmental disorder

247 ual processing region also identified in the Williams syndrome-typically developing comparison.

248 rizzled gene, FZD3, now renamed FZD9, in the Williams-Beuren syndrome (WBS) deletion region at chromo

249 niofacial and cognitive abnormalities in the Williams-Beuren syndrome.

250 These include the Williams-Landel-Ferry model, the activation model, and t

251 eoselectively is a Lewis acid variant of the Williams' three-component coupling.

252 we determined the expression profile of the Williams-Beuren syndrome critical region-deleted genes a

253 rsonality that typify Williams syndrome, the Williams syndrome cohort exhibited opposite patterns of

254 ISWI, and WCRF180, a protein related to the Williams syndrome transcription factor.

255 ygous microdeletion distally adjacent to the Williams-Beuren syndrome region on chromosome 7q11.23.

256 of the primate-specific inversion within the Williams-Beuren syndrome critical region.

257 of chromosome 12, where Wm82.a6 matches the 'Williams' haplotype while the other two near-gapless ass

258 a common symptom in patients with tinnitus, Williams syndrome, autism, and other neurologic diseases

259 ply with increasing temperature according to Williams-Landel-Ferry (WLF) behavior.

260 at haploinsufficiency in BEN is causative to Williams-Beuren syndrome, these results may further lead

261 pment and suggest how it could contribute to Williams-Beuren syndrome.

262 a patient with deletion of elastin owing to Williams-Beuren syndrome.

263 FZD9 (Frizzled9), a Wnt receptor related to Williams syndrome, is localized in the postsynaptic regi

264 7q11.23, usually associated with the typical Williams-Beuren syndrome.

265 ment and hypersocial personality that typify Williams syndrome, the Williams syndrome cohort exhibite

266 Unlike Williams syndrome, we found no chromosomal inversions fl

267 the yellow seeds produced by the unmodified Williams 82 parental cultivar.

268 model constructed based on only one variable,Williams plot interestingly showed that all 8061 data po

269 tomics on soybean hairy roots of the variety Williams 82 and imbibing seeds of Harosoy 63 upon treatm

270 dynamic interaction involving mainly Vaughan-Williams class III AAD as many commonly used drug classe

271 The Vaughn Williams classification divides antiarrhythmic agents in

272 region on 1q21.1 and duplication at the WBS (Williams-Beuren syndrome) region at 7q11.23.

273 cortex (V1) in high-functioning adults with Williams syndrome and age- and IQ-matched control partic

274 cardiovascular complications associated with Williams-Beuren syndrome and isolated supravalvular aort

275 ntribute to certain deficits associated with Williams-Beuren syndrome.

276 ogy of intellectually disabled children with Williams (WS) syndrome and its relationship to the behav

277 on mathematics achievement by children with Williams syndrome (WS) has been very limited.

278 = 510) were performed: (i) 20 children with Williams syndrome compared to 20 age- and sex-matched ty

279 vity were calculated comparing children with Williams syndrome to matched typically developing childr

280 nd voice hoarsening in a baby diagnosed with Williams-Beuren syndrome that was born premature and req

281 The association of the Limk1 gene with Williams Syndrome indicates that proteins of this family

282 ndaries were more variable in the group with Williams syndrome.

283 l and ventral streams among individuals with Williams syndrome (WS) compared with two control groups

284 Individuals with Williams syndrome are hemizygous for the elastin gene, o

285 edback improved learning in individuals with Williams syndrome but not in typically developing contro

286 and deleted hemizygously in individuals with Williams syndrome, a dominant genetic condition characte

287 is deleted hemizygously in individuals with Williams Syndrome, an autosomal dominant genetic conditi

288 functional connectivity in individuals with Williams syndrome, in whom LIMK1 is hemideleted, with ty

289 the general population and individuals with Williams syndrome.

290 nation between controls and individuals with Williams, Smith-Magenis, 22q11 deletion, or Noonan syndr

291 dings from two experiments with infants with Williams syndrome (a phenotype selected to bolster innat

292 ners given impoverished input, learners with Williams syndrome, specific language-impaired learners,

293 al and behavioral phenotype of patients with Williams syndrome.

294 SVAS severity varies among patients with Williams-Beuren syndrome (WBS), a rare disorder that rem

295 rtic stenosis (SVAS), and five patients with Williams-Beuren syndrome (WBS).

296 or both proteins are deleted in persons with Williams-Beuren syndrome, who often manifest muscle weak

297 ties in the cerebral cortex of subjects with Williams syndrome (WS), a genetically based developmenta

298 ) Ogston, and finally back at Wisconsin with Williams and Lou Gosting.

299 one variant H2A.X is phosphorylated by WSTF (Williams-Beuren syndrome transcription factor), a compon

300 a new regulatory mechanism mediated by WSTF (Williams-Beuren syndrome transcription factor, also know